Puswhisperer 1

Please allow me to introduce myself

Please allow me to introduce myself.

I'm a man of wealth and taste.

I've been around for a long, long year.

As an Infectious Disease doctor.

Not quite Sympathy for the Devil.

As of 2010, I have been practicing infectious diseases (ID) for almost 25 years, if you include the fellowship.

ID is relentlessly cool. Every day I see a cool case, or something unusual, or read an interesting article. I learn something new almost every day. Infectious diseases appear in history, in politics, everywhere. I have never understood why anyone would do anything else. Except, of course, if they want an income.

Why keep all this cool stuff to myself? So I started a blog, Rubor, Dolor, Calor, Tumor, first at pusware.com, then I moved over to Medscape (http://blogs.medscape.com/rdct). Included are ratholes, bad puns, and obscure references. In medical school my evaluations contained 5 flips, a flippant and a glib. Consider yourself warned.

The goal is simple. Every other day, depending on what I see on rounds, I write a short, referenced entry that covers one factoid. The one curious disease of the day. With emphasis on short. Just long enough to be read on the toilet, presuming no constipation. And at least one stupid attempt at humor, often repeated.

This book is a collection of my first years blog entries, reworked, rewritten and most of the typos corrected. Ha. All the numerous mistakes are mine.

Of course the entries focus on the clinical triumphs that give me the appearance of House like infallibility.

But I guarantee (1) you will be thrilled and amazed with a year in the life of a Puswhisperer.

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(1). The information is not meant to diagnose, treat, cure or prevent any disease and is not intended for self-diagnosis or self-treatment of medical conditions that should be managed by a qualified health care provider.

All demographic data was changed in the patients.

Hanging Chad

Published Sun, 07 Sep 2008

I saw a case of the Hanging Chad Disease this week, at least that is what I call it.

What is Hanging Chad Disease?

Eight years ago there was an election in Florida that was decided, in part, because of punch card ballots that, like the wardrobes of the time, malfunctioned.

Little bits of paper did not separate cleanly from the ballot and it was uncertain how to count them, at least to the Secretary of State of Florida.

So the hanging chad lead to the election being sent to the Supreme Court who decided he election went to Bush who decided there were weapons of mass destruction in Iraq which lead to an invasion of a part of the world where Leishmania is endemic.

What I saw was a case of old world Leishmania, a parasite that causes, among other things, a chronic ulcer on the skin. The patient had a half dollar sized ulcer on his upper arm for three months that had not responded to a variety of antibiotics, and then it was biopsied. Once the Leishmania was discovered, he was sent to me.

This patient was not a soldier, but a refugee from Afghanistan by way of Iraq and Pakistan, all places where Leishmania thrives.

Leishmania is spread by the sand fly bite. There are three species of Old World Leishmania (and many more New World species) and I am waiting for the culture at the CDC to grow and tell me which type of Leishmania he has before starting a course of therapy.

I anticipate he will get pentavalent antimony, which is often the treatment for Leishmania.

I expect we will see some cases in our returning soldiers, either soon, or in 100 years, depending on the results of November.

This is why ID (for this blog, ID stands for Infectious Diseases, not Intelligent Design) is the coolyist of subspecialties as it has connections to everything.

Infection Control

Published Tue, 09 Sep 2008

Amongst my many jobs (my grandmother always said that a job is what a dog does on the carpet) is the task of infection control at my various hospitals. Infections, as many of you are aware, are an infrequent complication of hospitalization but cause significant morbidity and mortality. I have been the Chair of our Infection Control (we now call it Infection Prevention, but for some things I am just too damn old to change) program for 19 years and have seen the continuous improvement in a variety of hospital-acquired infections, much to the detriment of my bottom line. After all, I get paid to take care of infections.

Some days I just feel like RJ Reynolds telling people to stop smoking. The one area that has made some improvement is hand hygiene, but often it seems difficult to get people to wash their hands or to use one of the many hand sensitizers. I suspect that in their heart of hearts, people do not believe in germs. They can’t see germs after all, so the probably the germs are not there. Believing in things you cannot see is more the topic of the Science-Based Medicine blog.

About 40% of hospital infections are due to germs carried on the hands (and probably the stethoscope and the beeper and rings and the white coat and the cell phone and the neck tie, all of which have been cultured and can carry pathogens. I am starting to think rounds should be like the Greek Olympics, done naked. It could decrease the spread of infections and, as a side effect, decrease obesity), so clean hands are important. It is estimated that it takes about 10 years for new medical information to be disseminated, so I have to cut people a little slack; we have only know the importance of hand washing for 160 years.

I suspect that part of the reason is that people do not wash their hands are just too damn busy to remember. Modern medicine is intense and complex and people are busy and at most can only remember about 6 things at any given time.

About 5 months ago I was taking the kids to school at 7:30 in the morning and I have to make a right onto a four-lane busy street and then an immediate left across traffic. Talking to the kids and drinking coffee, I made the maneuver with no problems only to find a cop pulling me over. What I did not do was stop at the light and what I did not see was the cop in the car on my left, right there in plain view. The turn was safe, there were just too many things for me to keep track of, including the cop and that pesky stop light.

Same problem with hand hygiene. We may have alcohol canisters and soap everywhere, but in the busy driving of modern medicine, washing your hands may be an illegal right-hand turn with an unseen cop on your left. They call me Dr. Metaphor. So while you should expect your health care provider to wash their hands, they may simply not remember. As the poster says, ‘It’s OK to Ask’ if they washed their hands. It’s like flying in an airplane. I always ask the pilot if the wheels are down when he starts his decent. Just want to be safe...

Powerful Antibiotics

Published Tue, 09 Sep 2008

Big Gun.

Strong.

Powerful.

There are adjectives that are often used to describe antibiotics. There are few things in medicine that are 100%. But if a physician uses the above adjectives to describe an antibiotic they do not know a burro from a burrow (1). It is 100% sensitive and 100% specific that the speaker is a moron when it comes to antibiotic use, is a sucker for drug company commercials, and/or is blowing smoke up your butt.

These are advertising terms. Antibiotics have no intrinsic power. They are marketed that way to fool clinicians into thinking they are doing right by their patient. My patient has what appears to be a serious infection. Should I have give a strong, powerful, big gun, and heavily detailed antibiotic? Like Cipro, whose web site says ‘19 years of Power and Confidence’ Or Zosyn, which features a lightning bolt, presumptively from the gods, hitting an agar plate? Can’t get stronger than a lightning bolt. Or Ertapenem, whose motto is the ‘Power of One. ’ Me? I thought one was the loneliest number I ever knew. It is my considered opinion that two can be as sad as one, it’s the loneliest number since the number one. Ohhhh. Of course I’ll give one of those antibiotics. They have POWER.

The question is rather, what is the best antibiotic that will optimally kill an organism in a given body space. It may well be one of those antibiotics. It may not. It depends, curiously enough, not on some mystical 'power,' but whether a given organism is susceptible to being killed by the antibiotic and whether that antibiotic gets killing levels where the infection is. And you know that from the local microbiology and the pharmacokinetics of an antibiotic, not a marketing slogan.

Antibiotics can be considered strong not because of marketing, but due to a mistaken tradition. Vancomycin is considered, incorrectly, a strong antibiotic. Now, if I had neurosyphilis, (and there may be those readers who, after reading a mere three blog entries, thinks that I do), treatment with vancomycin would have zero effect. Nothing strong about vancomycin with it comes to syphilis.

Sometimes, because of resistance, all we have to offer is a half-assed antibiotic. Vancomycin is an archetype of a lousy antibiotic: toxic, poor pharmacokinetics, bacteriostatic, and, when compared against a penicillin, always inferior. Over the last decade, the use of vancomycin has increased as it is one of the few drugs we have to treat methicillin resistant Staphylococcus aureus, the dread MRSA. I hate pronouncing it mursa. Sounds like a Texan trying to say thanks in French. It’s Em-Ar-Ess-Ay.

Vancomycin's lack of reliable efficacy is demonstrated in a recent retrospective study (one of many):

"Two-hundred and fifteen cases were included. Vancomycin monotherapy was given in 73%. Failure rates by infection site were as follows: osteomyelitis 37/81 (46%), epidural abscess five/18 (28%), surgical wound four/15 (27%), pneumonia eight/45 (18%), endocarditis five/32 (16%), bloodstream five/42 (12%), joint 1/23 (4%), and meningitis 0/1 (0%)."

As a treatment for infection, those response rates stink on ice. So much for a strong, powerful, big gun antibiotic. Instead, give the appropriate antibiotic.

Rationalization

(1) Burro = ass, burrow= hole in the ground.

Clinical failures of appropriately-treated methicillin-resistant Staphylococcus aureus infections (http://www.ncbi.nlm.nih.gov/pubmed/18533269). Journal of Infection Volume 57, Issue 2, August 2008, Pages 110-115.

Genetics of Infection

Published Wed, 10 Sep 2008

" The fault, dear Brutus, lies not in our stars, but in ourselves if we are underlings ."- Edward de Vere, the Earl of Oxford.

I do not necessarily want to blame the patient, but someone has to be at fault when things go badly. I used to have a policy of always blaming nursing, but now it is the genome where all that action is.

This century has been filled with fascinating advances in understanding the role of polymorphisms in the host immune system and the subsequent risk and outcomes of various infections. We have always known that everyone is not immunologically identical any more than we have the same height or hair color or sense of humor. Would you believe there are actually people who do find these posts funny?

Why some people live or die, why some people get an infections and others do not, has been a mystery. Certainly, there is variability in the virulence of different strains of, say, E. coli. The variation in mortality and morbidity you see clinically seems more than can be accounted for by variations in the organism. In outbreaks from the same strain of pathogen there is always variability in the effects on the host. Not all people have the same predilection to infection or the ability to withstand an infection. A 65 yo diabetic with lupus on prednisone just isn’t going to do as well with a blood stream infection as a young, healthy person. But the gross assessment that sicker people do worse with infection never seems to be enough to account for the great variability in outcomes in disease.

What is increasingly clear that it is often small, but profound, changes in the genes that may determine whether we live or die from an infection. Genes code for proteins. There can be single mutations in the genes, normal variations, that are called polymorphisms. Your gene that codes for a protein is not always the same gene that I have. Your gene may make more of a protein, or less of a protein, or one with greater or lessor affinity for its substrate. These variations are some of the clay upon which evolution molds its change. Remember. I have a degree in metaphorableness.

Some of these polymorphism can make people much more susceptible to dying from infections. Take mannan-binding lectin. Please. Anyone reading this know who Henny Youngman was? Anyway.

To quote the Wikipedia:

"The Mannan-binding lectin pathway (also known as the Ali/Krueger Pathway) is homologous to the classical complement pathway. This pathway uses a protein similar to C1q of the classical complement pathway, which binds to mannose residues and other sugars in a pattern that allows binding on multiple pathogens. Mannan-binding lectin (MBL; also called mannose-binding lectin) is a protein belonging to the collectin family that is produced by the liver and can initiate the complement cascade by binding to pathogen surfaces. MBL is a 2-6 headed molecule that forms a complex with MASP-I (Mannan-binding lectin Associated Serine Protease) and MASP-II, two protease zymogens. MASP-I and MASP-II are very similar to C1r and C1s molecules of the classical complement pathway and are thought to have a common evolutionary ancestor. When the carbohydrate-recognizing heads of MBL bind to specifically arranged mannose residues on the phospholipid bilayer of a pathogen, MASP-I and MASP-II are activated to cleave complement components C4 and C2 into C4a, C4b, C2a, and C2b. C4b and C2a combine on the surface of the pathogen to form C3 convertase (C4b and C2a), while C4a and C2b act as chemoattractants."

Say what? Bacteria have on their outside a variety of sugars, including a sugar called mannose, Mannan-binding lectin is a protein that recognizes these sugars and activates a wing of the immune system called the complement system to pop the bacteria like a zit and to help bring in white cells for the kill. Cool.

Another wing of the immune system that cannot be boosted but can have mutations that render the patient at risk for infection. There have been increasing studies that have shown that a decrease in mannan-binding lectin is associated with increased risk of infection, but an interesting study was published in 2008. This study found that polymorphisms that lead to decreased serum levels of mannan-binding lectin lead to a 2 fold increase in death from pneumococcal bacteremia. 25% of them what had low levels died vrs 12% of them what didn’t.

Pneumococcus is a one of many kinds of streptococci, one of the more common pathogens in humans and in other animals as well. Your genes may be different than mine, and that may make all the difference of living or dying. The threads that keep us alive are often thinner than we know.

All well and good, but what makes it all the more cool is in the accompanying editorial:

"Five hundred sixty-five million years ago, when the world was empty and barren because animal life had not colonized land yet, a common ancestor that we share with sea squirts (Ascidians) inhabited the seas. One of the genes that we still share with sea squirts today is a gene for mannose-binding lectin (MBL), signifying that this gene has existed for 565 million years and, thus, has been highly conserved throughout animal evolution."

The fact that our ancient ancestors, the sea squirt, and humans all have to protect ourselves from Streptococci and use, in part, the same defensive mechanism, I find particularly satisfying. The connections between infections and the host response are one of the compelling lines of evidence of evolution. And yet another reason that Infectious Diseases is the coolyest specialty in medicine

Rationalization

Low serum mannose-binding lectin increases the risk of death from pneumococcal infection. (http://www.ncbi.nlm.nih.gov/pubmed/18611155) Eisen DP, Dean MM, Boermeester MA, et al. Clin Infect Dis 2008; 47:510

Virus R Me

Published Fri, 12 Sep 2008

I'm sick today. One would think that I wouldn't get ill given my job. My eldest had a cold, and now he has passed it on to me. Sore throat, whopping headache, no legs when I try to bound up the steps. At least I do not have a stuffy nose and can taste my food. I would bet on an enteroviral infection and bet if I had a spinal tap it would be slightly positive.

I am unlikely to ever get a spinal tap as I am DNR (do not resuscitate), DNI (intubate), DNF (Foley), DNRT (rectal tube) and DNST (spinal tap).

It is the enteroviral season. I just hope I am not going to the index case for West Nile here in Portland. As of 9/12/08 we still haven't had the epidemic that has been four years in coming.

And the worst of the illness is the foggy brain. The neurons firing like they are immersed in molasses. Slow on the uptake, words hard to find, a total ‘tell me about the rabbits George ’state of mind. It must be how it feels to attend the RNC.

The worst is there is not a damn thing to do about it but suffer. There are cold treatments, but they are usually worse than the disease. And I know that while NSAIDS can take away the headache, the inflammatory response I am having is important. Most studies that have looked at the treatment of fevers and acute viral infections have demonstrated that treating the fever makes the illness last longer, and the last thing I want is this illness to bleed into the weekend.

So I suffer in silence, unless you know not consider this blog silence.

So, rather than be original, in honor of my viral infection I will republish an essay I used to have on the Quackcast (http://moremark.squarespace.com) site so it can continue to live:

Deconstructing Airborne: How to recognize medical nonsense.

Medicine is complicated. It is estimated that it takes a decade of training before anyone can truly be an expert in a field. You probably do not have 10 years to spend getting to know the ins and outs of medicine. How, then, to recognize when a medical therapy is legitimate, questionable, or total garbage?

There are some rules of thumb (although I think they would be rules of thumbs, since I count on the thumbs) that are reliable indicators that the medical intervention you are being asked to spend your hard-earned money on is worthless. Airborne is a popular 'cold remedy' that by some accounts sells 100 million dollars a year of product. Using Airborne as an example, let’s go through these rules of thumb (1).

Rule 1. The therapy pitches the claim directly to the media.

Given the glut of direct-to-consumer advertising by "legitimate" pharmaceutical companies, this may be a wee bit more difficult to use as a criteria. I will also mention in passing that I am one of those zealots who think big Pharma reps and their advertising represent the biggest impediment to good medical practice currently going and the medical literature is replete with good evidence of the pernicious evil that occurs when physicians interact with drug reps. Good doctors practice good medicine, but to have good doctors practice bad medicine requires an expensive dinner at a steak house with a cute rep. I have not taken so much as a pen in 20 years, so my opinions are pure as Oregon rain.

With prescription pharmaceuticals, you can quickly discover if the indication is backed by legitimate scientific studies: look it up in the Physicians Drug Reference (The PDR). Every drug indication in the PDR has been studied and approved by the FDA.

Not so with the directly marketed products. Thanks to the Congress, herbal supplements and vitamins are under NO requirement to have proven safety and efficacy against any disease or condition. None. As long as they have the disclaimer to the effect that "These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease."

These words are taken from the Airborne box (2) where they are in teeny tiny letters that I can't see unless I take off my bifocals and squint.

Read the box and the advertising. If they have the above words or something similar, its garbage. By law they can say anything they want as long as they include this disclaimer. It’s no different from a shaving commercial where the use of the particular razor will get you a partially clad supermodel. You know that is not true. I mean, you do, don't you? These products are no different. If it looks too good to be true, then it probably is.

Real, effective, medications are backed by randomized, placebo-controlled clinical studies published in peer-reviewed medical journals and the results are in the PDR.

Rule 2. The discoverer says that a powerful establishment is trying to suppress his or her work.

While the makers of Airborne do not make this claim, at the monthly secret meeting of the Medicine Subcommittee of the Tri-Lateral commission, we work hard to suppress the information that the ingredients in Airborne are effective. Just do a Google search on the ingredients of airborne. It is safe to say we are failing miserably.

It is often said that big Pharma suppresses data on the effectiveness of herbal preparations and will not do the studies because when clinical trials prove the efficacy of these supplements, people will use the cheap supplements instead of expensive pharmaceuticals. Unfortunately, many of these supplement companies are owned by big Pharma, so they win either way, and, at $7 for 8 tablets, I am not so certain that Airborne is all that inexpensive.

Rule 3. The scientific effect involved is always at the very limit of detection.

Evidence to support Airborne? I quote from the website:

"Each ingredient in the Airborne formula has been repeatedly documented in published studies to contribute to a strong, healthy immune system."

This is true in the same way I am related to the Queen of England. I am. But it will take a whole lot of death before the crown devolves on to my head.

Only by the world’s largest stretch of the imagination can it be said the ingredients in Airborne have been repeatedly documented in published studies to contribute to a strong, healthy immune system. Try it yourself. Enter the ingredients of Airborne into Pubmed and search the medical literature. Be impressed with what you do not find.

"Additionally, we conducted a study in 2003 that showed Airborne had a marked effect on reducing the duration of symptoms. Our Medical Advisory Board members are currently formulating a study that in addition to the studies in the literature, will further support Airborne's immune-boosting properties."

I assume the last sentence was not meant for humorous effect, but I laugh out loud every time I read it. Which is it? Does it boost immune function? Or does it reduce the duration of symptoms. Ain't the same thing.

The key words are " contribute to a strong, healthy immune system." What does that mean? Zip. Zilch. Nil. Nada. Nothing. That is a meaningless assertion. Immune boosting. Healthy immune system.

This whole concept of boosting the immune system baffles me. The immune system is not a biceps that you can build up by lifting weights or taking steroids. It’s an amazingly complex series interacting proteins and cells. There is no meaningful way to measure the immune system in a normal person, much less boost it.

Normal people have normal immune systems, and as long as you have reasonable diet and exercise, there is no way to boost.

But it is so vague and sounds so good and beneficial, it doesn't matter that it cannot be disproved. It could be argued that many severe vitamin deficiencies lead to poor immune function, so, yes, the vitamin and minerals in Airborne are good for the immune system, in the very basic and generic way taking a multivitamin is good for the immune system. But they are not saying that the Vitamin C is being used to treat scurvy or they are treating other deficiency states.

It’s like oxygen. Breathing strengthens the immune system. Don't breathe for 10 minutes and your immune system will weaken. I am surprised they don't put the oxygen in the bottle as part of the immune-boosting ingredients. Given them time.

You cannot find the study the company touts that specifically proves Airborne is effective. According to ABC news "GNG (the people who did the study to prove Airborne's efficacy) is actually a two-man operation started up just to do the Airborne study. There was no clinic, no scientists and no doctors. The man who ran things said he had lots of clinical trial experience. He added that he had a degree from Indiana University, but the school says he never graduated."

What is in Airborne? Vitamins, herbal extracts, and amino acids that do not do anything to prevent or treat a cold. Echinacea and Vitamin C, the most commonly touted cold remedies, when tested in careful clinical studies, do not work. Sorry. The data is in and Vitamin C and Echinacea do not do diddly.

Looking at the list on the package, only zinc, as a lozenge sucked every two hours, but not as an effervescent tablet, has been effective in decreasing cold symptoms. Zinc is their gateway drug. As long as these products contain zinc, they can say something to the effect that the active ingredient has been proven in clinical trials to decrease cold symptoms and not be called a liar. Most of these cold remedies have zinc in one form or another. At best, it is like taking a very expensive and not very complete multivitamin.

Rule 4. Evidence for a discovery is anecdotal.

I hear it all the time. I thought I had a cold coming on, I took 'fill in the blank,' and I did not get a cold. Or the flu. I am just glad people don't use this reasoning in choosing contraception. Or, given the population of the planet, maybe they do.

People love anecdotes, especially if they come from someone like, oh, I don't know, Oprah. Remember. The plural of anecdote is anecdotes, not data. Memory is faulty and biased. Just remember the argument in the car you had with your spouse over their behavior at the last party you attended. Who had the correct memory? We remember hits not misses, we remember events that confirm our bias and ignore the contradictory, and we grossly underestimate the role of chance. Combine these with the emphasis we put on the stories of others and you can see why anecdotes are worthless for judging the efficacy of medical interventions.

I always tell the residents that the three most dangerous words in medicine, especially when applied to treatments, are 'in my experience.' The problem with anecdotes in medicine is they suggest a causality where none exists.

Causality is a difficult thing to prove, although I will confess I have a pair of special shoes. I take care of infections all day. Ever since I bought the pair of shoes I wear to work each day I do not remember getting an infection. In fact, when I was getting ready for work this morning I thought I was getting a cold, but after I put on my Rockports, my symptoms faded. You would probably dismiss my claim that my shoes prevent infection. Apply that skepticism to all forms of medical claims. My shoes are no different from any other form of questionable medicine: beware of faulty causality.

Humans love anecdotes. A single story for most people is far more impressive than the best clinical trial ever published. Even though "40,000 customers contact (Airborne) every year," that is meaningless to support that Airborne works. What separates humans from other animals is self-delusion. 40,000 times zero is zero.

Rule 5. The discoverer says a belief is credible because it has endured for centuries.

This is especially true of traditional Chinese medicine. They used it for thousands of years, it must be effective. Never mind that the life expectancy for the Chinese was less than 40 years until, in part, the use of Western medicine at the beginning of the 20th century.

Airborne contains a hodgepodge of Chinese herbs used for the most part for a variety of infectious disease. Most have never been tested rigorously or, in the case of Echinacea, definitively shown not to work.

There is little from 2000 years ago, or 200 years ago, or even 20 years ago that I would use today. I would not wear 2000-year-old clothes, travel in 2000-year-old vehicles, use 2000-year-old heating, grow food with 2000-year-old farming techniques. Why use 2000-year-old medical therapies? Unless, of course, I want to get sick and die. Our ancestors were invariably wrong in large part as they did not use the scientific method to understand the world. And they died young as a result.

But I feel good in know that the herb Chinese Videx in Airborne has been used for 2500 years for PMS. That's a cold alright. Just like PMS.

Rule 6. The discoverer has worked in isolation.

Many forms of quackery were invented out of whole cloth by one goofball (I know, an ad hominem attack. If the shoe fits...), examples include Hanneman and homeopathy or D.D. Palmer and chiropractic. And their system, like the word of God, is never questioned or altered, despite data that may or may not modify or contradict it.

In the case of Airborne, it was "created by a second-grade teacher." A teacher and a second-grade teacher at that. While we don't necessarily support them financially, teachers have a certain cachet in this country, and those that take care of our young children are thought of are especially highly. If it had been created by a community college creative writing professor, would you have been as impressed?

Americans do love the idea of the lone inventor, toiling away in the basement before becoming rich with the pet rock or MS-DOS.

Certainly, when I think of cutting edge health care research I think do not think of the NIH or big Pharma; I think a second grade teacher. Especially since US students are ranked 17th and falling in science when compared to the rest of the world. I suppose that those who have the most exposure to snotty noses are those most expert in avoiding and treating them. By the same reasoning, I should own a brewery: experience in an area does not mean expertise.

Rule 7. The discoverer must propose new laws of nature to explain an observation.

This is common to all of quackery: they all violate what is known about chemistry, physiology, anatomy, and physics. Either 500 years of scientific progress is right OR alternative medicines represents insights into the nature of the universe that surpass all we have learned to date. The alt-med proponents either self deluded buffoons or future Nobel prize winners. Guess what I think.

Besides boosting the immune system, here are some words to watch for that guarantee that the speaker is a quack: any reference to energy of any kind: blockage, flowing, vibrating, harmonic, holistic. They all sound good. They all mean squat. Energy is not this vague, shimmery cloud that can be tapped into. Energy is a defined attribute of physical systems: the ability to do work.

Beware of any therapy that maps the entire body on to one area: the iris, the foot, bumps on the head. I saw an ad in the Gadget universe catalog where all the acupuncture sites are actually located in the hand. Makes it easier to apply therapy I suppose, but I get worried now whenever I clap my hands.

Natural: Infections are natural. Death is natural. Natural is neither good nor bad. But like organic, it sounds good.

Above all, beware of anyone who suggests the therapeutic effects are due to quantum mechanics, especially if they mention quantum entanglement to explain their nonsense: they are blowing smoke up your Heisenberg. Quantum mechanics is a surefire way to intimidate and overwhelm and is never an answer for systems bigger than an electron. I was a physics major in college and have spent my time with the concepts of quantum mechanics. It doesn't apply to the world you and I see and hear.

So those are the seven ways, with some examples, to recognize quackery and worthless medications. The rules are widely applicable to all kinds of hokum. Apply as needed.

Rationalization

1. Modified from The Seven Warning Signs of Bogus Science (http://www.quackwatch.com/01QuackeryRelatedTopics/signs.html) By Robert L. Park

2. From the Airborne box.

Go Yeast Old Man

Published Sat, 13 Sep 2008

The week is over and my virus lasted only a day. Thank you Rockport (1).

Five days of doing my best to kill kill kill. Kill viruses. Kill spirochetes. Kill bacteria. Kill yeasts. I hope PETA never goes microscopic.

If my work day has been successful, I have left a swath of unicellular death that makes Ghengis Kahn look like a piker. I am sure I have killed billions upon billions of creatures in my day.

But now it’s the weekend and I get to enjoy the best that the microbial world has to offer.

Saccharomyces cerevisiae is a common yeast. "Saccharomyces" comes from Greek, and means "sugar mold" and "cerevisiae" comes from Latin, and means "of beer." Put the two words together and they spell heaven. Saccharomyces is used to brew beer and to raise bread.

Occasionally Saccharomyces is a pathogen in humans. The only time I have seen disease due to Saccharomyces is in the ICU when patients are treated for their diarrhea with probiotics that contain S accharomyces boulardii, the primary yeast in Chef Boulardii products. Very rare, but reported in the literature, and why I do not treat diarrhea in the ICU with probiotics, although the literature to support its use as a preventative is good.

Years ago, when I was a fellow (and, no I have not had a sex change, a fellow is a doctor training in a subspecialty) I had an AIDS patient who was a home brewer and he developed a fungemia with Saccharomyces, the same one he used to brew beer. You could say I knew what aled him.

Thank you, I'll be here all week. Try the prime rib and don't forget to tip your ID doc.

It is extremely rare to get a fungemia with the yeast used for brewing and baking and it is a good thing as both are needed for two of the great pleasures of life.

The Pacific NW is the center of the microbrew world and tonight I enjoyed the brewers sampler at the local pub: blond, heffiweizen, amber, seasonal, IPA, Brown and Porter. One would think that if there were Karma, after a week of killing these organisms, I would get sour beer. Nope. No karma. The beers were perfect.

The other pleasure of yeast will come in the morning from waffles, which I make every weekend for my kids. This comes from How to Cook Everything and makes the best waffles ever. All thanks to Saccharomyces.

2 cups milk

2 cups flour

1 Tb sugar

1/2 tsp salt

1/2 tsp yeast

Mix together.

Add 1 stick of melted butter. Yes butter. You can have a good life or a long life. I choose good.

Let me sit in a warm place over night.

In the morning, separate 2 eggs, add the yolks, along with 1 or 2 or 3 tsp of vanilla to the batter. I like lots of vanilla, especially Watkins vanilla.

Whip the egg whites and fold them in.

Make a waffle with whatever iron you use. Mine is 50 years old with a fabric insulated electric cord, so you know I am soon to die of electrocution. And use real maple syrup, not that fake stuff. Even better with fresh blackberries, raspberries, peaches, or Oregon strawberries, not the wooden crap from California.

It will be the best thing you can do with your mouth in public.

The microbiologic world. One minute I am trying to kill it off, the next I am enjoying its excrement.

No matter where you look, you find an infectious disease, even in a good breakfast.

Rationalization

(1) See the prior essay.

Chicken Feed

Published Sat, 13 Sep 2008

Last call of the day yesterday, before I turned off my beeper for a weekend of kids’ soccer and Saccharomyces, concerned a bad case of colitis. An elderly man had been admitted to the hospital with a case of bloody diarrhea, so bad they were worried he had bowel ischemia. He was placed on ciprofloxacin and metronidazole, didn't get better, had a CAT scan that demonstrated a severe pan-colitis. After a couple of days his stool cultures had grown Campylobacter jejuni. No big deal, case closed. The patient had a relatively common cause of bacillary diarrhea.

What is interesting is that the organism is resistant to ciprofloxacin, and what is even more interesting is the why.

Antibiotic resistance can occur from many mechanisms. Most of our antibiotics are derived from molecules that exist in bacteria and their ilk. The microbiologic world is in constant competition with each other, and some compete by producing antibiotics that kill off the competition. The drug companies modify these natural antibiotics so that they have better pharmacologic properties. But as a defense in the wild, other organisms make molecules that destroy the antibiotics so they are not killed by the antibiotics made by other organisms or by the antibiotics they themselves make. There is an ongoing low-grade battle in the dirt and in your colon between the production of antibiotics and anti-antibiotics.

Articles in Science suggest that the number of potential resistance genes seen clinically pales in comparison to the amount of resistance genes available in the wild. Bacteria species can fairly easily acquire genes from other species and put them to use, so there is a large reservoir of resistance genes just waiting to jump into human pathogens given the right opportunity. Infectious disease is nothing if not applied evolution.

The other way we breed resistance is to induce new mutations in organisms by exposing them to low levels of antibiotics. In the microbial world what doesn't kill you truly makes you stronger. Low levels of antibiotics can lead to a variety of mutations that make antibiotics less active, a mechanism independent of new gene acquisition.

The Borg were wrong. Resistance is not futile, it is inevitable. And because the bacteria out multiply us, they have an evolutionary advantage over any antibiotic we can throw at them. I once did a rough back of the envelope calculation and figured that 30 years of reproduction for a bacteria is equal to 6 million years for humans. We have come along way in 6 million years. Can you say Lucy? I thought you could.

We intensify this battle by adding huge amounts of antibiotics into the world, some in people, but even more in agriculture. In the US, 70% (yep seventy. seven-zero) of antibiotics are used in agriculture as low levels of antibiotics in chicken feed (and other animal and vegetable feed) lead to bigger, healthier (someone will argue this point) animals that go to slaughter sooner. Your cheap 8 lb. fryer at Safeway gets that way in part because there have been small amounts of antibiotics in the chicken feed.

And that leads back to the Campylobacter. When quinolones are used in chicken feed resistance develops from a simple amino acid substitution at the antibiotic binding site which occurs in days and lasts for weeks, even after the antibiotics are stopped. Resistant organisms can be found in the chicken at the time of slaughter. Some studies have found resistance Campylobacter in grocery chickens approaching 50% of chickens tested.

The agricultural industry has long argued that there is no proven connection between animal antibiotics and human pathogen resistance, and fought for years any attempt to ban them. Go Bayer. But for quinolones (ciprofloxacin is a class of antibiotics called a quinolone) the data was clear enough that the Campylobacter resistance seen in human disease was from the use of quinolones in animal feed that the use of these antibiotics was banned in 2005.

This ban is a good thing and many of the bacterial causes of diarrhea ( Campylobacter, Salmonella) are often found in the colons of the animals we love to eat and to whom we give tons of antibiotics, breeding further resistance. I always bear in mind that everything we eat has a fine lay of human and/or animal stool on it. The last act of every animal when it dies, including you, is to release its bowels, and if the animal is to be eaten, some part of the final BM ends up in the food. Bon appetite.

One hopes that without the ongoing pressure of quinolones in the chicken feed that, because resistance is costly to the organisms, that Campylobacter will revert to susceptible again. It helped in Australia. But maybe not, but that is the topic of a future post.

Rationalization

Science 20 January 2006: Vol. 311. no. 5759, pp. 374 - 377. Sampling the Antibiotic Resistome (http://www.ncbi.nlm.nih.gov/pubmed/16424339).

Science 321, 365-367. Antibiotics and Antibiotic Resistance Genes in Natural Environments (http://www.sciencemag.org/cgi/content/abstract/sci;321/5887/365).

Germ Theory

Published Sun, 14 Sep 2008

The germ theory of disease is not just a theory. It’s the law. For infectious diseases it is the cornerstone of the subspecialty. It should be called the germ fact. I sometimes think that there are only three causes of disease: infectious, genetic and wear and tear.

Not everyone understands the concepts of infection and contagion as a cause of disease. Some think that disease is caused by blocked meridians or blocked innate intelligence or some other kind of nonsensical magical thinking.

Fine. There are all sorts of goofy stuff in the world, and that gives fodder for blogs such as Science-Based Medicine. Hint hint (http://www.sciencebasedmedicine.org).

One would expect that if a practitioner believes that disease is caused by blocked meridians and are trying to unblock them, perhaps such a practitioner would have no truck with those pesky science based disease concepts like germs, and that perhaps such a practitioner would not be so fastidious about practicing interventions that would prevent the spread of infection.

Staphylococcus aureus is a particularly virulent organism and it loves nothing better than finding a hole in your skin to use as a portal for invasion. Needles are good at causing holes for Staph to take advantage of. Dialysis needles. Diabetes needles. IVDA needles. And acupuncture needles.

It turns out a medical practitioner was colonized with MRSA (methicillin resistant Staphylococcus aureus) and was sloppy with his acupuncture technique and, along with unblocking the qi, dragged a little MRSA into his patients.

"Eight cases of invasive MRSA infection were identified. Seven cases occurred as a cluster in May 2004; another case (identified retrospectively) occurred approximately 15 months earlier in February 2003. The primary sites of infection were the neck, shoulder, lower back, and hip: 5 patients had septic arthritis and bursitis, and 3 had pyomyositis; 3 patients had bacteremia, including 1 patient with possible endocarditis. The medical practitioner was found to be colonized with the same MRSA clone [ST22-MRSA-IV (EMRSA-15)] at 2 time points: shortly after the first case of infection in March 2003 and again in May 2004. After the medical practitioner's premises and practices were audited and he himself received MRSA decolonization therapy, no further cases were identified."

If you get bored, and why would you be bored when you have this, Google photos of acupuncture. There is a distinct lack of pictures of practitioners using gloves, even though they touch the skin bare-handed to locate the puncture site and their fingers are often right next to the needle insertion. Our local acupuncture school had a photograph of the teacher and student placing needles sans gloves, sans foam, sans sterile technique, sans everything. An acupuncturist trying to generate a practice sent me a picture of her at work, putting in a needle without gloves. I wonder if acupuncturists use contraception. Probably not condoms.

It is not all that unusual for infections to occur from quackery of all kinds, and will be the focus of a future and more detailed entry at the aforementioned science-based medicine blog. It is not uncommon for SCAM (Supplements, Complementary and Alternative Medicine) practitioners to have little to no understanding in the concepts of infections, and what understanding they do have is often erroneous.

In my career I have seen several infections, including a joint infection, due to acupuncture.

You should not be reassured by SCAM practitioners just because they call themselves doctor. The following are doctors: Dr. Demento, Dr. Doom and Dr. Horrible. Do you suppose they know the basics of germ theory and hand hygiene? I think not. Well, the last two do wear gauntlets or gloves. You cannot expect someone who treats disease by SCAM methodologies to understand infections or to practice good infection control techniques. It’s hard enough to get real health care practitioners to wash their hands, and they understand germ theory. Or so one supposes.

Germs do not care what your theory of your disease is when it comes to causing disease. Modern Infection Control techniques are the only reliable way to prevent their spread. Ignore them at your peril, and my gain.

Rationalization

Infect Control Hosp Epidemiol 2008;29:859-865. Outbreak of Invasive Methicillin-Resistant Staphylococcus aureus Infection Associated With Acupuncture and Joint Injection (http://www.ncbi.nlm.nih.gov/pubmed/18684094)

MRSA Questions

Published Tue, 16 Sep 2008

One definition of an expert is someone who knows more and more about less and less until she knows everything about nothing.

For me, it is the opposite. I seem to know less and less about more and more until one day I will know nothing about everything.

Take MRSA. Please.

Today was another day of community-acquired methicillin resistant Staphylococcus aureus infections. No big deal, it is our plague of toads for the 21st century. Resistant bacteria are no surprise. Antibiotics are used, the organisms mutate or acquire new genes to compensate, they become resistance. Simple intellig,.... I mean evolution.

But here is what I do not understand.

Resistance is costly for the organisms. It takes more energy to reproduce, it takes more energy to make the resistance proteins, resistant organisms often multiply slower. As a rule, in an antibiotic free environment, MRSA should be out competed by sensitive stains and should not survive in the community. Hospitals, yes. Nursing homes, yes. Pig farms, yes. These are antibiotic rich environments and should select for MRSA.

But the community? Not only is MRSA surviving in the community, it is apparently supplanting the sensitive strains. MRSA infections are on the rise and here in StumpTown, 80% of community-acquired Staph infections are MRSA. The community-acquired MRSA is a new strain as well, called the USA 300 strain.

USA. USA. USA. Hmm. Maybe the wrong time to be jingoistic. The USA strain had not been reported prior to 2000. Hmmm. The real Y2k bug?

So why is it that a resistant organism (and MRSA is resistant to many antibiotics besides methicillin) is so easily out competing the wild type strains? New virulence genes? New ecological niche? Lack of herd immunity to a new stain? I don’t know. Probably all of the above.

And that leads me to another question.

I had a 78-year-old male who had broken his leg when he was 16 playing football and 60 years later the S. aureus, which had been hibernating all these years, finally cut loose and became symptomatic. Not a real surprise, 60 years between trauma and symptomatic infection is not even close to the reported record.

I knew it was probably a 60-year-old Staph as it was susceptible to all antibiotics, including penicillin. It was like looking in the backyard and seeing a Neanderthal wander by.

The last 50 years have seen the intense pressure of antibiotics and other medical interventions on Staphylococcus: better nutrition, antibiotics, etc. have all helped to make it harder for Staphylococcus to infect humans. Is the MRSA of today really the same Staphylococcus of 50 years ago? I mentioned in a prior entry that 50 years for bacteria is about the equivalent to 6 million years of human doubling. We were a 3-foot-high hominid 6 million years ago, aka Lucy. What changes have occurred in Staphylococcus during the 50 years of the antibiotic era?

Do we have a new species? Is it still the same _S_. aureus as 50 years ago or has there been enough change in the DNA of the organism we should declare a new species? Have we missed the evolution of a new species? Is the new MRSA the equivalent of _H. sapien_s pushing out Neanderthals? Have I had one IPA too many? Inquiring minds want to know.

I have asked many a microbiologist these questions and all I get is a 'what the hell are you talking about?' look.

Rationalization

Journal of Antimicrobial Chemotherapy Volume 64, Issue3 Pp. 441-446. Methicillin-resistant Staphylococcus aureus strain USA300: origin and epidemiology. http://jac.oxfordjournals.org/content/64/3/441.long

Best. Ringtone. Ever.

Published Wed, 17 Sep 2008

When I was a fellow I remember an attending telling me about the time the national meetings were in Las Vegas and he was waiting for a ride in the hotel bar and a lady came up to him and asked him if he was interested in a 'date.' Wink. Wink. Nudge. Nudge. Know what I mean.

He respectfully declined and she asked, "What kind of meeting is this? Business is the slowest it has been in weeks."

No one is less likely to participate in the world’s oldest pastime than an Infectious Disease doc. We are all too aware of what we might bring home. Like HIV and syphilis, not everything stays in Vegas.

The risk of HIV from sex is dependent on when in the course of HIV you attempt transmission: HIV is

"26 and 7 times, respectively, more infectious than asymptomatic infection. High infectiousness during primary infection was estimated to last for 3 months after seroconversion, whereas high infectiousness during late-stage infection was estimated to be concentrated between 19 months and 10 months before death."

There are a lot of factors that go into HIV transmission: kind of sex, having other sexually transmitted diseases, whether the person is on HAART or not. Even if your viral load is suppressed to unmeasurable, there is still a small risk of HIV transmission: if a couple that has 100 sexual encounters per year, the cumulative annual probability of HIV transmission is 0.0022 for female-to-male transmission, 0.0043 for male-to-female transmission, and 0.043 for male-to-male transmission. 100 sexual encounters a year. Sigh. I will avoid over-sharing at this point.

I am never ever going to be the Pope because I think condoms are GREEEAAAAAAAT. Thank you T. Tiger.

Condoms prevent pregnancy and prevent sexually transmitted diseases and help prevent the transmission of HIV.

Condoms, unlike the Pope, are not infallible, but it is my considered professional opinion, and you may disagree with me on this, that people like to have sex. And if they are going to have sex, it is better than not to wear a condom. Prevent HIV, prevent horrible deaths. Amazing what a simple piece of latex can do. Even more amazing that anyone would object to their use.

Part of the issue with sex is the various taboos and stigmas associated with it. In India they are trying to break down the taboo of talking about condoms by getting the conversation started with a ring tone for cell phones that is the Best. Ringtone. Ever.

Go to http://www.condomcondom.org and download the best ringtone ever.

Rationalization

HIV-1 Transmission, by Stage of Infection. (http://www.ncbi.nlm.nih.gov/pubmed/18662132) The Journal of Infectious Diseases 2008; 198:687-93.

Relation between HIV viral load and infectiousness: a model-based analysis. (http://www.ncbi.nlm.nih.gov/pubmed/18657710) Lancet. 2008 Jul 26;372(9635):314-20.

Legionella. It’s not just for legionnaires any more.

Published Thu, 18 Sep 2008

My medical career started around the time of the first cases of toxic shock syndrome, HIV and the first outbreak of Legionnaires in Philadelphia. I am that old. Or mature. Or overripe. I gave a lecture at the Med School this week and there were students who were not yet born when I received my MD. At least I do not (yet) smell of mothballs.

The hotel where the first outbreak at an American Legion Convention has been demolished; no one would stay there. Curiously, my brother, on a trip to China, stayed at the hotel where there was a SARS outbreak and business is booming.

Legionella are, from a disease etiology perspective, cool. They are found in fresh water, such as lakes and streams, where the bacteria needs free-living amoeba as hosts for survival and multiplication. Neat. It needs amoeba to live. Not only is Legionella found in lakes and streams, but shower heads, decorative fountains, nuclear cooling towers, and potting soils, all of which have been implicated in transmission of the disease. I see a cooling tower, I think Legionella. I suppose it will kill Homer some day.

Here in the Great Pacific Northwest, despite the penchant for rain and other forms of wet, we do not have much Legionnaire’s pneumonia. It is not for lack of looking; we spend thousands every year testing for Legionella and maybe get a case a year at the hospitals where I practice.

It turns out that our lack of Legionella is even odder than I had supposed as Legionella is having an upswing in the rest of the USA this century:

".A total of 23,076 cases of legionellosis were reported to the Centers for Disease Control and Prevention from 1990 through 2005. The number of reported cases increased by 70% from 1310 cases in 2002 to 2223 cases in 2003, with a sustained increase to 12,000 cases per year from 2003 through 2005. The eastern United States showed most of the increases in age-adjusted incidence rates after 2002, with the mean rate in the Middle Atlantic states during 2003-2005 exceeding that during 1990-2002 by 96%."

Why is that? And why not in the Great Pacific Northwest? I think the good beers are protective. But then I always credit beer.

The other interesting thing is when Legionella occurs. Rates of infection increase after hot, humid, weather. Thundershower weather. If you have those meteorological conditions, then 6 to 10 days later you get a spike in Legionella cases. Hot, wet, humid weather is not the hallmark of Oregon. Historically we get the long, cold drizzle. I remember a Ray Bradbury story about a kid who lived on a planet where it stopped raining only once every 100 years and everyone went out for the one day of sun. Except for the protagonist who was locked in a closet by his classmates. That is what Oregon winters are like. Lots of rain, not being locked in a closet.

But the last two years we have had more summer days like Minnesota: hot and humid with thundershowers. I always challenge the house staff to find me a Legionella after a thundershower, and they usually do. And they get a Scooby Snack. Good boy. It may be due to increased surveillance for the disease, but it is a fun predictor none the less and gets the residents interested. Climate scientists are predicting with global warming there will be more hot, humid, wet, thundershowers here in the Great Pacific Northwest (tired of my chauvinism yet?), so I wonder if we will also see an upswing of Legionella in the last half of this decade. Bet we do.

How, and even if, climate change is going to increase or decrease local incidence of Legionella is not yet well worked out. However, this is only one of many diseases that have the potential to increase with climate change. But that will be the subject of future posts.

Rationalization

Increasing Incidence of Legionellosis in the United States, 1990-2005: Changing Epidemiologic Trends (http://www.ncbi.nlm.nih.gov/pubmed/18665818). Clinical Infectious Diseases 2008; 47:591-9.

It's not the heat, it's the humidity: wet weather increases legionellosis risk in the greater Philadelphia metropolitan area. (http://www.ncbi.nlm.nih.gov/pubmed/16288369) J Infect Dis 2005; 192:2066-73.

Ask me no question, I'll tell you no lice

Published Thu, 18 Sep 2008

Last year my youngest child's class had a head lice outbreak. Snicker all you want, it WILL happen to you too, and when it does hope you have a boy rather than a girl, because it is so much easier to shave a boy’s head, and so much simper than using RID to eradicate the bugs.

With resistance increasing to the more commonly used anti-head lice medications, it is nice that an enterprising pediatrician figured out that hot air blown onto the head and trapped in a shower cap can kill off the lice better than medications. It’s better to cook ‘em than to poison ’em. Given the presidential debates are about to occur, I expect no end of hot air in the short term, so the incidence of head lice may transiently decrease, especially in those states with many electoral votes.

Head lice are common in all people, all ages, all socioeconomic groups now and for all time. People think lice are associated with being poor, but a recent meta-analysis of head lice prevalence suggests that being female (more hair? No wonder I never got the lice from my son) and crowding were more important factors than poverty. Depending on the population studied, prevalence rates in various parts of the world vary from .4% to 65%.

Pardon me for a moment while I scratch my head.

Lice, while freaking everyone out, are also good vectors for both Typhus and Relapsing fever, interesting but rare diseases in the US.

It is interesting how much the body resembles a forest or other ecological system. There are a variety of streptococci in the mouth and they each prefer to live in one distinct area of the mouth: one strep prefers the tongue, another the teeth, another the back of the throat. Each part of the body is an isolated Galapagodian (is that a word? It should be) island where one organism or another has evolved to occupy its own niche.

Same with lice. In the lab you cannot tell the difference between a head louse (Pediculus humanus capitis) and a body louse ( Pediculus humanus humanus). Head lice and body lice can be forced to breed in the lab in some odd parasitical version of "The Menagerie." They have evolved different survival strategies to survive as head lice, for example, lay their eggs and stick them to hair while the body louse lays its eggs in clothes.

Louse classification becomes even more complicated:

"Mitochondrial DNA (mtDNA) studies have shown that there are 3 distinctly different clade phylotypes of P. humanus found among modern humans.

The most common mtDNA phylotype is found among both head and body lice (type A) and is worldwide in distribution. The second mtDNA group (type B) occurs only in head lice and has been found in the New World, Europe, and Australia. The third type (type C) has been found only among head lice from Nepal and Ethiopia."

And that's not even mentioning the issue of pubic lice, which are most similar to the gorilla pubic louse. I do not even want to go there.

Given that lice are as common on humans as fleas on a dog, looking at the evolution of lice can lead to interesting observations about the evolution of humans and the dissemination of humans across the planet.

Lice evolution has helped define when humans and chimpanzees split (our respective lice split with us) and have helped date the out-of-Africa migration. And since the body louse lays its eggs in clothes, they have estimated, based on louse evolution that humans because wearing clothes about 100,000 to 72,000 years ago. Concert T-shirts followed later.

And most recently, it was mummies. Peruvian mummies to be exact. One thousand-year-old Peruvian mummies with mummified head lice. They collected these 1000-year-old head lice, isolated and typed their DNA. They found by DNA analysis that all the 1000-year-old Peruvian lice were all Type A (and premed) and it was the oldest louse DNA ever analyzed (until they analyze Rumsfeld's). Since these lice predated Europeans, it is concluded that the type A louse spread across the world with human migration and was not brought over with Columbus.

"The most likely theory is that phylotype A, issued from Africa, was distributed worldwide. Phylotype B may have survived and developed only in North and Central America, before Columbus, and is now spreading in the world, carried back by Europeans returning from the Americas. Type C is confined to highly mountainous countries of the Old World. In any case, the present work shows that there are several phylotypes of lice with geographical restrictions and that this was true before the arrival of Columbus in the Americas."

Nifty. Lice are more than a pain in the cranium and a source of low-level hysteria for the parents of young children. They help us understand our evolution and our wanderings over the planet. Like so much of infectious diseases, little things, even our vermin, have broader implications in understanding our past as well as why we get sick.

And my head still itches.

Rationalization

Hot Air May Be an Effective Nonchemical Treatment of Head Lice. (http://www.ncbi.nlm.nih.gov/pubmed/17079567) Pediatrics. 2006;118:1962-1970.

Molecular Evolution of Pediculus humanus and the Origin of Clothing (http://www.ncbi.nlm.nih.gov/pubmed/12932325). Current Biology , Volume 13, Issue 16 , Pages 1414 - 1417.

Worldwide Prevalence of Head Lice. (http://www.ncbi.nlm.nih.gov/pubmed/18760032) Emerging Infectious Diseases. Vol. 14, No. 9, September 2008 pg 1493.

Molecular Identification of Lice from Pre-Columbian Mummies (http://www.ncbi.nlm.nih.gov/pubmed/18254682). The Journal of Infectious Diseases 2008; 197:535- 43.

Caniculares Dies

Published Sat, 20 Sep 2008

It’s Latin.

I finally saw an organism I have read about for 25 years. That's the problem with Infectious Diseases. There are so many germs out there and many of them only rarely cause disease, often in patients with an altered immune system. There are over 500 species of bacteria in your gut alone, most of which are not pathogenic. And there are the bacteria on your skin and in your mouth and in and on your friends and family. Lots of bacteria. If you just live long enough, however, eventually you will see every bug.

There are, as I have mentioned before, 10 to 100 times more bacteria in and on you than there are cells of you. We are awash in a sea of the bacteria that make up out own bacterial flora, and occasionally the bacterial seas of other animals wash up upon our shore. Talk about a strained metaphor. I am going to wrap it in an ACE, ice it, and hope it gets better.

Our pets are a source for bacteria. Pets can harbor bacteria that are commonly pathogenic in humans as well as harbor their own bacteria that, under the right circumstances, can infect us.

For example, Escherichia coli, known as E. coli as no one can spell Escherichia without a dictionary. E. coli is one of the primary bacteria in human colons. A common cause of urinary tract infections, this organism is passed back and forth from person to person and from person to pet and back. We live in a thin haze of our own fecal flora and the fecal flora of the humans and animals around us.

One study assessed

"The fecal E. coli flora of 228 individuals from 63 households. We documented extensive within-household sharing of fecal E. coli, including within 3 of 5 UTI (Urinary Tract Infections) households. Our findings both confirm the results of previous smaller studies and extend them by demonstrating that within-household E. coli strain sharing is widely prevalent (being essentially a normal condition) and commonly occurs among pets, humans, and non sex partners, as well as between sex partners."

Seventeen percent of humans and dogs shared the same E. coli. E. coli is not the only pathogen that dogs can carry. Dogs have also been found to carry methicillin resistant staph,Clostridium difficile and vancomycin resistant Enterococcus. It is why I am not so sanguine about having dogs in my hospitals for pet 'therapy.' I have observed that dogs have a habit of licking their butts and elsewhere, so how do we know they haven't transferred a pathogen from butt to fur by way of the mouth? I never let a dog lick me if I can help it, it is the equivalent of shaking the hand of someone who just scratched their butt. Ick. If a dog has a germ, it may pass it on to you. Bacteria, the gift that keeps on giving.

Dogs have organisms in their mouths that usually do not cause disease in humans, like Pasteurella species and Capnocytophagia canimorsus. And it is this last organism I saw for the first time this week. If you are unlucky enough to have your spleen out and are exposed to Capnocytophagia canimorsus, it can go berserk, causing sepsis, all your organs to shut down and the patient gets a form of vascular thrombosis called DIC and purpura fulminans. It is a particularly nasty form of sepsis as patients can lose fingers, toes, arms, legs and their nose from the massive arterial clotting which this (and other) organisms can cause.

Which is what this poor person had. Years ago he lost a spleen to an accident and had frequent exposure to a slobbery dog. Capnocytophagia canimorsus, which lives in the mouth of dogs, managed, probably through small unnoticed breaks in the skin, to gain access to his blood stream and it really tried to kill him. What was particularly impressive was the amount of thrombosis of toes and fingers, although in the end he survived, thanks to all that the modern ICU has to offer, and did not lose a digit.

I have read about Capnocytophagia (it may be on your Boards, btw) for years, and have finally seen a case. I hope it’s the last. If you have a dog and you do not have a spleen, be wary of bites. Every animal can and will, under the right conditions, spread an odd disease or two to humans. The best way to sterilize your dog or cat is the autoclave, but for some reason people actually like their pets. Go figure.

Do we have a pet? Nope. My kids want a dog, but I know I will be the one to end up taking care of it, i.e., cleaning up the crap. Pass. They did have a hamster, which promptly bit me (Hamsters can carry Lymphocytic choriomeningitis virus), then escaped, fell down a heating duct and died on the heating coil, filling the house with the smell of roasting, rotting hamster in January and costing $400 to fix. I cannot imagine the smell and cost if a dog or a cat fell down the duct.

Rationalization

Escherichia coli Colonization Patterns among Human Household Members and Pets, with Attention to Acute Urinary Tract Infection. (http://www.ncbi.nlm.nih.gov/pubmed/18179385) Journal of Infectious Diseases 2008; 197:218-24.

Caniculares Dies: dog days.

Infectious Body Art

Published Sat, 20 Sep 2008

What marks me as an old geezer is that I do not understand hip hop. Or visible underwear. Or goatees. Or those hideous rectangular glasses that seem to be de rigueur, but make everyone who wears them look dorky without adding style. And body art. I am deep into mid-life, and perhaps I should acquire one of the above as part of my midlife crisis. I'm thinking of a bar code on my forehead. I am due.

Of course, given my body, there is no art short of a large bag that could improve my aesthetics, and older guys like me can only look lame with a tattoo or a diamond stud in a body part. But maybe a pony tail...

When I was a resident, tattoos were a sure sign of psychopathology. Only ex-prisoners and sailors had tattoos. And only the lobe of the ear was pierced. Nowadays everyone under 30 has a tat and all parts of the body are open to piercing. And they open up people with all sorts of unexpected and interesting infections.

Hepatitis from tattoo parlors are old hat, and, thankfully uncommon with good technique, but given the fine coating of bacteria we all have, and the fact that body surfaces cannot be sterilized, just be made very, very, very clean, seeing the odd bacterial infection from piercing and tattoos would be expected

I have seen two people lose an ear from getting the upper part of the ear pierced. Mark Anthony went on to do body art, I suppose. The lobe is made of fat, but the upper ear is cartilage and if a bacteria reaches the cartilage with a piercing it rips through the ear faster than antibiotics can keep up. Both Staphylococcus, from the patient's skin, and Pseudomonas, from the ice and water sometimes used for anesthetic and cleaning, are the common bacteria. Plastic surgeons can make a new ear for you later using a piece of rib cartilage, but the Van Gogh look, even if temporary, is so 19th century.

There are also, not unsurprisingly, local infections and abscesses depending on where the piercing was done, the belly button is the residual of the umbilical cord. In some people there is a residual cyst from the umbilical cord, called a urachal cyst. I had a patient that had a belly button abscess as a complication of the ring passing through the unknown urachal cyst and she developed a big abscess that needed to be surgically removed and, in the process, lost her belly button. It is my understanding she later had one reconstructed, but for a period of time was unable to practice omphaloskepsis.

The most worrisome infection from piercing is endocarditis, which is an infection of the heart valve. Endocarditis is not a trivial disease, 100% fatal if not treated and it is not unusual for the disease have significant morbidity including strokes and valve replacement.

Not unsurprisingly body art has a low, but real, chance of leading to endocarditis.

"In all, 22 specific cases of IE spanning 1991-2007 have been reported that were associated with piercing the tongue (seven), ear lobes (six), navel (five), lip (one), nose (one), and nipple (one), and reported in one heavily tattooed person; other general IE cases have also been mentioned. Twelve cases were in females, and one patient died; nine of these individuals had CHD (congenital heart disease). Twenty-one cases have been published in the 10 years from 1997-2007."

There are probably more case reports out there as cases tend to be under-reported as it is such a pain to write them up. I am always amazed at how the little things, the seemingly inconsequential choices we make, can lead to infectious disasters. Yesterday it was a dog in the lap, today a piercing. Dem dare bugs are always waiting to kill us, dontcha know.

One of the cooler blogs is Street Anatomy, where there is a nice collection of tattoos that reflect the underlying anatomy. It would be particularly appropriate if someone with the tattoo of a heart got a heart infection as a consequence. I like that kind of symmetry. Not that I would wish such a disease on anyone. I guess I'll have to come up with an alternative for my mid-life crisis. Perhaps I'll start a blog...

Rationalization

Infective Endocarditis After Body Art: A Review of the Literature and Concerns (http://www.ncbi.nlm.nih.gov/pubmed/18710675). Journal of Adolescent Health. Volume 43, Issue 3, September 2008, Pages 217-225

http://streetanatomy.com/blog/

Unknown unknowns

Published Sun, 21 Sep 2008

"There are known knowns. There are things we know that we know. There are known unknowns. That is to say, there are things that we now know we don't know. But there are also unknown unknowns. There are things we do not know we don't know. "

~ Donald Rumsfeld

Who knew?

That's the problem with fighting terrorists abroad so that they will not attack here at home, or at least not attack us again. All those unknowns. War wounds are expected. Whatever bacteria are in the soil, or on the skin, or on the uniform, or in the water can be drug/dragged into humans by whatever projectile is trying to kill them. Post-traumatic infections are part of trauma, although good care can keep them at a minimum.

One of the now known knowns from our most recent war, but was a prior unknown unknown was the fact many of these war wounds are due to a relatively unusual organism, Acinetobacter. In the US Acinetobacter is an occasional ICU acquired infection; it is not usually seen in patients from outside the hospital. Iraq is a little different. One US military hospital ship had 57 Acinetobacter infections occurring in 211 inpatients admitted from March through May 2003.

That’s a lot of Acinetobacter infections. We don't see that many a decade in my hospitals. These organisms cause a wide variety of trauma associated infections with a relatively high mortality rate and, worst of all, tend to be resistant to almost all antibiotics except carbepenams and colistin, a detergent used as an antibiotic in the 1960s. You know you are in a world of hurt if you have to recall to duty antibiotics that were retired in the 1970's.

The source of these wound infections seems to be field hospitals where the wounded first receive care. This organism is ubiquitous in the environment:

"Thirty-six were isolated from samples of the hospital environment, and 1 was isolated from soil surrounding the hospital. Most (68%) were collected in critical care treatment areas (11 from intensive care units, 7 from operating rooms, and 7 from emergency departments). In patient care areas, ABC isolates were recovered from operating room equipment (anesthesia machine [ n = 2], operating room table [ n = 1] and light [ n = 1], unspecified locations in the operating room [n = 2], environmental control units [i.e., heaters and air conditioners; n = 2], patient beds [ n = 12], sinks [ n = 8], and tent walls [ n = 2]). ABC isolates were also recovered from other locations, including an environmental control unit ( n = 1), environmental control unit drip lines or soil bags ( n = 4), a drinking water source ( n = 1), and soil outside a field hospital nutrition care section ( n = 1). No ABC organisms were re covered from the 31 archived soil samples. Twenty-Five (20%) of the 125 environmental samples collected from the Dogwood, Mosul, Tikrit, and Balad hospital locations yielded ABC isolates."

With so much Acinetobacter in the environment, it is not surprising there were wound and other infections, organisms such as Acinetobacter do love to take advantage of traumatized flesh. There is one case of where Acinetobacter was spread from an infected soldier to a healthy nurse.

Antibiotic resistance is also a worry, some isolates being resistant to all antibiotics.

"A. baumannii strain AYE exhibits an 86-kb genomic region termed a resistance island‚ the largest identified to date‚ in which 45 resistance genes are clustered. At the homologous location, the SDF strain exhibits a 20 kb-genomic island flanked by transposases but devoid of resistance markers. Such a switching genomic structure might be a hotspot that could explain the rapid acquisition of resistance markers under antimicrobial pressure. Sequence similarity and phylogenetic analyses confirm that most of the resistance genes found in the A. baumannii strain AYE have been recently acquired from bacteria of the genera Pseudomonas, Salmonella, or Escherichia."

45 resistance genes. Holy cannoli. That is a lot of resistance genes. It is a chest pain-inducing amount of resistance genes. If I were prone to anxiety, this would make me anxious. The Thorazine does keep me calmer, and the voices a little softer.

If you see the words 'resistance islands," think plate tectonics. These islands will drift to other places, or, to mangle yet another metaphor, explode like Krakatoa. Bacterial genes do not stay put. Bacteria can easily exchange resistance genes, and these organisms could be a source for future antibiotic resistance in other bacteria. Why Iraq has bred such resistant organisms is a mystery.

Resistance is costly for organisms; resistance does not develop without a reason. I wonder, half-seriously, if the Acinetobacter was the result of genetic engineering by the Iraqi's gone bad. Acinetobacter would be a poor choice for a biologic weapon, but accidents do happen when people are less than fastidious about their technique. But science prevails over paranoid conspiracy theories. Never attribute to malice that which is adequately explained by stupidity. It was probably a natural occurrence:

"Genomic islands are unstable regions and hotspots for the successive integration of resistance determinants in Salmonella spp., Escherichia coli, or Streptococcus thermophilus. We can safely assume that the mosaic-like structure of the AbaR1 island is the result of successive acquisitions of DNA fragments from different hosts, mainly Pseudomonas spp., Salmonella spp., and E. coli. "

The world is always odder than we can imagine.

Bacteria do so love to acquire other genes and use them. And pass them on. It is why we always lose the race between new antibiotics and resistance.

I wonder what bacteria lurk in the country of... never mind.

Rationalization

Acinetobacter baumannii Skin and Soft-Tissue Infection Associated with War Trauma (http://www.ncbi.nlm.nih.gov/pubmed/18611157). Clinical Infectious Diseases 2008; 47:444-9

An outbreak of multidrug-resistant Acinetobacter baumannii-calcoaceticus complex infection in the US military health care system associated with military operations in Iraq. (http://www.ncbi.nlm.nih.gov/pubmed/17516401) Clin Infect Dis 2007; 44:1577-84.

http://www.wired.com/wired/archive/15.02/enemy.html

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020007

Cleanliness is next to sumpthin'

Published Tue, 23 Sep 2008

Hand hygiene is an important part of infection control, although you wouldn't know it from some of the studies that look at hand hygiene rates. It takes about a decade for new information to get disseminated in the medical field, and so I have to cut health care providers some slack as we have only known about the importance of clean hands for, oh, I don't know, 160 years.

I suspect that at some level people have trouble believing, at a gut level, in the germ theory. Germs are just so damn small. If you can't see it, it doesn't exist. As part of my duties as Chair of Infection Control, we have made great progress at increasing compliance of hand hygiene, and have seen infections fall accordingly.

Especially beneficial is the use of the alcohol form, a pressurized canister that squirts out a ball of foam on your hand about the consistency of whipped cream; imagine my surprise to discover that the foam was supposed to be used topically. I had been using it like cheese whiz. When I was a kid, to take a whiz was to urinate. Does that make anyone other than me wonder what's in the can of cheese whiz?

Anyway.

Part of the campaign to increase hand hygiene is the motto, "It's OK to ask," allegedly empowering patients to ask their provider if they have washed their hands. As if. For entertainment’s sake, I spent a couple of hours asking patients if they understood the signs (they did) and if they would ask (they most certainly would not). When asked why, most said something to the effect they did not want to risk alienating their nurse or doctor. Not a bad policy; I wouldn't want to piss off the person who was bringing me my morphine.

I am suspicious that the approach to hand hygiene suggested by the "It's OK to ask" campaign is fundamentally bankrupt. If the airlines had a similar campaign about flying and that it was OK to ask whether the wheels were down at landing because the pilot just maybe forgot, no one would fly. The secret, if there is one, to these complicated problems is to make the default action hand washing.

Hands are not the only problem, and if push comes to shove we can always have them removed. Heh, heh, heh. More than hands have been associated with carrying bacterial pathogens.

Two studies have found pathogens on neck ties. I have been looking for a reason to give up on those worthless pieces of cloth and no longer wear a tie. I suppose I could go with a bow tie, but it takes far more panache than I possess to look good with a bow tie. And string ties, well, no one looks good in a string tie.

Other intimate objects in the hospital can carry bacteria:

- public phones

"Twelve different types of bacteria were found on the surface of telephones. The level of bacterial contamination for the telephone mouthpiece was increased to its highest point in October from its lowest value in August. It was also found that the micromouthpiece was about twice the contamination of earpiece."

- keyboards and mice

"In all 14 patients' rooms we collected a total of 1118 samples: 222 samples from keyboards and mice, 214 from infusion pumps and 174 from the ward's trolley. From the central ward 16 samples per fomites were obtained (computer keyboard and mouse at the physician's workstation and the ward's intercom and telephone receiver). Microbacterial analysis from samples in patients' rooms yielded 26 contaminated samples from keyboard and mouse (5.9%) compared with 18 positive results from other fomites within patients' rooms (3.0%; p < 0.02). At the physician's computer terminal two samples obtained from the mouse (6.3%) showed positive microbial testing."

- beepers

"Microorganisms were isolated from all pagers; 21% yielded Staphylococcus aureus, of which 14% were methicillin resistant. Cleaning with alcohol reduced the total colony count by an average of 94%. "

- stethoscopes

"All but six bacterial cultures were positive (85.7%). Staphylococcal species were the most common contaminants (47.5%). One case of methicillin-resistant Staphylococcus aureus was encountered. Gram-negative organisms were isolated in nine different samples (21%) including one case of Acinetobacter baumannii in the neonatal intensive care unit."

I think rounds in the hospital should be like the ancient Greek Olympics with everyone nude. It would also have the benefit of increasing weight loss in employees.

The world is a more filthy place than you can even begin to imagine. And you do not want to know what is in your mouth if you are a germaphobe you may never kiss again. In the real world it is no big deal, but in the hospital? I wish germs were the size of those creatures that were put into Chekov's ear. At least we could see them. I try and alcohol foam all my accessories, except my cell phone, even though it is a piece of crap Windows mobile and I am impatiently waiting for my Verizon contract to die so I can get my iPhone.

I wonder about these touch phones, the Blackberries, the other electronic devices in our pockets that we use while sitting in the bathroom. Not me. I don't even pick my nose. But I am sure others do. I am not sure I want to douse my iPhone in alcohol. But how else to clean it? I put my iTouch in the wash by mistake and it was detrimental to its functioning, although it was temporarily cleaner.

So many contaminated surfaces, so little time to disinfect.

Rationalization

The stethoscope as a vector of infectious diseases in the paediatric division. (http://www.ncbi.nlm.nih.gov/pubmed/18554272) Acta Paediatr. 2008 Sep;97(9):1253-5. Epub 2008 Jun 12.

Microbiology of public telephones. (http://www.ncbi.nlm.nih.gov/pubmed/16343633) Journal of Infection Volume 53, Issue 2 , August 2006, Pages 140-143.

Computer keyboard and mouse as a reservoir of pathogens in an intensive care unit (http://www.ncbi.nlm.nih.gov/pubmed/15139578). J Clin Monit Comput. 2004 Feb;18(1):7-12.

Gross. A true story.

Published Wed, 24 Sep 2008

My children love stories about work, especially gross stories, and the grosser the better.

The schedule said my next patient had parasites. Always a bad sign if you practice in Portland, Oregon. The Pacific Northwest is parasite free, and, unless the patient had been traveling abroad lately, the patient was likely to be crazy, or, at a minimum, uninformed. There are other diagnoses on the schedule that give one pause: Lyme, fatigue, and chronic Candida. You know in advance that the chance of a good doctor-patient interaction is slim.

Walking in the room the smell of garlic was overpowering. Sitting there was a slightly disheveled elderly man, who, while we talked, continually ate raw garlic cloves, one after another, as if they were jelly beans. At least that is how I eat jelly beans. In the small, often overly warm, exam rooms, the smell was intense. I like garlic. When I cook I always triple the amount of garlic and one of my favorite recipes is chicken with 40 cloves of garlic. I thought there could never be too much garlic. Wrong.

Talking with the patient revealed that parasites floated in the air and would land on his skin, burrow in, then travel through his body and finally come out his nose. Yes, his nose. You may guess where this is going.

I asked how he knew they were parasites, and he said he pulled them out of his nose. It was the garlic that kept the parasites at bay, forcing them to escape out his nose.

I asked, hesitantly, if he had a sample of the parasite, and he produced a large brown jar that rattled when he shook it. He unscrewed the lid and dumped about two cups of dried boogers onto the exam table.

To my credit I neither screamed nor puked. I explained to him that he did not have parasites and why. He did not believe me and left with his jar of dried parasites.

I can eat garlic now, and enjoy it, but for a long while the smell of garlic made my stomach churn.

The patient had delusions of parasitosis, not an uncommon problem for infectious disease doctors. Most doctors, when confronted with these patients, do not have enough background in parasitology to recognize that these 'parasites' have a life cycle that makes no sense. When examined under the microscope, the parasites always look like clothing threads or non-specific organic detritus. So they send them to me, both the patients and the pseudo-parasites. The treatment is antipsychotics, which I have never had a patient agree to take, much less see a psychiatrist. There is no doubt the disease causes suffering, but getting the patient treated in problematic.

The current popular incarnation of this syndrome is Morgellon's, a idee fixe that sure looks like delusions of parasitosis to these bifocaled eyes.

Occasionally it is not a delusional state that brings a patient in with a parasite, but someone who is misinterpreting the data. I had a patient who thought he had passed a worm, but it was just an earthworm that had fallen out of his pants; he had been working in the garden and was much relieved to know that he was not infected with worms. At least not earthworms.

Vermin Bites

Published Wed, 24 Sep 2008

Pets. I don't want one. But I am glad others do as it makes my job more interesting.

You don't really want to stick your hand near an animals mouth.

"Here kitty kitty kitty nice kitty damn, it done bit me on the hand."

Cats, especially, like to cause deep injuries. Unlike dawgs, which tend to cause tearing injuries, cats teeth are filthy solid needles that inject bacteria and whatever is in the mouth deep into tissues, gaining access to the joints of the hands and the tendon sheaths, neither of which is a good place to have bacteria.

A common bacteria in the mouths of cats, and to a lessor extent the mouths of dogs, is Pasteurella multocida and other members of the Pasteurella family. Pasteurella loves to cause soft tissue infections after bites, and often needs surgical debridement (pronounced de breed. not dee bride. Dee bride is de woman who walks down de aisle of de church). As did the patient I saw today whose cat inadvertently bit her on the thumb. Some surgery, a few days in the hospital, and some antibiotics later she is slowly getting better. And I thought my hamster was expensive.

Pasteurella can show up in other body parts, depending on the exposure. Remember Pig Pen from Charley Brown, always in a cloud of dirt? I think of animals that way, and I include humans as animals. All are in a cloud of bacteria. So if the cat wanders around your environment, it will leave little bacillary presents in its wake, that, with a little bad luck, will infect you.

I had a patient who developed a Pasteurella foot abscess. She denied any bites to her feet, but did like to walk barefoot through her house where she had 30 or so cats.

I had the peritoneal dialysis patient who developed Pasteurella peritonitis. The cat liked to sleep in the bag warmer where the dialysate was warmed prior to being infused into the peritoneum.

I had a patient whose cat chewed off the end of her Groshong catheter while she slept (I suppose it liked the taste of blood) and the catheter grew Pasteurella.

My all-time favorite was the teenaged girl who liked to put tuna on her nose and have her ever so cute kitty cat lick it off. The veins of the face drain back to the central nervous system, and she was unfortunate enough to get meningitis from Pasteurella. She did fine, but it was not a pleasant experience.

We live in close contact with a variety of animals, and with the animals come their bacteria and the infections those bacteria cause.

Seizures

Published Fri, 26 Sep 2008

The call today was about a patient with an Hispanic surname and a seizure. In my world that combination is cysticercosis, from the pork tape worm, Taenia solium. Pork. The other white meat.

Turns out that pigs have their very own tape worm. If you eat under-cooked pork, then you get the Taeniae larva, which travels to your brain where it forms marble sized, fluid filled cysts with a little parasite in them. Or you can acquire it from inadvertently (one hopes) eating human poo from a carrier. Sometimes you can see the parasite on the CAT scan, looking like a teeny fetus in a womb.

The parasite can live up to 25 years (can you say ick), but eventually all good things come to an end, the parasite dies, the cyst breaks down releasing parasite parts, the immune system attacks, the brain becomes inflamed and headache and seizures result.

Or after they die they calcify which also results in a focus for seizures.

In the U.S. pork tapeworm is not a problem, but South of the border it is a very common cause of seizures. It may not be a problem in the U.S. but one of the rare times I have sent food back is when the pork loin was rare. Just couldn't eat it. I also do not like pigeon rare, but for aesthetic reasons.

The results of treatment are problematic, and while I would not want a live parasite in my head, the literature suggests that the best you can get is a decrease in the seizure rates.

You say, well, I don't eat pork. I am of the Orthodox Jewish faith. No such luck. There was an outbreak in a New York city Orthodox Jewish community where 4 people had neurocysticercosis and several others had serologic evidence of disease. The source? Domestic help that had recently immigrated from Latin America, where Taenia is endemic. It was in the stool of the workers and was passed from worker to food to family.

Even if you do not eat the food or travel to where the disease is found, the infection can still come to you.

Also of interest, DNA analysis of tapeworm suggests that prehumans acquired Taenia from hyenas and cats (the definitive host) from eating antelopes (the intermediate host) and passed it to pigs and cattle later when we domesticated them. In evolutionary scheme of things, we gave the tapeworm to the pig. So really, pigs are just giving back what we originally gave them. What comes around, goes around.

My patient, unfortunately, does not have the typical MRI findings of cysticercosis and may have a low-grade brain tumor. He had a brain biopsy because of the unusual appearance of the MRI, but final pathology is pending. It's a bummer. An infection I could cure, and brain tumor, not so much.

Rationalization

Cool pictures: http://www.stanford.edu/group/parasites/ParaSites2004/Taeniasis/index.htm

Neurocysticercosis in an Orthodox Jewish community in New York City (http://www.ncbi.nlm.nih.gov/pubmed/1495521). NEJM Volume 327:692-695 September 3, 1992 Number 10.

Calor?

Published Fri, 26 Sep 2008

A Winner, The Open Laboratory 2008 (http://scienceblogs.com/clock/2009/01/the\_open\_laboratory\_2008\_and\_t.php).

"My normal temperature is 97, so 98.6 is a fever for me."

I hear a version of this phrase at least once a week. But is it true? What is normal body temperature?

98.6. A Boy Band? Average IQ of the Bush administration? The marking on a mercury thermometer? You remember mercury thermometers? No? Back in the day we had thermometers that used mercury and had a red mark at 98.6, and if your temperature went above the red mark, you got to stay home from school. We loved to crack thermometers open and play with the mercury, which may explain why I have a passing resemblance to the Mad Hatter.

Let's go back in time.

In 1868 Carl Reinhold August Wunderlich published "Das Verhalten der Eigenwärme in Krankenheiten" (The Course of Temperature in Diseases). Wunderlich gave “37 °C (98.6 °F) special significance with respect to normal body temperature,” based on a million observations in about 25,000 people. He found a mean of 98.6 °F without an electronic calculator to aid in the calculation. Only those living in the Victorian age were devoted enough to spend that kind of time calculating the average of a million numbers. Wunderlich gave 38 °C (100.4 °F) as the upper limit of the normal range, so a temperature greater than 100.4 was the first quantitative definition of a fever.

Tests conducted with one of Wunderlich's thermometers demonstrated they were mis-calibrated by as much as 1.4 to 2.2 °C (2.6 to 4.0 °F) higher than today's instruments. Therefore 98.6 is based on data collected with bad thermometers.

So what is normal temperature?

A study in 1992 measured 700 oral temperatures in 148 healthy men and women between the ages of 18 and 40, using modern thermometers. There was a range of temperatures from 35.6 °C (96.0 °F) to 38.2 °C (100.8 °F):

• a mean of 36.8 ± 0.4 °C (98.2 ± 0.7 °F).

• a median of 36.8 °C (98.2 °F).

• a mode of 36.7 °C (98.0 °F).

Mean, median, mode. Does that you take you back? I had to look them up to help my son with his math homework. But it is 98.2, not 98.6, that is the average temperature.

The mean temperature varies during the day: lowest at 6 a.m. (37.2 °C (98.9 °F)) and highest at 4 to 6 p.m. (37.7 °C (99.9 °F)). Like a stopped clock being right twice a day, people are 98.6 twice a day: once on the way up and once on the way down.

The important exception is ovulating females, who are above the mean, or warm, in the early morning. People use this fact, called the rhythm method, as a form of birth control. The medical term for these people is 'parents.'

Women had a slightly higher (women are hotter than men?) average oral temperature than men (men are cooler than women?) 36.9 °C (98.4 °F) versus 36.7 °C (98.1 °F). Black subjects had a slightly higher mean temperature but slightly lower diurnal oscillations compared with white subjects (36.8 °C (98.2 °F) versus 36.7 °C (98.1 °F) and 0.51 °C (0.93 °F) versus 0.61 °C (1.09 °F), respectively): these differences approached, but did not quite reach, statistical significance. Oral temperature recordings of smokers did not differ significantly from those of nonsmokers.

So what's a fever? Depends on the time of day.

"Fever is most appropriately defined as an early-morning temperature of 37.2 °C (99.0 °F) or greater OR a temperature of 37.8 °C (100 °F) or greater at any time during the day."

The other way to judge a fever is to have my wife hold her hand against your forehead. At least where the children are concerned, she says it is more reliable than the thermometer.

This is of practical importance as I see a couple of patients a year with the diagnosis of fever of unknown origin who, it turns out, took their temperature at 4 in the afternoon and, by golly, it was 99.9, as it was on each subsequent day. Normal temperature is 98.6. They have a fever. Patients can get thousands of dollars wasted on the workup of their nonexistent fever.

Normal temperature is 98.6 is a medical myth.

Rationalization

A critical appraisal of 98.6 degrees F, the upper limit of the normal body temperature, and other legacies of Carl Reinhold August Wunderlich (http://www.ncbi.nlm.nih.gov/pubmed/1302471). JAMA Vol. 268 No. 12, September 23, 1992.

Zombies

Published Sun, 28 Sep 2008

I am tired. I moved 1345 pounds of pea gravel from Home Depot to the car to the back yard. Why my wife cannot decorate with styrofoam, I do not know, but my new rule is that if the sack of rocks weighs more than my age, I am not lifting it.

Last night I finished World War Z. An oral history of the Zombie War by Max Brooks. If you like that sort of thing, and I do, it is a fun read. What, you may ask, does a book about Zombies have to do with Infectious Disease. Dude. Everything as something to do with infectious diseases. ID is the Kevin Bacon of connectedness.

Infections, of course, have done more to change the world than most people realize and if you pay any attention to the history of the world you quickly notice it is also the history of infections. Plagues of all kinds have continually swept through the world and killed enormous numbers of humans. Up to 2/3's of Europe died of a plague in the Middle Ages. The 1918-1919 flu pandemic killed about 2% of the world's population. That flu pandemic was by a bird flu strain, and if history repeats itself, if the next strain kills 2% of the world, well, 2% of 6 billion is a lot of people.

In WWZ the zombie plague is spread by the bite of a zombie, it infects the bitten, who die, and then are reanimated as a zombie that eat the living and are only killed by having their brains destroyed. Typical zombie fare, but the story takes place after a zombie pandemic that almost annihilates the human race and is told from the perspective of the survivors.

As an ID doc, it is you could substitute flu, or smallpox, or bubonic plague and see the book as a metaphor for the effects of a world-wide contagion. The world is primed for a huge pandemic. We were lucky that SARS was not that infectious and that it came to the county with a first-class health care system like Canada and not one with a second-rate system like, oh, I don't know, the US. Large populations with widespread travel would make it easy for a plague to rapidly spread across the world. The 1918 pandemic swept the world before air travel. If you have ever wandered the rat warrens of Chicago O'Hare, and imagined if some lunatic terrorist decided to infect himself and wander the airport, how quickly you could infect huge numbers of people.

ID docs, and those in public health, do worry about pandemics and, in a just-in-time economy, what would happen if, as is expected, half your workforce does not come to work due to an influenza or zombie pandemic. It has the potential to be a real nightmare.

One of the better chapters of the book from a medical point of view (as opposed to the creepy zombie army attacking and eating your innards point of view) is early in the book Breckenridge Scott is interviewed. He made a fortune selling a fake zombie cure called Phalanx. The character is the archetype of every purveyor of supplements in the US, from Airborne to Enzyte and I need to see if I can get the whole chapter reprinted.

A good horror novel, or any other work of fiction, needs to stand on its own. This book is a fun, creepy read. A great piece of fiction has a broader understanding of the human condition, and read as a possible example of any post plague existence, WWZ works at the higher level as well.

Read it for fun, read it to be creeped out, read it to look at how our world could react to a global catastrophe of, oh, climate change and the resulting spread of many forms of zombies, er, I mean, infections.

Mmmmmmmmmmm. Brains.

WNV

Published Mon, 29 Sep 2008

It has been a slow year for West Nile Virus (WNV) and, while it is a good thing, the CDC isn't sure why.

368 severe cases, only (only? I hate referring to any death as an only) 18 deaths. Not bad compared to prior years like 2007, when there were more than 1,200 cases of severe West Nile illness with 124 deaths. The peak in cases was in 2002 and 2003, when there were 3000 severe illnesses and more than 260 deaths. Not much compared to hand guns and cars, but enough.

Why the decline in cases?

It could be fewer mosquitoes. At least here in Oregon it has been a dry summer and the kids have had far fewer bug bites this year. My children, especially the youngest, are sentinel chickens for mosquitoes. The US drought monitor suggests the US has had less rain, which would lead to fewer mosquitoes which would lead to less West Nile. I can't see that mosquitoes are counted in the US, so perhaps this isn't true. Someone go out there and start counting mosquitoes please.

An increase in the decrease (huh?) in rainfall always leads to changes in infectious disease incidence of all kinds. Wet seasons have led to increases in the cases of Hantavirus (more rain leads to more plants leads to more seed leads to more mice which carry the virus that were in contact with people and gave them the disease). Only one of many examples. The changes in the seasons and the climate mean changes in infections.

It may be that the birds are not dying. Mosquitoes prefer to feed on birds and go after humans only when the birds are dead. If the remaining birds are less likely to die from WNL, as survivors of prior WNL seasons would be, then they would still be around for the mosquitoes to feed on. I don't know if this is true either.

I doubt it has anything to do with a change in the human populations. We haven't been exposed to enough WNL long enough and we are a secondary host for the virus.

So we had a slow year. Good. Let’s hope it stays slow.

Rationalization

http://drought.unl.edu/dm/monitor.html

Cellulitis

Published Wed, 01 Oct 2008

Yesterday was one of those inundations of consults that occur on occasion, and by the time I got home, took care of real life, it was time for bed and no spare time for a post. Life does have a way of requiring one’s attention.

Today was less busy, but I had a common consult: is it cellulitis or not?

Vasculitis is inflammation of the vascular tree.

Pneumonitis is inflammation of the lungs or pneuma, Greek for breath.

Hepatitis is inflammation of the liver, or hepta, some ancient word or other for liver. I prefer pate.

Cellulitis is inflammation of the cellula, which is god knows what, but is the word from the Latin cellula, which means a small cell, so what this has to do with a skin infection, I have never been able to find out. It is also, evidently, a prostitute’s cubicle, and, while you can get all sorts of inflammation from that kind of cellula, it has nothing to do with the case at hand.

The 3 most dangerous words in medicine are "In my experience," especially when it comes to treatments, but I am going to delve into those three most dangerous words in medicine, because there are pearls about cellulitis that can help one distinguish infection from other causes of rubor, dolor, calor, tumor in an extremity (I finally work those words into a post, I feel like Groucho should give me a twenty).

Here are pearls, prepare to make a necklace:

Cellulitis patients always have a fever or an increased white count. Always.

Cellulitis is never ever never never ever ever bilateral. Never ever. Now you may say to yourself, I have seen bilateral cellulitis, Crislip is wrong. And you may ask yourself, How did I get here? And you may ask yourself, am I right? am I wrong? My god, what have I done? And in this case you were wrong. It was a misdiagnosis. It wasn't bilateral cellulitis, you had a misdiagnosis. Live with it.

Here is a key point: the rubor, dolor, calor, tumor of cellulitis does not resolve with elevation and the rubor, dolor, calor, tumor of stasis/edema does. I have never seen this fact in print, so if some fellow wants to do a clinical study, just give me a nod in the footnotes. The problem is cellulitis leads to temporary swelling and redness in a leg from edema, and the patient goes to the doctor and says I am not getting better, it’s still red. And they get more and more expensive (but not more powerful) antibiotics until they are all Fanny Mae from the expense, and then they are sent to me, I elevate the leg higher than the heart and the 'cellulitis' is gone in a couple of minutes.

Never evaluate a leg for cellulitis in a dependent position. You will be misled.

For every 50 lbs the patient is over the ideal body weight, it takes one day more to get better.

Cellulitis on therapy progresses for one day, stabilizes for one day, then on the third day it starts to regress. You need patience with the patient.

Group A Strep cellulitis will start with severe groin pain on the affected side several hours before any rubor, dolor, calor, tumor of the leg; I presume this is from local lymphatic inflammation.

All the pearls mentioned above have, to my knowledge, not been subjected to rigorous clinical trials, so take them or leave them as you see fit. My consult today had neither fever nor leukocytosis, it was bilateral and disappeared with elevation. I stopped his antibiotics.

What is interesting is that the microbiology of acute cellulitis may be changing. It is taught that most cellulitis is due to Group A strep, Streptococcus pyogenes, the same bug that causes strep throat.

An interesting study in Finland looked at the microbiology of cellulitis and found

"Beta Hemolytic streptococci were isolated from 26 (29%) of 90 patients, 2 isolates of which were blood-culture positive for group G streptococci, and 24 patients had culture-positive skin lesions. Group G Streptococcus (Streptococcus dysgalactiae subsp. equisimilis) was found most often and was isolated from 22% of patient samples of either skin lesions or blood, followed by group A Streptococcus, which was found in 7% of patients."

I wonder if this true in the US as well. I seem to be seeing more Group G streptococci lately, but have yet to find a resident who wants to repeat this study with our local data. One considered it, but has yet to commit. I sure hate a strep tease.

Rationalization

Acute Bacterial, Nonnecrotizing Cellulitis in Finland: Microbiological Findings (http://www.ncbi.nlm.nih.gov/pubmed/18260753). Clinical Infectious Diseases 2008;46:855-861.

Measles: Where is MY angry mob?

Published Thu, 02 Oct 2008

In my world there are facts and practices that are so ingrained, such a major part of the underlying structure of Infectious Diseases, that challenging them can only be viewed as jaw-dropping ridiculousness.

If you are a physicist, you take relativity as a given.

Chemists, I suppose, take atomic theory as a given.

In medicine, anatomy is a constant.

In infectious diseases, germs cause disease. Duh. To fight the diseases there are two options: antibiotics and the immune system. Of the two, the immune system is far superior, and without a good immune system, as AIDS and cancer chemotherapy have proven with depressing regularity, all the antibiotics in the world will not stop you from dying of infection if your immune system cannot be reconstituted.

The best use of the immune system is to have preexisting immunity so when exposed to an infection, you do not get it. From, say, a vaccine. The efficacy of vaccines is, to an ID doctor, beyond question.

They work. Vaccines, along with nutrition and flush toilets, are why we all get to live to our 80s and we do not have to have 9 children in the hope that one or two will survive to adultery.

Take measles, a nasty disease.

In the not so good old days there were 400,000 cases a year in the US with 400 deaths and to this day there are 25 to 30 million children infected each year in the world and it kills 345,000.

Vaccine efficacy is 90-95%. I have seen exactly one case of measles in 25 years or so of Infectious Diseases, and it was imported into the US (yet another failure of border patrol).

The vaccine is safe with little in the way of side effects: not autism, allergic reaction in 1 in a million.

In 2000 measles was declared eliminated in the US. Gone. No more local disease.

Crap.

I make a living from infections and their complications and the elimination of measles represents yet another vanished income opportunity. You think Fanny Mae has issues, try being an ID doc. Damn you vaccines. Where is MY bailout?

But good news is always around the corner. There is a group of people who think vaccines, despite voluminous data to the contrary, causes autism. And they have a small, but vocal, following. People like me rely on science and reason to make medical decisions. Pesky things like facts and data and clinical studies.

Those who support the Infectious Disease Employment Act, i.e., the anti-vaccination folks have a different way to determine the proper course of medical interventions: the angry mob "...because there is an angry mob on my side, and I like the fact that I can say she is completely wrong," saith Jenny McCarthy discussing my Hero, Amanda Peet and her support of vaccines. And we all know the ongoing benefits to society brought about by angry mobs. Ask the monster.

I am thinking that it would be a good research modality for The National Center for Complementary and Alternative Medicine (NCCAM). After millions spent investigating SCAMs, they have yet to discover a use for these modalities using the scientific method. Perhaps, instead, they should use the 'angry mob' as the way to validate homeopathy, acupuncture, etc.

Thanks to religious exemptions and anti-vaccine wackaloons, we have had a small resurgence of measles this year. Not much. Only 131 cases, of which 91% were in kids who were not vaccinated. It is a small beginning. But I am hopeful. If Jenny could just be against flush toilets...

Rationalization

http://www.unicef.org/immunization/index_measles.html

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5733a1.htm

http://www.sciencebasedmedicine.org/?p=186

http://www.ecorazzi.com/2008/09/30/jenny-mccarthy-strikes-back-at-amanda-peet-over-child-vaccinations/

Warning: there was some sarcasm in the above post that will likely be unnoticed by many readers.

Popcorn and Abscesses

Published Fri, 03 Oct 2008

Not all Streptococci are the same. Most do not cause abscesses, but the S. anginosus group can, and often does, cause abscesses.

S. anginosus (old name S. milleri. Microbiologists love to get together, get drunk, and change the names of bugs. Keeps them employed I suppose) is part of the normal flora of the mouth and, if it gains access to the blood it can go to the liver or brain or spine and cause an abscess. If it is accidentally inhaled into the lung, it will cause a lung abscess.

And, like the patient today, it somehow manages to get into the soft tissues of the neck, a retropharyngeal (behind the throat) abscess. The neck has numerous tissue planes down which the strep can invade, so these tend to be big abscesses that dissect down into the chest and, in the process, cut off the airway. I do not know yet why this patient has a S. anginosus abscess, he cannot talk due to a tracheostomy, but relatively minor trauma is often all that is needed. The most curious case I had was someone who, while a wee bit drunk, failed to chew his nacho chip sufficiently and it cut clean through his esophagus when he swallowed it.

The curious thing about S. anginosus is not the diseases it causes, or the drugs used to treat it. It is the smell. It smells like buttered popcorn. I have never smelled it. For some reason I cannot bring myself to smell a culture plate. When I was a fellow one of my colleagues ran down to the lab to smell a plate and it turned out to be Coccidiomycosis. Turns out Coccidiomycosis is very infectious under these conditions (it wasn't known that it was Coccidiomycosis when it was smelled (smelt?)), and one is not supposed to smell it. That person is the only living human who knows what Coccidiomycosis smells like. And it ain't Teen Spirit.

Why does S. anginosus smell like popcorn? It makes diacetyl. Lots of diacetyl.

"The caramel odor associated with the "Streptococcus milleri" group was shown to be attributable to the formation of the metabolite diacetyl. Levels of diacetyl in the 22- to 200-mg/liter range were produced by 68 strains of the "S. milleri" group."

What is cool is that the reason it smells like buttered popcorn is that diacetyl is one of the compounds that gives butter that butter smell. Next time you have that fake butter spread, think to yourself, "I can't believe it’s not S. anginosus tm."

Small amounts of diacetyl are found in beer and wine from the yeast fermentation and it is what gives beer and wine a slipperiness. Or so says the Wikipedia, which also says

"Concentrations from 0.005 mg/L to 1.7 mg/L were measured in Chardonnay wines, and the amount needed for the flavor to be noticed is at least 0.2 mg/L."

So the bacteria make 10 to 100 times (I know, sloppy math) the amount of diacetyl found in wine. Why it makes so much dactyl, I cannot discover.

Oregon beers are many things (best anywhere), but slippery is not one of them. Makers of Chardonnay try and maximize the amount of diacetyl to give the wine that buttery taste and slipperiness. Or maybe it’s really pureed slugs. A new smoothy flavor for the local Jamba Juice? Give me a good Bordeaux any day.

So next time you have that microwave popcorn and a glass of Chardonnay, remember that the buttery richness is also is the smell of abscesses.

Bon appetite.

Rationalization

Detection of diacetyl (caramel odor) in presumptive identification of the "Streptococcus milleri" group. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC270577/)J Clin Microbiol. 1992 November; 30(11): 3028.

http://en.wikipedia.org/wiki/Diacetyl

Hamlet Act 3, scene 1, 55

Published Sat, 04 Oct 2008

Saw a bad case of tuberculosis today. As opposed, I guess, to a good case of TB. Bad for him, good for me. Multiple involved lobes of the lung, consumption and coughing up blood. Fortunately, he is from the Western hemisphere, so I do not have to worry much about resistant TB. He should get better with antibiotics and time. Although he has no insurance, TB is one of those diseases that will be taken care of.

People always act surprised when I mention that I saw a case of active tuberculosis as they think it is a disease of the past, a killer of artists and musicians. I learned as I wrote this that WC Fields died of TB. The heck. Unfortunately, TB is alive and well in the world. It kills about 1.5 million people a year, one third of the world’s population is infected with TB and there is a person infected every second. And boy is he pissed.

The US and western Europe do not have much TB. It has been on the decline for decades. Most of the cases of TB are in the developing and Third World. But.

I think of humans as surrounded by a sea of germs and most of our energy output is to keep these germs from consuming us. Which they will eventually. I have the unproven idea that doctors die of their subspecialty, so I am certain to die of an infection. At least I am not an OB doc. I have told my wife to cremate me immediately upon death so the bacteria I have spent a lifetime killing do not get their chance to eat me.

And the US is like a person. We are an island of low infection rates for diseases that infect most world. Good nutrition, flush toilets and public health departments across the country have kept these infections at bay. I wonder for how long. If you want to get good and anxious, read the books by Laurie Garrett. You will want to pull the covers over your head and stay in bed.

The problem with TB is that it is infectious, the method of spread is coughing and in this country no one ever worries about covering their cough. Turn your head and cough. Why turn your head? It doesn't make it easier to find the hernia, it is so the patient doesn't cough TB (or some other infection) on you. Every couple of years we get a patient with active TB who has spent the prior month’s coughing on everyone they meet, spreading TB. Coughing is an efficient way to spread disease.

The other problem with TB is resistance. The way you breed resistant TB is gave intermittent and inadequate therapy for long periods of time and that is just how TB is treated outside the West. Most US patients with infectious TB receive DOT: directly observed therapy, so we can help insure all the medications are taken. Not so in the rest of the world where half of people who even get therapy for TB receive inadequate or intermittent therapy to guarantee the organisms develop resistance.

The result?

Worldwide, 20% of TB is multidrug resistant (MDRTB) and 2% of TB are extremely drug resistant (XDRTB) and I expect those numbers will get worse. Most of these cases are in Korea, China and the Old Soviet Union. If you visit those countries, do not inhale.

And they will come our way. They always do.

Today, at least, I can still treat TB. Even if I can't treat some MRSA and E. coli.

Rationalization

Laurie Garrett. The Coming Plague and Betrayal of Trust.

WHO Tuberculosis. (http://www.who.int/mediacentre/factsheets/fs104/en/)

http://en.wikipedia.org/wiki/List_of_tuberculosis_victims

I don't know

Published Mon, 06 Oct 2008

Call weekends, which was this weekend, are long. I cover 2 states and 8 hospitals, and I get to see great cases, but I am glad I can to back to my mere three hospitals tomorrow. I think my nick name should be ppd, the peripatetic pus doc.

ID consults have fallen into 2 general categories:

1) How and for how long to you treat an already defined infection.

2) What the heck is this germ and what do I do with it.

3) What the hell does this patient have.

I enjoy type 3. I still cannot count. They are the most fun and offer the greatest opportunity to use those three words that increasingly define my practice:

"I don't know."

House seems to figure out each case in about an hour, although the route by which he gets to the denouement almost always gives me conniption fits. And as I always say, if the conniption fits, wear it. It’s why I do not watch medical shows, they get it wrong. Except for Scrubs, which is closer to reality, at least my reality, of any TV show. Every year I know more and more. I read 1200 articles a year, attend 10 plus conferences a month. And each year I seem increasingly unsure about what is going on with my patients. In the skeptical world, they talk about the arrogance of ignorance (aka Jenny McCarthy syndrome) where the people who know the least on a topic think they are the most knowledgeable (it is really called the Dunning-Kruger effect). I have the opposite problem.

So much of the time I can't figure out what the patient has, but they get better, and I make sure I get all the credit. If things go badly, of course, I blame nursing. It is a curious phenomenon that knowledge breeds uncertainly. However, part of being a specialist is too ignorant with panache. I have beaucoup buckets of panache.

I tell patients that as long as they are getting better, it is probably a good thing I cannot make a diagnosis. In medicine we are very good at diagnosing diseases that will kill or injure you but no good at diagnosing the trivial self-limiting illnesses. So most of the time no diagnosis is a good diagnosis.

Problem is when it comes to billing I need a diagnosis and a diagnosis code. You can know a doctor by the codes she knows by heart. Here are some of mine.

S. aureus bacteremia: 038.11.

Fever: 780.6.

UTI: 595.

Endocarditis: 421.

There are codes for everything. Every disease. There is a code for being electrocuted in a bath tub. There is a code for being sucked into a jet engine. There is even a code for weightlessness. I am really looking forward to the first patient that presents with that complaint.

"So, what can I do for you?"

"Doc. I'm weightless."

What I really need, and the one thing for which there is no code, is the diagnosis 'I don't know.'

Or maybe I just don't know it.

Rationalization

http://en.wikipedia.org/wiki/Dunning%E2%80%93Kruger_effect

165 degrees

Published Tue, 07 Oct 2008

The microwave oven is great for heating left overs, wonderful for melting butter, handy for warming a cold cup of coffee. And the one in our house, when popping corn, I notice it blocks the thought waves beamed into the radio receiver in my head, or is that too much information?

The problem with a microwave is that it is too easy to give a half-assed cooking of food and not kill any bacteria.

Salmonella is back. 32 people in Minnesota and 11 in other states have developed Salmonella by eating chicken pot pies that were microwaved instead of cooked in the oven. The package didn't say you could microwave it, but these folks did it anyway. You get hungry deer in Minnesota, doncha know?

"Frozen, raw, breaded and pre-browned stuffed chicken products covered by this alert and similar products, may be stuffed or filled, breaded or browned and therefore appear to be cooked. These items may be labeled "chicken cordon bleu," "chicken kiev" or chicken breast stuffed with cheese, vegetables or other items."

The chicken isn't cooked, just browned. Twice cooked chicken is rubbery and tasteless, so they make the pot pie and you cook it, supposedly in the oven.

The same thing happened last year when 165 people got Salmonella from chicken pot pies that were not cooked enough.

This is no surprise as Salmonella are commonly found in food products and are part of the food chain. How common? Depends on the study and how the prevalence of Salmonella is determined. In a representative study,

"Overall, 9 (64%) of 14 lots and 42 (31%) of 135 of the (chicken) carcasses were positive for Salmonella."

As long as we eat chicken and chicken by-products (eggs) we will be exposed to Salmonella and the 400,000 cases a year will continue.

Heat kills, and if you get your food to 165 degrees the bacteria will die. Microwaves are particularly bad in that they heat unevenly so that one part is cold and another part is hot and the food is not sterilized.

Not only Salmonella, but Listeria can survive both freezing and microwaving. Food is dangerous and it will be until we switch to Soylent Green.

You could irradiate your food as well, but the public has issues with radiation, even though no one at Three Mile Island ever developed Salmonella.

ALWAYS eat your food deep-fried, it’s better to die of heart disease than infection. Besides, my Dad is a cardiologist.

Rationalization

http://www.fsis.usda.gov/News_&_Events/NR_100308_01/index.asp

Salmonella prevalence in free-range and certified organic chickens. (http://www.ncbi.nlm.nih.gov/pubmed/16300088) J Food Prot. 2005 Nov;68(11):2451-3.

Prevalence and risk factors for Salmonella and Campylobacter spp. carcass contamination in broiler chickens slaughtered in Quebec, Canada (http://www.ncbi.nlm.nih.gov/pubmed/17803137). J Food Prot. 2007 Aug;70(8):1820-8.

Incurable

Published Wed, 08 Oct 2008

Long day, short post.

I had a consult today for something that used to never happen, but I am seeing with increasing frequency: a Staphylococcal infection I cannot cure.

The problem is MRSA. Some strains are resistant to damn near everything and when combined with a poor host (immunologically, not financially) and allergies, treatment options get limited.

I have a patient with an infection of her arm bone, the humerus (no joke here) with an MRSA that is sensitive to vancomycin, linezolid and daptomycin only. She developed an allergic reaction to vancomycin that shut down her kidneys, a rash to linezolid and has relapsed after a 6-week course of daptomycin. A problem with daptomycin is that resistance can develop on therapy, so I am less than sanguine that I will still have that antibiotic when testing comes back. I really do not want to amputate her arm to cure her.

The reason that S. aureus is resistant to methicillin (the M in MRSA) is an alteration in the binding site on the surface of the bacteria were the antibiotic sticks. It called PBP-2a. (Short of Penicillin Binding Protein Two aaaaaa; named by the Fonz). So no beta-lactam works. Not a cephalosporin, not a penicillin, not a carbapenem.

All the remaining antibiotics are equally lousy for treating MRSA and have higher failure rates than beta-lactams. There are new cephalosporins coming down the pike that are designed to bind to PBP-2a. I really hope these antibiotics are as good for MRSA as cefazolin is for MSSA. Ceftobiprole is one of a class of agents that I am sure will be heavily detailed when it is released. As a rule new antibiotics are rarely as good as the companies say they are, they almost never live up to the hype. No one can hype a piece of crap better than a drug rep, but I so badly need a drug that will kill MRSA I am hoping that for once I am wrong and ceftobiprole will be all I need it to be. I want to be able to kill again.

You watch. It is going to cost a fortune. It will not be as active against MRSA as touted. I am sure to have my heart broken. Again.

1982

Published Wed, 08 Oct 2008

In 1982 I was a third-year medical student and the first report of Gay Related ImmunoDeficiency (GRID) was published in the MMWR. It did not, as I remember, make an impression at the time, a series of obscure diseases when I was still trying to learn the basics of medicine.

Two years later I was taking care of my first AIDS patients as a medicine resident in Minnesota. Those cases made an impression: a 25 yo male who died of disseminated Mycobacterium avium and a middle-aged dwarf who died of Cryptococcal meningitis.

At the time we had no idea what was causing the disease, we only knew it was linked to drugs, sex and Haiti. Both my patients had thousands (yes thousands) of sexual partners and both had used drugs, so they had the tentative diagnosis of GRID, now AIDS. We all felt moderately comfortable that it was not spread casually, but I still remember declining a piece of chocolate from the young male with the excuse that I wasn't hungry. I also remember him telling me that I could not get the disease from him unless "we had sex or I spit in your mouth." That conversation has stuck all these years.

That same year, 1984, HTLV-3 was discovered, since renamed HIV. Once the virus was discovered, the pathophysiology known and the epidemiology understood, I have felt more comfortable eating my patient's chocolate, but I still do not want anyone to spit in my mouth.

The AIDS epidemic has been a major part of my career. The early years of death after awful death. The initial waves of optimism then pessimism as medications were developed, tried, succeeded, then failed. Now with HAART I have had one death this century from AIDS. We have gone from a nine-month life expectancy to an almost normal life expectancy for U.S. AIDS patients. Some residents will go through a three-year training program and never see an infectious complication of HIV. The progress has been astounding, at least for those who can afford the medications. I have seen far too many deaths because patients can afford their medications and come in dying of AIDS.

All these advances stem from the discovery of the virus by Franoise Barre-Sinoussi and Luc Montagnier for which they received a well-deserved Nobel this week. The depth and breadth of understanding that can be rapidly brought to bear on new pathogens is astounding, as HIV and SARS have demonstrated. What has always been depressing about HIV is the numbers of people who really should never have died. Science and epidemiology were ignored in favor of politics and religion. 25 million people have died so far from AIDS, most of the deaths unpleasant and in the young. Simple preventatives could have done much to attenuate the early epidemic: condoms, needle exchange and closing down bath houses.

To this day, the 2007 statement by the Catholic Bishop Maputo Archbishop Francisco Chimoio of Mozambique that condoms were deliberately infected by HIV to finish off Africans has still not be repudiated by the Church. How many extra will die in a country where these 500 people are newly infected each day?

Pisses me off.

Rationalization

http://www.avert.org/worldstats.htm

http://news.bbc.co.uk/2/hi/Africa/7014335.stm

A Budget of Dumb Asses

Published Thu, 09 Oct 2008

This is updated and republished on Medscape (http://blogs.medscape.com/rdct) (where these entries are born) every October.

I had my flu shot today. Well, my anti-flu shot. Protected me and my patients from death for another year. Whew. I wonder if you are one of those dumb asses who do not get the flu shot each year. Yes. Dumb Ass. Big D, big A. You may be allergic to the vaccine, you may have had Guillain Barre, in which case I will cut you some slack. But if you don't have those conditions and you work in health care and you don't get a vaccine for one of the following reasons, you are a dumb ass.

1. The vaccine gives me the flu . Dumb ass. It is a killed vaccine. It cannot give you the influenza. It is impossible to get flu from the influenza vaccine.

2. I never get the flu, so I don't need the vaccine. Irresponsible dumb ass . I never had a car accident, but I wear my seat belt. And you probably don't use a condom either. So far you have been lucky, and you are a potential winner of a Darwin Award.

3. Only old people get the flu. Selfish dumb ass . Influenza can infect anyone, and one of the groups who die of influenza are the very young. Often those most likely to die from influenza are those least able, due to age or underlying diseases, to respond to the vaccine. You can help prevent your old, sickly grandmother or your newborn daughter from getting influenza by getting the vaccine, so you do not get the flu and pass it one to her.

4. I can prevent influenza or treat it by taking Echinacea, vitamin C or Airborne. Gullible dumb ass cubed then squared . None of these concoctions has any efficacy whatsoever against influenza. They neither prevent nor treat influenza.

5. Flu isn't all that bad a disease. Underestimating dumb ass . Part of the problem with the term 'flu' is that it is used both as a generic term for damn near any viral illness with a fever and is also used for a severe viral pneumonia. Medical people are just as inaccurate about using the term as the general public. The influenza virus kills 30,000 people and leads to hospitalization of 200,000 in the US each year. Influenza is a nasty lung illness. And what is stomach 'flu'? No such thing.

6. I am not at risk for flu. Denying dumb ass . If your breathe, you are at risk for influenza. Here are the groups of people who should not get the flu vaccine (outside of people with severe adverse reactions to the vaccine): children younger than 6 months and "completely healthy adults who have no contact with someone who isn't [healthy]." And zombies. And former President Clinton, who evidently doesn't inhale.

7. The vaccine is worse than the disease. Dumb ass AND a wimp . What a combination. Your mother must be proud. Unless you think a sore deltoid for a day is too high a price to pay to prevent two weeks of high fevers, severe muscles aches, and intractable cough.

8. I had the vaccine last year, so I do not need it this year . Uneducated dumb ass. Each year new stains of influenza circulate across the world. Last years vaccine at best provides only partial protection. Every year you need a new shot.

9. The vaccine costs too much . _Cheap dumb as_s. The vaccine costs less than a funeral, less than the Tamiflu, less than a week in the hospital.

10. The government puts tracking nanobots in the vaccine and well as RFID chips as part of the mark of the beast, and the vaccine doesn't work since it is part of a big government sponsored conspiracy to line the pockets of big pharma and inject the American sheeple with exotic new infections. Well, that excuse is at least reasonable. Paranoid dumb ass.

So get the vaccine. Or be a dumb ass. One of these days I'll let you know how I really feel about the flu vaccine.

Death by Cold Sore

Published Sat, 11 Oct 2008

Maximus : [laughing] You knew Marcus Aurelius?

Proximo : [very quickly and defensively] I didn't say I knew him, I said he touched me on the shoulder once! He gave me Herpes.

~ Gladiator. Kind of.

Herpes simplex is a common virus. About 80% of Americans have HSV 1 and 20% have HSV 2. Type 1 causes mostly cold sores and type 2 causes mostly genital disease, although on occasion type one 1 can cause genital disease and type 2 will cause oral lesions. How these strains switch places has never been adequately explained to me.

People who have close, traumatic contact can spread the virus to each other, the archetype being wrestlers, where hot, sweaty, bloody grappling can pass Herpes. That’s wrestling I am discussing. It has a name in wrestlers, Herpes gladiatorum. I prefer the British name, Scrumpox, as it sounds much more disgusting and funny. Scrum. Heh, heh, heh. A bumper sticker I sometimes see says "Rugby Players Eat Their Dead," so perhaps that is how type 2 Herpes gets to the lips. Cannibalism.

There is now a new variant of Herpes in Japan called BgKL that has been spreading among Sumo wrestlers. It has infected 39 Sumo wrestlers over a 5 year period and actually killed 2 of them. Considering there are only about 700 professional Sumo wrestlers in Japan, that is impressive. How they died is not specifically mentioned (pneumonia or hepatitis or embarrassment), but it was apparently from the Herpes infection rather than a secondary infection.

BgKL is more virulent than your average bear. This strain reactivates more often, spreads more efficiently, has higher virus levels in the lips and skin and causes more severe symptoms than other strains. The photos on the interwebs show widespread skin lesions, far more than you usually see with the more common strain of Herpes. I wouldn't touch them, much less try to push them out of a ring. Sumo wrestlers live and train together, helping to increase viral spread. They live in stables, or so all the reports say, like Kobe beef cows, so I suppose horsing around helped spread the virus. There are puns I cannot avoid making.

They postulate that this mutated form of Herpes 1, because it is more infectious, is replacing the less virulent strains seen before in Japan.

"The BgKL frequency decreases in a geographical gradient suggest that this HSV-1 variant was dispersed from Shikoku to the surrounding regions and then to more distant regions."

So it is spreading out in Japan from an epicenter.

Yet another in an endless series of examples in the microbial world of evolution, with organisms taking advantage of changes in their environment, us, to multiply and spread. Staph does it, E. coli does it, even uneducated Flu's do it. Let’s do it. Let’s evolve.

So if your travel plans include Japan, might I suggest no kissing the Sumo wrestlers.

Rationalization

Analysis of herpes simplex virus type 1 restriction fragment length polymorphism variants associated with herpes gladiatorum and Kaposi's varicelliform eruption in sumo wrestlers (http://www.ncbi.nlm.nih.gov/pubmed?term=18796708). J Gen Virol 89 (2008), 2410-2415.

The herpes simplex virus type 1 BgKL variant, unlike the BgOL variant, shows a higher association with orolabial infection than with infections at other sites, supporting the variant-dispersion-replacement hypothesis. (http://www.ncbi.nlm.nih.gov/pubmed?term=17475752) J Clin Microbiol. 2007 Jul;45(7):2183-90. Epub 2007 May 2.

Contrasting geographic distribution profiles of the herpes simplex virus type 1 BgOL and BgKL variants in Japan suggest dispersion and replacement. (http://www.ncbi.nlm.nih.gov/pubmed?term=17215348)J Clin Microbiol. 2007 Mar;45(3):771-82. Epub 2007 Jan 10.

Geographical distribution of the herpes simplex virus type 1 BgKL variant in Japan suggests gradual dispersion of the virus from Shikoku Island to the other Islands (http://www.ncbi.nlm.nih.gov/pubmed/16757606). J Clin Microbiol. 2006 Jun;44(6):2109-18.

Is Insanity Infectious

Published Sat, 11 Oct 2008

Every couple of years I get a consult as to whether or not the etiology of someone's insanity is infectious or not.

It is a previously healthy person, with no personal or family psychiatric history, who has a psychotic break, either becoming schizophrenic or manic. They do not respond as expected to medications or have an atypical presentation, and they get a spinal tap that is abnormal, suggesting a meningitis of some sort, so they call me.

Is insanity infectious? Maybe. Stupidity sure is. Insanity is, like heart disease, multifactorial in etiology, so it is hard to tease out infection as a cause. There has been a suggestion for years that some mental illness is due to infections. Part of the problem with neurology is they do not have good access to the diseased organ. When in doubt you can always biopsy a liver or a lung or a bone marrow. The cranium tends to get in the way and removing even small bits of brain is not a good idea. It is a popular myth that people only use 10% of their brain (sometimes it seems less), but I would hate for the neurosurgeon to inadvertently remove third grade.

Anecdotally I have seen a few infections present as new onset insanity. One guy was admitted naked and catatonic, screening CXR showed large potato shaped lymph nodes in the chest, he had an LP and was found to have sarcoidosis. His psychosis melted away with steroids.

Neurosyphilis, rare, can also show up as mental illness. In my practice it has been primarily in elderly widows whose husbands brought more home from the war than medals and memorabilia.

Cat Scratch Disease (Bartonella henselae) can present as an agitated psychosis followed by coma for a few days. One case I had awoke from his three-day coma, went home after a 10-day uninsured hospitalization, and killed his girlfriend’s cats. I wonder if they are still together.

Other diseases are problematic: toxoplasma can cause behavioral changes in mice, making them less fearful of cats so they are eaten and the parasite can complete its life cycle in the cat. Can it cause mental illness in normal people? Maybe.

Perinatal infections are linked with the development of schizophrenia, especially if the infection occurs in the first trimester. But which virus? CMV? Influenza? Some things as of yet undiscovered? Many viruses have been associated with schizophrenia. And is there a genetic predisposition? Probably.

Maybe it’s a post-infectious disease. Post streptococcal diseases include chorea, a movement disorder, and there has been some data to suggest it can lead to OCD as well.

There is also epidemiologic data to suggest that schizophrenia is associated with the Borna virus, which is associated with a range of neurologic symptoms in a variety of animals. And it leads to TNTC Borna again puns in the literature.

Dr. David Gilbert has said for years that the etiology of all diseases are either genetic, wear and tear, or infectious, and I am strongly drawn to this idea.

My consult this week? Acute psychosis in a young woman and a spinal tap/MRI that could be infectious. Evaluation so far is negative for infection, which always makes the case harder. It is nice to find an infection you can treat, but the sad truth is that the brain doesn't do all that well with even minor trauma, and the thought that your child's insanity could be an infectious gives the often false hope they will get better. They usually don't. I hate that.

Rationalization

A nice "popular' review: http://www.sciam.com/article.cfm?id=infected-with-insanity

Incompletely Inured

Published Tue, 14 Oct 2008

Yesterday, Sunday, was a busy day, that in no way had anything whatsoever to do with Infectious Diseases. Hard to believe that I could spend an entire day and not see something that was related to infections. I guess I wasn't looking hard enough to notice some germ or other. Monday, back to work, and no shortage of infections.

Acute care medicine gets you used to all sorts of human conditions. Four of the six senses (I am psychic) are stimulated (fortunately not taste), often unpleasantly, during rounds. We all get good at switching off those parts of the brain that lead to a less than professional response to the various sights, sounds and odors that flood the hospital. Patients do not want to see their provider puking.

Sometimes you will walk onto a ward and the distinctive tang of melena (bloody diarrhea) will hit the first nerve. You inhale deeply and with appreciation: it is the fragrance of internal medicine, you are home, in your element, the hospital. Ahhhh.

Today there were two sensory assaults I have not experienced for many years.

The first was wet gangrene in a diabetic foot. The smell of putrefying flesh when it is still attached to the patient is distinctive. You know the microbiology of the infection instantly, as only the combination of anaerobes plus aerobes in dead tissue make that smell. It is a mixed infection with stool organisms and there are people who have done the olfactory studies to elucidate the microbiology of stench, sometimes using technology in lieu of their own nose. It is probably Bacteroides spp. that accounts for most of the funk, but the research is curiously minimal, and what chemical(s) cause the smell I cannot find. It is probably a complex melange like a good red wine. The treatment, like most anaerobic infections, is surgical not antibiotics. I have become good a keeping my expression calm, not wrinkling my nose to the acrid smell coming from the foot of the bed or the foot in the bed. The patients probably think I have Parkinson's. That Dr. Crislip is so unexpressive.

The other I still, after 25 years, cannot deal with. When someone with acute pneumonia gives one of those deep, hacking, wet coughs and brings up a large specimen, expels it into a tissue, and offers it to me to examine, I lose it. Still brings on my gag reflex better than a bottle of ipecac. As a medical student I had mentioned to my attending that I had an issue with sputum production and he had been kind enough to provide, as my final in the history and physical class, a patient with tri-lobar pneumonia who coughed up his body weight in green sputum while I did my final exam. Tears literally ran down my face as I (successfully) tried not to vomit. I passed. And not out.

Today was a little easier. The patient honked up a big wet loogy and offered it to me. I long ago learned to avert my eyes, stare in the middle distance, and politely decline the offer, explaining that sputum is one of my peccadilloes and that the patient probably did not want to examine my last meal in exchange. They have always understood and seem to appreciate my honesty. Or they are too kind to call me a wimp.

The respiratory therapists and the nurses derive no end of pleasure from my inability to deal with pulmonary secretions, enjoying the occasional opportunity to display a juicy sputum specimen to me. As an ID doc, they tell me, I should be comfortable with all things pus, including sputum. I always tell them that as an infectious disease doc pus is a theoretical construct (and my vanity license plate). Others collect it for me, the lab analyzes it, and I determine what to do with it. I want to keep it that way.

Rationalization

Microbial involvement in chronic wound malodour. (http://www.ncbi.nlm.nih.gov/pubmed/10531934) J Wound Care. 1999 May;8(5):216-8.

Clinical and microbiological features of necrotizing fasciitis (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC228417/). J Clin Microbiol. 1995 Sep;33(9):2382-7.

Association of odor from infected root canal analyzed by an electronic nose with isolated bacteria (http://www.ncbi.nlm.nih.gov/pubmed/17931944). J Endod. 2007 Sep;33(9):1106-9.

Thai Food Wimp

Published Wed, 15 Oct 2008

My family loves Thai food. My kids would rather eat Thai than any other style of food. And while I enjoy Thai, when it comes to heat, I am a total wimp. There is nothing I want less on my food than capsaicin, especially when it comes out the other end. But that is a story for another time.

But if it was not for infectious moulds, there wouldn't be hot foods at all. Really.

Some plants make noxious molecules to prevent getting et by insects, fungi, and bacteria.

Fusarium is a mould common in the environment. It is found in rotting organic material and occasionally infects the profoundly immunocompromised. At bestI have seen a handful of cases in my career. Fusarium, however, is a major cause of death of chili seeds. It kills the seeds in the chili before they can be spread to start a new plant. Bad thing, killing off the offspring before they can sprout. Hard to propagate the species. Except in the case of the Jolly Green Giant. Too bad Fusarium didn't get to him before he made his sprout.

Fusarium is bad for chili's and it would be in the plant’s best interest, although not mine, for it to have a defense against Fusarium. Which it does.

How does the chili protect itself from Fusarium? It makes capsaicin, the molecule that makes chili's hot. And capsaicin kills Fusarium.

How does the fungus get to the chili's in the first place? By way of scavenging hemipteran's (hemiptari?) which are leafhoppers, treehoppers, cicadas, aphids, scales, and true bugs. These bugs, in the process of looking for food, drag the mould into the chili, where it grows and kills the chili seeds.

How does all this relate?

They found that that the more scavenging bugs there were, the more potent the wild chili's are.

"These results suggest that the pungency in chilies may be an adaptive response to selection by a microbial pathogen, supporting the influence of microbial consumers on fruit chemistry."

Lots of bugs leads to more Fusarium which leads to more capsaicin.

Capsaicin may also be involved with seed dispersal as mammals, such as me, do not like capsaicin as it is an irritant (boy is it ever), but birds evidently have no ill effects from the chemical. It means that the chili's will be eaten by birds, which pass the seeds undigested over longer distances, rather than by mammals, which would digest the seeds and/or crap closer to home.

Evolution and infection in action to make Thai food unpleasant for non-masochistic mammals. Cool. Despite the heat.

Rationalization

Evolutionary ecology of pungency in wild chilies (http://www.ncbi.nlm.nih.gov/pubmed/18695236). Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11808-11.

Seed dispersal: Directed deterrence by capsaicin in chilies (http://www.ncbi.nlm.nih.gov/pubmed/11473305). Nature, 412 (6845), 403-4

Bad Singing

Published Thu, 16 Oct 2008

You think chili's have it tough, try being human. Malaria (a redundant name from the Italian, mal: bad and aria: opera song) has probably had more impact on the human genome than any other organism.

I once heard a Nobel laureate declare that half of everyone who has ever died from malaria. I have never been able to confirm that estimation, but it doesn't stop me from passing it on. Who am I to contradict a Nobel winner, even if his prize was in the wimpy (at least compared to medicine) field of physics.

Malaria is endlessly interesting. Its manifestations, its treatment, its history, its evolution, its resistance to antibiotics, and its impact on human evolution and history. I can, and eventually will, babble about this parasite for pages.

Everyone in medicine learns about sickle cell disease, a mutation in hemoglobin, the molecule that carries oxygen. It is found in some Africans and the mutation protects against malaria. In Asia there is thalassemia, which has the same protective effect.

But what. There's more. And it is not a streak knife.

The molecule that powers the body is ATP. There is an enzyme, pyruvate kinase, that converts phosphoenolpyruvate to pyruvate with the production of one molecule of ATP.

Most cells make their ATP in the mitochondria, but red cells do not have mitochondria and need pyruvate kinase to make ATP to make energy.

"Pyruvate kinase deficiency is the most frequent abnormality of the glycolytic pathway and, together with a deficiency in glucose 6 phosphate dehydrogenase (G6PD), is the most common cause of nonspherocytic hemolytic anemia.... The prevalence of homozygous pyruvate kinase deficiency is estimated at 1 case per 20,000 persons; more than 158 mutations have been described."

That’s a lot of mutations in one enzyme, I wonder why. Hey. Malaria in an infection of red blood cells. Could there be a link? Of course.

"Pyruvate kinase deficiency has a protective effect against replication of the malarial parasite in human erythrocytes. We have described a dual mechanism for protection against P. falciparum in pyruvate kinase deficiency that included an invasion defect of erythrocytes from case subjects (observed in those with a homozygous mutation) and preferential macrophage clearance of ring stage infected erythrocytes from case subjects (observed in both homozygotes and heterozygotes)."

So if you have this mutation, while you are not a potential X-man, you are more resistant to getting malaria and if you get malaria, you clear it better.

How this works, I either cannot understand or find. Perhaps it is simple starvation. Or perhaps there is more. In normal animals, malaria induces a new pyruvate kinase that alters glucose metabolism in its favor.

Malaria is still a major health problem, with half a billion cases a year in the world and million deaths, so it is probably exerting a evolutionary pressure on the human genome. I hope it makes us smarter.

Rationalization

Pyruvate Kinase Deficiency and Malaria (http://www.ncbi.nlm.nih.gov/pubmed/18420493). N Engl J Med 2008;358:1805-10.

Pyruvate kinase in malaria host-parasite interaction (http://www.ncbi.nlm.nih.gov/pubmed/805379). Nature 255, 345 - 347 (22 May 1975).

Hereditary red cell disorders and malaria resistance. (http://www.ncbi.nlm.nih.gov/pubmed/18591619) Haematologica, Vol 93, Issue 7, 961-963.

Wrong. Again. And again. And again.

Published Fri, 17 Oct 2008

Short post. Busy day, tired, up late finishing a novel I just had to know how it ended. Lonely Werewolf Girl, if you have to ask. The protagonist is a werewolf, addicted to opiates, homeless, depressed, with an eating disorder. Except for the werewolf part, not unlike a lot of the druggies I take care of. At least I assume they are not werewolves...

I was wrong three times this month, and the month is only half over. Fortunately, it was at three different hospitals, so unless they read this blog, no one will see a pattern.

First case was a young male back from Vietnam, with bad crampy bloody diarrhea and positive blood cultures. He has a gram-negative rods in his blood, I am told, what do you think he has?

Salmonella I replied. Most common cause of bacteremia with a bacillary diarrhea.

He grew Campylobacter.

The next week I had an elderly man with no risks present with diarrhea and fever. He has gram-negative rods in his blood. What do you think he has?

Well, I say, I saw a case of Campylobacter last week, but the most common cause of bacteremia with bacillary diarrhea is Salmonella.

He grew Campylobacter.

This week I get a call about a young woman with bad lupus on steroids who comes in with abdominal pain and diarrhea and has gram-negative rods in her blood. What is it, they ask?

I say it's Campylobacter. Although the most common cause of bacteremia with bacillary diarrhea is Salmonella, and, although I am not superstitious, things do come in threes, so it has to be Campylobacter.

It was Yersinia.

You can't win. That’s why ID keeps you humble (well, maybe you, not me). No matter what a hot shit you think you are as a diagnostician, the cultures will pop positive with some germ out of left field that you didn't expect and make all your erudite pontifications turn to dust in your mouth. Mmmmmmm. Humble pie. It is also why ID is so much fun.

It is why my motto is "Frequently in Error, Never in Doubt."

Belt and Suspenders

Published Sun, 19 Oct 2008

A resident hit me up for a curbside after Grand Rounds. A curbside is where a doc asks you a question about a case, but does not want a formal consult. I like that term. Formal consult. Like I should wear a tux. It is a way of giving me liability without remuneration, but is an important way that physicians learn.

He had a patient with a case of MRSA and gave the patient two antibiotics because he wanted to 'double cover' the staph. Was that the right choice? Maybe. An enduring medical myth, that you need to give two antibiotics for infections.

I think this evolved from tuberculosis therapy where it is critical to give at least two antibiotics to prevent the emergence of resistant organisms. Or perhaps from the early cancer chemotherapy era when we had lousy drugs for Pseudomonas and two antibiotics were given. The mechanism for prevention of resistance in TB does not apply to the treatment of bacteria. In TB there are already preexisting resistant strains that are selected for by the antibiotic, generally (and there are always exceptions) this is not true for bacterial infections.

There are occasional bacterial infections that require two antibiotics: prosthetic valve endocarditis, prosthetic joint infections, toxic shock syndrome, and some kinds of streptococcal native valve endocarditis come to mind. But for routine staphylococcal and other infections there is no reason to give more than one antibiotic once you know the susceptibility. If you don't know the susceptibility of the organisms as it is still growing in the lab and there is a high probability that the organism is resistant to one of the empiric antibiotics, it is reasonable to give two antibiotics to cya, or cypa. In infected people, chose the wrong antibiotic up front and the patient has a much higher chance of dying.

You gotta double cover Pseudomonas. No. You don't. It’s a myth. Most of the time one drug (as long as it is not Zosin), if the organism is susceptible, is sufficient. Combination therapy does not increase cure rates or prevent the emergence of resistance. Double coverage does increase toxicity and expense, and is only of benefit in sepsis from gram-negative rods.

The more intense the environmental pressure, the faster organisms will evolve to survive. Some bacteria have mechanisms that increase their mutation rates in the face of environmental stress. Antibiotics are an environmental stressor for bacteria. Combination antibiotics can have four effects in killing bacteria: the combination has no extra killing (it has no more killing than one antibiotic (1+1 = 1)), the combination can have additive killing (1+1 = 2), the combination can have synergistic killing (1+1 = 5) or the combination can be antagonistic (1+1 = 0).

It turns out, at least in E. coli, that combination antibiotic therapy leads to faster development of resistance compared to single antibiotic therapy. I had always thought the main way to get resistant organisms was to give a little amount of antibiotic for a long time, the application of the dictum "what doesn't kill you makes you stronger."

In a recent study, they discovered that the more effective the combination of antibiotics was at killing bacteria, the faster the bacteria developed resistance. The better antibiotics are at killing bacteria, the faster it pushes the evolution of resistance. Bummer.

"We found a correlation between synergy and the rate of adaptation, whereby evolution in more synergistic drug combinations, typically preferred in clinical settings, is faster than evolution in antagonistic combinations. We also found that resistance to some synergistic combinations evolves faster than resistance to individual drugs."

Not only does double coverage not increase efficacy nor does it decrease the development of resistance, in E. coli, it accelerates the development of resistance. There are times when the evidence demands the use of combination therapy to improve outcomes. Outside of those conditions monotherapy should suffice and has less impact on the local microbial resistance. As we slowly slide into the post-antibiotic era, avoiding combination antibiotics when they are not needed may help prevent the emergence of resistant bacteria.

It is always the rule in medicine: No good deed ever goes unpunished. The sooner you understand that little pearl, the less harm you will do.

Rationalization

Accelerated evolution of resistance in multidrug environments (http://www.ncbi.nlm.nih.gov/pubmed/18779569). Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13977-81. Epub 2008 Sep 8.

cya: cover your ass

cypa: cover your patient’s ass

Warm October

Published Tue, 21 Oct 2008

My son has a fall break, and I have taken a few days off to have father-son time at the Oregon Coast. We have been coming to the beach for 40 years, and, while my memory can be faulty on many issues, the beach has changed in my lifetime. The low tides are not as low as I remember them, the high tides are higher. The ocean seems to have risen. The interwebs say the oceans have risen 0.05 mm a year for the last 40 years. That would be 2 mm since I started walking the Arch Cape beach. Doesn't seem like one whole heck of a lot on paper, but my fallible memory seems to remember low tides that were, well, low. Really low. Vast expanses of beach. Now, even on a minus tide, there isn't that much walking beach.

Oceans rise because of melting ice, and warm water expands. Warm water takes up more room and thermal expansion is part of why sea levels are rising. With warm water brings, you guessed it, infections.

I am on a sea food diet. I see food, I eat it. At the beach we eat sea food, at least for the short term. Except oysters. I am chicken to eat raw oysters. I have eaten deep-fried grasshoppers and raw horse. Poor Mr. Ed. He did not taste like chicken. Raw oysters are home for Norwalk and Vibrio species, all causes of gastroenteritis.

Back when I was a youngster first walking up and down the beach, I did not have to worry about Vibrio as the water was too cold. That was a problem for the warm waters of the Gulf Coast, where the water was greater than 15 degrees, the lower limit of temperature for Vibrio parahaemolyticus.

No longer. There was an outbreak of Vibrio parahaemolyticus gastroenteritis on a cruise ship in Alaska that was associated with eating raw oysters. Never before had the Alaskan waters been warm enough to support the growth of Vibrio parahaemolyticus.

"Mean daily marine water temperatures at Farm A in July and August from 1997 to 2004 showed a 0.21 C increase per year (r2 = 0.14, P<0.001); data-preserve-html-node="true" water temperatures in July and August were significantly warmer in 2004 than in each of the six previous years examined (P < 001). Mean yearly surface-water temperatures from 1976 to 2004 in the Gulf of Alaska also showed a trend of increasing water temperatures."

Warm water leads to warm water infections.

"This report documents a large outbreak of V. parahaemolyticus serotype O6:K18 in the United States, and it expands the range of epidemiologically confirmed V. parahaemolyticus illness to a latitude higher than 60 degrees‚ more than 1000 km north of British Columbia, previously the northernmost area reported to have locally acquired illness. Furthermore, our findings provide evidence to support the hypothesis that a water temperature above 15.0 degrees C at the time of oyster harvest is an appropriate threshold indicator of increased risk of V. parahaemolyticus infection from the consumption of raw oysters. Although water temperatures have reached 15.0 C at Farm A each year since 1997, 2004 was unusual because mean temperatures were above 15.0 C for a much longer period and were almost 2 C warmer than during any of the previous years."

Tonight I had a BLT with onion rings. I hope tomorrow there will be enough beach for a nice long walk. It will not be there much longer.

Rationalization

Outbreak of Vibrio parahaemolyticus Gastroenteritis Associated with Alaskan Oysters. (http://www.ncbi.nlm.nih.gov/pubmed/16207848) NEJM. Volume 353:1463-1470. October 6, 2005.

Intestinal Infections

Published Wed, 22 Oct 2008

A few days off with my youngest continues, and the Oregon Coast is infection free. At least as far as I can tell. We walked in the beach, watched Speed Racer, played golf, and went to dinner. Nothing that appeared to be related to infections in any way occurred. Such is vacation time. If only we had a plague here at the beach, it would give me something to write about.

Except the Web. CNN tells me that Mr. Blackwell died of complications of an intestinal infection. But nowhere can I find just what intestinal infection. The inexactness of the news always bugs me. I know one thing reasonably well, and its infectious diseases, and the news almost always either get it wrong or is incomplete. How am I supposed to trust the rest of the news? Help me, Mr. Harvey. I know that Mr. Blackwell's publicist is under no requirement to give details as to the exact nature of his illness, but as an ID doc I hate the uncertainty.

I am not a big fan of fashion (although thanks to my wife I have seen more of American's Next Top Model than I should probably admit). I am a fan of infections and an even bigger fan of knowing. So what was it?

I would bet first on C. difficile, a diarrhea commonly acquired in the hospital due to the use of antibiotics. Quinolones and clindamycin kill off the normal bacteria of the colon, letting the_Clostridium difficile_ overgrow and cause infection. C. diff, as we call it in the biz, makes a toxin that can cause necrosis of the colon, causing the colon to perforate and kill the patient. The organism is becoming resistant to common antibiotics and some strains are hyper-producers of the toxin, leading to increase in colectomies and deaths from the disease.

The other intestinal infection that would kill would be a perforated diverticular abscess with peritonitis.

All the other infections that could kill seem less likely. I want details and I cannot find them, and probably never will.

Anyone knows the real answer, let me know.

Rationalization

A Predominantly Clonal Multi-Institutional Outbreak of Clostridium difficile‚ Associated Diarrhea with High Morbidity and Mortality (http://www.ncbi.nlm.nih.gov/pubmed/16322602). NEJM Volume 354:2200 May 18, 2006 Number 20.

Drug Fever

Published Fri, 24 Oct 2008

All the glitters is not gold

All who wander are not lost

All who are febrile are not infected.

--ancient Elvis saying.

Fever, fever, fever. 780.6.

Why does the patient have a fever?

This week, one of the patients had a fever due to drugs. She came in infected, the infection resolved, the white count decreased, she felt better and, after a period of time, the fever returned. Routine work up was negative so they called me.

I didn't find any infection to account for either, so I looked at the drug list. Could it be drug fever? Vancomycin and Zosin were the only drugs to worry about.

When do you worry about drug fever? The patient has a fever and they are on a drug. Hence the name. There are other hints. Continuous fever, where it temperature does not fall to normal, is an inconsistent finding. Eosinophilia is another. It can be any drug, any time, first dose or the hundredth.

You have to play the odds: antibiotics are common causes, and vancomycin, which, due to MRSA, I have had to use by the bucketful, seems a very common cause, as are beta-lactams and sulfa. Of the unimportant (i.e., non-antibiotic drugs) H2 blockers and anti-seizure drugs lead the list.

In the end you have to stop the drug and see if the fever goes away, usually in about four half-lives of the drug. The only way to prove it is drug fever is to re-challenge, which, since it is not an allergic reaction, you can do safely, but is rarely needed. The rare time there is re-challenge has occurred when there is a change-of-house staff and they inadvertently restart the medication. Oops.

After stopping the antibiotics her fever curve drifted down over 48 hours. Probably the vancomycin. He shoots. He scores. No fever for 48 hours, then, just to piss me off, she has a fever. Just one that doesn't recur. It was a mustache on the Mona Lisa of my diagnosis.

Rationalization .

Drug fever. (http://www.ncbi.nlm.nih.gov/pubmed/8698996) Infect Dis Clin North Am. 1996 Mar;10(1):85-91. Review.

Endocarditis, Bacteremia and Dental Work

Published Sat, 25 Oct 2008

Bacteremia is common after dental work. Real common, even after tooth brushing. 20% of the time with toothbrushing and 60% of the time if the dentist yanks a tooth you can find bacteria in the bloodstream if you look hard enough. And that is the frequency of bacteremia after doing something as primitive as blood cultures.

If you do more sophisticated 21st-century methods of looking for bacteria, brushing and tooth extraction releases a flood of bacteria:

"Sequence analysis of 16S rRNA genes identified 98 different bacterial species recovered from 151 bacteremic subjects. Of interest, 48 of the isolates represented 19 novel species of Prevotella, Fusobacterium, Streptococcus, Actinomyces, Capnocytophaga, Selenomonas, and Veillonella."

Icky, poopy, Guadeloupe as we say in our house. And you kiss your spouse with that mouth? But it does bring home the fact that your mouth is a rich biological microenvironment, only a flossing away from your bloodstream.

The worry is bacteria seeding abnormal heart valves, especially around the time of dental extraction, and the American Heart Association (made up of Real Americans, I might mention 10 days before the election) recommends prophylactic antibiotics to prevent endocarditis, even though amoxicillin only decreases the bacteremia by half.

Do dental extractions increase the risk of endocarditis? I am not so certain. There has been epidemiological data to suggest that dental work does not increase endocarditis risk and prophylactic antibiotics are not effective in endocarditis prevention, but the studies are unreadable by all but other epidemiologists. Another epidemiologic study was published last month again demonstrates (I guess) that dental extraction is not a risk for endocarditis.

"The study population was composed of 170 hospitalized patients with infective endocarditis. The frequency of dental procedures during the 3-month period immediately before admission was compared with the frequency of such procedures during earlier 3-month control periods (when no endocarditis developed), using the case-crossover design. Thirty-four out of 98 patients with available information (35%) had 81 dental procedures during the 2 years before hospitalization, 12 (12%) of whom had 14 procedures during the 3 months before admission. The number and types of dental procedures performed during this 3-month period were not statistically different from those carried out during any earlier 3-month period, which served as a control period. Dental procedures do not significantly increase the risk of IE."

Dental work is not the risk it is cracked up to be for endocarditis and the big risk for developing endocarditis is life. It's why I no longer brush my teeth.

I have been told that the US has 30% of the world’s lawyers and the American Heart Association Guidelines are easy to find (to prove it, I'll let you google it). Published, did I mention, by Real Americans from Real America. So until the guidelines change, don't run the risk of running afoul with the ABA. Follow them. The guidelines, not the ABA.

Rationalization

Bacteremia Associated With Toothbrushing and Dental Extraction (http://www.ncbi.nlm.nih.gov/pubmed/18541739). Circulation. 2008;117:3118-3125.

Diverse and novel oral bacterial species in blood following dental procedures. J (http://www.ncbi.nlm.nih.gov/pubmed/18434561) Clin Microbiol. 2008 Jun;46(6):2129-32. Epub 2008 Apr 23.

Are dental procedures an important risk factor for infective endocarditis? A case-crossover study (http://www.ncbi.nlm.nih.gov/pubmed/18797944). Eur J Clin Microbiol Infect Dis. 2008 Sep 17.

Bee Frage and diarrhea

Published Sun, 26 Oct 2008

I wish I knew half as much as I think I do. There are about 10,000 articles in Pubmed each year related to infectious diseases. If I were to read one an hour, boy would I be bored.

It is not only new things to learn, but I am constantly surprised by things I thought I knew, but didn't. They are rarely of clinical importance, but it really seems the more I know, the less I know. It is that old definition of a specialist: she knows more and more about less and less until she knows everything about nothing.

Take Bacteroides fragilis. It is the major anaerobic bacteria isolated in infections related to gastrointestinal perforation and an important germ in the formation of abscesses. When killing anaerobes you want to make sure you kill B. frag, as we call it in the biz.

Because it is a common pathogen, I assumed it was a common anaerobe of the GI tract. I was wring, wrang, ronge, wrung, well, you know what I am trying to say.

B. fragilis makes up a small percentage of the fecal flora and only 40% of humans are colonized with B. fragilis. Rather than being a predominant and common part of the colon, as I thought, it is a minor colonic constituent and can be uncommon.

The other thing I thought about B. fragilis is that it did not cause disease unless it escaped the colon. That, based on new information, is also in error. B. fragilis is a new described cause of gastroenteritis, aka the Hershey squirts, in humans.

There is an Enterotoxigenic Bacteroides fragilis (ETBF) that causes an inflammatory diarrhea. The organism is evidently endemic in Bangladesh, where the study was done. Enterotoxigenic means it secretes a toxin into the bowel to cause disease, a common mechanism for bowel pathogens to cause diarrhea, since it is the diarrhea that allows the organism to spread. Much of the world now, and all of the world in the past, uses the same water source for drinking and waste disposal. Where do you think Coor's light comes from?

"ETBF was identified to cause a clinical syndrome with marked abdominal pain and nonfebrile inflammatory diarrhea in both children (age, 11 years) and adults. Fecal leukocytes, lactoferrin, and pro-inflammatory cytokines (interleukin 8, tumor necrosis factor)‚ well as B. fragilis toxin systemic antitoxin responses‚ increased rapidly in ETBF-infected patients. Evidence of intestinal inflammation often persisted for at least 3 weeks, despite antibiotic therapy."

I bet we have all seen a case or two of this, patients who have diarrhea, "substantial abdominal pain and tenesmus," no fever and negative studies for the cause of the diarrhea. Growing B. fragilis from the stool would be considered normal flora and not considered a pathogen. To confuse issues, evidently up to 40% of controls will carry ETBF (and there is, maybe, an association with bowel cancer, perhaps due to chronic inflammation).

The depressing thing about these ETBF's is that 7% are resistant to metronidazole (Flagyl for those of you who have sold their soul and speak brand name only). I also thought metronidazole resistance was unheard of.

Maybe I finally have a reason to order fecal leukocytes, usually a test that adds nothing to the diagnosis of diarrhea. Negative work up with positive stool WBCs could be a hint of ETBF, although there is no diagnostic tests yet for us lowly clinicians. But if you are going to Bangladesh for vacation, don't consume any stool.

Ha.

Rationalization

Association of Enterotoxigenic Bacteroides fragilis Infection with Inflammatory Diarrhea. (http://www.ncbi.nlm.nih.gov/pubmed/18680416) Clinical Infectious Diseases 2008; 47:797-803.

Water is wet, fire is hot, media is biased

Published Mon, 27 Oct 2008

Captain Renault : I'm shocked, shocked to find that gambling is going on in here!

[a croupier hands Renault a pile of money]

Croupier : Your winnings, sir.

Captain Renault: [sotto voce] Oh, thank you very much.

[aloud]

Captain Renault: Everybody out at once!

~ Casablanca

There is one area of knowledge I know reasonably well, and that is Infectious Diseases. My local newspaper, the Oregonian, usually gets some details wrong on their stories about infectious diseases. One wonders how I can believe the veracity of the rest of the information reported in our fine daily.

The other issue is bias in reporting. It is certainly an issue in clinical trials as the outcome is in part determined by who pays for the study. If the study is funded completely by a pharmaceutical company, it is much more likely to be favorable to the study drug than if the funding is independent. You have to know who is paying for the study to accurately judge the result.

I am always wary of bias in the medical literature, which is part of the reason I have had no interactions and have accepted no gifts from pharmaceutical companies for my entire career. Well, not entirely true. A few years ago the Uni-sin rep sent me a Fleets enema with his company sticker on it. I still display it proudly on my desk.

Unfortunately, the media is not good at reporting the potential sources of bias in clinical studies.

In a recent JAMA study they looked at 306 news articles from a variety of sources and found:

42% did not mention if there was pharmaceutical company funding and

67% referred to the study drug by their brand names more than half the time.

Most did not have written policies to address these issues.

The problem? Given that who provides the funding introduces (probably unconscious) bias into a study, you have to discount at least part of the results based on who is paying for it. It is a curiosity that even in studies where the results do not reach statistical significance between two study drugs, the non-significant data almost always looks better for the study drug. If the potential source of bias is not reported, and, more importantly, the bias explained, consumers are not given important information to help evaluate a drug and its purported efficacy.

When I evaluate a study and see that the funding is all from one company or that the investigators are drug company whores, I mean speakers, I discount the result by a fudge factor, 10 - 20%, with no data to back me up. But it seems about right.

As to brand names vrs generic, I am a bit more skeptical as to any adverse effect for consumers, although I do make the house staff speak only generic. Some patients do think that generic medications are worse than brand name medication, but that is not true. A drug is a drug is a drug. Brand names are just more expensive. And the price? I realize that bringing drugs to market is very expensive and that they need to make back their R&D and make a nice profit as well. That is the American way. But so often the price of unique drugs appears to be made more on what the market will bare rather than what is reasonable, as if I know what reasonable is. And I need to make some pun about a bear market and just can't do it.

Bias is ubiquitous in medical studies, but fortunately physicians are immune to its effects and easily recognize when they are being manipulated. HAHAHAHAHAHAHAHAHAHAHAHAHA.

God, I am funny.

Rationalization

Reporting Pharmaceutical Company Funding and Use of Generic Medication Names (http://jama.ama-assn.org/cgi/content/abstract/300/13/1544). JAMA. 2008;300(13):1544;550.

http://www.medscape.com/viewarticle/581368

I Bow Down to my Bacterial Overlords.

Published Tue, 28 Oct 2008

My professional life is spent killing things: bacteria and fungi and parasites. I am not so certain I kill viruses. If there is indeed karma to be lost or gained in this life, I have piled up a heap o' bad karma with all the microbial death I have wrought in the last 25 years.

Life on earth is mostly single-celled and bacteria predated humans and will live on long after the earth is rendered uninhabitable for humans. Bacteria live damn near everywhere and those that live in harsh environments are called extremophiles. Bacteria live miles underground, in boiling water, and have been found to thrive in the La Brea tar pits. I would not be surprised to find that bacteria are on the moons of Saturn, the polar caps of Mars, or in the most uninhabitable place known, my children's bedroom.

We greatly underestimate the number of organisms out there if we rely on counting just those organisms we can grow. The clinical microbiology lab can grow only a tiny fraction of the bacteria and many species, like humans, cannot be cultivated. Some estimates suggest we can grow about 1% of the bacteria on the planet, and when they use genomic techniques the number of bacteria in always staggering. Most of the biomass of the planet is bacteria, and there are 10 to 100 times as many bacteria in and on us than there are cells of us, most of which we cannot grow and can only find using biogenetic analysis. It is a bacteria's world. James Brown had it wrong.

I was listening to the SGU podcast this weekend and an interview with Phil Plait and I guess the time for bacteria to rule again is sooner than I had thought. I had always thought that life on earth was doomed when the sun went supernova in another 6 billion years or so. A long time. But it turns out the sun is slowly heating up from a natural effect of nuclear fusion, and that in a mere 2 billion years (he said 100 million on the show, but corrected himself on his blog) the oceans will have boiled away.

I know that seems like a long time, especially when me and everyone I know and can know will be dead, gone and forgotten in less than 200 years. Deep time makes the brain hurt. Two billion is a number I can kind of sort of maybe wrap my brain around. One of the few books I have read twice is John McPhee's _Annals of the Former Worl_d, and it will give you a taste of a flavor of a hint of what 2 billion years means.

If Earth's history was a 12 hour clock, it is now 4:30 am. In half an hour, the time of animals and plants will be gone, and in three hours the oceans will be gone. But I bet the bacteria survive until the sun goes nova, and who knows, maybe continuing on past the supernova event, surviving deep in the earth living on chemical reactions instead of photosynthesis, life on earth continuing until the planet reaches the temperature of space.

Not only will I eventually be consumed by the organisms I spent a lifetime killing, in the end they will outlast me and everything we do.

But at least they have me beer.

Rationalization

http://www.washington.edu/newsroom/news/2003archive/01-03archive/k011303a.html

http://www.stephenjaygould.org/library/gould_bacteria.html

A Rich Microbiologic Stew

Published Wed, 29 Oct 2008

I see a lot of intravenous drug abusers (IVDA, the PC term is injection drug users, not abusers, but if the shoe fits...) and I am going to go out on a limb here and suggest that it is not a healthy lifestyle (btw, when do I get a style with my life? At 51 I think I should get to have more than a life, I should have style).

It is estimated that the average drug addict lives 15 to 20 years from the onset of their disease, and I have seen innumerable lives wasted and cut short from all kinds of drug use. Everyone dies, but when a 20-year-old dies of drug use it is particularly sad. I am sure some asshole will read this and say they deserved to die, but dead people have no chance to turn their lives around. With time, many a user can, and will, kick the habit.

Take the recent patient, a 20-year history of heroin and cocaine use, now presents with an abscess from injecting into the soft tissues of the abdominal wall and some sort of abscess in the periphery of her lungs. I am still trying to sort out the potential microbiology of her infections, but with IVDA's the list of potential organisms is long. Heroin is rich in microorganisms:

"Fifty-eight heroin samples were tested by citric acid solubilization and 34 by the MRD suspension technique. Fifteen different gram-positive species of four genera were recognized. No fungi were isolated. Aerobic endospore-forming bacteria (Bacillus spp. and Paenibacillus macerans) were the predominant microflora isolated and at least one species was isolated from each sample. B. cereus was the most common species and was isolated from 95% of all samples, with B. licheniformis isolated from 40%. Between one and five samples yielded cultures of B. coagulans, B. laterosporus, B. pumilus, B. subtilis and P. macerans. Staphylococcus spp. were isolated from 23 (40%) samples; S. warneri and S. epidermidis were the most common and were cultured from 13 (22%) and 6 (10%) samples respectively. One or two samples yielded cultures of S. aureus, S. capitis and S. haemolyticus. The remainder of the flora detected comprised two samples contaminated with C. perfringens and two samples with either C. sordellii or C. tertium. Multiple bacterial species were isolated from 43 (74%) samples, a single species from the remaining 15. In 13 samples B. cereus alone was isolated, in one B. subtilis alone and in one sample B. pumilus alone. C. botulinum and C. novyi were not isolated from any of the heroin samples."

It is why heroin users get Bacillus infections of the eye, Clostridial gas gangrene from skin popping, Staphylococcal endocarditis, polymicrobial soft tissue abscesses, and the occasional wound botulism. Almost any germ can be injected along with the heroin and travel to any body site. It is hard to say that heroin is contaminated with bacteria, as that presupposes a sterile product.

While this study did not culture yeast, there have been outbreaks of Candida associated with heroin. I had a 68-year-old man who started using heroin at age 64 when his son turned him on the joys of being high. He eventually died of Candida parapsilosis endocarditis. I prefer to golf with my kids, although after some rounds I think heroin may be better.

Black tar heroin, a cheap and particularly filthy form of heroin (I saw one chunk of black tar with a banana peel in it), is used for skin popping and is associated with multiple deaths from gas gangrene.

But wait. There is more.

Many heroin addicts lick their needles to help them slide in easier as the needle point dulls, injecting mouth bacteria into their skin or blood stream. Heroin needs to be dissolved before injection, so tap water, toilet water, river water and puddle water have been used by at least one patient of mine. I had one patient who had Acinetobacter bacteremia every time she used the bottled water in the lobby of the local youth hostel, when she switched to burger restaurant water (from the faucet in the bathroom) the bacteremias ceased.

I had one patient who mixed his heroin with tap water, as soon as he got blood return the syringe jammed, so he took off the needle and squirted the blood/water/heroin mixture into a used coffee cup. While he was out and about getting a new syringe the mixture clotted, so he dissolved the clot in spit, then injected it. Curiously, he developed a fever and got sick.

It is a credit to the immune system how rarely these patients get infections. My idea is to call heroin a probiotic and market as an immune system booster to support immunological health. I'll make fortune and my patients will always come back for more.

Rationalization

An investigation into the microflora of heroin Journal of medical microbiology. (http://jmm.sgmjournals.org/content/51/11/1001.short) 2002, vol. 51, no11, pp. 1001-1008.

Postscript: No similar microbiologic studies have been done, to my knowledge on the microbiology of cocaine and meth, but when you see how meth is made, you wonder how anything could survive the manufacturing process.

By the sea, by the sea, its VRE

Published Thu, 30 Oct 2008

This week the national Infectious Disease meetings were in Washington, DC, and this year I couldn't make it. I am stuck with seeing what comes over the interwebs, and it is interesting to see what gets reported from the hundreds of studies presented at the meeting.

Of course the first one I see is a most vexatious report from Bloomberg news, " Beaches in U.S. Host Drug-Resistant Bacteria, Researchers Find." Cue the Drama Prairie Dog (http://www.youtube.com/watch?v=jHjFxJVeCQs).

I do not have the actual study, but evidently the researchers cultured the water and beaches of California and Washington and found VRE, vancomycin resistant Enterococcus.

Let’s see. We have Enterococcus in our stool. We flush it down the toilet where it goes to the processing plant, then into the river and out into the ocean. Would you be surprised to find stool organisms in and on the beaches? Not me, especially an organism as hearty as the enterococcus.

It is not uncommon to find this organism in runoff, especially near the high human density of SoCal.

"Species identification was determined for 1413 presumptive Enterococcus isolates from urban runoff, bay, ocean and sewage water samples. The most frequently isolated species were Enterococcus faecalis, Enterococcus faecium, Enterococcus hirae, Enterococcus casseliflavus and Enterococcus mundtii. All five of these species were isolated from ocean and bay water with a frequency ranging from 7% to 36% . Enterococcus casseliflavus was the most frequently isolated species in urban runoff making up 36-65% of isolates while E. faecium was the most frequently isolated species in sewage making up 53-78% of isolates. The similar distribution of species in urban runoff and receiving water suggests that urban runoff may be the source of Enterococcus. No vancomycin or high-level gentamicin resistance was detected in E. faecalis and E. faecium isolate"

That some VRE are isolated from water is not a surprise, although it is a first to find vancomycin resistance, given that this organism is being heavily selected for with the buckets of vancomycin we are using to treat MRSA. VRE itself is probably not much to worry about in the environment as, despite the quasi-apocalyptic tone of the report, VRE is a risk only to the sickest of the sick in the hospital.

"If people with compromised immune systems, such as those who have undergone cancer therapy, play in sand with the bacteria, they could potentially contaminate themselves or their households, the researchers said."

The only way people can avoid being exposed to the organisms found in human stool is to lock themselves in a bubble and never venture out. Stool organisms are everywhere.

However, more worrisome, is the resistance genes to vancomycin, of which there are at least 5, have been known to jump from the_Enterococcus_ to MRSA, giving us VRSA, vancomycin resistant Staphylococcus aureus. Vancomycin resistant MRSA is a bug to worry about.

Antibiotic resistance genes are common, even in areas that are not exposed to antibiotics. Most antibiotics are based on a bacterial and fungal products, and the organisms have resistance genes to protect themselves from their own antibiotic production and the antibiotic attacks of other organisms.

One study collected dirt across Canada (the country not the yeast), and isolated 480 different strains of Streptomyces, the source for many of our common antibiotics and tested them against 21 different antibiotics. These dirts (I once lost a scrabble game saying the plural of dirt is dirts, and lost the challenge. Stupid Webster. I have vowed to use the word dirts until it becomes part of the language) was pristine and it was unlikely the organisms had ever been exposed to man-made antibiotics. The Streptomyces were resistant to seven or eight antibiotics on average and two were resistant to 15 drugs.

The Borg were half right. Resistance is inevitable. And everywhere.

Rationalization

Species distribution and antimicrobial resistance of enterococci isolated from surface and ocean water (http://www.ncbi.nlm.nih.gov/pubmed/18422952). Journal of Applied Microbiology, Volume 105, Number 4, October 2008 , pp. 1017-1025(9).

Sampling the antibiotic resistome (http://www.ncbi.nlm.nih.gov/pubmed/16424339). D'Costa VM, McGrann KM, Hughes DW, Wright GD. Science. 2006 Jan 20;311(5759):374-7.

Drama Prairie Dog (http://www.youtube.com/watch?v=jHjFxJVeCQs).

Crazy MRSA: A Biochemical Curiosity

Published Fri, 31 Oct 2008

The voices in my head are different than most people's. Mine tell me how wonderful I am, and who am I to disagree? The antipsychotics were never of much help, they made my lips smack too much.

Maybe I will need to get back on my thioridazine (mellaril), an old-school antipsychotic, as the drug, at least in a test tube, has a curious effect on S. aureus methicillin resistance: it reverses methicillin resistance.

Methicillin resistance is mediated by a gene, mecA, that produces penicillin-binding protein 2a (pbp2a), a protein on the cell surface that has a markedly decreased affinity for all beta lactams. Penicillins are a class of antibiotics called beta-lactams. Methicillin was the first anti-staphylococcal beta lactam and not surprisingly, the first anti staphylococcal antibiotic to which S. aureus became resistant. Use it and lose it. But that is why it is called MRSA, and not ORSA or NRSA, the other anti staphylococcal penicillins being oxacillin and nafcillin.

Thioridazine decreases the production of the pbp2a by decreasing the transcription of the mecA gene.

"Transcription of mecA was reduced with increasing concentrations of thioridazine in the presence of a fixed amount of oxacillin. Furthermore, the protein level of PBP2a was reduced when bacteria were treated with the combination of oxacillin and thioridazine."

Thioridazine decreases mRNA levels of the beta-lactamase gene. Whether this is useful is not known, but the effect does occur at drug levels that are relevant for antipsychotics. It just might be worth suppressing the voices, which tell me such good things, to treat an MRSA.

Rationalization

Reversal of methicillin resistance in Staphylococcus aureus by thioridazine (http://www.ncbi.nlm.nih.gov/pubmed/18836185). J Antimicrob Chemother. 2008 Oct 3.

Ocean Spray. It’s not Just for Cranberry Juice

Published Sun, 02 Nov 2008

Halloween is a busy day with two kids that live to trick or treat and we always have a Halloween party with real food before they disappear into a week of sugar fueled lethargy. And of course, the one day I needed it to be slow, it was busy, and I had two consults with infections due to Serratia marcescens.

S. marcescens is not that unusual as a pathogen, causing hospital acquired infections of all kinds. What is interesting about the bug is it makes a reddish-orange pigment called prodigiosin. It can kind of look like blood.

It is the prodigiosin pigment that makes Serratia easy to identify, much to the distress of San Francisco.

In the 1950's the military wanted to know how biologic warfare agents were spread in an urban environment. In Operation Ocean Spray (nothing to do with the color of cranberry juice) they placed agar plates throughout San Francisco and sprayed Serratia over SF from offshore. Some reports say they released balloons filled with the organism and popped them over the city. Serratia would be easy to track through the city since all they had to do was look for red/orange bacteria growing on the drop plates. The military thought Serratia was not a pathogen, and they were wrong. Shortly thereafter there was an increase in Serratia infections in the Bay area, 11 patients had pneumonia with one death from endocarditis.

One report suggests that people were breathing 5000 bacteria or more for hours after the spraying and the spraying covered about 117 square miles.

So when the wackaloons say the condensation trails (Con Trails) from airplanes are not water, but are really the government spraying us with bacteria and nanobots, it is hard to counter with the assertion that the government would never do anything so stupid.

Fast forward a decade and the increase in the drug culture. San Francisco became the home of Serratia endocarditis in IVDA's, presumably as it was in the water of the Bay area. I have heard, but cannot confirm, that the strains that caused endocarditis were not the same as the strain sprayed over San Francisco.

But that is just what the men in black would want you to think.

Rationalization

Serratia marcescens endocarditis: a regional illness associated with intravenous drug abuse. (http://www.ncbi.nlm.nih.gov/pubmed/1106290)Ann Intern Med. 1976 Jan;84(1):29-35.

Tony Montana would not like these studies

Published Mon, 03 Nov 2008

It has been suggested that cockroaches will some day rule the world. They are so hardy, so resilient, that they will survive a nuclear holocaust. I say look out for them today.

This study came out of Ethiopia where they looked at cockroaches as a source for intestinal parasites. Now if you think you are having a bad day, think of these poor researchers. They trapped 6480 cockroaches of three different cockroach species. Ick.

Then they did " microscopic examination of the external body washes of pooled cockroaches and individual gut contents ."

What did you do today? Body washed cockroaches. Followed by a light massage and manicure.

They also did a microscopic evaluation of the guts of the cockroaches, although how they made the tiny endoscopes I do not know.

And they found pathogens:

"..cockroaches are carriers of Entamoeba coli and Entamoeba histolytica/dispar cysts as well as Enterobius vermicularis, Trichuris trichiura, Taenia spp. and Ascaris lumbricoides ova."

All parasites that infect the human colon and cause diarrhea.

This is not the first time pathogens have been found in cockroaches. In another study 305 cockroaches were evaluated for bacterial pathogens and Escherichia coli, Streptococcus Group D, Bacillus spp., Klebsiella pneumoniae, Proteus vulgaris, Citrobacter freundii, Staphylococcus aureus , and Streptococcus non-group A and B were found. Others have found Salmonella in/on cockroaches associated with an outbreak.

Yet another study found Candida, Aspergillus and Penicillium associated with the wee beasties.

Cockroaches live in intimate contact with humans and they have our bacteria, fungi, and parasites. They are more than disgusting. Bear Grylls better be careful what he eats, although only 30 of the 4000 species are human pests.

It is why I make a point of keeping my cockroach consumption to a minimum.

Rationalization

Transactions of the Royal Society of Tropical Medicine and Hygiene Volume 102, Issue 11, November 2008, Pages 1143-1147. Cockroaches as carriers of human intestinal parasites in two localities in Ethiopia. (http://www.ncbi.nlm.nih.gov/pubmed/18579170)

Vector Borne Zoonotic Dis. 2008 Oct 30. A Survey on Species and Prevalence Rate of Bacterial Agents Isolated from Cockroaches in Three Hospitals. (http://www.ncbi.nlm.nih.gov/pubmed/18973441)

Mycoses. 2006 Jan;49(1):23-5. Cockroaches as carriers of fungi of medical importance. (http://www.ncbi.nlm.nih.gov/pubmed/16367814)

Influenza deaths

Published Tue, 04 Nov 2008

It’s flu season. Quiet so far, most states with flu have only had sporadic cases.

Got my vaccine. You?

People die of influenza, both directly from the virus and from secondary bacterial infections. Some years have more deaths than others, and in modern times nothing has surpassed the mortality of the 1918-1919 influenza pandemic, where about 1/5 of the world was infected and 50 million died worldwide, 675,000 in the US.

Should history repeat itself (which it NEVER does, right?), they expect 2 million US deaths. What was the cause of death in the 1918 pandemic? The conventional wisdom is that since the 1918 pandemic was an avian (bird) flu, it was a primary influenza infection that killed everyone. This theory is supported in part by the fact that the reconstituted virus is particularly virulent in mice. BTW, Decon is cheaper.

But men are not mice, John Steinbeck not with standing.

So why did all those people die?

"In the present study, we have examined recut tissue specimens obtained during autopsy from 58 influenza victims in 1918-1919, and have reviewed epidemiologic, pathologic, and microbiologic data from published reports for 8398 postmortem examinations bearing on this question."

Those studies that reported the bacteriology of the patients who died almost always found pathogens: Streptococcus pneumoniae (24%), Streptococcus hemolyticus (17%), Staphylococcus aureus (9%), Bacillus influenzae (10%) and a smattering of other pathogens. Looks like those microbiologists have been changing names for over a century.

They also reviewed the lung specimens and they had the typical histopathologic changes of bacterial pneumonia. Death from bacterial superinfection was thought to be the case at the time:

"Although the cause of influenza was disputed in 1918, there was almost universal agreement among experts that deaths were virtually never caused by the unidentified etiologic agent itself, but resulted directly from severe secondary pneumonia caused by well-known bacterial pneumopathogens‚ that colonized the upper respiratory tract (predominantly pneumococci, streptococci, and staphylococci)."

Good news, right? We have antibiotics, and they didn't, so we will not die. I would not be so sanguine. Antibiotic resistance continues to increase and I continue to worry about the MRSA sweeping the world. There was a recent outbreak of linezolid resistant MRSA that killed half the patients. Resistance to daptomycin, our other MRSA drug, develops on therapy and, due to poor tissue penetration, cannot be used for pneumonia. While only 10% or so of the deaths in 1918 were due to S. aureus, I have seen a few post-viral secondary infections due to MRSA and the rapidity with which it killed my patients despite the best antibiotics we have was sobering. Not to imply that I wasn't sober.

A bad influenza year and relatively widespread MRSA colonization could be a perfect storm for a marked increase in pneumonia we can't treat and influenza deaths.

Glad I got my vaccine. You?

Rationalization

Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic : Influenza Implications for Pandemic Influenza Preparedness (http://www.ncbi.nlm.nih.gov/pubmed/18710327). The Journal of Infectious Diseases 2008; 198:962–70.

"Outbreak of Linezolid-Resistant Staphylococcus aureus in Intensive Care" ICAAC- IDSA 2008; Abstract C2-1835a.

Rash decisions

Published Wed, 05 Nov 2008

Fever and a rash. A common infectious disease problem. Most rashes are often neither diagnostic nor important, a curious epiphenomenon of the underlying infection.

There is one rash that makes me nervous: petechia. The patient this morning had a sudden onset of fevers and rigors shortly followed by a progressive petechial rash.

Cue the music from Jaws, as the issue of Neisseria meningitidis rears its ugly pili. Nasty bug, it can kill almost as fast as a great white. I have seen people go from normal to dead in less than 8 hours from this organism.

There are curious epidemiologic features around Neisseria meningitidis. The main disease causing serotypes are A,B,C, W-135, and Y. What happened in the lab for D through V and W-1 to 134 I have never discovered. Wolverine, beware, there is a new strain of meningococcus, X, that in 1992 accounted for over half of the cases in Niger; it had been considered a relatively non-virulent strain in the past. Does Speed Racer suspect?

The vaccine does not cover group B meningococcus. Cuba had an outbreak with group B and they developed a vaccine that has some efficacy. For reasons I cannot discover, Cuba has been unwilling to share the vaccine with the US. Go figure. Molecular epidemiology suggests Cuba did share the organism with the US. Outbreaks of group B meningococcus in Florida are thought to have reached the US with Cuban immigrants. Another failure of immigration officials. Never would have happened in Arizona.

Group B is thought to have started in Europe in the 1970's, then to Cuba, to South America (thanks Che) and then to my own state of Oregon, where we had an outbreak in 1992. We continue to have issues with group B disease.

Fortunately this bug is still easy to kill. Antibiotic resistance is reported, but is rare.

The other curiosity is there are a wide variety of reasons people can get ill with meningococcus: complement deficiencies, alternations in Toll-like receptors, but my favorite is variations in snot. If you have the wrong kind of snot, you are more likely to get meningococcus and die:

"Meningococcal disease occurs after colonization of the nasopharynx with Neisseria meningitidis. Surfactant protein (SP)-A and SP-D are pattern-recognition molecules of the respiratory tract that activate inflammatory and phagocytic defenses after binding to microbial sugars. Variation in the genes of the surfactant proteins affects the expression and function of these molecules. METHODS: Allele frequencies of SP-A1, SP-A2, and SP-D were determined by polymerase chain reaction in 303 patients with microbiologically proven meningococcal disease, including 18 patients who died, and 222 healthy control subjects. RESULTS: Homozygosity of allele 1A1 of SP-A2 increased the risk of meningococcal disease (odds ratio [OR], 7.4; 95% confidence interval [CI], 1.3-42.4); carriage of 1A5 reduced the risk (OR, 0.3; 95% CI, 0.1-0.97). An analysis of the multiple single-nucleotide polymorphisms in SP-A demonstrated that homozygosity for alleles encoding lysine (in 1A1) rather than glutamine (in 1A5) at amino acid 223 in the carbohydrate recognition domain was associated with an increased risk of meningococcal disease (OR, 6.7; 95% CI, 1.4-31.5). Carriage of alleles encoding lysine at residue 223 was found in 61% of patients who died, compared with 35% of those who survived (OR adjusted for age, 2.9; 95% CI, 1.1-7.7). Genetic variation of SP-A1 and SP-D was not associated with meningococcal disease.

CONCLUSIONS: Gene polymorphism resulting in the substitution of glutamine with lysine at residue 223 in the carbohydrate recognition domain of SP-A2 increases susceptibility to meningococcal disease, as well as the risk of death ."

Life and death often hinge on little things like a glutamine instead of a lysine in your mucous.

Patient today is fine thanks to prompt diagnosis and antibiotics.

Rationalization

Serogroup B Meningococcal Disease -- Oregon, 1994 (http://www.cdc.gov/mmwr/preview/mmwrhtml/00035870.htm).

Clin Infect Dis. 2006 Dec 1;43(11):1426-33. Genetic polymorphism of the binding domain of surfactant protein-A2 increases susceptibility to meningococcal disease. (http://www.ncbi.nlm.nih.gov/pubmed/17083016)

Meningococcal Meningitis: Unprecedented Incidence of Serogroup X-Related Cases in 2006 in Niger (http://www.ncbi.nlm.nih.gov/pubmed/17278055). Clinical Infectious Diseases 2007; 44:657-63.

Honey

Published Thu, 06 Nov 2008

Bees have a bad name amongst us skeptically inclined. Senator Harkin was under the delusion that bee pollen cured his hay fever and when a senator gets a bee in his bonnet, they pass bills. The result was The National Center for Complementary and Alternative Medicine (NCCAM), one of the biggest wastes of tax dollars ever. I know that you can't really blame the bees, they were not responsible, but still. With no irony, my spell checker suggests Occam for NCCAM.

Today I saw a lady with severe arterial insufficiency and as a result chronic lower leg ulcers that continually get super-infected. What to do. Long-term antibiotics are problematic as they lead to resistance and allergic reactions. The wound care people had her on Silvadeen/charcoal patches that were quite painful to take off. I gave my usual suggestion for a different form of wound care, which resulted in a rolling of the eyes.

I was told as a medical student by a plastic surgeon never put in a wound what you wouldn't put in your eyes. You don't want to damage new tissues, he said, and that's what most wound care does. As a result, for years I packed wounds with contact lenses. Soft, not hard.

In the first year of my practice I was writing a note on the nursing station when I heard a patient start screaming. This was before I learned to ignore the suffering of others as I became a full-fledged member of the medical-industrial complex. Investigating, I discovered that her surgeon had ordered sugar for the wound and the kitchen had mistakenly sent up salt. Talk about a metaphor come to life.

Upon further research I found there is a reasonably good literature to support both granulated sugar and honey in the treatment of wounds, ulcers and burns, and the data suggests that both therapies are equal to, if not better than, standard medications. Not a great literature, but good enough to draw some tentative conclusions.

Don't bacteria like sugar? Not at the concentrations found in honey. Ever been to France and seen the preserved fruits? They preserve them in sugar. Same reason there is sugar in strawberry PRESERVES. It’s why they are not called strawberry rotten from the Staphylococcus and E. coli.

Sugar and honey are inexpensive. They kill all the bacteria that often are pathogenic on the skin. It washes off painlessly. It doesn't kill new tissues and it absorbs all the gunk make by the wounds and bacteria. And you get to participate in the naturalistic fallacy with your patients. It is the wonder drug that works wonders. No, wait, that's aspirin. I doubt it is as good as a wound vac, but not everyone can afford a wound vac.

How is honey supposed to work?

"Honey has several well-known properties responsible for its antimicrobial activity. These include a high osmolarity due to the high concentration of sugars ( 80% wt/vol), a low pH (3.2 - 4.5 for undiluted honey), and the production of hydrogen peroxide, which, after dilution of honey, is produced by glucose oxidase originating from the bees. In addition, unknown Floral or bee components contribute to the activity."

Is it effective in wounds and burns? Yes, he says with a tentative quaver in his voice. Pubmed (like the verb Google) honey or sugar as a search term and you will find an interesting literature, filled with studies that are not all that great, but suggestive. Even the irascible Cochrane reviews concludes that

"Honey may improve healing times in mild to moderate superficial and partial thickness burns compared with some conventional dressings. Honey dressings as an adjuvant to compression do not significantly increase leg ulcer healing at 12 weeks. There is insufficient evidence to guide clinical practice in other areas."

Not a ringing endorsement for honey dressing, I will grant you, but I often chose the soup not the salad. But if you read all the literature, it is suggestive.

I found the CID article this year interesting on the effects of honey on skin pathogens. It kills them dead.

"Antibiotic-susceptible and resistant isolates of Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecium, Escherichia coli, Pseudomonas aeruginosa, Enterobacter cloacae, and Klebsiella oxytoca were killed within 24 h by 10% - 40% (vol/vol) honey. After 2 days of application of honey, the extent of forearm skin colonization in healthy volunteers was reduced 100-fold , and the numbers of cultures were reduced by 76%."

It is an interesting literature, made difficult by often small numbers and poor design and the lack a placebo control that looks like honey but isn't. Many of my patients have no insurance, little money, and fewer resources. There is enough data and biologic plausibility that I suggest it to some of my patients, although I spend more time on the caveats than usual.

The most dangerous words in medicine are "In my experience" and in my experience honey works. I am, of course, deluding myself. But at least there is some data and, unlike the homeopaths, I am not diluting myself.

Rationalization

Cochrane Database Syst Rev. 2008 Oct 8;(4):CD005083. Honey as a topical treatment for wounds (http://www.ncbi.nlm.nih.gov/pubmed/18843679).

Medical-Grade Honey Kills Antibiotic-Resistant Bacteria In Vitro and Eradicates Skin Colonization (http://www.ncbi.nlm.nih.gov/pubmed/18433338). Clinical Infectious Diseases 2008; 46:1677 - 82.

Outbreaks

Published Sat, 08 Nov 2008

I get to investigate infectious outbreaks. Most outbreaks occur in relative slow motion, a case this week, a case next week, a case the following week of the same organism or the same site. I help try and figure out why.

Some outbreaks come with the force and suddenness of a flash flood. Like Norovirus. This is the virus made famous by Disney cruises. Ever notice that Steamboat Willie didn't show a toilet? Walt wasn't looking after his creations. No place for Mickey to go should he dine in the buffet. I have dealt with several Norovirus outbreaks in various hospitals, where patients and staff come down with nausea, vomiting and diarrhea all within a few days.

There are many causes of infectious diarrhea and they all have their pathogenic peculiarities. Norovirus is no different.

The first is that Norovirus recently voted the world’s most infectious virus. It was on the November ballot as part of the Green Party candidate. Didn't you see it? It takes one viral particle to cause disease. One.

"We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date."

That’s it. It beats out Shigella, which takes as few as 10 organisms to cause disease. That’s infectious.

The second issue about Norovirus is how hardy it is. People have diarrhea, like shrimp and oyster fisherman (shouldn't you shrimp for shrimp and oyster for oysters if you want to be consistent?), who crap into the sea and Norovirus gets in the water and is filtered and concentrated in oysters. People then collect oysters, freeze them and send them all over the world. Problem is, freezing doesn't kill the norovirus. Neither does cooking.

"Norovirus is heat resistant, with viable virus surviving after heating at 60°C for 30 min. In other outbreak investigations, people eating well cooked or overcooked shellfish had a risk of becoming ill that was similar to that for people who ate raw shellfish. It is likely that the time and temperature of cooking required to inactivate norovirus in oysters may render the food unpalatable to consumers."

I will eat damn near anything, including raw horse when I was in Japan, but raw oysters are one of the few things I have not tried. I have also never eaten tongue, because they thought that the tongue would taste me while I tasted tongue. Freaks. Me. Out. Man.

The final cool thing about Norovirus is that it mutates in response to the host's antibody reaction to it. You get infected, your body develops antibody to the proteins that makes the virus virulent. The virus escapes the immune system by mutating at the sites where the antibodies bind. And the more the organisms can mutate, the longer the virus can be excreted in the stool.

"The greatest number of amino acid mutations in a given patient was 11; they were detected in NoV isolates recovered over a 119-day period and were mapped to positions at or near putative antigenetic sites. In the patient with most severe immune dysfunctions, only 5 amino acids mutated over 182 days, suggesting immune-driven selection."

So many cool things in one virus: infectivity, world trade, evolution. Now if someone could suggest a good book, I have to be heading to the toilet for a while.

Rationalization

Journal of Medical Virology Volume 80 Issue 8, Pages 1468 - 1476 Published Online: 12 Jun 2008 Norwalk virus: How infectious is it? (http://www.ncbi.nlm.nih.gov/pubmed/18551613)

Clinical Infectious Diseases 2007;44:1026;031. Internationally Distributed Frozen Oyster Meat Causing Multiple Outbreaks of Norovirus Infection in Australia. (http://www.ncbi.nlm.nih.gov/pubmed?term=17366444)

High Prevalence of Prolonged Norovirus Shedding and Illness among Hospitalized Patients: A Model for In Vivo Molecular Evolution. (http://www.ncbi.nlm.nih.gov/pubmed?term=18774885) J Infect Dis. 2008 Oct 1;198(7):994-1001.

Peer Pressure

Published Sun, 09 Nov 2008

This week I went to Employee Health and commandeered the influenza vaccine cart. We are a bit over 50% for employee flu shots, and I think it is important for as many people as possible to get the shot. It allows me to inject those government sponsored tracking nanobots.

Then I wandered from station to station offering flu shots.

Who, I would demand loudly, dares to refuse and flu shot from the great and powerful Chief of Infectious Diseases?

Most said they already had the shot, but in two hours I managed to give 13 flu shots. Actually, they are anti-flu shots. Sometimes a patient asks for something for pain, and I think, well, you could stub your toe. English is often imprecise.

It was fun. People were shocked that I was actually giving a shot. Several people thought I was a nurse, since a doctor giving a shot, actually doing the work instead of writing an order and walking away, is rare. Several nurses complimented me on the quality of my injection; I assume they were incredulous that I was competent to give a shot. Like a bear riding a bicycle, it is not that I do it well, but that I could do it at all.

I had the opportunity to talk to people about who should get the flu shot and about the disease. On every unit there was one person who would not make eye contact with me nor offer to get the shot. I presume they are the people who will not get the flu shot no matter what the reason but were unwilling to talk to the all-knowing Oz.

There is one nurse I still need to get. Evidently she NEVER gets the flu shot, and is proud of it, but she was off a few days. I will not put her name on the blog, but everyone on the unit knows I am gunning for her.

If there is anyone reading this who is an ID doc, I suggest you put aside a couple of hours one day and to do the same thing at your hospital. It will make an impression as to the importance of the flu shot and you will have a good time.

Down with Meningitis

Published Mon, 10 Nov 2008

A busy call weekend, with one consult on a case of bacterial meningitis due to S. pneumoniae. Not a surprise in that strep pneumo, as we call it in the biz, is the number one cause of meningitis in the adult. It was the patient that made the disease a curiosity. He had Down’s syndrome.

It is the Down's that make the case of interest.

A variety of functional immune deficiencies have been described in Down's:

- Decreased neutrophil and monocyte function (chemotaxis, phagocytosis and the oxidative burst), in some studies but not others.

- Increased IgG1 and IgG3 but decreased IgG2 and IgG4.

- Decreased specific antibody responses upon immunization. IgG has 4 subtypes and IgG2 is the antibody needed for a response to carbohydrate antigens, which is the one that is needed to kill pneumococcus.

Lots of good reasons to get infected. Downs, unfortunately, affects more than just the brain.

I also expect a resistant organisms as the patient developed the meningitis on cephalexin. And indeed it was resistant to penicillin.

That's four cases of meningitis this week, each from a different organism: viral, meningococcus, S. pneumoniae and a strep the lab is still identifying.

The wonder drug that works wonders. Wait. That's aspirin.

Published Tue, 11 Nov 2008

Statins are in the news today for the relatively unimportant reason that they prevent death from myocardial infarction, especially in a subgroup of people who have an elevated C reactive protein.

C-reactive protein (or CRP, and since it is ReActive, shouldn't the proper acronym be CRAP?) is a protein that is elevated when you are inflamed. Many processes will elevate your CRP, from infection to collagen vascular disease, but not being inflamed by religious or political fervor.

Inflammation is good in response to infection, but continued inflammation has the potential to cause vascular diseases and acute inflammation (such as pneumonia and urinary tract infections) is well known to increase the risk of angina, heart attacks, strokes, and pulmonary embolism.

Statins lower cholesterol, but probably more importantly statins work as an anti-inflammatory by a variety of mechanisms too complex for my tiny brain to comprehend.

What kills people with infections is often an overly brisk inflammatory response. Inflammation is like a Bordeaux: a little is good, a lot can kill you. Interestingly, retrospective studies have consistently demonstrated that people who get pneumonia while on statins have a decreased mortality compared to those not on statins.

Same result with a recent retrospective study:

They looked at 29,900 adults hospitalized with pneumonia of which 1372 were taking statins on admission.

"At 30 days, those patients taking statins who were hospitalized with pneumonia had a 31% lower risk of dying compared with patients not taking statins. By 90 days, the reduction in mortality was maintained, with those taking statins having a 25% lower risk of dying compared with those not on statin therapy."

Bad word, retrospective. What is needed is a randomized prospective placebo controlled trial to see if the results are really truly true.

There have also been studies with decreased mortality and sepsis for patients on stains.

The epidemiological data looks good so far, so when you wash down that aspirin a day with a glass of red, include a statin so when you pass out drunk and get a pneumonia, you are less likely to die.

Rationalization

Chest. 2003;124:740-743. Statins, Inflammation, and Sepsis. (http://chestjournal.chestpubs.org/content/124/2/740.abstract?ijkey=9e75abe5dfb0ceadbc8ec72bfd6b372181ebbffe&keytype2=tf\_ipsecsha)

Preadmission use of statins and outcomes after hospitalization with pneumonia (http://www.ncbi.nlm.nih.gov/pubmed/18955636). Arch Intern Med. 2008;168:2081-2087.

Statin Use Reduces Mortality After Hospitalization for Pneumonia (http://www.medscape.com/viewarticle/582611).

Second to none

Published Wed, 12 Nov 2008

Health care in the US is second to none. Probably because we are 29th.

"Among 33 industrialized nations, the United States is tied with Hungary, Malta, Poland and Slovakia with a death rate of nearly 5 per 1,000 babies, according to a new report. Latvia's rate is 6 per 1,000."

USA. USA. USA.

It is not just infant mortality. A fifth of US citizens do not have health care, and it you do not have insurance you should avoid the opportunity to get sick. The nice thing about the US health care 'system' is that I get to take care of all sorts of illnesses that people in advanced societies, who actually work together to help each other, do not get an opportunity to see.

Untreated hypertension, untreated diabetes, untreated syphilis, progressive HIV, advanced tuberculosis.

Because some people did not have health care and live from paycheck to paycheck, they let their health slide, sometimes ending up with advanced disease, sometimes dying. People die every now and then because they can't afford health care, often of infections. I sometimes want to put on the death certificate for cause of death: uninsured and too proud to seek care.

I don't have to travel back in time or go to Third World countries to see diseases that should be of historical interest in an advanced society.

Like today. A patient with an infected hip fracture who is insane and who did not seek health care.

In the olden times, when there were no antibiotics or surgery, patients with bone infections developed a large mass of scar tissue around the infected fracture that subsequently calcified. It would be a mass of calcium surrounding the fracture two or three times the size of the normal bone. That is what my patient had. A huge, calcified callus over the fracture. It is rare to see this response in the 21st century since we treat infections and fractures. At least if you have sanity and money. If you lack one or both, you get the rare opportunity to develop findings that were common in the 19th century.

Google the Flu

Published Thu, 13 Nov 2008

Google, as you may not know, tracks everything. Every search term, every search. They say the data can't be tracked back to you, and I trust Google. The home page is so cute, with the changing logo for every holiday. How could they do anything evil with their data?

Google does have a cool infectious disease application of all that data collection.

If people get the flu or there is flu in the community (you know, the dumb asses who didn't get the vaccine) people look for information about the influenza. And the first place they go is Google.

Google keeps track of those searches and they reported today that searches for flu, muscle aches‚ or fever‚ go up dramatically when there is flu circulating in the community and the searches go up about two weeks before the usual reporting mechanisms discover that flu is in the community. They used data going back to 2003 and the search terms paralleled the standard reporting data very closely. It appears that for flu, Google searches are a good early warning system for disease activity.

The data has yet to be published in a peer review journal, although the NY Times suggests they are looking at Nature for publication.

This is not the first time surrogate makers have indicated the presence of an infection outbreak.

Over-the-counter cold remedy sales increase when there are influenza-like illnesses in the community and sales of antidiarrheals such as Kaopectate increase when there have been cryptosporidia outbreaks, sales of each preceding recognition of the outbreak.

I expect clever people will discover other surrogates that can be tracked for early warning of outbreaks. As I type this it looks like the top Google search terms are Lady Antebellum, Martina Mcbride, Miranda Lambert, Rodney Atkins, Kelly Pickler and George Strait, suggesting we are about to have an outbreak of country music. The horror, the horror. If you thought Norovirus is bad, just you wait.

Rationalization

Google Flu Trends http://www.google.org/flutrends/

NYT: Google Uses Searches to Track Flu’s Spread (http://www.nytimes.com/2008/11/12/technology/internet/12flu.html)

MMWR: Monitoring Over-The-Counter Medication Sales for Early Detection of Disease Outbreaks --- New York City (http://www.cdc.gov/mmwr/preview/mmwrhtml/su5401a9.htm)

Vitamin D: Supporting Immune Health.

Published Fri, 14 Nov 2008

The rains stopped today. It has been Oregon weather: dark and wet, with seemingly endless rains. It has been weirdly warm for November; it hit 66 yesterday. It is like living in a Ray Bradbury story, the one where a planet has 4 hours of sunshine every 100 years.

Rain and clouds mean no sun and no sun means low vitamin D. Unless you eat lots of ice cream. I get frequent flyer miles from Baskin Robbins.

Today was a hip fracture with a wound infection in an old woman. As part of the work up on the fracture service, she had a vitamin D level what was not measurable. No surprise for an Oregonian, especially the institutionalized elderly, who do not get out in the sun, preferring to drive around the city at 20 miles an hour no matter that the posted speed limit.

Vitamin D is required for bone metabolism, so association with hip fracture is no surprise. What is interesting is that Vitamin D is also an important adjunct of the immune system, and there is growing evidence that deficiencies in vitamin D increase infections.

Vitamin D deficiency is associated with reactivation of TB, developing TB, viral upper respiratory infections, pneumonia, and bacterial infections in atopic dermatitis. Variations in vitamin D receptors (polymorphisms) are also associated with upper respiratory tract infections and TB.

The mechanism by which vitamin D is used by the immune system and the risks for infection are in their infancy. How much the lack of vitamin D is associated with post-operative hip infections, I cannot say. But I bet it is a factor and a future paper or someone.

There was a little bit of sun today. I thought about taking off my shirt to get a dose of sun and boost my vitamin D levels. Nope. Wasn't worth making other people sick. We are just getting over the Norovirus outbreak. I'll eat ice cream instead.

Rationalization

Thorax. 2007;62:1003-1007. Reactivation of tuberculosis and vitamin D deficiency: the contribution of diet and exposure to sunlight (http://www.ncbi.nlm.nih.gov/pubmed/17526677).

American Journal of Clinical Nutrition, Vol. 86, No. 3, 714-717, September 2007. An association of serum vitamin D concentrations < 40 nmol/L with acute respiratory tract infection in young Finnish men. (http://www.ncbi.nlm.nih.gov/pubmed/17823437)

Vitamin D May Help Prevent Infections With Atopic Dermatitis. http://www.medscape.com/viewarticle/581922 .

All Summer in a Day. (http://www.wssb.wa.gov/content/Classrooms/tate/content/freshman/All Summer In a Day/story.htm) By Ray Bradbury.

Often in error, never in doubt

Published Sat, 15 Nov 2008

On rounds today I got a curbside, someone asking me a question in an informal way.

One of the ICU nurses wanted to know what was going on with her eight-year-old. I get many such questions every day as I walk around my hospitals.

Her eight-year-old had played a particularly muddy soccer game at one of the local schools over the prior weekend and she noted that his shoes, which had been sitting uncleaned in the garage all week, now smelled like cat piss. Her words. I know of no infection that smells like cat piss.

And more interestingly her son was covered with pustules that looked like chickenpox, which he couldn't have because he had the disease and the vaccine twice. Look, I just report what people tell me.

We talked about it for a bit, how muddy the field was, and how my son was playing tomorrow, and I hoped the field dried out and I was uncertain what her son had and it didn't ring any bells. Then, as I walked away, a bell rang.

There is some infection associated with muddy Australian rugby players I said. What is it?

And where in the hell did that thought come from. That is one of the issues I have working in a teaching hospital. Some of the ideas I come up with do not arise in the conscious mind, and my later explanation of the diagnosis is an after-the-fact rationalization. Most of my best diagnoses come from some part of my brain that I have no control over. The thought burbles up through my brain like a bubble in a tar pit.

Pop. The patient has...

Google to the rescue. Google often makes me look smarter than I am, a quick search and the instant appearance of genius. Don't tell anyone that's my secret.

I entered Australia, rugby, mud, infection and viola (I can spell instruments better than French).

Outbreak of Aeromonas hydrophila Wound Infections Associated with Mud Football (http://www.ncbi.nlm.nih.gov/pubmed/15095211). Clinical Infectious Diseases 2004; 38:1084. I read this article one time, four years ago. Where is that memory stored and how did I access it? Got me.

I was almost right. It was mud football, not rugby, but almost the same thing.

"On 16 February 2002, a total of 26 people presented to the emergency department of the local hospital in the rural town of Collie in southwest Western Australia with many infected scratches and pustules distributed over their bodies . All of the patients had participated in a mud football, competition the previous day, in which there had been > 100 participants. One patient required the removal of an infected thumbnail, and another required surgical debridement of an infected toe. Aeromonas hydrophila was isolated from all 3 patients from whom swab specimens were obtained. To prepare the mud football fields, a paddock was irrigated with water that was pumped from an adjacent river during the 1-month period before the competition. A. hydrophila was subsequently isolated from a water sample obtained from the river. This is the first published report of an outbreak of A. hydrophila wound infections associated with exposure to mud."

Is this what the kid has? I don't know. There are other organisms that can cause pustules and folliculitis, some of which are associated with mud or water. I asked her to take her kid to the doc to culture the pustule. Perhaps it is another water-borne organism. I printed off the reference for her to take to the pediatrician.

I enjoy swinging for the fence for a diagnosis. People remember if you are spectacularly right. I am more often wrong than right, but everyone is always making a wrong diagnosis in medicine. Good docs are not those that are initially right, but those that do not stick to the initial ideas when they are wrong.

I hope I get a culture on this one. And the difference between Oregon and yogurt? Yogurt has culture.

Postscript: the kid got better and the pustule was never cultured. Crap.

Housing Market

Published Mon, 17 Nov 2008

The housing market is tanking, people cannot afford their mortgage payment and are losing their homes. Abandoned homes are not cared for. In California, that means that the backyard pool is also not being cared for. No chlorine, a big pool of stagnant, warm water is an ideal breeding ground for mosquitos and mosquitos are a vector for all sorts of diseases.

Like West Nile Virus.

And wouldn't you know it, Bakersfield, California, has a problem.

Despite the unusually dry and hot conditions, the mosquito populations in Bakersfield are booming.

The dry conditions have also led to a decrease in house finch populations that had previously had high herd (flock?) immunity to West Nile but a boom in the population of previously uninfected western scrub jays and house sparrows, which had no herd (flock?) immunity.

As a result, there was a West Nile epidemic in non-immune Jays and Sparrows, who died, then the mosquitos, needing to eat and unable to find birds to feed on, turned to humans. At the peak of the epidemic, 19 out of every 1000 mosquitos had West Nile and there was a 280% increase in human West Nile cases.

At the same time Bakersfield had a 300% increase in loan defaults leading to pool and hot tubes not being cared for. I guess for every 1% load default there is a 1% increase in West Nile.

"An aerial photograph of a representative Bakersfield neighborhood shows the extent of the problem, with 17% of the visible 42 pools and Jacuzzis appearing green and likely producing mosquitoes."

There is also a shift in the mosquito population as the pools are left untended.

"Alarmingly, during 2008, many of these unmaintained pools previously positive for Cx. p. quinquefasciatus were now occupied by Cx. tarsalis, a more competent vector of WNV than Cx. p. quinquefasciatus."

The abbreviations and Latiny words are the names of the mosquito strains

When I was a kid I thought the show Connections was the coolyest series ever, and I still love how odd connections can end up in an outbreak of disease in a Suessian cascade of events. Imagine what would have happened if a bug had sneezed

In this case it was all because of the financial meltdown.

Rationalization

Delinquent Mortgages, Neglected Swimming Pools, and West Nile Virus, California. (http://www.ncbi.nlm.nih.gov/pubmed/19239785) Emerging Infectious Diseases Vol. 14, No. 11, November 2008

The Continued MRSA Brouhahahahahahaha

Published Tue, 18 Nov 2008

There is a slow but continued pressure to do something about MRSA.

No doubt that MRSA is a problem. I cannot reliably kill it with the current antibiotics and it is becoming resistant to alternative agents.

Just this month there was an outbreak of linezolid resistant MRSA that killed half the patients who developed it. Not a surprise. Linezolid resistance should be easy enough for the organism to develop.

So we have to do something. But what?

Check patients for MRSA and isolate them when they are admitted? To adequately check each patient for MRSA you would have to culture nose, throat, rectum and skin. Four cultures. And if you were to use one swab to obtain 4 specimens, in what order do you do the collecting? The CDC guidelines say once an MRSA, always an MRSA and isolate the patient. Unlike love, MRSA is forever.

The problem is that Staph is more or less normal flora. It comes and goes depending on local conditions, and in the end it will be futile to try and isolate and eradicate normal flora. The patient who is MRSA negative today is positive tomorrow from a visitor. The doctor who is MRSA negative today is positive next week from the handshake from his psoriatic neighbor. Staph is everywhere you don't want it to be, the anti-VISA card.

Isolation of patients is not without its dangers. Patients who are in isolation get less care and have more complications and falls. No good deed ever goes unpunished.

The problem is not MRSA, which is a sentinel chicken of bad infection control practices. If there is transmission of pathogens in the hospital then the problem is not the pathogens, but the health care providers. We probably markedly under appreciate the number of organisms spread in the hospital, because it is expensive and time consuming to type organisms to look for relatedness in outbreaks.

The key to control of MRSA is proper infection control. Like hand washing.

If you have a problem with MRSA in your institution, the problem isn't the bug. Look in the mirror. Someone isn't serious about infection control.

Rationalization

"Outbreak of Linezolid-Resistant Staphylococcus aureus in Intensive Care" ICAAC- IDSA 2008; Abstract C2-1835a.

Wenzel RP, et al. " Screening for MRSA: A Flawed Hospital Infection Control Intervention (http://www.ncbi.nlm.nih.gov/pubmed/18937571)" Infect Control Hosp Epidemiol 2008; 29.

It’s Over. Norovirus that is.

Published Wed, 19 Nov 2008

The outbreak of norovirus on one of the units of one of my hospitals is over.

What a pain. The staff on the unit responded superbly and once the outbreak was identified and infection control procedures instituted, it remained confined to one unit and there were no cases past the incubation period. They really cut the infection off at the knees.

Infection control procedures work when applied correctly. Not everyone believes that assertion as evidently some staff would not enter the unit during the outbreak. They were afraid of catching the disease and evidently had no confidence in infection control procedures.

This does not surprise me.

A couple of years ago, during the height of the biologic terrorism fears, a young girl came down with monkeypox, which she caught from her pet rodent. Monkeypox looks just like smallpox and there was concern she might be the index case of a terrorist attack. I heard a lecture at a meeting by the MD who took care of her. He had the smallpox vaccine so it was safe for him to take care of her. However, he could get no one else to take care of the girl, MD or RN, so he was her sole provider until they had the correct diagnosis.

It is estimated that should there be another flu outbreak like the 1918 pandemic, about half of health care providers will not come to work. And a significant number think it’s OK.

"BACKGROUND: Conflicts between professional duties and fear of influenza transmission to family members may arise among health care professionals (HCP).

METHODS : We surveyed employees at our university hospital regarding ethical issues arising during the management of an influenza pandemic.

RESULTS : Of 644 respondents, 182 (28%) agreed that it would be professionally acceptable for HCP to abandon their workplace during a pandemic in order to protect themselves and their families, 337 (52%) disagreed with this statement and 125 (19%) had no opinion, with a higher rate of disagreement among physicians (65%) and nurses (54%) compared with administrators (32%). Of all respondents, 375 (58%) did not believe that the decision to report to work during a pandemic should be left to the individual HCP and 496 (77%) disagreed with the statement that HCP should be permanently dismissed for not reporting to work during a pandemic. Only 136 (21%) respondents agreed that HCW without children should primarily care for the influenza patients.

CONCLUSION : Our results suggest that a modest majority of HCP, but only a minority of hospital administrators, recognizes the obligation to treat patients despite the potential risks. Professional ethical guidelines allowing for balancing the needs of society with personal risks are needed to help HCP fulfill their duties in the case of a pandemic influenza."

I took care of AIDS patients before we knew it was what HTLV-3 (now HIV, that is how old I am), and we were not entirely certain how it was spread. I like to think that when the time comes, I will have the courage of my convictions and work through the next pandemic. I know infection control works.

But I do expect that at least half of my colleagues will not be there to help me. If they are worried about a little diarrhea (well, not so little) how are they going to respond to a plague?

Rationalization

BMC Public Health. 2006 Apr 18;6:99. Local public health workers' perceptions toward responding to an influenza pandemic (http://www.biomedcentral.com/1471-2458/6/99/abstract ).

BMC Public Health. 2006 Dec 28;6:311. Influenza pandemic and professional duty: family or patients first? A survey of hospital employees. (http://www.ncbi.nlm.nih.gov/pubmed/17192198 )

What and Why

Published Thu, 20 Nov 2008

What they have is easy. The culture or the serology or the syndrome often gives the diagnosis.

But why? Why do people get infections? Often it seems to be bad luck, wrong time, wrong place. Sometimes it's the patients. There is great variability in the human immune system. Yours is not the same as mine. Some people are born with more ability to respond to infections, others less so. Clinically, I have only the most primitive assays at my disposal to evaluate the immune system and I wager than in another 10 or 15 years I will have far more sophisticated genetic tests to determine why a patient has an infection.

I did have two 'whys?' answered this week.

One patient, who presented with pneumococcal meningitis, turned out to have an IgM deficiency. Not common at all, I cannot find that IgM is specifically associated with pneumococcal meningitis, but it is the first class of antibody to come on line for infection, so I am crediting IgM deficiency for his relatively slow response to therapy.

The other diagnosis is more common. A patient with recurrent sinopulmonary infections, sore throats, and "catches everything." A common complaint of patients.

Turns out this patient has an antibody deficiency as well: Total IgG, IgG subtypes 2 and 4, and IgA levels are half normal. While absolute antibody levels correlate poorly with infection, it seems reasonable to ascribe her recurrent minor infections to her low antibody levels.

Antibody deficiencies are probably more common than realized by most clinicians.

Data on 127,000 patients from the Rochester Epidemiology Project, found 158 of primary immunodeficiency cases over the 31-year study period.

B cell defects accounted for 78% of the cases, and were divided about equally between IgA deficiencies, IgG subclass deficiencies, general hypogammaglobulinemia, and miscellaneous defects.

That's a rate of 10.3 per 100,000, more common than tuberculosis.

The clinical hint is recurrent infections of any kind.

Anyone presents by my clinic with recurrent infections gets antibody levels and IgG subtypes as part of their evaluation, and I hit pay dirt a couple of times a year.

Rationalization

Joshi A, et al. " Incidence and temporal trends of primary immunodeficiency in Olmsted County, Minnesota, USA: a population-based cohort study (http://www.ncbi.nlm.nih.gov/pubmed/19121249)" ACAAI 2008; Abstract 50.

Infections in 252 Patients with Common Variable Immunodeficiency. (http://www.ncbi.nlm.nih.gov/pubmed/18419489) Clinical Infectious Diseases 2008; 46:1547–54

Hitchcock didn't know the half of it.

Published Sat, 22 Nov 2008

When I was a kid the most horrible scene in the movies, to my way of thinking, was the scene in Gone with the Wind where they lop off the soldiers gangrenous leg without anesthesia and Miss Scarlet goes running out of the hospital in a panic.

The second most horrible scene was the lady with her eyes pecked out in The Birds. I could not watch the Bob Newhart Show without thinking of Susanne Pleshette with bloody, empty eye sockets. It kind of detracted from the comedy, or maybe added to it, depending on my mood. The eyes are one area that I hate having anyone get near. It took years to get up the gumption to get contacts. And I won't even tell you about the lady with the pneumococcal eye infection that ruptured during the exam. Well, I guess I did. Still give me the willies.

While birds, of course, never swarm, attack and kill people, they are good at spreading disease. Right now the worry is avian flu, which will probably get the US by way of migrating birds, probably ducks, which are relatively resistant to dying from avian flu.

You can't stop a duck, and that has extra meaning to me as a University of Oregon grad, with the second-lamest mascot in the state. Number one is Oregon State. But what can you expect from a school with no sense of color?

Birds, it turns out, can carry more than avian flu.

In this study they looked at fecal or cloacal samples from 97 birds in northeastern Siberia; Point Barrow, Alaska, USA); and northern Greenland.

Sign me up. Let’s go somewhere to collect bird crap that's colder than hell (yes I know. Hell is hot. Nope. I spent three years in Minnesota for my medicine residency. Hell will be cold, I'll be wet, naked and there will be a brisk wind). And culture the bird crap. See. Was your day really all that bad?

They looked at the E. coli in the bird poo and found

"E. coli isolates from Arctic birds carried antimicrobial drug resistance determinants; among 17 antimicrobial drugs tested, resistance to 14 was detected. Resistance was observed in 8 isolates, 4 of which displayed resistance to >4 drugs, and occurred most often to ampicillin, sulfamethoxazole, trimethoprim, chloramphenicol, and tetracycline. Two resistant isolates displayed isolated fosfomycin resistance."

What is remarkable about the resistance is that these samples were collected from the arctic, one of the remotest and most hostile areas on earth, where there is no antibiotic use.

It is postulated that migrating birds picked up the E. coli when in more temperate areas and brought them north. Resistant E. coli have also been found in isolated human and animal populations that have little or no exposure to antibiotics, and migratory birds are a potential explanation for the resistance.

They suspect these resistant organisms were of clinical origin as they had the same pattern of resistance as E. coli in hospitals.

Yet another way for antibiotic resistance to spread, but at least Homeland Security, by watching our borders, can keep out the migrating birds. We just need a high enough wall.

Rationalization

Dissemination of multidrug-resistant bacteria into the Arctic. (http://www.ncbi.nlm.nih.gov/pubmed/18258081) Emerg Infect Dis. 2008 Jan;14(1):70-2.

All those in favor.

November 23rd, 2008

Bacteria communicate with each other. Really. They send each other information that subsequently changes their behavior.

It called quorum sensing and has probably been present in bacteria for a billion years. It’s called quorum sensing because the bacteria and yeast communicate with each other when the colony reaches a critical number of bacteria. They then alter their metabolism, make some virulence factors or start to form biofilms in response to communications with each other.

Hey. They are an awful lot is us here, let’s eat a little less, build us a home and invade the host.

There are at least a half-dozen quorum sensing systems in pathogenic bacteria, depending on the species, and others exist in other species.

Bacteria use small molecules and peptides to communicate with each, some of which suppress other strains of the same species to gain a local advantage in a disease.

Not only do bacteria communicate with each other, they may communicate with other colonies of organisms, other bacterial species and even with host cells. The strain of S. aureus that gets there the firstest with the mostest prevents other S. aureus from thriving. Not only does the fittest survive, the fittest prevent the weaker from growing. I bet this system help accelerate pathogenicity.

Some bacteria can sense host molecules like dynorphin or epinephrine and alter the production of their virulence factors to enhance infection. Host enzymes can degrade bacteria quorum sensing molecules to prevent the bacteria from plotting and taking you over.

Back and forth they chatter and we try and jam the communications. The cold war writ small.

I used to think I was hearing voices. I wasn’t. It’s the bacteria in and on me. Talking. Planning. Conspiring. There are out to get us, you know. In the end they will. Eat, drink and be merry, for tomorrow you will be bacterial dinner.

Rationalization

Quorum Sensing: Bacteria Talk Sense (http://cid.oxfordjournals.org/content/47/8/1070.abstract). Clinical Infectious Diseases 2008; 47:1070–6

Dung Fungus

Published Mon, 24 Nov 2008

Catchy title, huh?

The world of microorganisms is vast and there are fungi that live in dung. Dung hits the ground (or on occasion the fan) and if it was a long time ago the dung gets fossilized and the fungus growing on it gets fossilized right along with it.

You can tell something about the history of a region by looking at the number of fossilized fungal spores in dung and in the sediments.

For example, there is a fungus called Sporormiella. It grows in the dung of herbivores. If there are a lot of herbivores, you have a lot of_Sporormiella_, herbivores die off, and there are less Sporomiella. Living only in herbivore poo may not be a good long-term survival strategy, or, for me, a short-term survival strategy.

"These spores decline rapidly at the end of the Pleistocene at the approximate time of megafaunal extinctions and increase again in sediments of recent centuries after livestock introduction."

So by measuring the amount of this fossilized organisms in coprolites, you can get an idea of what happened a million years ago or more.

They did this on Madagascar and saw the spores plummet with the mass extinction of the megafauna in the Pleistocene and then a rise when livestock were introduced on the island. The spores have plummeted in the last 200 years as Madagascar has been stripped of its complex fauna and flora. Here is an idea of what can be inferred from the looking at fossilized dung fungus changes over time:

"i. The late Holocene before humans was a time of increasing aridity and perhaps seasonal or interannual dynamics that promoted changes in key megafaunal habitats such as wooded savanna.

ii. People arrived and hunted the naive megafauna, at least the ones that were slow on the ground such as many of the largest lemurs, to local extirpation and depressed the numbers of other megafauna.

iii. In the absence of the strong cropping regime imposed by hippos, tortoises, and ratites on the grasslands (and perhaps on woody vegetation by giant lemurs), savanna areas, forest edges, and understories would become increasingly flammable as plant biomass accumulated.

IV. The change in fire regimes would mean that preferred megafaunal habitats became increasingly fragmented as fire converted areas to simpler systems with less edible plant biomass (e.g., spiny bushland and steppe).

v. Humid forest and high-elevation areas were the last settled and converted by humans (as indeed they are still being transformed today at an alarming rate) (13), but they would have provided poor refugia for most of the savanna-adapted megafauna, and the less-swi t giant lemurs would have been vulnerable to hunting even within dense habitats."

The rise and fall of ecosystems all derived from looking at dung fungus and charcoal deposits over time.

I spend my day trying to kill bacteria and fungus; it amazes me what can be determined by looking at their corpses.

Rationalization

Sporormiella fungal spores, a palynological means of detecting herbivore density (http://linkinghub.elsevier.com/retrieve/pii/S0031018206001015). Palaeogeography, Palaeoclimatology, Palaeoecology Volume 237, Issue 1, 21 July 2006, Pages 40-50.

Sporormiella and the late Holocene extinctions in Madagascar. www.pnas.org/cgi/doi/10.1073/pnas.1534700100

Chicken Migration

Published Wed, 26 Nov 2008

Chickens are a great source of pathogens. Salmonella and Campylobacter lead the list. Chickens lead crowded, short lives, and their lives would be even shorter if farmers didn't put antibiotics in the chicken feed.

The good thing about small amounts of antibiotics in the feed is the chickens get bigger faster and you get a cheap fryer.

The downside is antibiotic resistance. 70% of antibiotics in the US are used in agriculture, about 25 million pounds a year. That’s total, not per animal. The rule is simple: expose a bacterial population to antibiotics, especially low levels of antibiotics, and the resistance is inevitable.

At least chickens do not fly and do not migrate, so the antibiotic resistance should be contained to the farm. Except.

Chickens do migrate. They take a truck, often in open cages, from the farm to the abattoir. The wind from the truck aerosolizes the chicken dander and poo, spraying the countryside, and the car behind the truck. They

"...collected air and surface samples from cars driving two to three car lengths behind the poultry trucks for a distance of 17 miles. The cars were driven with both air conditioners and fans turned off and with the windows fully opened. Air samples collected inside the cars, showed increased concentrations of bacteria (including antibiotic-resistant strains) that could be inhaled. The same bacteria were also found deposited on a soda can inside the car and on the outside door handle, where they could potentially be touched."

Some of the organisms were antibiotic resistant. Clinton was right not to inhale, he just picked the wrong situation.

Unfortunately I cannot yet access this journal through our library probably because this is the first issue. So I cannot find which pathogens were isolated and to which antibiotics they were resistant.

But it gives me pause. How many times have I been stuck behind a pick-up full of teenagers? The exposure risk is scary.

Rationalization

Transporting Broiler Chickens Could Spread Antibiotic-Resistant Organisms. (http://www.jhsph.edu/publichealthnews/press\_releases/2008/rule\_chicken\_transport.html)

Journal of Infection and Public Health Volume 1, Issue 1, Pages 33-39 (2008). Food animal transport: A potential source of community exposures to health hazards from industrial farming (CAFOs) (http://www.ncbi.nlm.nih.gov/pubmed/20701843).

Happy Thanksgiving

Published Thu, 27 Nov 2008

Happy Thanksgiving. My favorite holiday because it is associated with lots of infections. Kind of not true. My favorite holiday is really Halloween. But I need a lead for the blog.

Salmonella and Campylobacter go with poultry like, well Salmonella and Campylobacter go with poultry.

"This study was conducted to determine the prevalence and antimicrobial resistance of Campylobacter and Salmonella isolates from retail poultry meat in the UK during 2003-2005. Poultry meat (n = 2104) were more frequently contaminated with Campylobacter (57.3%) than with Salmonella (6.6%). Chicken exhibited the highest contamination from Campylobacter (60.9%), followed by duck (50.7%), turkey (33.7%) and other poultry meat (34.2%). Duck had the highest contamination from Salmonella (29.9%), compared with chicken (5.6%), turkey (5.6% ), and other poultry meat (8.6%). C. jejuni predominated in raw chicken, whereas C. coli predominated in turkey and duck. C. coli isolates were more likely to exhibit antimicrobial drug resistance, including quinolones, than C. jejuni. Salmonella Enteritidis was the most frequent Salmonella serotype isolated. Salmonella isolates from turkey exhibited higher rates of multiple drug resistance (55.6%) than isolates from chicken (20.9%) and duck (13.6%). The findings reinforce the importance of thorough cooking of poultry meat and good hygiene to avoid cross-contamination."

This is why the pop-out in your butterball is designed to not only cook the turkey, but overcook it. But who wants rare poultry? We are big time Francophiles in my family, but I still remember getting rare pigeon in France. It's the way it is served. One of the few things I could not eat and I ate raw horse in Japan (Mr. Ed we barely cooked ye), but raw poultry? Icky.

Most people do not get their infection from the cooked bird, but instead do not adequately clean the prep space and put culture media, I mean cooked food, where they prepared the turkey, re-inoculating the bird.

The only way to reliably eradicate these pathogens is to irradiate the food, and the advantage to this is a turkey with three legs.

You can also get Salmonella from infant formula, dog food, vacuum-packed rats (mmmmm, vacuum-packed rats), reptiles (I wish turtles and snakes were a Thanksgiving tradition) and tree sparrows, to name a few.

Being a vegan or vegetarian is no protection. Tomatoes, spinach, peppers, basil, cheese, milk, apples, peanut butter, cantaloupe, alfalfa sprouts, and almonds have all been implicated in Salmonella outbreaks.

Bon appetite.

Rationalization

Int J Environ Health Res. 2008 Dec;18(6):403-14. Prevalence, characterization and antimicrobial resistance of Campylobacter and Salmonella in raw poultry meat in the UK, 2003-2005. (http://www.ncbi.nlm.nih.gov/pubmed/19031145)

Good News in Bleak Times

Published Sat, 29 Nov 2008

Being an ID doc is not all roses and champagne. Not that the two go together. Work used to be busier. There used to be nosocomial infections and ventilator-associated pneumonia, but thanks to applying infection control procedures at my hospitals, I have ICU's that have gone for over a year without a ventilator-associated pneumonia. Damn. My kids are reaching college age.

New medications for transplant patients and G-CSF have made infections in cancer and transplant patients a relative rarity.

Don't get me started in AIDS. Thanks to HAART and prophylactic antibiotics, we can go for years without seeing an opportunistic infection. I haven't seen a cerebral toxoplasma or CMV retinitis this century. Oh for the bad old days.

I was sliding into a funk about the grim future in infectious diseases when good news arrived out of the United Kingdom.

Measles is increasing. One in 4 has not had an MMR and they are at risk for a measles epidemic as herd immunity wanes.

They estimate that England could see 30,000 to 100,000 measles cases. They will probably only see a tenth that many, but I can dream, can I not? My dreams are not as noble as Dr. Kings. The only downside is it that the problem is in England and in children. It is a good start, but I need an outbreak in US adults. I need a really bad epidemic of something, anything, infectious. Flu would be good, but it seems to be a relatively benign flu season so far.

The BBC credits the debunked vaccine-autism link as the reason for the poor vaccination uptake.

I hope that the anti-vaccine crew continue their good work in America and we have a plague or two here.

It is said that the anti-vaccine crowd does not want children to get diseases, suffer, and occasionally die from vaccine-related diseases. I am sure that tobacco farmers don't want their end users to get lung cancer, that handgun manufacturers are against children accidentally shooting themselves, and that alcohol producers don't want people to develop cirrhosis. It just happens to be the end result of what they are selling.

The Green our Vaccine folks say they just want safer vaccines. What they will get are measles outbreaks and maybe mumps and rubella as well, with all the concomitant morbidity and mortality these diseases, and others, have to offer. It just happens to be the end result of what they are selling. The only thing that will be green will be the grass on the graves who died of preventable infections.

Rationalization

Measles cases surge to new high (http://news.bbc.co.uk/2/hi/health/7753210.stm)

Half time

Published Sun, 30 Nov 2008

Its 37-17 at the half, my alma mater, University of Oregon, with the second-worst mascot, is trouncing Oregon State, with the worst mascot in college sports.

It's nice to know that football is, like so many human activities, filled with infections.

MRSA leads the list, thanks to the trauma (turf burns), cosmetic shaving (who says football players do not have a feminine side?) and close contact. One of the first outbreaks with the current USA 300 strain of MRSA was in a professional football team. But there are numerous other football associated outbreaks.

There have been infections associated with mouth guards, which, at least by culture, are perhaps more disgusting than a toilet seat.

Osteitis pubis, an infection usually seen in postpartum women, is reported in football players. A fair number of linebackers do look like they are in the third trimester.

Group A streptococcus has passed through a football team as has scabies, coxsackievirus B2 and echovirus 16, the latter two with aseptic meningitis.

Hot tub folliculitis has been reported due to whirlpool use.

Herpes is commonly spread in football, both on and off the field, and many in the stands watching the game will acquire it tonight in drunken celebration or drowning their sorrows. I suspect that will not be the only STD spread this weekend in the post game festivities.

Back to Football.

World AIDS Day

Published Tue, 02 Dec 2008

Today is world AIDS day. The start of the AIDS epidemic coincided with the start of my medical career. I do not want to suggest causality here. But to quote the Grateful Dead, what a long strange trip it’s been.

I took care of my first AIDS patient about 25 years ago and he died after a long wasting illness due to Mycobacterium avium. The autopsy showed tissues that were more acid-fast bacilli than human cells. It was like some sort of real life Invasion of the Body Snatchers. My second patient was a circus dwarf with cryptococcal meningitis who visited bath houses during his travels. The next 15 years were an endless parade of awful deaths in young people with occasional bursts of hope (AZT, then combo therapy) followed by disappointment as therapies failed and the death toll continued to mount. I never expected triple drug therapy to be so effective.

The deaths were all the more aggravating as we knew early on how the disease was spread: sex and drugs. The techniques to prevent the spread of disease are simple. Condoms and needle exchange. Both are still opposed by those who prefer their form of morality over preventing people from dying. African bishops declare that condoms spread HIV, not prevent it, with none of the higher-ups disagreeing or condemning the statements.

So many people who died needlessly. In the book The Band Played On the response to the early HIV epidemic is compared to toxic shock syndrome. It was too bad, the author said that the disease didn't start in freckle-faced red-headed children.

It is a changed landscape. I have had one AIDS death this century and the only opportunistic infections I have seen since 2000 are Pneumocystis. HAART, much to my happy surprise, really works. My patients no longer die. That's good.

Outside the industrialized West, deaths from HIV are still common, but at least there is hope that the disease can be controlled. All we need is worldwide peace and prosperity. Yeah. Right. Like that's going to happen.

Rare Bug, Rare Disease, Bad Outcome

Published Wed, 03 Dec 2008

Necrotizing fasciitis is not all that common and is often rapidly fatal. It comes in many flavors, metaphorically speaking. Taste is one of the sensory modalities I try to avoid using in evaluating infections. Usually nec fasc, as we call it in the biz, is due to Group A streptococcus or is a mixed synergistic necrotizing fasciitis, a polymicrobial infection that behaves, or misbehaves, like gas gangrene. Gas gangrene, the disease that most people fear, is rare outside of skin popper, heroin users who run out of veins and inject directly into the skin.

I have seen a variety of gram-negative rods cause necrotizing fasciitis over the years: Serratia, Yersinia, Vibrio.

MRSA is increasing as a cause of necrotizing fasciitis, probably, but arguably, due to strains that make the Panton-Valentine Leukocidin (PVL), a protein that dissolves tissues like water on the Wicked Witch of the West.

The PVL can turn meat into liquid and is part of the reason the current strain of MRSA makes abscess so commonly. I wonder if it would make a good meat tenderizer.

So when the patient came in with a rapidly progressive purple leg, septic shock and multi-organ system failure, I expected one of the above from cultures.

He was in end-stage liver disease and yellow, and the surgeons whisked him off to the OR and amputated his leg in an attempt to save his life. Post op he developed new areas of necrotizing fasciitis on his abdomen and his other leg, and within 24 hours he was dead.

All the cultures grew Streptococcus pneumoniae. Very odd. There are fewer than a dozen reported cases of necrotizing fasciitis due to Streptococcus pneumoniae in the medical literature, most with some sort of immunodeficiency. The organism was sensitive to all antibiotics, as if they did any good.

The other interesting feature about the case reports is the prior use of NSAIDS, like ibuprofen. There has long been an association between necrotizing fasciitis due to group A streptococci and NSAIDS. The drugs, being anti-inflammatory, probably help tilt the balance of power in favor of the bacteria. This patient was too sick to answer questions, so we will never know if we can point the finger at an NSAID or not. The severity of his disease can probably be attributed to his liver failure.

Rationalization

Necrotizing Fasciitis Due to Streptococcus pneumoniae after Intramuscular Injection of Nonsteroidal Anti-Inflammatory Drugs: Report of 2 Cases and Review (http://www.ncbi.nlm.nih.gov/pubmed/11486297). Clinical Infectious Diseases 2001;33:740

Staring me in the face Part 1

Published Thu, 04 Dec 2008

The patient has been in and out of the hospital three times this month with fevers, intermittent confusion, up and down renal dysfunction, pancytopenia, platelets to 30K and a rash that looks like maybe a drug rash. This time it looked like maybe a necrotizing fasciitis in the leg, but I&D showed only hematoma, probably from her Coumadin.

Being a transplant patient on cyclosporin and prednisone, I kept looking for an infection and could not find one.

Exam, review of systems, cultures, X-rays, bone marrow biopsies were negative, and tests for every opportunistic infection I could think of were negative. Yet the patient was sick and often getting sicker.

Medicine is hard. Really hard. Patients get sick and the diagnosis can be frustratingly, aggravatingly elusive. Sometimes I wake up in the middle of the night with a diagnosis, sometimes a diagnosis comes as I am driving home, but where they come from I do not know.

Today I had what I will call, for a lack of a better term, my Aha moment. After failing miserably for weeks to get a diagnosis, today it bubbled up some unknown place, all the information fell into place like a perfect Tetris game. I was looking at all the labs and exams and I said...

When I came up with the diagnosis everyone said at the same time "Of course that’s what it is. It couldn't be anything else."

What did I say?

I'll let you know tomorrow.

Care to take a swing at it? I'll answer any questions if you have them.

Staring me in the face Part Deux

Published Fri, 05 Dec 2008

Bingo. He had a case of bingo.

TTP from cyclosporin. Took a month to figure it out. TTP is short for thrombotic thrombocytopenic purpura.

When evaluating a patient, especially a complicated patient, you start from what is sometimes called the hinge point.

The hinge point is the symptom or lab finding or clinical feature that you think is the most important. In the case of this patient, it was the fact it was a liver transplant patient, i.e.,an immunocompromised patient, with a fever. She never really developed the purpura that would have served as the hinge point of developing a diagnosis of TTP. I thought maybe the lack of purpura was due to the Coumadin the patient is on for a prior pulmonary embolism, but hematology assures me I am wrong. How dare they.

When patients do not have the key finding that makes one think of a disease, the diagnosis can be delayed.

What is really annoying is how day after day I would look at all the data and see no pattern, no diagnosis. It is frustrating to have a sick patient, know there is something evil going on, and not being able to put your finger on it. Then, once I thought of TTP, that is all I could see in the same information. It is like staring at an optical illusion for days and not seeing the pattern and then, once the skull is seen instead of the lady at the mirror, all I can see is the skull. ARRRGGGHHHHHHH.

TTP is unusual, the CDC says there are only 1200 cases a year, and this would be the second case I have seen in 25 years, so I suppose I should cut myself some slack, but once you see the diagnosis, with the 20-20 vision of hindsight, it seems so obvious. It was staring me in the face.

Coincidence? I don't think so.

Published Sun, 07 Dec 2008

I do a lot of driving for my job. I am the only ID doc at four hospitals and I can spend several hours a day going from place to place in slow traffic. To while away the time I listen to books on tape (well, books on mp3) or podcasts. It is amazing how often I hear a word on the iPod then simultaneously see that word on a billboard or street sign. Someone must be sending me a message, it cannot just be random serendipity. It is too weird not to have an underlying meaning. Someone must be trying to tell me something. But what?

Another odd thing is how often I read an article and I see the disease I read about in the subsequent few weeks. Like today. I see a patient who was admitted with community-acquired Staphylococcus lugdunensis bacteremia. _S_. lugdunensis is a skin staph, one of many coagulase-negative staphylococci that make up our normal flora. There is also _S_. aureus, which is the coagulase positive Staphylococcus.

Just two weeks ago I read "Significance of Staphylococcus lugdunensis bacteremia: report of 28 cases and review of the literature" as part of the quasi-random literature reading I do for the Puscast (http://moremark.squarespace.com/puscast-pacid-podcast/). And, as so often happens, I then see a case of Staphylococcus lugdunensis bacteremia.

Coincidence? I don't think so.

Community acquired Staphylococcus lugdunensis bacteremia is often due to endocarditis (heart valve infection), so, although I heard no murmur, as I was writing my progress note, who was outside of the room of the patient next door? The ECHO tech, with his machine, getting ready to take a look at the heart of the patient next door. Co inky dink? No way. I told him I wanted an ECHO on my patient to look for endocarditis.

"A total of 28 patients with S. lugdunensis bacteremia were identified. Of the 13 patients with endocarditis, all were community acquired."

He called me an hour later to tell me the patient had endocarditis as there was a big vegetation on the patients tricuspid valve. This is the truth. When he called me I was in the drive though of the Jack in the Box ordering a chicken bowl (first time, the rice is odd tasting) and looking at the picture of the bowel that was vegetables in it. Whoa.

And yesterday my son was playing NBA Live on the PlayStation and in the video game Brandon Roy pulled a hamstring. And what happened in the Boston game last night? We got crushed. And Brandon pulled his hamstring. Too many coincidences. Someone, somewhere is trying to tell me something. Spooky man.

Of course, it’s all just a touch of confirmation bias, the tendency for humans to remember hits and forget misses. I heard thousands of words and read dozens of articles so I was bound, just by chance, to see or hear an unexpected correlation. If I were prone to finding meaning in random events, today would be full of portents. But I don't believe there is a hidden underlying meaning so I would not go camping in portents.

What I really need to read is an article about an infectious disease physician winning Powerball.

Rationalization

Significance of Staphylococcus lugdunensis bacteremia: report of 28 cases and review of the literature (http://www.ncbi.nlm.nih.gov/pubmed/18648747). Infection. 2008 Aug;36(4):314-21.

It's all in where you come from

Published Mon, 08 Dec 2008

The history reveals all. If you ask the right questions and listen, often you will figure out the right diagnosis and sometimes even predict the organism.

Ex-nurse has two years of a red, hot, painful, swollen knee. Doesn't respond to standard therapy. Doesn't get better after arthroscopy. Knee continues to degenerate so she gets a new knee. No better. So the knee is revised. Still no better. At each evaluation of the knee there are a smattering of WBC, but routine bacterial cultures are negative, so it is passed off as degenerative joint disease.

So this time ortho calls me and says he is going in again and do I have any ideas?

Nope.

Then he mentions that she is from the Philippines.

Two Burk You Losis.

Knee-jerk reaction, in this case a chronically red, hot, painful, swollen knee-jerk reaction.

If you say seizure and give me a Mexican last name, I'll say pork tape worm faster than you can eat a strip of bacon. Mmmmmm. Bacon.

If you say fever and trip to Africa, it will be malaria.

And if you say the Philippines, it's TB. Or not TB. That is the question.

So I said, well, I have never seen a case of TB in a knee, much less in a prosthetic knee, but you had better send off fungal and especially AFB (tuberculosis) cultures, just in case. If it is infected, it's from something that doesn't grow using usual techniques.

And it was TB.

I saw the patient the next day and not only was she from the Philippines, she has always had a positive PPD and never received therapy.

TB of artificial joints is rare, only a handful of cases have been reported. But as best I can gather the chances I will be able to salvage her joint are reasonable. We will see.

Ask and you will receive the diagnosis. Maybe the Secret is right after all.

Rationalization

South Med J. 2007 Jan;100(1):66-9. Prosthetic joint infection by Mycobacterium tuberculosis: an unusual case report with literature review. (http://www.ncbi.nlm.nih.gov/pubmed/17269530)

Addendum. As of 2012 the patient is functional, but still has a swollen, warm knee. Ortho tells me she can’t get another knee, so she is on chronic INH/Rifampin.

Slow

Published Tue, 09 Dec 2008

It is slow. It’s the lull between Thanksgiving and Christmas when the hospital slows down, but with the economy in the toilet, the hospitals seem even quieter than expected. You would think that the economy would make no difference in how often people get sick, but it does. In part people do not seek care but tough it out and, as a result, sometimes die. Hard times mean an increase in deaths in the uninsured, but it will take some time before the unemployed of today are the corpses of tomorrow.

Also, sadly, it is a slow influenza year. No influenza, no pneumonia, no death, no disease. Sigh. I can't speak for other institutions, but his year we have been especially good at getting our employees and patients immunized. So maybe the immunizations are working; herd immunity in action. It is such a pisser than when I we do our jobs right, we get less work.

Last week in clinic I saw a patient in their late 70's who had osteomyelitis of the femur as a teenager. 50 years later her leg pops open and starts to drain. Cultures growing S. aureus, no surprise, but it is sensitive to penicillin, which accounts for less than 2% of S. aureus these days.

It’s like finding a coelacanth or a caveman preserved and still alive in a block of ice.

Having S. aureus reactivate after 50 years is not that unusual and not even the record, or my personal record, which is 60 years. In the era of antibiotics, we rarely get to see a bone infection that festers for decades before becoming symptomatic.

What to do about it? Probably nothing. The only cure would be amputation and since there is no loss of structural integrity of the bone, it is best to beat it down with a little antibiotic.

I did a back-of-the-envelope calculation years ago that suggested that 50 years for bacteria was about the same as 3 million years for people in terms of doubling time. Three million years ago we were Lucy, a 2-foot-high hominid, wandering the plains in Ethiopia looking for a Wii console for Christmas. The Wii has been in short supply that long. Wii sports is why we evolved the opposable grip, as I understand it.

I wonder if the S. aureus of today is the same S. aureus of 50 years ago, or has it evolved enough to warrant being called a new species. I have looked in the literature and asked around, but no one has ever addressed the issue. They look at me like I am some sort of goof. Given all the genetic changes in the USA 300 strain of MRSA, is calling it_S. aureus_ akin to calling modern humans Australopithecus afarensis? Inquiring minds want to know.

Rationalization

J Am Geriatr Soc. 1999 Aug;47(8):1035-7. Reactivation of osteomyelitis caused by Staphylococcus aureus after 50 years. (http://www.ncbi.nlm.nih.gov/pubmed/10443871)

Chronic osteomyelitis caused by Klebsiella pneumoniae with a 50 year course. (http://www.ncbi.nlm.nih.gov/pubmed/8550716) Medicosurgical management] J Chir (Paris). 1995 Aug-Sep;132(8-9):342-5. French.

Recurrence of chronic osteomyelitis in a regenerated fibula after 65 years. (http://www.ncbi.nlm.nih.gov/pubmed/17539217 ) Orthopedics. 2007 May;30(5):403-4.

First recurrence of osteomyelitis eighty years after infection (http://www.ncbi.nlm.nih.gov/pubmed/14814172). J Bone Joint Surg Br. 1951 Feb;33-B(1):110-1

Lung Abscess

Published Wed, 10 Dec 2008

17 yo female, started one week prior to admission with RUQ pain and right chest pain that was pleuritic in nature, fevers, and chills.

You have pleurisy, here is some T3.

Next day, not better. You have costochondritis, here's some NSAIDS.

The next day a CXR is done and she has a lung abscess. Big one. Young people do not get lung abscesses.

Her past medical history is negative, she has 4 birds, two dogs and a cat. A high school student, no bad habits, plays saxophone. Only travel is to Eastern Europe 6 months ago.

Why the lung abscess?

She has cultures that grow Streptococcus anginosus and Eikenella corrodens. Mouth bugs. It is what you would expect in an aspiration lung abscess from rasty black stumps of rotten teeth. Her teeth look great and she has not been unconscious from drugs, alcohol, trauma or medical care. Or American Idol.

I think it’s from her saxophone.

Ever seen a brass instrument spit valve emptied? Big time ick.

When people play the sax they keep their epiglottis open and the tendency to tilt the head back for the long notes (the sax equivalent of the guitar face) would open a perfect pathway for the pooled spit to drip into the lung.

Sax players also use circular breathing where they keep the airway open so they can keep blowing that long mournful note, like in Jungleland:

"The epitome of the soulful saxophone ballad; the first note just freezes you. That first note just stretches out and a slow, unrushed passion emotes from Clarence's soul and sets Bruce up for his final tragic verse. The sax creates a sweet and bittersweet flavor that reaffirms the tragedy. I remember when I was a kid how my music teacher told me to play with feeling. This song defines that comment. Clarence uses every note to express the pain that Bruce sings about."

But you knew that already.

Circular breathing. The intake of breath fills the chest and stomach; cheeks and neck are inflated when air is halfway up the chest. While forcing air from cheeks and neck into the instrument, the player simultaneously breathes in through the nose to the bottom of the stomach.

Saxophone players may have a shorter life span than other musicians, and do you know what most jazz sax players die of? Besides heroin use? Lung disease.

It all comes together nicely.

This exemplifies the problem with unprotected teenage sax. It’s not the television, that’s for sure. At least my boys play guitar.

Rationalization

http://www.audioholics.com/news/editorials/exploration-of-the-best-rock-saxophone-solos

BMJ. 1999 December 18; 319(7225): 1612-1613. Unsafe sax: cohort study of the impact of too much sax on the mortality of famous jazz musicians (http://www.ncbi.nlm.nih.gov/pubmed/10600961)

J Voice. 1999 Jun;13(2):265-73. Laryngeal movements in saxophone playing: video-endoscopic investigations with saxophone players. (http://www.ncbi.nlm.nih.gov/pubmed/10442758)

Addendum . It turns out the BMJ reference is meant to be a joke that the Christmas issue is the US equivalent to April Fools. Sure fooled me.

Goat Cheese

Published Thu, 11 Dec 2008

Another teenager, this one with fevers for a month, progressive weight loss, night sweats, hepatosplenomegaly, increased liver tests and pancytopenia.

Extensive work up as an outpatient is negative and she is admitted to the hospital, and now has small gram-negative rods growing from her blood on the fifth day of her admission.

Interestingly, although her temperature is 104, her pulse does not go above 80. For those that play at home, it's Faget's (pronounced fah-jays; its French. Only use the hard ‘t ’if you are from Texas) sign.

Faget's sign is pulse temperature disassociation. Normally for every degree of temperature elevation the pulse should kick up 10 beats. Faget's classically occurs with only a handful of diseases: Typhoid, Brucella, yellow fever are the typical atypical infections to typically have this sign, although it can atypically occur with some more typical infections in the US like Legionella and Tularemia. Usually in the US it’s beta blockers that lead to Faget's.

Sure enough, the cultures grew Brucella melitensis, which has been eradicated in the US. To brag, (and what is this blog for if not to give the illusion of my infectious omnipotence?) when they called me for the consult I first said something to the effect that when we get the name of the bug we may have a hint as to its origin. I asked for the patient’s name and when they said a Hispanic surname, I said it had to be Brucella. She denied ever having left suburban Portland or eating any unusual foods. So why did she have this odd organism?

Brucella has a long history of killing people and has been called undulant fever as well as Mediterranean fever, Cyprus fever, Gibraltar fever, and Malta fever, a testament to the troubles it caused the British Empire. The British army, in the days before food preservation, kept supplies on the hoof and in the Mediterranean one of the few animals that could exist on those rocky outposts was the goat. So they got Brucella as well as an excellent chevre.

Prior to this case I had only seen one other case of Brucella in Oregon, a new immigrant (less than a month in the US) with orchitis (testicular infection). He had been a professional goat milker in Mexico and eventually needed a orchiectomy to cure the disease. I saw a smattering of cases in L.A. as a fellow and it set my personal record for the longest incubation of a bacteria, the blood culture turning positive on the 42nd, the last, day of incubation.

A month later I saw the patient, this time with her mother, in a follow-up. She was cured of her infection and her mother rather grudgingly admitted that the Uncle occasionally brought goat cheese with him when he visited from Mexico and that she had eaten some. No one else in the family, however, came down with the disease.

When I was a kid, I thought diseases were named after the source of the infection, as my best friend swore that you got Salmonella from eating salmon. What, I wonder now, would I eat to get Brucellosis?

Rationalization

JAMA. 1975 May 12;232(6):636-7. Brucellosis linked to Mexican cheese. (http://www.ncbi.nlm.nih.gov/pubmed/1173155) Eckman MR.

Clin Infect Dis. 2001 Dec 15;33(12):2017-22. Epididymoorchitis due to Brucella mellitensis: a retrospective study of 59 patients (http://www.ncbi.nlm.nih.gov/pubmed/11698991).

Frequently in error, never in doubt-- the ID motto.

Published Fri, 12 Dec 2008

45 yo male whose life is even less eventful than mine.

Works, raises a family, sleeps.

Has low back pain after some minor lifting. Don't we all at that age. Wait until you are my age, 357 in dog years. I am increasingly like the Tinman in the Wizard of Oz, except I can't seem to find the oil to get things loose again. I sympathize.

His back pain gets worser and worser (my sons parallel word with better) so he gets an MRI and he has a spinal epidural abscess. Odd in that he has no risks; usually this is a disease of needle users or at least a complication of an infection elsewhere. He has none of the above.

Then there is the lack disc space infection. Usually the bacteria are presumed to go to the disc first, as the disc at least has some blood flow, and from the disc the bacteria go into the epidural space.

Oh well, it's a common medical aphorism that patients do not read the textbooks before coming into the hospital and so do not know how to manifest their disease properly.

Epidural abscesses are usually due to Staphylococci and Streptococci, and I occasionally see those organisms causing disease for no damn good reason. So I say it's probably going to be one of those organisms.

Imagine my surprise when the lab says the pus shows a gram-negative rod. Staphylococcus and Streptococcus are gram-positive cocci. The heck. More oddities.

But I am up to the task, pontificating that, oh, it’s just after Thanksgiving, so this will probably be Salmonella. Tis the season and Salmonella occasionally likes to cause extra-intestinal infections. That’s the ticket. It's going to grow Salmonella.

Days pass and the lab says that whatever it is, it is only growing anaerobically. What? An anaerobe? Now I am stumped. I have two guesses and two misses, so I wait. Three strikes and you are made comfort care.

It is Prevotella species that finally grows.

And the reason? Once a bug is identified, killing it, or at least selecting an antibiotic, is simple. I want to know why. Why? Why, why, why, why, why? Luck! Blind, stupid, simple, doodah, clueless luck! " 'What' is interesting, but nothing satisfies more than knowing why. This time, no way, no why. I can't find the hint of a suggestion of a possibility of a reason for why.

A Pubmed reveals a grand total of zero spontaneous Prevotella epidural abscesses. So I have the first one. Ever. Yippie for me.

Bacteroides , the most common pathogenic anaerobe, has fewer reported cases of spontaneous epidural abscesses than I have fingers (12. 8 on the left, 4 on the right. Don't ask).

You just never know whatcha gonna grow. It’s the great thing about ID. You can blather on about how this and that bacteria should be causing the infection, and the cultures grow some unexpected germ that makes all your erudite pontifications wrong.

Another good case, curable with a course of antibiotics, but in the end slightly unsatisfactory.

All the way to the bank

Published Sun, 14 Dec 2008

As the cognoscenti are aware, I also pontificate, er, blog, over at Science-Based Medicine, where the issue from the anti-vaccine wackaloons are discussed at length. The need to defend vaccines has always stuck me as odd. It is like defending clean water or fresh air.

Of course, I have a variety of vested interests in promoting vaccines.

First, as I have mentioned in the past, is the opportunity to inject the new version (6.66 I believe) of tracking bots that are ATP powered. Much better and longer lasting than the old bots, they can pinpoint your location far better than those cell phone tracers.

But more important is all the money we doctors make from vaccines.

The anti-vaccine wackaloons often mention that it is the loads of cash we docs bring in from vaccinating people that keeps the vaccine’s coming. I was looking over my IRS forms for the last several years to tally up all the money I have made from vaccines and it was, um, carry the zero, add those columns up and it’s, yeah. Nothing. I didn't make dime one from giving any vaccines last year. I went around the hospital giving flu vaccines but I made the mistake of doing it for free because I think it is important people get vaccinated. Silly me. Not only did I not charge exorbitant fees for vaccinating my colleagues, they are not going to get sick and pass the flu to their patients. Crap. I could really make some money from a good flu outbreak, seeing as how I only get paid for seeing sick people.

Of course, it could be argued that I am in the thrall of the evil medical-industrial complex, and I am only serving my masters by promoting vaccines.

Let’s tally up all the money I have received from big pharma in the last 25 years: again, carry the zero, add the columns from 1985 to present and the sum is, yeah, zero. I don't do drug companies. Never talk to the reps, never take their food or pens or hospitality. I usually refer to them as lying bastards and for some reason I am not been asked to participate in their speakers bureau. I wonder why big pharma does not advertise on my podcasts or website.

I am an adult ID doc (meaning I take care of adults, not that I act like one. You are only young once, but you can be immature all your life, that's my motto). It is the pediatricians who make the bling from vaccines. The excessive vaccine schedule that weakens the immune system and causes all sorts of evil in children exists to make pediatricians wealthy. Heartless bastards. It’s the childreeeennnnnnn.

Turns out vaccines are not so lucrative after all.

It costs docs about $1500 dollars to purchase the vaccines. Given reimbursement, sometimes docs can't cover the cost of the vaccine, much less pay to keep the doors open. It costs somewhere around $100 an hour or more to run a medical office.

How much to docs make giving a vaccine?

"The net yield per dose -- calculated as the reimbursement minus price paid -- averaged from $2.90 for the Haemophilus influenzae type b vaccine PedvaxHIB to $24.34 for Pediarix. Across practices, the range of net yields varied from $10 for one vaccine to $90 for another. For the heptavalent pneumococcal conjugate vaccine alone, some practices had a positive net yield of up to almost $39.00 per dose whereas 11% had a negative net yield for the vaccine."

As a result, some practices are not purchasing the more expensive vaccines and others are considering no longer offering vaccination. That’s good news for me. Fewer vaccines may lead to a plague of some sort. Now that will make me some cash.

Rationalization

Freed GL, et al. Variation in provider vaccine purchase prices and payer reimbursement (http://www.ncbi.nlm.nih.gov/pubmed/19047253). Pediatrics 2008; 122: 1319-1324.

Freed GL, et al. Primary care Physician perspectives on reimbursement for childhood immunizations (http://www.ncbi.nlm.nih.gov/pubmed/19948578). Pediatrics 2008; 122: 1325-1331.

Berman S. Is our vaccine system at risk for a future financial 'meltdown? (http://www.ncbi.nlm.nih.gov/pubmed/19047260) Pediatrics 2008; 122: 1372-1373.

Cold

Published Tue, 16 Dec 2008

Cold, cold, cold. This week, in what is usually the mild Pacific NW, it is going to be below freezing. When I die and go to the hell that so many have promised me, it will not be fire and brimstone. It will be cold. And I will be naked. And wet. With a breeze in my face. In Chucky Cheese. And they are playing country music.

Now there are those you reading this who are calling me a wimp, but I spent my residency in Minnesota, where I learned to hate cold. But I was asked today, as I wandered the hospital stomping out illness, can you catch a cold? Nope. It’s a myth. Then I was asked, 'What's the data?'

Um. Er. Well.

I'll be damned. What IS the data.

It is old data. 1958. One year younger than me. So old it doesn't exist in electronic form. But people say it says that chilling doesn't increase cold risk.

A subsequent study in the NEJM had the same result. No increased incidence of cold's when chilled people are challenged with rhinovirus. When I ask my eldest what he was doing with his friends, he usually replies, "Chillin'." At least he will not be catching a cold. Or will he?

But then, in what was one of the odder studies I have found, some researchers did show that those who had their feet chilled were more likely to get cold symptoms;

"BACKGROUND: There is a common folklore that chilling of the body surface causes the development of common cold symptoms, but previous clinical research has failed to demonstrate any effect of cold exposure on susceptibility to infection with common cold viruses.

OBJECTIVE: This study will test the hypothesis that acute cooling of the feet causes the onset of common cold symptoms.

METHODS : 180 healthy subjects were randomized to receive either a foot chill or control procedure. All subjects were asked to score common cold symptoms, before and immediately after the procedures, and twice a day for 4/5 days.

RESULTS : 13/90 subjects who were chilled reported they were suffering from a cold in the 4/5 days after the procedure compared to 5/90 control subjects (P=0.047). There was no evidence that chilling caused any acute change in symptom scores (P=0.62). Mean total symptom score for days 1-4 following chilling was 5.16 (+/-5.63 s.d. n=87) compared to a score of 2.89 (+/-3.39 s.d. n=88) in the control group (P=0.013). The subjects who reported that they developed a cold (n=18) reported that they suffered from significantly more colds each year (P=0.007) compared to those subjects who did not develop a cold (n=162).

CONCLUSION : Acute chilling of the feet causes the onset of common cold symptoms in around 10% of subjects who are chilled. Further studies are needed to determine the relationship of symptom generation to any respiratory infection."

Lack of a placebo arm makes controlling for bias impossible. I have had a lot of cold feet in my dating days, but I do not remember a subsequent infection; those followed when I didn't get cold feet. But I share too much.

I suppose I should be convinced, but the data is not compelling and not relevant to 'the real world.' I just got it from my evening walk and my nose was congested and my throat dry. I seem primed for upper respiratory compromise with mechanical alterations that could make it easier for a rhinovirus, or other infections like Streptococcus pneumoniae, to gain a foot hold. Or a nose hold.

A good study would be to challenge people after a 3-mile trek on a below-freezing day in a 25-mile wind as I did today. That was a cold stress. The increase seen in the winter of respiratory disease is always attributed to crowding and easier transmission, but there is some, albeit contradictory information, that physical cold does increase the risk of bacterial infections.

Whether cold causes infection depends on how much stress the cold exposure causes.

"Psychological stress was associated in a dose-response manner with an increased risk of acute infectious respiratory illness, and this risk was attributable to increased rates of infection rather than to an increased frequency of symptoms after infection."

Does cold cause a cold? Maybe. I bet it does. It is too bad the other forms of temperature do not have names like beer, sex and golf. Those might be worth catching.

Besides, "a cold in the head cause less suffering than an idea."--Jules Renard

Rationalization

Am J Hyg. 1958 Jul;68(1):59-65. Transmission of the common cold to volunteers under controlled conditions. III. The effect of chilling of the subjects upon susceptibility (http://www.ncbi.nlm.nih.gov/pubmed/13559211).

Exposure to cold environment and rhinovirus common cold: Failure to demonstrate effect (http://www.nejm.org/doi/pdf/10.1056/NEJM196810032791404). N Engl J Med. 1968;279:743.

Fam Pract. 2005 Dec;22(6):608-13. Acute cooling of the feet and the onset of common cold symptoms (http://www.ncbi.nlm.nih.gov/pubmed/16286463).

N Engl J Med. 1991 Aug 29;325(9):606-12. Psychological stress and susceptibility to the common cold (http://www.ncbi.nlm.nih.gov/pubmed/1713648).

Failure

Published Wed, 17 Dec 2008

I hate failure. Even though I should expect it, the annoying thing about medicine is that you can do everything correctly and fail.

Eight weeks ago the patient came in with sustained staphylococcal bacteremia. Sustained bacteremia is the sine qua non of endocarditis and it was the dread MRSA. Worse than the dread Pirate Roberts.

He was treated with a 6-week course of vancomycin, and now he is back with another case of sustained bacteremia. Crap. To quote the dread poet Robert, "The best laid schemes of mice and men / Gang aft a-gley." I could not have said it better myself, although I try not to drink when I write poetry.

The problem with vancomycin is that all susceptible organisms are not the same.

The MIC (mean inhibitory concentration in micrograms per ml) for a susceptible S. aureus can be 0.5, 1.0, 1.5 and 2.0. As the MIC increases, the treatment success rates fall. His MRSA had an MIC of >= 1.0. Should have been fine. It wasn't. It could be that the heterogeneity of vancomycin resistance was a factor. Staph, like humans, can be a sloppy reproducer, and kick out mutant sub-populations that have slightly higher MICs to vancomycin and perhaps I have selected for these strains.

"Data from multiple laboratories demonstrated that the resistant subpopulations (i.e., vancomycin MICs of 8-16 mg/mL) typically represented;1 in 15 to 1 in 10^6 colony-forming units (CFUs)."

I hope I have not bred a vancomycin-resistant staph. Shouldn't happen, but one frets.

The outcome can hinge on as little as 0.5 micrograms per ml of vancomycin. Vancomycin just isn't all that great a drug, and the alternatives, linezolid and daptomycin, are, in head to head trials, no better. As best I can tell, them what I think the alternatives are better than vancomycin have drank deeply at the trough of big pharma.

Fortunately, we do have new drugs coming down the pike that are cephalosporins that specifically target the mutation that makes MRSA MRSA. I predict 1) it will be very expensive and 2) resistance will occur. On the bright side, I may be able to kill MRSA again, if only for a short period of time.

Rationalization

Relationship between vancomycin MIC and failure among patients with methicillin-resistant Staphylococcus aureus bacteremia treated with vancomycin (http://www.ncbi.nlm.nih.gov/pubmed/18591266). Antimicrob Agents Chemother. 2008 Sep;52(9):3315-20. Epub 2008 Jun 30.

The Rationale for Revising the Clinical and Laboratory Standards Institute Vancomycin Minimal Inhibitory Concentration Interpretive Criteria for Staphylococcus (http://www.ncbi.nlm.nih.gov/pubmed/17407040). Clinical Infectious Diseases 2007; 44:1208.

French Eponym

Published Fri, 19 Dec 2008

The French dominated infectious diseases for decades because of the head start afforded by Louis Pasteur, whose name is immortalized in the song Louie Louie, a little ditty recorded by the Kingston Trio in Portland, Oregon. The lyrics have a history of being obscure, and perhaps obscene, but I think the song is about the sterilization of food to prevent acute diarrhea.

"Louie Louie, oh no. Me gotta go. Aye-yi-yi-yi, I said. Louie Louie, oh baby. Me gotta go."

The application of Pasteurization has made food borne gastroenteritis less of a problem, but the downside has been fewer Top 40 hits with obscure, perhaps obscene, lyrics.

There are numerous eponyms for infectious diseases that carry the names of French physicians and they are all bad. The diseases, not the French physicians.

Today was one of the dreaded eponyms, Fournier's gangrene. Gangrene is bad enough, but add a dead French physician to it and you have disaster.

Fournier's is also called mixed synergistic necrotizing fasciitis.

Mixed as it is due to multiple organisms.

Synergistic as the organisms work together in a supportive environment to self-actualize and cause more damage than any single organism could. Usually it is a mixture of E .coli, Streptococci and anaerobes.

Necrotizing as it dissolves tissues.

Fasciitis as it is a deep, burrowing infection of the fascia, the connective tissue between the muscle and the skin.

Fournier's usually occurs in diabetics and in the perineum, the area you use to sit on a bicycle seat. It is one of many infections that liquify soft tissues. It is what accounts, I believe, for the death of Elphaba Thropp.

Antibiotics are all well and good, but the real treatment is widespread debridement (pronounced de-breed-mint, not da-bride-mont. Da bride is da woman who walks down da aisle of da church). The first case I saw was a young male that required removal of most of the soft tissue of his thighs and abdomen, including his scrotum. His testicles were resting on a damp towel; I cringe and curl up as I type this. All forms of gangrene require extensive and disfiguring surgery to cure the infection. But the only other alternative is rapid death.

The patient had their debridement and is doing well, albeit with a cantaloupe-sized chunk of flesh gone. It is important to make all metaphors in medicine related to food in someway.

It is the unstated goal of every doctor to become immortalized with an eponym, although in fairness it should be named after the patient rather than the doctor.

What, I wonder, will be Crislip's syndrome. Ideas?

Rationalization

eponyms.net/eponyms_January_2007.pdf (http://eponyms.net/)

Hypersensitive

Published Mon, 22 Dec 2008

The alleged stimulus for this blog is the cases I see at work.

However, work is slow. The holidays slow down as elective medical care is postponed until the new year and, therefore, the resultant infections are postponed as well.

The economy is slow, and ID has always been the reimbursement canary in the medical coal mine.

And finally Portland is shut down with the worst winter storm in my memory. We get freezing rain, which is impossible to move around in. I spent three years in hell, er, I mean, Minneapolis, and they never had weather like this. Plus, we have hills, an unknown geologic feature in the Midwest. Nothing gives that feeling of 'oh crap' quite like going down a hill, hitting the brakes, and accelerating due to gravity and ice.

Anyway. ID-wise there is not one whole heck of a lot going on to write about, so I turn to the interwebs.

The cool thing is that vaccines have the potential to prevent cancer, specifically cervical cancer, due to Human Papilloma virus (HPV). The vaccine will probably prevent anal, penile and oral cancers as well, as these can be caused by HPV, although how a cervical virus makes it to the oral pharynx no one has yet explained to me. I digress.

Early on there was a report that the vaccine was associated with an increase in hypersensitivity rates, which is an uber allergic reaction. Because of general fears about vaccines, this report did not help ease the minds of parents who were taking their daughters to get the vaccine.

However, researchers did another study and found (to quote from Medscape, published in the BMJ)

"From the 269,680 HPV vaccine doses administered in schools, 7 cases of anaphylaxis were identified, which represents an incidence rate of 2.6 per 100,000 doses (95% confidence interval [CI], 1.0 - 5.3 per 100,000), the researchers reported.

In comparison, they noted that the rate of identified anaphylaxis was 0.1 per 100,000 doses (95% CI, 0.003 - 0.700) for conjugated meningococcal C vaccination in a 2003 school-based program.

That report may have been an overestimate, however. The current study concludes that "true hypersensitivity" to the HPV vaccine is uncommon, and a detailed examination of case reports found only 2 cases of anaphylaxis after more than 380,000 vaccine doses."

And the association may not be causation, as kids will have other reasons for allergic reactions like asthma and bee stings. Every week in the US there are a large number of people who have a vaccine, by chance some will have a reaction after the vaccine, and blame the vaccine, when, in fact, the two are unrelated.

"They point out that 1 study estimated that if 80% of eligible American adolescent females were to receive a saline injection according to the vaccination schedule for HPV, 3 in 100,000 adolescents would require emergency care for asthma and allergy within 24 hours of vaccination (Pediatr Infect Dis J. 2007;26:979-984)."

17 of 18 girls who had a reaction to the first dose of the vaccine were skin test negative and tolerated the re-challenge no problemo.

So it looks like the vaccine is safe, especially in Australians. Who, I might add, are an exceptionally intelligent group of people, judging by those who listen to my podcasts.

Now if we can just figure out a way to prevent the vaccine from making them hyper-sexual. Or so the interwebs tell me. And I thought that was due to the contrails. Or was the fluoride? It is so hard to keep these things straight.

Rationalization

True Hypersensitivity to HPV Vaccine Uncommon http://www.medscape.com/viewarticle/584651

Unintended Goodness

Published Wed, 24 Dec 2008

I actually got out of the house today. And there was work! The joy of a good infection. I sometimes feel a tich guilty over how much fun I have at work, since part of enjoyment is derived from the fact some poor unfortunate has to get a disease odd enough or interesting enough to warrant an infectious disease consultation.

Today was something I have not seen for a while, a S. pneumoniae pneumonia. What was odd about it was the organism was intermediate to penicillin.

Resistance in the pneumococcus has two flavors: intermediate (MIC [mean inhibitory concentration] to penicillin between .1 and 1 micrograms per ml) and resistant with MIC >= 2.

These forms of resistance have different mechanisms. The intermediate strains have DNA point mutations that have lead single amino acid substitutions at one of the three binding sites of penicillin which results in a slight increase in the MIC to penicillin. The more point mutations, the higher the MIC. It is why the mean MIC to penicillin of _S_. pneumoniae has been slowly increasing since the discovery of penicillin.

Resistant strains have acquired a new chunk of DNA from another bacteria that leads to complete resistance to penicillin and to several other common antibiotics as well. Which is a story for another day. Suffice it to say I wish I could acquire the hair gene from another human with equal ease, I am tired of my scalp getting sunburned every summer.

Here is yet another cool thing, in an endless list of cool things, in ID.

There are 82 + serotypes of S. pneumoniae. The most common disease causing strains tend to be the resistant strains. The old pneumococcal vaccine is not all that great a vaccine, it does not so much prevent disease as prevent you from dying if you get the disease, which is not that bad an outcome. There is a newer pneumococcal vaccine that is given to children and targets the 7 most common invasive pneumococcal strains, which are also the strains most likely to be resistant to penicillin. The new vaccine is excellent and prevents disease in kids, as well as decreasing the number of kids who carry the bug.

The use of this vaccine in children has resulted in invasive disease plummeting in kids and, as a side effect, disease due to these strains has decreased in adults. It appears that kids are the vectors that serve as a source of pneumococcal infection in adults.

"The rate of antibiotic-resistant invasive pneumococcal infections decreased in young children and older persons after the introduction of the conjugate vaccine. There was an increase in infections caused by serotypes not included in the vaccine..."

and

"...the introduction of a pneumococcal conjugate vaccine for children has reduced the population rate of adult pneumococcal bacteremia due to vaccine serotypes and is associated with a reduced risk of bacteremic pneumococcal pneumonia for adults with children in the home."

One cannot, however, autoclave your kids to prevent infection.

Giving the vaccine to kids has resulted in a decrease in disease in adults and overall decrease in disease from resistant strains. Which is a nice change, as usually when you try something new you worry about unintended bad consequences. No good deed ever goes unpunished in medicine.

It is why I have not seen a resistant S. pneumoniae for a while. But it will be short-lived. The ecological niche is being filled by strains not covered by the vaccine and resistance is not futile, but inevitable. See ' On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (http://www.talkorigins.org/faqs/origin.html)’ for a complete explanation.

For a short period of time we have had a vacation from S. pneumoniae. All vacations end. And I want to go to Hawaii.

Rationalization

Vaccine. 2006 Jan 23;24(4):468-75. Epub 2005 Aug 15. Impact of pediatric vaccination with pneumococcal conjugate vaccine on the risk of bacteremic pneumococcal pneumonia in adults. (http://www.ncbi.nlm.nih.gov/pubmed/16125826)

N Engl J Med. 2006 Apr 6;354(14):1455-63. Effect of introduction of the pneumococcal conjugate vaccine on drug-resistant Streptococcus pneumoniae. (http://www.nejm.org/doi/full/10.1056/NEJMoa051642)

Zoe Sin

Published Tue, 30 Dec 2008

The holidays are over, so it is back to reality.

The ICU fellow said to me, so, I hear you do not think much of Zosin.

True story. I can count on one finger, probably the middle one, the number of times I have prescribed Zosyn, aka piperacillin/tazobactam.

I don't trust it, or any of the other penicillin/beta-lactamase inhibitors, Timentin (ticarcillin/clavulanate) or Unisin (my spelling for ampicillin/clavulanate).

Why you might ask? Because the beta-lactamase inhibitor once said there were WMDs, and when I looked, well, no WMDs. So I can't trust them. As our soon-to-be ex said so eloquently, "There's an old saying in Tennessee‚ I know it's in Texas, probably in Tennessee, that says, fool me once, shame on, shame on you. Fool me, you can't get fooled again." He must of been thinking of The Who. Greatest rock band of all time.

For you all that are unaware, this is a class of antibiotics that contain two drugs. One, the antibiotic. One of the mechanisms by which bacteria are resistant to antibiotics is to make enzymes, called beta-lactamases, that degrade antibiotics. Makes them wear bunny suits; very degrading. The antibiotic is combined with a drug, a beta-lactamase inhibitor, that prevents the antibiotic from being degraded by inactivating the beta-lactamase. Builds its self esteem as it were.

My problem?

Several.

The antibiotic and the inhibitor have different pharmacokinetics, so you are always hoping that there is enough inhibitor around to allow the antibiotic to kill. Antibiotics are referred to as bullets, but that is a bad metaphor, as I can kill you with one bullet, but it takes hundreds or thousands of antibiotic molecules to kill a bacteria. Rather than a bullet, antibiotic are more akin to death by a thousand cuts. I worry that there is enough inhibitor around to allow the thousand cuts needed to kill the bacteria.

If the organism makes a beta-lactamase that is not affected by the beta-lactamase inhibitor, and many beta-lactamases are not inhibited by the current beta-lactamase inhibitors, then the inhibitor actually slightly inhibits the antibiotic instead. Pseudomonas does not make a beta-lactamase that is inhibited by tazobactam, as a result the combo drug is less active than piperacillin alone.

The result of this may be death. Most antibiotics are given before the cultures come back. If you delay therapy in sick patients, they have 30% higher death rates, so you give the best antibiotic you can think of for the presumed organisms.

If that infecting organism is Pseudomonas and you gave ZoSin, then your patient is more likely to die.

"A total of 34 bacteremia episodes were identified involving isolates with reduced susceptibility to piperacillin-tazobactam (minimum inhibitory concentration, 32 or 64 mg/L, reported as susceptible); piperacillin-tazobactam was empirically given in 7 episodes. There was no significant difference in baseline characteristics between the 2 groups. Thirty-day mortality was found to be 85.7% in the piperacillin-tazobactam group and 22.2% in the control group (P = .004). Time to hospital mortality was also found to be shorter in the piperacillin-tazobactam group (P =; .001). In the multivariate analysis, 30-day mortality was found to be associated with empirical piperacillin-tazobactam therapy (odds ratio, 220.5; 95% confidence interval, 3.8-12707.4; P = .009), after adjustment for differences in age and APACHE II score."

I recognize that when I choose my empiric antibiotic, sometimes I am literally betting my patient’s life that I can choose right.

I do not like losing that bet. So I never give Zosin, especially if I do not know what bacterium is trying to kill my patient.

Rationalization

Clin Infect Dis. 2008 Mar 15;46(6):862-7. Outcomes of bacteremia due to Pseudomonas aeruginosa with reduced susceptibility to piperacillin-tazobactam: implications on the appropriateness of the resistance breakpoint (http://www.ncbi.nlm.nih.gov/pubmed/18279040).

It's Back

Published Wed, 31 Dec 2008

I have determined, through long observation, that the use of intravenous heroin is not conducive of a healthy lifestyle.

Which I need. A lifestyle that is. Not heroin. I have a life, but it seems to lack style. Of course, I wore bell-bottom cords well into my 30's, so perhaps I have a style known as 'dork.'

There are few infections that are 100% fatal in humans. Rabies for one, the other is bacterial endocarditis.

If you do not treat it correctly it will always kill the patient. Always. The closest I ever came to a spontaneous cure was a patient who came in with streptococcal endocarditis, received 2 doses of ceftriaxone and then remembered he was a Christian Scientist and refused further therapy. He survived, and came back a month later disease free, giving credit to the Big Scientist, but I still think the two doses of the long-acting antibiotic were enough to cure him.

The problem is that if you want heroin, you may not hang around the hospital to get your antibiotics, especially if the doctors have been kind enough to give you direct access to the central veins of the body for easy delivery of antibiotics.

And so the patient today, with Staph on the aortic valve, decides that rather than stay at the nursing home for nafcillin, skipped to get some drugs and relapsed her infection. Back to square one. I emphasized the universally fatal nature of the disease to her, so perhaps this time she will complete the therapy, this time with some drug rehab thrown in. But if past behavior predicts the future, I would not be optimistic that she will survive.

I have read somewhere, but cannot find where, that the average IVDA in NYC lives for 5 years and dies of murder or infection. Like I say, not a healthy lifestyle.

The worst case of endocarditis was that of Alfred S. Reinhart, who developed his heart infection as a result of rheumatic heart disease and had the misfortune of being alive in the pre-antibiotic era and being a medical student.

As such he had insight into all the details of his disease and could recognize and predict his future. He kept a diary of his disease until a few days before he died and it is one of the saddest of all medical writings. I don't worry so much about being dead, but the process of getting there has never appeared to be all that pleasant.

When he developed the embolic events that characterize the disease, he was with his sister-in-law and told her, "I shall be dead in 6 months." Alfred S. Reinhart saw the bullet coming for months, Matrix style. Ugh.

"I felt sure that I was going to collapse momentarily from sheer exhaustion induced by lack of sleep and the intense pain. I cannot deny that I had visions of the end, nevertheless, I knew that morphine would soon take the edge off my pain ... standing orders permitting me to call for reasonable doses of morphine within proper limits of time as I should find it necessary, proved a great boon in these days. I utilized this privilege comparatively little in the past, but was only too ready to ask for one quarter of morphine at this time to relieve the intense distress which was gripping me. This dose seemed to take the edge off the pain sufficiently to allow me to lie on my right side for perhaps ten or fifteen minutes during which time I readily fell into a sleep following the exhausting experiences of the past hours"

Dead at 24 from acute heart failure.

If you think you are having a bad day, read about Mr. Reinhart: www.cmaj.ca/cgi/reprint/167/12/1379.pdf

Every time I read it I get all bummed out.

I am going to go listen to the Cure. Always a good choice when depressed.

Isn't that special?

Published Thu, 01 Jan 2009

I am a specialist, not as in special education. What makes me a specialist, an expert in Infectious Diseases? Time and education. I took all the requisite classes, was a fellow, took and passed my Infectious Disease Boards, blah blah blah. According to The Man, I am qualified to be an Infectious Disease specialist.

In the old days that was enough and more to be expert in a field. Time and experience and everyone had to bow down to your greatness, whether or not you really knew the difference between a burro and a burrow (1).

Now days, it is not so easy. Now days, what makes me expert is an ongoing attempt to have mastery of the Infectious Disease literature, which is really a good definition of futility. Sisyphus had it easy, he had the same boulder. Every year the amount of information in medicine increases and my brain has progressive age-related atrophy. Maybe 10,000 neurons die a day, more if I have to watch Bill O'Reiley.

Last year there were 37,452 articles related to infections on Pubmed. I would have to read 102 articles a day to read them all, or 4 an hour. I skim about 500 articles, and read about 100 in depth every month to prepare for the Puscast (http://moremark.squarespace.com). I go to Grand Rounds, ID conference, noon report, and the national conferences. And every year I get further and further behind. It boggles my tiny brain that after almost 25 years of ID there are infections I have yet to see, or a bug I have never heard of. My two most common phrases at work (after "one maple bar please") seems to be "I didn't know that" and "I don't know, I'll look it up." But that is the definition of an expert: she knows more and more about less and less until she knows everything about nothing.

It takes a lot to keep up in medicine, to know what is going on in your field and to try and apply it to the complexity and uncertainty of clinical medicine. It is an impossible task. What makes me expert is the ongoing attempt to master science-based medicine; I therefore am a master of the impossible. Sounds like a DC title.

There were, in contrast, 184 articles on chiropractic, 116 on homeopathy, 805 on acupuncture and 365 on herbs last year.

Damn. I should have been an alternative medical provider. So little to learn. So easy to keep up.

I mention this because today is the one-year anniversary of the Science-Based Medicine (http://sciencebasedmedicine.com) blog, where I am a more or less bimonthly contributor. Send presents, gift cards and cake to Steve Novella, David Gorski, Kim Atwood, Harriet Hall, and Wally Sampson. To save on postage, might I suggest a homeopathic present?

Happy Birthday to us. I would wish everyone a happy New Year as well, but I am on the Mayan calendar. July 19th is my New Year, with the end of the world scheduled for 2012.

Rationalization

1) an ass and a hole in the ground.

Cocci

Published Fri, 02 Jan 2009

Last night was the first time in 20 years I was awake at midnight for New Years. Mr. Clark is looking pretty good given his stroke, but the bands that played were who? Fergie, The Jonas Brothers, Taylor Swift, and the Pussycat Dolls? I am so out of touch. The reason I was up as I had to pick up my 15-year-old from a party. After midnight. And all too soon he will be driving. And dating. What have I done?

Cocci. This is pronounced cox-e, not cox eyes. As in Coccidioidomycosis, or Valley fever.

An endlessly interesting disease, it is a fungus found in the soil of the American SW as well as in S. America. The first case ever reported was a disseminated infection in a South American cowboy, Domingo Ezcurra, who eventually died of the disease. His pickled head is still available for observation, in a jar at a S. American medical school. It's here ( botit.botany.wisc.edu/toms_fungi/images/ezcurra.jpg (http://botit.botany.wisc.edu/toms\_fungi/images/ezcurra.jpg)) if you want to be grossed out. What other science blog gives you the opportunity to see not just a pickled head, but an historically important pickled head?

My current patient is not going to be that unfortunate, but he does have chronic Cocci pneumonia with cavities that is not responding as it should to high dose oral fluconazole. He is probably not improving as his diabetes is not under the best of control, but then the infection makes it hard to control the diabetes, so around and around we go.

But, after a good college try, it is time to declare a fluconazole failure and try intravenous amphotericin B.

I wonder if there is a difference in diabetics with Cocci that makes them less responsive to medications due to differences in the Cocci rather than the usual worser white cell function of the diabetic: they are more likely to have mycelial forms of the disease.

"Type 2 diabetic patients with pulmonary coccidioidomycosis were four times more likely than non-diabetics to develop parasitic mycelial forms. We formulated a comprehensive definition based on the results as follows: patients with pulmonary coccidioidomycosis with an evolution longer than 8 months, cough, hemoptysis, radiological evidence of a cavitary lesion, and type 2 diabetes mellitus, develop parasitic mycelial forms of Coccidioides spp. Based on microscopic images of patient specimens, we propose incorporating mycelial forms into the parasitic phase of Coccidioides spp. in patients with type 2 diabetes mellitus and chronic and cavitary pulmonary coccidioidomycosis."

Way back in the last century, when I was a young ID fellow with hair and vision, I was taught there was one Cocci, found in the New World. But that makes no sense. The Cocci of S. America evolved separately from the Cocci in the San Juaquin valley, and should be different. And indeed they are. The U.S. Cocci is Coccidioides immitis while that in South and Central America is C. posadasii. They are treated the same and are probably clinically the same. But they are not the same. Like the Patty Duke show.

This patient got his Cocci the old-fashioned way: wintering in Arizona. When I go to the American SW, I make a point of not inhaling. However, exposures to Cocci can be brief. I have seen two people get a lung resected for worry of cancer: smoking truckers with big lymph nodes on their chest on CT, weight loss and chronic pneumonia. In both cases the bronchoscopy showed atypical cells that could be cancer, so, given the history, off to the OR to take a lung out. It was only on the deep pathology that the classic spherules of Cocci were seen. There is no Cocci here in Oregon, but these truckers drove I-5 to L.A., right through the heart of Cocci territory.

Take-home message: don't take out a lung until after you have taken a good history.

Rationalization

Eur J Clin Microbiol Infect Dis. 2008 Sep;27(9):813-20. Epub 2008 May 30. Mycelial forms of Coccidioides spp. in the parasitic phase associated to pulmonary coccidioidomycosis with type 2 diabetes mellitus. (http://www.ncbi.nlm.nih.gov/pubmed?term=18512089)

Hamsters

Published Sat, 03 Jan 2009

I went and saw Bolt with my 11-year-old today. Entertaining movie, but the 3D animated effects are jaw-dropping.

It is the story of the adventures of three infectious disease vectors: a dog, a cat and a hamster. As is often the case after we see movies with animals in them my son asks for a pet, and, as is usual, I demur. Not because I worry about infections, but prior experience with vermin, I mean pets, has demonstrated that the responsibility for their care usually devolves on to me.

Hamsters are a source for the LCM (Lymphocytic Choriomeningitis) virus, a disease that causes aseptic meningitis. Hamsters have also been associated with the spread of multi-drug resistant Salmonella. And I don't think they taste near as good as a Guinea Pig.

LCM is spread from hamsters to humans, and can be fatal in the immunoincompetent, although it is often asymptomatic in normal people.

There have been occasional outbreaks, but the most curious case was the patient who died and had their organs harvested (the live ones tend to resist) and the recipients of the organs developed LCM. This has happened at least twice.

In one outbreak

"The epidemiologic investigation revealed that a member of the donor's household had brought home a pet hamster three weeks before the donor died. Although the donor had not been the primary caretaker of the hamster, she had contact with the rodent's environment on multiple occasions."

The donor was asymptomatic at the time of the organ donation.

I am always amazed at what can be transient exposure to pathogens yet patients still get disease.

We did have a hamster once. My eldest son bought one and proudly brought it home.

Here dad, hold it.

I did, and the damn thing promptly bit me, drawing blood.

A couple of months later, in the dead of winter, the rodent escaped its cage, fell down the heating duct, and promptly died on one of the electric hearing coils, filling the house with the smell of cooking, then cooking and rotting, hamster.

It costs 400 dollars for the heating guy to disassemble the system and clean up the decomposing hamster. He barfed at least once.

Just imagine what a dog or cat would smell like if it did the same. Nope. No pets for us.

Rationalization

Lymphocytic Choriomeningitis Virus Infection in Organ Transplant Recipients --- Massachusetts, Rhode Island, 2005 (http://www.ncbi.nlm.nih.gov/pubmed?term=15931158)

Transmission of Lymphocytic Choriomeningitis Virus by Organ Transplantation. (http://www.ncbi.nlm.nih.gov/pubmed/16723615) N Engl J Med 2006; 354:2235-2249

My awesomeness recognized

(by someone besides my youngest child)

Published Sun, 04 Jan 2009

Many thanks to the lunatic, er, I mean, perspicacious reader who nominated me for one of the best science blog entries for 2008. I actually won. My 11-year-old is psyched.

See all the winners at http://scienceblogs.com/clock/2009/01/the_open_laboratory_2008_and_t.php

Zits

Published Tue, 06 Jan 2009

Infected artificial hips are a major source of morbidity for the patient.

At a minimum they need to have the hip washed out and a long course of IV and oral antibiotics.

At a maximum the have to have the joint taken out and they go jointless for 3 months or more, which will never do for Willie Nelson.

These infections are usually Staphylococci of one sort or another, but this patient had gram-positive rods in a three-year-old prosthetic hip.

Propionibacterium acnes is a bug of greasy, hairy males.

Propionibacterium acnes is an anaerobe that grows in the oils of hair follicles, men tending to the furry and the oily side. It lives in a protected site in that the antibiotic scrubs do not get into the follicle, the IV antibiotic does not get into the follicle, and so the bug is protected from all our measures to prevent operative infections.

The best protection is to be a hairless female, but that hardly seems worth it.

This bug done gets dragged into the wound and, if there is artificial material or devitalized bone, it hunkers down and causes the most indolent of infections. It is not unheard of to have 5, 6, 7 years elapse between the surgery and the clinical presentation of the infection.

I had one case with 8 years between the craniotomy and the presentation of the brain abscess that the surgeon said looked (but did not taste) like scrambled eggs and grew P. acnes.

Treatment is problematic. For CNS shunt infections, vancomycin plus ceftriaxone may be best. In my experience ('in my experience' being the three most dangerous words in medicine) clindamycin works better than penicillin, and it is one of the few anaerobes that are resistant to metronidazole.

The lowly zit bug. When you are young it messes the mirror, when you are old it messes with your hip.

Rationalization

J Infect. 2007 Aug;55(2):119-24. Propionibacterium acnes: an agent of prosthetic joint infection and colonization. (http://www.ncbi.nlm.nih.gov/pubmed/17418419)

BBF. Blood and Body Fluid.

Published Wed, 07 Jan 2009

One of the few huge fights my wife and I have had was when we were taking childbirth classes and the leader had the men and women separate into groups and share our feeling about what it meant to be a parent.

I said that feelings are like blood and body fluids: I don't share them with strangers.

For some curious reason I was thereafter considered the class asshole. Go figure.

BBF's are not something you want to be inadvertently exposed to at work and probably not in your spare time either. BBF's carry infectious diseases like hepatitis B, hepatitis C and HIV.

In the hospital we have many clever ways to prevent needle sticks, the most common work associated mechanism whereby our employees get a BBF exposure, although splashes are becoming more common.

Murphy was an optimist and somehow we still manage to get the occasional needle stick despite needleless systems and needle guards. I think the hand has an attraction to being poked by sharp needles.

Needle sticks are probably under-reported, especially in the OR and surgeons, and I strongly advise safe sex with any surgical resident until you know their infection status, not that I have sex with residents mind you, just sayin'.

The risk of infection from a needle stick depends on whether or not it is a hollow bore (the needle, not the surgeon), whether there is visible blood, how deep the injury is, and whether gloves are worn.

The risks are variably reported, but for needlestick injuries involving blood-contaminated with HIV, needles can spread the virus in 0.3% of cases. The risk of transmission of HBV from a needlestick injury varies from 1% to 40%. Hep B is the one to worry about, so I hope you got your vaccine. The risk for hepatitis C virus transmission from a needle stick is about 1.8% (range 0% to 7%).

If you get a needle stick, you need testing then medications to try and prevent HIV. So far we have not had an HIV transmission from a needle stick, knock on faux wood veneer.

What is curious is all the calls I get for odd BBF exposures.

Many times cleaners get stuck from needles left in restrooms and hotel rooms. Usually it is insulin syringes, but IVDA are not particularly fastidious at properly disposing of their drug paraphernalia.

There have been those that have had a one night stand and are worried about bringing something home to the wife. It is always a man. Men are pigs, in case you are interested.

My old boss liked to tell the story of when the ID meetings were in Las Vegas. He was at the hotel bar waiting for a friend and a lady asked him if he was interested in a 'date,' which he declined. She asked what kind of meeting was in the hotel as business was particularly slow. ID docs know too much to be swine.

People have been stuck with needles cleaning up parks, one kid was stuck when someone put their needle in a coin return and he stuck his finger in looking for change. Cops have been stuck and bit wrestling with the crazy and the felonious.

The call today was someone who was helping at a halfway house and a junkie stumbled and fell on him, jabbing his thigh with a syringe.

My all-time favorite was a guy at a strip club and the performer was lactating, and when she gave a spin he got milk in his eye. I was asked by the ER if he needed HIV prevention. I was laughing so hard I do not think I ever gave an answer.

Rationalization

N Engl J Med. 2007 Jun 28;356(26):2693-9. Needlestick injuries among surgeons in training. (http://www.ncbi.nlm.nih.gov/pubmed/17596603)

Leaks

Published Thu, 08 Jan 2009

What the patient has is often easy in ID. They grow something from a fluid that should not have bacteria in it. In this case, it was S. pneumoniae in both the blood and the spinal fluid. Easy enough. Bacteremia with meningitis.

The hard part is why. "Why? Why, why, why, why, why? Luck! Blind, stupid, simple, doodah, clueless luck!" Usually the patient has bad luck and that is not a very satisfying answer to the question.

There are well-known risk factors for developing S. pneumoniae bacteremia in the adult, the big two being HIV and something wrong with immunoglobulins, and in my world that means a hematologic cancer like multiple myeloma or Waldenstroms. Anytime I have a patient with S. pneumoniae in the blood, especially someone who shouldn't (i.e., a nonsmoker/drinker) I check an HIV and an SPEP, and more often than not I hit pay dirt.

However, in this case neither of these risk factors are probably going to be the reason as the patient is too young.

One of the curiosities of meningitis is that the etiology of meningitis in CSF leaks is usually S. pneumoniae. The first case and the second and the third. One would think that if your spinal fluid was leaking into your nose or throat that you would get meningitis from the common organisms of that part of the body, but the answer to the question: what is the cause of recurrent S. pneumoniae bacterial meningitis? A CSF leak. Remember that. Not that I have any inside information, but it could be a bored question. Er. Board question.

Finding CSF leaks is both hard and easy. Easy as the patient often has sweet (yes, people taste their snot), clear chronic runny nose from one nostril and a history of head trauma.

Years ago, trying to dodge a sprinkler one evening I ducked right into the back of a metal chair splitting my head open. Ever since I have had a chronic left sided nasal drainage. Or do I? Am I just paranoid doctor? Can you see me through my iSight camera? You can, can't you? Spies everywhere, out to get me...Thank you, I will take my Thorazine now.

Hard in that the leak can be tiny and finding and fixing it is technically difficult. One patient, when he was told that to fix his leak they had to pop off his skull, lift his brain, and stuff the leak with something to block the leak (the neurosurgeon didn't use quite these words) the patient said no way, they are not doing that to him, and he has now had 7 cases of bacterial meningitis (he now works as a president of GM.). And that is not the record. The problem is each episode leaves him a little more brain-damaged and less able to make a rational decision; it’s hard to change your mind when it has been damaged.

The case has a history of head trauma of the worst kind, a gunshot wound to the head a decade ago, and it looks like the buckshot may have eroded though the bone, leaving a tunnel from the infected sinus to the brain. A good reason to develop meningitis, and a hard one to fix. She will be seeing a surgeon soon, in the mean time I will make sure she gets both of the S. pneumoniae vaccines, as that is her best bet for prevention of recurrence.

Rationalization

Twelve episodes of meningitis in the same patient (http://www.ncbi.nlm.nih.gov/pubmed/18604029)! Kathmandu Univ Med J (KUMJ). Apr 2007-Jun;5(2):243-6.

Prophylaxis?

Published Fri, 09 Jan 2009

Few diseases freak the ER out more than a case on meningococcal meningitis. The reason is not the rapid, horrible death of the patient, but that this is one of the few diseases that casual contact with the index case, aka the patients, increases your risk of getting the disease yourself. Then you get to have a rapid, horrible death.

If you are a household contact with a case of meningococcal meningitis then your risk of getting the disease is 500 to 800 times that of the general population.

Because of this, it is recommended that anyone who has been in a room for 4 or more hours with a person with meningococcus without a mask or has contact with the patient’s spit, needs chemoprophylaxis: rifampin or ciprofloxacin or ceftriaxone.

It is also recommended that them what have sat next to an index case on an airplane get prophylaxis as well, not that there has been a case of meningococcus spread this way, although there has been spread of TB. It is a recurrent theme of this blog: just do not inhale. It only gets you in trouble.

No doctor has EVER spent 4 hours in a room with a patient, although we do get exposed to the odd bit o' spittle now and then, mouth to mouth resuscitation being the classic exposure. So it is rare that a doc needs prophylaxis, and most other health care providers do not need prophylaxis as well, especially if they are wearing a mask. However, if there is a case of meningitis, before the cultures are back, many of the providers are in panic mode and in the ER looking for an antibiotic.

The family of the case mentioned in yesterday’s post ended up in the ER asking for prophylaxis, which they did not need as the meningitis was not due to meningococcus.

The interesting question that arises with the need for prophylaxis is whether the reason family members need prophylaxis is not that the strain causing the meningitis is more virulent but that the host is more susceptible.

There are several genetic variations in the immune system, aka polymorphisms, that predispose patients to developing meningococcal meningitis: my favorite, as I have mentioned before, being alterations in snot, or as the more scientific among us call it, surfactant protein-A2. If I ever get a parrot, I am going to teach it to say, "Polly wants a morphism." Just as if I ever get a monochromatic dog, it will be named Spot.

The reason we get sick and die is often in our genes. I have a vial of MRSA in my Calvin Klines. For homeland security, if you are reading this, that was meant to be a joke

It may be that the health care professional, as well as the talented amateur, does not need the prophylaxis. Perhaps a genetic predisposition in families is the reason why families have in increased risk of disease and not the exposure in and of itself. Perhaps we are inappropriately extrapolating family data to health care workers who screw up on basic infection control procedures.

On the other hand I had a patient with meningococcus whose only exposure was sharing a beer three week prior with his friend who subsequently had meningococcus. As is often the case, the answer in not clear cut, although the take home here may be to not drink from a friend’s longneck.

Rationalization

Exposure to Patients With Meningococcal Disease on Aircrafts (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5023a2.htm). MMWR

Clin Infect Dis. 2006 Dec 1;43(11):1426-33. Epub 2006 Oct 31. Genetic polymorphism of the binding domain of surfactant protein-A2 increases susceptibility to meningococcal disease. (http://www.ncbi.nlm.nih.gov/pubmed/17083016)

Relevance of Fcgamma receptor and interleukin-10 polymorphisms for meningococcal disease. (http://www.ncbi.nlm.nih.gov/pubmed/11740730) J Infect Dis. 2001 Dec 15;184(12):1548-55. Epub 2001 Dec 3.

Dead Parrot Sketch

Published Sun, 11 Jan 2009

People are always stranger than I can possibly imagine. In medicine we get to see doozies, and one of the aspects that makes being a doc fun and interesting is that I get to see all kinds of people, from crazy street people to presidents of banks, but I do not have to go home and have dinner with them.

When you have spent a quarter of a century in medicine, and in particular Infectious Diseases, you become comfortable that infectious diseases are due to germs. There are lots of different germs, and they cause a variety of diseases. Group A streptococci causes cellulitis, P. falciparum causes malaria and HIV causes AIDS.

HIV has been a particularly interesting one because I have watched it from the beginning. The first cases of HIV were reported in the MMWR in 1981, when I was in my second year of medical school. By the time I was a resident I was seeing cases of young gay men dying of some sort of disease, but what it was and how it killed them was a mystery. Then they discovered what was at first called HTLV then HIV. We knew what was killing our patients but we couldn't do squat to prevent it. Then there was roller coaster years as new HIV medications were developed that worked for a short period of time, failed, and then the inevitable death.

Over the last 25 years we have gone from a 9-month life expectancy to, in many patients, an almost normal life expectancy due to the application of a remarkable understanding of the physiology of the HIV virus and the development of HAART. It has been an astounding change.

This week I saw one of my HIV patients who presented in 1999 dying of AIDS with CD4 cells of 90, PCP and an HIV viral load of 300,000. Now is virus is suppressed, his immune system is normal and he has a productive, happy life.

It is immensely satisfying to know he has a good chance of outliving me.

It is why I find the HIV deniers so baffling. Christine Maggiore died last week of untreated AIDS. She was one of the leaders of the HIV deniers and she so believed that HIV did not cause AIDS that she evidently let her daughter acquire and die of AIDS.

It is sad and odd. The information that supports HIV/AIDS is enormous, with almost 194,000 references on HIV in Pubmed as of today. When I read the web sites of those who deny HIV as the cause of AIDS, it is like reading papers from bizarro world, with a twisted alternative understanding of what I would call the real world. The willful disregard of reality is mind-boggling, akin to denying gravity or the inability to breathe under water, then behaving accordingly. And dying. I am reminded of a Monty Python bit, where one of the characters refuses to recognize reality, be it the Black Knight (it's only a flesh wound) or a pet shop owner. More of Monty Python meets the Twilight Zone, really, given the outcome.

You unlock this door with the key of imagination. Beyond it is another dimension - a dimension of sound, a dimension of sight, a dimension of mind. You're moving into a land of both shadow and substance, of things and ideas. You've just crossed over into the Twilight Zone. Submitted for your consideration, a parrot dies of AIDS.

Dead Parrot Sketch

The cast:

MR. PRALINE

John Cleese

HIV Denier

Michael Palin

The sketch:

A customer enters a pet shop.

Mr. Praline: 'Ello, I wish to register a complaint.

(the owner does not respond).

Mr. Praline: 'Ello, Miss?

HIV Denier: What do you mean "miss"?

Mr. Praline: I'm sorry, I have a cold. I wish to make a complaint!

HIV Denier: We're closin' for lunch.

Mr. Praline: Never mind that, my lad. I wish to complain about this parrot what I purchased not half an hour ago from this very boutique.

HIV Denier: Oh yes, the, uh, the Norwegian Blue...What's,uh...What's wrong with it?

Mr. Praline: I'll tell you what's wrong with it, my lad. 'E's dead from HIV, that's what's wrong with it!

HIV Denier: No, no, 'e's uh,...he's resting.

Mr. Praline: Look, matey, I know a dead parrot when I see one, and I'm looking at one right now.

HIV Denier: No no he's not dead, he's, he's restin'! Remarkable bird, the Norwegian Blue, idn'it, ay? Beautiful plumage!

Mr. Praline: The plumage don't enter into it. It's stone dead from HIV.

HIV Denier: Nononono, no, no! 'E's resting!

Mr. Praline: All right then, if he's restin', I'll wake him up! (shouting at the cage) 'Ello, Mister Polly Parrot! I've got a lovely fresh cuttle fish for you if you show...

(HIV Denier hits the cage)

HIV Denier: There, he moved!

Mr. Praline: No, he didn't, that was you hitting the cage!

HIV Denier: I never!!

Mr. Praline: Yes, you did!

HIV Denier: I never, never did anything...

Mr. Praline: (yelling and hitting the cage repeatedly) 'ELLO POLLY!!!!! Testing! Testing! Testing! Testing! This is your nine o'clock alarm call!

(Takes parrot out of the cage and thumps its head on the counter. Throws it up in the air and watches it plummet to the floor).

Mr. Praline: Now that's what I call a dead parrot.

HIV Denier: No, no.....No, 'e's stunned!

Mr. Praline: STUNNED?!?

HIV Denier: Yeah! You stunned him, just as he was wakin' up! Norwegian Blues stun easily, major.

Mr. Praline: Um...now look...now look, mate, I've definitely 'ad enough of this. That parrot is definitely deceased, and when I purchased it not 'alf an hour ago, you assured me that its total lack of movement was due to it bein' tired and shagged out following a prolonged squawk. Turns out e 'as AIDS.

HIV Denier: Well, he's...he's, ah...probably pining for the fjords.

Mr. Praline: PININ' for the FJORDS?!?!?!? What kind of talk is that?, look, why did he fall flat on his back the moment I got 'im home?

HIV Denier: The Norwegian Blue prefers keepin' on it's back! Remarkable bird, id'nit, squire? Lovely plumage!

Mr. Praline: Look, I took the liberty of examining that parrot when I got it home, and I discovered the only reason that it had been sitting on its perch in the first place was that it had been NAILED there.

(pause)

HIV Denier: Well, o'course it was nailed there! If I hadn't nailed that bird down, it would have nuzzled up to those bars, bent 'em apart with its beak, and VOOM! Feeweeweewee!

Mr. Praline: "VOOM"?!? Mate, this bird wouldn't "voom" if you put four million volts through it! 'E's bleedin' demised!

HIV Denier: No no! 'E's pining!

Mr. Praline: 'E's not pinin'! 'E's got AIDS E's passed on! This parrot is no more! He has ceased to be! 'E's expired and gone to meet 'is maker! 'E's a stiff! Bereft of life, 'e rests in peace! If you hadn't nailed 'im to the perch 'e'd be pushing up the daisies! 'Is metabolic processes are now 'istory! 'E's off the twig! 'E's kicked the bucket, 'e's shuffled off 'is mortal coil, run down the curtain and joined the bleedin' choir invisible!! THIS IS AN EX- HIV INFECTED PARROT!!

(pause)

HIV Denier: Well, I'd better replace it, then. (he takes a quick peek behind the counter) Sorry squire, I've had a look 'round the back of the shop, and uh,we're right out of parrots.

Mr. Praline: I see. I see, I get the picture.

HIV Denier: I got a slug.

(pause)

Mr. Praline: Pray, does it talk?

HIV Denier: Nnnnot really.

Mr. Praline: WELL IT'S HARDLY A BLOODY REPLACEMENT, IS IT?!!???!!?

HIV Denier: N-no, I guess not. (gets ashamed, looks at his feet)

Mr. Praline: Well.

(pause)

HIV Denier: (quietly) D'you.... d'you want to come back to my place?

Mr. Praline: (looks around) Yeah, all right, sure.

And I bet they didn't use a condom.

See Em Vee

Published Tue, 13 Jan 2009

CMV. Sounds like a Honda sedan. It stands for Cytomegalovirus. A disease of children, AIDS and organ transplant patients, it is rarely seen in normal people. Or is it?

The middle-aged single male needed to have a diverting colostomy, too, well, divert. Stuff. The particulars are not relevant to the case.

As part of the preparation he had a colonoscopy and, much to the surprise of the person looking up the old colon, there were small ulcerations and a patchy, angry red colon.

The patient had no symptoms of colonic problems, so the findings were unexpected.

The biopsy was even more unexpected: CMV.

The heck.

CMV colitis is seen in end-stage AIDS patients and bone marrow transplant patients. It is not a disease of normal people. I think.

He appears to be immunologically normal, and his HIV is a negative.

Thank goodness for Pubmed. It is what makes every consultant look more knowledgeable than they are.

Turns out CMV can cause both severe and mild colitis in normal people. Most of the case reports are severe disease, and given the commonness of the Hershey squirts, I bet these represent the tip of a diarrheal iceberg. I shudder to think what damage a diarrheal iceberg would do to an ocean liner. The Titanic had it easy.

The few reported cases of mild disease suggest CMV colitis is probably self-limited. My patient has no symptoms, so I will check his immune system as best I can and watch. ID docs are the only physicians who do not have to treat every culture that comes their way.

But I wonder if mild colitis, maybe often with minimal or no symptoms, is a common manifestation of CMV that we miss since the ubiquity of diarrhea makes it unlikely that people would receive a diagnostic colonoscopy.

Now I am going to have a peanut butter sandwich. No CMV, just the risk of Salmonella.

Rationalization

Viol J. 2008 Mar 27;5:47. Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review. (http://www.ncbi.nlm.nih.gov/pubmed/18371229 ) Dig Dis Sci. 2005 Apr;50(4):609-16.

Serologies

Published Wed, 14 Jan 2009

Diagnosing infectious diseases with serology is sketchy.

Infections will lead to an antibody response and, by measuring the type of antibody and the increase in the titer of antibodies and what bacterial structures have caused an antibody response, you may be able to identify an infection with something you cannot grow.

The problem is that serology can be unreliable.

Patients may make antibody that you cannot measure.

Patients may not make antibody to the infection.

Patients may have a positive test, but it is cross reacting to another organism, resulting in a false positive test. HIV is screened with an ELISA test, which has a high false positive rate because there are similar viruses (viri? Pleural like Elvis?) that are not pathogenic but cause a similar reaction on a blood test. You have to confirm the HIV diagnosis with a Western blot (there is a Southern blot, but back in the day when I did these blots in the lab, there were no Eastern or Northern blots, things have changed. All the points of the compass current have a blot. But I am but mad when I blot north-north-west: when the blot is southerly I know a hawk from a handsaw), which is less sensitive but more specific.

If you live in an area where a disease does not exist, like Lyme in Portland, Oregon, then a positive Lyme test is more likely to be a false positive than a true positive. You have to interpret the test in the context of the patient’s symptoms. Making a diagnosis based on serologies alone is stupid.

Then there is the issue of labs out there that will run any test they want and seem to always have a positive test. These labs are beloved by naturopaths and other quacks as they will run tests that have no validation and always seem to be positive. Laboratories that are self-fulfilling prophecies, they specialize in worthless unvalidated tests, and naturopaths and their ilk send multiple serologies for diseases that patients have no risk or reason to have. And the tests are almost always positive, but that is probably confirmation bias, as the patient then come to me. I lost confidence in one lab when they sent me a picture of Babesia with a big arrow pointing to a platelet clump.

Lyme is particularly problematic. I saw a patient today who has no good exposure history for Lyme and a symptom complex that is not consistent with Lyme, but the Lyme serology was sent by the naturopath, to -I am too chicken to mention it as the US has 30% of the world’s lawyers- labs and it was positive. As it always is.

I remember one of these labs, and I cannot find the reference, had a test for Lyme that was positive in everyone tested, and they concluded that everyone had Lyme, not that the test was worthless.

I have two rules of thumb (rule of thumbs?).

2) Use serology to confirm what you think the diagnosis is based on the history.

1) If the serology doesn't support the clinical diagnosis, it is probably the serology that is wrong.

You are what you eat

Published Fri, 16 Jan 2009

Even after 25 years, I am still amazed at people will do to themselves to get high.

Some things are mythical. Like Jenkum. Supposedly people put human waste in a jar with a balloon on top and let it ferment, then inhale the fumes to get high. The better name is butthash, and this one I do not believe. It sounds like an urban myth that was generated just to see how stupid some people can be.

But Pruno? That made Emerging Infectious Diseases and it was not the April 1 edition either.

Pruno. What a name.

It is a prison alcoholic drink made from peeled potatoes smuggled from the kitchen, apples from lunches, one old peach, jelly, and ketchup. Inmates use heated water with an immersion heater and added it to the mixture. Ketchup, but not catsup, appears to be a key ingredient in the concoction, as is fruit. One prison banned fresh fruit to prevent the production of pruno. Like that will work.

The result is magenta in color and smelling like baby poop. Mmmmmmmmmm. Pruno.

The consequence of drinking the pruno is initially a drunk, followed in this case by Botulism, type A. I assume there was some serious vomiting as well.

The source of the botulism is probably from the potato skins. Clostridium botulinum is found in the soil as are potatoes, and there have been other outbreaks of type A botulism associated with baked potatoes and potato salad.

I have only seen a smattering of botulism in my career, all but one from home-canned foods. I saw one case as a fellow where the patient had C. botulinum in his sinus from snorting coke. There has been an outbreak with carrot juice and another with eating fermented beaver tail and paw. I prefer my beaver tail and paw stir-fried. I love those organic foods.

I am sticking with French Bordeaux's.

Rationalization

Botulism from Drinking Pruno (http://www.cdc.gov/eid/content/15/1/69.htm) Emerging Infectious Diseases. Vol. 15, No. 1, January 2009.

J Infect Dis. 1998 Jul;178(1):172-7 A large outbreak of botulism: the hazardous baked potato (http://www.ncbi.nlm.nih.gov/pubmed/9652437).

Am J Epidemiol. 1981 Apr;113(4):436-44. Restaurant-associated type A botulism: transmission by potato salad (http://www.ncbi.nlm.nih.gov/pubmed/7010999).

Botulism Associated with Commercial Carrot Juice --- Georgia and Florida, September 2006 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm55d106a1.htm). MMWR.

If you only learn one thing

Published Sat, 17 Jan 2009

My goal for each post is one factoid or cool infectious disease issue. Just one. If I can offer one new piece of information, then at the end of a year I figure my readers have had the opportunity to forget almost 365 facts. It is not often you can have the opportunity to forget so much information so effortlessly.

Call week end. Blah. Call means lots of phone calls from lots of docs with a quick curbside.

The curbside is where they ask you a question but do not want a formal consult, which is just as well on the weekend as my tux is at the cleaners, making a formal consult difficult. The term curbside, or curbstone as some call it, evidently comes from stock advice given on Wall Street by investors who could not afford an office. The past is becoming the future from the looks of things. How that got translated to medicine, I don't know. And who takes financial advice from someone who sits curbside?

So I got a phone call about S. aureus in the blood stream of a patient, probably from a catheter infection, and I told them to have the catheter pulled and placed on vancomycin pending the results of the sensitivity. The doc said, "Then give them 10 days or so of po antibiotics, right?"

Now here is the one thing I want you to learn from this blog, sear it into your brain such that when you are a drooling, mindless, demented patient in the ICU at age 102 and the medical student asks you, "How long do you treat catheter related S. aureus bacteremia?" even in your addled state you reply

"The minimum minimum minimum duration of IV therapy for S. aureus bacteremia from a line is two weeks of intravenous antibiotics," then lapse back into your confused dementia.

Got that? Two weeks IV. Minimum. If diabetic, prolonged fever, MRSA, and a variety of other confounding issues you go 4 or 6 weeks of IV. But the MINIMUM duration of IV is 2 weeks.

I suggested that they get a formal ID consult on Monday when the susceptibility testing is back.

As a self-serving aside, ID consults for S. aureus bacteremia are in the patient’s benefit. Not just my saying so, see

Impact of Routine Infectious Diseases Service Consultation on the Evaluation, Management, and Outcomes of Staphylococcus aureus Bacteremia. (http://www.ncbi.nlm.nih.gov/pubmed/18444816 )Clinical infectious diseases. 2008, vol. 46, no7, pp. 1000-1008.

Background . Staphylococcus aureus bacteremia causes considerable morbidity and mortality, and strategies to improve management and outcomes of this disease are needed.

Methods . Routine consultation with an infectious diseases specialist for cases of S. aureus bacteremia was mandated at our institution in May 2005. We compared the evaluation, management, and outcomes of cases before and after this policy change. All comparisons are by period (i.e., before or after initiation of the policy of routine consultation).

Results . In the year before and the year after the implementation of routine consultation, 134 and 100 cases of S. aureus bacteremia, respectively, were evaluated. Consultation rates increased from 53% of cases before to 90% of cases after the policy change (P < .001). Echocardiography (57% vs. 73%; P =.01) and radiographic studies (81% vs. 91%; P =.04) were used more frequently during the period of routine consultation, and infective endocarditis or metastatic infections were diagnosed more frequently (33% vs. 46%; P =.04). All 4 standards of care (removal of intravascular foci of infection, obtaining follow-up blood culture samples, use of parenteral B-lactam therapy when possible, and administration of ‚ 28 days of therapy for complicated infections) were adhered to more frequently with routine consultation (40% vs. 74%; P <.001). data-preserve-html-node="true" Treatment failure (microbiological failure, recurrent bacteremia, late metastatic infection, or death) occurred less often during the intervention year (17% vs. 12%), but this difference was not statistically significant (P =.27).

Conclusions . A policy of routine consultation with an infectious diseases specialist for patients with S. aureus bacteremia resulted in more detailed evaluation, more-frequent detection of endocarditis and metastatic infection, and improved adherence to standards of care.

Of course, the study was done by ID docs, so the results are self-serving, but have been confirmed in several other studies. Also done by ID docs. We have to look after our own.

As one last warning, note the two 'n's in annals. If you are looking for this reference on the wards and forget the second 'n', be prepared to do some 'splainin. I though the .org was for philanthropic organizations and that the hospital firewall blocked access to NSFW sites. I can't log on to Facebook, but anals.org is OK? Who knew.

So three things learned today, one of which you can never, ever, never ever forget.

1) give a minimum of two weeks IV therapy for catheter-related line S. aureus bacteremia.

2) get an ID consult for S. aureus bacteremia.

3) annals has 2 n's.

Rationalization

The review as too short course therapy for S. aureus bacteremia is at http://www.annals.org/cgi/content/abstract/119/4/304 .

Dogs

Published Tue, 20 Jan 2009

The residents say I hate dogs. Not true. I love dogs, although I do need a new recipe. I grow weary of deep-fried. I hate dog owners. Well, maybe hate is too strong a word. But as best as I can tell, there is no such thing as a considerate dog owner. Now someone is going to kvetch about kids, but I do not have to listen to kids bark all day, kids do not run up to me yipping at my heels as I walk, and kids certainly do not crap on my lawn. At least I think they don't.

Dog owners seem to think their personal vermin should be allowed access to the hospital, and increasingly these clueless goobers bring their dog into the hospital. I saw several dogs wandering the hospital with their owners this weekend.

I am not talking about seeing eye dogs, or service animals or even 'Pet Therapy' dogs, who I have my concerns about. Just regular old pets. People think that their pet should accompany them into the hospital.

Why should I care?

For one, you never know when these things will bite or crap, and I want to participate in neither.

From an infectious disease point of view people pet dogs and then do not wash their hands afterwards. It is a myth that a dog’s mouth is cleaner than a humans. It isn't. Dogs mouths are far worse than ours in terms of number and type of bacteria because they do not brush their teeth and they lick their butt. Then they lick everywhere else, including your face and hands. If I touch a patient, I wash my hands. I have yet to see a dog washed after interacting with a patient or staff, and they every bit a potential vector for infection as your physicians.

Not only can dogs carry pathogenic bacteria, but they can carry MRSA and C. difficile , both significant hospital pathogens. I do not want them, animals or their bacteria, in my hospital. I have enough trouble controlling human to human spread of disease, and do not want to add the added worry about whatever Fifi the wonder poodle is bringing into the hospital.

Ask people nicely to please take their dog outside, you might as well have asked them to eat the dog. It does not surprise me. At least here in Oregon, people care far more for their dogs than they do for their fellow humans.

Rationalization

Asymptomatic nasal carriage of mupirocin-resistant, methicillin-resistant Staphylococcus aureus (MRSA) in a pet dog associated with MRSA infection in household contacts. (http://www.ncbi.nlm.nih.gov/pubmed/12522764) Clin Infect Dis. 2003 Jan 15;36(2).

An Epidemic of Malassezia pachydermatous in an Intensive Care Nursery Associated with Colonization of Health Care Workers' Pet Dogs. (http://www.ncbi.nlm.nih.gov/pubmed?term=9494146) NEJM. 1998.

Rash Decisions

Published Wed, 21 Jan 2009

The call was to see a NHL (non-Hodgkin's Lymphoma, not National Hockey League) on the second round of chemo.

While neutropenic he developed numerous red nodules all over his body while he was recovering his neutropenia. As always, they had him on G-CSF to help his WBC return.

The worry when a neutropenic has red bump disease, as I like to call it, is that it could be a manifestation of a disseminated infection, especially a mould of some sort, and so, although he was afebrile, he had two of the lesions on the leg biopsied.

All the lesions faded except the two on his legs at the biopsy site, which developed painful ulcers with necrotic edges and surrounding redness and edema. His WBC shot to 60K presumably from the G-CSF. He did not develop a fever and looked otherwise OK.

The biopsy was negative for mould and showed vasculitis/panniculitis.

I think the patient has pyoderma gangrenosum. Dermatology always has such gross names.

It looked like pyoderma (do a Google image search if you want to get an idea what they look like) but the patient did not have a reason for the disease, or so I thought. The 'usual' underlying conditions for this uncommon disease include ulcerative colitis, Crohn's disease, rheumatoid arthritis, and myelocytic leukemia.

The interesting thing about pyoderma is that if you operate on it or biopsy it, the lesion gets worse with increased pain and ulceration, and that is what happened to that patient.

Pubmed (the consultant’s secret weapon) to the rescue, as always.

There are a smattering of cases of pyoderma associated with lymphoma. Here is the cool part: it is associated with the long-acting GCSF, Neulasta, which he was on.

There are a whopping 2 other reported cases. So here is a third case to languish in obscurity.

Rationalization

Br J Haematol. 2006 Jan;132(1):115-6. Pyoderma gangrenosum complicating pegylated granulocyte colony-stimulating factor in Hodgkin lymphoma. (http://www.ncbi.nlm.nih.gov/pubmed/16371028)

Skinmed. 2006 Mar-Apr;5(2):96-8. Pyoderma gangrenosum related to a new granulocyte colony-stimulating factor. (http://www.ncbi.nlm.nih.gov/pubmed/16603845)

True True and Related?

Published Thu, 22 Jan 2009

Group B streptococcus bacteremia is not all that uncommon, at least in my world. BUT in my world every surgery gets infected; I have a skewed outlook on the medical world. Usually Group B occurs in babies and moms around the time of delivery or in older diabetics and alcoholics for no damn good reason. Group B strep is also known as Streptococcus agalactiae. When I took my internship boards, I missed a question about Streptococcus agalactiae, which I had never heard of. I did know all about Group B strep, but did not know they were one and the same. Bastards.

The presumed pathophysiology is new GI colonization by a strain to which you have no antibody and it manages to sneak into the blood stream, often, in the older patient, seeding a joint or two.

This patient is not old, nor immunoincompetent nor peripartum, but still has a group B streptococcus in the blood.

Again my usual question: why? What is a good question, but I want to know why.

When the patient developed bacteremia she was taking a course of metronidazole for C. difficile colitis. Could they be related? I don't know. Her colon is inflamed and filled with bacteria. It could be that she had the misfortune of being colonized (no pun intended for the first and only time in this blog) at the same time she developed colitis and had the resultant bacteremia from the organisms leaking into her blood stream from the inflamed colon.

To make it even more unusual, the patient developed endocarditis that, while cured microbiologically, has required valve repair. There are fewer than 200 reported cases of endocarditis due to Streptococcus agalactiae (did I mention Streptococcus agalactiae is also called Group B strep? I would hate to miss a test question because I didn't know that. Bitter much? Ask me about neuroanatomy in med school if you want a real rant), accounting for < 2% of causes of endocarditis. Weirdness squared. Someone owes this patient a string of good luck.

Is C. difficile associated with endocarditis? Nope. Not that I can find. But chronic bowel inflammation is. And there is the well-known association between S. bovis endocarditis and bowel cancer; well known to me at least, but if you are going to be taking your medicine boards, don't say I didn't tell you.

My hypothesis is the patient seeded their valve as a complication of the C. difficile colitis. If so, it is the first case ever. You heard it here first. Since I am first, we will name it after me. And about time too.

Rationalization

Am J Med. 1992 Apr;92(4):391-5. Increased risk of bacterial endocarditis in inflammatory bowel disease. (http://www.ncbi.nlm.nih.gov/pubmed/1307218)

Clin Infect Dis. 2002 Jun 15;34(12):1576-84. Epub 2002 May 24. Streptococcus agalactiae infective endocarditis: analysis of 30 cases and review of the literature, 1962-1998 (http://www.ncbi.nlm.nih.gov/pubmed/12032892).

There is no place like Ghon

Published Fri, 23 Jan 2009

83 yo lady with recent pleural effusions fluid between the lung and the chest wall. Maybe pneumonia, she responded to a course of moxifloxacin, a quinolone antibiotic, last admission, and is back with more of the same.

Interesting CT: large pleural effusion with a large calcified something-or-other in the right middle lobe.

Large, calcified something-or-others in the right middle lobe (RML) are often old TB. When you first inhale TB it most often goes to the RML, and sets up the primary infection. After the immune system gets the TB under control, over time the initial infection calcifies, leaving the Ghon complex, named after Dr. Ghon. Crohn and Ghon share an ‘h’ that should not be there and that I can never remember where to put it.

Her history is interesting. She lived her entire life in Oregon, but the family of playmates as a child all had TB, and it (TB, not the playmates) evidently killed a couple of them.

She tells me she as always had this bit of calcium in her lungs. Even though the Ghon complex is calcified, there are probably still live organisms in the center. Unlike love, TB is forever.

The pleural fluid is mid way between exudate and transudate, and has 30% eosinophils.

Some pleural effusions from TB occur when an old pleural granuloma ruptures into the pleural space causing an intense allergic response, not unlike a PPD. The result is recurrent pleural fluid.

So we are sending off the tests looking for TB.

Here is the interesting thing: she got better for a while on a quinolone. These antibiotics are excellent therapy against TB and taking them for routine pneumonia leads to the delay in the diagnosis of TB. The patients with TB gets better and the treating physician thinks it is due to the treatment of routine bacterial pneumonia. They relapse their tuberculosis when the antibiotic is stopped.

“The aim of this study was to assess the effect of empiric fluoroquinolone therapy on delays in diagnosis in patients with PTB initially misdiagnosed as bacterial pneumonia...

In the fluoroquinolone group, eight patients (89%) improved clinically or radiographically, whereas only eight patients (42%) in the non-fluoroquinolone group improved (P = 0.04). The delay in initiation of anti-tuberculosis medication was longer in the fluoroquinolone group than in the non-fluoroquinolone group.”

Remind me in a month when we have all the studies back, I'll let you know if she really has TB.

Rationalization

Impact of fluoroquinolones on the diagnosis of pulmonary tuberculosis initially treated as bacterial pneumonia (http://www.ncbi.nlm.nih.gov/pubmed/16333927). The International Journal of Tuberculosis and Lung Disease, Volume 9, Number 11, November 2005 , pp. 1215-1219(5).

Empiric Treatment of Community Acquired Pneumonia with Fluoroquinolones, and Delays in the Treatment of Tuberculosis (http://www.ncbi.nlm.nih.gov/pubmed/12032896). Clinical Infectious Diseases 2002;34:1607;612.

Postscript: It wasn’t TB.

Sourdough

Published Sun, 25 Jan 2009

I had that microbial gift that keeps on giving this week. No, not gonorrhea.

Sourdough.

For years I had a sourdough starter that followed me from college to med school to Minnesota to LA and was lost, tragically, when I dropped the jar on my move home to Portland for my current job.

So for 19 years I have been sourdough free. I somehow never got the gumption back to begin another starter. I was in mourning.

Until this week. The head of my clinic has 100-year-old sourdough starter and this week she gave me a cup of ancient yeast.

I am back in business. This morning was sourdough pancakes and tomorrow it will be biscuits.

The good news is sourdough supports nutritional health. Snicker.

In studies sourdough increases the availability of nutrients, minerals and improves glycemic control in diabetics. And Saccharomyces cerevisiae is a probiotic, so it supports immune and GI health. As if my immune system is a sagging collection of flesh that needs support. Crislip’s rule number 314159. If a product is said to ‘support’ any kind of health, the only thing the product will support is the bank account of the producer of the product.

Since my yeast colony is 100 years old, it predates bioengineering and is a more natural product.

So shortly I am going to market my special Detox Immune Enhancing Sourdough starter and diet.

I am going to make a fortune.

If you can get a good sourdough going at home, do it, it is so much better than the products you buy at the store.

Rationalization

Nutrition. 2003 Jun;19(6):524-30. Making bread with sourdough improves mineral bioavailability from reconstituted whole wheat flour in rats. (http://www.ncbi.nlm.nih.gov/pubmed/12781853)

Acta Diabetol. 2008 Jun;45(2):91-6. Sourdough-leavened bread improves postprandial glucose and insulin plasma levels in subjects with impaired glucose tolerance. (http://www.ncbi.nlm.nih.gov/pubmed/18317680)

Live Blood

Published Tue, 27 Jan 2009

Most of my consults come from other doctors: the patient has an odd infection and the doc wants my involvement.

It is less common to get to see a patient in consultation at the patient's request. Usually these are "hand-holding" consults where the primary doctor has it under control, but the patient wants expert confirmation from a second opinion.

Doctor: "I'm afraid you are crazy"

Patient: "I want a second opinion."

Doctor: "OK. You are ugly too."

The outpatient today was billed as a blood stream infection. So I immediately start thinking as I walk to the room: Staph? Strep? Endocarditis? Something exotic and travel related? Most patients with blood stream infection are ill and in the hospital and bacteremia is not a subtle clinical problem. The med list contains no antibiotics, so it appears that if the patient does have an infection they either have not yet been treated, which would be odd, or they have finished treatment.

In the room is a healthy appearing young human with a thick sheaf of papers that do not look like standard lab reports.

After routine introductions, I ask my standard, "What can I do for you?"

"I have a blood stream infection."

He doesn't look ill to me.

"What kind? How was it diagnosed?"

"Well, I was having problems and since I don't have insurance I went to a naturopath who ran a bunch of tests. One of them was live blood analysis. They take a drop of blood and put it on a microscope, and they can see your immune system attacking infections in your blood stream. He showed them to me. He wanted to give me a colon detox treatment, but I thought I would see a real doctor first."

Damn.

He had a copy of the photograph of his live blood analysis. I asked him to point out the infections. He couldn't. Neither could I.

A review of his symptoms and a few physical exam findings later revealed no infectious diseases, but a moderate case of asthma and allergies to account for his symptoms.

I rarely get a referral from quacks, er, naturopaths and chiropractors. I wonder why. After I told the patient that live blood analysis is total crap (the word I used) I do not think I will see patients from that ND again. ND is short for ‘Not a Doctor’.

Live blood analysis is one of those forms of quackery where real and imaginary medicine overlap. There are a smattering of diseases, non-infectious and infectious, that can be diagnosed on blood smear: leukemia, some forms of anemia. For infections to be seen, you usually have to use stains to see malaria or leptospirosis. The vast majority of infections do no show up in a smear of the blood.

If you can see one organism per high-power field on a light microscope you have 100,000 bacteria per ml. In infected persons that degree of bacteria in the blood leads to what we call rapid death.

I perused some sample web sites of live blood analysis practitioners and they were a remarkable trip into nonsense and incompetence. They were calling the usual dirt and debris that appear on slides as pathogens.

My favorite is

“Fibrous Thallus. Indicates a nationalization of garbage,‚ like bacteria, yeast/fungus, mould, and their acid wastes and acid crystals lying in a dormant/inactive state. The diet is too high in protein, carbohydrate (sugar), and junk food, experimentation with recreational drugs and/or use of prescription drugs.”

It reminded me of the ancients who would sacrifice an animal and examine its entrails for auguries of the future. Live blood analysis is a high-tech equivalent.

Total crap.

The patient also had a collection of his labs in a bound notebook from his DC/NP with an explanation of each lab. For his CO2, which was normal, there was the comment. "Normal. Keep breathing healthy." As if he had a choice.

He paid hundreds of dollars for nonsense and didn't even get his asthma diagnosed correctly.

At least he avoided the detox colonic.

Rationalization

http://www.quackwatch.com/01QuackeryRelatedTopics/Tests/livecell.html

Ceviche

Published Wed, 28 Jan 2009

About two years ago I had a patient who had a period of nausea and vomiting and then developed at chronic lump on her skin. On biopsy it was some sort of parasite. It was too degenerated to say for sure what it was.

Today I saw a patient in clinic who has had intermittent nausea and vomiting, with a 30 lb. weight loss, and a completely negative GI work up.

By history she has the same exposure as the patient of two years ago. Both ate a lot of ceviche, a citrus marinated raw fish, while in Mexico. How can that make you sick?

The raw fish carries a parasite, Gnathostoma spinigerum, that is not killed by the lemon juice, which causes Gnathostomiasis. Which just sounds unpleasant.

G. spinigerum used to be is SE Asia, but it may have come to Mexico as part of the Tilapia fish farming.

"The life cycle of this parasite is as follows: Adult parasites of G. spinigerum are found in the stomach of mammals (e.g., dogs and cats), feces containing ova. Ova reach the water (i.e., when domestic parasitized animals live at the shore of a lagoon). Free-swimming first-stage larvae are formed, which are ingested by the minute copepod copepod: see crustacean. Any of the 10,000 known species of crustaceans in the subclass Copepoda. Copepods are widely distributed and ecologicaly important. Most of the 44,000 crustacean species are marine, but there are many freshwater forms. cyclops, and become second-stage larvae. Freshwater fish eating cyclops are the second intermediate host. Larvae develop to the third state (L3) in the fish muscles. Consumption of this fish by cats, dogs, or other mammals results in development of adults in the gut, closing the cycle. Humans acquire the infection by consuming raw or undercooked freshwater fish. When a larva is ingested by a human host, no further development occurs, but the larva migrates through subcutaneous tissue and internal organs where it produces migratory swelling in the skin and other symptoms depending on the site or organ affected. In most cases, symptoms are not serious; however, if the parasite migrates to vital organs of the host, it can cause severe illness or even death"

G. spinigerum is noted to cause eosinophilic meningitis and migratory itchy skin rashes as the parasite wanders through your tissues looking for a place to live. It can cause gastrointestinal symptoms, which has been the patient’s primary complaint, although there are features of the presentation (lack of eosinophilia) that make me doubt the diagnosis and I have been pursuing some other ideas.

But as the first reference states,

"A diagnosis of gnathostomiasis should be considered for patients with a history of transient, migratory cutaneous or subcutaneous swellings, or nonspecific gastrointestinal symptoms for which a potential epidemiologic exposure is identified ."

The main point of this entry?

Ooooo icky poopy, a worm.

The only good fish is a fried fish.

The best thing of all? If I am right, I will have aced the diagnosis that another local ID doc missed. My enormous ego needs constant feeding.

Mmmmmmmm. Right diagnosis.

Rationalization

Moore DAJ, McCrodden J, DeKumyoy P, Chiodini PL. Gnathostomiasis: an emerging imported disease. (http://wwwnc.cdc.gov/eid/article/9/6/02-0625.htm) Emerg Infect Dis [serial online] 2003 Jun [date cited].

Emerg Infect Dis. 1999 Mar-Apr;5(2):264-6. Gnathostomosis, an emerging foodborne zoonotic disease in Acapulco, Mexico. (http://wwwnc.cdc.gov/eid/article/5/2/99-0211\_article.htm)

Shazam!

Published Wed, 28 Jan 2009

Keeping healthy is not necessarily a process filled with comfort and dignity. Women have to endure the pelvic exam when they are young. Men get the prostate exam as they age. Note the word is prostate. Not prostrate. Although sometimes you have to be the latter to get the former evaluated. If you have problems peeing from prostate obstruction and the urine gets infected, those bacteria have to go somewhere. If not into the urinal, they will get into the blood stream.

There is a vascular connection between the bladder/prostate and the spine, called Batson's plexus, named after Billy Batson, aka Captain Marvel. It is a set of valveless veins that go from the bladder to the lumbar spine. This can be a highway to the spinal cord for bacteria, as the patient this week demonstrated. He, and it is always a he, as it is the rare female who gets bladder outlet obstruction from an enlarged prostate, had progressive difficulty urinating, then got infected, then developed back pain and had discitis and a spinal epidural abscess.

Most of the infections that occur for this reason had E. coli as the cause, since E. coli is the most common cause of urinary tract infections. Not so in this case, as the epidural and the urine grew out Streptococcus agalactiae, aka Group B streptococcus.

Odd as there are a whopping three cases in adults in the literature of this organism causing epidural abscesses. As a cause of UTI in non-pregnant females, it is also uncommon and even more unusual in non-pregnant men. I cannot find data on pregnant men, of which we currently have one in Oregon.

Now drained, I expect a cure with a long course of antibiotics. At least I can still kill a Group B strep.

It is good to pee.

Rationalization

Enferm Infecc Microbiol Clin. 2004 Feb;22(2):89-91. Clinical significance of Streptococcus agalactiae isolation from urine samples of outpatients from health care centers. (http://www.ncbi.nlm.nih.gov/pubmed/14756990)

Fooled Again

Published Fri, 30 Jan 2009

When young females present with fevers and flank pain, you think: pyelonephritis. Common things are common in medicine and tautologies are tautological.

And that is what the outpatient docs thought. However, she was no better on several days of oral ciprofloxacin so she was admitted for IV therapy.

Her WBC kept going up (35,000) so they called me.

Part of the purpose of this blog is to alter events to make me look like SuperDoc ™, and this will be no different.

There were several curious features when I saw her.

While her urine dip (not for potato chips) was positive for WBC, her microscopic exam demonstrated no pyuria; the negative cultures were attributed to the oral antibiotics.

Her CT of her kidneys on admission had no stones and no abscess.

And boy did she have flank pain. The lightest of thumps on the right flank elicited extreme pain. She said that the pain radiated abound her back and into her right lower quadrant. Just like a kidney stone. But she looked surprisingly nontoxic for someone with a WBC of 35K, and not much of a fever.

I bet she had an appendix gone south and CT showed a huge abscess due to a ruptured appendix that the surgeon described in the OR as looking like a grenade had gone off in her peritoneum.

The flank pain that fooled everyone? The abscess had dissected into her paraspinous muscles.

A classic H&P for pyelonephritis that turned out to be something else.

And lest you think I am always right, yesterday I bet that a patient had Legionella pneumonia. The confirmatory test today? Negative. A swing and a miss.

When you are a consultant it is fun to try and predict the diagnosis and the odd time you are right will impress people far out of proportion to the more numerous misses. It is the ID equivalent of what Biggest Douche Bag in the Universe does.

Years ago I saw an 18 yo girl with known valvular heart disease with the question of whether or not she had endocarditis.

She had 5 days of fevers, headache, myalgias, that left for five days, recurred for five days and left for 5, then recurred yet again.

For fun I asked, "How was your vacation at Black Butte?"

The look of shock and awe (TradeMark: Harlan K. Ullman and James P. Wade ) on her face when she asked "How did you know I was at Black Butte" was one of the more satisfying responses of my career.

She had the history suggestive of relapsing fever and the one place in Oregon with this disease is Black Butte.

Home run with the bases loaded.

Few remember that Babe Ruth also led in strikeouts for several seasons.

Rationalization

Radiographics. 2004 Oct;24 Suppl 1:S11-28; discussion S28-33. Mimics of renal colic: alternative diagnoses at unenhanced helical CT (http://www.ncbi.nlm.nih.gov/pubmed/15486235).

Grand Rounds Part 1: Where is Ra's al Ghul when we need him?

Published Sat, 31 Jan 2009

Friday the 6th I will participate in Grand Rounds as part of a panel discussing the medical complications of global warming.

To kill two stones with one bird, what I prepare for the lecture I will translate into a quick blog entry.

Everyone knows that the burning of fossil fuels combined with the endless flatulence of humans and our domestic animals are part of the cause of the increase in the greenhouse gasses and subsequent global heating.

It has been made famous with the readings of CO2 on Mauna Loa in Hawaii with the yearly increase in CO2 since 1960 and the correlation with increasing average temperature:

What is more cool, or hot, is that these changes in greenhouse gasses can be measured in ice cores going back thousands of years. The interesting results of these measurements include:

"Beginning 8,000 years ago, humans reversed an expected decrease in CO2 by clearing forests in Europe, China, and India for croplands and pasture.

Beginning 5,000 years ago, humans reversed an expected decrease in methane by diverting water to irrigate rice and by tending large herds of livestock.

In the last few thousand years, the size of the climatic warming caused by these early greenhouse emissions may have grown large enough to prevent a glaciation that climate models predict should have begun in northeast Canada.

Abrupt reversals of the slow CO2 rise caused by deforestation correlate with bubonic plague and other pandemics near 200-600, 1300-1400 and 1500-1700 AD. Historical records show that high mortality rates caused by plague led to massive abandonment of farms. Forest regrowth on the untended farms pulled CO2 out of the atmosphere and caused CO2 levels to fall. In time, the plagues abated, the farms were reoccupied, and the newly re-grown forests were cut, returning the CO2 to the atmosphere."

Two thirds of Europe died in the 1300s from bubonic plague and estimates of New World deaths from new infections are as high as 95% of the population in the 1500s. The result was a slow down in global warming. Dead people make less gas.

So there may be hope for the reversal for global warming. Anyone want to get in line to participate in the great human die off?

I didn't think so.

Rationalization

THE ANTHROPOGENIC GREENHOUSE ERA BEGAN THOUSANDS OF YEARS AGO (http://stephenschneider.stanford.edu/index.html). WILLIAM F. RUDDIMAN

Grand Rounds Part Deux

Published Sun, 01 Feb 2009

Everyone complains about the weather, but no one tries to change it.

Long-term climate change will affect ecosystems to increase or decrease disease spread, and along the way there may be changes in weather to facilitate the spread to disease. Oregon is wet, but we lack much in the way of Legionella. As I have discussed once before, Legionella is spread when there is hot, humid, thundershower weather. In Oregon we have cold, wet rain. Or at least we used to.

Climate change models, and perhaps even supermodels, suggest Oregon will get warmer and wetter in the winter.

The cold is important. Legionella do not grow nearly as well in amoebas (part of their life cycle in the wild) when the temperature is less than 20 degrees. That's centigrade, not Kelvin.

Warm wet weather? Don't inhale. Curiously there are no cases associated with bongs although it is suggested that tetrahydrocannabinol increases your risk for Legionella. David Gilbert once presented a case at conference of a Legionella from a humidifier used to treat a head cold. Close enough? Legionella

"... cases occurred with striking summertime seasonality. Occurrence of cases was associated wit monthly average temperature and increase in relative humidity. However, case-crossover analysis identified an acute association with precipitation and increased humidity 6-10 days before occurrence of cases."

The association with increased rainfall has been confirmed in other studies.

But it is more than just the rainfall. The warm, moist weather facilitates the spread of Legionella from environmental reservoirs.

There have been outbreaks of Legionella associated with cooling towers, and the warm wet weather helps spread the contaminated mists from the cooling towers downwind, spreading the disease for miles. Sort of a macro-bong effect.

Legionella are also associated with fountains of all kinds, whirlpools, showers, wash basins, lakes, ponds, streams, and rainwater collected on roofs.

WC Fields said he didn't drink water because fish poop in it. Maybe he was on the right track after all.

Rationalization

Euro Surveill. 2007 Mar 1;12(3):223. Community outbreak of Legionnaires disease in Vic-Gurb, Spain in October and November 2005 (http://www.ncbi.nlm.nih.gov/pubmed/17439808).

Epidemiol Infect. 2007 Jul;135(5):811-7. Increased rainfall is associated with increased risk for legionellosis (http://www.ncbi.nlm.nih.gov/pubmed/17121693).

Proc Soc Exp Biol Med. 1995 Jul;209(3):205-12. delta 9-Tetrahydrocannabinol, cytokines, and immunity to Legionella pneumophila (http://www.ncbi.nlm.nih.gov/pubmed/7777582).

Grand Round Part Tois

Published Tue, 03 Feb 2009

There are two factors that may increase or decrease infections with global warming.

The first is people will need to move and they will bring diseases with them. Water is what is going to make them move. Large numbers of people live along coastlines and as the oceans rise, people will move, with the possible exception of the Canute family.

As someone said, we can out run sea level change.

The other reason people will move is looking for drinking water. As one example, 30 million people get their drinking water from the Andes glaciers, most of which will be gone in perhaps 30 years. They will not be drinking bottled water as a substitute.

Climate change will alter the distribution of many vectors of infections, most importantly mosquitos. It has been estimated that more than half of everyone who has ever died has died of a mosquito borne illness. To get a the hint of our future (this is a US centric blog) look at, but do not move to, Brownsville, Texas, where 40% of the residents are now seropositive for dengue. Dengue is classically a disease of central America, but as the environment becomes more hospitable for mosquitos, they go north, bringing with them their diseases. Where is Horace Greeley when you need him? Climate models suggest that a 4 degree rise in temperature could lead to the spread of dengue as far north as Chicago and Winnipeg. Malaria could reach as far north as Maine.

Disease spread is not just limited to mosquitos.

In Belgium (sorry for the language Mr. Beeblebrox), there has been increased temperature, which has lead to increased broad leaf trees, which has lead to increased seeds, which has lead to increased voles which eat the seeds, which carry Hanta, which infected humans, which lead to an increase in renal failure from Hanta virus. The old lady who swallowed a fly had nothing on that series of events.

On the bright side, the RSV season may be shortening. As an ID doc, that is a trade I will take any day: RSV for malaria, dengue and Hanta virus. Oh my.

Rationalization

Emerg Infect Dis. 2007 Oct;13(10):1477-83. Dengue fever seroprevalence and risk factors, Texas-Mexico border, 2004 (http://www.ncbi.nlm.nih.gov/pubmed/18257990).

My Favorite Nun

Published Wed, 04 Feb 2009

Phone call from the ER.

Seizures.

New immigrant.

Diagnosis always at the top of the list is cysticercoses, or the pork tape worm Taenia solium.

CT is unenhanced, but shows at least 20 areas of calcification through out the brain and one area of edema and swelling in the temporal/parietal lobe.

Unenhanced CT's do not give enough detail to make the diagnosis, but the MRI today does: numerous 1 cm fluid filled cysts scattered through out the brain, and in each one, like a teeny tiny fetus, is a worm.

I will pause here while you shudder.

The life cycle is simple enough. You eat pig poo containing eggs, and the worm goes to your brain where it sets up cysts.

The organism lives quietly for years, like a psycho in your apartment complex. He was so nice and kept to himself, who would have thought he could do such a thing. Then one day it dies, and as it dies it causes an inflammatory response and you get headaches and seizures. In some parts of the world, like Mexico, cysticercoses is the number one cause of seizures.

Treatment is albendazole or praziquantel, the one drug evidently named after an Aztec god. When you treat the patient gets much worse as dying organisms lead to further inflammation so antibiotics need to be combined with steroids. Longterm, treated patients may have fewer seizures, but the need to kill with worms is still uncertain. Still, who wants a live worm in their brain. Except Mister Mind (http://en.wikipedia.org/wiki/Mister\_Mind\_and\_the\_Monster\_Society\_of\_Evil)?

Take home: don't eat pig poo. But I bet you knew that.

Rationalization

Ann Intern Med. 2006 Jul 4;145(1):43-51.Jan;3(1):22-3. Meta-analysis: Cysticidal drugs for neurocysticercosis: albendazole and praziquantel (http://www.ncbi.nlm.nih.gov/pubmed/16818928).

Not a bacteria for a 'real' man

Published Wed, 04 Feb 2009

The patient has known valvular heart disease and part of the evaluation as an outpatient is an ECHO.

It shows a small vegetation on the aortic valve, confirmed on a transesophageal ECHO.

Years ago, in my L.A. days, I was called about what to do because the surgeon had worn her mask around her neck during lunch, and in the middle of the case a broccoli floweret fell onto the heart. Largest vegetation I had ever seen.

History and exam do not really support a heart valve infection, but it is hard to deny the reality of a floppy vegetation.

For four days the blood cultures are negative. Damn. No risks for the odd organisms that cause culture negative endocarditis. Then there are gram-positive cocci in clusters. Coagulase negative staph? Maybe, but then it turns out to be Micrococcus.

Huh. Micrococcus is a gram-positive coccus that forms tetrads, which makes it sound like some sort of Ninja. Micrococcus is found in soil, water, beer (Oh. My. God.), marine sediments, dry Italian sausages, miso, and Spanish dry-cured ham. Pretty much my favorite dinner. Mostly a part of the human skin and mouth, it is what cause the smell in a stinking foot. The organism responsible for the Scholl's fortune.

Endocarditis from Micrococcus is unusual: 17 cases or so in the literature. And I suppose it could be contaminant, but I will treat it.

Rationalization

Zentralbl Bakteriol. 1995 Oct;282(4):431-5. Micrococcus luteus endocarditis (http://www.ncbi.nlm.nih.gov/pubmed/9810667) : case report and review of the literature.

Postscript: he was cured with antibiotics. Whether is would have been cured without them, we shall never know.

My liver quiver

Published Sat, 07 Feb 2009

My liver quivers.

~ Bob Marley

Rearrange your liver to the silent mental grace.

~ Yes.

The liver is not well represented in popular music. Send in better lyrics if you know any.

The liver, however, is well represented in infectious disease. Today was a liver abscess, bacterial, from a diverticular abscess.

Most liver abscesses are due to some sort of biliary disease and it is odd to see one due to colonic disease in this century. It was a more common cause in the old days, before CAT scans and antibiotics.

This patient had a risk factor that lead to his liver abscesses: he is single.

He had symptoms for over two months of a diverticular abscess, and he kept expecting it would go away.

The first question I often ask a patient is some version of "What brings you to the hospital?"

Often in men it is some variation of "My wife/girlfriend made me."

(BTW: anyone who answers "My car" is instantly eligible for physician assisted suicide, as is anyone who says "My fingers" in response to the question "How do you feel?" Be original, puh leaze).

Not having a girlfriend to make him come to the hospital, he let it fester. Fester. That's a great word. I did not realize that Uncles Fester from the Addams Family had an odd name until well into medical school.

We older XY's would probably not survive to senescence except for the XX's 'making' us go to the hospital.

The other curiosity of the liver abscess is he had time to develop a thrombus in his portal vein. His is bland, but occasionally these are infected thrombi (therefore the pleural of Elvis is Elvi). In my experience (the most dangerous words in medicine) I do not see many portal or hepatic vein thrombosis, despite what the references say. Perhaps they have a hospital filled with single men.

Rationalization

AJR Am J Roentgenol. 2005 Oct;185(4):1015-23. Hepatic attenuation differences associated with obstruction of the portal or hepatic veins in patients with hepatic abscess. (http://www.ncbi.nlm.nih.gov/pubmed/16177426)

Leukocytosis

Published Mon, 09 Feb 2009

The patient is initially admitted with urosepsis. Multi-organ system failure, she requires three days of blood pressure support that keeps her alive, if somewhat cool and mottled in her extremities due to the clamp down of her arteries from the pressors.

Levophed makes the toes blue and cold, especially in patients with underlying vascular disease.

She slowly improves and is weaned off her pressors and then, four days into her hospitalization, she gets a fever for a day and her WBC jumps to 29,000.

New infection? Undrained abscess? Complication of her bacteremia?

Work up is negative for all of the above. Here is what I bet is happening.

It is not that unusual to see patients bump their WBC and get a fever after prolonged hypotension. More often than sepsis, I occasionally get called to see a patient with a fever and leukocytosis after coronary artery bypass surgery (CABG). While on the bypass pump, patients are relatively hypotensive for an hour or so, and they have a decrease blood flow to the abdominal organs.

I think what happens is that hypotension leads to tissue damage and the reperfusion results in a flood of WBC into the tissues to clean up the dead meat. The result is a brief inflammatory response with a fever and an increase in the WBC.

This is an extrapolation from studies that demonstrate reperfusion of the heart is associated with a fever. There are a variety of animal models that show reperfusion of heart or lung or liver leads to fever and leukocytosis. Ischemic colitis and pancreatitis are occasionally seen after CABG, both of which are causes of fever.

I tend to see this syndrome more in people who have underlying vascular disease or reasons for underlying vascular disease: diabetes and hypertension. I can't prove it, unfortunately, for like diarrhea, the diagnosis is made by a process of elimination. At least one fact and one bad pun per post. That's my goal.

If there is an article on post sepsis/hypotension leukocytosis that is not infectious, I can't find it.

Feel free to do the study, just make me the lead author. Call it Crislip's syndrome.

We did nothing and she got better. It is the importance of time wounding all heels, or something to that effect. As in intern, it is don't just stand there, do something. As an attending, it is don't just do something, stand there. And as my wife can attest, I am excellent at doing nothing.

Rationalization

Cardiology. 2005;103(4):169-73. Epub 2005 Mar 21. Body temperature - a marker of infarct size in the era of early reperfusion (http://www.ncbi.nlm.nih.gov/pubmed/15785024).

Ann Thorac Cardiovasc Surg. 2005 Feb;11(1):25-8. Gastrointestinal complications in patients undergoing coronary artery bypass grafting (http://www.ncbi.nlm.nih.gov/pubmed/15788965).

Influence of prolonged cardiopulmonary bypass times on splanchnic perfusion and markers of splanchnic organ function. (http://www.ncbi.nlm.nih.gov/pubmed/12735579) Ann Thorac Surg. 2003;75:1558–1564.

True True Related

Published Wed, 11 Feb 2009

Laboratory results on the Whipple's patient came back today.

The patient has no measurable vitamin D. Interesting. Whipple's is associated with malabsorption, but the patient has no weight loss or other symptoms associated with malabsorption.

Makes one (me being that one) wonder about cause and effect. Malabsorption from Whipple's could lead to a decrease in the vitamin D levels OR perhaps the low vitamin D helped to put him at risk for the disease, since he is not at genetic risk as best I can tell from HLA testing.

Vitamin D deficiency increased the risk for a variety of infections, so perhaps in Whipple's as well. Pubmed suggests no one else has ever looked.

The other issue is where does the Whipple's bacillus come from? It is environmental, but if you think your job has its downsides, consider this study.

“Whipple's disease is a systemic disorder in which a gram-positive rod-shaped bacterium is constantly present in infected tissues. After numerous unsuccessful attempts to culture this bacterium, it was eventually characterized by 16S rRNA gene analysis to be a member of the actinomycetes. The name Tropheryma whippelii was proposed. Until now, the bacterium has only been found in infected human tissues, but there is no evidence for human-to-human transmission. Here we report the detection of DNA specific for the Whipple's disease bacterium in 25 of 38 wastewater samples from five different sewage treatment plants in the area of Heidelberg, Germany. These findings provide the first evidence that T. whippelii occurs in the environment, within a polymicrobial community. This is in accordance with the phylogenetic relationship of this bacterium as well as with known epidemiological aspects of Whipple's disease. Our data argue for an environmental source for infection with the Whipple's disease bacterium.”

And you think you job is bad.

Rationalization

Appl Environ Microbiol. 1998 Feb;64(2):760-2. Environmental occurrence of the Whipple's disease bacterium (Tropheryma whippelii) (http://www.ncbi.nlm.nih.gov/pubmed/9464419).

The New Pig Pen

Published Sat, 14 Feb 2009

Infections are somewhat inevitable. Surgery is not a sterile procedure, since the skin cannot be sterilized. Surgery is just very very very clean. That's three very's, so you know it is clean. Everyone has bacteria in and on them, but some people have more than others.

Infected artificial hips are no fun for the patient, and if due to S. aureus, often result in a need to remove the hip for several months while we attempt to eradicate the staph, such as occurred with today's consult.

But why the staph infection?

The answer lies on the skin, where the patient has a moderate case of psoriasis. Normal skin does not have much, if any, S. aureus on it, but if you have any kind of skin disease: eczema, psoriasis, atopic dermatitis, or use needles, which damages the skin, your S. aureus carriage rate goes from zero to almost 100 %.

If you have lots of skin disease, you have lots of S. aureus. The problem is that if you are heavily colonized with S. aureus, the is little if anything that can be done to get rid of all the bacteria. Think Pig Pen from Charlie Brown, except instead of dirt, the patient is in a haze of bacteria. Once the surgery is over, what S. aureus you might have beaten down rapidly grows back.

Staph just love to take advantage of breaks in the skin and invade.

I had one poor lady who had recurrent boils due to MRSA and her 3 year old daughter had horrible skin disease. There was no way to get MRSA out of the family.

If you need to operate on a patient with bad skin disease, it is probably reasonable to give the patient a chlorhexidine shower before they go to the OR, but it didn't help with this patient. Don't be surprised when then get an infection. There is just so much we can do to prevent infections and when they occur, of course, Medicare will not pay for it. Not every infection is necessarily our fault.

Rationalization

Br J Dermatol. 2006 Oct;155(4):680-7. Skin colonization by Staphylococcus aureus in patients with eczema and atopic dermatitis and relevant combined topical therapy: a double-blind multicentre randomized controlled trial. (http://www.ncbi.nlm.nih.gov/pubmed/16965415)

Growing Lung Nodule

Published Thu, 19 Feb 2009

Back from 4 days at the Oregon Coast with my youngest. No infections for 4 days. No broadband for 4 days. Very odd to be on dial up, but we always have a good time together. The party is over and it's back to work.

The patient has an odd lymphoma for which he is getting chemotherapy. As part of his followup he has a CT every few months and he has a small round nodule on the CT. A few months later it is bigger. What is it? The only way to know is to put a needle into it and it grows Cryptococcus neoformans. This is not an uncommon cause of a round lesion in chest CT, and I have seen at least one lung removed thinking the fungus was a tumor.

Unlike lung cancer, Cryptococcus is curable, at least most of the time. The literature suggests that pulmonary Cryptococcus is unusual in normal people although I bet that symptomatic disease is uncommon in normal people. If the fungus is in your environment, then I bet a lot of people get asymptomatic infections, such as this patient, who had no pulmonary or infection symptoms whatsoever.

Normal people, if such a thing exists, probably need no therapy, but in the immunoincompetent the yeast can disseminate to cause meningitis. He had a negative blood and spinal tap, so he only needs a course of oral fluconazole.

The more interesting thing is that there are two forms of Cryptococcus: neoformans and gattii.

C. gattii is new to the NW and is now endemic on Vancouver Island (part of Canada, so Homeland Security will keep it out of the US). It is more virulent than the_neoformans_ strain and less responsive to therapy. C. gattii was associated with eucalyptus trees, but this strain is found in the fir trees of the NW and is perhaps one of the infections associated with global warming. It has found a new ecological niche to fill, and has now caused hundreds of cases in B.C. in humans and many more in animals. Visitors to the Island need to be careful to not inhale.

One would think that Koala bears, which subsist entirely in eucalyptus leaves, would be immune, but Cryptococcus is the number two killer of this animal. Also, and I am uncertain why I find this delightful, but the strain in Vancouver is the result of same sex mating. I will let you come to your own conclusion as to what, if any, significance that fact has.

Rationalization

Cryptococcus gattii risk for tourists visiting Vancouver Island, Canada (http://www.cdc.gov/ncidod/EID/13/1/178.htm) [letter]. Emerg Infect Dis. 2007 Jan.

Nature. 2005 Oct 27;437(7063):1360-4. Epub 2005 Oct 9. Same-sex mating and the origin of the Vancouver Island Cryptococcus gattii outbreak. (http://www.ncbi.nlm.nih.gov/pubmed/16222245)

The Joint Ain't Jumpin'

Published Fri, 20 Feb 2009

Every organism can grow in any space. That is what makes ID endlessly entertaining and interesting.

Most septic prosthetic joints are due to Staph of one sort or another, and early infection after joint replacement tend to be coagulase-negative staph or P. acnes.

Five months after a new knee the patient develops sudden onset of, can you guess what?

Rubor, dolor, calor, tumor in the knee. Where have I heard those words before? It is odd to see an infected knee 5 or 6 months in, and often it is a peculiar organism.

A tap shows some WBC and a few days later she is growing Streptococcus intermedius from the cultures.

I thought, huh, that’s odd, but it is part of mouth flora and people are bacteremic all the time, so why not _S_. intermedius?

Back last century I would have had to plow though the Index Medicus to find how often this bug has been reported in a joint. Quick PubMed and... the heck. Only one case in the literature, and that in a normal joint. So here is the first case ever of _S_. intermedius in a prosthetic knee. We shall henceforth call it Crislip's Disease. Let the call go out.

Part of the problem with S. intermedius is that while it can be grown, it did not grow well enough to get antibiotic sensitivities.

As part of the human mouth, the milleri group of which intermedius is part, have been exposed to beaucoup antibiotics and being intermediate to penicillin is not uncommon. Makes me nervous, but in attempt to salvage the knee without taking it out I am going to give ceftriaxone for 6 weeks.

Rationalization

J Rheumatol. 1980 Jan-Feb;7(1):89-92. Streptococcus MG-intermedius (Streptococcus milleri) septic arthritis in a patient with rheumatoid arthritis. (http://www.ncbi.nlm.nih.gov/pubmed/7354474)

J Infect Chemother. 2002 Jun;8(2):134-7. Trends in antimicrobial susceptibility of the Streptococcus milleri group. (http://www.ncbi.nlm.nih.gov/pubmed/12111565)

Postscript: It worked. Knee salvaged.

Inside Out or Outside In?

Published Sat, 21 Feb 2009

Elderly patient with progressive shoulder pain. It was on the side where he had decreased movement secondary to a stroke, but over several weeks his range of motion was decreased due to pain in the shoulder. He was seen in the ER, the shoulder had no pathology, so he was treated for muscle strain. He had no other symptoms.

Then, about two weeks in, he developed increased pleuritic chest pain, i.e. pain with breathing.

Still no other symptoms, including cough or shortness of breath.

This lead to a CT, which showed a paraspinous mass infiltrating into the pleural space near the apex of the lung. Pancoast tumor? He had been a smoker.

So a biopsy is set up and in 5 days he develops a huge lung abscess, has his first fever, and his blood grows S. anginosis.

His teeth are fine and he has no loss of consciousness nor infiltrate to suggest that he had pneumonia, so here is my hypothesis.

He had primary pyomyositis of the paraspinous muscles that eroded into this pleural space and then into the lung.

This is bass ackwards (lysdexics untied!) of the usual order of events, but the history suggests I am right as does the CT which shows osteomyelitis of the rib, more likely if he had a long standing muscle infection rather than a primary pulmonary infection. I will admit that rib osteo is rare as hens teeth.

It alll started as a paraspinous phegmon, then five days later, man oh man.

A huge abscess formed in five days. Impressive. Then he had a fever as it ruptured into the lung and he stated to have a productive cough.

Against the pathophysiology is that there is only one S. anginosis pyomyositis in the literature, but in my favor is the fact that I never let reality get in the way of a great diagnosis. I have seen a smattering of spontaneous pyomyositisesi (what is the pleural of pyomyositis?) due to S. milleri.

That's two Strep milleri group infections in two days. Will tomorrow be three? I am not going to say. You could call that a strep tease.

Rationalization

J Rheumatol. 1993 Mar;20(3):521-4. Pyomyositis: early detection and treatment. (http://www.ncbi.nlm.nih.gov/pubmed/8478863)

Yeast in the Urine

Published Tue, 24 Feb 2009

There are diseases that are difficult to treat. Candida in the bladder is probably self-limited, but upper tract disease is problematic and there are no satisfactory therapies, especially for non albicans Candida.

If you have a diabetic with kidney stones and post obstructive pyelonephritis due to C. tropicalis, like todays consult, what do you treat the patient with? Which preposition is best to end a sentence? First, of course, relieve the obstruction. But what antifungal?

Non albicans Candida are relatively resistant to fluconazole.

The echinocandidans are great everywhere but the urine, where they get no urinary levels. For a UTI, caspofungin is a piss poor drug. Wha wha wha wha.

Amphotericin B is great for killing Candida, but it can also kill the kidney. I am not a fan of calling it amphoterrible, as if you know what you are doing and are judicious in your use of the drug, most of the time bad side effects can be avoided. Most of the time. If I have a 90 yo with diabetic nephropathy in their one transplanted kidney and on cyclosporin, well, maybe there is not much you can do to protect the three remaining nephrons.

Decisions. Decisions.

Perhaps I could get away with caspofungin, as there was a series of cases reported in CID of caspofungin used successfully in Candida cystitis, but it was by Merck minions and the lead author gets many dollars from Merck.

"Manuscript preparation. Merck initially submitted case record forms of patients with candiduria to J.D.S. but had no role in selection of the patients described. Potential conflicts of interest. J.D.S. has received recent funding support from Pfizer, Merck Research Laboratories, and Astellas Pharmaceuticals, has previously participated in multicenter clinical research with and studies funded by Merck, and has served as a consultant to and is on the speakers‚ bureau for Merck. S.K.B., C.J.L., and N.A.K. are all employees of Merck Research Laboratories. "

It did not inspire confidence for a study free of bias.

Best bet is probably amphotericin B, and the if I give a small amount (0.3 mg/kg a day) using constant infusion, I may avoid the nephrotoxicity.

I am not that big a fan of lipid complexed amphotericin. It costs a mint (about 400 dollars a dose. Yes, $400. How else is that 'free' pizza paid for at conference), is not more effective, and for most cases only somewhat less toxic. If I am treating a kidney infection, I WANT my ampho in the kidney where it can kill some yeast rather than complexed to fat. I prefer regular amphotericin if the patient can tolerate it, and with constant infusion they often do.

Rationalization

Clinical Infectious Diseases 2007;44:e46. Caspofungin in the Treatment of Symptomatic Candiduria (http://www.ncbi.nlm.nih.gov/pubmed/17278048).

Clinical Infectious Diseases 2003;36:943. Continuous Infusion of Escalated Doses of Amphotericin B Deoxycholate: An Open Label Observational Study (http://www.ncbi.nlm.nih.gov/pubmed/12684904).

It is good to have a spleen

Published Wed, 25 Feb 2009

Female in her 40's has a fever to 105, feels awful, then shows up in the ER. Hypotension, renal insufficiency, low platelets (18,000) with scattered petechiae.

She spleen had been removed about five years ago for what turned out to be a benign condition. People without spleens to not get more frequent infections, but when they do, man can they go to stink with rapidity.

The most common severe infection is _S_. pneumoniae and I bet that would grow on blood cultures, although she does have dogs, one of which licks her with great frequency.

Up front I put her ceftriaxone and azithromycin, but after 48 hours her blood cultures were negative. Then a thin, long gram-negative rod slowly grew.

It is growing Capnocytophagia of some sort, maybe C. canimorus. That's two in less than 6 months, after never having seen a Capnocytophagia before.

Patients can have their spleen removed for a variety of reasons, but there are may conditions where the patients functionally behave as if they had no spleen:

Alcoholism, amyloidosis, autoimmune hemolytic anemia, biliary cirrhosis, bone marrow transplantation, celiac disease, chronic active hepatitis, chronic graft vs. host reaction, chronic myelogenous leukemia, collagenous colitis, essential thrombocythemia, Graves' disease, hairy cell leukemia, hashimoto's thyroiditis, hemangiosarcoma of the spleen, hemophilia, hematologic diseases, hereditary spherocytosis, Hodgkin's disease, idiopathic thrombocytopenic purpura, non-hodgkin's lymphoma, ovarian carcinoma, portal hypertension, rheumatoid arthritis, right sided heart failure, sarcoidosis, Sjögren's syndrome, splenic irradiation, systemic lupus erythematosus, thalassemia, ulcerative colitis, Whipple's disease.

Whoa. Talk about venting ones spleen.

There are 874 references pertaining to Capnocytophagia on PubMed. That's a lot of cases, many in ostensibly normal people. Given the number of dogs I bet this disease is under-reported. At our weekly infectious disease conference they presented a 9 month old with sepsis and meningitis that turned out to be due to Capnocytophagia. The family dawg evidently licked the child's head like I would a Tootsie roll pop, trying, I suppose, to get to the tasty center.

I always remember that if nothing else, a dog licks their butt. Why would I want it to then lick me? It is part of the reason I am leery about dawgs in the hospital as part of pet 'therapy’.

"Zoonotic agents were isolated from 80 out of 102 (80%) dogs. The primary pathogen was Clostridium difficile, which was isolated from 58 (58%) faecal specimens. Seventy-one percent (41/58) of these isolates were toxigenic. Extended-spectrum beta-lactamase Escherichia coli was isolated from one (1%) dog, extended-spectrum cephalosporinase E. coli was isolated from three (3%) dogs, and organisms of the genus Salmonella were isolated from three (3%) dogs. Pasteurella multocida or Pasteurella canis was isolated from 29 (29%) oral swabs , and Malassezia pachydermatous was isolated from eight (8%) aural swabs. Giardia antigen was present in the faeces of seven (7%) dogs, while Toxocara canis and Ancylostoma caninum were detected in two (2%) dogs and one (1%) dog, respectively."

MRSA is also carried in pets as well. It is just a matter of time before some poor patient gets something from the visiting dawg.

But people seem to love dawgs more than each other, so I expect to see a few more of these before I retire.

Rationalization

J Hosp Infect. 2006 Apr;62(4):458-66. Epub 2006 Feb 7. Prevalence of zoonotic agents in dogs visiting hospitalized people in Ontario: implications for infection control. (http://www.ncbi.nlm.nih.gov/pubmed/16466831)

Leukemoid

Published Wed, 25 Feb 2009

The higher the white count, the more you fret. This patient was admitted with a WBC of 1800 thanks to the magic of chemotherapy, and C. difficile diarrhea thanks to the magic of antibiotics. Within 4 days the WBC had jumped to 106,000 with a nasty differential. Myelocytes and metamyelocytes and I have never metamyelocyte I liked. Thank you Will Rodgers.

One would think she is heading to have her colon removed due to severe colitis, at least to judge from her WBC. And yet. She is stable. No fevers, no hypotension, her belly is slightly distended but moderately tender. The flat plate has no toxic mega colon. Should she go to the OR? If she is heading for perforation, the sooner the colectomy, the better. What might be happening instead is that she has a form of IRIS, Immune reconstitution inflammatory syndrome, first described in AIDS when patients would become symptomatic with preexisting infections as their immune system returned on HAART and recognized pre-existing pathogens.

In the neutropenics IRIS is described in them what have Aspergillus lung disease, and getting sicker when the WBC returns is a good prognostic sign. It has also been described in postpartum, since pregnancy is an immunosuppressive state. Could IRIS be occurring in her colon? If so, she needs time, not an operation. There is a real disconnect between the highest non-leukemia WBC of my career and how clinically good she looks. Time to nervously drum my fingers on the table.

And time, that wonder of all heals, worked yet again. The patient did fine: like this sentence she has a colon.

Rationalization

Immune reconstitution inflammatory syndrome in cancer patients with pulmonary aspergillosis recovering from neutropenia: Proof of principle, description, and clinical and research implications. (http://www.ncbi.nlm.nih.gov/pubmed/17525971) Cancer. 2007 Jul 1;110(1):112-20.

Bacterial Boogers

Published Sat, 28 Feb 2009

I really do not remember why I went to medical school. What delusion I was suffering under at the time that made me pick medicine, I do not know. I occasionally talk to premed's and they are so clueless about the practice of medicine. Maybe I am a doc because my Dad is a doc; beware of role models.

Don't get me wrong. I love what I do. I have the best gig in the city, the sole ID doc (if I were in South Korean doc, I would be the Seoul ID doc) at 4 hospitals, I get to see all the cool cases and rarely do I get called to see something dull. I get all the clinical gold and little of the pyrite.

It is a nice part of the job that I meet nice people (Its nice to be nice to the nice -Frank Burns, MD) and help get them better. But it is not what gets me up in the dark to head off to work. What I enjoy more than anything else is figuring things out. I love to call the diagnosis before the confirming tests. I know I know I know. Arrogant self centered bastard who uses his blog to trumpet his clinical triumphs. But it is fun to get the diagnosis before the confirmatory tests.

I am more often wrong than right, but no one ever remembers when you are wrong, because in medicine you are always wrong. Babe Ruth also lead the league in strikeouts.

65 yo diabetic female with cardiac arrest on dialysis. Survives (obviously, else why would I see her? I have had one post mortem consult in my career, but usually those are reserved for the pathologist). She is febrile and her blood cultures grow Enterococcus and Klebsiella. ROS has a month or two of sweats, she has right upper quadrant pain and her transaminases are 3x normal.

Diabetics plus Klebsiella equals liver abscess. Simple math. Why, I wonder, is the English math plural, maths? They have such a singular way of talking.

But not just any Klebsiella, there is a strain that started in Taiwan and is hypermucoviscous. Ugh. What does this mean? It means it's like snot on a plate, and the hypermucous probably inhibits the ability of WBC to kill the beast. It also makes it more likely to cause eye and brain infections. Snot bad. Bacterial snot worse.

So the CT did show what looks to be a liver abscess or a liver tumor or both; as always there are confounding factors that obscure the diagnosis until we can do a liver biopsy.

Unfortunately (for me, not for her), the Klebsiella is not the hypermucous strain, just a regular old Klebsiella.

I'll give me half credit.

Rationalization

Scand J Infect Dis. 2007;39(9):828-30.C Pyogenic liver abscess caused by hypermucoviscous Klebsiella pneumoniae (http://www.ncbi.nlm.nih.gov/pubmed/17701725).

J Clin Microbiol. 2008 Dec;46(12):4061-3. Evidence for clonal dissemination of the serotype K1 Klebsiella pneumoniae strain causing invasive liver abscesses in Korea. (http://www.ncbi.nlm.nih.gov/pubmed/18971367)

Eur J Clin Microbiol Infect Dis. 2009 Jan;28(1):109-11. Risk factor analysis of invasive liver abscess caused by the K1 serotype Klebsiella pneumoniae (http://www.ncbi.nlm.nih.gov/pubmed/18663497).

Never Heard of It

Published Sun, 01 Mar 2009

Almost a quarter of a century. That’s how long I have been an MD. I realized that there is only one other doc older than me in the Department of Medicine at Good Samaritan, and he is my boss. I now get to complain in a querulous old voice about how much better it was back in the day.

But even after all this time I am still called upon to kill things I have never heard of.

Another urinary obstruction. I seem to have a run on these, with a yeast in the nephrostomy tubes and acute renal failure.

I expect some sort of Candida or other, but after 5 days the labs says it is..

Cue up the dramatic prairie dog (http://www.youtube.com/watch?v=jHjFxJVeCQs).

Trichosporon asahii .

Never heard of it. Well, I have, evidently, as it is in the Compendium, but I will be damned if I remember writing about it.

Pubmed is not of much use, although evidently it is a common yeast in Japan, I have never seen a case in the US. Is there a genetic or environmental reason for the disease in Japan? Or is it found in the Japanese beer? And no, not Kirin. Asahi means morning sun in Japanese, in case you wanted to know. So I assume it is the rising sun Trichosporin.

In Japan, it acts like Candida, causing a variety of infections in patients with poor immunity, but I can't find much on therapy.

Thank goodness for Dr. Fungus (http://www.doctorfungus.org/). If you have a weird ass fungus and no clue as to what to do, search Dr. Fungus.

Voriconazole is evidently the best of breed and amphotericin canna be trusted.

So voriconazole it is.

But don't forget Dr. Fungus, even if it sounds like one of Spiderman's rogues.

Herpes on the Brain

Published Tue, 03 Mar 2009

Herpes encephalitis is a bad disease. It melts your brain, necrosing your temporal-parietal area until you are tuned into a Limbaugh.

A lot of you (not me) have Herpes. One in four Americans have Herpes simplex 2 (the mostly genital herpes) and only 10% or so know it. Most herpes is asymptomatic and is shed and passed from person to person with no one aware.

This is important in the clinic, as well as when you get drunk and stagger out of the bar with a person of uncertain provenance.

Lets say you have a couple A and B. They have been together for a few months and A has never had Herpes. B now has a whopping case of Herpes for the first time ever.

A thinks B is a cheatin' pig, and a bald face liar to boot, because where else could that Herpes have come from if not from foolin' around (this sounds like it may make a good country song), but the more likely scenario is that A has asymptomatic disease and gave it to B. Check the Herpes serology on A, and if positive, will be suggestive that A in fact was the Herpes donor to B. But if B is a male, well, he may be a cheaten' pig and a bald face liar as well, but that is not an ID issue.

All men (except me) are pigs. My wife says she wished she had known that in her younger days; it would have resulted, perhaps, in less heart ache.

But what about the patient from the weekend? Comes in with viral meningitis, not encephalitis, and after a few days the PCR for HSV (LSMFT) is positive.

Do you treat Herpes meningitis? Herpes is a cause of benign recurrent aseptic meningitis, or Mollaret's meningitis, but as it is the first episode, I can't call it recurrent yet.

The ID textbook, Mandell, says

"Among immunocompetent persons, aseptic meningitis associated with genital herpes is usually a benign (albeit uncomfortable) disease and gradually resolves without sequelae. Controlled trials of intravenous acyclovir for established HSV meningitis have not been conducted. However, intravenous acyclovir 5 mg/kg every 8 hours is recommended for hospitalized symptomatic patients. Most series have reported a low frequency of neurologic sequelae."

Where is the damn reference? I can't find squat on a PubMed search to support that assertion. Pisses. me. off.

So should I treat? Sometimes I do, and sometimes I don't. If they are ill and have bad lesions I do, if it is just a headache I may not. Drugs are not without their toxicity's.

Rationalization

Reactivation of genital herpes simplex virus type 2 infection in asymptomatic seropositive persons. (http://www.ncbi.nlm.nih.gov/pubmed/10727588) N Engl J Med. 2000 Mar 23;342(12):844-50.

Fever on the fifth day

Published Wed, 04 Mar 2009

The following is opinion with no references. So take it with a grain of salt substitute.

Patient had a big abscess that was percutaneously drained and a few hours later he spikes fever. So he gets more antibiotics piled on. Eh. Not that he needs them. Remember, give Tylenol for a fever, give antibiotics to kill a bacteria. Not the same thing.

Abscesses are not amenable to cure without draining. In the abscess the organisms are not growing, and when they are not growing they canna be killed. Almost all of our antibiotics kill organisms as they divide. Kind of mean, really, who wants to be killed during reproduction? (BTW: I am currently reading Mary Roach's 'Bonk,' hilarious, which is what brought the prior thought to mind).

When you drain an abscess, the organisms start dividing, and when they divide, you kill them.

When bacteria die, they dump endotoxin into the blood, which leads to an inflammatory response and, vwa-la, people have a fever.

The febrile response is what you expect shortly after draining any abscess.

Speaking, or writing, of fever, what about the 5 day fever? Not a fever that lasts for five days, but the fever that is seen on about day five of hospitalization.

People come in with a fever/infection and get better, then about the fifth hospital day they have a single fever.

Back in the old days, people would have their crisis during pneumococcal pneumonia and either live or die. The crisis marked the onset of the IgM response, needed for efficient killing of encapsulated organisms. The crisis would occur about day 10 of illness.

Here is what I wonder about: most of these fevers occur around day 10 of the infection, often day 5 or so of hospitalization. I think this fever marks the onset of the IgM response to whatever is ailing the patient; hence the fever.

Someone wants to do the study to prove this, feel free. Just mention me in the acknowledgements as the genius behind the study.

Lactobacillus

Published Fri, 06 Mar 2009

Lactobacillus is a gram-positive rod, a normal part of the lower GI tract and the female genital tract. It is a rare cause of serious infections, like endocarditis.

The patient has a history of a Whipple's, where the pancreas is removed, and has nothing to do with soft, squeezable toilet paper, 5 years ago. Now he has fever and mid epigastric pain and CT shows an abscess.

It is drained, and both the abscess and the blood grows Lactobacillus, as you might have guessed from the title.

It is a curious case. Lactobacillus is also a probiotic (given what they cost, they are certainly not amateur-biotics), and there has been the occasional odd case on Pubmed of Lactobacillus in the blood and a liver abscess due to Lactobacillus. Generally, however, it is thought that probiotic Lactobacilli are safe. He has eaten yogurt, so maybe the source. The Lactobacillus in yogurt and probiotics is often a different strain than those found in and on normal humans. Unfortunately, I have to easy way to see if the source of his bug is life or Yoplait.

I presume the patient has a leak somewhere causing this abscess, but as of today we have not been able to find one.

There are a smattering human cases of Lactobacillus abdominal abscess on a Pubmed search, both associated with gastric perforation.

Drain and antibiotics, and expect I will cure him as long as he does not have a leak.

And best of all, his immune system is being boosted and/ or supported by the Lactobacillus in his peritoneum and blood. I assume he is getting far more immune boosting than if he were merely eating the probiotic as DanActive. Right?

Rationalization

Obes Surg. 2006 Jan;16(1):102-4. Intra-abdominal abscess in the course of intragastric migration of an adjustable gastric band: a potentially life-threatening complication (http://www.ncbi.nlm.nih.gov/pubmed/16417767).

If you can’t be self-aggrandizing, what’s the point of having a blog?

QuackCast 22. (http://www.pusware.com/quackcast/quackcast22.mp3) Boost your immune system. And die. A cursory review of the immune system and then a review of some medical literature that suggests boosting it will cause you to die die die die die die die die die die die die die........ Got carried away. Were all gonna DIE!!!!!!!!!!!! Sorry. I panic easy.

QuackCast 16. (http://www.pusware.com/quackcast/quackcast16.mp3) Probiotics. A review of probiotics: theory, use and complications.

Doctors are not supposed to get sick.

Published Tue, 10 Mar 2009

Especially Infectious Disease docs. I am punctilious about infection prevention. I wash my hands at rates that make lady MacBeth look like an amateur. But not for the same reason. I have no blood on my hands. I have been lucky that way. I got my flu vaccine the day after it came out.

My mistake was taking vitamin C and Echinacea. When ever I do, I always get a virus.

I have three days of fevers, bad headache, achy eyes, and a slight cough. Just an occasional cough. Barely anything, but a deep, raspy, painful cough when it hit. It was gone in three days and transitioned into a stuffy nose with continued sneezing.

Is it flu? I canna get the flu. It would be like the Pope getting AIDS. Just should not happen and I do not participate in risk behaviors and do all the appropriate prophylactics.

Problem is, I may have had an attenuated clinical course because, yet again, they picked the wrong strain for the vaccine.

The vaccine has both A and B influenza and they pick the strains in the vaccine from circulating virus from the year before. They do that because it takes a long time to manufacture each vaccine dose. One flu shot is grown in one chicken egg, and it takes that one poor chicken a long time to lay all those eggs. She sure walks funny at the end of the flu season.

There are two major lineages of type B flu: B Victoria and B Yamagata. Last year, they put the Victoria lineage in the vaccine and 98% of type B flu was due to the Yamagata lineage.

Crap.

So this year, they made the vaccine protective against Yamagata, but now 2/3 of the type B flu in circulation is from the Victoria lineage. Unfortunately, not the VIctoria's secret lineage.

Double crap.

So perhaps I had the flu, shortened and attenuated by last years vaccine. Or perhaps I had another virus. Either way, I stayed home and got caught up on the Sara Conner Chronicles.

The triple crap is flu season is peaking the past several weeks.

So wash your hands and don't inhale.

Rationalization

CDC "FluView: 2008-2009 Influenza Season, Week 5 ending February 7, 2009."

" 2007-08 U.S. Influenza Season Summary (http://www.cdc.gov/flu/weekly/weeklyarchives2007-2008/07-08summary.htm)."

Sine qua non

Published Wed, 11 Mar 2009

Still the clinging brain fog of post-viral recovery. Good thing I am a professional and can fake it as needed. It makes the typing slllllloooooooowwwwwwwwwww. Tell me about the rabbits George.

I like that phase. _Sine qua non i_s a Latin legal term for "that without which it could not be."

There are symptoms or tests that define an illness. For an endovascular infection, the sine qua non is sustained bacteremia. Most infections result in intermittent bacteremia, but if the infection is in the bloodstream, then it seeds the blood continuously and the blood cultures are positive day after day, hour after hour.

Blood cultures two week apart for the same organism, Enterococcus in this case, means an endovascular infection, which usually means a heart valve infection. This patient has a pacemaker, so maybe that would be the source of bacteremia.

You tend to see enterococcal endocarditis in old men, and is probably the gift of an enlarging prostate (pronounced prostrate). It leads to obstruction with may push the bug into the blood, and hence to the valve. It is my understanding the women folk don't have a prostrate, and I have seen one case of enterococcal endocarditis in a female.

There are two ways to give a rabbit endocarditis. One, make it a heroin addict. As Hef knows, nothing sadder than a junkie bunny. Two, put a wire across a valve and give the rabbit a bolus of bacteria. The valve, whacking against the valve 60 times a minute, gets a little rough, resulting in platelet-thrombin deposition, a place for the bug to grab a hold and, then, endocarditis.

Pacers give that roughened valve, but most patients don't get a bolus of bacteria. Unless they have that pesky prostate. That reminds me, I need to have mine removed to be safe. I no longer need it. Or is that oversharing?

On transesophageal ECHO, he had an infection on the tricuspid valve, right where the valve bumped ugly with the pacer wire.

Now I can occasionally salvage an infected catheter, prosthetic joint, or artificial valve. But for whatever reason, the literature suggests you just can't save an infected pacer system. I have always failed when asked to try, no matter what magic cocktail of antibiotics I tried.

Once I had a patient with an infected pacer and cardiology told me no way can we take it out without killing the patient. In a flash of genius, I thought, the problem is the pacer wire is covered with clot. It I can strip off the clot with tPA, then I can cure the infection.

Bad idea.

Not only did I strip off clot, the bacteria followed and he got a touch septic, he says with deliberate understatement. He had the pacer pulled and did just fine as they always do. I have since learned that, despite their protestations that they will kill the patient, cardiologists are actually quite incompetent at the task and have never followed through on the promise.

This patients pacer will come out later in the week, and he should be the better for it.

Rationalization

Thorax. 1969 July; 24(4): 498‚ 499. Adhesions of pacing catheter to tricuspid valve: adhesive endocarditis (http://www.ncbi.nlm.nih.gov/pubmed/5795653).

Int J Antimicrob Agents. 2007 Nov; 30 Suppl 1:S42-50. Infection of intravascular prostheses: how to treat other than surgery (http://www.ncbi.nlm.nih.gov/pubmed/17869069).

Postscript: Pacer came out with no complications.

A new personal record

Published Thu, 12 Mar 2009

I tell my older patients that for each day you are in bed with a fever, it is three days to get your strength back. It isn't supposed to apply to me. I am young, yes I am, only 357 in dog years. Everyday I hit a wall at about 3 and need a nap, which I get on the drive home. But at least, thanks to the swimming in molasses speed I am moving at this week, I hit that wall slowly.

Today I saw a 62 yo with classic meningitis, and the spinal fluid grew N. meningitidis. Old people get S. pneumoniae, and the oldest I have seen N. meningitidis cause meningitis is about 45. It is rare in folks my age, with an attack rate of 0.1/100,000 in the elderly.

He has no immunoincompetancy and has no good exposure or travel history (subSaharan Africa and the Haj are popular ways to acquire meningococcus). So I guess this falls under the title: fecal matter occurs.

I bet it will be type B, the strain that predominates here in the NW, and the strain not covered by the vaccine. Other parts of the world have other strains, and sub-Saharan Africa is having an issue with type X. Perhaps that type will not been seen in people under 21 or only be available on hotel cable.

When there is an exposure to the index case of meningococcus, the exposed needs to take an antibiotic to prevent disease. Significant exposure is if you have spent greater than 4 hours in the room with a patient, so no doctor has ever had an exposure. Problem is the current prophylaxis is ciprofloxacin, and there are now reported cases of ciprofloxacin resistance.

In one case, the ciprofloxacin resistance is due to a point mutation in the binding site of the antibiotic. The other went and got new genes from a Neisseria lactima to become resistant. I hates it when they get new genes.

I still have the beta-lactams, so I will be able to kill this bug for a while yet.

Rationalization

Clinical Infectious Diseases 2007;44:657‚ 663. Meningococcal Meningitis: Unprecedented Incidence of Serogroup X‚ Related Cases in 2006 in Niger (http://www.ncbi.nlm.nih.gov/pubmed/17278055).

N Engl J Med. 2009 Feb 26;360(9):886-92. Emergence of ciprofloxacin-resistant Neisseria meningitidis in North America. (http://www.ncbi.nlm.nih.gov/pubmed/19246360)

Hyperventilation

Published Fri, 13 Mar 2009

Respiratory rate of 35 to 40 in my meningitis patients. No fever, WBC better, no cardiac or pulmonary reasons for the increased respirations. Repeat CT shows no herniation or basal ganglia stroke.

Why the increased respiratory rate?

One hint from Pubmed:

“We present the case of a 57 year old man who developed a B-cell lymphoma which involved his lymph nodes, liver, spleen, bone marrow, and peripheral blood. Shortly after attaining a complete remission with chemotherapy, the patient developed profound hyperventilation with no apparent cardiac or pulmonary cause. After one month, the patient developed a 7th nerve palsy and a subsequent work up demonstrated that he had lymphomatous meningitis. The hyperventilation resolved completely with intrathecal chemotherapy, although the patient eventually died of widely disseminated lymphoma."

Whether a similar issue occurs with bacterial meningitis, I cannot say. Endotoxin can lead to hyperventilation by a variety of mechanisms, both central and peripheral. Few diseases dump endotoxin into the body like meningococcus, so perhaps I can postulate a flood of CNS endotoxin is driving his respiratory rate by, oh, evil humors.

I found this as well. I would have thought the opposite is true as I think of meningococcus as endotoxin production central.

“Endotoxin is liberated following antibiotic killing of Gram-negative rods, and antibiotics may differ in this respect. Although the amount of filterable endotoxin has also been reported to increase following antibiotic killing of meningococci, it is unknown how this influences the host response. We investigated the influence of three antibiotics on levels of free endotoxin in culture medium and cytokine production in whole blood ex vivo during killing of four strains of meningococci. Bacterial killing was significantly more efficient with penicillin or ceftriaxone than with chloramphenicol, and free endotoxin levels were lower after exposure to antibiotics as compared with no treatment (ANOVA, P < 0.001). Endotoxin levels were lowest after exposure to chloramphenicol. In three of the four strains exposure to antibiotics resulted in considerably lower cytokine levels (ANOVA, P < 0.001), and TNF-alpha levels were significantly lower after exposure to penicillin or ceftriaxone than after chloramphenicol treatment. Only in the strain that induced the lowest levels of TNF-alpha were cytokine levels comparable for untreated and treated samples. We conclude that fear of excessive endotoxin release or cytokine production caused by effective antibiotics is not justified in the treatment of meningococcal infections."

The heck.

Rationalization

J Neurooncol. 1992 Jun;13(2):173-5. Hyperventilation as the initial manifestation of lymphomatous meningitis (http://www.ncbi.nlm.nih.gov/pubmed/1279132).

J Antimicrob Chemother. 1997 Jan;39(1):13-8. No increase in endotoxin release during antibiotic killing of meningococci (http://www.ncbi.nlm.nih.gov/pubmed/9044022).

Lemierre's syndrome

Published Tue, 17 Mar 2009

This virus is hanging on like Norm Coleman, it just will not admit defeat. I just want to reach down my bronchus and scratch scratch scratch.

The French dominated infectious diseases for years, and you can tell that long tradition in many of the eponyms for infectious diseases. Many contain the name of the famous Frenchman who first described the disease, or at least were able to get it into print.

Take Andre Lemierre. He doesn't seem to warrant an internet biography, even if he does have a street named after him in Paris. In 1936 he described a series of patients in the Lancet with sepsis from infected clot in the neck. Occurring after a sore throat (angina means neck pain in the ancient language, for those spell casters in Alagaesia), it was called post anginal sepsis and was due to Fusobacterium necrophorum, a mouth anaerobe. Part of the disease complication is bits of infected clot break off and travel to the lung to cause multiple lung abscesses.

I see a case of this every couple of years in a person with poor dentition and no insurance. The latter is important since thy cannot afford a doctor to the antibiotics that would, perhaps, prevent it.

However, to have anaerobes in the mouth you have to have teeth, and the patient today in sans teeth. So what is the cause of the clot in the neck and multiple lung abscesses?

Our friend, the Staphylococcus aureus. It isn't called coagulase positive staph for nothing, and this organism knows now to clot blood. This is the second Lemierre's I have seen due to S. aureus, so I almost have a series; that would require three.

There are 5 staphylococcal Lemierre’s reported in Pubmed. I bet there are more cases out there. I have said for years that we need a searchable online cool ID case site where these cases can be reported. No one listens to me. And why should they?

Rationalization

Lemierre syndrome: a case of a rarely isolated microorganism, Staphylococcus aureus. (http://www.ncbi.nlm.nih.gov/pubmed/19247251) Ceylan B, Yavuz L, Baydar CL, Tuz M, Eroglu F, Kiris I, Akcam FZ, Erdem B. Med Sci Monit. 2009 Mar;15(3):CS58-61.

Multiple peritonsillar abscesses caused by Arcanobacterium haemolyticum in a young female. (http://www.ncbi.nlm.nih.gov/pubmed/19142834) Bomke AK, Steiner S, Podbielski A. Dtsch Med Wochenschr. 2009 Jan;134(3):75-8. Epub 2009 Jan 13. German.

A Lemierre syndrome variant caused by Staphylococcus aureus (http://www.ncbi.nlm.nih.gov/pubmed/18358967). Puymirat E, Biais M, Camou F, Lefavre J, Guisset O, Gabinski C. Am J Emerg Med. 2008 Mar;26(3):380.e5-7.

Lemierre syndrome variant: Staphylococcus aureus associated with thrombosis of both the right internal jugular vein and the splenic vein after the exploration of a river cave (http://www.ncbi.nlm.nih.gov/pubmed/17221323). Boga C, Ozdogu H, Diri B, Oguzkurt L, Asma S, Yeral M. J Thromb Thrombolysis. 2007 Apr;23(2):151-4. Epub 2007 Jan 13.

Lemierre syndrome due to non-multiresistant methicillin-resistant Staphylococcus aureus (http://www.ncbi.nlm.nih.gov/pubmed/12047702). Fong SM, Watson M. J Paediatr Child Health. 2002 Jun;38(3):305-7.

Drunken Microbiologists

Published Wed, 18 Mar 2009

Here's my theory, completely unsupported by facts. Every year all the microbiologists meet somewhere nice, get really really drunk and then, to hoots and giggles, change the names and classification of organisms. And they do it just to bug me.

Today was a patient with an infection in the facet joint of her thoracic spine. Odd place to get an infection, I have seen a pair of these that I can remember, both of which had had radiation in the area and both grew a viridans streptococcus.

Today's patient had no such prior trauma, but the MRI showed osteomyelitis and a fluid collection. At my behest they stuck a needle in it and it grew...

Streptococcus infantarius . Sounds like a Palestinian uprising. But I had never heard of the bug. Pubmed tells me it is the bacteria formally known as S. bovis. That I know.

Here is the breakdown (http://pusware.com/rdct/wp-content/uploads/2009/03/200903171740.jpg) of which group D strep is which.

Note they call it "simplified." Yeah, right.

For those of you dying to know the biochemicals (http://pusware.com/rdct/wp-content/uploads/2009/03/200903171754.jpg) (from the first reference),

Still, like the formally all encompassing S. bovis, Streptococcus infantarius is associated with bowel cancer, so at some point the patient will need a colonoscopy.

It also may be associated with non-colonic GI cancers. Part of the problem is all the epidemiological studies are going to have to be repeated with the new classification to see which group D streptococci are associated with which which cancers, if any.

See what happens when microbiologists get drunk? We all suffer.

At least I can kill Streptococcus infantarius, and kill it I will.

Rationalization

Streptococcus infantarius sp. nov. related to S. bovis and S. equinus (http://www.ncbi.nlm.nih.gov/pubmed/9331678). Adv Exp Med Biol 1997; 418 : 393-5.

J Clin Microbiol. 2008 April; 46(4): 1570. Association between Streptococcus infantarius (Formerly S. bovis II/1) Bacteremia and Noncolonic Cancer. (http://www.ncbi.nlm.nih.gov/pubmed/18256231)

Candida parapsilosis

Published Thu, 19 Mar 2009

There are a bunch of Candida out there (Can da da, not can DEE da).

When I was a young whippersnapper all clinical isolates of Candida were C. albicans, but there has been a slow shift away from C. albicans to non-albicans Candida causing disease. Like the patient in the ICU leaking bile into his peritoneum. He is growing C. parapsilosis and has had a fever and increased white count, so it is probably the real deal.

But what to treat him with?

C. parapsilosis has higher MIC's to fluconazole, so I get nervous with that agent, although he will probably be just fine if I use it, given that he has no other issues with his immune system.

The echinocandidins are a good bet, and as a rule all the Candida are sensitive, except, it turns out, some C. parapsilosis, which isn't your fathers C. parapsilosis.

C. parapsilosis is actually three in one, a trinity of Candida: C. parapsilosis sensu stricto, Candida orthopsilosis, and Candida metapsilosis. My lab can't tell the difference, but depending on which one it really is, there is different susceptibilities to the various antifungals.

Voriconazole or posaconazole may be a good choice, but are pricey, and like so many patients, uninsured.

Decisions decisions, and the problem is no clinical trials, just _in_ vitro susceptibility, to guide therapy. I think I will call a psychic to guide my decision. The first five minutes are free.

Rationalization

Diagn Microbiol Infect Dis. 2008 Sep;62(1):106-9. Significant differences in drug susceptibility among species in the Candida parapsilosis group. (http://www.ncbi.nlm.nih.gov/pubmed/18555634 )

J Med Microbiol. 2009 Feb;58(Pt 2):185-91. Molecular differentiation and antifungal susceptibilities of Candida parapsilosis isolated from patients with bloodstream infections. (http://www.ncbi.nlm.nih.gov/pubmed/19141735)

Postscript: Patient did fine on high dose fluconazole. The benefits of a normal immune system and draining the pus.

A surprise

Published Sat, 21 Mar 2009

My elderly (well, greater than 50 is often considered elderly, so I fit) patient with the Neisseria meningiditis meningitis awoke and now has elbow pain and swelling.

The state tells me the serotype is B, which is the most common Neisseria serotype in Oregon. The big four serotypes being A, B, C, and, after skipping D though V and 1 through 134, W-135. B is also the serotype not covered by the vaccine.

We (meaning someone else. I don't do anything that requires a needle) tapped his painful elbow and there were 92,000 white cells and no crystals. He has an infected joint. How often does that occur with meningococcus? Rarely in kids, and less often in adults. Meningococcus is a rare cause of disease in adults, and a septic joint is a rare complication of the disease, so this is rare squared.

Curiously, some strains of meningococcus have an increased propensity for seeding joints, mostly W-135. Why? One of the many mysteries in medicine.

For those of you taking medicine boreds, remember the underlying immunologic defect in patients with recurrent meningococcus is terminal complement deficiency.

Rationalization

Clin Infect Dis. 2003 Dec 15;37(12):1639-42. Epub 2003 Nov 17. The role of particular strains of Neisseria meningitidis in meningococcal arthritis, pericarditis, and pneumonia. (http://www.ncbi.nlm.nih.gov/pubmed/14689345)

Red lips, bloody nose, septic knee.

Published Tue, 24 Mar 2009

That's the patient. He has a long history of a bloody nose for the 7 decades of his life and he has red dots at the vermilion border of this lips. And spiders. Not the arachnid, Mr. Parker.

And now he has a knee with rubor, dolor, calor or, tumor (I have to work the title of the blog in somewhere). The knee is tapped and filled with pus (that makes it sound like we injected pus; we withdrew pus just to make things clear) and the fluid grew methicillin sensitive S. aureus.

It is odd how when I read an article in a journal and I see a case shortly thereafter. I suppose if I never read, I would never see anything new. The reading causes new cases to appear; I am convinced of the cause and effect.

Patient has Osler-Weber-Rendu, now called Osler-Rendu-Weber, I do not know why they changed the name order since I was a medical student. And the CID article calls it Rendu-Osler, poor Weber is aced out. Osler better watch his back. OWR is congenital form of arterial venous malformations (AVM's), and wouldn't you know it, they get infections. Brain abscesses and infected joints.

"Thirty two patients experienced 45 extracerebral severe infections. Extracerebral infections accounted for 45 (67%) of all 67 severe infections. They included septicemia (9 infections [13.4%]), arthritis and osteomyelitis (6 [8.9% ]), skin infection (abscesses and erysipelas; 6 [8.9%]), muscular abscesses (5 [7.4%]), spondylodiskitis (4 [6.3%]), hepatic abscesses (5 [7.4%]), and other severe infections (endocarditis, pneumoniae, pyelonephritis, tuberculosis, rickettsiose, and acute appendicitis with peritonitis; 10 [15%]). S. aureus was identified in 14 cases , 1 case of septicemia was due to Enterococcus faecalis and Pseudomonas aeruginosa (after a urinary infection), and 2 cases of muscular abscesses were due to Streptococcus species and Pseudomonas aeruginosa (in one case) and to Streptococcus viridans and anaerobes (in the other)."

The presumed pathogenesis is noses get colonized with staph and the prolonged nose bleeds lead to staph gaining access to the blood stream. The brain abscess occurs because the pulmonary AVM's allow the bacteria to bypass the 'filter' of the lungs and lodge in the brain.

The joints? Got me. There are evidently articular involvement with OWR, but I can't find details on the interwebs and the Pubmed references have no abstracts.

What is amazing is how often and how long these patients can bleed from their nose: days and months.

Man, this is one group that wants to keep the index finger as far from the nose as possible.

Rationalization

Clin Infect Dis. 2007 Mar 15;44(6):841-5. Hemorrhagic hereditary telangiectasia (Rendu-Osler disease) and infectious diseases: an underestimated association. (http://www.ncbi.nlm.nih.gov/pubmed/17304458)

Punch me in the Nose

Published Sat, 28 Mar 2009

Been a busy week. Many consults, lots of family stuff and the Science-Based Medicine (SBM) post to write. I remain in awe of my co-conspirators, er, co-bloggers at SBM and their ability to churn out reams of quality prose in short order. But now I have time to noodle around with this blog.

Today I saw a case of endocarditis. Nothing odd except it was a pan-sensitive coagulase negative Staphylococcus, generically referred to as coag negative staph.

Probably a health care associated disease, as he is on dialysis, and the use of central lines is associated with bacteremia and subsequent seeding of the heart valve.

Health care associated is the current preferred term, rather than hospital acquired or god damn it, it wasn't my fault associated, since a lot of health care is now provided outside the hospital. The term they really use is nosohusia, but that sounds like some sort of nasal problem in an elephant, and I can't say nosohusial without giggling.

Health care associated endocarditis is not an insignificant problem with a high death rate and coag negative staph are a common cause of the infection. In the series referenced below,

"Staphylococcus aureus was the most frequently isolated microorganism (28 cases; 33.7%), followed by Enterococcus species (19 cases; 22.9%) and coagulase-negative staphylococci (18 cases; 21.7%)"

I don't consider acupuncture to be healthcare, that would be quack associated endocarditis. Quackahusia?

What is odd about the case for me is that I have taken care of him twice in the past: both for infected knees. Evidently we had a bad interaction on the first go round, as today he said, yeah, he remembers me from three years ago and he wants to punch me in the nose. I do not remember the interaction, but evidently I sent him home from clinic saying his knee was OK when in fact it was not. Hence the interest in punching me.

Still. I try and get along with my patients, and I am discomforted by his need to rearrange my nose.

Of course I apologized, but kept more than an arms length away.

Rationalization

Clin Infect Dis. 2008 Nov 15;47(10):1287-97. Contemporary epidemiology and prognosis of health care-associated infective endocarditis. (http://www.ncbi.nlm.nih.gov/pubmed/18834314)

Cocci. Again.

Published Sat, 28 Mar 2009

I am not a big fan of weekend call, and as I slide into advanced decrepitude, it has less and less allure.

I know. Whine whine whine. But since I am on call, it can't be wine wine wine.

No matter how much I am not a fan of working weekends, at least I get to see interesting cases when I make it to the hospital.

The patient has a dense pneumonia, fevers, cough unresponsive to antibiotics.

History revealed that she was just back from two months in Arizona and Coccidiomycosis is a common cause of (missed) outpatient pneumonia. Cocci is also increasing in incidence, and may be one of those diseases that increases with global warming. Or not. Hard to know what to make of a three-year trend, but the incidence has been increasing in California as well.

Cocci, aka Valley Fever, is an endlessly interesting fungus found in the soil of the American SW, and one of its manifestations is pneumonia, often associated (not in this case, although she did have a rash) with the skin disease erythema nodosum. Dermatomes can't use real words to describe disease, just Latin terms, so they can sound infallible, a pope-y way of doing things. It just means red bumps, but you can't look smart if you tell a patient, yeah, you have red bumps. The patient knows that already, but did not know they have erythema nodosum . I had one patient with acute Cocci with about 90% of her body having red bumps.

Cocci is a self-limited disease in most normal people, and the patient is getting better with no specific fungal therapy.

The motto of Arizona is Ditat Deus, with is Latin for God gives you Cocci. The key thing is that if you go to Arizona, do not inhale. Ever.

And when your patients come back from wintering in the SW, beware of Cocci.

Rationalization

Emerg Infect Dis. 2009 Mar;15(3):397-401. Coccidioidal pneumonia, Phoenix, Arizona, USA, 2000-2004 (http://www.ncbi.nlm.nih.gov/pubmed/19239751).

J Infect Dis. 2005 Jun 1;191(11):1981-7. Epub 2005 Apr 20. An epidemic of coccidioidomycosis in Arizona associated with climatic changes, 1998-2001. (http://www.ncbi.nlm.nih.gov/pubmed/15871133)

MMWR Morb Mortal Wkly Rep. 2009 Feb 13;58(5):105-9. Increase in Coccidioidomycosis - California, 2000-2007 (http://www.ncbi.nlm.nih.gov/pubmed/19214158).

Do you have blue mold rot?

Published Tue, 31 Mar 2009

Young female with months of itching and a discharge with yeast on the vaginal prep. Candida is the usual reason, so she is given fluconazole. She doesn't get better so another round of fluconazole, and still not better.

So a culture is sent, thinking maybe it is a non albicans Candida, since it is full of yeast, and no germ tubes are seen. Maybe C. glabrata.

Nope. Cryptococcus, and not even neoformans but Cryptococcus laurentii.

Where did that come from?

Cryptococcus laurentii is a soil organism, but occasionally is seen causing disease in the profoundly immunoincompetent, like AIDS and leukemia, not that there are many cases of this yeast causing disease in the lit-tra-ture.

No cases of vaginitis reported with this organism, so mine would be the first. I wonder how many firsts I have reported in this blog, not that this is considered peer reviewed and a legitimate source for the announcement of new discoveries.

How to treat is also a problem. Cryptococcus laurentii has higher MIC's to fluconazole, but voriconazole, to which it is more susceptible, costs an arm, a leg, and your first born's left kidney. The right kidney is reserved for linezolid.

So I will try high dose fluconazole first, which she can afford and to which she had some response to low doses.

Oh, and if you have some blue mold rot on your apples, due to Penicillium expansum, Cryptococcus laurentii is an effective biological agent against blue mold rot. One never knows when one will be on Jeopardy and it will be fruit diseases for 500.

Rationalization

Med Mycol. 2009 Feb 23:1-7. Susceptibility profile of clinical isolates of non-Cryptococcus neoformans/non-Cryptococcus gattii Cryptococcus species and literature review. (http://www.ncbi.nlm.nih.gov/pubmed/19235546)

Postscript: High dose fluconazole worked.

Hypnagogic Rat Hole

Published Tue, 31 Mar 2009

As you may have gathered, I have in interest not only in infectious diseases, but in the area of quackery and also what is generally considered skepticism. I have read about hypnagogia, where there is a waking dream. And I actually had one last night. I usually detest hearing about dreams.

ROMEO

I had a dream last night.

MERCUTIO

So did I.

ROMEO

Well, what was your dream?

MERCUTIO

My dream told me that dreamers often lie .

That sums it up for me. But last night I woke up to see a white, tall, thin glowing person at the foot of the bed looking at me, and I could not move or talk. My first though was, shit, who is in the room. Then I realized, I am have a hypnagogic dream. Cool. It looked like like an alien or a ghost and it had me paralyzed. Then I really woke up and it went away.

I can really see after last night how someone could think they had seen a space alien if they did not know what hypnogogia was. It sure looked like the real deal, but I had read too may Skeptical Inquirer's I suppose, and my rational brain took over far too fast.

No infectious disease pearls today, instead I had to prepare a talk for Thursday. Back to pus tomorrow, unless it really was an alien and they come back tonight to get me. I am not sanguine space aliens sterilize those anal probes between uses. There have been outbreaks associated with colonics

“Persons who were given colonic irrigation immediately after a person with bloody diarrhea received it were at the highest risk for the development of amebiasis. Tests of the colonic-irrigation machine after routine cleaning showed heavy contamination with fecal coliform bacteria.”

and that would alienate me.

Rationalization

An Outbreak of Amebiasis Spread by Colonic Irrigation at a Chiropractic Clinic. (http://www.nejm.org/doi/pdf/10.1056/NEJM198208053070603) N Engl J Med 1982; 307:339-342. August 5, 1982.

Ignorance with Style

Published Wed, 01 Apr 2009

Ignorance with Style. That is what being an ID doc is all about. So often there is an infection and I know what the patient has, but not why. I can almost always come up with a plausible reason, based on anatomy, physiology and microbiology about why this particular infection in this particular patient. But plausible does’t mean it is true. Sometimes it feels like I am making up 'just so' stories to explain what is going on, all sound and fury, signifying nothing. And sometimes I got nothing.

For you meat fans, the iliopsoas muscle is the pork loin in pigs. Mmmmm. Pork loin. Especially grilled.

In humans the ileopsoas usually gets infected after a groin pull, which has no resemblance to what they do to make taffy. Someone dives for a loose ball, or lifts a heavy object, or twists funny. Not ha ha funny, although when I do the twist it is ha ha funny. The presumption is the trauma leads to a little bleeding into the meat, er, muscle, and it is seeded by the blood, usually with S. aureus. It is hard to infect muscle without trauma. The rabbit model of pyomyositis, I have been told, involves hitting a rabbit leg with a hammer, for without the trauma infection never occurs. A cat I could see, but a wittle bunny wabbit? I am glad I do not do animal research.

Iliopsoas infections are usually unilateral unless the infection originates from the low back. A low back infection, especially with TB, can cause bilateral disease as the ileopsoas inserts at the spine. The infection tracks down the muscle from the spine.

Male, prior trauma, unilateral disease, acutely ill, S. aureus. Defines the usual ileopsoas abscess I see in the U.S.

So I have a female, bilateral iliopsoas abscesses, big as softballs, sub-acutely ill. These abscess are so large they have obstructed both ureters. At least it grew S. aureus. And did I mention no trauma? There is hardware in the back, but no radiographic changes or clinical history to suggest that the back is infected and the source of infection. Best as I can tell from Pubmed, bilateral ileopsoas from S. aureus are almost unreported.

And odder still: the S. aureus is penicillin sensitive; this century only a few percent of Staph can still be killed with penicillin.

How to put it all together? I can't. It has to be from the spine, but I can't prove it. I'll just have to kill it. Better than pork loin is a penicillin sensitive S. aureus. There is great pleasure "To crush yoah S. aureus, see dem driven befoah you, and to hear de lammentation of de vimmin!"

If there is karma, and you generate bad karma from killing living things, I am toast. Another billion organisms soon to die at my order.

Rationalization

Medicine (Baltimore). 2009 Mar;88(2):120-30. Microbiology and outcome of iliopsoas abscess in 124 patients. (http://www.ncbi.nlm.nih.gov/pubmed/19282703)

Spinal Cord. 2006 Apr;44(4):258-9. Paraplegia caused by spinal infection after acupuncture. (http://www.ncbi.nlm.nih.gov/pubmed/16151454)

Gangrene

Published Sat, 04 Apr 2009

One the most memorable scenes I have seen in the movies was in Gone with the Wind where they had to amputate the leg with only whiskey, not even acupuncture (snort) for anesthesia because of gangrene. I was about 14 when I first saw GWTW and it really creeped me out. I do not blame Miss Scarlet from running away. Euw. And I certainly never wanted to know nothin' about birthin' babies.

Gas Gangrene is usually due to Clostridium perfringens, and Clostridium perfringens is an odd bug. Either it causes a rapidly progressive necrotizing infection with an equally rapid progression to death OR it is nothing important.

But when people get _C_. perfringens in a cultures, it results in a quasi-urgent call to your friendly neighborhood ID doc.

Patient on Friday had a hip wound that, thanks to some bad post-operative diarrhea, became infected. So the surgeon cleans it out and the cultures grow stool organisms including _C_. perfringens.

Patient is fine. No necrosis, not sepsis, no gas in the tissues.

Under these circumstances, the _C_. perfringens is just sitting there, doing nothing, like a teenager on a Saturday afternoon, and not pathogenic, unlike a teenager. It is estimated that half of _C_.perfringens isolates are colonization/contaminants. _C_. perfringens s is part of the normal GI flora, and will show up as a fellow traveler in wounds, gallbladders and the blood, especially post delivery. It has been found in every soil sample except, evidently, the Sahara desert. So it is not surprising that after a gunshot wound and a fall into the dirt, that gangrene was not an usual complication of war wounds like the poor sod in GWTW. It kills impressively fast, I have seen skin poppers (when heroin users run out of veins they ‘pop’ heroin under the skin and the heroin, especially the black tar kind, is rich in _C_. perfringens ) go from fine to dead in less than a day.

Gas gangrenes can also occur from _C_. septicum when the organism invades into bowel cancer. Since the infection starts internally and burrows out, it is hard to diagnose early, and is the source of the one and only post-mortem consult I have ever had. The patient came in multi-organ system failure septic shock and died in about an hour after reaching the ICU. As they were preparing the body for transport, he developed a spreading, necrotic infection over his right hip and they called me worried that something communicable was happening. It turned out that the patient had _C_. septicum of the right colon that burrowed out through the hip. A quick gram strain showed the boxcar shaped gram-positive rods and I could reassure the nurses they had nothing to worry about. Well, nothing as far as acquiring an infection from this patient was concerned.

Over the years I have seen a handful of patients with lymphoma that involved the gut get chemo, killing the gut lymphoma, giving both _C_. perfringens s or _C_. septicum a chance to cut loose. One patient refused antibiotics and wanted to be comfort care. And he survived. It was like falling out of an airplane without a parachute and surviving because you landed in swamp mud. In Nevada. Amazing.

The other Clostridium that kills you quickly, and I hope never to see, is Clostridium sordellii which causes sepsis after medical abortion using mifepristone and intravaginal misoprostol.

Those darn Clostridia, lurking everywhere, just waiting to kill us.

Oh yeah. Go Ducks. The Gang Green.

Rationalization

Clostridium sordellii Toxic Shock Syndrome After Medical Abortion with Mifepristone and Intravaginal Misoprostol --- United States and Canada, 2001--2005 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5429a3.htm )

Am J Hematol. 2002 Jun;70(2):145-8. Spontaneous gas gangrene in malignant lymphoma: an under-reported complication (http://www.ncbi.nlm.nih.gov/pubmed/12111788)?

Onkologie. 2009 Mar;32(3):115-8. Epub 2009 Feb 18. Fatal Clostridium septicum infection in a patient with non-Hodgkin's lymphoma undergoing multimodal oncologic therapy. (http://www.ncbi.nlm.nih.gov/pubmed/12111788)

IRIS

Published Wed, 08 Apr 2009

Pregnancy is a weird state. Slightly immunosuppressive, pregnant women, but interestingly not pregnant men, are prone to a variety of odd infections such as TB and Listeria. If you make it through the pregnancy with no infectious complications, you still have the delivery to deal with, and post-partum sepsis has a special place in the hearts of ID docs everywhere. It was in post -partum females that hospital infection control had its beginning. The principal that contaminated hands could spread infections and that sterilizing hands could prevent the spread of infection was established. A discovery that is only just now, 150 years after its discovery by Ignaz Philipp Semmelweis, being routinely used by health care providers.

Sigh. Do not get me started on hand hygiene. You have better things to do.

The patient today is transferred in septic as all get out 3 days after a C-section and her abdomen is cherry red, and I bet this is group A strep cellulitis.

One wonders (the One being me, not Harry Potter) if her post pregnancy state is making her more ill than she might otherwise be.

IRIS (Immune Reconstitution Inflammatory Syndrome) was popularized with HIV disease. When patients get HIV medications and their immune system returns, it (the immune system) attacks preexisting infections and patient become ill. Often our symptoms are not due to the bug, but the host immune reaction to the bug.

IRIS has been described in recovering neutropenics (there is no 12 step) and in pregnancy.

It may be, and it may not be. But perhaps her robust response to whatever she is infected with is due in part to a over-reaction of her immune system now that she has delivered.

A rebound immunologic overcompensation. That’s my story and I am sticking to it.

Rationalization

Immune Reconstitution Syndrome and Exacerbation of Infections after Pregnancy (http://www.ncbi.nlm.nih.gov/pubmed/17918082). Nina Singh and John R. Perfect. Clinical Infectious Diseases. Volume 45, Issue 9, Page 1192;199, Nov 2007

A Cold

Published Thu, 09 Apr 2009

I took my Echinacea, I took my vitamin C, I took my Airborne, I took my zinc, and I boosted by immune system with Dannon. And I still got a cold today. Stuffy, runny, scratchy, I am a living Niquil commercial. So I spent my day wearing a mask. Everyone said I looked better.

As usual, lots of cases that I have not yet, and maybe never will, figure out.

Like the 45 year old with a history of asthma, maybe acute pneumonia on CXR (but CT has some nodules), febrile, and a creatinine of 5.

The weird thing is the proptosis. Both of her eyes are bugging out. It will probably be Graves disease, common things commonly being common. Tautologies being taut? Doesn’t work, but I tried. Blame the interferon.

But.

If it turns out she does have an pulmonary-renal syndrome, then maybe the proptosis is a manifestations of Wegener's, as I learned today thanks to the magic of Pubmed. It would tie it all together nicely.

Ask me in a week, I will let you know if the ANCA is positive.

Rationalization

Am J Med. 1977 Jul;63(1):131-41. T he ocular manifestations of Wegener's granulomatosis. Fifteen years experience and review of the literature (http://www.ncbi.nlm.nih.gov/pubmed/327802).

Postscript: And it wasn't Wegeners, it was Graves.

Overlap

Published Fri, 10 Apr 2009

I wear multiple hats, mostly to cover the bald spot on my head.

As I am sure you know, besides being an ID doc and babbling away on this blog, I have an interest in medical woo, or Supplements, and Complementary and Alternative Medicine (SCAM's).

Although I ask my patients if they see a quack, er, I mean alternative (alternative to what, effective therapy?) providers, it is rare that my patients see anything beyond a chiropractor for low back pain.

Occasionally they see a naturopath, and their care is limited to herbs. I thought I had heard it all until my patient with chronic sinusitis told me her naturopath told her to wear wet socks to bed. As the socks dry, the evaporating moisture draws the fluid out of the sinusitis and out the feet. She thought it sounded hinky, and did not do it.

I lost my composure and burst out laughing. I could not believe this was the real deal. It is. From swanznaturopathy.blogspot.com

"Wet Socks - a must have hydrotherapy treatment

This sounds much more difficult to implement than it actually is. Most people worry about sleep quality, but then report that their sleep actually improves with the wet socks. It is an old folk remedy, tested and true. It is great for colds, sinus infections, sore throats, ear infections, coughs, and much more. I have personally used it to support healing in the legs after a sprained ankle. I know first hand how effective the treatment can be for infections and when sick, I am often discouraged that I did not put the wet socks on a day earlier and potentially avoid the later symptoms of the infection. It is great for kids. Surprisingly, they typically don't complain about having cold wet socks put on their feet.

Supplies:

1 pair white cotton socks

1 pair thick wool socks - as close to 100% wool as you have

Directions:

1. Wet cotton socks and soak them completely with cold water. Be sure to wring the socks out thoroughly so they do not drip. If you desire, place wet socks in the freezer for 3 to 5 minutes (do not freeze if using this treatment on children).

2. While cotton socks are chilling, warm your feet. This is very important to increase the efficacy of the treatment. Warming can be accomplished by soaking your feet in warm water for at least 5-10 minutes, massaging the feet vigorously, using a heating pad, etc.

3. Dry the feet off completely.

4. Place cold wet socks on feet. Cover with thick wool socks. Go directly to bed. Avoid getting chilled.

5. Keep the socks on overnight. The cotton socks should be dry in the morning.

This treatment works by forcing an increase in circulation down through the legs at night to dry the socks from the inside. The increased circulation supports drainage in the sinuses and throat at night while you sleep. Typically during the night our circulation throughout the body is very stagnant. Wet socks changes that normal dynamic. It works. Try it sooner than later."

The author of this won an award for naturopathic excellence (http://www.lifeevents.org/common-cold-cure.htm). Really.

Another site suggests it as a cold remedy and concludes "The next morning your cold will be gone. Congratulations! If you feel sniffles by the end of the day, perform the procedure each night until you feel relief."

Well, duh. Treat a self-limited disease every day and eventually it will get better.

Bastyr (http://www.bastyrcenter.org/content/view/197) (Not how I would spell it) University says

"The body reacts to the cold socks by increasing blood circulation, which also stimulates the immune system. You have to rev up the immune system, so it’s ready for battle against the affliction or condition.

This treatment acts to reflexively increase the circulation and decrease congestion in the upper respiratory passages, head and throat. It also has a sedating action, and many patients report that they sleep much better during the treatment. The treatment is also effective for pain relief and increases the healing response during acute infections. The wet sock treatment is used in conjunction with other modalities to treat inflammation, infection or soreness of the throat, headaches, migraines, nasal congestion, upper respiratory infections, coughs, bronchitis and sinus infections."

This is an institution of ‘higher’ learnin’. Is it any wonder I have no respect for their teachings?

Some humor writes itself. You just can't make this stuff up. And in Oregon they have prescriptive privileges.

A return to days of yore.

Published Tue, 14 Apr 2009

Been very busy the last few weeks. We have a French exchange student staying with us, so my evenings are spent showing him the different variations of rain that are available in Portland. It is said, incorrectly, that Eskimo's have 4 million words for snow, or some such number. In the Pacific NW we have far more words for rain, all starting with God Damn, and moving down the list. But the bottom line is sometimes there is little time for blogging.

I have a case of something I have not seen in years: PJP. One never says PJP pneumonia, since the second P stands for pneumonia. It is like saying ATM machine. He is an AIDS patient who has not been on HAART for reasons I cannot yet discover, but his immune system has been destroyed to the point where he has PJP.

PJP is short for peanut butter and jelly, no, sorry, Pneumocystis jirovecii Pneumonia, a disease that, thanks to prophylaxis and HAART is almost a disease of historical interest in AIDS. I do not think I have seen an AIDS related case this century, although, thanks to anti-TNF antibodies and other immunosuppressive agents, I have seen PJP in patients being treated for Lupus, rheumatoid arthritis, and other such diseases.

Back in day, when nickels had bumble bees and the style was to wear an onion on your belt, there were always a few PJP patients in the hospital. Now, residents can go an entire career and not see one.

Another triumph of modern medicine I really do not not want it to come back.

Rationalization

Chest. 2009 Mar 2. Trends in Hospitalizations for AIDS-Associated Pneumocystis jirovecii Pneumonia in the United States (1986-2005). (http://www.ncbi.nlm.nih.gov/pubmed/19255292)

More yeast

Published Wed, 15 Apr 2009

Patient has _S_. aureus bacteremia from heroin use. No surprise. Has a vegetation on the mitral valve, so the diagnosis is not in doubt. Endocarditis.

I once, years ago in another city, got called from a surgeon who had a price of broccoli fall out of her mask and on the heart. Biggest vegetation I have ever seen. Where is a rim shot when I need one? Or a wilhelm scream (http://instantrimshot.com/)?

So she is sent to the nursing home for treatment of endocarditis and comes in three weeks later with Candida albicans in her blood. Still, suprizingly, using heroin. Who would have figured? Presumptively the Candida is from using her line (heroin often has Candida in it), so we pull the line, wait a day, and repeat the blood cultures. At day 3 they pop positive. Repeat echo show no new or changed vegetation, but now she has clot in her jugular vein.

Probable fungal septic thrombophlebitis. Crap. Evidently there are less than 20 cases ever reported on Pubmed.

The take home is that sustained positive blood cultures over time means some sort of endovascular infection, usually endocarditis or a catheter infection, but the vascular tree is big and sometimes you have to look around to find the source.

Some Coumadin and antifungals and, one hopes, no more heroin, and the patient will get better.

Rationalization

Intern Med J. 2009 Jan;39(1):61-3. Thrombolytic therapy for management of complicated catheter-related Candida albicans thrombophlebitis (http://www.ncbi.nlm.nih.gov/pubmed/19290985).

Clin Infect Dis. 1998 Feb;26(2):393-7. Management of candidal thrombophlebitis of the central veins: case report and review. (http://www.ncbi.nlm.nih.gov/pubmed/9502461)

Postscript. She did. Get better.

4 A's or 5?

Published Fri, 17 Apr 2009

When I started in practice, my father, a cardiologist, told me the 4 A's of being a consultant: Appearance, Affability, Ability and Availability. Three out of four ain't bad. If you are going to be an ID doc, the 5th A is Amaze them.

Doctors tend to blather on and on about the possible diseases a patient could have. If you can, on minimal information, before the diagnosis is given, blurt out the answer. If you are right, it will impress people to no end, and if you are wrong, well, hell, you are always wrong at the beginning. It is why we blather on and on and order a boat load of tests.

I was scheduled to see a patient in clinic Friday with a headache and fevers of a month or so duration. The primary care physician had asked me about the case on the phone, and at that time I had no good ideas.

But he got sicker and went to the ER and I got a call from the ER doc. He ran through the same history I already knew, and then said "We did a spinal tap, and there are 240 WBC's, mostly monos and lymphs, the glucose is 15 and the protein is 226, and the gram stain ..."

Here is where you butt in.

"It showed yeast." I said.

He was flabbergasted. He asked if I was looking at the labs on the computer.

Nope.

Then how did I know?

I said it is what ID docs do.

Who needs false modesty, right?

Patient has Cryptococcal pneumonia with meningitis.

I try to do this about once a week and I succeed one a year. But everyone remembers when Babe Ruth pointed to left field, and then went they and had a candy bar. No one remembers that he lead the league in strikeouts.

ID is perhaps unique in the opportunity to come up with an odd diagnosis with a few facts and a educated lucky guess. It is the medical equivalent of a cold reading.

When John Edwards does it, he makes millions talking to the dead. When I do it, I get the medicare discount rate.

But if you can get the diagnosis on minimal data occasionally, it will impress everyone.

Where did he get the yeast? Maybe a horse barn, he has extensive exposure to horse barns. Maybe not. Cryptococcus will be one of the endemic fungi in the Pacific NW, imported from Vancouver. But pigeon poo and barns are not uncommonly a source for Cryptococcus.

Rationalization

Clin Exp Dermatol. 2004 Mar;29(2):159-60. Primary cutaneous cryptococcosis in an elderly man (http://www.ncbi.nlm.nih.gov/pubmed/14987274).

The prevalence of Cryptococcus neoformans in various natural habitats (http://www.ncbi.nlm.nih.gov/pubmed/5679667). Medical Mycology, Volume 6, Issue 3 1968 , pages 213 - 217

I can't leave even for a few days...

Published Tue, 28 Apr 2009

I had five days off with my youngest for his spring break, and we spent the time at the Oregon Coast. Great time. No TV, only dial up internet, no newspaper, no contact with the real world. So I get back on Sunday and my wife tells me we are in a State of Emergency.

What?

We have closed the borders with Mexico

No way. Why?

Because of Swine Flu.

Huh? Flu season is over. Where in the hell did that come from?

Whether or not this is going to be a pandemic strain, and whether it is going to kill off 2% of the world like the 1919 pandemic, I can't say. It may just dribble off the court and be a false alarm. I hope so.

However, people seem to be in panic mode real soon. As I write this there are 40 cases in the US, no deaths. People are wearing masks around town and asking for oseltamivir. Some people are keeping there kids home from school, even though no cases reported in Oregon.

We are just finishing the flu season. There were about 30,000 documented cases of flu, 55 deaths documented in kids, and thousands of extra deaths in adults. And it was a slow year.

There is a Cinco de Mayo party coming up (what day is that?) and concern was expressed about having the kids attend. Maybe 30,000 people die each year in car accidents. If you really want to protect you kids you would make sure they got a flu shot and not let them in a car. And don't get me started on deaths from guns.

Swine flu? We will see. "Prediction is very hard, especially when it's about the future" - Yogi Berra" Or perhaps it was "I predict the future to be full of pic-a-nic baskets, Boo-Boo." Ask a psychic, not me.

I would prefer the government to over-react than under-react with infections. They (infections not government. Or did I get it backwards?) can spread to fast and kill too quickly. It is better safe than sorry. One of these days, be it avian flu, or this swine flu, or another strain, flu will come out of nowhere and kill a boatload of people. If it is going to kill lots of people, there is not much we can do for now except not inhale. Worked for President Clinton.

Postscript: an interesting bit of personal history, my first reaction to H1N1.

Half time

Published Wed, 29 Apr 2009

NBA playoff time and, here in PDX, the Blazers are it. If we lose, its oh-va. So its quickie pearl time here in Rip City.

38 yo IV meth user has three days of severe low back and thigh pain. Rather than heroin, he takes enough aspirin to get a level of 300 and it is the ringing in the ears that brings him to the hospital. MRI of the back is negative.

All the blood cultures grow S. aureus.

The clinical pearl?

About 30% of S. aureus bacteremias will present as severe musculoskeletal, especially low back, pain.

That is it. I have a game to watch.

Its coming

Published Thu, 30 Apr 2009

No, not flu. Well, maybe. It’s too soon to tell whether the swine flu is going to be a pandemic disaster that kills millions or fizzles. I hope the later. But hard information about the swine flu is rare and the reports on the TV define histrionic. However, I am dining primarily on pork. Ribs and loin and chops and bacon.

No swine, no swine flu, so I am doing my part.

No, something wicked this way comes, and it isn't, yet, a virus.

Very old male with a right lung filled with something. It is a near total white out, and, while short of breath, he is surprisingly non-toxic. His bronchoscopy has heavy growth Cryptococcus. That's two cases of Cryptococcus in less than two weeks.

Since 1999 _C_. neoformans has been newly established on Vancouver Island and causing disease in Canadians. Thanks to a strong show of force by HomeLand Security, it has not been a problem in the U.S. Until now. The prevailing winds and the local environment are carrying the yeast our, meaning my, way. This may be the start of something bad.

Here are the cases (http://pusware.com/rdct/wp-content/uploads/2009/04/200904292104.jpg).

And how they got here (http://pusware.com/rdct/wp-content/uploads/2009/04/200904292105.jpg). Looks like the invasion plans for Iraq.

I wish border patrol was a bit more selective in what it lets through. I expect the NW will become endemic for Cryptococcus unless we get lucky and global warming turns the area into a desert. Take that, Cryptococcus.

Rationalization

J Infect Dis. 2009 Apr 1;199(7):1081-6. Molecular evidence that the range of the Vancouver Island outbreak of Cryptococcus gattii infection has expanded into the Pacific Northwest in the United States. (http://www.ncbi.nlm.nih.gov/pubmed/19220140)

Oh poo.

Published Fri, 01 May 2009

The Blazers are eliminated.

Poo.

We have our first case of Swine flu in the state.

Poo.

I spent my afternoon in Swine flu meetings.

Poo.

So more Pooh. It sums up my attitude today.

Due to uncetain copyright issues, here is the link to flu Pooh (http://pusware.com/rdct/wp-content/uploads/2009/05/poohflu.jpg).

Flu for you

Published Sat, 02 May 2009

I have been hesitant to write about the bacon, er, swine flu. So little data, so much hysteria. If you want to hear me babble on about Swine flu, listen the Skeptics Guide to the Universe number 197, (available on iTunes). I hope Steve Novella has his usual psychic ability and edits out all the dumbass things I say.

I have worried for most of my career about another influenza pandemic that repeats the 1919 pandemic, and, as the body count has not risen, I think we have maybe maybe maybe dodged a bullet.

Maybe.

As the body count has not increased (as I write, 367 cases and no deaths in the industrialized West except for a case acquired in Mexico), it would appear that hope hope hope it is not a particularly virulent strain of flu if you can get proper medical care.

Maybe.

To get a pandemic like 1919 that infected half the world and killed maybe 2 to 5% of the world, you need a strain of flu that is both very infectious and very virulent. Looks like swine is infectious but not virulent. It causes, maybe, mostly mild flu. Flu that does not kill you.

"There are some genetic tests that have shown the virus we are dealing with right now does not have the factors that we think made the 1918 virus so bad," said Julie Gerberding, former head of the CDC, in an interview yesterday on ABC News. "But we have to be careful not to over-rely on that information, because these flu viruses always evolve."

There is a suspicion, yet to be proved, that severe, fatal, flu is the exception, not the rule.

However.

Influenza is one pain in the ass, or the lung.

It has segmented DNA, so what happens is that a pig gets simultaneously infected with human, pig and, say, bird flu. Then, as it reassembles, it takes a few DNA segments from the bird, a few from the human and a few from the pig and, voila, a new strain of flu.

So I am still nervous.

We (may) have an strain of flu, the bacon flu, that is (maybe) infectious but not virulent.

For the last several years we have had a very virulent (killed 257 of 421 cases, about a 61% death rate) avian flu wandering though the world. But the avian flu is not infectious. You have to wallow in bird flu to get infected.

Worst case: the avian and the swine and a human flu will meet in a pig somewhere and recombine like some sort of horrible transporter accident and we get the worst of both worlds: an infectious AND virulent new strain of flu.

It could happen. And if it can happen, eventually it well. In nature, if it is not forbidden to occur, it is required to occur.

So maybe maybe maybe this is the start of a huge shit storm. I watched I Am Legend too many times.

Infected Infarctions

Published Tue, 05 May 2009

Hepatocellular carcinomas are bad. Often you can't cut them out and they are not particularly responsive to chemotherapy. They are preventable, as many hepatomas are due to chronic hepatitis B, and are found in hepcats. The consult today is an elderly female from SE Asia with a lifetime of chronic hepatitis B and now a mass in her liver.

What they do to kill these tumors is cut off its blood supply and they do that mechanically: stuff the hepatic artery that feeds the tumor with beads and gelfoam and the artery clots off and the tumor dies. It works, but is not without its potential problems. Like bacterial seeding of the dead liver and a subsequent pockets of pus.

She had several days of fevers, chills, fatigue and, after admission,E. coli in the blood. A CT looking for the source of the E. coli demonstrated that the tumor, which was embolized about a month ago, now has a pocket of gas in it. The liver is downstream from the colon, which is filled with hundreds of species in the feces of bacteria. Sometimes the bacteria relax, turn off their minds, and float downstream and lodge in the liver. Tomorrow never knows when that will happen.

Only way to get gas in the dead tumor is if something is making gas, and, as my 12 year old likes to demonstrate loudly, to be alive is to make gas. While one worries with gas about gas gangrene, the end by product of all metabolism is gas, and every organism, from anaerobes to E. coli to Candida can make gas. The worst gas forming infection I have ever seen, at least in term of quantity of gas made, was a S. aureus infection that looked like a seltzer bottle had been released in his muscles.

Infected infarctions are also problematic to treat as the dead tissue is a huge foreign body with no antibiotic penetration, so they tend to respond poorly to drainage and antibiotics. I am not optimistic that I can cure the infection.

Rationalization

Br J Surg. 2005 Oct;92(10):1248-54. Adverse effects of radiofrequency ablation of liver tumours in the Netherlands. (http://www.ncbi.nlm.nih.gov/pubmed/15997440)

Postscript: No follow up. Patient had a change in insurance which lead to a change in hospital systems.

Incidentaloma

Published Sat, 09 May 2009

Technology becomes increasingly inexpensive and available. I heard that there is now a ultrasound probe that uses your iPhone as the screen. I am sitting in the parking lot at the mall, with my netbook in my lap as my children look for a Mothers Day present, writing this blog.

And the anesthesiologists have transesophageal echocardiograms and they can check out cardiac function any time they please, and this time they pleased.

Patient has a chronic foot infection that needs debridement and in the OR the anesthesiologists slip that old probe down the esophagus and there is the heart, beating away nicely and there is that aortic valve and, hey, what the..?

A vegetation.

Really. I looked at the ECHO and it sure looks like a veggy to me, a 6 mm clot on the tip on the aortic valve, flopping in and out.

Once I get to talk to him and examine him he has no constitutional symptoms, no murmur, no emboli, no lab findings of endocarditis. Nothing to suggest endocarditis but a really abnormal TEE.

Blood cultures are negative, but he is on antibiotics for the foot infection.

Classically, an incidentaloma is an adrenal mass found on CT when you were not expecting it.

It does not typically refer to a vegetation on a valve, but I have been called twice this year about unexpected clots on valves. The other was a 1.4 cm aortic vegetation that was found on a routine ECHO obtained for other reasons.

So what is it? Treated endocarditis? Partially treated endocarditis? Culture negative endocarditis? Murantic endocarditis (sterile vegetations from a hypercoagulable state)? A really really really odd tumor on the valve? I don't know. Only way to know with certainty is to cut it out, and that hardly seems worth it. The heart is one of the few place I can’t get my interventional cardiologists to biopsy. Go figure.

If the cultures remain negative I will send of all the serologies that in 20 years have yet to strike pay dirt. In the end he have to be treated for culture negative endocarditis, safe is better than sorry.

Rationalization

Ann Cardiol Angeiol (Paris). 2001 Oct;50(6):316-8. Cardiac incidentaloma. (http://www.ncbi.nlm.nih.gov/pubmed/12555622)

Medicine (Baltimore). 2005 May;84(3):162-73. Blood culture-negative endocarditis in a reference center: etiologic diagnosis of 348 cases. (http://www.ncbi.nlm.nih.gov/pubmed/15879906)

Postscript: patient never had a diagnosis and the endocarditis was a cure, if one can cure a disease you are not certain they really had.

Strawberries

Published Tue, 12 May 2009

Oregon is the best place to live on earth. Period. But don't tell anyone, it will be our little secret. One of the delights are the strawberries, which are not the fibrous only slightly sweet posers that come from California. Oregon strawberries are luscious, but do not travel, going bad in less than 48 hours after picking. The season usually doesn't begin to June, but for me the season started early.

Fevers, hypotension, acute renal failure, altered mental status, a diffuse erythroderma that included the palms and sole, red conjunctiva and the tongue. The tongue was cool. It looked like a strawberry. Not the best I have seen, that being in a case of post partum toxic shock syndrome (yes, it was a case of Staphylococcal toxic shock syndrome) where the tongue looked like a big Hood River strawberry. Didn't taste like it, though. (Just joking).

Strawberry tongue has a limited differential: Toxic shock syndrome (TSS), both Staphylococcal and Streptococcal, Scarlet fever, and Kawasaki's.

There is also, evidently, a recurrent familial form. And there can be a white strawberry and a red strawberry, but not a chocolate covered, strawberry tongue. Well, I guess there could be, if a Kawasaki’s patient ate a Hershey bar, but not as a clinical sign.

Google images is full of examples (http://www.officialpsds.com/images/thumbs/Strawberry-tongue-psd36882.png&imgrefurl=http://www.officialpsds.com/strawberry-tongue-PSD36882.html&usg=\_\_SFELhNzJd0XI7vHqnJV4EsGub8Y=&h=325&w=400&sz=279&hl=en&start=0&sig2=LFcyWfHVsCjm02dKL7VtmA&zoom=1&tbnid=NduNpQBAYf7YwM:&tbnh=126&tbnw=155&ei=uAHqTN-7AoaisAO504WxCw&prev=/images?q=strawberry+tongue&um=1&hl=en&sa=N&biw=1185&bih=766&tbs=isch:1&um=1&itbs=1&iact=hc&vpx=421&vpy=475&dur=967&hovh=202&hovw=249&tx=170&ty=136&oei=uAHqTN-7AoaisAO504WxCw&esq=1&page=1&ndsp=24&ved=1t:429,r:20,s:0).

I cannot find why TSS causes a strawberry tongue and cannot find reports of a tongue biopsy, as well as why Kawasaki's cause the same physical finding. What does Kawasaki's have in common with TSS? Got me.

But I did find Baboon syndrome, where you get a rash that looks like a baboon butt. Cool. It can be due to the same toxin that causes scarlet fever, so there is a link.

Rationalization

Clin Exp Dermatol. 2009 Apr;34(3):355-7. Epub 2008 Aug 9. SDRIFE (baboon syndrome) induced by penicillin (http://www.ncbi.nlm.nih.gov/pubmed/18699835).

J Dermatol. 2003 Jan;30(1):69-71. A case of baboon syndrome associated with group a streptococcal infection (http://www.ncbi.nlm.nih.gov/pubmed/12598713).

Potato Potatoe

Published Wed, 13 May 2009

There is an ongoing 'discussion' in my family of what is better: rice or potatoes. I am a rice fan, my wife prefers potatoes. Mashed, fried, boiled or baked, she like her hot potatoes.

And that brings us to the clinical sign of the hot potato voice.

What is it about old time Doctors and their urge to describe everything after one food or another? Makes eating less enjoyable.

Todays patient had fever, bad sore throat, was toxic appearing with a marked left shift. There was also a soft, deeper than usual, whispery voice, the hot potato voice, so called because it sounds as if the patient talks as if there is a hot potato in their mouth. This is a sign of peritonsillar abscess or cellulitis.

And sure enough the CT showed two early tonsillar abscesses and peritonsillar inflammation, and, though the magic of antibiotics, the patient is getting better.

However. Let's see a show of hands: everyone who has listened to someone talk with their mouth full of hot potato. I thought so. Nobody.

Is the peculiar way of talking with a peritonsillar abscess really like talking with a hot potato in your mouth? There is no question in medicine that is not worth a study. Dr MF Bhutta compared the talking of people with tonsillitis to them what had a hot potato in their mouth and the sounds were different:

The study, Hot Potato Voice in Peritonsillitis: A Misnomer, appeared in the Journal of Voice.

“Voice changes are a well-recognised symptom in patients suffering from peritonsillitis," it says. "The voice is said to be thick and muffled, and is described as a 'hot potato voice,' because it is believed to resemble the voice of someone with a hot potato in [their] mouth. There have been few studies analyzing ... the voice changes in tonsillitis or peritonsillitis and none that have compared these changes with those that occur with a hot potato in the oral cavity."

To remedy this lack of knowledge, the three doctors recruited two sets of volunteers. The first group comprised 10 hospital patients whose suffering related to their tonsils. Each volunteer pronounced three particular vowel sounds, which the doctors recorded and subsequently analyzed using special software.

The second group were 10 healthy hospital staffers, "with each of these participants placing a British new potato of approximately 50 grams in their oral cavity, warmed by microwave to a 'hot,' but not uncomfortable, temperature."

The doctors detected unmistakable differences. The unique sound of someone burdened with an actual potato, they explain, "is related to interference with the anterior tongue function from the physical presence of the potato."

There are obvious flaws in the study. The potato should have been an Idaho baker, not an English new potato. Wrong thermodynamics. Part of the reason people with tonsillitis talk that way is to decrease the pain they have when talking. The potato should have been HOT, not hot. It should hurt.

They need to repeat the study, or use hot pizza instead.

Baboon butts and hot potatoes, this blog has it all.

Rationalization

http://www.guardian.co.uk/education/2009/jan/13/improbable-research-mahmood-bhutta

J Voice. 2006 Dec;20(4):616-22. Epub 2005 Dec 19. "Hot potato voice" in peritonsillitis: a misnomer. (http://www.ncbi.nlm.nih.gov/pubmed/16360301)

Right again

Published Wed, 13 May 2009

I no long remember why I became a doctor, it was too long ago and I barely remember yesterday anymore. But I do remember why I remain one, and it is because being an ID doc is so cool. Not cool, like what my kids consider cool, since as a human I am the antithesis of cool. Cool as in fun and interesting.

It is nice to make people better and talk with them and help them, don't get me wrong. But the fun, what really bakes my potato, is figuring out the diagnosis before the cultures pop positive.

Like the patient today. Old heart transplant, as an outpatient he has a new temporal headache, and, despite the negative biopsy (which are known to have a high false negative rate) he is put on high dose prednisone for temporal arteritis.

He declines, has hemoptysis, a nodular upper lobe infiltrate on CT and develops petechiae on his legs.

He is admitted, his blood cultures grow a yeast and he is transferred to my hospital.

I am far more often wrong than I am right, and it is always annoying how often reality gets in the way of a good diagnosis. I wish I were a CAM provider and did not have to worry about reality.

I said that it will be Cryptococcus, that it is the ONLY diagnosis possible, and by gosh and by golly his serum cryptococcal antigen is > 1:2048. CNS evaluation is in process.

It always impresses people when you hit one out the ballpark.

In my mind there are two take homes from this case.

One. And I can't prove this by any data that I can find, but my local rheumatologist agrees. If you are on transplant medications, you cannot develop a vasculitis. I wonder if the temporal arteritis was, in fact, early cryptococcal disease.

B. Disseminated Cryptococcus causes petechiae. I didn't know that. Red bumps and molluscum contagiosum like lesions are the most common skin manifestations of Cryptococcus. Ulcers and cellulitis less so, and while I cannot find petechaie on Pubmed, doing the Google on the interwebs finds all sorts of references.

III. 3 out of 2 people do not understand arithmetic, but everyone seemed to worry it might be Candida. Candida does not get in the blood stream unless there is a intravascular catheter, which he does not have. Just because he has a heart transplant doesn't mean he is equally at risk for all fungi. Candida just ain't on the list.

That is now four cases of Cryptococcus, three in less than a month.

This will be the year of Cryptococcus and West Nile in Oregon. Something wicked this way comes.

Cue up the music from Jaws.

Rationalization

Arch Dermatol. 1996 May;132(5):545-8. Cutaneous Cryptococcus infection and AIDS. Report of 12 cases and review of the literature.

Postscript: as of 2010, we are still lacking in West Nile in Oregon.

Saepius in Erroris, Nunquam in Nuto.

Published Tue, 19 May 2009

Busy busy busy.

Sometimes life keeps me away from the computer, but then, is that really living? There are things that need to be done away from the interwebs, at least until I become one with Matrix.

I spent a chunk of my day teaching residents as one of my hospitals has an internal medicine residency program. The problem is I often do not know here my ideas for a diagnosis come from. Like today.

I was asked to see a patient with a hematologic malignancy and fevers for five days despite ceftriaxone and azithromycin for the not really there pneumonia. The kind of sort of maybe infiltrate that has increased in frequency since OMPRO started measuring time to first antibiotic as a quality indicator. As a result, a lot of iffy pneumonias are treated instead of waiting, proving yet again that no good deed goes unpunished.

I know from a quick chart review that the white cells have gone form 6 to 1.7, his platelets from 230k to 90, and his hemoglobin has dropped 2 points. Rest of his labs are OK.

So the patient tells me he has teeth chattering rigors (which he has during the interview), fevers, severe myalgias, and abdominal pain. Otherwise no localizing symptoms

Hmmmm.

PMH: Waldenstrom’s, but no treatment for a year.

Animals? Dogs.

Travel outside Portland?

We were at our cabin in Eastern Oregon, near Bend, at 4900 feet.

Why he mentioned the elevation, I do not know, but my ears perk up.

So, any ticks?

Yeah. 4 tick bites, and his wife volunteers that they are swarmed with ticks this time of years.

And like a bubble floating up out of the bath and popping, I could smell what he had. But I do not know where the thought came from. The diagnosis is made far below conscious thought, then I do a rapid song and dance to justify the potential diagnosis.

I should mention that I have yet to confirm the diagnosis, and like many great diagnoses I make, reality often contradicts me. Pesky reality.

My motto: Saepius in Erroris, Nunquam in Nuto: Frequently in Error, Never in Doubt.

I will probably report in a few weeks I was wrong.

But for now I am calling it Colorado Tick Fever. Everything fits perfectly.

Rationalization

www.oregon.gov/DHS/ph/acd/diseases/ctf/facts.shtml#more

Postscript. Colorado tick fever serology was negative, and he either got better on his own or due to the doxycycline he received. However, Waldenstrom’s is a disease of abnomal antibody production, so maybe I was right and the serologies are wrong. Yeah. The serologies are wrong. That’s the ticket.

Cross Reaction

Published Wed, 20 May 2009

I spent the day watching my son in the state golf tournament. He did OK. First time to State. No infections on the golf course.

My latest Cryptococcus case? Doing great thanks to amphotericin B and flucytosine.

When the patient first came in he had nodules on his chest CT and was coughing up blood. In the differential is Aspergillus infection and the pulmonologist sent of both cultures and a serum Aspergillus galactomannan assay.

The galactomannan assay is a reasonable way to determine if a patient has invasive Aspergillus. Galactomannan is one of the cell wall constituents and when the organisms gets in the blood, bits of the cell wall flake off into the blood, like dandruff, and can be measured.

His was positive at 0.56, just above the cut off of 0.5.

Does he have fleas and lice? Flice? Lleaes (pronounced like llama, or the way George Hrab can say yes).

Nope.

The galactomannan assay can be false positive with, of all things, piperacillin/tazobactam. Sometimes a bored question. Yawn.

And it turns out the Cryptococcus makes glactoxylomannan which cross reacts with the assay, so it is not really a false positive, it is true positive for the wrong fungus.

Since the patient has a serum cryptococcal antigen titer > 1:2048, I am not surprised the assay was positive, os it is a a true false positive? A false true positive? Something like that, if you know what I mean, and I am sure you do.

More importantly, since the patient who is at risk for Aspergillus is also at risk for Cryptococcus, a positive galactomannan assay in the right host should probably result in a serum cryptococcal antigen as well.

Rationalization

J Clin Microbiol. 2005 Jun;43(6):2929-31. Cryptococcus neoformans Galactoxylomannan contains an epitope(s) that is cross-reactive with Aspergillus Galactomannan. (http://www.ncbi.nlm.nih.gov/pubmed/15956422)

N Engl J Med. 2003 Dec 11;349(24):2366-7. False positive test for aspergillus antigenemia related to concomitant administration of piperacillin and tazobactam. (http://www.ncbi.nlm.nih.gov/pubmed/14668472)

Onycomycosis gone bad

Published Fri, 22 May 2009

Patient rolls his car. It is always a bad idea to roll your own. Something, just what is not certain, maybe his dogs nail, punctured his palm. His hand, not the PDA.

Since then he has had ongoing pain and erythema on the palm of his hand and when he moves his middle finger.

I do not know about you, but I have trouble driving if I cannot fully extend my middle finger.

He received several courses of oraql antibiotics without resolution, and then to a hand surgeon, and then to me.

The striking feature on exam is all his nails were heavily involved with a fungal infection. It had cleared years ago after a course of terfinibine, but relapsed almost immediately after stopping the medication. At least as immediately as a nail can grow.

The surgeon opened it up and it was a low-grade gooey mess, not typical of a bacterial infection.

I made sure that the cultures were sent for fungal cultures as well as for AFB, but now the cultures are growing a Trichophyton species.

I bet whatever penetrated his palm (probably his nail, not the dog's) dragged in his nail mould and caused a tenosynovitis, since the most common pathogens for nail infections are the dermatophytes Trichophyton rubrum and Trichophyton mentagrophytes .

There are at best 18 references on Pubmed of soft tissue infections with these organisms, almost all in the profoundly immuno-incompetent and no cases of tenosynovitis.

The NEJM suggests the best therapy is itraconazole as the best treatment. In ID the answer to the cause of the infection is all in the exposure history. You get infected with what you are exposed to. My wife, fortunately, has an infectious smile, so I am safe for the time being.

Rationalization

N Engl J Med. 2009 May 14;360(20):2108-16. Clinical practice. Fungal nail disease. (http://www.ncbi.nlm.nih.gov/pubmed/19439745)

Why?

Published Wed, 27 May 2009

I sometimes get asked what: what does the patient have.

Sometimes I get asked how: how to treat the patient. That was todays patients. The patient had a fever the day after he has his laparoscopic mesenteric biopsy and three days later his blood cultures popped positive for Candida glabrata of all things.

They asked be about the best antibiotic to use (I picked caspofungin).

But the interesting question is why.

Preop, he had no symptoms.

Past medical history includes diabetes, pacemaker dependent, obesity with chronic 'diaper rash' in his skin folds. His pacer is three years old.

His exam is negative.

The classic risk factors for Candida in the blood are central lines, hyperalimentation, broad spectrum antibiotics, neutropenia and a major surgery. He had none of the above.

The only reason he could have positive blood cultures is if he had seeded his pacer system from his intermittently oozy groin. Unfortunately his TEE today showed probable infection on the wires.

Crap.

I can't cure a bacterial pacer infection, much less a Candida infection, medically and if the pacer system comes out, he has no rhythm. He has no rhythm, who could ask for anything more? Me. It is why I am glad I am not a cardiologist.

There is exactly one case of C. glabrata pacer infection in the lit-tra-chure and a smattering of a handful of a smidgin of other Candida species on pacers. Like all infections of pacers, the system absolutely, positively has to be removed. Unlike prosthetic valve endocarditis, the literature suggests you are as likely to cure a pacer infection medically as you are to get an accounting of the money spent to bail out Fanny Mae.

Rationalization

J Infect. 2000 Sep;41(2):176-8. Medical treatment of a pacemaker endocarditis due to Candida albicans and to Candida glabrata. (http://www.ncbi.nlm.nih.gov/pubmed/11023765)

Postscript: The pacer came out without incident and the wires grew Candida. He did fine.

The Secret

Published Thu, 28 May 2009

Sometimes you suspect the diagnosis as soon as you walk in the room.

The patient was billed as chronic cough with an elevated white count. Why?

He was thin and tanned, the latter odd for Oregon at this time of the year. What was striking was his clubbed fingers. The most impressive I have seen in years.

I take the history: slight non-productive cough, 10 pound weight loss, his long bones have been aching for couple of months. 2 pack a day smoker for years.

Labs showed an elevated white count, 14 to 16, 000, but otherwise normal. His chest x-ray is OK.

His exam is negative except for the clubbing and muscle wasting. He says his fingers have always been that way. There is congenital clubbing, but no way is this is congenital, although I hope so. I go looking for the cancer that should be there.

CT scan shows a 4 cm mass, some sort of cancer, in his mediastinum, right behind his heart where it could not be seen on CXR. The clubbing was the hint.

"Of patients with idiopathic pulmonary fibrosis, 65% have clinical digital clubbing. In these patients, an increased occurrence has been shown in patients with higher grades of smooth muscle proliferation in the lungs.

Clubbing has been reported in 29% of patients with lung cancer and is observed more commonly in patients with non-small cell lung carcinoma (35%) than in patients with small cell lung carcinoma (4%). Digital clubbing was reported in 38% of patients with Crohn disease, 15% of patients with ulcerative colitis, and 8% of patients with proctitis. Clubbing was observed in up to one third of Ugandan patients with pulmonary tuberculosis.)"

The long bone pain is probably pulmonary osteopathy, an unusual cause of bone pain. All his symptoms are from his cancer, which will be biopsied later in the week.

The reason I recognized this case is I compulsively go to noon report where the residents present interesting cases as unknowns and the Chief of Medicine, Dr. Jones, discusses the case, with input from the house-staff.

Not five days earlier they had presented a similar case and Dr. Jones finished by saying, "Some people say it is a waste of time teaching these rare diseases, but you never know when one will walk into clinic."

And sure enough, there was a case in the office less than a week later. Weird. Or can you say confirmation bias? Sure, I thought you could.

I am disinclined towards the supernatural, but it is spooky how often you hear about a good case or read about something new, and you see a similar case a week or two later. I always wonder how many similar cases I have missed over the years because I did not know about the disease. It is why I try to say "I have never diagnosed a case" rather than "I have never seen a case." I wonder how many I have seen and not known it. The Secret is true. Just by knowing about a disease, the universe delivers it up to you. The Secret doesn't create health and wealth, it creates cancer, infection and death. A much more interesting, if awful, result.

Rationalization

Clubbing of the Nails (http://emedicine.medscape.com/article/1105946-overview)

Kiss my Aspergillus

Published Thu, 29 May 2009

Aspergillus is everywhere. It can be the mold on your bread, the mold on your cheese, and the mold on the cup of coffee that is left out for three or four weeks. My wife, and most females, have curiously never seen mold on a cup of coffee left out for weeks. Most males have. I don't know why, but when I was single I would let the dishes sit in the sink until the growth on them evolved into a life form that wanted to clean itself. I don't do that anymore.

So when Aspergillus is in a bronchoscopy culture, you have to ask if it as real or a contaminant, and Ella Fitzgerald can't help you with that.

The patient has had Wegeners for 5 months and is on dialysis, prednisone, and just finished the Cytoxan that cleared up the pulmonary infiltrates on her CT. Now back in the hospital, she has cavitating pulmonary nodules, the BAL from the bronchoscopy is growing Aspergillus after only three days. She is a touch short of breath, but no hemoptysis.

The gold standard for invasive Aspergillus is biopsy showing invasion of the organisms, but the bronch biopsy did not show this.

Open lung? Treat?

The BAL had Aspergillus on staining, so it must be a fairly high concentrations and she had no prior structural lung disease to predispose to heavy colonization. The chance that the Aspergillus is the real deal is about 25%.

"Organisms such as cytomegalovirus, Aspergillus, and Candida were frequently identified in BAL specimens but were eventually proved to be pathogens in only 24%, 25%, and 0% of cases, respectively."

Not good odds. But it is a compatible CT, host and large amounts of Aspergillus that grew rapidly. If the galactomannan assay is positive, then the diagnosis is clinched.

So she is on voriconazole and we shall see. That’s the royal we, not the multiple personality we. You don’t want to see my goth cowgirl. Trust me.

Rationalization

Clinical utility of bronchoalveolar lavage in immunocompromised hosts (http://www.ncbi.nlm.nih.gov/pubmed/1545588). Mayo Clin Proc. 1992 Mar;67(3):221-7.L

Oprah wants your children dead and I am moving

Published Mon, 01 Jun 2009

Well, Oprah really doesn't want your children to die. At least I do not think so. But one wonders. If you spend anytime at all in the antivax world then you are aware of Jenny McCarthy, who believes, despite all the evidence to the contrary, that vaccines are dangerous and cause autism. She has even go so far as stating in her Time interview that

"I do believe sadly it's going to take some diseases coming back to realize that we need to change and develop vaccines that are safe. If the vaccine companies are not listening to us, it's their f\__ing fault that the diseases are coming back. They're making a product that's s___. If you give us a safe vaccine, we'll use it. It shouldn't be polio versus autism."_

It isn't. Holy False dichotomy, Batman. Vaccines are safe. The diseases they prevent are bad. Real bad. We do not want them back.

Time does not approve of 'uck' or 'hit' but has not problem giving antivax wackaloons space.

But the wise and powerful O has hired Ms McCarthy for, perhaps, a talk show where she can take her vaccine delusions to an even wider audience. And kids will die. And, in the end, Oprah will need to be added to the Jenny McCarthy body count.

"Everyone look under your seats. Everyone here gets a child dead from pertussis."

When it comes to health care, and woo, Oprah is a goof; there is a nice evaluation over at Newsweek. Go to www.oprah.com/contactus. Let her know that indirectly killing babies by supporting antivaccine nonsense is a bad idea. Let her know it will make her fat. But let her know.

So. This is my last entry at this site.

About a month ago I was contacted by the folks at Medscape asking if I would be interested in being their Infectious Disease blogger. Do the same thing I do here, but do it on Medscape, with a much bigger audience.

I said sure.

So starting this week I have sold my soul to the company store (my goal in life) and Rubor Dolor Calor Tumor will now be over at Medscape (http://www.medscape.com/public/blogs).

See you there.

Rationalization

Jenny McCarthy on Autism and Vaccines. www.time.com/time/health/article/0,8599,1888718,00.html

Don't change the litter box before driving.

Published 1 June 2009

Note: first Medscape, add the polls

In Oregon, in case you are interested, if you get three photo radar tickets and a car accident in less than three months, the State looks unkindly upon you. I get to enjoy public transportation for the next month, much to the amusement of my coworkers (a word I always see as cow orkers, although I have no idea what orking a cow would entail). Amongst other things, if, in the following 12 months you get another moving violation, they suspend your license for a year. It is a good reason to drive very, very carefully. And kids are always pointing out the police cars.

Toxoplasma is an interesting parasite. In the wild it infects small animals like mice, but it needs to complete its life cycle in a cat or other carnivore. So the parasite goes to the brain of the mouse and causes an encephalitis, which slows the mouse down and increases the chance it will be captured and et by a cat. This is only one on many examples where an infection changes the behavior of its host to help increase its chances of reproducing.

Toxoplasmosis is supposed to be asymptomatic in humans, or so I thought. Turns out that patients infected with toxo are not all that normal. Toxo seropositive people have slower reaction times and as a results are more prone to car accidents, not that car accidents will help the organism reproduce. Although one wonders if our ancient forebears were more likely to be consumed by lions as a result of toxoplasmosis. And I would prefer my neurosurgeon to be toxo negative.

As always, it is not that simple. All Tanzanian military recruits are screened for toxo, and those that are seropositive had an increased car accident rate only if they were blood type RhD negative. Blood type RhD positive was protective from toxo associated car accidents.

"Our results show that RhD-negative subjects with high titers of anti-Toxoplasma antibodies had a probability of a traffic accident of about 16.7 %, i.e. a more than six times higher rate than Toxoplasma-free or RhD-positive subjects. "

Why the Rh association? They don't know.

"It must also be noted that the effect of latent toxoplasmosis on reaction times varies across testing minutes ....The authors speculated that two effects of infection might interplay in Toxoplasma-infected men. Latent toxoplasmosis is known 1) to impair reaction times in infected men and animals and also 2) to increase the concentration of testosterone in infected men. Increased concentration of testosterone positively influences the level of personality trait competitiveness in men, which, in turn, could enhance performance under certain circumstances. Therefore, the negative effects of latent toxoplasmosis on psychomotor performance in men could influence the rate of traffic accidents under certain conditions only, which could explain some differences in results between the published case-control studies and present cohort study."

Officer, the parasite in my brain increased my testosterone levels and decreased my reflexes and made me a more aggressive, but sloppier, driver.

If you know anyone in, say, Oregon who could be at risk for a one-year license suspension, let them know about this. It might be a mitigating factor that, combined with Twinkie consumption, could be the difference between driving and public transportation.

Rationalization

Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study. (http://www.biomedcentral.com/1471-2334/9/72) BMC Infectious Diseases 2009, 9:72.

Hyperhidrosis, or Sweating with the ID doc

Published 2 June 2009

There are symptoms that, by themselves, are difficult to evaluate. The hardest is sweats.

Night sweats occur frequently and may be a sign of infections: endocarditis is the leading infectious reason in the west. However, any infection can cause a drenching sweat, usually to break a fever. The standard pattern is a rigor then a fever then sweat to break the fever.

The patient today never has a fever, just 6 years of occasional drenching sweats that occur out of nowhere, anytime day or night, and have no other associated symptoms. Over the last two months the symptoms have crescendoed to occur 5 to 10 times a day.

The patient sweats enough to raise his BUN and creatinine. That's a lot of water loss. It's almost like the Axe deodorant commercials that have been on during the NBA playoffs.

Go Orlando. Sorry. I am in Portland. I can never, ever root for L.A. for any reason. But I digress.

No other symptoms. The referring docs have looked for infections, collagen vascular disease, and neuroendocrine causes and come up with nothing.

The patient has an extensive travel history to the lands of Chagas, Old and New World Leishmania, and malaria, but there is nothing to suggests these diseases are present. P. malariae has been known to become symptomatic decades after leaving an endemic area, but usually with fevers and chills as well as sweats.

But it seems a real stretch that these sweats are infectious, especially as they have been going on for 6 years. If the sweats are not due to fevers, not due to infections, and not due to collagen vascular disease or Hodgkins, then what is it?

I think perhaps maybe its autonomic dysfunction, as the patient has carried the diagnosis of multiple scleroses for 15 years, although no other symptoms of MS.

Pubmed is not that helpful for other case reports of sweats and MS: one of decreased sweating, one of unilateral sweating, but nowhere can I find out of control sweating as the only symptom of the MS. Thermoregulatory issues are common in the disease, but are mostly reported to raise the sweating threshold.

However, the MS sites have many testimonials of patients with MS and hyperhidrosis. The plural of anecdote is anecdotes, not data. And the pleural of empyema is... never mind.

So maybe MS is the reason for the sweats. But I hate a diagnosis that made by exclusion.

Go Magic.

Rationalization

J Appl Physiol 92: 1779-1780, 2002. Multiple sclerosis and thermoregulatory dysfunction. (http://www.ncbi.nlm.nih.gov/pubmed/20671034)

Zebras are so last century

Published 3 Jun 2009

There are those in medicine that love to hunt zebras. Not me. Too mundane. I prefer to hunt zebra unicorns with red and yellow stripes.

Like the consult today.

Diabetic with 5 days of leg cellulitis that is getting worse on vancomycin and pipercillan-tazobactam. More redness, more pain, white cell count climbing.

A leg with, well, there is no other way to say it: rubor, dolor, calor, and tumor. And today he has developed two areas of small hemorrhagic bullae on his calf and thigh.

The probable reason for the worsening symptoms is undrained pus. Common things are usually common. That's why they are commonly referred to as common.

But. But. But.

It turns out that all this occurred shortly after a hike in the Mt. Hood Wilderness marked by time spent in the Bagby Hot Springs. Bagby Hot Springs are a series of hot tubs fed by geothermal heated water where hippies go to get stoned and soak neckid in the wilderness, or so I am told. I try to avoid stoned neckid hippies.

Cool hint. Or really hot. What infections do you get from hot springs? Besides sexually transmitted diseases?

Hemorrhagic bullae make an ID doc think of Vibrio infections, but that occurs after salt water exposure.

Pseudomonas causes folliculitis after hot tub use, but not, as a rule, cellulitis.

Aeromonas is a cause of soft tissue infection with necrosis after fresh water exposure. But that should have responded to pip-tazo.

So Pubmed to the rescue.

Acanthamoeba , fungi I can neither spell nor pronounce, and an outbreak of a gram-negative rods that could not be identified have been reported as hot spring associated infections.

I am not surprised that the gram-negative rods could not be identified. Most organisms that grow in hot water, thermophiles, have evolved to survive only at higher temperatures and probably would not grow at the lower temperatures of the micro lab.

But I did not know until I went looking that Legionella has caused cellulitis and when you think of fresh, hot water, you should always think of Legionella. And tea.

So that's the red and yellow striped unicorn I went hunting today. Legionella studies are pending. Listen carefully. If, in a few days, you hear a triumphant shout of "yes," that was me.

As I am sure will happen, at great diagnosis will be ruined by the reality of the lab results.

But it is the journey not the destination that is fun.

That's a lie. I just want to be right.

Rationalization

J Toxicol Environ Health A. 2007 Jan;70(1):84-7. Environmental survey of Legionella pneumophila in hot springs in Taiwan. (http://www.ncbi.nlm.nih.gov/pubmed/17162501)

Clin Infect Dis. 1993 Jan;16(1):51-3. Cellulitis caused by Legionella pneumophila. (http://www.ncbi.nlm.nih.gov/pubmed/8448318)

Necrotizing cellulitis caused by Legionella micdadei. (http://www.ncbi.nlm.nih.gov/pubmed/1731498) Am J Med. 1992 Jan;92(1):104-6.

Osteo, Cancer and Insurance

Published 6 Jun 2009

Health care in the US is second to none. Because we are 17th. Or worse. The patient this week is a laborer and never had health insurance. Ever.

Over 15 years ago he developed a pimple on this shoulder. He doctored it himself. Over the next 15 years it progressed to the point where he has a dinner plate sized defect over his shoulder. You can see his humerus, his clavicle, and his whole shoulder joint, all of which is infected, at the bottom of an enormous soft tissue divot.

His plain x-ray is great/awful. All the bones of this shoulder are mottled and look like a rat has been gnawing on the bones. Very chronic osteomyelitis.

Even more impressive is the huge amounts of heterotopic bone. He has more calcium in the soft tissues of his arm than he does in the bone. Heterotopic bone is bone deposition in soft tissues and is only seen in chronic, untreated osteomyelitis of years duration. It used to be seen in the pre-antibiotic era, but is extremely rare where people have access to good health care.

Like not here. When asked, he said the reason he never had it cared for is that he did not want to incur the cost. It was health care or food and rent. He chose to eat. Now the only chance of cure is to amputate his arm and the upper chest. Not a good outcome.

The odd thing is how this process ate way all the soft tissues of his shoulder. It looked like a hyaena had been having at go at his shoulder. Chronic osteomyelitis is not usually so destructive, more often having recurrent sinus tracts and drainage.

Years ago, back last century, I wore an onion on my belt....which was the style at the time...you couldn't get those white ones, you could only get those big yellow ones ... , there was a case of a patient who let his Basal cell? Squamous cell? I cannot quite remember which, eat away his entire abdominal wall skin and fat leaving the underlying muscle exposed.

I am amazed at the amount to soft tissue destruction, and wonder if it started as an underlying skin cancer.

Alternatively, chronic osteomyelitis is associated with various cancers of the draining sinus tract. For you eponym mavins (Steve?), it is called Marjolin's ulcer.

To quote from the reference below:

"A Marjolin ulcer‚ is identified as a squamous cell carcinoma that develops in post-traumatic scars and chronic wounds. It has been well documented that it was first described by Jean Nicholas Marjolin in 1828, and then Hawkins reported in 1835 a case of squamous cell carcinoma that appeared to have originated from a site of chronic osteomyelitis. Although well described, squamous cell carcinoma consistent with the diagnosis of a Marjolin's type is an uncommon entity. Its incidence ranges from 0.23% to 1.7% . Cases of chronic osteomyelitis that may develop into squamous cell carcinoma have an incidence range of 0.2;.7% . It most often occurs in Caucasian males, age range 18 -40 years. The average reported duration of osteomyelitis before the development of the squamous cell carcinoma is 27-30 years, but ranges from 18 to 72 years. Mean latency period is 30.5 years."

I like the fact the mean latency period can be longer than the ages of the patients who develop the disease. Probably some sort of time travel involved.

Squamous cell carcinomas are not the only cancers associated with osteomyelitis: all the cell lines in the skin have resulted in at least one case report.

Rationalization

Hand. 2006 December; 1(2): 89–93. Marjolin’s Ulcer Arising at the Elbow: A Case Report and Literature Review (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2526029/?tool=pubmed).

50:50

Published 8 Jun 2009

Follow ups.

It was not Legionella that caused the cellulitis. All the studies are negative. He went to the OR as there was no improvement, and there was no necrotizing disease or abscess and all the gram stains and cultures are negative. Serology and urinary antigen for Legionella were also negative.

Another beautiful hypothesis killed by facts.

Could this be a non-infectious disease? I don't think so, but thermophiles from a hot spring may not be grown in the micro lab, but then why would they grow in a cool leg?

I suppose of the other disease that can mimic cellulitis, Sweet's is most likely, and the pathology of the debridement is pending.

"The Sweet syndrome (acute febrile neutrophilic dermatosis) is characterized by papules that coalesce to form inflammatory plaques. These lesions are erythematous and tender; they most commonly occur on the upper extremities, face, and neck. Associated findings include fever, conjunctivitis or iridocyclitis, oral aphthae, and arthralgia or arthritis. Patients also have moderate neutrophilia and dermal infiltration by polymorphonuclear leukocytes. Sometimes the syndrome is mistaken for infectious cellulitis. Ten percent of patients with the syndrome also have an associated malignant condition, usually acute myelogenous leukemia. Immunologic disorders, such as rheumatoid arthritis and inflammatory bowel disease, have also been implicated. Corticosteroids remain the mainstay of treatment."

The other destructive shoulder cellulitis with underlying osteo was found to have basal cell carcinoma in all the biopsies: skin and bone. Fifteen years or so of letting a malignancy slowly eat away his shoulder.

Whoa.

I have seen some impressively destructive cancers ignored by patients over the years. I remember (25 years in medicine gives me the right to tell stories. And I have my AARP card, so I can complain about anything, anytime. Get off my lawn and turn off that damn hip-hop) when I was a medical student doing my ER rotation a guy came in with a hemoglobin of 5, feeling light headed (the patient, not me). So I did the usually excessive medical student history and review of systems and found nothing, then on exam found a cancer the size and shape of a large mushroom on his back oozing blood (melanoma on later biopsy). He totally dismissed it when I asked him about it. Oh, nothing.

As our former President said, denial is more than a river in Syria.

As those who work with me know, there is no part of medicine I enjoy more than making an unlikely diagnosis. I do feel a tad guilty exulting in being right as it usually means someone also has a terrible illness.

All the best cases are someone else's tragedy.

Rationalization

Narrative Review: Diseases That Masquerade as Infectious Cellulitis. (http://www.annals.org/cgi/content/full/142/1/47) 4 January 2005. Volume 142 Issue 1. Pages 47-55.

Hey. Look at my cool case.

Published 9 Jun 2009

I love noon report. The residents often present cool non ID cases (yes, surprisingly there are cool cases that are not infectious in nature. Who da thunk it?).

Today they had a case of a 27 year old with a huge stomach from a midgut volvulus from malrotation from a Ladd's band. The CT, when scrolled though, looked just like the gut was being sucked down a whirlpool, hence the whirlpool sign.

It reminds me there needs to be a journal entitled "Hey. Look at my cool case."

Recently I had a youngish (now that I'm 52, what used to be elderly is now youngish) guy who had a day of intractable vomiting, probably food poisoning.

At the end of the vomit marathon he reached up to wipe the sweat from his forehead only to find pus draining from his scalp.

25 years ago he had seizure surgery (say THAT five times as fast as you can, worse than toy boat) and he had a chunk of plastic in place of his skull and the pus is draining from the most anterior part of the plastic.

He had no trauma, and CT shows infection over the plastic, confirmed at surgery when it was debrided (pronounced dee breed. De bride is da woman getting married in da church) and the flap removed. (Do not let the patient know he could have had a V8 (http://www.youtube.com/watch?v=ShcbV31tcAk)).

There are the occasional Staphylococcus or P. acnes infections that can fester (I did not realize the significance of the name in the Adams family until I did my ID fellowship) for years. But it didn't grow those organisms.

It grew Streptococcus pneumoniae of all things.

I thought maybe it leaked in from the frontal sinus, bursting through with the increased pressure from the vomiting, but CT and neurosurgery all attested to the integrity of his sinus. I so wanted this to be a Potts puffy tumor (chronic frontal sinusitis) because I like to pop my p's, but that was a dead end diagnosis. He also had no immune defect that I could find.

So he received a course of antibiotics for a flap infection.

Streptococcus pneumonia e is distinctly odd to cause cellulitis in adults (causing periorbital cellulitis in kids) and has never been reported to cause a flap infection.

So. Hey. Look at my cool case.

May be that could have been the name of the blog.

Rationalization

Eur J Clin Microbiol Infect Dis. 2007 Apr;26(4):247-53. Streptococcus pneumoniae skin and soft tissue infections: characterization of causative strains and clinical illness. (http://www.ncbi.nlm.nih.gov/pubmed/17372776)

Scand J Infect Dis. 2000;32(2):133-6. Clinical syndromes associated with adult pneumococcal cellulitis (http://www.ncbi.nlm.nih.gov/pubmed/10826896).

780.6

Published 12 Jun 2009

You can tell what a doctor does for a living by the ICD-9 codes they have memorized.

780.6. Fever. My personal favorite.

There is a code for everything. Weightlessness is 994.9. Decapitation (by guillotine): E978. There, I suppose, in case Marat returns from the dead. Ready for a zombie French revolution? 666 is postpartum hemorrhage. Draw your own conclusions. A code for everything but my most common diagnosis: I don't know.

I don't know is my most frequent conclusion. For every great diagnosis I make, I have 100 shoulder shrugs. It is the least satisfactory answer for the patient and not billable. At least I always have 780.6 to fall back on.

Today was yet another shrug of the shoulders (I do it with Gallic exaggeration). Elderly female with fevers, chills, sweats. No focality on exam, on labs, on review of systems, on X-rays.

Pan cultures (including cultures of the wine flagon and goat hooves) all negative.

Probably viral, but the look from patient and daughter when I said 'probably viral' was one of 'can you get me a real doctor who knows what they are doing?'

Part of the problem is fevers in the elderly are often the only manifestation of serious underlying medical problems.

I remember back when I was an intern I had an elderly woman admitted to me in the middle of the night with just a fever. I thought, in the immortal words of Betty Davis, what a dump. As I wheeled her to her room (at the county hospital we did transportation at night if we wanted the patients expedited to their room) she dropped her pressure and almost coded. She grew Staph in her blood that next day. That's when I learned that fever in the elderly can be significant.

However, I can't find a reason for her fever, so I am betting that it is a self-limited nothing. I have a routine with patients under these circumstances. I tell them that in medicine we are good at diagnosing serious life threatening or injuring illnesses that we can treat and are no good at putting a name on the self limited, ultimately trivial illness (not life threatening or injuring, just life inconveniencing), so it is good that we do not have an answer.

Most of the time patients understand and appreciate that explanation.

This time the daughter looked at me like I was too stupid for words.

Oh well. As long as she gets better.

Rationalization

Am J Emerg Med. 2003 May;21(3):230-5. Unexplained fever in the ED: analysis of 139 patients. (http://www.ncbi.nlm.nih.gov/pubmed/12811720)

Ann Emerg Med. 1995 Jul;26(1):18-24. Fever in geriatric emergency patients: clinical features associated with serious illness. (http://www.ncbi.nlm.nih.gov/pubmed/7793715)

Infections in Asterix

Published 14 Jun 2009

I am on call this weekend. Whine whine whine cry cry cry. Boo and hoo. Poor me. Call is the one downside of being a doc. But at least I get to see some good cases.

You are a tropical rain forest. Really. You have a complex ecosystem in and on you. There are 10 to 100 times more bacterial cells in and on you than there are cells of you. You may think you are a hot shot ID doc (I certainly do), but in reality you are a sentient transport system for bacteria and in the end you will be consumed by the bacteria you spent a lifetime killing. Unless, I suppose, you are at ground zero of a thermonuclear weapon.

Today I saw a patient with an infected knee after two taps for gout.

It grew Staphylococcus lugdunensis, a coagulase-negative staph. This century the lab has started to speciate some of the coagulase-negative staphylococci and lugdunensis has been popping up in the occasional cultures. Blood, a knee here, an abscess there. It may be more common as a recent study suggests it is not an uncommon isolate in sort tissue infections. Studies from 2002 suggested it is a cause of abscesses in the pelvic girdle. Clinically it seems to like to cause disease below the belly button, esp. the toes. And that may be for good reason.

Like many bacteria, lugdunensis has a niche in your body. You are not covered in a schmear of bacteria, rather, each bug has its own area where it prefers to live. Location location location are the top three selling characteristics of real estate, but somehow the nail bed of the first toe doesn't seem to be all that desirable a place to live to me. But that is the preferred location for S. lugdunensis. Toe > legs > groin.

I have been informed that the characteristic smell of lugdunensis is bleach, so you will never discover an outbreak in a Clorox factory.

Treat it like a S. aureus. It is more virulent than the usual coagulase negative staph, and if you grow it, hey, give your local ID doc a call. At least you can't pick your nose with your toes and spread the organism.

BTW, from Wikipedia:

"Lugdunensis was a province of the Roman Empire in what is now the modern country of France, part of the Celtic territory of Gaul. It is named after its capital Lugdunum."

Which is now Lyon, where the organism was first described. And I thought it was from lug nuts.

Someone want to send me to Lyon to investigate further?

Rationalization

J Clin Microbiol. 2009 Apr;47(4):946-50. Staphylococcus lugdunensis, a common cause of skin and soft tissue infections in the community (http://www.ncbi.nlm.nih.gov/pubmed/19244465).

Clin Microbiol Infect. 2009 Jun 6. Staphylococcus lugdunensis in several niches of the normal skin flora (http://www.ncbi.nlm.nih.gov/pubmed/19519842).

True, true and probably unrelated

Published 16 Jun 2009

I have this middle-aged female who months and months ago presented with endocarditis from viridans strep. She had the usual therapy and, as best I can tell, is a cure.

Several weeks after therapy ended she developed pain in her left hip and on MRI was found to have inflammation of the left pelvic girdle muscles. No fevers, no increase in the CK, no leukocytosis. The reading on the MRI was myositis, maybe, maybe not, pyomyositis.

She improved on clindamycin (penicillin allergic) and then relapsed after a 4 week course. MRI showed more of the same, so she was then placed on a longer course of clindamycin. And, after 6 months was finally pain free and the MRI showed it was all better.

I know. Probably should have done a biopsy. During the prolonged clindamycin she was also diagnosed with scleroderma.

Now the plot really thickens.

Two weeks or so off the clindamycin and the pain, but nothing else, is back.

Why?

There is a myositis/scleroderma overlap, as there is with all rheumatologic syndromes. Everything overlaps in rheumatology. So maybe this is relapsing myositis from scleroderma. But why the apparent response to the clindamycin?

Here is where I go off the deep end. I sure hope there is some water in there.

I used to think that the clinical significance of the immunomodulatory effects of macrolides were a heap of fetid dingoes kidneys.

However, there have been two clinical studies and one animal study to show survival benefit of macrolides even when the organism is resistant to the clindamycin. Probably from the immunomodulatory effects of the antibiotics rather than any antibacterial effect. They are ever so slightly immunosuppressive. Since what people die from in sepsis is an excessive inflammatory response (if you say cytokine storm, I will slap you upside the head. Long story), if you can take the edge off the inflammation, you take an edge off the death rates.

So maybe, maybe the effects on the myositis are due to the immunomodulatory effects of the clindamycin on the myositis/scleroderma. Just wee bit o' immune suppression from the clindamycin and the myositis improves. Stop the macrolide and the myositis returns. Or not. I can find nothing on Pubmed to support my hypothesis. But as I am sure you are aware by now, I don't let those pesky facts get in the way of a good story.

But it is a curious association. Probably nothing, no causality, but if there is, it is to be called the Crislip effect. I want something named after me before I die, and it is not the glove breaking on the prostate exam.

I am repeating the MRI and, if positive, will get a muscle biopsy. I will let you know.

Rationalization

Clin Infect Dis. 2008 Apr 15;46(8):1157-64. Effect of clarithromycin in patients with sepsis and ventilator-associated pneumonia. (http://www.ncbi.nlm.nih.gov/pubmed/18444850)

Respir J 2009; 33:153-159. Impact of macrolide therapy on mortality for patients with severe sepsis due to pneumonia. (http://www.ncbi.nlm.nih.gov/pubmed/18768577)

J Infect Dis. 2009 Feb 1;199(3):311-9. Treatment with protein synthesis inhibitors improves outcomes of secondary bacterial pneumonia after influenza. (http://www.ncbi.nlm.nih.gov/pubmed/19113989)

Unexpecting

Published 17 Jun 2009

I have an hour to kill, waiting to give the residents their ID bored review. Spelled correctly. I can't wait to see their eyes glaze over as I go over the pearls they need to pass the boreds, drool flowing from the corner of their mouths.

I will probably go to internal medicine hell for this, but I don't find the physical exam all that helpful. Do NOT let Steve Jones know I said this. The physical can be fun, and occasionally you will pick up a finding that makes the diagnosis. But for me the three important parts to making a diagnosis are history, history and history. Cultures, labs, and X-rays should only confirm what you figured out after talking to the patient. It is why it always frys my bacon a little when patients tell me to read the chart instead of talking to them.

There are exceptions: endocarditis, heart failure, and cellulitis are diseases where the exam is of help. As is pelvic pain.

Middled aged female with group B streptococcus (GBS) in her blood for no reason except diabetes, which is probably reason enough. Most group B strep bacteremia I see is without a source and is almost never due to endocarditis. While she has a long history of joint pain, now she can't get out of bed due to the severe back pain.

Usually exam will elicit exactly where the pain is coming from: hip, bursa, iliopsoas, paraspinous, spine, saccoiliac (SI) joint. Simple maneuvers can quickly tell where the infection is, since new pain in a bacteremic patient is usually pus under pressure.

I thought, by exam, she had an saccoiliac joint infection, in part by the location of the pain, in part by all the negative findings on exam and in part by the predilection for group B strep to go to joints in the elderly, or at least a pseudo-joint in the case of the SI.

Bone scan was negative in the SI, but lit up in the L 3-4 paraspinous area.

The heck. Group B strep is not a cause of myositis or abscess as a rule, so I got an MRI.

I hate the phrase‚ expect the unexpected. If you expect it, it is no longer unexpected, and to say expect the expected is a lame tautology. Unexpect the unexpected? Naw.

MRI showed an L 3-4 epidural and paraspinous abscess.

Now THAT was unexpected. This is not, as a rule, what GBS does in adults. Even more odd was no discitis or osteomyelitis that is nearly always the proximate cause of epidural abscesses.

How commonly does Group B Streptococcus cause an epidural abscess? Rare as a fair election in Iran. Or Florida for that matter. It is nice to see we have been successful in bringing our form of government to at least one country in the Mideast.

A grand total of five or so GBS epidural abscesses are reported on Pubmed. It looks like most cases started with a facet joint infection, which my patient did not have, and how they could tell it started in the facet joint I cannot say.

Take home: I can't trust the exam for pelvic pain either.

Rationalization

J Spinal Disord Tech. 2005 Oct;18(5):458-61. Lumbar facet joint infection associated with epidural and paraspinal abscess: a case report with review of the literature (http://www.ncbi.nlm.nih.gov/pubmed/16189461).

Clin Infect Dis. 2005 Sep 15;41(6):839-47. . Group B streptococcal infections in elderly adults. (http://www.ncbi.nlm.nih.gov/pubmed/16107984)

Answer these questions three

Published 18 Jun 2009

Three questions. Not name, quest and favorite color.

Every infection comes with three questions that I should try an answer:

What is the bug?

How best to kill it?

How did it get there?

The last is often the more interesting question. The name of the bug often will be the hint as to where it came from. Infections have patterns.

Years ago I was called by the nurse to see a patient in the ICU.

He has Candida in his chest tube drainage‚ she told me.

I'm on my way in. In the meantime have him drink methylene blue.

When I walked into the Unit a quick glance at the chest tube revealed that all the fluid was blue. He had an esophageal-pleural fistula.

Oh, said the nurse. That's why his chest tube output went up every time he had a glass of water.

If you get Candida in a pleural space, it is due to a bronchopleural fistula. Candida pneumonia is rare as hens teeth, so it is odd to see it reach the pleural space by way of the lung. A hole connecting the esophagus and pleural space, an esophageal-pleural fistula, is just about the only reliable way Candida can get to the pleural space.

This month I have two Candida empyemas in the ICU. One is a C. tropicalis due to an esophageal leak after removal of an esophageal cancer. The fluid also grew lactobacillus. Radiographic studies only confirmed what the microbiology suggested must be present. The patient has upper and lower dentures, which are often heavily colonized with Candida. Perhaps the source?

The other is more unusual: C. albicans that occurred after an aspiration lung abscess ruptured into the pleural space. In the space of five days he went from clear chest x-ray to large round fluid density to big pleural collection. At VAT's the surgeon said he had a lung abscess that perforated into the pleura. The patient not the surgeon. Candida is not a common cause of aspiration lung abscess (maybe 8 reported cases), but he had upper dentures and lower poor dentition. I bet the Candida came from his dentures as well. Not that there is much literature to confirm my hypothesis. Anyway, that's my story and I am sticking to it.

Rationalization

Denture and candida. (http://sciencelinks.jp/j-east/article/200209/000020020901A1031146.php) Medicine & Drug Journal VOL.37;NO.10;PAGE.3009-3015(2001)

Chest. 2000 Jun;117(6):1672-8. Fungal empyema thoracis: an emerging clinical entity (http://www.ncbi.nlm.nih.gov/pubmed/10858401).

Bridgekeeper : STOP!

He who would cross the Bridge of Death

Must answer me

These questions three

Ere the other side he see.

Sir Galahad : (swallowing) Ask me your questions, Bridgekeeper...I am not afraid...

Bridgekeeper : What...is your name?

Galahad : (nervous) Sir Galahad...

Bridgekeeper : What...is your quest?

Galahad : (really nervous) To seek the Grail...

Bridgekeeper: What...is your favorite color?

Galahad : (relieved) Blue! (starts across; oops) NO!

YELLOOOOOOOOOOOOOOOOWWW!!!!

Boutonneuse hibou

Published 21 Jun 2009

I was pooped yesterday. The prior weekend I was on call, so I worked 12 days in a row. As I age, well, wines age and get better, I am more ripening (over ripe?) than aging, I fade at the end of the second week.

Two consults at the end of the day. The first was a cellulitis, and the second was billed as a fever. The resident wanted to know why the fever.

I was yawning as a read the chart and talked the case over with the resident. I had an idea after talking with her, but I wanted to see to the patient first.

Fevers to 104, worst headache of his life, normal CBC, mild trans-aminitis. But. But but but. He has just returned from a bicycling trip in Italy.

And then the hinge point, the finding around which the diagnosis revolves: he had a black eschar with surrounding erythema on his lower leg.

The fatigue fell away. The hunt was on, the games afoot Watson, or at least the games a calf.

I think I know what he might have.

Evidently not everyone gets as jazzed at a great case as I do. When I see what may be a zebra, a case of something I have never seen before, I get a surge of excitement. I get pumped.

The year of medicine I had the most fun was my internship because everything was new and interesting. As the years go by, some diseases are no longer that interesting. Heart failure. COPD. Stroke. They are mostly slight variations on a theme. Kind of, well, dull.

But infections. There are so many infections and I am nowhere close to seeing them all. Birders have it far easier. There are a paltry 10,000 birds species. Bo-ring. Easy to see them all. Just look up. Nothing compared to potential infections. There are a dozen Rickettsia that can infect humans and I have seen one to date: Rocky mountain spotted fever. Well, perhaps I should say I have diagnosed one to date; if I have seen others, I missed it.

Until yesterday.

I think I have my first case of R. conorii or Boutonneuse fever, which is an increasing problem Italy. It was the black eschar that may be the hint. That is the infamous tache noir I have read about for 15 years and have never seen.

No sooner do I whine that the physical exam is less than revealing and I get a case where they physical exam is key to the diagnosis. Figures. Sometime I wonder why I ever bother to pontificate on a topic as I am sure to be proven wrong in the next 48 hours. Unfortunately he has no boutonneuse (French for spotty), at least not yet.

But he is on doxycycline and serology is pending. I will get the results back about the time I retire.

Rationalization

Minerva Med. 1981 Sep 1;72(31):2063-70. [ Current endemic expansion of boutonneuse fever in Italy (http://www.ncbi.nlm.nih.gov/pubmed/6894788)\].

Parassitologia. 2006 Jun;48(1-2):131-3. Epidemiology and clinical features of Mediterranean spotted fever in Italy (http://www.ncbi.nlm.nih.gov/pubmed/16881414).

Postscript: he responded rapidly to doxycycline, acute serology was negative and he was lost to follow up.

Bacterial artha-ritis

Published 22 Jun 2009

The alphabet soup of streptococci. A and B and C and D and E and F and G.

Gee. Dr. Lansfield was a wonderful microbiologist, but all these letters do not help me to remember which is which. Bacteria need names. Fred. Barney. Wilma.

Group G strep is beta hemolytic, like the strep of strep throat and is found in the nasopharynx, skin, GU, and GI tract of normal people. It occasionally pops loose to cause disease.

Out of nowhere the patient had rapid onset of rubor, dolor, calor, tumor, of his knee. Unlike most patients with an infected joint he had no prior trauma to the knee and no risk factors for infectious artha-ritis: cancer or diabetes or alcoholic liver disease or anything. His life is as uneventful as mine.

Yet, the tap of the knee grew Group G strep. A little I&D and some IV beta lactam should take care of it.

So where did it come from? Just prior he had been hiking in the Mt. Hood Forrest and took a shower in a camp ground. The water did not drain well and he stood in a few inches of undrained shower water, probably mixed with the effluent of prior showerers. He had some foot erythema after the exposure to the shower and just prior to the infection of his knee. So I guess it went downstream from a cellulitis to the knee, not, by any means, a common occurrence.

That would be an intriguing source for the Group G strep. Not much in Pubmed to suggest this is the right reason. But there are articles from the developing world and from olden days to suggest that streptococci are often found in swimming pools with less than adequate maintenance.

An article from 1927 suggests that microorganisms besides B. coli (this is old. B. coli is now E. coli) are commonly found in pools are Staphylococcus and Streptococci which were undoubtedly introduced into the pool by the bathers. Streptococcus was found in four pools studied. Practically every sample of water that was polluted with B. coli contained Streptococcus... Ick.

Streptococci are constant indicators of intestinal pollution and the number found in the pool parallels the amount of pollution as indicated by the number of bathers.

Ick again. I don't want to swim no more. Pools are like sausages. You do not what to know what is in them. The fetid shower water is, perhaps, the equivalent of a swimming pool and would be an intriguing source for the strep.

Rationalization

American Journal of Public Health. Mallmann 18 (6): 771. (1928). Streptococcus as an Indicator of Swimming Pool Pollution (http://www.ajph.org/cgi/reprint/18/6/771).

Streptococcal septic arthritis in adults. A study of 55 cases with a literature review. (http://www.ncbi.nlm.nih.gov/pubmed/15288856) Dubost JJ, Soubrier M, De Champs C, Ristori JM, Sauvezie B.

J Rheumatol. 1982 May-Jun;9(3):424-7. Group G streptococcal arthritis (http://www.ncbi.nlm.nih.gov/pubmed/7120237).

Changing a tire

Published 23 Jun 2009

When I started practice late last century I wore the standard white coat. After awhile, for reasons I no longer remember, but are probably related to my wife's continued attempts to give me some style (if they ever have a male on’ What not to Wear’, it should be me), I changed to the sport coat and tie look.

Years passed and the sport coats are looking a little ratty. They are pricey. Even at Goodwill, my preferred shopping store, a good sport coat will run 80 bucks, and at Nordstroms, well, lets say you don't want to be an ID doc in a down economy.

So I went back to the white coat look, which my wife says is slimming (ha) and it has generated lots of comments, mostly good.

From an infection control perspective, what should one wear in the hospital? While I am unaware of outbreaks, many routine articles of clothing have been found to carry bacteria.

Ties are the best documented carriers of bacteria, and should be abandoned. Ties are never cleaned and when you push them out of the way so they are not dipped into the patient, they pick up whatever is on your hands. They are saturated with months of bacteria and soup. I have up ties from the 90's.

Beepers, rings, watches (very rare), phones, artificial nails and stethoscopes have all been cultured and found to contain pathogens. Probably lab coats as well, since they are not laundered very frequently, and are exposed to pus, patients, and hospital food. At least beepers, cell phones (not my Droid, no way) and stethoscopes can be alcohol foamed. I wonder how many people check their email on their iPhone while sitting on the toilet? Icky poopy.

So what to wear? Look professional or be relatively bacteria free? The British have gone to the extreme of allowing nothing below the elbows (except hands) and no ties. We may be heading that way, but I need pockets and a belt to carry my electronic doodads, at least until I get that Ethernet jack in the back of my skull. Neo had the right idea.

I think medicine should be practiced in the same garb as ancient Greek Olympic athletes: nude. Plus, it would save on ipecac AND combat obesity in the work place.

Rationalization

Hospital Scrubs Are a Germy, Deadly Mess (http://online.wsj.com/article/SB123137245971962641.html)

Half of doctors' neckties contained dangerous bacteria, new study

Pediatr Infect Dis J. 2006 Nov;25(11):1074-5. Bacterial contamination of health care workers' pagers and the efficacy of various disinfecting agents. (http://www.ncbi.nlm.nih.gov/pubmed/17072134)

Anaesthesia. 2009 Jun;64(6):620-4. Bacterial contamination of stethoscopes on the intensive care unit. (http://www.ncbi.nlm.nih.gov/pubmed/19453315)

Int J Nurs Stud. 2008 Nov;45(11):1572-6. A prospective comparative study of the relationship between different types of ring and microbial hand colonization among pediatric intensive care unit nurses. (http://www.ncbi.nlm.nih.gov/pubmed/18479684)

Bacterial colonization of wristwatches worn by health care personnel (http://www.ncbi.nlm.nih.gov/pubmed/19243858). Am J Infect Control. 2009 Aug;37(6):476-7.

Word History

Published 24 Jun 2009

Most of my great diagnoses exist only in my head. Not that it is bad, as my internal reality is far superior to the external one.

For many patients I see, I try, for fun, to come up with three lists.

One is the list of diseases the patient probably has, common things, oddly, being common.

Another is the list of things the patient cannot afford to have missed: pulmonary embolism or meningitis. Maybe unlikely based on the history and physical, but if that is the diagnosis, the patient is in a world of hurt.

Last, of course, is the list of cool things, which are usually neither common nor fatal.

I have a routine I go thorough with every patient, asking about this and that, looking over the chart and the labs and then, boom. One thing jumps out that may be the hinge-point upon which the entire diagnosis in the clouds is built.

The patient today: Fevers to 103, worst headache of their life (German sausage makers get the wurst headaches of anyone), right lower lobe interstitial pneumonia, mild increase in transaminases. No response to standard community acquired pneumonia therapy.

Temperature is 103, pulse 80.

Any animal exposure? I ask.

Nope.

Been around any...then I rattle of a list of animals what would make Noah proud.

I went hiking around wild goats is the response.

The temp of 103 and the pulse of 80 is the hinge-point and the goat is the door and oh my god do I need to work on my metaphors.

But usually for every degree the temperature increases, the pulse increases by 10.

When it doesn't, its called pulse-temperature disassociation, or Faget's sign. Soft g. Fah-jay. It's French.

Faget's sign is named after Dr. George Snelling. Not really.

"Jean-Charles Faget was born to French parents in New Orleans. He studied in Paris from 1837 to 1845, and after receiving his doctorate in 1844 settled in New Orleans. He stayed in Paris 1866-1867 and subsequently lived in New Orleans for the rest of his life. In 1858 he discovered a specific pathognomonic sign of yellow fever, a slow pulse at high fever. "

Classically it is a sign of yellow fever, it can also be seen in Typhoid fever, Brucella, dengue, Q fever, tularemia, chlamydia, Legionella and is reported with a smattering of other diseases. In the US it is usually due to beta blockers.

I am betting Q fever from the goats. It may not take much of an exposure to get Q fever if you get the right animal infected. Coxiella burnetii is the cause of Q fever, which gets its name, to quote the ever helpful wikipedia:

"The "Q" stands for "query" and was applied at a time when the causative agent was unknown; it was chosen over suggestions of "abattoir fever" and "Queensland rickettsial fever," to avoid directing negative connotations at either the cattle industry or the state of Queensland."

I like abattoir fever more.

The patient had the exposure, it is the right clinical pattern, so now I await the serology. That's two serologies I am waiting on.

If you are a resident or medical student, remember the differential for Faget's. You may shine at a pimping session.

Rationalization

Jean-Charles Faget (http://www.whonamedit.com/doctor.cfm/3090.html)

BMC Infect Dis. 2006 Oct 6;6:147. A super-spreading ewe infects hundreds with Q fever at a farmers' market in Germany (http://www.ncbi.nlm.nih.gov/pubmed/17026751).

The Art of the Pimp (http://web.med.harvard.edu/sites/murmur/html/articles/012604/012604\_mschoen.asp)

Postscript: Q fever serology was negative. Another great diagnosis sunk by reality.

I am fat to avoid TB.

Published 25 Jun 2009

A cool thing (I do use the word cool a lot, phat is a synonym in the dictionary, but I doubt I could use that without looking like an even bigger dork than I am) about ID is that the effect of germs upon humans goes well beyond the acute infections.

Humans and germs have evolved together for millions of years, the bugs have left their footprints in our genome.

It is estimated that a serious chunk of our DNA, maybe 10%, is viral that got incorporated into our genome and never got out, now coming along for the ride. They have even resurrected a fossil retrovirus from our DNA. The real Jurassic park.

Malaria also has had a serious impact on our genome with multiple mutations that confer resistance to the infection, the most famous of which is sickle cell.

Todays JAMA has a commentary that postulates that obesity and atherosclerotic consequences of the metabolic syndrome are an adaptation to both tuberculosis and starvation.

Most of human times have seen a shortage of food and those who could pack on the fat are more likely to survive lean times. So we have a propensity to be fat, especially in the reproductive years.

Also in most of historical times TB was ubiquitous and accounted for at least 25% of deaths. TB has killed more people than any organism but malaria, with more than a billion people having died from TB.

As I understand it, putting on fat signaled both fertility and an associated inflammatory response to keep TB in check. Fat became linked fertility and a pro-inflammatory response. Putting on fat signaled that you were able to bring a baby to term. Having a pro-inflammatory response was important for short-term survival in a breeding population. It kept the TB at bay.

When you were fat and fertile, you were also had a 'boosted immune system," to use the favored quack term. They postulate that the short-term benefits outweighed the long-term atherosclerotic complications since they occurred after the reproductive years. We live longer and eat more and what was once of benefit is now pathologic.

They further postulate that there will be downstream triggers in the obesity/inflammation pathways that, when discovered, will be manipulated to decrease both fat and the metabolic syndrome.

I commend to you reading the original, which is full of leptins, and TNF and adipokines, oh my. It is an interesting and testable hypothesis.

In the end all diseases are due to infection or genetics. Sometimes both.

Rationalization

Evolutionary speculation about tuberculosis and the metabolic and inflammatory processes of obesity. (http://www.ncbi.nlm.nih.gov/pubmed/19549976) JAMA. 2009 Jun 24;301(24):2586-8.

Fossils Resurrected! (http://news.softpedia.com/news/Fossils-Resurrected-48353.shtml)

Look. Up in the sky. It's a bird. It's a plane. It's...

Published 30 Jun 2009

IDman. Pronounced eye-dee, not id, like the Freudian dealybob.

Like Superman, I have powers. Special powers. Not like special education.

I am the only doctor who can stop an antibiotic. I am the only doctor who can ignore cultures.

Today, I had the opportunity to do both. While I was gone this weekend one of my patients had a bronchoscopy and the cultures grew Candida tropicalis. The patients was started on caspofungin. I stopped the caspofungin with my superhuman powers. Next up is leaping over a tall building.

Candida in the sputum can virtually always be ignored.

My wife likes to garden. More, I think, than anything else. Her favorite garden tool is the chipper-shredder and she can spend hours stuffing plants into it, making mulch. It worries me that her favorite movie is Fargo, and she says it is due to the fact she is a Minnesotan. I am not so sure and I keep my distance when she is chipper-shreddin’.

Now if I were to be involved with a tragic chipper-shredder accident and lose all but both thumbs, I could easily count the number of true Candida pneumonias I have seen in my 25 or so years as a superhuman infectious disease physician.

One was a massive aspiration in a patient with severe Candida esophagitis and there was Candida in the alveoli at autopsy. The other was what I thought was an Aspergillus fungus ball, but when it was resected it was a big ball o' Candida.

Candida just almost never ever causes a lung infection in mostly normal patients. Well, sometimes it will infect the hematologic malignancy patient, especially if they have profound neutropenia. But these patients can grow anything in any site.

If you grow Candida in a sputum of a normal patient, pay no attention to it. Especially do not go starting Caspofungin. That stuff runs 2 to 3 hundred dollars a dose.

Be my sidekick. IDlad, ignore the Candida.

Rationalization

Intensive Care Med. 2009 Apr 9. Significance of the isolation of Candida species from airway samples in critically ill patients: a prospective, autopsy study (http://www.ncbi.nlm.nih.gov/pubmed/19357832).

Medicine (Baltimore). 1993 May;72(3):137-42. Primary Candida pneumonia. Experience at a large cancer center and review of the literature (http://www.ncbi.nlm.nih.gov/pubmed/8502166).

Premature Closure

Published 1 Jul 2009

I need a self-aggrandizing title.

There is ‘Americans Pediatrician’ and ‘Americas most Read Pediatrician’ and there is the ‘Conscience of Modern Medicine’. I am not trademarked and I am neither a world-renowned leader nor a pioneer. No one calls me Dr. Mark (well one ICU nurse does). And I don't wear scrubs outside the hospital. I suspect I need to work on my image if I want to get some product endorsements. Unfortunately, to quote Dr. Gag Helfrunt, "Vell, I'm just zis guy, you know?"

The nice thing about being a doc is that every day is a chance to say "Huh. I didn't know that." I remember back with I had to use the Index Medicus to find information. Now I am a Google away. Not a Bing. A Google. I lack a Google of knowledge, not a Bing. I do lack a bing of cherries.

Today I was asked to see an AIDS patient of 15 years with CD4 counts of 50 who had just resumed taking his HAART after a year off medications, and now has a fever. So they called me. He had a white cell count of 41K, hgb of 9 and platelets of 61 and a marked left shift. He has new, rapidly growing lymph nodes everywhere.

CT showed lots of adenopathy in the chest and abdomen, so it was thought he has some sort of HIV related infection or tumor. They wanted me to figure out which one.

There is a process in medicine called premature closure, and I will let you make your own inappropriate comment. It is where the brain stops thinking about the problem at hand because you think you know the diagnosis. It is really common in evaluation of HIV patients and people returning from foreign counties. Whatever the problem is, it has to be related to either HIV or travel. Common or unrelated illnesses are not considered.

Todays patient had 17% blasts in the differential and he probably has AML, unrelated to HIV. Just bad, awful, terrible, crappy, luck. I sure do hate leukemia, but I see a biased subpopulation: those that get infected and often die. Just like I am certain that every surgery leads to infection. I wish. I try to remember there is a confirmation bias in my practice, since they do not call me when patients do not have infections.

What I didn't know was that leukemia can occasionally present like an aggressive lymphoma with rapidly progressive lymphadenopathy, mimicking Hodgkin's. Its rare, but what he has. Unfortunately Occam’s razor is unreliable in HIV, you have to follow Hickam's Dictum. So he may yet have two or more illnesses, but for now it looks like it is all AML.

Rationalization

Gag Helfrunt (http://en.wikipedia.org/wiki/List\_of\_minor\_The\_Hitchhiker's\_Guide\_to\_the\_Galaxy\_characters#Gag\_Halfrunt)

AIDS. 2002 Apr 12;16(6):865-76. Acute myeloid leukemia in patients infected with HIV-1 (http://www.ncbi.nlm.nih.gov/pubmed/11919488).

Am J Hematol. 1986 Jan;21(1):89-98. Acute myelocytic leukemia manifested by prominent generalized lymphadenopathy: report of two cases with immunological, ultrastructural, and cytochemical studies (http://www.ncbi.nlm.nih.gov/pubmed/3458362).

Occam’s razor (http://en.wikipedia.org/wiki/Occam's\_razor)

Hickam's Dictum (http://en.wikipedia.org/wiki/Hickam's\_dictum)

Why Why Why

Published 1 Jul 2009

Summer time and the living is easy. Except if you have bacteremic pneumococcal pneumonia. It is a bad disease, and people feel mighty poorly when they have it.

That was todays patient, who had a classic URI, then cough, the rigors and fevers and a marked increase in the cough with chest pain. He had 'e' to 'a' changes on exam, which is always a fun finding.

The magic that is a beta-lactam, and the patient is all better. Except. Why? Why does a 30ish yo otherwise healthy human get streptococcal bacteremia?

One. HIV. Nope.

Two. Immunoglobulin issues.

Always a worry. In older adults I always check for multiple myeloma or other related malignancies in any bacteremic pneumococcal disease, and I hit pay dirt a couple of times a year. Pneumococcus in the blood equals SPEP.

The patient's IgG levels are low. IgG1 and IgG3 are mostly against protein antigens and IgG2 is mostly against carbohydrates, so maybe she has an IgG2 deficiency; levels are pending.

Three. This one I didn't know: Pregnancy, which is an issue in this patient. Pregnant women, but not pregnant men, have an increased risk for many infections, including S. pneumoniae. The rate of pneumococcal bacteremia is markedly higher among pregnant women, homeless persons, and those in prison. So if you go to jail, do not get pregnant. And have a place to live, although I suppose jail could be considered home.

Fortunately I rarely have to see infected pregnant patients, although pregnancy is a weird immunosuppressive state, in the U.S. odd infections are not a common issue.

Rationalization

Medicine (Baltimore). 2005 May;84(3):147-61 Bacteremic pneumococcal pneumonia: a prospective study in Edmonton and neighboring municipalities (http://www.ncbi.nlm.nih.gov/pubmed/15879905).

Postscript: Immunoglobulin levels were normal.

I talk the talk, but they don' walk the walk

Published 4 Jul 2009

It is the 4th of July and Portland has shut down, at least as far as infections go. I am just back from the Zydeco portion of the Blues festival after a slow work day.

So I will make an observation. No references, no pearls, no wisdom.

This week the new house staff started.

Bright eyed, bushy tailed, and scared spitless.

We get good residents. It is rare to have a dud. They work hard, are nice people, and are excellent at feigning interest when I launch into an endless rant about the stupidity of "big gun" antibiotics or "low-grade fever."

But they all have one feature in common: They don't try and keep up.

Everyone who has been a resident knows the routine. They present the cases, then we discuss it (i.e. I blather on and on about the case) then we go see the patient. I usually continue to talk as we walk to see the patient. And the residents almost never try and match my pace. I do walk briskly. But as I talk they fall father and farther behind until I stop and they catch up.

At some point I mention that when I was a resident, I would automatically match the pace of my attending. I would never fall behind. But these days? They always fall further and further behind until I mention it.

So what gives? I think I will start sprinting and see what happens.

Real ID returns next week. Enjoy the 4th and don’t blow off a finger.

Bad Air

Published 6 Jul 2009

There are diseases that are endlessly interesting because of the variations of the presentation. Endocarditis is one of those diseases. But endocarditis is an odd disease, in the West a result of intravenous drug use (it is now use, not abuse) or aging.

Other disease are not so interesting in their presentation but are fascinating due to their impact on culture or history or genetics.

Patient today is freshly returned from a 10 month long trip to sub Saharan Africa and presents to the ER with fevers to 104, chills, sweats, cytopenias and 1% of her red cells have Plasmodium falciparum. Nothing unusual about the case as malaria. Fairly typical. I would bet from the timing that she had her mosquito bite the day she left Africa, so she had gone months dodging the malaria bullet until the end of the trip. Unfortunately the patient could not tolerate the prophylaxis.

Malaria is endless interesting as a disease for its impact on human cultures. I have read that half of everyone who as ever died has died of malaria and it still accounts for 500 million infections a year and a million deaths, mostly in children. About 1% of people who get malaria die from it.

It still kills the occasional traveler. Most illness is due to infection with the potentially fatal falciparum strain. There are between five and 15 deaths due to malaria reported every year in the UK. In 2006 there were 1,758 reported malaria cases, with eight deaths. All the UK deaths were due to falciparum malaria caught in Africa. That's a pretty good death rate for a trip to Kenya or Niger.

Many malaria deaths are essentially murder. About half the antimalarials, and other antibiotics, sold in Asia and Africa are counterfeits that contain no active ingredients. They are placebos and placebos are not particularly effective against life threatening infections. It is hard to imagine the kind of slime mold (and I apologize to slime mold everywhere) that would manufacture fake antibiotics, which probably helps kill hundreds of thousands of children worldwide each year who are given fake medications. We bitch about the high price a drugs in the US, but at least we know that when we are getting gouged for linezolid (fifty dollars a tab), we are getting gouged for the real deal.

There are also people who sell homeopathic antimalarials. That boggles the mind. Water used to prevent and treat a disease that in most of the world has at least a 1% mortality rate.

But if you are going to travel outside of the industrialized nations, buy your antibiotics before you go. And stay away from homeopathy. Unless you want to die.

Rationalization

J Travel Med. 1996 Mar 1;3(1):62. Homeopathic Resistant Malaria. (http://www.ncbi.nlm.nih.gov/pubmed/9815426)

http://www.blueturtlegroup.com/catalog/3

Bad Air Redux

Published 8 Jul 2009

I have said before that being an ID doc is like being a birder, and I keep a mental list of the infections I have yet to see. Unlike identifying birds, seeing a new infection is actually interesting. Just kidding. Birds are cool. I had some Ivory-billed Woodpecker for dinner this weekend, and hope to have Spotted Owl next month. And Condor egg omelet? To become extinct for.

Today was a first for me, a new bird, the IV treatment of severe malaria.

My malaria patient had 1.1% of the red cells infected yesterday. Today? More than 10%. Whoa. The tech called to say she had never seen so many parasitized red cells. The patient was clinically perhaps a bit better, and certainly no worse, but greater than 10% qualifies as severe malaria. Sometimes there a delay between the therapy and a decrease in the parasitemia, but more than 10% was too much.

For years quinine was the treatment for malaria, but there is no IV quinine in the US. There is a touch of quinine in tonic water, but not enough to do anything against malaria, so a gin and tonic is not considered a reasonable therapeutic intervention for the patient, although it may help calm the doctor.

But there is the anti-arrhythmic quinidine. I used quinidine as a resident late last century when we treated the occasional PVC with an acute MI. Quinidine also kills malaria as it the dextrorotatory diastereoisomer of quinine. But of course I state the obvious.

I have never given IV quinidine for malaria, but did back in the day when we treated any ectopy in the ICU. I guess we know better now, I do not think I know a resident that has ever given IV quinidine or lidocaine. Too old school.

I called the CDC just to double check, the wise heads agreed with the IV quinidine and doxycycline. Whew. Its nice to have the CDC.

So IV quinidine it is. I feel like an intern again.

Rationalization

MMWR April 19, 1991 / 40(RR-4);21-23. Treatment with Quinidine Gluconate of Persons with Severe Plasmodium falciparum Infection: Discontinuation of Parenteral Quinine. (http://www.cdc.gov/mmwr/preview/mmwrhtml/00043932.htm)

A True Story

Published 8 Jul 2009

Years ago the national ID meetings were in Las Vegas.

An attending of mine was waiting at the bar for a ride when a young lady sidled up to him and asked if he were interested in a 'date.'

He declined the opportunity, to which she replied, "What is it with this meeting? Business is the slowest it has ever been."

5,000 ID docs in the city. We know too much and what we could bring home. No 'dates' for ID folk. I often say that while people are pigs, ID docs probably have the highest rates of not messing around in the medical world. No data to support that assertion of course. But "What happens in Vegas stays in Vegas" doesn't apply to gonorrhea.

I mention this in passing as I am off to The Amazing Meeting 7 in Vegas with my father in a few hours where I am going to talk on Lyme. Probably no new entries until next week.

And my malaria patient is doing better.

See you next week.

Old OI's Return

Published 14 Jul 2009

ID is a depressing field. They keep figuring out ways to decrease infections. Best practice bundles have almost wiped out hospital acquired infections at all my institutions. Colony stimulating factors have made prolonged neutropenia and their resultant infections almost a thing of the past. Thanks to HAART, HIV related opportunistic infections have become rarities. I am tempted to stand at a street corner with a sign that says "Will do ID for food" or "Why Lie? I want to treat an infection." Thank goodness for the likes of Jenny McCarthy. At least the pediatric ID docs will get to see some of the almost extinct vaccine preventable illnesses. Sadly, I will not benefit much from a plague of measles or pertussis. Most of my patients are already immune.

Ahh, but thank goodness for Rituxan and its ilk. It just takes the edge off of immune competence and results in patients with the immunological function of a moderate AIDS patient. Rituxan is an antibody that kills of CD20 cells that predominate in NHL (NonHodgkins Lymphoma, nothing can target the National Hockey League). If you combine the immunosuppression of lymphoma with the immunosuppression of Rituxan, you get the Infectious Disease recovery act .

Patient today had NHL treated with Rituxan and comes in with seizures. Her brain his filled with too numerous to count (not really, if I took my time I could probably count the hundreds of small white matter lesions scattered through out the MRI) something-or-others.

What are they? The two impressive features were 1) the lack of mental status changes, b) the lack of mass effect on the MRI and iii) the mostly normal LP, with just a tich of elevation in the protein. And my inability to count.

It is probably PML (Progressive multi focal leukoencephalopathy), brought on by the JC virus. The JC virus, or John Cunningham virus (named after Richie's Uncle, who discovered it in the Fonz; it was why he jumped the shark) will reactivate in patients who receive Rituxan for rheumatologic diseases, or occasionally in NHL, to cause PML. The JC virus directly kills the oligodendrocytes, the cells that make the myelin that insulates your nerves, the cells that make you. So your brain melts, and you go with it. It is a horrible disease. I was glad to see it go.

I used to see PML all the time in AIDS patients, but I have not seen a case this century. The treatment is to reverse the immunosuppression, and since she is done with her chemotherapy, I hope she will get better with time.

And remember, you or someone you know received Rituxan treatment and have suffered serious side effects, you need to consult our dedicated and experienced defective drug attorneys immediately. You could be entitled to compensation for your pain and suffering, but if you hesitate the statute of limitations in your state could end your case before it has a chance to begin. Let us help you get the justice you deserve.‚ I wish that was .

Rationalization

http://www.kerrysteigerwalt.com/public/defectivedrugs/rituxan.html

Int J Hematol. 2008 Nov;88(4):443-7. Epub 2008 Oct 15. Progressive multifocal leukoencephalopathy in a patient with B-cell lymphoma during rituximab-containing chemotherapy: case report and review of the literature (http://www.ncbi.nlm.nih.gov/pubmed/18855101).

Have to ask the right question.

Published 15 Jul 2009

When I was a kid I was told by a friend that you got Salmonella from eating salmon. Seemed reasonable to me at the time, I did not realize it was named after Sal Mon, one of the top level Pokemon. God know what you get from eating spotted dick (http://en.wikipedia.org/wiki/Spotted\_dick).

The patient I saw yesterday had Salmonella in both her diarrhea and her blood. Simple enough, but why? Everyone assumed she picked it up on her trip to SE Asia, but that had been 6 weeks prior and that was a wee bit too long an incubation period.

So you start asking exposures, since Salmonella has many ways to get into the food supply and cause diarrhea. There seems to be a new outbreak every month.

Unusual foods? Nope.

Pistachios? Nope.

Peanut butter? Nope.

Tomatoes or Fresh salads? Nope.

Pets or animals at home? Nope.

Any reptiles? Nope.

Any folk remedies? Nope.

Hows about chickens or eggs? We raise chickens.

Odd response given the pet or animal question that preceded it. Once there was a patient who admitted with fevers and diffuse granulomatous lymphadenopathy. Everyone asked him if he had pets or animals at home, and he said no. My boss, on Chief of Service Rounds, asked the patient if he was around any animals, and he said his roommate had a half-dozen cats. HE didn't have animals, it was his roommate. It is all in how you ask the question. The patient had Ted Nugents disease, or Cat Scratch Fever.

She probably got the Salmonella from her chickens, as it came before the eggs. She was not enamored with the idea that she developed Salmonella from her chickens, since she had chickens for years and never developed an infection before. The final flush of the toilet to make the diagnosis was she had recently been started on a proton pump inhibitor (PPI) after returning to the US, and so for the first time had no stomach acid barrier to prevent infection. As noted in the rationalizations, "There is an association between acid suppression and an increased risk of enteric infection."

Once you start a PPI, stay away from the raw eggs unless you have a lot of reading you want to get done.

Rationalization

Am J Gastroenterol. 2007 Sep;102(9):2047-56. Systematic review of the risk of enteric infection in patients taking acid suppression. (http://www.ncbi.nlm.nih.gov/pubmed/17509031)

Swimming in Body Fluids

Published 16 Jul 2009

Vacation means swimming. In lakes. In rivers. In oceans. In pools. Swim in a pool, you are swimming in the microbial flora of everyone else in the pool. And chlorine does not kill everything.

The family had returned from a 2 week trip to the tropics where they swam in the hotel pool with many a young child.

First one child gets sick with nausea, vomiting and headache.

Then the next child gets nausea, vomiting and a headache.

Dad gets lip blisters.

Mom then gets nausea, vomiting and a headache. She goes to the ER and has a lumbar puncture (LP) aka spinal tap. Me? I am never going to use the word 'headache' in an ER. I do not want an LP. Ever. The thought gives me the willies. She had a classic aseptic/viral meningitis and went home after a few days. Then she has progressive shortness of breath and gets admitted to my hospital with large, bilateral pleural effusions, prolonged PR on EKG, but normal cardiac function. I was called, the sound of trumpets announcing my arrival.

I was betting on leptospirosis more than the eventual diagnosis because of the pleural effusions. Their tropical travels had taken them to areas that are endemic for leptospirosis and leptospirosis is a common cause of aseptic meningitis. There were other features against leptospirosis: no protein in the urine, no increase in bilirubin, no conjunctival suffusion (eyes that look like you have been smoking a whole baggie of pot).

However the other disease spread by the shared pool water is the enterovirus, and we asked the outside hospital to run a PCR for enterovirus on the CSF and it was positive. Pools are a great source of the enteroviruses as they are often resistant to chlorine. The classic in the old days was polio, the most feared of the enteroviruses. Formaldehyde is better at killing the virus, but no one wants to swim in that.

So all her symptoms were due to the enterovirus, but I have some splainin' to do with the pleural effusions. I can't find where enterovirus causes pleural effusions in normal people without heart failure. Is it due to direct invasion of the pleural space or a immunologic post infectious disease? I don't know. I need to browbeat the lab into running a PCR on the pleural fluid.

Rationalization

An outbreak of aseptic meningitis due to echovirus 30 associated with attending school and swimming in pools (http://www.ncbi.nlm.nih.gov/pubmed/16458563). Int J Infect Dis. 2006 Jul;10(4):291-7. Epub 2006 Feb 3.

An outbreak of viral meningitis associated with a public swimming pond. (http://www.ncbi.nlm.nih.gov/pubmed/15816154) Epidemiol Infect. 2005 Apr;133(2):291-8.

Aseptic meningitis outbreak associated with echovirus 9 among recreational vehicle campers--Connecticut, 2003. (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5331a2.htm)

MMWR Morb Mortal Wkly Rep. 2004 Aug 13;53(31):710-3.

An outbreak of an enterovirus-like illness at a community wading pool: implications for public health inspection programs. (http://www.ncbi.nlm.nih.gov/pubmed/2735481) Am J Public Health. 1989 Jul;79(7):889-90.

Bad Air Re Re Dux Dux

Published 16 Jul 2009

The intravenous quinidine worked perfectly for the malaria . Within a day her parasitemia was zero.

But.

When I went off to TAM she was looking great in the ICU, ready for transfer, I thought everything was going perfect.

I returned from Vegas and the sign-out list said: On a vent, pressors, ECMO (Extracorporeal membrane oxygenation), moved to trauma ICU.

I felt all the blood drain from my face and my heart fell into my shoes. I thought I was going to puke. What the hell had happened?

It is often not the organism, but the inflammatory response to the organism, that kills us. There is an old observation that after antibiotics, patients worsen. Antibiotics shatter the organism and there is a flood of endotoxin and other bacterial parts and the body responds with a tsunami of cytokines and the patient will transiently worsen about 4 hours later. It happens all the time. All you can do is hang on and support the patient.

Three percent of Westerners who get malaria die of the disease, the risk is not trivial. Depending on your destination, rates of malaria can be 1–357 per 100,000. It gasters my flabber that there are them what will sell a homeopathic preventative for malaria. Last I looked, water had no effect against Plasmodia.

With malaria, the response is delayed about 24 hours. But when there is a big die off of the organisms, there can be a delayed, and massive, systemic inflammatory response (SIRS), ironically due to the antibiotics. And she had a massive SIRS. Thank goodness for modern ICU's, if she had worsened in most other hospitals, given the rarity of ECMO, she would have died.

Fortunately, she is much better now and on the mend. But. oh. shit. I get anxious just thinking about it. PTSD.

My dad is a retired cardiologist and he used to say what kept him awake at night was not the calls but the worry. I have understood that for years, and that sick feeling that occurs when patients do unexpectedly badly keeps me up at night as well.

Rationalization

Krause G, Schöneberg I, Altmann D, Stark K. Chemoprophylaxis and malaria death rates. Emerg Infect Dis [serial on the Internet]. 2006 Mar [date cited]. Available from http://www.cdc.gov/ncidod/EID/vol12no03/05-0736.htm

It's a gas.

Published 18 Jul 2009

When I was a kid I saw Gone with the Wind on a big screen. The scene where they had to lop off a gangrenous leg without anesthesia, not even acupuncture, but just a shot of whiskey, was for me one of the most horrific pieces of movie making I had seen. I think I am scarred for life.

Gas Gangrene is one of those diseases that can kill with remarkable rapidity, and I have seen people go from healthy to dead in less than 24 hours as they were rapidly consumed by Clostridium perfringens, the classic cause of gas gangrene. Gas in tissues is one of those red alert, danger Will Robinson findings. But while all that glitters is not gold, all that is gas is not Clostridium. But all who wander are lost.

Young female who twisted her ankle and 24 hours later had abrupt onset marked rubor, dolor, calor, tumor of her leg from ankle to knee. And lots of pain. She was seen in the ER and plain films had gas. CT was obtained, and there was even more gas, all up and down her calf. Patient was surprisingly non toxic and no underlying medical problems, but was whisked off to the OR for fasciotomies. No gas gangrene, the tissues looked fine and the gram stain had gram-positive cocci. I am betting group A strep (which it was).

Gas in tissues is always worrisome, but when you think about it (I will go get a beer while you do), the end point of all metabolism is the production of gas. Anyone with a 12 year old boy at home recognizes the volumes of gas that can be loudly expelled in the course of a day amidst great hilarity.

With gas gangrene, by the time you see the gas it is probably too late, it is a late finding of the disease and you better call the coroner. I have seen much larger volumes of gas over the years for _S_. aureus, Group A Streptococcus and Candida than I ever have from _C_. perfringens. I have seen one other case of acute cellulitis with lots of gas in a cook who stabbed their hand.

It would appear from Pubmed that gas with cellulitis but no necrosis is infrequency reported, but in emphysematous pyelonephritis there is lots of gas produced from a wide variety of organisms. And often there is gas in abscesses, presumably from the infecting organisms.

Gas bad. But sometimes maybe not all that bad only a vigorous bacterial farting.

Time flies like an arrow, fruit flies like a banana

Published 20 Jul 2009

I was searching for information on Pubmed this morning and let out a big sigh. It occurred to me that the first time I searched for this topic was 27 years ago as a fourth year medical student on my infectious disease rotation when I had to talk on warfarin and endocarditis. Dint have no ECHO back in my day. We had to diagnose endocarditis with history and physical. And he didn't have those highfalutin’ third generation cephalosporins neither. Men were real men, doctors were real doctors and small furry creatures from alpha centrui were REAL small furry creatures from alpha centuri. But where does the time go?

I had a patient over the weekend who presented with acute back pain after lifting her walker and was admitted for intractable pain. MRI showed maybe an epidural abscess, maybe a discitis, but not that impressive. She is on immunosuppressives for newly diagnosed myasthenia gravis, but I was less than thrilled by exam (no spinal tenderness) and MRI that she had an infection.

But we got blood cultures.

And wouldn't you know that all the cultures are positive 24 hours apart for an enterococcus. My motto: frequently in error, never in doubt. Proven wrong again by the cultures.

The sine qua non of endocarditis is sustained bacteremia, so ECHO or no, she will need to be treated for endocarditis. She is also on warfarin for history of pulmonary embolism. Since vegetations are mostly clot, I keep wondering if prior use of warfarin will lead to false negative ECHO's, since they can't form clot. No one has done that study yet. There's a paper for a budding cardiologist.

Interestingly, while warfarin makes endocarditis worse (they shower emboli), prior use of anitplatelet agents improves outcomes.

"There was a trend for lower mortality among patients started on antiplatelet drugs after admission (AOR 0.29, 95% CI 0.08-1.13). The effect of aspirin on mortality was much the same in patients who received 325 or 80 mg daily. Chronic antiplatelet therapy was not associated with a significantly lower risk of major embolism"

Here is a pearl. Aminoglycosides are neuro-endplate blockers, so I may make her myasthenia worse with the gentamicin.

Yes, some of us still use gentamicin. But I have given up on theophylline. I am making progress.

Rationalization

Clin Microbiol Infect. 2009 Feb;15(2):193-9. Chronic antiplatelet therapy and mortality among patients with infective endocarditis (http://www.ncbi.nlm.nih.gov/pubmed/19196260).

Clin Infect Dis. 2007 May 1;44(9):1180-6. Impact of prior antiplatelet therapy on risk of embolism in infective endocarditis (http://www.ncbi.nlm.nih.gov/pubmed/17407036).

J Huazhong Univ Sci Technolog Med Sci. 2005;25(3):294-6. Investigation on the mechanism of exacerbation of myasthenia gravis by aminoglycoside antibiotics in mouse model (http://www.ncbi.nlm.nih.gov/pubmed/16201276).

Do the feet smell?

Published 21 Jul 2009

Middle aged man with athaletes feet (its atha-lete, not athlete) who gets a spontaneous foot cellulitis and maybe a touch of abscess. No risk factors, to trauma, no reason for the infection.

He doesn't respond to a oral beta-lactam, and eventually gets betterish on vancomycin. Cultures of the abscess grow coagulase negative Staphylococcus. Ignore it, right? Riiiiiiggggghhhht.

That's what I would have said last year, but not this year.

Turns out there is a _S._ lugdunensis, a coagulase-negative staphylococcus, that is not an uncommon cause of lower extremity infections. On the rare times I have seen lugdunensis, it has been the etiology of endocarditis or a post-operative knee infection. Unfortunately the lab usually doesn't look for lugdunensis in skin infections because it is thought to be a contaminant/normal flora.

However, we are all a tropical rain forest of microorganisms, and each organism has a niche on a body. S. lugdunensis likes live below the waist, especially on the big toe. I prefer beach front property myself.

It is one those organisms that has a unique smell. And what does it smell like, you ask? Teen Spirit? No. Bleach. Oh, Never mind. Did he smell like bleach? I don't know. Pushkin I am not, so I did not sniff the foot and the lab made no note of any odor. I do know the organism is not acquired in utero.

Next time you call me with a foot cellulitis, sniff the foot first. Let me know if it smells like the Y.

Rationalization

Clin Microbiol Infect. 2009 Jun 6. Staphylococcus lugdunensis in several niches of the normal skin flora (http://www.ncbi.nlm.nih.gov/pubmed/19519842).

J Clin Microbiol. 2009 Apr;47(4):946-50. Staphylococcus lugdunensis, a common cause of skin and soft tissue infections in the community (http://www.ncbi.nlm.nih.gov/pubmed/19244465). PMID: 19244465

Enferm Infecc Microbiol Clin. 2009 Mar;27(3):148-52. [Evaluation of methods for studying susceptibility to oxacillin and penicillin in 60 Staphylococcus lugdunensis isolates.] (http://www.ncbi.nlm.nih.gov/pubmed/19306714)

Postscript: They eventually identified the organism as _S._ lugdunensis.

At least it is not called Pansy Fever

Published 23 Jul 2009

It is summer in Oregon and people are going from floating corpse white to freshly boiled lobster. However, you are not supposed to get a sunburn where the sun don't shine, unless, of course, you have been to Rooster Rock, the local clothing optional beach. And in Oregon, clothing should always be the option. The glare off the large expanses of glistening white skin can damage vision and is a more common cause of blindness in the NW than hiking on glaciers without sunglasses.

The patient comes in after a cardiac arrest and develops bilateral pneumonia on CXR. Two days into the hospitalization, as she starts reperfusing her ischemic tissues, she gets a sunburn. Her body turns bright cherry red, including her buttocks, palms and soles.

There is, interestingly, sparing around the eyes and lips, her conjunctiva are injected and, unfortunately, I can't see the tongue well due to various support tubes. I think it is normal.

What is the causing the erythroderma? I hate making rash decisions. Not many things cause a sunburn rash that involves the palms and the soles. It could be sunburn, but she has been in the ICU for two days. Syphilis? Maybe, but the VDRL was negative. If it could be lues, don't touch the rash as cutaneous syphilis is a sea of wiggling spirochetes. I don't think your spouse will be reassured when you say you got the Great Pox from touching a patient. It will just sound wrong.

It looks like a toxic shock rash, but she is not toxic or shocky: blood pressure and kidney function are within normal operating parameters.

There is no skin fragility (Nikolsky sign: stroking of the skin causes the it to separate at the epidermis) so I do not think it is staph scalded skin syndrome, a disease of children, although I have seen one case in a old man.

Scarlet fever? That is streptococcal, and she is growing staph. The rash does not feel like sandpaper to me, which is what the skin of Scarlet fever is supposed to feel like. But Staphylococcus can cause a scarlet fever like rash. According to the peds texts, Staph causes neither circumoral pallor (which she had) nor strawberry tongue (which I could not see clearly).

She has yet to exfoliate, which will probably make the diagnosis of Staph pneumonia with a scarlet fever rash.

Rationalization

Infect Immun. 1981 February; 31(2): 732-736. Staphylococcal scarlet fever (http://www.ncbi.nlm.nih.gov/pubmed/7216472): role of pyrogenic exotoxins.

Postscript: she did exfoliate so the rash was probably from the Staphylococcus.

Warts

Published 25 Jul 2009

One of the many infrequently mentioned benefits of working in a hospital is the people you work with. Good, smart people tend to go into health care. One of the ongoing pleasures of work is the docs and nurses and social workers and nutritionists and techs and I am sure if I try to make an inclusive list I will forget a group, so I will say etc etc and etc.

As a result of long association, people seem comfortable curbsiding me with their infectious disease issues. Like yesterday I got to see a wart. A big wart that was inflamed and annoying to its owner.

How, I was asked, do I treat it?

Compound W works, and you could have it burned off with liquid nitrogen, but given its location on the hand I wouldn't burn it off.

How come if you use cold it is called burning it off?

Got me. Language is funny (both in the ha ha and odd meanings of the word) that way.

Then someone suggested duct tape. Now I know that duct tape is a useful product outside of medicine, but warts?

I was skeptical. Hard to believe, I know.

The theory proffered on the ward was it cuts off oxygen so the wart dies. Didn't seem likely since the oxygen gets to the wart by way of the blood supply, although I duct tape embolism would work.

So off to Pubmed, and oh yeah you betcha, there are 24 references about removing warts with duct tape.

The some studies says it does not work, some studies demonstrate efficacy. I refer the Tom Sawyer technique

“Why, you take your cat and go and get in the graveyard 'long about midnight when somebody that was wicked has been buried; and when it's midnight a devil will come, or maybe two or three, but you can't see'em, you can only hear something like the wind, or maybe hear'em talk; and when they're taking that feller away, you heave your cat after'em and say, Devil follow corpse, cat follow devil, warts follow cat, I'm done with ye!”

It hasn't failed me yet. A dead cat is always a plus.

Duct tape? I don't know. Just doesn't seem plausible to me, but more papers than not suggest that it is effective. But I am not treating genital warts with it.

Rationalization

Arch Pediatr Adolesc Med. 2002 Oct;156(10):971-4. The efficacy of duct tape vs cryotherapy in the treatment of verruca vulgaris (the common wart) (http://www.ncbi.nlm.nih.gov/pubmed/12361440).

Arch Pediatr Adolesc Med. 2006 Nov;160(11):1121-5. Efficacy of duct tape vs placebo in the treatment of verruca vulgaris (warts) in primary school children (http://www.ncbi.nlm.nih.gov/pubmed/17088514).

Arch Dermatol. 2007 Mar;143(3):309-13. Duct tape for the treatment of common warts in adults: a double-blind randomized controlled trial (http://www.ncbi.nlm.nih.gov/pubmed/1737209).

Br J Dermatol. 2007 Apr;156(4):687-92. To freeze or not to freeze: a cost-effectiveness analysis of wart treatment (http://www.ncbi.nlm.nih.gov/pubmed/17326748).

Cringe Worthy

Published 28 Jul 2009

There are a lot of French eponyms in Infectious Diseases. Thanks, I assume, to Pasteur, the French dominated Infectious Diseases for years. And thanks, in part to all the wars, the French had ample opportunity to learn about infections back in the day, perhaps to come again, when infectious diseases was a surgical subspecialty. Before penicillin, a chance to cut was a chance to cure. As resistance is slowly increasing in all the major pathogens, I expect I may have to relearn how to scrub into a case. Ick.

Fournier has a sign, a tibia and a gangrene named after him, not bad for a life studying syphilis.

Fournier’s is a mixed synergistic necrotizing fasciitis of the perineum, usually occurring in diabetics. The colonic flora work together to act like gas gangrene and eat up the rectum, scrotum and surrounding tissues. I still remember the first case I saw as a fellow, a young male who was missing the soft tissue of this thighs, rectum, abdominal wall, and scrotum, the testicles sitting on a moistened towel. I cringe 20 plus years later, although long term, thanks to the magic of plastic surgery, he had a pretty good cosmetic result.

The microbiology is usually a little strep, a little gram-negative rod (usually _E_. coli) and a lot of anaerobes. There have been increased cases of MRSA causing necrotizing fascitis, but only few Fournier’s.

The patient came in with rapidly progressive necrotizing infection and was treated rapidly with aggressive debridement and broad spectrum antibiotics. Much to my surprise, all the cultures grew methicillin sensitive Staphylococcus (MSSA). Not the typical organism. The key for patient survival is rapid and extensive debridement. Pronounced dee-breed. Not dee-bride, who is the person who walks down the aisle of the church. And they found 'frank pus.' What the hell is frank pus? There is frank bleeding which is contrasted with occult bleeding. But there is not occult pus, so there is no reason to ever append the adjective ‘frank’ to the noun ‘pus’.

MSSA is reported in a smattering of cases of Fournier’s, but is my first causing this disease.

There are three reported cases of Fournier’s after vasectomy, although with vasectomy they report the more typical of group A strep post op necrotizing fascitis than the classic mixed microbiology.

Still. Hardly seem like a good trade off to be sterile.

Rationalization

J Urol. 1992 Jun;147(6):1613-4. Lethal Fournier's gangrene following vasectomy (http://www.ncbi.nlm.nih.gov/pubmed/1593699).

Neither A nor B nor C nor D

Published 28 Jul 2009

I'm not talking med school grades here.

So many infections I have yet to see. I have mentioned somewhere before that being an ID doc is like being a birder, only ID is actually interesting. You will find that I have a limited comedic repertoire, so I will repeat myself on occasion. Think you have it bad, think of the poor residents who have to listen to three years of my repetitive blathering and can't jump to Fark. Like a birder I have my lifetime list of infections I have seen and infections that I hope to see, despite the fact it means someone will have to suffer for me to add to the list. I am not silly enough to believe that my thinking it makes it so. I'll leave that to the goofs who practice the Secret.

Today, I done diagnosed something I had never seen before. Other posts have discussed the recent case of severe malaria. Upon admit the patient was not that ill, but had elevated transaminases (about 5 x normal) and bilirubin (3) to an extent that I thought was more than could be accounted for by the severity of the malaria. As if I have a vast experience of treating malaria in the Portland, Oregon, although if predictions of global heating are correct, malaria could make a comeback in my neck of the woods.

Hepatitis is known to occur with severe malaria and is a bad prognostic sign. However, it wasn't all that severe for the first three days, so I wondered about other causes of hepatitis from sub-Saharan Africa: yellow fever and Hepatitis A,B,C, and E. I sent off all the serologies and the ABC was negative (good thing we do not send our specimens to the Sesame Street Lab), but I was called by the State today: Hepatitis E IgG negative, IgM repeatedly positive, consistent with acute hepatitis. She had malaria AND hepatitis E.

He shoots, he scores, the crowd goes wild.

Hepatitis E is spread by fecal-oral (such an appetizing term, n'est pas?) that is found in sub-Saharan Africa in the water and there have been huge outbreaks in refugee camps. It has a nasty predilection for killing pregnant females.

Interestingly, it is also probably more common than previously suspected in the West. In Europe it is spread by pigs and eating pig livers or hunting wild swine. Who knew there were still wild swine in Europe.

In the US, a recent article in Journal of Infectious DIsseases showed that 21% of Americans are seropositive for hepatitis E. The risks in the US are eating organ meats and having a pet, and I assume the two are mutually exclusive. Mmmmmm pet liver.

So look for Hepatitis E. Way cooler than a Condor. And more common.

Rationalization

J Coll Physicians Surg Pak. 2009 Jun;19(6):367-70. Malarial hepatopathy in falciparum malaria (http://www.ncbi.nlm.nih.gov/pubmed/19486576).

Vet Microbiol. 2009 Jun 26. High HEV presence in four different wild boar populations in East and West Germany (http://www.ncbi.nlm.nih.gov/pubmed/19595519).

J Infect Dis. 2009 Jul 1;200(1):48-56. Epidemiology of hepatitis E virus in the United States: results from the Third National Health and Nutrition Examination Survey, 1988-1994. (http://www.ncbi.nlm.nih.gov/pubmed/19473098)

Sorry, nothing to learn here. Keep moving. A content free post.

Published 29 Jul 2009

One of the purposes of this blog is to give the illusion of near omniscience (in fact I am omnivorous). Case after triumphant case where, with a combination of House, Welby and Holmes, I find the correct diagnosis.

I wish that were reality.

More typical is the case I have right now: a foreign born kidney transplant patient back from a trip to Idaho with fevers to 103 and 5 to 6 profuse watery diarrheal stools a day.

Easy right?

Maybe. Diarrhea can cause fevers but fevers can cause diarrhea. I figure, probably incorrectly, that throughout most of history we ate questionable food and many infections came from food. So getting rid of contaminated food would be an important evolved response to infection. It is why, perhaps, when tumor necrosis factor (TNF) is injected into rats, it makes them grab a book and head to the toilet, as it gives them diarrhea. But that may be a just so story.

The patient has no risks or symptoms for opportunistic infections. One member of the family had a similar illness, but it lasted only 48 hours

So we work up the fever: stool for WBC (waste of time, but others do it) are negative. O&P negative. Bacterial cultures negative. And the fevers and diarrhea continue. Slight crackles develop on exam (I never heard them) which lead to a CXR and then a CT of the chest. There are patchy left sided infiltrates but no pulmonary symptoms at all. Nothing. Is the diarrhea an epiphenomena of the pneumonia and TNF induced fever response?

Sputum is unimpressive, and he has a mild hemolysis.

Mycoplasma ?!? CXR worse than the patient and hemolysis smells of that organism, but it is not a disease of the elderly and this kind of diarrhea is not usually part of the disease, although who really knows with the immunosuppressives he is on.

Legionella is pending and his fever is drifting down, whether from the macrolide or time I do not yet know.

Often the diagnosis is like a piñata. It's there, somewhere, a treasure, and I am swinging the bat with a suspicion of where it is and I hope I do not connect with someone's head by mistake.

And that is why they call me Dr. Metaphor. Well, not really.

Sometimes I am slightly envious of the cardiologist. A quick cath and the issue of coronary artery disease is put to rest.

Oh well. I'll let you know what I get.

Postscript: there was never a diagnosis and the patient got better. The preferred result, as a diagnosis with a dead patient somehow ever satisfies.

Sine qua non part deux

Published 31 Jul 2009

Sine qua non , Latin for ‘that without which it could not be’.

Sustained bacteremia is the sine qua non of endocarditis, or to be picky, an endovasular infection. As a rule, only infections in the vascular tree (endocarditis, infected aneurysms, septic thrombophlebitis, etc.) give positive blood cultures day after day.

So in the right patient, no matter what the studies, like some crappy negative transthoracic echo (TTE), if the blood cultures are positive day after day, it has to be an endovascular infection. And BTW. Never let a negative TTE exclude endocarditis. TTE’s are usually only useful if positive for endocarditis.

The patient is admitted with 6 weeks of fevers, chills, night sweats, failure to thrive, malaise, and a prosthetic valve. He was seen in the ER and blood cultures were positive, so he was called back in and the repeat blood cultures were positive again.

Prosthetic valve endocarditis is not that unusual, occurring in about .8% of patients per year, at least those with a prosthetic valve. It is more unusual to get a prosthetic valve infection in a patient without a prosthetic valve.

But the blood grew a gram-negative rod. Maybe. After several days the lab could not identify it, so they sent it on.

It was Aeromonas. No, wait, maybe a Neisseria of some sort, but still not fer sure. But at least I have sensitivities on the organism. I may not know what it is, but at least I can try and kill it.

Where did the Neisseria come from? Neisseria are normal oral flora. He had some dental work several months before and took the usual prophylactic antibiotic, not like it really works. The clinical data to support antibiotic prophylaxis is nonexistent at best, but I would do it as prophylactic antibiotics are the standard of care.

There are a whopping 7 cases of Neisseria reported as a cause of prosthetic valve endocarditis, several of which were cured with medical therapy. There was one case of _N_. meningitidis and one of _N_. gonorrhoeae, proving yet again you must be careful to whom you give your heart.

The patient is improving on a third generation cephlosporin and an aminoglycoside, so I am cautiously optimistic. But I am not optimistically cautious. That's a one way street.

Rationalization

Cochrane Database Syst Rev. 2008 Oct 8;(4):CD003813. Antibiotics for the prophylaxis of bacterial endocarditis in dentistry (http://www.ncbi.nlm.nih.gov/pubmed/18843649).

S. aureus pays my mortgage.

Published 8 Aug 2009

All but two of my consults this week were due to S. aureus. If it wasn't for S. aureus I would be standing at a freeway off-ramp with a sign that says "Will do ID for Food."

Sine qua non again. Sustained bacteremia is always an important clinical finding as it usually means an endovascular infection. Only an infection whose focus is in the vascular tree will have a sustained bacteremia. And sustained can be for days. It usually means endocarditis, but not always. It could be due to a line infection. It could be an infection elsewhere. As an intern my attending diagnosed an infected aneurysm as a result of a splenectomy. The stump of the vascular supply to the spleen had been tied off and a arterial-venous malformation had formed, which was subsequently seeded with Staph. He had heard a bruit over where the spleen had been, a physical finding missed by everyone else. No way would I make that diagnosis without finding it accidentally on a CT.

ID docs love to know if round purple things in the blood are transient or sustained in the blood stream and nothing gripes my cookies more than when one set of blood cultures are growing a gram-positive bacteria and antibiotics are started without repeating the blood cultures first.

Always always always repeat blood cultures before treating gram-positive bacteria in the blood. Always. It will decrease the aggravation in your ID doc no end. And really, there is nothing more important than making your ID doc, i.e. me, happy.

The patient on Friday is a dialysis patient who came in with fevers, as do most of my patients, and S. aureus in the blood. His catheter was pulled and he still had persisting fevers, positive blood cultures and neck pain and chest pain. ECHO did not show a vegetation, but CT showed both a big clot in the internal jugular vein and a peripheral cavitating lesion in the lung.

What he has is a nosocomial Lemmier’s, septic thrombophlebitis of the internal jugular, with septic emboli to the lung. Usually Lemmier’s is due to mouth anaerobes (it is also called post anginal sepsis, angina in the old times was neck pain, but, due to medical plate tectonics, angina has moved its position over time. If enough time passes, angina will eventually refer headache) but there are increasing cases of Lemmier’s due to S. aureus.

Antibiotics and anticoagulation are usually curative as was the case in this patient

It is curious how rarely I see septic thrombophlebitis given how common both clot and S. aureus are in the blood stream.

In a study of 1275 surgical ICU patients who were evaluated for DVT, more clot was found in the upper extremity veins than the lower:

"DVT was confirmed in 39 patients. The incidence of upper-extremity DVT was higher than that of lower-extremity DVT (17% vs 11%; P = .11). Four-extremity scans diagnosed more DVT than 2-extremity scans (33% vs 7%; P < .001).

There was a significantly higher incidence of upper-extremity DVT in patients with sepsis or central lines. They had higher APACHE III scores on admission to the ICU, longer hospital stays, and higher in-hospital mortality rates than patients with DVTs.

Sepsis was present in 72% of patients with upper-extremity DVT, compared with 53% of patients with lower-extremity DVT (P < 0.001), and 86% of upper-extremity DVT was associated with central venous catheters."

I get a fair number of ultrasounds looking for clot associated with line infections, this study suggests I should get more.

Rationalization

Upper-Extremity DVT in ICU Patients (http://www.medscape.com/viewarticle/587835). Society of Critical Care Medicine (SCCM) 38th Critical Care Congress: Abstract 305. Presented February 2 2009.

Bovis, part one.

Published 10 Aug 2009

Back when I was a resident, there were Group D Streptococci and they were divided into enterococcal and non enterococcal streptococcus.

Easy. You only had to remember two things.

The problem with modernity is they have increasingly sophisticated ways of analyzing bacteria and separating them into different groups.

There also used to be S. bovis, a non enterococcal Group D streptococcus. S. bovis in the blood means bowel cancer and the patient needs a colonoscopy to look for GI pathology to account for the bloodstream infection. Not only is this a practical piece of information, but it is the kind of thing they like to ask on the boards, so make note of it. I would hate to have you miss a question because you were not paying attention.

The patient was found down, how long we do not know. It is my clinical impression (aka I am probably wrong and the victim of confirmation bias) that transient bacteremia is common in people found down for prolonged periods of time. Normal skin organisms leak into the blood stream and the they have a transient bacteremia. However, that tidbit is unsupported by any literature I can find, so get to work someone and generate a paper that verifies my insightful observation.

The patient is a heavy alcoholic and not particularly well kept, so when he was found down and febrile, he had blood cultures that grew_S. gallolyticus_, a sub type of S. bovis. S. bovis is a bowel bug, not a skin bug, but perhaps it leaked from the skin for to judge from the smell, fecal flora may not have been confined to just his gi tract. It was only one of three sets, so he did not have endocarditis, but still needed a colonoscopy. It was negative for malignancy, but he does have cirrhosis with varices and maybe that is why he has bacteremia.

Liver disease may also be a risk for S. bovis bacteremia.

Not all bacteria are equal in the ability to cause disease and the better they are identified, the better you can evaluate the patient.

Rationalization

J Infect. 2001 Feb;42(2):116-9. Prevalence of liver disease in patients with Streptococcus bovis bacteraemia. (http://www.ncbi.nlm.nih.gov/pubmed/11531317)

Pathology. 2009 Feb;41(2):183-6. Streptococcus bovis bacteraemia: identification within organism complex and association with endocarditis and colonic malignancy. (http://www.ncbi.nlm.nih.gov/pubmed/18972318)

Bovis, yet again.

Published 11 Aug 2009

That prosthetic valve endocarditis from a while back that had no name? It is Neisseria elongota. Took elong time to identify it. I'm tired. They can’t all be gems.

75 year old with a new diagnosis of inflammatory bowel disease early this year.

He has had a progressively painful hip since the diagnosis of IBS and failure to thrive. He has a TIA and is admitted. Blood cultures are growing two of two streptococcus. He has a known flail mitral valve.

Positive blood cultures, abnormal valve, emboli, sounds like endocarditis to me.

He had one blood culture on a prior admission that had both a coagulase negative Staphylococcus and a _S_. alactolyticus, yet another group D Streptococcus in the bovis family. It was dismissed as contaminant, which is not unreasonable as there are no cases of any disease outside of cavities in humans. He has had some dental work, and don't we all? It is a common bug in pigs and chickens, of which he has no contacts.

There are no reported cases of endocarditis yet with this organism. I got the first one. Lets hear it more me.

But the more interesting feature of the case is that his systemic symptoms started around the time he was diagnosed with Crohn's. IBD is associated with endocarditis, so maybe that is why he has endocarditis. And we still have to determine if the hip is infected as well. Then I also have the first case of septic arthritis with this organism.

Rationalization

Am J Med. 1992 Apr;92(4):391-5. Increased risk of bacterial endocarditis in inflammatory bowel disease. (http://www.ncbi.nlm.nih.gov/pubmed/1307218)

Z Gastroenterol. 1992 Jun;30(6):397-402. [ An increased incidence of bacterial endocarditis in chronic inflammatory bowel diseases (http://www.ncbi.nlm.nih.gov/pubmed/1636271)\]

Lookin' Good

Published 14 Aug 2009

Shh. Gather round. I am going to tell the secret of looking good as a consultant. Besides the white coat. For years I wore sport coats, but they wore out and it is pricey, even at Goodwill, to get new ones. So of late I have gone to the white lab coat. It is slimming and matches my hair.

The patient, a two pint a day vodka drinker is admitted with ETOH withdrawal when he decides to quit drinking on his own.

In the ER he is febrile and blood cultures are done.

Next day his cultures pop positive, both sets with a gram-negative rod that the lab is calling funny, not ha ha but odd.

So I see the patient, whose mental status has cleared, and he cannot move either shoulder or his ankle, although he has little rubor, calor or tumor in any of the joints, he howls with pain with passive movement of the joints. He also has a cellulitis of his right leg.

So I call the lab and ask what they think.

They don't know what it is. Its small, funny looking, gram negative and oxidase positive and its in the Identification machine, they will tell me what it is in the morning.

So here is my secret. Don't tell anyone.

I Google or Pubmed everything. I put gram-negative, rod oxidase positive, pleomorphic (med speak for funny looking) in the search box and up comes a list, and on the list is Pasteurella, and the patient has a cat.

So I write in my note, say it's probably Pasteurella, and it was. I look like a god. Minor deity. Like Pan.

Babe Ruth lead the league in strikeouts, as do I, but everyone remembers his pointing at the stands and knocking it out of the stadium.

So to look good? Google or Pubmed everything, then commit to a diagnosis.

Unfortunately, the patient is refusing debridement and antibiotics, so the outcome not looking so good.

Also, and of interest, is that liver disease (his bili is 9.0) is a risk for Pasteurella and septic joints. And you do not need to get a cat bite to get exposed to Pasteurella. He denies any bites. Cats lick everywhere and where the cat licks, Pasteurella follows. I once had a young girl who put tuna on the tip of her nose and had her cat lick it off. She got Pasteurella meningitis. I had another who let her cat sleep in her CAPD bag warmer, and she got CAPD peritonitis. People wonder why I don't want pets in my ICU's.

Rationalization

Adv Med Sci. 2009 Apr 14;54:1-4. Pasteurella multocida infection in a cirrhotic patient: case report, microbiological aspects and a review of literature. (http://www.ncbi.nlm.nih.gov/pubmed/19366651)

Infections Destroys All

Published 16 Aug 2009

Half a lifetime of taking care of infectious diseases and I am still impressed with what acute infections can do.

Allegedly normal 28 year old male, has fevers and is seen in the ER and gets a course of antibiotics without a diagnosis. You know he is going to get worse. He does. Fevers, stiff neck, altered mental status, he comes back to the ER.

WBC 25,000 in the blood, 900 in CSF, he has a purpuric rash on his soles and conjunctiva.

Meningococcus? He is admitted to the ICU as meningitis and given lots o' antibiotics.

Next day he has a new loud diastolic murmur and all his blood cultures have gram-positive cocci in clusters.

ECHO shows a bicuspid aortic valve with a large vegetation and a 1.5 cm abscess in the heart. TEE shows the abscess extending up into the aorta.

All in just two days. Abscesses in the heart are bad, usually incurable with antibiotics and one of the few locations I cannot get interventional radiology to stick a needle in. Something about trying to hit a moving target, if you ask me they are just a bunch of wimps.

He has a surgical repair and has survived. The operative report describes extensive abscess in the heart and aorta that has to be reconstructed. I am SO glad I am not a surgeon. It is all methicillin resistant Staphylococcus aureus.

Talking with the patient pre-op he had a festering splinter on his finger and it is not the first time I have seen catastrophic endocarditis in a patient with unsuspected bicuspid aortic valve. Bicuspid valves do not tolerate the stress of infection well at all, with abscess formation and rapid valve decompensation common.

10% or so of ascending aortic dissections have underlying bicuspid valve and the abnormality is associated with cystic medical necrosis of the aorta. Which may be why bicuspid aortic valve endocarditis seems to form abscesses with endocarditis with such frequency.

Rationalization

Curr Probl Cardiol. 2005 Sep;30(9):470-522. The bicuspid aortic valve (http://www.ncbi.nlm.nih.gov/pubmed/16129122).

Damned if you do, Damned if you don't

Published 17 Aug 2009

What do you do when all the solutions stink on ice? Do something? Do nothing? Both?

Patient has bad (as opposed to the good?) methicillin resistant Staphylococcus endocarditis (MRSA) endocarditis (yet another) with a large vegetation on the mitral valve and emboli everywhere. Also, he has seeded both his eyes.

His MRSA is resistant to all the standard antibiotics but vancomycin and that with an MIC of 2.

Once the MIC to vancomycin exceeds 1.0, failure rates start to increase and it becomes impossible to safely dose vancomycin. So do you hold? Change? I have zero confidence in linezolid for endocarditis, at least when used as monotherapy, so I reasoned that if daptomycin is noninferior to vancomycin when the MIC to vancomycin ain't so bad, it should be better if the MIC to vancomycin is higher.

All men die. Socrates was a man. All dead men are Socrates. So much for reasoning. Daptomycin has no indication for left sided endocarditis either, but then none of the newer agents do. New antibiotics are usually approved for skin and soft tissue infections, which an antibiotic shampoo would probably cure.

So with trepidation I changed him to daptomycin. Whether or not it was the change (I do not think it was) he progressed his endocarditis and has destroyed his valve and remains bacteremic.

He is, for a variety of reasons, a horrible surgical candidate.

So now what?

Clinical Infectious Diseases this month suggests the best option is linezolid with a carbapenem for salvage and he has responded to that therapy. I had a similar patient with refractory MRSA endocarditis who I cured with linezolid and ertapenem. Not my first choice, but I suppose reasonable if the patient is failing. Better than daptomycin? Eh.

I want the new MRSA cephalosporins, so called fifth generation (and I can always use fifth), to come out yesterday. I know they are going to charge an arm, leg and kidney for them (someone has to pay for that pizza at conference), but to be able to kill MRSA. Ah 'tis a consummation Devoutly to be wished.

Rationalization

Clinical Infectious Diseases. 2009;49:395-401. Salvage Treatment for Persistent Methicillin Resistant Staphylococcus aureus Bacteremia: Efficacy of Linezolid With or Without Carbapenem. (http://www.ncbi.nlm.nih.gov/pubmed/19569970)

Postscript: he was cured with a combination of linezolid and ertapenem and there is in vitro data to suggest the combination is synergistic. Two cures. I could say that in “in case after case” the combination is effective. If I can get three, I have a series.

Bloody Bullae

Published 19 Aug 2009

Hemorrhagic bullae.

If you are an ID doc, hemorrhagic bullae makes you think of Vibrio vulnificus. Sometime last century the Annals published the classic (as if medical articles have the same cachet as Dickens or Twain) article on hemorrhagic bullae and their relationship with liver disease, sepsis and V. vulnificus.

My patient has an increasing cellulitis, hemorrhagic bullae, and is on dexamethasone, a steroid, for cancer It’s nice to have a risk for the infection. V. vulnificus is associated with warm salt water exposure or oyster consumption, but he has been nowhere near the sea. The closest he has been to the ocean is a fillet o'fish sandwich from the local fast food eatery.

A quick Pubmed reveals that Aeromonas, a fresh water pathogen, has been associated with hemorrhagic bullae, but he has not been in a lake or a pond of late either.

So we treat him for cellulitis and Vibrio vulnificus and he gets better. The next day the blood cultures are growing a gram-negative rod, so I think, maybe my first V. vulnificus?

His leg improves and we narrow his antibiotics. Thing is, he grows Pseudomonas aeruginosa from his blood and for 48 hours he has improved on therapies with zero activity against his infecting organism. Maybe it was the dexamethasone that prevented him from going septic, maybe his genes, maybe just luck, who knows. Sometimes people just get better. My rule is, when people improve, take credit. When things go ill, blame nursing. Just kidding. I had a patient with Pseudomonas sepsis as a resident who refused therapy due to underlying advanced cancer, and he got better without therapy. Even this most nasty of bugs does not kill everyone, everytime.

Also odd is that he does not, as best as can be determined, have a necrotizing fasciitis, which is usually what gram-negative rod soft tissues infections cause. And there are no reports in Pubmed of hemorrhagic bullae from Pseudomonas. So probably another fluke case.

He has been changed to an anti-pseudomonal antibiotic and continues to get better, not that is was due to anything I have done. But I am still taking the credit.

Sing-Along

With apologies to Sam (http://www.youtube.com/watch?v=MHF558u6Q\_8).

Uno, dos, one, two, tres, quatro

Matty told Hatty about a thing she saw.

Had a cellulitic leg and ate oyster raw.

Bloody Bullae, Bloody Bullae.

Bloody Bullae, Bloody Bullae, Bloody Bullae.

Hatty told Matty, "Let's don't take no chance.

Let's not be L-seven, the blister need a lance."

Bloody Bullae, Bloody Bullae

Bloody Bullae, Bullae Bullae, Bloody Bullae.

Matty told Hatty, "That's the thing to do.

Got to kill that Vibrio before it kill you."

Bloody Bullae, Bloody Bullae.

Bloody Bullae, Bloody Bullae, Bloody Bullae.

Rationalization

Ann Intern Med. 1988 Aug 15;109(4):318-23. Syndromes of Vibrio vulnificus infections. Clinical and epidemiologic features in Florida cases, 1981-1987 (http://www.ncbi.nlm.nih.gov/pubmed/3260760).

Shock

Published 21 Aug 2009

Shock.

Septic? Toxic? Cardiogenic? Hemorrhagic? Electrical? Marilyn Manson?

So many ways to go into shock.

A middle-aged patient is admitted in what looks like septic shock: multi-organ system failure, DIC, platelets of 30, pressor dependent blood pressure.

Exam, labs and X-rays reveals none of the big three usual causes of infection: pneumonia, urinary tract infection, or soft tissue infection, which has the nice acronym PUS.

Not a lot of things cause non-focal rapid onset sepsis: Meningococcus, plague, Group A Streptococcus, maybe S. aureus lead the list, but the patient has no reason for any of the above.

So we treat for everything and next day all the cultures are negative.

Talking with the family reveals that the patient had axillary pain before admission that was thought to be due to minor trauma. Looking at the arm pit was initially unimpressive, but perhaps disgusting, as all arm pits lack a certain aesthetic appeal. As his blood pressure improved, cellulitis becomes evident in the axilla as well as a faint, diffuse erythroderma that involved the palms and soles. I suppose his blood pressure was so low he could not perfuse his tissue enough to get red in either the infected arm pit or what looked like a toxic shock rash.

He was whisked off to the OR for debridement. Streptococci are seen in the tissues that were edematous but there was no necrotizing fasciitis. So far cultures are negative.

It is an odd case of both septic shock (but the blood cultures are negative) and toxic shock (TSS) (but no strawberry tongue, necrotizing cellulitis and only a brief erythroderma). And the signs of TSS occurred in slow motion, over three or four days, and manifested late in the course of the disease. But the patient is slowly getting better.

There was an interesting recent case of Streptococcal TSS jumping from patient to a health care worker, so remember the droplet and contact isolation. My specialty is called INFECTIOUS diseases for a reason.

Rationalization

Clin Infect Dis. 2009 Aug 1;49(3):354-7. Nosocomial transmission of invasive group a streptococcus from patient to health care worker (http://www.ncbi.nlm.nih.gov/pubmed/19580415).

Ra's al Ghul was not so far off

Published 26 Aug 2009

I am on vacation this week, so I do not have much to write about. You may get Gonorrhea or malaria on vacation, but I old and have no risks for either. Golf and hiking is mostly infection free.

Now don't get any ideas about visiting my house while I am on vacation; I am spending most of my time on the front porch with a bottle of Jack Daniels and a loaded shotgun, yelling incoherently about the giverment and health care. I am, at least, a step up from the barking dogs in the neighborhood.

Before I left I helped with a Grand Rounds presentation on the potential health effects of global heating.

It is an interesting topic, and global warming is good for me. While paying work is going down thanks to a combination of the economy and all the infection control bundles, the changing climate may increase some diseases in the U.S. like malaria and dengue. The downside of global warming is that in England, and maybe else where, the respiratory syncytial virus (RSV) season is decreasing. A good trade off in my book. More malaria, less RSV. There are numerous reasons why climate change is going to increase infections, but the perhaps most important is an increase in the range of mosquitoes that carry diseases.

Although infections may increase with global warming, infections may also be the solution of global warming. There have been times when global warming has slowed: when large plagues that have killed off massive numbers of people. Fewer people mean less burning, less agriculture derived gases, more CO2 sequestration as the forests grow back.

"Abrupt reversals of the slow CO2 rise caused by deforestation correlate with bubonic plague and other pandemics near 200-600, 1300-1400 and 1500-1700 A.D. Historical records show that high mortality rates caused by plague led to massive abandonment of farms. Forest regrowth on the untended farms pulled CO2 out of the atmosphere and caused CO2 levels to fall. In time, the plagues abated, the farms were reoccupied, and the newly re-grown forests were cut, returning the CO2 to the atmosphere."

Not the most elegant solution to global warming, but probably worth it; who really wants to drive a Prius?

See you next week.

Rationalization

Clin Infect Dis. 2006 Mar 1;42(5):677-9. Epub 2006 Jan 25. Climate change and the end of the respiratory syncytial virus season (http://www.ncbi.nlm.nih.gov/pubmed/16447114).

Survival of the Fittest

Published 31 Aug 2009

I saw a patient today who by all rights should be dead. She is a homeless heroin user who has had at least a dozen different bacteremias this century. To add to her medical problems she is on dialysis for unrelated reasons and comes in intermittently at best. Not a good combination for longevity. I have read somewhere that the average life expectancy of an IV heroin user is 5 years and they die of murder or infection. Anyone know if this has a reference, or did I pull it out of a donkey?

I took care of her a couple of years ago when, over a 6 month period, she kept being admitted for a recurrent yet transient Acinetobacter bacteremia. Febrile and shaking, she would be admitted and have positive blood cultures that were negative upon repeat. She was worked up for a focus of infection and one was never found. No abscess, no endocarditis, repeat cultures negative.

Taking a history I found she used two water sources for mixing her heroin: the ladies room at a local burger joint and the water cooler at the local hostel. I never got either cultured, but I bet on the water cooler, and she stopped using both and the problem went away.

Acinetobacters are an increasing problem as they can be pan-resistant (no Greek theater criticism for this bug) and has been a major problem in wound infections in our troops.

Now she is in with Elizabethkingia meningoseptica in the blood. What is Elizabethkingia meningoseptica you ask? It used to be called Chryseobacterium (now its clear, right?), but genetics and the pathetic need for drunken microbiologists to change pathogen names to keep us clinicians squirming, has lead to a new designation. I think those are the two reasons that bacteria classification keeps changing. And Elizabeth was/is Queen, not King.

Elizabethkingia meningoseptica is also found in tap water, so I need to find out where she is getting her water for shooting up. Her water is probably the source of her bacteremia.

In the meantime, a touch of antibiotics and she is already much improved.

Rationalization

J Clin Microbiol. 2009 Jul 8. Association between contaminated faucets and colonization or infection by non-fermenting gram-negative bacteria in intensive care units in Taiwan (http://www.ncbi.nlm.nih.gov/pubmed/19587299).

Clin Infect Dis. 2007 Jun 15;44(12):1577-84. An outbreak of multidrug-resistant Acinetobacter baumannii-calcoaceticus complex infection in the US military health care system associated with military operations in Iraq (http://www.ncbi.nlm.nih.gov/pubmed/17516401).

Elizabeth O. King (http://www.bacterio.cict.fr/e/elizabethkingia.html), an American bacteriologist at the CDC.

Postscript: She left AMA (against medical advice, not American Medical Association) before I could ask where she was getting her water.

ECHO echo echo

Published 2 Sep 2009

I am a grouchy old fart and and have the AARP card to prove it. Get off my lawn punk. I have been a Mac user from day one and still have a functioning 128K original Mac. Dark Castle anyone? But this upgrade to Snow Leopard has pissed away a day. Argh. So much not working right. Double argh. Every time I have upgraded in the past everything has worked better, not worse. Triple Argh.

I am old enough to have treated many an endocarditis without benefit of echocardiography. Really. There was once a time when we did not have an ECHO and had to rely on physical and, most importantly, positive blood cultures for an organism that is known to cause endocarditis. I also walked to the hospital, uphill and barefoot in the snow and made my own penicillin from mould that grew on old bread and coffee grounds.

These days there is a shift in how medicine is done. Back in the day, we were trained to do things a step at a time and wait for results before moving on to the next test. However, that would lead to a prolonged length of stay and the real cost, I am told, is keeping people in the hospital. As a result, it seems that every possible test is done on every patient to reach a diagnosis as fast as possible.

So as result, if you have someone with a risk for endocarditis, you do not wait for the blood cultures to come back positive to order an ECHO to 'rule out endocarditis.’ Sometimes, even if they do not have a risk for endocarditis, an ECHO may be ordered. If I had my way I would never allow an ECHO that had the indication ‘rule out endocarditis.’

The problem is that an ECHO in the absence of the classic findings of endocarditis, like, say, positive blood cultures and emboli, is of little utility and is more likely to have a false rather than a true positive. If your pretest probability of a disease is low, the chance that a test is a true positive is low.

Like today. Patient has end-stage liver disease and comes in septic. ECHO, to rule out endocarditis, shows a possible abnormality. Blood cultures grow E. coli and the patient responds rapidly to therapy. There are, since 1909, 36 cases of native valve endocarditis reported in the literature due to E. coli. Given the maybe 250,000 cases of E. coli bacteremia in the US each year, the odds that the questionable goober on the valve is due to infection from E. coli is neither clinically nor statistically likely. The patient goes on to a TEE which shows a sclerotic valve. No endocarditis. No surprise.

Endocarditis is still a mostly clinical diagnosis, based on sustained positive blood cultures, exam and risks. The ECHO never need be done to ‘rule out' endocarditis.

“Thus echocardiography is useful in confirming the clinical diagnosis of infective endocarditis, but only rarely detects vegetations in patients who lack the characteristic clinical features of endocarditis, regardless of whether they have positive negative blood cultures.”

A waste of time and money, both of which are better spent on ID docs.

Rationalization

Clin Microbiol Infect. 2007 Feb;13(2):216. Escherichia coli native valve endocarditis (http://www.ncbi.nlm.nih.gov/pubmed/16643514)

Eur Heart J. 1984 Oct;5 Suppl C:53-7. The role of echocardiography in suspected bacterial endocarditis. (http://www.ncbi.nlm.nih.gov/pubmed/6519087)

Something Wicked This Way Comes

Published 4 Sep 2009

One of the last patients I saw before vacation was an elderly female with end-stage liver disease who was admitted with several days of progressive shortness of breath. Her liver disease was due to some autoimmune process and she had recently been started on moderate doses of prednisone, but her bilirubin continued to climb and was 19 when I saw her.

She had been on a ventilator for a few days, afebrile, but with increasing oxygen requirements and her CXR had bilateral infiltrates that looked more like congestive heart failure than infection.

She had no risks for odd infections (travel, etc.) and all her cultures were negative. Her bronchoscopy was growing a yeast to be identified, but Candida is common in the upper airway, and can be ignored in the sputum of about 99.99%, or more, of patients.

I ordered diagnostic tests looking for the typical atypical organisms that cause culture negative pneumonia and left for vacation. Within the next 24 hours the patient had died.

Several days later her sputum grew not Candida, but Cryptococcus gattii. They sent some of her blood for testing, but the serum cryptococcal antigen was negative, so this was primary cryptococcal pneumonia.

There are two types of Cryptococcus: neoformans, which has been around forever, and gattii, named for the NY mob boss, which is new to North America. Cryptococcus gattii came to Vancouver Island at the beginning of the century from the tropics and, thanks to the prevailing winds and an inattentive border patrol, _C_ . gattii has slowly been moving south. Unlike neoformans, which grows in eucalyptus trees (and is a significant pathogen in koalas; one would have thought they would have evolved resistance since they live entirely on eucalyptus leaves. That is the last time I am going to let the kids complain about eating leftovers), Cryptococcus gattii likes to live in firs, and there is no shortage of firs in the great Pacific Northwest. Next year the IDSA meetings are in Vancouver, BC. If I go, I am not going to inhale.

Recent reports in Emerging Infection Diseases suggest that _C._ gattii is increasingly common in Washington and Oregon (you can tell when someone is not from around these parts as they call it Washington State not Washington. The capital is Washington DC. And there is no ‘r’ in Washington. Unlike neoformans, _C_. gattii likes to infect normal people as well as the immunoincompetent and is also more refractory to treatment. A bad combination.

Looks like after years of being relatively dull, Oregon may be perking up with odd infections. Just don't tell any potential tourists. The joke used to be “What is the difference between Oregon and yogurt? Yogurt has culture. No longer.

Rationalization

Spread of Cryptococcus gattii into Pacific Northwest region of the United States (http://www.cdc.gov/EID/content/15/8/1185.htm). Emerg Infect Dis. 2009 Aug.

The Misery of a Mystery

Published 6 Sep 2009

I get to work the three-day weekend, lucky me. But things are not too bad, a few consults each day, and my kids have reached that age where they prefer to spend time with their friends rather than with their dorky parents.

I had left one hospital today and was on my way to the next when I got called back to the ER to look at a most peculiar case.

For five days he has had bilateral red, swollen very painful ears, both his arms have a rash and he has some anterior chest pain.

Exam? Funny you should ask. Both his ears have rumor, dolor, calor, tumor, with some subcutaneous ecchymosis but no blisters. The arms look like a folliculitis, if anything, with crusting. His sternoclavicular joint is tender to palpation.

Labs are OK, rest of exam negative, no past medical history of note. He does not look systemically ill, like patients with a serious infection.

What the hell is it?

If it is Zoster (Shingles), it is bilateral and Zoster is never bilateral, and there is no lesions that look like Chicken Pox.

Relapsing polychondritis? Would explain the ears and the chest wall tenderness, but not the rash, although the interwebs give a variety of rashes with polychondritis. And he has not relapsed yet.

Cellulitis? Never, ever, bilateral, and why the ears? Does not look like a strep infection and he is non-toxic.

The one hint, maybe, perhaps, is that he lives on a boat and 24 hours before the onset he had taken a bath in the Columbia river. Rivers are not the cleanest source of water, even in the Pacific NW.

Aeromonas ? It could be, especially with the ecchymosis. Aeromonas is a fresh water organism that causes a cellulitis, but why the bilateral ears and arm involvement? And I think of Aeromonas as a systemic illness with more local tissue damage.

What is it? I'll be damned if I know. I await cultures with interest.

Rationalization

J Infect. 2000 May;40(3):267-73. Clinical features and therapeutic implications of 104 episodes of monomicrobial Aeromonas bacteraemia. (http://www.ncbi.nlm.nih.gov/pubmed/10908022)

Postscript: I never did get a diagnosis. Where is House when you need him?

26 Nov 2010

That is it. One year of Puswhispering. I continue to whisper to pus about every other day over at Medscape.com if this has been an insufficient amount of infectious diseases blathering.

And the amazing thing? Something different every post. ID is so cool.

There will be a year two, and a yaer three until I die or retire, which ever is first.