Dedication

To Bradley, my youngest.

He will likely never read this.

Foreword

The pus keeps flowing.

Here are the collected Medscape essays from September 2013 to September 2014 year 6 of my blog.

I am now to be called the Head of the Morbers

Sep 2, 2013

I had call for the three-day weekend, it is a holiday, and I feel like slacking and grilling instead of writing a blog entry.

Still, while doing my Puscast this afternoon I came across a wonderful article in Emerging Infectious Diseases, Quinto Tiberio Angelerio and New Measures for Controlling Plague in 16th-Century Alghero, Sardinia. One of the many fun aspects of ID is its history. Infections, unlike other diseases, have a long and rich history.

I hope to use the following as a basis for infection control in the hospital, especially for MRSA. Everywhere they mention plague, I substituted MRDO. I especially like XXIII as it relates to cats. The more things change, the more they stay the same.

And call me Head of the Morbers.

MRDO Guidelines

I Because the disease is considered a divine punishment, fasts, prayers, vows, and good actions are prescribed to appease the wrath of God.

II The town must be divided into 10 wards. Each ward must be controlled by a Health Deputy, a person with a high reputation who is invested with full powers. The Health Deputies have the power and the means to 1) punish disobedient citizens without the need to ask for any Magistrate’s advice; 2) set fire to all objects suspected to be infected with MRDO; 3) close the houses in which MRDO casualties had occurred; and 4) provide the guards and adopt any mandatory measure needed to guarantee the public health.

III Through edicts, the population must be warned that citizens who do not declare new MRDO cases—cases that occur in their houses and in other houses—within 6 hours will be prosecuted.

IV It is strictly forbidden to have contact with a person suspected to have contracted MRDO before a physician has ruled out the suspicion.

V The MRDO hospital must be kept closed by establishing strict guards, thus avoiding the risk that MRDO patients will mingle with the rest of the population. All patients will be provided all supplies and medicine needed.

VI The Health Deputies and the Morbers must gather twice a day in the so-called “City House” to follow the course of the epidemic and to transmit the information to the Councilors who are assisted by the physicians.

VII Fire must be set to mattresses, fittings, and furniture from all houses in which MRDO cases have been registered.

VIII If paupers become ill of a “common” disease and do not want to leave their houses, the city government must provide them with the supplies and medicine that are commonly guaranteed in the hospital.

IX Meetings, dances, and entertainments are strictly forbidden.

X When a person is suspected to have died of MRDO, the corpse must be checked by physicians or surgeons to establish whether the deceased person actually died of MRDO. If the cause of the death is indeed MRDO, the relatives of the deceased person must carry the corpse in the courtyard or leave it outside the door.

XI Two secluded infirmaries must be chosen where persons with MRDO or suspected to have MRDO can be isolated. Until these sites are assigned, these persons will be allowed to live in their own houses. However, they should keep themselves separate from the rest of their families as much as possible. Guards will watch over their houses.

XII Gravediggers should be selected from among persons who had contracted and survived MRDO during a previous outbreak in another town. Gravediggers must live separately from the rest of the community and far from the hospital. They are not allowed to leave their houses unless accompanied by a Health Deputy.

XIII Furniture and fittings that are not used must be put aside so that they do not get infected; this will occur until the whole city undergoes disinfection.

XIV The Councilors and the Jurors of the city of Barcelona (with whom the city has many commercial exchanges) must be immediately informed that a MRDO outbreak is occurring in Alghero.

XV Selling entrails of old animals, meat from ill animals, pool fishes, and any other kind of low-quality meat is forbidden.

XVI Each day, the Morbers and the physicians are compelled to visit all houses suspected to have MRDO patients and to arrange the hospitalization of these persons into the isolation center.

XVII Persons from a house with persons suspected to have MRDO are forbidden to leave their premises to reach the core of the city. The Morbers are charged to fulfill their needs.

XVIII If MRDO affects a person living in a house suspected to have persons with MRDO, gravediggers must take the patient to the hospital or to the isolation place by moving him/her and the bed in which he/she lies. Leaving a MRDO patient in his/her own house is absolutely forbidden. The transfer to the tancat has to take place immediately. If the patient is a distinguished person, he is allowed to stay in his own house.

XIX A red cross must be painted on the doors of houses known or suspected to have persons with MRDO so that the rest of the population will keep its distance.

XX The surgeons are not allowed to leave the hospital or the isolation center. They are allowed to leave those structures only to assist other MRDO patients, and they must be accompanied by the Morbers and the guards.

XXI Trustworthy persons must be elected to stay in the isolation center and to assist MRDO patients.

XXII The pharmacists must provide the poorest with the necessary treatments. A list of the supplied treatments and a list of the citizens must be kept to distinguish between the poorer and the richer. The richer will pay for their treatments, and the city government will pay for the paupers.

XXIII The city must be cleaned every week from rags and dead things; leather not tanned and rotten raw wool must be put in isolated places; turkeys and cats must be killed and thrown in the sea.

XXIV It is compulsory to use the Armenian bole for the disinfection of wells and wine casks. Every month, a sack of Armenian bole must be poured in each well. A certain amount also must be added to the wine casks so that they are preserved from the bad quality and corruption of the MRDO humors.

XXV A good supply of wood must be provided to light fires in the city and in the houses during the days and nights. Persons must wear perfumes to eliminate or to mitigate the bad quality of the corrupted air.

XXVI Fire must be set to the infected objects with no peculiar value. High-value furniture must be washed; exposed to the wind; or even better, disinfected in dry heated stoves/ovens.

XXVII Frequent inventories must be carried out in the pharmacies to guarantee a large stock of medicines and their availability.

XXVIII Proclamations must be performed to prevent the citizens from going out of their premises and not move from one house to another. It is forbidden to set fire to furniture and fittings without the respective permission. Those not complying with these instructions will be prosecuted.

XXIX Bells must be rung and cannon balls and artillery fired to purify the air.

XXX When the physicians diagnose a new MRDO case, the Morbers must be immediately alerted. They will have the custody of the patient and will take care of him/her.

XXXI It is compulsory to shut the windows and close the doors of all houses when a person with MRDO or suspected to have MRDO is taken to the tancat or to the lazaretto or when a person who died of MRDO is taken to the cemetery. Perfumes must be worn and bells must be rung so that the citizens pay attention not to contract the bad air (disaura) and, hence, the contagion.

XXXII It is mandatory to bury MRDO victims within 6 hours after their death. The corpses must be buried in secluded cemeteries. Long and deep trenches must be excavated, and the corpses must be covered with lime to avoid the air corruption and mephitic vapors. It is forbidden to bury MRDO victims inside the churches. Citizens who die outside the city walls must be buried in secluded areas.

XXXIII During the Mass, it is highly recommended to be careful when shaking hands in token of peace.

XXXIV The beggars and the homeless must be kept outside the city walls during the day to reduce as much as possible their contact with other citizens.

XXXV All citizens are compelled not to leave their houses. Only 1 member per household is allowed to go out for shopping. Permission to go out has to be granted by the Morber of the area.

XXXVI People allowed to go out must bear with them a cane measuring 6 feet long. It is mandatory that people keep this distance from one another.

XXXVII Physicians are compelled to visit all patients. The richest will pay in due time, and the city Councilors will provide for the poorest.

XXXVIII A large rail, called parabanda, must be positioned in front of the counters in the shops in which meat, bread, wine, and foodstuff are sold so that citizens will keep their distance from the counter itself.

XXXIX It is mandatory to keep dry stoves/ovens always on. These stoves/ovens are similar to those used to cook the flat tiles (rejolas). The oven’s chamber must be filled with infected textiles/objects after those ones have been washed under the Morbers’ supervision. The chamber must be constantly heated by an underlying lighted fire.

XL To allow people to confess, 3-window portable confessionals must be prepared. Two windows are positioned laterally and 1 anteriorly so that the confessor is not reached by the patients’ bad breath. For the confessor’s sake, the confessional must be perfumed and kept locked in a chapel not accessible to the common people. When sacraments are administered, the confessional must be transported by the gravediggers directly at the patient’s bedside and must be taken immediately back to the chapel.

XLI The weekly Head of the Morbers is charged to list all the things entering the lazaretto and the tancat during the week and to attend to all the patients’ needs. Similarly, the Morbers are charged to fulfill the needs of persons suspected to have MRDO who must stay isolated in their own houses and watched over by the guards.

XLII The weekly Head of the Morbers must keep the inventory of all the beds, fittings, and furniture that enter into the tancat and the lazaretto. Things showing a good state of preservation will be used to fulfill the patients’ needs, whereas the rest will be burned to avoid the spread of contagion and to avoid robberies.

XLIII Citizens are forbidden to attempt to cure themselves in their own premises. All ill persons and persons suspected to have MRDO must be carried to the tancat or to the lazaretto. Guards must accompany these persons and keep other citizens away during the transfer.

XLIV All infected textiles and objects from the lazaretto must undergo laundry and then disinfection in the dry oven.

XLV During summertime, bonfires must be set in wooden areas to purify the air taking care not to damage the land’s owners.

XLVI Infected infants who are orphans or do not have a wet nurse must be bottle fed by using the milk of well-fed goats. For this purpose, goats will be allowed to live inside the lazaretto.

XLVII The buboes of MRDO patients must be cut open or cauterized. Those who are reluctant must be tied so that surgeons can intervene.

XLVIII People suspected to be infected and convalescents must undergo quarantine before they are allowed to get back in contact with healthy inhabitants.

XLIX When the MRDO epidemic is close to its end, a high number of male and female goats will have to be introduced within the city walls during the night. The animals will be placed inside the houses of the MRDO patients, and this operation will be repeated for several nights. However, for the population’s sake, the houses also will undergo whitewashing. Whitewashing will be performed by painters who survived the contagion. For the less suspected houses, it is required that the windows be kept wide open and that perfumes be sprayed and all surfaces washed with vinegar.

L People living in the surroundings are forbidden to enter the city walls unless their health status has been carefully checked and permission from the Morbers granted. The Morbers are entrusted to check that these persons’ belongings be washed and disinfected in the oven. Once these persons have been proved to be healthy, they will be admitted to live in their new houses but only after their own disinfection. Once they have settled down in their new houses, these persons are compelled to stay isolated from the rest of the population for some days.

LI The houses’ owners and the lodgers are compelled to disinfect, whitewash, ventilate, and water their residences. In case they do not attend the task, the city government will have to bear the costs.

LII It is strictly forbidden to sell linen, silk, cotton, and wool textiles without permission from the Morber of the area.

LIII The Morbers are compelled to carry out the complete disinfection of the city afterward and house after house. The darkest houses and those lacking aeration will be whitewashed, perfumed, and cleaned with vinegar. Bonfires will be set all around. Similar precautions will be applied to the houses whose walls are covered with golden slivers and leathers. Silk, cotton, linen, and woolly textiles must be washed and disinfected in the oven.

LIV Once all these precautions have been taken, the Councilors, the Deputies, the hospital attendants, and the physician Angelerio himself [the other anonymous physician had already died of the MRDO] must visit all the Alghero inhabitants, house after house. The citizens will be asked under oath if the Morbers had indeed disinfected their houses properly. In case disinfection had not properly been performed, another will be carried out within the following 6 days.

LXV It is compulsory that all citizens expose to the wind the furniture and fittings from their houses for 10 days. When the Counselors visit the citizens, at the end of the epidemic, everything must be in order.

LXVI Each citizen who is aware that his neighbors have not carried out the disinfection properly must notify it to the Councilors and Morbers. The latter will keep the secret and will pay the honest citizen with a money consideration.

LXVII It is compulsory to disinfect the tancat and the lazaretto located outside the city walls by using the same methods described in Instruction LIII. Fire must be set to every object kept inside the above structures. The persons who have survived and complied with the quarantine will be allowed to return to the city wearing new and disinfected clothes. The main city hospital, Sant’ Antonio, must be disinfected and reordered. The hospital will be reopened to all the population and will go back to its standard use.

Rationalization

Quinto Tiberio Angelerio and New Measures for Controlling Plague in 16th-Century Alghero, Sardinia

(<https: data-preserve-html-node="true"//wwwnc.cdc.gov/eid/article/19/9/12-0311_article>)

The Yeast Tells All

Sep 4, 2013

Cultures don't lie, and, according to Rasheed Wallace, neither does the ball. The name of the bug will often give a hint as to why the patient has a particular infection.

The patient has an aortic aneurysm repair, and post-op has multiple medical issues including pneumonia with a recurrent empyema. The cultures? They grew C. albicans and Lactobacillus. So, there is one reason why those organisms, especially the Candida, gets into the pleural space. There has to be an esophageal-pleural fistula. Has to.

So, we ordered a gastrograffin study and sure enough at the bottom of the esophagus was a leak into the pleural space. It is distant from the AAA repair, so why there was a hole is not certain. And of note, the nurse noticed that every time the patient tried to vomit the quality of the chest tube drainage altered to a greenish tinge.

Years ago, I was called about a Candida empyema. I told the nurse to give the patient a little methylene blue, and I would be in a bit to see the patient. When I arrived, the chest tube fluid was blue.

Oh, said the nurse after I pointed out the reason the fluid was blue. That's why the chest tube output went up every time he had a glass of water.

In the OR they repaired the leak, but no good explanation for why is forthcoming, although he had many procedures down the esophagus and it would be hard to credit which one, if any, led to the hole.

I suspect the Lactobacillus was probiotic in origin as it is very rare to find that organism in the pleural space and another suggestion of a leak, although it did not occur to me at the time.

Surgical repair and antibiotics and the patient slowly improved.

Cultures don't lie if you know what they are trying to tell you.

Rationalization

Eur Respir J. 1989 Nov;2(10):1021. Lactobacilli and pleuropulmonary infection.

https://www.ncbi.nlm.nih.gov/pubmed/2606189

Ann Fr Anesth Reanim. 2003 May;22(5):470-3. [Candida albicans induced empyema: mode of revelation of a spontaneous oesophageal disrupture].

<https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/12831975>

Does the Ball Lie? A Review

https://www.theringer.com/2017/3/1/16046350/does-the-ball-lie-1b09e7bebe48

Jon Snow Redux

Sep 6, 2013

Although the variety of ID in phenomenal, there are some diseases that recur. S. aureus pays my mortgage, and if there is one organism that is my arch enemy, it would be S. aureus.

ID is also unusual as competency and knowledge of infections for non-specialists gradually shifts from knowing what they are doing to totally messing up, and for many docs, it is like slowing boiling a frog. Before they are aware, they have crossed into Jon Snow territory.

And S. aureus is the one bug where people mess up the most. Recently I had a twofer. A patient is admitted with recurring MSSA bacteremia after receiving 2 weeks of vancomycin for a dialysis catheter infection where the catheter was not removed. Another who was about to be sent home on 10 days of oral TMP-Sulfa for MRSA bacteremia from a boil.

It is a sign of my age that this just irritates the hell out of me. It is not like there is no data on how to approach S. aureus bacteremia or that my colleagues and I are a page away.

Here are some rules with S. aureus bacteremia to help guide you. References available upon searching PubMed, and how hard is that? Evidently very. There are exceptions, subtleties, and nuance to all of these rules, of course. But if you have not mastered the rules, you are not ready for the exceptions. Ask your local ID doc for clarification. There is only one rule in medicine that is 100% (1).

\1) Community acquired S. aureus bacteremia with no focus is ALWAYS endocarditis. Period. No matter what the ECHO etc.

\2) S. aureus in the urine gets there hematogenously about 30% of the time. It is not S. aureus urosepsis, it is S. aureus sepsis seeding the urine

\3) S. aureus bacteremia ALWAYS gets iv therapy. Or another way to think about it: never treat with oral antibiotics.

\4) NEVER give a non-beta-lactam (usually vancomycin) for MSSA for ease of use. Vancomycin has a 30% higher failure rate. And never, ever, use clindamycin.

\5) NEVER give a beta-lactam that is not cefazolin or nafcillin/oxacillin for MSSA. Anti-staphylococcal beta-lactams are superior to all other agents for MSSA.

5a) If the MIC to vancomycin is 1.0 or greater, depending on the infection and host, consider an alternative antibiotic. Which one? Ask ID.

\6) If the patient has endovascular hardware, usually a valve or pacer, the endovascular hardware is presumed infected. And if the line is the source, pull the damn line.

\7) The only patient who gets two weeks of IV for bacteremia is a totally normal host with a removable focus, usually a line or cellulitis/abscess, and has MSSA. Everyone else should get at least 4 weeks of IV therapy.

\8) In the literature ID consultation for S. aureus bacteremia results in less cost and better outcomes in multiple studies and phone consults are not equal to a formal consult.

Seriously. We know more than you about the topic. I used to think that was not the case, but given what I have seen the last few months, I am not so certain it applies to everyone.

And if you are bored, take the opportunity to email this to, well, you know who needs it.

(1) The only rule that is 100%? Anyone who refers to antibiotics as 'strong', 'big gun' or 'powerful' is an idjet who truly knows nothing about the treatment of infectious diseases. I have yet to find an exception.

That is Sodium with an 'N'

Sep 10, 2013

I have a love-hate with infections. I love the challenge of diagnosis, but I hate the morbidity and mortality of infections. Most of the great cases I write about are someone else's disaster. Kind of awful really.

TB is the disease I hate and love the most. As a diagnostic and therapeutic challenge, few diseases are as tricky and subtle, which is fun as a doctor. For human misery, few diseases have had the impact of TB, perhaps second only to malaria. And after all this time our ability to diagnose the infection with alacrity stinks on ice.

The patient is a young male from West Africa who has 2 weeks of fever, an upper lobe infiltrate on CT and CXR, a positive QuantiFERON and a low sodium. But no pulmonary symptoms.

Other facts: no old chest films. Maybe a negative one 7 years ago in Spain. Oddly, they will not send me to collect the old films.

Maybe a negative ppd 3 years ago when he came to the US. Maybe. He is uncertain.

So is this TB? Is it progressive primary disease? Early reactivation? Old inactive Tb and scarring.

I don't know. It would be so much easier if there were an old CXR or a quick and easy way to diagnose TB.

What sways me in the end is the low sodium. There is no reason for the low sodium, and it is a common manifestation of pulmonary TB, and in the old days TB was the most common cause of Addison's.

"The mean serum sodium concentration was 134.54 ± 4.95 mmol/L and more than half of subjects (51%) have shown hyponatremia."

Right where his sodium has been all week. And when you look up sodium do you go to 'N' in the dictionary? And 'K' for potassium? I do.

So, I suggested we get a bronchoscopy to make sure there is no active TB. I hate sending people to bronchoscopy to make the diagnosis, but it is the only way in this case. I am also biased as I had a similar case this year that grew MTB on cultures and that patient did not even have a fever.

It could also be M. africanum, which is endemic in West Africa. Which would also make it funner. Yes funner. I'll let you know if I remember.

Rationalization

Hyponatremia due to pulmonary tuberculosis: review of 200 cases. Jonaidi Jafari N, Izadi M, Sarrafzadeh F, Heidari A, Ranjbar R, Saburi A.Nephrourol Mon. 2013 Winter;5(1):687-91. doi: 10.5812/numonthly.7091. Epub 2012 Dec 15.

<https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/23577332>

PLoS Negl Trop Dis. 2010 Sep 28;4(9):e744. doi: 10.1371/journal.pntd.0000744. Mycobacterium africanum--review of an important cause of human tuberculosis in West Africa.

https://www.ncbi.nlm.nih.gov/pubmed/20927191

POLL RESULTS

I have a love-hate relationship with

• TB 11%
• My significant other. 5%
• Medicine. 27%
• Insurance companies. No wait. That would be hate-hate. 42%
• Mass produced lagers. 11%
• Other Answers 4%
  • chicken wings

Big and Cold

Sep 11, 2013

104 today in Portland. Hot for a September day in the Great Pacific Northwest and I am going to let it cool off before I go my daily constitutional.

I expect heat at work. Rubor, dolor, calor, tumor describe infections, and this blog. Red, painful, hot, and swollen. My gaster is always flabbered when infections fail to inflame and are cold.

Three years ago, I treated the patient, successfully, for a RUQ Pseudomonas infection as a complication of a kidney transplant. Since then, she has had no issues. Then over the next month, she had progressive RUQ pain. No fevers, no chills, no other symptoms but a progressive pain and then decreased intake as eventually eating increased the pain.

Finally, she saw her doc who got a CT: big abscess in the RUQ. No fevers, no leukocytosis, no nothing. The patient was admitted for diagnosis and treatment of the abscess.

No exposure or other history to suggest an opportunistic infection related to her immunosuppressives and her exam is only modestly tender in the RUQ. No way is it Pseudomonas again after all this time and her lack of symptoms. It will be something indolent, coagulase-negative Staphylococcus or P. acnes, and I put by money on the latter given its propensity to manifest years after inoculation. Maybe actinomycosis or even Nocarida. So IR (not the baboon) drains a liter plus of pus. The patient feels much better, and it grows...

MRSA. Did not see that coming.

Cold abscesses are classically due to TB, especially of the spine, but I sometimes see them due to S. aureus and it always surprises me. My first case was over 30 years ago as an intern in a patient who had what was thought to be a Pancoast tumor but turned out to have a cold S. aureus abscess. And every couple of years I see a huge abscess that lacks rubor, dolor, calor with maybe a touch of tumor. And it is S. aureus.

Cold abscesses due to a smattering of other bacteria are reported in the Pubmeds, but S. aureus does not occur with the frequency that my confirmation bias would expect.

IR and antibiotics and the patient improves.

Rationalization

Pacing Clin Electrophysiol. 1985 Nov;8(6):897-9. Osteomyelitis of the first rib presenting as a cold abscess nine months after subclavian venous catheterization.

https://www.ncbi.nlm.nih.gov/pubmed/2415943

J Surg Tech Case Rep. 2012 Jul;4(2):115-7. doi: 10.4103/2006-8808.110254. Melioidosis of chest wall masquerading as a tubercular cold abscess.

<https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pmc/articles/PMC3673354/>

I am Weasel

<https: data-preserve-html-node="true"//en.wikipedia.org/wiki/I_Am_WeaselCharacters>

It's the Iron, Man

Sep 13, 2013

The patient is an elderly male who presents with fevers, rigors, and MOSF. His blood cultures, over the next 24 hours, are repeatedly positive for MSSA.

Presumptive endocarditis: community-acquired S. aureus bacteremia with no focus. Been there, done that. And the TTE is suggestive for a mitral valve vegetation.

But is it without a focus? He has been getting monthly iron shots from his PMD, and the episodes started within an hour of the last injection. He is convinced the infection is due to the injection.

Could be. He has no rubor, dolor, calor or tumor over the injection site, but cutaneous trauma is a good way for S. aureus to gain access to the vascular system, so I might grant that.

And the iron. Iron is an important growth factor for pathogens, and the body keeps it tightly sequestered from bacteremia. Iron overload states increase the risk of many infections, but how about iron dextran? Not much:

" A few small, human studies in a population with chronic kidney disease suggest a possible increased risk of developing an infection associated with intravenous iron; however, prospective human data directly linking intravenous iron to exacerbation of existing infection or infection-related mortality are lacking. In vitro data suggest that increased transferrin saturation related to iron administration may result in polymorphonuclear leukocyte dysfunction and decreased inhibition of bacterial growth. Sparse animal data have linked intravenous iron therapy with morbidity and mortality in sepsis models."

But I always fret when they give iron in the ICU to septic patients. And it may have helped the S. aureus get a toe hold. S. aureus needs iron and has systems in place to get it from humans. If given a free lunch, it may have taken advantage of the situation, although I can find no PubMed examples of S. aureus infections directly attributable to iv/im iron use as opposed to iron-overload states.

Probably a perfect storm: trauma plus iron plus an aged immune system and then endocarditis.

Rationalization

Ann Pharmacother. 2007 Sep;41(9):1476-80. Epub 2007 Jul 31. Risk of infection with intravenous iron therapy.

https://www.ncbi.nlm.nih.gov/pubmed/17666575

J Vis Exp. 2013 Feb 7;(72). pii: 50072. doi: 10.3791/50072. Staphylococcus aureus growth using human hemoglobin as an iron source.

https://www.ncbi.nlm.nih.gov/pubmed/23426144

Microbes Infect. 2012 Mar;14(3):217-27. doi: 10.1016/j.micinf.2011.11.001. Epub 2011 Nov 15. A battle for iron: host sequestration and Staphylococcus aureus acquisition.

https://www.ncbi.nlm.nih.gov/pubmed/22123296

Prog Transplant. 2007 Dec;17(4):332-6. Hepatic iron content and the risk of Staphylococcus aureus bacteremia in liver transplant recipients.

https://www.ncbi.nlm.nih.gov/pubmed/18240700

Science. 2004 Sep 10;305(5690):1626-8. Iron-source preference of Staphylococcus aureus infections.

https://www.ncbi.nlm.nih.gov/pubmed/15361626

The RUQ sucks. Or so I was always told.

Sep 16, 2013

The patient had a cecum resection that resulted i an anastomotic leak. The leak was repaired, but she represented with RUQ pain, fever, and leukocytosis.

A CT showed a large abscess between the diaphragm and the liver. It is drained and grows colon bugs. The microbiology is no surprise. But why the abscess so far from the original insult?

Curtis and Fitz-Hugh noted the propensity for Gonorrhea to travel from the fallopian tubes all the way to perihepatic space. Their original descriptions make for interesting reading.

Supposedly respiration leads to a negative pressure in the RUQ and infection and cancer metastases are sucked into the area. The RUQ has the lowest pressure and sucks the most.

I found multiple statements to the effect that

"The location of intra-peritoneal spread of disease is influenced by gravity and the negative sub-diaphragmatic pressure caused by respiratory motion."

But I can't find the original measurements and papers that demonstrate the RUQ slurping up infectious material. Maybe my Google-fu is off. Or maybe it is as Stephen Jay Gould said:

"No scientific falsehood is more difficult to expunge than textbook dogma endlessly repeated in tabular epitome without the original data."

So if the RUQ truly sucks, I can't find the proof. I am sure someone will set me straight.

Rationalization

Am Surg. 2001 Mar;67(3):243-8. What is normal intra-abdominal pressure?

A CAUSE OF ADHESIONS IN THE RIGHT UPPER QUADRANT ARTHUR H. CURTIS, M.D. JAMA. 1930;94(16):1221-1222. doi:10.1001/jama.1930.02710420033012.

https://jamanetwork.com/journals/jama/article-abstract/235357

ACUTE GONOCOCCIC PERITONITIS OF THE RIGHT UPPER QUADRANT IN WOMEN THOMAS FITZ-HUGH Jr., M.D. JAMA.1934;102(25):2094-2096. doi:10.1001/jama.1934.02750250020010.

https://jamanetwork.com/journals/jama/article-abstract/251262

Patterns of peritoneal spread of tumor in the abdomen and pelvis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650201/

Cow Pie

Sep 18, 2013

I do not know why you get up every day and trudge off to work. The fame? The glory? The money? A lack of better options? Me? I just have a great job. I work with good people in good hospitals, and I fell into a subspecialty that suits my temperament. I say fell, since 32 years ago I did an ID rotation as a fourth-year medical student as a fluke, the rotation I had wanted to do not being available. I was hooked by the end of the four weeks and have never looked back.

ID has novelty, and I am bored very easily. As this blog amply demonstrates, ID has variety. ID cures, and longitudinal care, while nice, is not high on my professional needs. I am very much a fix it and move on kind of person.

But above all, I like to figure things out. Either the diagnosis or why the patient has a given infection. If you spend even a little time on the Pubmeds or the Googles, there is no end of information you can discover if you have even a smidgeon of curiosity. There is an endless opportunity to learn.

Often it is the name of the bug that leads to the why and wherefore of the disease.

The patient has been on dialysis for a couple of years waiting for a transplant and comes in with fevers and chills. Almost certainly the catheter, all lines eventually break or get infected. You are not supposed to have a plastic tube in your chest for months at a time.

Gram-negative rods. Hm. Not usual, but not unexpected. Then the lab calls it Aeromonas hydrophila and they call me.

Sometimes taking a history is controlled aggravation. I want to jump straight to the question that might solve the case, but I remain patient and go through the routine. And at the end of the routine of travel, pets, diet, water exposure there is nothing.

But it is Aeromonas. There has to be a good water exposure.

So, no water I ask? No hot tubs, swimming pools, lakes, rivers, well water, non-city water?

Nope.

I ask, I tell the patient, because Aeromonas is a water bug. Freshwater. Have you been in freshwater?

I suppose third time is the charm because he then remembered that a few days before the onset of his illness he had been fishing along the banks of the Tillamook River and got up to his knees in muddy river water.

And Bingo was his name-o.

Tillamook, for those of you unlucky enough to live outside the great Pacific Northwest, is on the Oregon Coast and is famous for their cheese. The Tillamook High mascot, and Oregon does excel in lame mascots (my kids are the Aardvarks), is the Cheesemakers. The Tillamook River flows through a plain surrounded by cows, the source of milk for the most excellent cheddar. "The county has been called "a natural cow pasture" by Sunset Magazine." And cows make cow pies, which are an excellent source for Aeromonas, washing into the river with the perpetual Oregon rains.

Depending on the study and how they are isolated, 40 to 99% of cow pies contain Aeromonas, and it is often found in the water around cows.

So, I am calling the source of infection the cow pie water of the Tillamook, and there is no one to gainsay me.

I do not see many Aeromonas infections despite the surfeit of freshwater in the great Pacific NW. This is perhaps the 4th Aeromonas in 23 years. One was presumptive, a curbside from a nurse whose son had a wound infection after a muddy soccer game.

We removed the line, and the patient improved immediately and will receive a short course of antibiotics.

Rationalization

J Hyg (Lond). 1984 Jun;92(3):365-75. Aeromonas hydrophila in livestock: incidence, biochemical characteristics and antibiotic susceptibility.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129318/

Clin Infect Dis. 2004 Apr 15;38(8):1084-9. Epub 2004 Mar 29. Outbreak of Aeromonas hydrophila wound infections associated with mud football.

https://www.ncbi.nlm.nih.gov/pubmed/15095211

Tillamook River

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

Another Just So Story?

Sep 20, 2013

The patient is an IVDA, heroin, who comes in with fevers, severe abdominal pain, and both legs with a petechial rash that looks like lots of emboli. It is going to be endocarditis. What else?

Exam had no murmur and no emboli anywhere else, which is odd if it is emboli in the legs as they many should be found everywhere.

CT showed a section of small bowel, and a section of large bowel was thickened, but nothing in the kidneys and spleen. Also, odd to have abdominal emboli without the classic wedge-shaped lesions in the kidneys and spleen.

The patient was febrile once and but resolved after 24 hours, perhaps due to the vancomycin.

After several days the BC remained negative, and I am starting to get suspicious about the diagnosis.

Maybe it is fungal endocarditis, but the beta-glucan and the galactomannan are negative.

Is this a vasculitis? She has known hepatitis C, supposedly in remission. Abdominal pain is a common manifestation of vasculitis.

We finally get TEE (don't ask, there were a variety of issues with getting diagnostic studies accomplished in a timely manner) and the valves were pristine. But. There was a patent foramen ovale, allowing gradeaux to pass from the right to left side of the heart and then downstream to the legs.

Have you ever looked at pictures of black tar heroin? I hope you have not been seeing it in the wild due to personal use. It is nasty stuff, filled with all sorts of particulate matter. Ick.

"Heroin has several characteristics that affect how it is used and even how it is distributed: colour, physical state; water solubility, pH balance, heat stability, weight/volume and purity (Ciccarone & Bourgois, 2003). The colour palette of heroin is summed in the title of this paper: brown, black and white; with a high degree of spectral variability. The extremes of black and white are heroins stereotypically coming from Mexico and Southeast Asia, respectively. Brown heroin can come from any of the source regions, but typically is seen coming from Southwest Asia. Physically, most of the world's heroin is in powdered form; the only exception being the solid form of heroin coming from Mexico called "black tar" heroin. Water solubility varies, with type-4 heroin, a highly purified heroin traditionally stemming from Southeast Asia, having the highest water solubility. On the acid-base spectrum, the chemically basic form (pH > 7) of heroin comes exclusively from Afghanistan/Pakistan; all other heroin forms are in a chemically acidic (pH < 7) form. The basic form of heroin is heat stable; it therefore begins to burn and subsequently vaporize (sublime) at a higher temperature. Black tar heroin also appears somewhat heat stable. Powdered heroin, again most the world's heroin, is light with minimal volume by weight. Light weight/low volume heroin is distributed, as one would expect, over greater distances, usually by air transport, than the one solid heroin-black tar heroin. The heavier weight and higher volume black tar heroin is only distributed to the US and mostly by land routes. Distribution at the retail level also varies by physical form of heroin: powered heroins are sold in glassine folds or tiny plastic zip baggies, while solid black heroin is wrapped in plastic and sealed in tiny balloons for sale (unpublished data). Finally, heroin purity, while highly variable, seems to have some limits by form: black tar heroin seems to plateau at about 25-30% pure (National Drug Intelligence Center, 2000), which may have a purity limit based on manufacturing.

To sum up source and heroin type: Southeast Asian heroin is stereotypically white, powdered, highly water soluble and acidic; Southwest Asian heroin is typically a brown coarse powder with poor water solubility (until acidified from its basic form by the addition of an acid) and good heat stability; Colombian heroin is off-white to light brown, powdered and acidic with good water solubility; Mexican heroin is dark brown to black, solid, vaporisable, of lower purity and despite its acidity, requires heat to go into aqueous solution."

Heroin is not sterile by any means, and if cultured will grow a variety of microorganisms. See all the things you learn from this blog? It is why I so enjoy ID. So many opportunities to learn.

I wonder if what we are seeing is paradoxical emboli of particulate matter or infectious material. In the old days, when I was a resident, and all the heroin was white and adulterated with talc and dry milk, we would see many patients with pulmonary hypertension from talc getting wedged in the pulmonary vasculature. You kids today have much better-quality drugs. There is one case of disseminated granulomatosis disease due to a PFO reported, so my hypothesis is not entirely off base.

There was not enough to data to support the treatment of endocarditis, so I stopped the antibiotics and so far, there has been no relapse.

Rationalization

Am J Forensic Med Pathol. 1987 Dec;8(4):326-33. Disseminated granulomatosis through a patent foramen ovale in an intravenous drug user with pulmonary hypertension.

https://www.ncbi.nlm.nih.gov/pubmed/2449073

Am J Med. 1976 May 10;60(5):711-8.Intravenous injection of talc-containing drugs intended for oral use. A cause of pulmonary granulomatosis and pulmonary hypertension.

https://www.ncbi.nlm.nih.gov/pubmed/1020758

Int J Drug Policy. 2009 May;20(3):277-82. doi: 10.1016/j.drugpo.2008.08.003. Epub 2008 Oct 21. Heroin in brown, black and white: structural factors and medical consequences in the US heroin market.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704563/

A Microbiologic Second Puberty

Sep 23, 2013

The patient is an elderly male with has a routine CABG and sent home after an uneventful post-op course.

8 days later he is admitted short of breath, an ECHO showing tamponade physiology and he was taken off to the OR for a presumed hemopericardium.

No fevers, no chills, no constitutional symptoms. And no blood in the pericardial space. There was a large amount of slightly cloudy yellow fluid that after just a few days was growing lots of P. acnes.

Again.

I swear I never saw P. acnes in the last century, but it has been a common, and problematic, cause of all sorts of surgical infections.

It is problematic in that I can’t think of a way to prevent it. It is resistant to cefazolin and it lives in the oil of hair follicles, so it is protected from both topical antiseptics and the preoperative antibiotics. And it is why it occurs in men: we are the greasy, hairy gender.

Then a scalpel drags it into the joint or the back or the shunt or the hardware or the pericardium. Being part of the normal cutaneous microbiome, the immune system doesn’t recognize it as foreign with the same robust inflammation, so simmering without the classic signs of infection is common for the organism, sometimes taking years to manifest. P. acnes defines fester. BTW. It wasn’t until I was well into my 40s that I realized the origin/meaning of the name Uncle Fester.

It has been a long time since I have taken care of a case of bacterial pericarditis and all of mine have been either S. pneumoniae or S. aureus. Guess I am unusual (no comments from the gallery):

“The most frequently identified causative organisms were Propionibacterium acnes (P. acnes), staphylococci and streptococci. A common predisposing factor was an immune-compromised state, followed by cardiac surgery. Fifty-five patients were treated with antibiotics (medical group) while 63 cases (surgical group) underwent surgical drainage (pericardial window) and/or pericardiectomy… CONCLUSIONS: In contradistinction to the literature reports, the most prevalent organism for IP was P. acnes”

He is doing fine with drainage and antibiotics.

More and more P. acnes. I thought I was done with this bug when I was 14.

Rationalization

Acta Cardiol. 2009 Jun;64(3):297–302. Infectious pericarditis: an experience spanning a decade.

<https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/19593938>

Uncle Fester

https://en.wikipedia.org/wiki/Uncle\_Fester

Any Bug in Any Place

Sep 25, 2013

The patient is a middle-aged female with steroid dependent lupus related lung disease. She has been on prednisone for several years with no infectious complications until this admission when she developed the abrupt onset of a red, hot, swollen, tender leg. All of a sudden, whomp, the whole lower leg was involved, and she is admitted to the hospital, delirious with infection.

Besides the steroids and chronic edema, there is no unusual exposures to suggest some odd organism as the cause of the cellulitis, so I would have bet on S. pyogenes, and I would have lost the bet.

All the blood cultures grew Acinetobacter baumannii. The heck.

It is distinctly rare for gram-negative rods to cause a non-necrotizing soft tissue infection, but one or another does rear its ugly head every year or so, almost always in people with immunologic or bio-mechanical risks. in this case, I would blame the steroids.

Of course, any bug can cause any disease. Acinetobacter’s claim to fame is soft tissue infections after war-related trauma, but there are a number of reports of it causing soft tissue infections in civilians:

“Acinetobacter baumannii is rarely encountered as a pathogen causing community-acquired skin and soft tissue infection. A 79-year-old man had a fever for 3 days accompanied by pain and swelling over the left leg around an old scar caused by a dog bite 10 years ago. Two sets of blood cultures and a wound culture all yielded A. baumannii. The patient’s condition deteriorated initially but recovered completely after 3 weeks of meropenem treatment. This case suggests that A. baumannii should be included among pathogens with the potential to cause complicated skin infection in the community.”

I hate that last line and it, as well as similar sentences, should be banned from the literature. Someone gets some weird bug causing an infection, writes a paper, and then suggests it should be considered in cases in the future. No, it shouldn’t. Every bug is a potential pathogen; in medicine you treat the probable pathogens. And I bet the authors are going to bore their residents forever with each case of cellulitis. “It’s usually Group A Streptococcus, but I had this case of Acinetobacter once blah blah blah blah.” I know how Peppermint Patty feels.

When I find Acinetobacter I wonder about an environmental/water source, but history yielded little. She does live in a trailer park but does not use the holding tank for the water, getting it from a hose that is piped into the unit. Is that the source? Don’t know and cannot get a culture. Besides the well-known propensity to attract tornadoes (not) I can find no reported medical issues with mobile home/trailer parks on either the Googles or PubMed.

Antibiotics remain the wonder drug that works wonders (not ASA), and she improved rapidly with therapy.

Rationalization

J Formos Med Assoc. 2003 Sep;102(9):650–2. Community-acquired bacteremic cellulitis caused by Acinetobacter baumannii.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/14625612>

Charlie Brown's teacher

https://www.youtube.com/watch?v=q\_BU5hR9gXE

Some Things Change for the Better

Oct 7, 2013

I’m back from ID Weak. Sigh. Lots of CME but relatively little learnin’. With all the reading I do for the blog and podcast, I do a reasonably good job of keeping up in my field. Wheat mostly. Time spent for information gathered, meetings are really not efficient, but the eating in SF is almost as good as in PDX. And the rule still holds that every day away from work generates 2 days' worth of paperwork and lab results upon return.

There are occasionally talks with a historical perspective, and I enjoy those as I am now old enough to remember how things were back in the day. Medicine has changed dramatically over the course of my career. The first 15 years were marked by endless AIDS related deaths, and I have seen only one of AIDS death this century. I do not think I ever cured an invasive mold infection in the old days; now I am surprised if I can’t.

The patient is an elderly male with a hematologic malignancy, on prednisone, who comes in with a week of eye pain then double vision because of a partially fixed eye. He has no proptosis, and labs show a WBC of 0.8 from chemotherapy. Not good.

CT shows a mass in the adjacent sinus, and the medial eye muscles next to the sinus are edematous. Not good.

The worry is rhinocerebral mucor. I have only seen a pair, both last century and both fatal. It is one of those “Oh, expletive deleted” diagnoses where you expect nothing but badness. But that was then; this is now.

He received one antibiotic in each class, a technique usually reserved for surgical residents, and he was whisked off to the OR.

There was a large mass in the sinus that was debrided, and it was mostly mucous and some sort of mold on the gram stain and after a couple of days it grew Aspergillus. The patient did fabulously. It is amazing how well patients do with the newer azoles. And surgery. And stopping steroids. And having the WBC return with GCSF. But his pain vanished and his functioned returned, and he is now on an arbitrary but prolonged course of voriconazole. The good news is he is done with chemo for now, so I do have to worry about recurrence with more neutropenia.

While not as common as mucor, there are cases of rhinocerebral Aspergillus. My patient was lucky as the mold did not move beyond the extraocular muscles into the brain, and we could reverse much of his immunosuppression. But I still like me that voriconazole.

The newer azoles, the post ketoconazole medications (I guess some are not so new anymore), have slowly changed mycology treatment. One by one, cryptococcosis, coccidioidomycosis, histoplasmosis, aspergillosis, and mucormycosis have been picked off by evolving azoles, going from often fatal to often cured. It has been a welcome change.

Rationalization

BMJ Case Rep. 2013 Feb 5;2013. pii: bcr2012008552. doi: 10.1136/bcr–2013–008552. Rhinocerebral mucormycosis: literature review apropos of a rare entity

http://www.ncbi.nlm.nih.gov/pubmed/23389725

Indian J Otolaryngol Head Neck Surg. 1998 Jan;50(1):26–32. doi: 10.1007/BF02996763. Rhinocerebral invasive aspergillosis.

http://www.ncbi.nlm.nih.gov/pubmed/23119372

Probiotic Fail

Oct 9, 2013

Infections are a balance between the virulence of the organism, the efficacy of the antibiotics and, most importantly, the host response. Even the most pathetic of organisms can cause infections in the immunocompetent, and we are all an immune system away from being consumed by bacteria and fungi.

The patient is an AIDS patient, CD4s currently around 200, has a renal transplant who has three months of consumption: low-grade fevers, 30 lb. weight loss and fatigue but minimal pulmonary symptoms. A CXR finds a large thick-walled upper lobe lung abscess, confirmed on CT.

ID exposure history is bland, as is often the case here in the great Pacific NW, but a doubly immunosuppressed patient can have a wide variety of organisms causing a lung abscess. These are Captain Renault cases; I have to round up all the usual suspects.

And all the usual suspects were negative. No AFB, Fungi, no Rhodococcus, no nothing except the bacterial cultures from the bronchoscopy: 2 + gram-positive rods that, on quantitative cultures grew > 100,000 Lactobacillus most closely resembling L. salivarius.

Hard to believe the Lactobacillus is the pathogen, given no prior cases of human infections in the lung, but she responded nicely to ampicillin, so I am inclined to think it is the real deal.

Why? The host I assume, and there are a smattering of other Lactobacillus species causing lung abscesses and pneumonia, so it is not completely out of the picture.

L. salivarius is mostly used as a probiotic to prevent respiratory infections in some studies, although of questionable efficacy. I would call this an epic fail although he was not taking a probiotic preadmit and the organism can be found in the GI tract of humans. Any bug can and will infect any organ given the opportunity. I suppose to prevent antibiotic-associated diarrhea, all he needs do is cough and swallow.

Maybe she could get a course of po to cure the infection, but given a host, whose immune system was so poor that this wimpy organism could cause disease, I am going for a course of IV.

Rationalization

Int J Sport Nutr Exerc Metab. 2012 Aug;22(4):235–42. Epub 2012 May 10. Effects of a Lactobacillus salivarius probiotic intervention on infection, cold symptom duration and severity, and mucosal immunity in endurance athletes.

http://www.ncbi.nlm.nih.gov/pubmed/22645171

Pediatr Infect Dis J. 2013 Aug;32(8):810–4. doi: 10.1097/INF.0b013e31828df4f3. Probiotics and prebiotics in preventing episodes of acute otitis media in high-risk children: a randomized, double-blind, placebo-controlled study.

http://www.ncbi.nlm.nih.gov/pubmed/23429555

Thorax. 1992 Nov;47(11):992. Fatal lung abscess due to Lactobacillus casei ss rhamnosus.

http://www.ncbi.nlm.nih.gov/pubmed/1465766

Pharmacotherapy. 2002 Sep;22(9):1180–2. Lactobacillus species as a cause of ventilator-associated pneumonia in a critically ill trauma patient.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/12222555>

"Round Up The Usual Suspects!"

https://www.youtube.com/watch?v=vtSmfws0\_To

Stewardship

Oct 14, 2013

I have been doing antibiotic stewardship at one of my hospitals for about 4 months now. It is a one-person show. I review the chart of anyone on antibiotics for more than 72 hours and make suggestions. It is interesting to see what others are doing with antibiotics. Most are doing fine, but sometimes…

Infections are odd. No one would treat an MI without a cardiologist or cancer without an oncologist or deliver a baby without an obstetrician. But infections can and are treated by anyone, sometimes quite, well, creatively. Probably because infections slide from simple to over your head like boiling a frog, so gradually the treating physician doesn't even notice they cross the line into not knowing what the hell they are doing.

I know before physicians can perform conscious sedation; they have to take a test to prove they understand the process. Sometimes I think the same should be required before antibiotics can be prescribed. ID really is more than having access to the culture and sensitivity.

There are some common patterns:

\1) Antibiotics are rarely changed to less expensive/broad-spectrum therapy even if the susceptibilities allow.

\2) If evil bugs are not isolated (MRSA or the dread bacteria Pseudomonas), the vancomycin/anti-pseudomonal is continued since the patient improved.

\3) For some docs no organism can go untreated. Doesn't matter the source of the culture or the lack plausibility that the organism is causing disease. A bug is grown, and it must be treated.

\4) When a patient has an aspiration, metronidazole is given. This one, in particular, drives me nuts. Most of the time, an aspiration event is NOT the same as an aspiration pneumonia. The latter is usually a chronic lung abscess in someone with rotten teeth who loses consciousness.

And then there are the usual, same old same old approaches to infections. Back in 1989, a classic was published in the American Journal of Medicine: Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy. It was one the intellectual epiphanies of my career. I have discussed this article elsewhere. Everyone should read it, memorize it, and take to heart with the same passion they do their favorite basketball team. I think no one has.

The fallacies in antibiotic therapy are

• Broader is better.
• Failure to respond is failure to cover.
• When in doubt, change or add another.
• Sickness requires immediate treatment.
• Response implies diagnosis.
• Bigger disease, bigger drugs.
• Bigger disease, newer drugs.
• Antibiotics are non-toxic.

To which I will add my own.

• Once started, an antibiotic cannot be stopped.
• Once a class of antibiotic is started, you need to stay in class.
• Gotta double cover (i.e. give two antibiotics) a particular organism.

The primary reason a particular antibiotic is given is ‘I like it.’

As I wander the EMR doing antibiotic stewardship, we do a reasonably good job, but 24 years after publication I still run across all the above. Plus ça change, plus cest la même chose.

Rationalization

N Engl J Med. 1975 Dec 18;293(25):12915. Testing the physicians knowledge of antibiotic use: Self-assessment and learning via videotape.

http://www.ncbi.nlm.nih.gov/pubmed/1186823

Spoiler alert: Ygritte would have a field day.

Am J Med. 1989 Aug;87(2):2016. Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/2667357>

A Medical-Skeptical Classic

https://sciencebasedmedicine.org/a-medical-skeptical-classic/

I see it as often as a short-period comet

Oct 16, 2013

“If one is master of one thing and understands one thing well, one has at the same time, insight into and understanding of many things.” - Vincent Van Gogh

Once, for hoots and giggles, I added up the number of pathogens whose presentation and treatment I need to know for my job. I came up with 1375. A very rough estimate depending on whether you are a lumper or a splitter. There are over 2400 serotypes of Salmonella, but I counted that as one, even though not all Salmonella are the same in terms of pathogenicity.

So, call it 1300. Doesn’t seem like a lot to know to me, even when you add in all the antibiotics. Once you start adding in all the weird and wondrous permutations and the interactions with less interesting diseases, then the field rapidly becomes jaw-droppingly complex, maybe 1300 factorial? Or more. And damn near anything that can grow at 98.4 F is a potential pathogen if the immune system is compromised enough.

Most of my day is spent killing S. aureus, and the other bugs rear their ugly heads less often. Some bugs I see as often as a short-period comet, maybe every decade or so.

The patient comes in neutropenic from MDS, septic, and in MOSF. No good cause is found, and over a week's course in the ICU, he slowly improves. Then a fever to 103 and the WBC is 35,000 presumptively from the G-CSF. His ALP, which had been in the 300’s, goes to the 500’s and the blood cultures grow yeast.

I get all excited, as I often do when I think I am going to see an unusual manifestation of a pathogen. I tell the housestaff that this is going to be Candida albicans, and it is heptatosplenic Candida (HSC). Fevers, rebound leukocytosis, increase in the ALP. Gotta be. Classic I say, with the pompous assurance of the zebra hunting specialist as I explain the disease presentation, sometimes a Board topic, to the residents.

Well, Babe Ruth did lead the league in strikeouts

There was no HSC. The ALP was mostly chronic, and the increase WBC was from the stimulating factors. And the yeast? C. krusei. Have not seen that in a decade or more, another short-period comet, since I have no Wayampi Amerindians in my practice.

By contrast, Candida krusei and Saccharomyces cerevisiae were detected in over 30% of (Wayampi Amerindian) carriers.

While textbooks mention C. krusei as a cause of HSC, the Pubmeds yield nothing. Probably the government shutdown.

C. krusei is one those problematic Candida, with variable susceptibilities to all of the antifungals, most notoriously resistant to fluconazole. So we pulled all his lines (culture negative as were repeat blood cultures), and he responded rapidly to micafungin. We (I leave using the royal we) will finish up a 14-day course and call it good.

Rationalization

Mycoses. 2012 May;55(3):e74–84. doi: 10.1111/j.1439–0507.2012.02182.x. Epub 2012 Feb 24. New insights into hepatosplenic candidosis, a manifestation of chronic disseminated candidosis.

http://www.ncbi.nlm.nih.gov/pubmed/22360318

J Infect Dis. 2013 Sep 9. [Epub ahead of print] Candida albicans Is Not Always the Preferential Yeast Colonizing Humans: A Study in Wayampi Amerindians.

http://www.ncbi.nlm.nih.gov/pubmed/23904289

J Infect. 2013 Mar;66(3):278–84. doi: 10.1016/j.jinf.2012.11.002. Epub 2012 Nov 19. Risk factors and outcomes of Candida krusei bloodstream infection: a matched, case-control study.

http://www.ncbi.nlm.nih.gov/pubmed/23174708

Non falsifiable

Oct 21, 2013

All that is gold does not glitter,

Not all those who wander are lost;

Not all who are febrile are infected.

Antibiotics and cultures have cost.

~ JRR Tolkien

Someone mentioned in a review of my collected essays that my 'humor' tends to repeat itself. Guilty. Partly it is I cannot remember what I have written over the years of this blog and partly because I am just not that clever. I know I have used the above quote before, but some concepts are worth repeating. And repeating. Some days I feel like a Chatty Cathy doll, pull the string and I go on and on about, say, S. aureus bacteremia. Or the cause of fevers.

Fevers are a common result of many pathophysiologic pathways, and the wise doctor bears that in mind. Or me. I try to remember the noninfectious causes of fever, even when they are not particularly interesting.

Over the weekend, I had two cases of fever that I thought were not infectious in etiology.

One was an IVDA with MSSA righted sided endocarditis and TNTC septic pulmonary emboli who, after a week of therapy, remained febrile despite draining all the pus and correct antibiotics. It was the pattern of the fever that was suspect. Rather than the usual up and down hectic fever it was continuous, never falling below 39. I figured it might be drug fever, perhaps the famotidine, and I suggested that, among other interventions, they stop the H2 blocker and within 12 hours the fevers fell for the first time, and he remained afebrile.

For all of 18 hours. Then it was back 39. Oh well. A swing and a miss.

The other was an acute femoral fracture who developed high fevers, respiratory failure, and a leukocytosis within 18 hours after admission, with delay the repair of the fracture while his SIRS/MOSF was controlled.

He was pan-cultured, broad-spectrumed, and the infectious evaluation for a source for the fever was negative, and over 48 hours he slowly improved. This time I think his SIRS was due to emboli from his fracture.

“Bone marrow itself is a tremendous stimulus for activation of the clotting system. As a result, hypercoagulation and venous stasis in the draining veins generate mixed macroemboli from the initial bone-marrow microemboli. Bone-marrow embolization of the lung in phase I leads to mechanical obstruction of pulmonary arteries. In phase II, release of local mediators, triggered by a systemic inflammatory response (SIR) of the lungs, causes damage to the pulmonary membranes. Disturbed gas exchange and respiratory insufficiency with possible cardiac and cerebral decompensation are the result. In most cases an FES may not be detected clinically, and any mild cardiorespiratory changes are treated easily with oxygen insufflation and usually disappear within 48 h.”

This is not a falsifiable diagnosis, unlike the drug fever, so I am sticking with it.

Most of my institutions have yet to jump on the procalcitonin bandwagon. The one that does seem to use the test with abandon in cases that are obviously infected. There are times I would like a procalcitonin, and this would have been a nice case where, if negative, everyone would be happy stopping the antibiotics. So, we did it the old-fashioned way: clinical acumen. Seems to work just fine.

Rationalization

Orthopade. 1995 Apr;24(2):84–93. [Pathophysiology of fat embolisms in orthopedics and traumatology].

http://www.ncbi.nlm.nih.gov/pubmed/7753543

POLL RESULTS

I

• live and die by the procalcitonin 12%
• use the less expensive amateurcalcitonin 19%
• rely on my clinical acumen 19%
• never stop an antibiotic if the patient gets better 9%
• defer to the wisdom that is ID 40%
• Other Answers 2%
  • dip more frequently into my knowledge of Latin to cover up my cluelessness.

I expected more

Oct 23, 2013

As I have mentioned in the past, work has slowly declined over the last decade. Fewer neutropenics, no AIDS opportunistic infections, many fewer hospital-acquired infections, etc. etc. There are fewer infections to take care of combined with those damn hospitalists. When you have bright doctors running the inpatient service instead of clinic docs there is less fear, uncertainty, and doubt and FUD drives consults. My inpatient volume is down at least 50% compared to the turn of the century. I am not complaining, mind you, just commenting. I do not want to work like I did when I was a young whippersnapper, full of vim and vigor. My vim levels have declined at least 50%, and only supplementation keeps my vigor levels barely therapeutic.

Still, we have the biologics, the various antibodies that mess with immune function to treat cancers and collagen vascular diseases. Developed, I hope, to help keep ID docs busy.

The patient is on infliximab, aka Remicade, for his rheumatoid arthritis. He has a CXR for a chronic cough productive of green curds. Ick. I get gaggy with sputum as it is; I am glad he did not offer to show me said green curds.

There was a peripheral cavity in the upper lobe on plain film, and CT revealed two smaller ones in other lungs and a bronchoscopy yielded nothing. All the studies, including fungal antigen testing, were negative.

So, they took it out, and it was Aspergillus fumigatis, as it should be. I am kind of puzzled at the negative galactomannan, but the lesion was very peripheral, and perhaps the bronchcoscopist was washing out the wrong area. It is a good test, but not a great one with a sensitivity of 87%:

The summary estimates of pooled DOR, SEN, SPE, PLR, and NLR of the BAL-GM assay (cutoff value 0.5) for proven or probable IA were 52.7 (95% confidence interval (CI) 31.8 87.3), 0.87 (95% CI 0.79 0.92), 0.89 (95% CI 0.85 0.92), 8.0 (95% CI 5.7 11.1) and 0.15 (95% CI 0.10 0.23) respectively

The patient is a gardener, so perhaps it was acquired from mulching. Or perhaps just life, given the ubiquity of Aspergillus. We inhale 100 spores a day, so there is no end of potential exposure. But finding cavities in three different lobes suggests a greater than average inhalational inoculum, such as one finds stirring up a mulch pile. It would not be the first multi-lobar pneumonia due to Aspergillus I have seen from mulching.

The other nice thing about the last decade besides less work is the new azoles. Before voriconazole I never cured an Aspergillus. Since voriconazole I have never failed to cure Aspergillus. Maybe a bit of an exaggeration combined with a faulty memory, but not much.

I had expected to find a tonne (2,205 lbs) of references concerning infliximab and invasive pulmonary Aspergillus. Nope. Two specific hits on the Pubmeds and some fretting. The lack of literature kind of surprised me given all the other issues with the biologics and fungi.

He did just fine.

Rationalization

Tumor Necrosis Factor Inhibition and Invasive Fungal Infections

http://cid.oxfordjournals.org/content/41/Supplement\_3/S208.full

N Engl J Med. 2001 Apr 5;344(14):1099 100. Invasive pulmonary aspergillosis associated with infliximab therapy.

http://www.ncbi.nlm.nih.gov/pubmed/11291675

Clin Infect Dis. 2007 Sep 15;45(6):673 81. Epub 2007 Aug 8. Fulminant mulch pneumonitis: an emergency presentation of chronic granulomatous disease.

http://www.ncbi.nlm.nih.gov/pubmed/17712749

PLoS One. 2012;7(8):e43347. doi: 10.1371/journal.pone.0043347. Epub 2012 Aug 14. Systematic review and meta-analysis of detecting galactomannan in bronchoalveolar lavage fluid for diagnosing invasive aspergillosis.

http://www.ncbi.nlm.nih.gov/pubmed/22905261

POLL RESULTS

As I get on in years most of my decline has been in

• vim 3%
• vigor 13%
• gumption 24%
• concentration 16%
• word finding 32%
• Other Answers 13%
  • Giveadamns.
  • drive, all kinds
  • Sanity.

Yet another unexpected pathogen

Oct 25, 2013

Common things are, of course, common. Hence the tautology. It is what gets me through the day. If every case I had were something unusual or odd, I would never get home, spending all my time on the Pubmeds learning about weirdness. You young whippersnappers have no idea how good you have it with Pubmed and the Googles. Bifocals would not help me read an Index Medicus.

The patient has a long history of intermittent low back pain. It usually lasts three days, and he has a routine he uses to relieve the symptoms. This time was different. Rather than getting better over the three days, the pain became increasingly severe, and off he went to the ER.

He had no other complaints. Not a fever or a chill or an infection anywhere else. Nothing. But the MRI showed an epidural abscess with discitis, which was debrided, and they called me.

OK. Gram-positive cocci in the specimen. Probably a mouth Streptococcus. As a recent study suggests, it is not all that uncommon for the transient bacteremia's of life to seed damaged backs:

“In total, microbiological cultures were positive in 28 (46 %) patients. Anaerobic cultures were positive in 26 (43 %) patients, and of these 4 (7 %) had dual microbial infections, containing both one aerobic and one anaerobic culture.”

This study did not surprise me overmuch as it is within the spectrum of spontaneous infected backs I see, although my sense is I see more Streptococci and Staphylococci, probably since that is what the lab can grow.

And it grew?

S. pneumoniae. Both the epidural space and the urine. Now I am flummoxed. That is a rare event, the CID title notwithstanding. They report 8 spinal infections of all kinds in a 12-year period and make mention of 20 more. It would be my first pneumococcal epidural abscess. I suppose the English have a different definition of rare that I do.

And I think it is the first time I have seen S. pneumoniae in the urine as well. An S. pneumoniae UTI in adults is also rare, and he was asymptomatic. I doubt this organism would fall under the rubric of asymptomatic bacteriuria and be ignored.

I assume the S. pneumoniae was transiently in the blood (negative cultures) then to both urine and epidural, although I suppose it could have been a UTI that seeded the epidural space by way of Batson’s plexus.

Labs suggest neither a paraproteinemia nor HIV as a potential risk, but the SPEP is pending. At least it is a bug I can kill, and he will get a course of ceftriaxone.

Rationalization

Eur Spine J. 2013 Apr;22(4):690–6. doi: 10.1007/s00586–013–2674-z. Epub 2013 Feb 10. Does nuclear tissue infected with bacteria following disc herniations lead to Modic changes in the adjacent vertebrae?

http://www.ncbi.nlm.nih.gov/pubmed/23397187

Clin Infect Dis. 1999 Apr;28(4):873–81. Streptococcus pneumoniae spinal infection in Nottingham, United Kingdom: not a rare event.

http://www.ncbi.nlm.nih.gov/pubmed/10825053

Indian J Med Microbiol. 2012 Jan-Mar;30(1):96–8. doi: 10.4103/0255–0857.93056. Pneumococcusuria: From bench to bedside

http://www.ncbi.nlm.nih.gov/pubmed/22361770

J Clin Microbiol. 2004 Sep;42(9):4383–5. Pyelonephritis and urosepsis caused by Streptococcus pneumoniae.

http://www.ncbi.nlm.nih.gov/pubmed/15365050

From the Tips

Oct 28, 2013

I don’t charge to remove central lines. I just take tips. Nah. A variation of an old circumcision joke that doesn’t really work. They can’t all be gems.

The patient is admitted with pus around the PICC line. She has been on antibiotics for 3 weeks for recurrent MSSA bacteremia with no source identified despite an extensive workup. We are working our way towards a PET scan at some point, pending insurance approval.

She is afebrile, and blood cultures are negative, but the tip of the PICC grows both Pseudomonas and Enterobacter. To make issues even more interesting, the patient has had two tendon ruptures while on ciprofloxacin in the past, has an itchy red rash on nafcillin and the care facility will not take her back if we treat the MSSA bacteremia with daptomycin since each dose costs a small fortune.

Having a line tip positive with S. aureus, Candida or other organisms may be a harbinger of badness to come:

“Among 125 patients from whose CVC tips the above four organisms were grown, seven (12.3%) of 57 patients who did not receive appropriate antibiotic therapy within 48 h after CVC removal subsequently developed BSI, but only one (1.5%) of 68 patients who did receive appropriate therapy developed BSI (OR 0.11, p 0.02).”

Central line tip cultures that are positive with negative blood cultures are problematic. They are probably associated with a small increased risk of bacteremia, but how long to treat and with what is not known.

So what to do? I opted for 5 days of cefepime which is probably more than enough since she was not yet bacteremic:

"Among bacteremic patients receiving shorter (5-7 days) versus longer (7-21 days) antibiotic therapy, no significant difference was detected with respect to rates of clinical cure (45/52 versus 47/49, risk ratio 0.88, 95% confidence interval [CI] 0.77-1.01), microbiologic cure (28/28 versus 30/32, risk ratio 1.05, 95% CI 0.91-1.21), and survival (15/17 versus 26/29, risk ratio 0.97, 95% CI 0.76-1.23)."

Then change to cefazolin to finish up the treatment of the MSSA bacteremia. I do not think I will lose any ground in the treatment of the S. aureus infection, where ever it may be hiding out, and I can keep the beta-lactams going.

I suppose there will be as many other options offered as doctors reading this; when there is a paucity of data for every three doctors, you will get four opinions.

Rationalization

Diagn Microbiol Infect Dis. 2012 Jun;73(2):157–61. doi: 10.1016/j.diagmicrobio.2012.03.002. Epub 2012 Apr 5. Clinical significance of Candida colonization of intravascular catheters in the absence of documented candidemia.

http://www.ncbi.nlm.nih.gov/pubmed/22483190

Clin Microbiol Infect. 2010 Jun;16(6):742–6. doi: 10.1111/j.1469–0691.2009.02926.x. Epub 2009 Sep 11. Development of bacteraemia or fungaemia after removal of colonized central venous catheters in patients with negative concomitant blood cultures.

http://www.ncbi.nlm.nih.gov/pubmed/19747217

Clin Microbiol Infect. 2006 Sep;12(9):933–6. Clinical significance of isolated Staphylococcus aureus central venous catheter tip cultures.

http://www.ncbi.nlm.nih.gov/pubmed/16882304

Failure

Oct 30, 2013

I am not used to failure. Well, professional failure. Well, failing to kill bugs. A nice aspect of ID is that we usually cure infections, or they get better on their own, and I can take the credit. Long term, I always fail. I always keep in the back of my mind that someday, unless I am cremated, I will be consumed by the organisms I have spent my professional life killing. For the short term, we usually triumph over the infection, an outcome that will undoubtedly become less assured as we slide into the post-antibiotic era.

The patient is a poorly controlled diabetic admitted with foot infection and bacteremia. She is homeless and schizophrenic as well, another triumph our ability to help those who cannot help themselves. Infections tend to inordinately affect and kill the disadvantaged, poor, and uninsured, as a quick google will confirm. It reflects poorly on the US, but as a society, we have long ago abandoned the "rising tide lifts all boats” in favor of "screw you, I got mine". I tend to favor any hideous abomination from hell that will decrease morbidity and mortality in my patients.

The cultures grow MRSA with an MIC to vancomycin of 1.0, repeat blood cultures and ECHO are negative, and I opt for 4 weeks of vancomycin which she gets at a local nursing home.

Six days after stopping the antibiotics, she has a new onset of severe back pain, and an MRI shows thoracic osteomyelitis and epidural abscess. Expletive deleted. Debridement finds MRSA, and now the MIC is 2.0. Given the pharmacokinetics of vancomycin I suspect all it was doing was annoying the Staph, giving the beast a chance to evolve higher MICs.

Concentrations of vancomycin in bones of 14 patients undergoing total hip arthroplasty (group 1) and 5 patients with osteomyelitis (group 2) were studied. Group 1 received vancomycin, 15 mg/kg intravenously, 1 h prior to anesthesia. Group 2 received doses adjusted to achieve peak levels in serum of 20 to 30 micrograms/ml and trough levels of less than 12 micrograms/ml; bone specimens were collected during surgical debridement. The specimens were pulverized and eluted into phosphate buffer, and the supernatants were analyzed for vancomycin content by fluorescence polarization immunoassay. In group 1, vancomycin was detectable in all cancellous specimens with a mean concentration of 2.3 +/- 4.0 micrograms/g (range, 0.5 to 16 micrograms/g); 10 of 14 cortical specimens had detectable vancomycin; the mean cortical concentration was 1.1 +/- 0.8 micrograms/g (range, not detectable to 2.6 micrograms/g). In group 2, vancomycin was detectable in only two of five cortical bone specimens (mean concentration, 5.9 +/- 3.5 micrograms/g). Cancellous bone was obtained in one patient; the vancomycin concentration was 3.6 micrograms/g.

Although there is some conflicting data, the preponderance of the information suggests that as the MIC goes up from .5 to 1 to 1.5 to 2 to vancomycin, clinical success falls.

But what is the best antibiotic(s) to treat MRSA with an increased MIC to vancomycin? Got me. The arguable order for treating severe MRSA infections based on the available data may be vancomycin > linezolid=daptomycin > ceftaroline, with linezolid winning for pneumonia and daptomycin for bacteremia. I suspect that the real order, if we ever get good clinical data, will be ceftaroline > daptomycin = linezolid with vancomycin bringing up the rear. We often get away with vancomycin, especially if we get have good source control and/or a good host. But I want to practice best medicine, not what I can get away with and we so lack good comparative clinical trials on how to treat MRSA.

Still, I have a failure with vancomycin that only made the bacteria more resistant or, as the current language has it, non-un-less-susceptible. I have good source control, so I used ceftaroline this time around. It may be the best option for killing the MRSA, her one problem I think I have a solution for, although it will be of no help with the diabetes, mental illness, and homelessness.

Rationalization

Antimicrob Agents Chemother. 1988 September; 32(9): 13201322. PMCID: PMC175859 Vancomycin concentrations in infected and noninfected human bone. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC175859/

Diagn Microbiol Infect Dis. 2008 Apr;60(4):43740. Epub 2007 Dec 21. Diminished vancomycin and daptomycin susceptibility during prolonged bacteremia with methicillin-resistant Staphylococcus aureus.

http://www.ncbi.nlm.nih.gov/pubmed/18096352

J Infect Chemother. 2013 Feb;19(1):429. doi: 10.1007/s1015601204499. Epub 2012 Jul 14. The use of ceftaroline fosamil in methicillin-resistant Staphylococcus aureus endocarditis and deep-seated MRSA infections: a retrospective case series of 10 patients.

http://www.ncbi.nlm.nih.gov/pubmed/22797874

Poll Results

For the poor, the mentally ill and the otherwise disadvantaged

• as a society we should help care for them 84%
• as a society we should help care for them as long as it doesn't come from my pocket 1%
• screw 'em. People get what they deserve. 2%
• solutions are too complex for me to know what to do 6%
• I have strong opinions on the subject devoid of data and/or morality. 4%
• Other Answers 3%
  • les s money on war and more for the poor

Weight Gain

Nov 5, 2013

The patient is finishing a course of vancomycin for an infected septic hip from Enterococcus, resistant to ampicillin

The infected prosthesis was removed, a spacer placed, and the patient has been biding his time at a nursing home. He has done quite well clinically, with no signs of infection, lab work peachy keen, but pain and a lack of a real hip have limited his activity.

His only complaint was weight gain. He was up 20 lbs, which is to be expected with his decreased activity. Or is it?

It is interesting that antibiotics can affect animal growth. Farmers have been putting antibiotics into animal feed for years in part because it helps the animals fatten up faster.

There is a fascinating literature, beyond the scope of this blog, demonstrating how the constituents of the bowel microbiome can promote weight gain and messing with a normal microbiome can shift the balance in favor of obesity. Like some antibiotics:

“A major and significant weight gain can occur after a six-week intravenous treatment by vancomycin plus gentamicin for IE with a risk of obesity, especially in males older than 65 who have not undergone surgery. We speculate on the role of the gut colonization by Lactobacillus sp, a microorganism intrinsically resistant to vancomycin, used as a growth promoter in animals, and found at a high concentration in the feces of obese patients.”

A finding confirmed in another study:

“The acquired obesity observed in patients treated with vancomycin may be related to a modulation of the gut microbiota rather than a direct antibiotic effect. L. reuteri, which is resistant to vancomycin and produces broad bacteriocins, may have an instrumental role in this effect.”

I am not in the habit of warning patients that they could gain weight, perhaps due to antibiotics; perhaps I should. It is early in the understanding of how the microbiome influences human health and disease, and I need to get in on the ground floor with the Microbiome Diet & Cookbook and make a killing. Too bad I have ethics. And I wish I could blame my own colonic flora for my weight, but having no colon makes that difficult. I know that it is my weakness for maple bars and ice cream. No alternation of the microbiome could overcome that.

Rationalization

Clin Microbiol Infect. 2013 Apr;19(4):305–13. doi: 10.1111/1469–0691.12172. Epub 2013 Mar 2. Gut bacterial microbiota and obesity.

http://www.ncbi.nlm.nih.gov/pubmed/23452229

PLoS One. 2010 Feb 10;5(2):e9074. doi: 10.1371/journal.pone.0009074. Vancomycin treatment of infective endocarditis is linked with recently acquired obesity.

http://www.ncbi.nlm.nih.gov/pubmed/20161775

Nutr Diabetes. 2013 Sep 9;3:e87. doi: 10.1038/nutd.2013.28. Lactobacillus reuteri and Escherichia coli in the human gut microbiota may predict weight gain associated with vancomycin treatment.

http://www.ncbi.nlm.nih.gov/pubmed/24018615

POLL RESULTS

I gain weight because

• I have the wrong gut flora 8%
• I eat too much and move to little 49%
• I photosynthesize 14%
• I am a vancomycin junkie 5%
• I am an adipose magnet 19%
• Other Answers 5%
  • The gravitational pull on my home planet is much less than here on Earth.
  • I have the metabolism of a snail
  • All of the above. Plus genetics. It's not my fault.

Infected Hole

Nov 6, 2013

About 10 days ago the patient had chest pain. For a variety of reasons, it took some time for her to seek medical care, and it was primarily progressive dyspnea and recurrence of chest pain that led her to the ER. That led to the cath lab and an ECHO, both of which demonstrated a left ventricular pseudoaneurysm. And so, to the OR where at the time of repair, it was noted that there was a “fibrinous pericarditis.” Probably a bad Dressler's, but the surgeon sent of cultures of the necrotic myocardium and the pericardial fluid.

And it had moderate growth Streptococcus intermedius although a paucity of white cells.

So, they called me.

The patient had no symptoms of infection, nor did she have any bacteremia inducing trauma, just poorly controlled diabetes. Her dentition is fine.

If real, it would be very rare. I can find four cases of infected MI’s, two with purulent pericarditis (3 S. aureus and an E. coli) and two cases of infected pseudoaneurysms (S. aureus and Salmonella).

Bacteremia is a daily occurrence in humans from a variety of sources and dead tissue would be fertile soil for a bacterium to seed and grow in the extremely unlucky. I would bet that most patients who seed a myocardial infarction die quickly, the death is attributed to the MI and as a result may be less rare than reports would suggest.

It is hard to ignore moderate growth of a pathogen in what should be a sterile area, especially now that the infection site has sutures holding the heart together. I suppose I will treat it like Streptococcal prosthetic endocarditis. And from the narrow ID perspective, she did just fine.

Rationalization

Abscess of the Myocardium Complicating Infarction Report of Two Cases. Can Med Assoc J. 1964 December 5; 91(23): 1225–1227.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1928485/

Microbiology of Odontogenic Bacteremia: beyond Endocarditis Clin. Microbiol. Rev. January 2009 vol. 22 no. 1 46–64.

http://cmr.asm.org/content/22/1/46.full

A Connecticut Yankee

Nov 8, 2013

The patient had an aortic valve replacement 6 months ago and has been doing great until a month before admission when he developed fevers and malaise but nothing else.

He saw his PMD who noted a change in his murmur which led to an ECHO that showed a small vegetation and probably a large ring abscess. He was admitted, and after three days, his blood cultures remained negative. He went to the OR where infections and necrotic tissue was found around half the valve ring.

Gram stain and cultures were negative, and he had zero risks for culture negative endocarditis. What was striking clinically is how little infection symptoms he had given the degree of valve infection, and he continued to work out and work with no problems.

On day 6, the blood cultures started to pop positive with gram-positive rods that were identified as P. acnes. I had put that organism at the top of my list in my initial consultation, and it impressed everyone. Sometimes I feel like a Connecticut Yankee in King Authors Court, making knowledge look like magic, amazing and confounding the non-ID savages. As I have mentioned before to you young whippersnappers out there, always commit to the odd bug. No one will remember if you are wrong, but everyone will remember if you call the zebra before the cultures. It can give you a reputation.

P. acnes prosthetic valve infections are rare, with 18 hits on the Pubmeds, mostly aortic valves. It is indolent, presenting late with a ring abscess.

I do not know what to do to prevent P. acnes surgical infections. Living in the oils of hair follicles, it is protected from all the maneuvers we employ to prevent surgical infections. As a percentage of prosthetic SSI's, I would wager it now accounts for a majority, or at least a plurality, of the infections I see, although I will admit I have not done a careful epidemiology.

At IDSA, I talked to one of the SSI prevention gurus about ideas to prevent P. acnes infections. He had nothing. I always presume, perhaps erroneously, that P. acnes is acquired at the time of surgery as I usually see it in hairy men. There is also the possibility of bacteremia from the mouth. Although P. acnes in the blood may be ignored as a contaminant, the recent suggestions of its involvement in herniated discs makes calling P. acnes a contaminant problematic.

Now that the valve is replaced, he will get a course of penicillin for prosthetic valve endocarditis.

Rationalization

J Clin Microbiol. 2007 January; 45(1): 259–261. Published online 2006 October 25. doi: 10.1128/JCM.01598–06 PMCID: PMC1828954 Propionibacterium acnes as a Cause of Prosthetic Valve Aortic Root Abscess.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828954/

J Clin Microbiol. 2011 Apr;49(4):1598–601. doi: 10.1128/JCM.01842–10. Epub 2011 Feb 16. Clinical significance of Propionibacterium acnes recovered from blood cultures: analysis of 524 episodes.

http://www.ncbi.nlm.nih.gov/pubmed/21325550

Eur Spine J. 2013 Apr;22(4):690–6. doi: 10.1007/s00586–013–2674-z. Epub 2013 Feb 10. Does nuclear tissue infected with bacteria following disc herniations lead to Modic changes in the adjacent vertebrae?

http://www.ncbi.nlm.nih.gov/pubmed/23397187

Am J Med Sci. 2005 Apr;329(4):178–80. Incidence of bacteremia after routine tooth brushing.

http://www.ncbi.nlm.nih.gov/pubmed/15832100

Fortuitous

Nov 13, 2013

The patient had an implantable cardioverter-defibrillator (ICD) placed for recurrent ventricular fibrillation and was doing well except for a growing fluid collection over the pocket site. No constitutional symptoms, normal labs, and on exam, the unit was floating in some sort of fluid, blood? pus? but it was not the typical abscess seen with pocket infections. There was no rubor, dolor, or calor.

So rather than taking it out we tapped it. Bloody pus but no organisms seen. I was betting on P. acnes as it was a hairy male, but after 5 days, it was growing partially acid-fast gram-positive rod. Nocardia?

So, we (meaning not me. I remember the old days when the cardiologist grabbed the lead and gave it a yank like starting a mower, and you could see the whole heart move up in the chest under fluoroscopy. These days they have lead extraction systems that make removal much safer) took out the system, and after 10 days it is identified as M. fortuitum.

Huh. Not a common cause of pacer pocket infections with about 10 cases in the Pubmeds.

“Most cases developed within 6 months from implantation suggesting nosocomial acquisition. Wound discharge, fever, and pain at the generator site were the most common presenting features. At presentation they had a median duration of symptoms of 34 days. Concomitant bacteremia was present in half of the cases. Antibiotics therapy and removal of the pacemaker system were needed to achieve cure in the majority of cases. Clarithromycin and fluoroquinolones were the most commonly used antibiotics.”

Not certain where his came from, although he lives and works on a farm and has exposure to lot of organic material that could contain M. fortuitum, the organism being found in soil, dust, rivers, lakes, and tap water i.e., everywhere. We have not had a second case to suggest an issue with the hospital water supply.

While awaiting ID of the organism, I started him on TMP-Sulfa, thinking it was Nocardia. Now what? Quinolones and macrolides are the mainstays of therapy but also mess with the cardiac conduction system leading to death, and he is without his ICD. My plan is to start the antibiotics when he gets the ICD reimplanted since blood cultures are negative, and he is clinically doing well. And taking out the generator is likely curative. Once he can be defibrillated, I can probably treat safely while I await sensitivities.

He did fine.

Rationalization

Pediatr Infect Dis J. 2009 Nov;28(11):1032–4. doi: 10.1097/INF.0b013e3181aa6592. Myocardial abscess and bacteremia complicating Mycobacterium fortuitum pacemaker infection: case report and review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/19859019

N Engl J Med. 2012 May 17;366(20):1881–90. doi: 10.1056/NEJMoa1003833. Azithromycin and the risk of cardiovascular death.

http://www.ncbi.nlm.nih.gov/pubmed/22591294

Cardiology. 2011;120(2):103–10. doi: 10.1159/000334441. Epub 2011 Dec 13. QT prolongation and torsade de pointes induced by fluoroquinolones: infrequent side effects from commonly used medications.

http://www.ncbi.nlm.nih.gov/pubmed/22156660

Infect Control Hosp Epidemiol. 1999 May;20(5):343–5. Hospital water supply as a source of disseminated Mycobacterium fortuitum infection in a leukemia patient.

http://www.ncbi.nlm.nih.gov/pubmed/10349952

Life Lessons

Nov 21, 2013

The patient is an IVDA. Two years ago, he had a mitral valve replacement due to endocarditis, and, such is the power of addiction, he relapsed.

He comes to the ER for an I&D of two large arm abscesses and, while not febrile, all four blood cultures bottle of cultures grow Corynebacterium and S. salivarious so he is admitted, and they call me.

I tell the patient I am worried about endocarditis, that without the right therapy, his disease is 100% fatal, but if we do it right, we have a reasonable shot at a cure. The few cases of prosthetic valve endocarditis reported suggests medical cure is possible, depending on which Corynebacterium. Some cases were evidently cured with daptomycin.

129 cases of Corynebacterium endocarditis involving nine species met inclusion criteria. Corynebacterium endocarditis typically infects the left heart of adult males and nearly one third of patients have underlying valvular disease. One quarter of patients required valve replacement and one half of patients died. Toxigenic C. diphtheriae is associated with pediatric infections (p < 0.001). Only C. amycolatum has a predilection for women (p = 0.024), while C. pseudodiphtheriticum infections are most frequent in men (p = 0.023). C. striatum, C. jeikeium and C. hemolyticum are associated with nosocomial risk factors (p < 0.001, 0.028, and 0.024, respectively). No species was found to have a predilection for any particular heart valve. C. pseudodiphtheriticum is associated with a previous prosthetic valve replacement (p = 0.004). C. jeikeium infections are more likely to require valve replacement (p = 0.026). Infections involving toxigenic C. diphtheriae and C. pseudodiphtheriticum are associated with decreased survival (p = 0.001 and 0.032, respectively).

I try to impart the seriousness of his disease. He is more concerned about when he can eat, being NPO for a TEE. Several hours later, he has gone, back to the streets and continued IVDA and an almost guaranteed death at age 24. Not everyone learns the lessons life offers.

I know there will be those reading this whose attitude towards a relapsed heroin user will be a combination of contempt and superiority. Me? I mostly feel sorry for people throwing away their lives. It is sad, you get one life, and you piss it away with addictions. And I wonder how horrible your life is that heroin is a good option.

My life lessons are so much easier as an employed, middle-class male. Make sure my right rear window is all the way up when going through the car wash. The water comes in fast and furious otherwise. That was the life lesson I learned today. I have it so easy. You?

Rationalization

J Infect. 2006 May;52(5):e13941. Epub 2005 Oct 19. First report of prosthetic mitral valve endocarditis due to Corynebacterium striatum: Successful medical treatment. Case report and literature review.

http://www.ncbi.nlm.nih.gov/pubmed/16236359

BMC Infect Dis. 2007 Feb 6;7:4. Corynebacterium endocarditis species-specific risk factors and outcomes.

http://www.ncbi.nlm.nih.gov/pubmed/17284316

POLL RESULTS

Life lessons

• are rarely learned from others 34%
• should be multiple choice 16%
• should be graded on a curve 7%
• are for the weak and feeble. 3%
• are valuable, at least you didn't leave the sunroof open. Idjet. 36%
• Other Answers 4%
  • are usually learned after their value has been lost through the passage of time and trouble.
  • are wasted on experience

More Snot in the Wrong Place

Nov 23, 2013

The patient is an elderly male with a history of cholangiocarcinoma who presented with acute on chronic RUQ pain and dyspnea with SIRS. The WBC is 15K, but his LFTs are normal.

So, a CT is done, and it reveals several large cavitating lung masses, a large liver abscess, and some partial clot in the inferior vena cava.

Yet another liver abscess with normal transaminases. Very annoying. The liver abscess is drained, there is pus, and it grows K. pneumonia as does the blood. Again.

I call the lab, and yep, it is mucoid, with the snot test: touch a loop to the culture and lift. It leaves a long string of mucoid Klebsiella as the wire is pulled away. Looks just like snot. If you don’t believe me, look at a picture. Ick.

It is probably confirmation bias, but I get the sense I am seeing more mucoid Klebsiella causing liver abscess. These organisms, which started in Taiwan, are known for causing liver abscesses with metastatic complications such as endophthalmitis. The mucoid capsule inhibits phagocytosis, increasing pathogenicity. If you were a white cell, would you want to eat Klebsiella snot? Not me.

I figure the clot in IVC is infected, and the lung findings are septic pulmonary emboli. He improved rapidly on ceftriaxone after drainage.

The patient had no exposures except life to acquire a mucoid Klebsiella. I suppose something wicked this way comes from Asia. Hard to defend against an organism that can move around the world in the colon. As I have mentioned before, while we may think we are hot stuff, in the end we are sentient transport media for bacteria.

Rationalization

Hypermucoviscosity: An Extremely Sticky Phenotype of Klebsiella pneumonia Associated with Emerging Destructive Tissue Abscess Syndrome. Clinical Infectious Diseases 2006; 42:1359–61

http://cid.oxfordjournals.org/content/42/10/1359.full.pdf

J Chin Med Assoc. 2008 Sep;71(9):442-7. doi: 10.1016/S1726-4901(08)70146-1.

Pyogenic liver abscess associated with septic pulmonary embolism.

http://www.ncbi.nlm.nih.gov/pubmed/18818136

How Sweet It Is

Dec 5, 2013

It has been a while. I like to write for the blog three times a week, MWF, but I need to be working to have grist for the mill. I spent a long Thanksgiving weekend in Minnesota with the in-laws. I hate the cold I hate the cold I hate the cold. I wish my wife were from Hawaii. But I am back to work with some great cases, and awaaay we go!

Before I left, I saw an unusual case of relapsing cellulitis. The patient has myelodysplastic syndrome and had been admitted for an arm cellulitis at the start of November that required debridement, but the cultures were negative. I did not see her that admission. She was stable at the nursing home receiving wound care when the fevers recurred as well as the skin infection.

First on the leg, then on the arm, then on the abdomen, over the next 24 hours, she developed hemorrhagic cellulitis with bullae. She was both neutropenic and thrombocytopenic and was readmitted.

They call me, and sure enough, it is hemorrhagic bullae. The classic bored question has a case of hemorrhagic bullae in a cirrhotic who eats shellfish, and the answer is Vibrio vulnificans. However, the patient has none of those risks.

Other organisms and processes can cause hemorrhagic bullae including

“Necrotizing fasciitis, Bullous impetigo, Echthyma gangrenosum, menigococcemia (late stage), Staph Scalded Skin, Herpes, Zoster, Gas gangrene Autoimmune - bullous pemphigoid vs pemphigoid vulgaris, pyoderma gangrenosum Drug reaction (TEN and SJS), contact dermatitis”

So, we culture the blood, put her on antibiotics that should kill what might kill her, and call the surgeons, who do a debridement and biopsy.

Gram stain and cultures are negative for organisms, and the hospitalist calls it before the pathology returns.

Sweet’s, or febrile neutrophilic dermatosis. There is idiopathic, malignancy-related (including MDS), and drug-related,

“Sweet’s syndrome (the eponym for acute febrile neutrophilic dermatosis) is characterized by a constellation of clinical symptoms, physical features, and pathologic findings which include fever, neutrophilia, tender erythematous skin lesions (papules, nodules, and plaques), and a diffuse infiltrate consisting predominantly of mature neutrophils that are typically located in the upper dermis…. In patients with malignancy-associated Sweet’s syndrome, the lesions may appear bullous, become ulcerated, and/or mimic the morphologic features of pyoderma gangrenosum.”

There is also a smattering of bullous forms of Sweet's reported, and the hemorrhagic component was more likely due to the thrombocytopenia and misled me. We stopped the antibiotics, and she improved with steroids.

Rationalization

Am J Emerg Med. 2008 Mar;26(3):316–9. doi: 10.1016/j.ajem.2007.07.014. Hemorrhagic bullae are not only skin deep.

http://www.ncbi.nlm.nih.gov/pubmed/18358943

Orphanet J Rare Dis. 2007 Jul 26;2:34. Sweet’s syndrome–a comprehensive review of an acute febrile neutrophilic dermatosis.

http://www.ncbi.nlm.nih.gov/pubmed/17655751

Reumatol Clin. 2013 Jul-Aug;9(4):246–7. doi: 10.1016/j.reuma.2012.01.014. Epub 2012 Jun 30. Sweet syndrome associated with myelodysplastic syndrome: report of a case. Review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/22749728

Double Vision

Dec 6, 2013

Ooh-ooh (oooh) ooh-ooh, double vision

(Oooh) I need double vision

(Oooh, double vision) it takes me out of my head, takin’ me out of my head

(Oooh, double vision) I get my double vision, woa-oah

(Oooh, double vision) seeing double double, double vision

(Oooh, double vision) oh-oh my my double vision

(Oooh, double vision) double vision, yeah-ah-ah eah-eah eah-eah ah

(Oooh, double vision) I get double vision, oooh

How, how?

~Foreigner

How, how indeed.

The patient presents with double vision and a descending weakness. On exam, the patient is best described as floppy, he cannot bring his head forward off the pillow on his own, and his head bobbles like it is on a spring. His eyes drift apart like an old married couple. No, I am not over-sharing.

That presentation has a very narrow differential diagnosis: Miller-Fischer variant of Guillain-Barré and botulism.

Botulism has two forms: food and wound. She is homeless and not eating home-canned good, Alaskan fermented beaver tail or beached whale. Mmmmm. Fermented beaver tail. Botulism is a problem in the native populations of Alaska due to food preparation techniques, which is conducive to C. botulinum growth.

“The traditional preparation involves placing meat and fat tissues into skin bags (puurtaq), which are sewn shut and aged for weeks or months under rocks or buried under gravel. However, it has become common practice in the Nunavik region and elsewhere to use either plastic bags or buckets, metal barrels, or glass containers in place of the skin pouch. Among Pacific Coast First Nations people and Alaska Natives in southeast Alaska, foodborne botulism is caused by salmon eggs (“stink eggs”) aged in airtight jars.”

In this case, it is from a more mundane cause, intramuscular injection of black tar heroin, although the organism is not usually isolated from heroin. His shoulder was indurated and tender and grew C. botulinim from the I&D. He was lucky, never progressing to intubation, and has been slowly improving on penicillin G and anti-toxin. Despite the popularity of black tar heroin, it is the first botulism I have seen from that source.

Another fun fact about the disease:

“Justinus Kerner described botulinum toxin as a ”sausage poison“ and ”fatty poison“, because the bacterium that produces the toxin often caused poisoning by growing in improperly handled or prepared meat products. It was Kerner, a physician, who first conceived a possible therapeutic use of botulinum toxin and coined the name botulism (from Latin botulus meaning ”sausage“).

One thing I have wondered about for years and have never been able to find an answer to is what is the ‘real’ function of botulism and tetanus toxin. There is no way these proteins evolved to cause disease in animals; causing botulism and tetanus has no survival benefit that I can imagine. The best I can find is their origin, not their purpose:

“ …it is proposed that the ancestral function of the neurotoxin gene cluster may have been related to collagen binding and degradation, a hypothesis that places CNT sequence, structure, and function within the broader context of other clostridial toxins and the evolution of clostridial pathogenesis.”

These toxins must have another survival function in the wild, but what? So many curiosities and unanswered questions in ID.

Rationalization

West J Med. 1990 October; 153(4): 390–393. PMCID: PMC1002567 Botulism among Alaska Natives. The role of changing food preparation and consumption practices.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1002567/

Volume 10, Number 9—September 2004 MMWR Botulism Type E Outbreak Associated with Eating a Beached Whale, Alaska

http://wwwnc.cdc.gov/eid/article/10/9/04–0131\_article.htm

Botulism in the North: A Disease Without Borders Clin Infect Dis. (2011) 52 (5): 593–594.

http://cid.oxfordjournals.org/content/52/5/593.full

JAMA. 1998 Mar 18;279(11):859–63. Wound botulism associated with black tar heroin among injecting drug users.

http://www.ncbi.nlm.nih.gov/pubmed/9516001

J Med Microbiol. 2002 Nov;51(11):1001–8. An investigation into the microflora of heroin.

http://www.ncbi.nlm.nih.gov/pubmed/12448685

Insights into the evolutionary origins of clostridial neurotoxins from analysis of the Clostridium botulinum strain A neurotoxin gene cluster. BMC Evolutionary Biology 2008, 8:316.

http://www.biomedcentral.com/1471–2148/8/316

The Bird That Wasn't There

Dec 9, 2013

I have mentioned in the past that ID is a lot like birding. I have a life list of diseases I have seen, or I want to see, before I retire. Unlike birding, ID is interesting. Just kidding. I almost rear-ended a car recently when I saw a bald eagle flying along the Willamette. Sometimes I think I might see a rare bird, only to be proven wrong by testing, a form of medical pareidolia where I want the pattern to resolve into a zebra bird.

The patient has 2 years of marked cachexia, losing an enormous amount of weight and now has a BMI of 10. He has alcoholic liver disease and a variety of other medical problems, including mental illness, organic brain injury, homelessness, and no teeth that make adequate food consumption problematic.

I am asked to see him to answer the question as to whether his cachexia is due to TB, as there is a vague history of a partial course of treatment in the past.

Evaluation puts TB at the bottom of the list. There is nothing to suggest he has TB, pulmonary, or extra-pulmonary.

But.

He has a known cardiomyopathy with an ejection fraction of 15%. And, for reasons that were obscure, a large, dilated colon. He has spent most of his adult life homeless, mostly in the Southern US.

I put all together as Chaga’s. Yep, Chaga's. Trypanosoma cruzi.

The parasite is endemic in the Southern US as is the vector.

“The southern states have enzootic T. cruzi transmission that involves at least 11 triatomine species and hosts such as raccoons, opossums, and domestic dogs.”

There are two reasons we do not see much disease in the US despite the fact it is common in the environment. One is likely air conditioning. Our houses are too tight to let bugs in. But more importantly, US triatomine bugs are fastidious. T. cruzi is spread in insect's stool. In S. America, the bugs feed and defecates at the same time, and the parasite is then scratched into the skin to cause disease. In the US, the bugs are more careful, not relieving themselves where they eat:

“The defecation patterns of the bugs were studied while feeding upon immobilized mice. Wild-caught adult male and female triatomines were observed feeding one to three times for a total of 71 observed feedings. T. rubida (15 bugs) appeared to be more aggressive, beginning feeding shortly after being placed in proximity to the host (within 2.3 min) whereas Triatoma protracta (12 bugs) was more deliberate, beginning feeding, on average, at 4 min. There were 40 observations of T. rubida, which fed for 27.9+/–13.6 min, whereas T. protracta fed for 22.8+/–7.5 min (n=31). Bugs were weighed pre- and post-feeding and T. rubida females ingested>T. protracta females>T. rubida males>T. protracta males. Weight gain did not correspond to the feeding duration. Defecation occurred on 42% of the feedings (30 of 71), and no bugs defecated on the host. The majority of the defecations occurred within 1 min of feeding, usually at the time of repletion. A large proportion of defecations occurred after the bugs left the vicinity of the host. All bugs and at least one fecal smear from each feeding bug were tested for Trypanosoma cruzi and 21% of T. protracta were positive by PCR (4 bugs and 1 feces). No T. rubida tested positive for T. cruzi.”

Mighty considerate of the wee beasties. And if you are having a bad day, just be glad you do not have to collect and measure Triatoma poo.

So, I sent off the serology, and they repeated his ECHO, and the EF is now 60%. And the serology came back negative.

Gosh golly gee willikers. But if you do not think about a disease, you will never diagnose it. In my case even when I think about a disease, I can't diagnosis it. Maybe next time.

Rationalization

An Estimate of the Burden of Chagas Disease in the United States. Clin Infect Dis. (2009) 49 (5): e52-e54.

http://cid.oxfordjournals.org/content/49/5/e52.full

Volume 18, Number 4—April 2012 Vector Blood Meals and Chagas Disease Transmission Potential, United States

http://wwwnc.cdc.gov/eid/article/18/4/11–1396\_article.htm

Acta Trop. 2009 Aug;111(2):114–8. doi: 10.1016/j.actatropica.2009.03.003. Epub 2009 Mar 24. Feeding behavior of triatomines from the southwestern United States: an update on potential risk for transmission of Chagas disease.

http://www.ncbi.nlm.nih.gov/pubmed/19524078

Volume 13, Number 4—April 2007. Autochthonous Transmission of Trypanosoma cruzi, Louisiana.

http://wwwnc.cdc.gov/eid/article/13/4/06–1002_article.htm

POLL RESULTS

Diagnostically

• I look for horses 29%

• I look for zebras. 13%

• I look for unicorns. Multicolored unicorns in fact. Then I give homeopathic detox. 14%

• I do not let those pesky labs get in the way of a good clinical diagnosis. 30%

• I order a bunch of tests and hope for pay dirt. 13%

• Other Answers 2%

⁃ iron maiden

Leukemoid

Dec 11, 2013

The patient is admitted with an exacerbation of COPD and has the usual workup and treatment, including steroids.

Everything was negative for infection on admit except an admitting WBC of 55 K. Three months ago, the CBC was normal. For the next 5 days, the WBC fluctuated between 55k and 66K, and they called me.

There are three diseases on the short differential for a leukemoid reaction: an infection the size of my ego, miliary Tb, and cancer. There are, of course, other causes of a leukemoid reaction:

“Infection was the most common cause of LR (n = 83, 47.9%; 95% confidence interval, 40.7–55.4), followed by ischemia/stress (27.7%), inflammation (6.9%), and obstetric diagnoses (6.9%). Higher WBC counts were significantly associated with positive blood cultures (P = .017) or a positive Clostridium difficile toxin (P = .001).”

One of my favorite zebras to look for causing a leukemoid reaction is carcinoma of the bladder, which curiously can make G-CSF, although it is not the only tumor that does.

One process that does not cause a sky-high WBC is steroids; 20 to 25,000 should be the maximum white cell count from prednisone, and they should be mature cells, the WBC goes up from steroids because the steroids prevent egress from the vascular tree.

In this case, it was the differential that was the key: promyelocytes and a few blasts. You do not see a left shift like that outside of leukemia except in extreme physiologic stress in the ICU.

I suggested an oncology evaluation would be in order since leukemia is one of the few diseases that is not due to infections.

Rationalization

Leukemoid Reaction: Spectrum and Prognosis of 173 Adult Patients. Clin Infect Dis. (2013) 57 (11): e177-e181.

http://cid.oxfordjournals.org/content/57/11/e177.

Cytokines Cell Mol Ther. 1998 Jun;4(2):113–20. G-CSF production in human bladder cancer and its ability to promote autocrine growth: a review.

http://www.ncbi.nlm.nih.gov/pubmed/9681250

Am J Med. 1981 Nov;71(5):773–8. Prednisone-induced leukocytosis. Influence of dosage, method and duration of administration on the degree of leukocytosis.

http://www.ncbi.nlm.nih.gov/pubmed/7304648

J Clin Invest. 1975 Oct;56(4):808–13. Comparison of agents producing a neutrophilic leukocytosis in man. Hydrocortisone, prednisone, endotoxin, and etiocholanolone.

http://www.ncbi.nlm.nih.gov/pubmed/1159089

Record Delay

Dec 17, 2013

The patient had a robot prostatectomy (I always imagine the robot from Lost in Space doing the procedure, waving its arms about wildly) a little over two years ago, and after he never felt quite right. He had chronic dull left lower quadrant and never got his mojo back. He would try and exercise and be active, but he tired easily.

Evaluation of this abdomen revealed a lymphocele, a not uncommon complication of the procedure, occurring in a fifth of patients. He had no fever, chills, or weight loss; just some night sweats that started a week before admission. They had been following the lymphocele intermittently, and it had not changed, but this time, there may have been an inflammatory rim suggesting abscess around it, so it was tapped.

And there was pus, gram-positive cocci on the gram stain, and it grew a coagulase-negative Staphylococcus.

He had no recent infections, trauma, or potentially bacteremia inducing procedures in the last two years, although low grade, occasional bacteremia is part of the human condition.

The interesting thing is now that the lymphoceles are drained, he feels much better, and the pain is gone.

So, has this been festering two years? History would suggest it, and I always evaluate my etiologic hypotheses through the patient's history. It sure sounds it has been going on that long. Coagulase-negative Staphylococci can certainly fester for years when associated with prosthetic joints with minimal constitutional symptoms. It just seems unlikely with a purely soft tissue infection.

Or was it infected from transient bacteremia only recently? More likely, but I have trouble thinking of coagulase-negative Staphylococci seeding this late. I do wonder how often those coagulase-negative Staphylococcal bacteremia's that are declared "contamination’ are instead a real, but clinically unimportant, bacteremia. It is not likely to ever be a knowable factoid.

There are a smattering of cases of late infected lymphocele, although mine would be a world record. Where is Guinness when you need it?

Rationalization

Urology. 1996 Jan;47(1):140–2. Delayed infection of a pelvic lymphocele following pelvic lymphadenectomy.

http://www.ncbi.nlm.nih.gov/pubmed/8560652

Int J Urol. 2013 Dec;20(12):1169–76. doi: 10.1111/iju.12144. Epub 2013 Mar 21. Lymphocele after extraperitoneal robot-assisted radical prostatectomy: A propensity score-matching study.

http://www.ncbi.nlm.nih.gov/pubmed/23521086

Urol Int. 2009;83(4):479–81. doi: 10.1159/000251192. Epub 2009 Dec 8. Delayed infection of a pelvic lymphocele following robotic radical prostatectomy and pelvic lymphadenectomy: two cases.

http://www.ncbi.nlm.nih.gov/pubmed/19996659

Reactivation

Dec 18, 2013

I was initially called by the hospitalist about a psoas abscess. It was an elderly male with fevers and abdominal pain, and the CT showed a right psoas abscess on the same side he was having a diabetic foot ulcer worked on.

Should be S. aureus, I said, does he have back pain?

Some.

Check an MRI. Sometimes iliopsoas abscess come from, or can spread to, the lumbar spine, and there can be a concomitant discitis or epidural abscess. And there was. The epidural and the iliopsoas were drained, and it all grew MSSA.

The patient was otherwise well, no other complaints suggesting infection elsewhere, so we set him up for a course of nafcillin, and off he went to the nursing home to finish the antibiotics.

Two weeks later, I get a call from the ICU. He is re-admitted. I hate that sinking 'oh crap I hope I didn’t screw up and miss something' feeling that comes with a re-admission.

He is back with obtundation, and the evaluation shows a severe case of shingles in a mid-thoracic dermatome. It is probably VZV encephalitis, but there is a fresh wound right over where the LP would be done, but the MRI of the brain is suggestive.

But here is what I did not expect. This time they did an MRI of the entire spine and found two other epidural abscesses, both small, both causing no cord compression, in the thoracic spine. These too were debrided, and pus was found although the cultures were negative. At no time did he complain of thoracic pain.

Epidurals can be multi-level, but usually there is pain in the area. Finding a pair of previously undiagnosed epidural abscesses was a bit of surprise, but it can occur in about half of patients. The record I could find was abscesses 13 separate levels.

The other issue is the zoster. It reactivated at the same level one of the abscesses, and I so want to blame the infection, but I could find no case reports where an epidural abscess resulted in a VZV reactivation. Seems reasonable but is more likely to be true-true and unrelated.

Rationalization

Spine J. 2013 Nov 11. pii: S1529–9430(13)01652–5. doi: 10.1016/j.spinee.2013.10.046. [Epub ahead of print] Spinal Epidural Abscesses: Risk Factors, Medical vs Surgical Management, A Retrospective Review of 128 Cases.

http://www.ncbi.nlm.nih.gov/pubmed/24231778

J Emerg Med. 2004 Jan;26(1):51–6. Spinal epidural abscess presenting as intra-abdominal pathology: a case report and literature review.

http://www.ncbi.nlm.nih.gov/pubmed/14751478

Eur Spine J. 2011 December; 20(12): 2228–2234. Spinal epidural abscess: aetiology, predisponent factors and clinical outcomes in a 4-year prospective study.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229722/

Increasing cost and toxicity without benefiting the patient.

Dec 23, 2013

It is flu season. H1N1 has reared its ever so ugly head the last few weeks, and there have been at least two deaths in young people because of influenza complications. Two too many. You can always tell an anti-vaccine wackaloon as they often put the adjective ‘only’ in front of some vaccine-preventable death rate. Me? I have never had a death that was an ‘only.’

There is something about flu that really brings out the rant in me, be it vaccine use in health care workers, isolation, or treatment.

I was asked today about increasing the dose of oseltamivir to treat influenza. Standard dose oseltamivir decreases mortality in hospitalized patients with influenza. It is not like penicillin and group A Streptococcus, but it is better than nothing.

If a little is good, a lot is better, right?

Double dose oseltamivir in one study did nothing and in another study had almost no difference in outcomes except for

“Subanalysis of influenza B patients showed faster RNA decline rate (analysis of variance, F = 4.14; P = .05) and clearance (day 5, 80.0% vs 57.1%) with higher-dose treatment.”

Subgroup analysis usually leads to false-positive results and is part of the reason Why Most Published Research Findings Are False. Every time you read the results of a clinical trial, go back, and re-read Ioannidis. Your enthusiasm will fade. And although statistics makes my head hurt, a p of 0.05 may be statistically significant, and it is unlikely to be clinically relevant.

The cut-off of significance, 0.05, it should be emphasized, is an arbitrary boundary that was established by Fischer in 1925 but has since become dogma set in rebar-reinforced cement.

And what is significant, at least as initially formulated by Fischer?

"Personally, the writer prefers to set a low standard of significance at the 5 percent point … A scientific fact should be regarded as experimentally established only if a properly designed experiment rarely fails to give this level of significance.

In other words, the operational meaning of a P value less than .05 was merely that one should repeat the experiment. If subsequent studies also yielded significant P values, one could conclude that the observed effects were unlikely to be the result of chance alone. So “significance” is merely that: worthy of attention in the form of meriting more experimentation, but not proof in itself."

And a p of 0.05 is probably not enough to reject the null hypothesis for most studies. For biologic studies it has been suggested that a p of 0.005 and p 0.0001 are better indicators that the results are ‘true.’ Given all the flaws in medical studies, a p of 0.05 is probably just noise to be ignored until validated with further, better, studies.

Well, if double doesn’t work, then triple must be better, right? Well, triple dose also doesn’t make a difference for patient outcomes but does lead to more rapid clearance of the virus. Bee. Eff. Dee.

Several years ago, it was suggested that we get a UA on every patient on admission since if pyuria or bacteriuria were present on admit we would not get dinged if they had a subsequent UTI. I argued that it was not ethical to order a test on a patient for our benefit if there was no clinical indication. We would inflict upon the patient cost and potential complications of further testing and treatment when the patient had no symptoms.

Similarly, I would argue that a decline in the viral excretion, if not accompanied by improved outcomes for the patient, is not an ethical reason to treat a patient. We would offer increased cost and toxicity with no benefit. I can’t see that double or triple dose oseltamivir therapy would not violate the medical ethical principles of beneficence and non-maleficence.

So, I am sticking with standard-dose oseltamivir.

Rationalization

Clin Infect Dis. 2013 Dec;57(11):1511–9. doi: 10.1093/cid/cit597. Epub 2013 Sep 17. A prospective intervention study on higher-dose oseltamivir treatment in adults hospitalized with influenza a and B infections.

http://www.ncbi.nlm.nih.gov/pubmed/24046309

BMJ. 2013 May 30;346:f3039. doi: 10.1136/bmj.f3039. Effect of double dose oseltamivir on clinical and virological outcomes in children and adults admitted to hospital with severe influenza: double blind randomised controlled trial.

http://www.ncbi.nlm.nih.gov/pubmed/23723457

Triple-Dose Flu Remedy Hastens H1N1 Viral Clearance

https://www.medscape.com/viewarticle/811132

A Dirty Dozen: Twelve P-Value Misconceptions Steven Goodman

http://www.tc.umn.edu/alonso/Goodman\_Semin\_Hemat\_2008.pdf

Revised standards for statistical evidence. Valen E. Johnson PNAS November 26, 2013 vol. 110 no. 48 19313–19317.

<http: data-preserve-html-node="true"//www.pnas.org/content/110/48/19313>

Why Most Published Research Findings Are False

https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124

Bugs don't care

Dec 25, 2013

A generic nondenominational seasonal greeting to all my readers. I worked today, Christmas, since the germs, like the honey badger, don’t care. It may be time for peace on earth and goodwill towards men, but as far as the bacteria are concerned, every day is an opportunity to try and kill another human.

The patient had a relatively minor fall off a moving skateboard, skinning his knee and getting banged up. Over the next several days, he has increasing pain in his knee and leg. In the ER, it is felt he has a traumatic infected bursa, which is drained, but the patient does not improve.

He is febrile, pus draining from the incisions, and still has a lot of pain in his thigh, so they call me. His thigh is twice normal size, red, and very tender. The bursa cultures are growing S. anginosus group. I figure he has infection tracking up into the thigh. S. anginosus group likes to cause abscesses, and the multiple collections of pus are confirmed by an MRI. In the OR, there are not only many abscesses, but the surgeon calls it a necrotizing fasciitis and myositis, with destruction of muscle and tendon. And still, it only grows S. anginosus.

The next day the infection has spread up his buttocks and back all the way to the scapula, and he is transferred to a burn unit. And all that grows is S. anginosus.

I am amazed, even after 30 years of medicine, what havoc bacteria can inflict. Necrotizing fasciitis from S. anginosus group is reported, but there are only a hand full of cases. I suspect it was more the trauma than the bacteria, and he probably had more blood/hematoma from his skateboard injury than was suspected. The injury led to a fertile soil in which the bacteria grew to cause damage. I do not think there is a fascial plane that goes from the knee all the way to the scapula along which the bacteria could travel.

Debridement is still better than antibiotics for infections, and a burn center is a great place for that kind of expertise.

Rationalization

Rev Med Chir Soc Med Nat Iasi. 1995 Jul-Dec;99(3–4):215–9. [Pyogenic infections with different locations caused by Streptococcus anginosus alone or in association with anaerobic bacteria].

http://www.ncbi.nlm.nih.gov/pubmed/9455370

Ann Emerg Med. 2011 Dec;58(6):574, 578. doi: 10.1016/j.annemergmed.2011.04.003. Man with shoulder pain after a fall. Necrotizing fasciitis.

http://www.ncbi.nlm.nih.gov/pubmed/22098998

Good Eponym

Dec 27, 2013

I have mixed feelings about eponyms. Sometimes eponyms serve to obscure, sometimes eponyms honor a discoverer, and sometimes eponyms are anachronistically cool or poetic.

The patient has three months of new cluster headaches over the right eye. He sees a neurologist and gets the pain under reasonable control. For a month leading into his admission, he has increased swelling over under his eyebrow, the same place as the headaches.

No constitutional symptoms or other medical problems, he has a CT that shows his right frontal sinus is filled with something, and it has eroded through the bone and out towards the air.

Potts puffy tumor. That is an eponym that is both archaic and somewhat poetic. I’ll keep that one. From the Wikipedia:

“Pott’s puffy tumor, first described by Sir Percivall Pott in 1760, is a rare clinical entity characterized by subperiosteal abscess associated with osteomyelitis. It is characterized by an osteomyelitis of the frontal bone… This results in a swelling on the forehead, hence the name.”

These are usually bacterial in etiology, but in the OR it was a black mass eating through the bone that eventually grew Aspergillus.

That is odd. There are only two other Pott’s puffy tumors due to Aspergillus in the literature. History and labs do not suggest any immunodeficiency, although the patient does like to garden, so perhaps that is the exposure, a real stretch given the ubiquity of that mold.

Now an arbitrary course of the effective but ever-so-pricy voriconazole, and I would anticipate a cure.

And it was.

Rationalization

Mycoses. 2005 Jul;48(4):235–7. Primary frontal sinus aspergillosis: an uncommon occurrence.

http://www.ncbi.nlm.nih.gov/pubmed/15982203

J Craniofac Surg. 2008 Nov;19(6):1694–7. doi: 10.1097/SCS.0b013e31818b432e. Pott’s puffy tumor.

http://www.ncbi.nlm.nih.gov/pubmed/19098585

Medical eponyms

https://en.wikipedia.org/wiki/Medical\_eponyms

POLL RESULTS

Eponyms

• are fun 18%
• are great for pimping interns 33%
• have no place in medicine as they only obscure 3%
• should be avoided unless it is named after me. Crislip's sign/syndrome/disease/triad. There so needs to be one. 28%
• should be avoided if it derives from Nazi's and other criminals 10%
• Other Answers 8%
  • are confusing
  • great for 'pimping' medical students

Hand to Mouth Disease

Dec 30, 2013

I see the patient in follow up from the ER. He had an abscess on the palmar aspect of his index finger, and the cultures grew S. milleri. By the time I saw him, the infection was gone, he was on the last day of his antibiotics, and there was nothing for me to do.

So, I chatted with the patient about how he got the infection.

I told him that infection was a mouth Streptococcus, and whenever I am working and get minor hand trauma, the first thing I do is wipe my hand on my jeans and then lick the wound clean. Yeah. I know. And me an ID doc.

So, I said, did you put your finger in your mouth?

He had.

I explained to the patient that is how he got the infection, but it was cured with drainage and antibiotics. And then it became curious.

The reason he was worrying his finger with his teeth is he has these hard, black (he is African American) half-millimeter nodules in all the creases of his hands and fingers. They hurt at times, so he digs them out, and they leave little pits in his skin. He had had them since he was 9, and no one had ever taken any interest in them.

I had never seen anything like it. While the patient was in the room, I Googled it and found nothing. I suggested he see a dermatologist because I had no clue what it was.

But tonight, I used different search criteria and found a perfect match.

It is palmoplantar keratoderma with punctate hyperkeratosis Turns out it is a classic presentation of the disease:

“Keratosis punctata of the palmar creases is characterized by the development of small round keratotic papules, electively and exclusively found in the palmar, digital, and uncommonly soles creases. The etiology is unknown. The frequency is higher in the black population. Although considered as an hereditary palmoplantar keratoderma with autosomal dominant transmission, familial cases with localizations on the soles is uncommon.”

The interwebs are such a great resource to help figuring out the unusual. Google everything. I do and am always better for it.

Rationalization

Ann Dermatol Venereol. 1998 Dec;125(12):898–901. [Focal familial palmoplantar keratoderma with punctate hyperkeratosis of the palmar creases].

http://www.ncbi.nlm.nih.gov/pubmed/9922864

J Am Acad Dermatol. 1990 Mar;22(3):468–76. Punctate keratoses of the palms and soles and keratotic pits of the palmar creases.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/2138179>

Happy New Year

Jan 1, 2014

I hope the year started with drunken debauchery for you. Not me. I worked, although I did participate in our traditional New Years' past time watching the Twilight Zone marathon on the SciFi channel. Do I live an exciting life, or what?

I was bemoaning with some non-health care workers today that we had to work New Years, and he said he didn't mind, he was getting double-time pay. I remember about 15 years ago a friend mentioned he received comp time, credit for every hour worked. Wish that existed in medicine, I could have retired years ago.

So often, I get questions for which I have no good answers, and I feel that part of being a sub-specialist is being clueless with style.

The patient had a month of progressive back and hip pain, which was credited to chronic back issues. It became so severe that she could not rise and was transported to the ER where a non-displaced hip fracture was found. No trauma to account for the fracture, but she is an elderly small Caucasian female, so perhaps reason enough.

In the OR, it looked odd: new bone formation, no pus or necrosis, and the surgeon thought it was going to be bone tumor. Since I am writing this, you know it isn't. So, he removed the whole femoral head, biopsied the odd bone, tossed it all in formalin (arrrrrrrrrggggghhhhhhhhhhhhhhhhh, but I can't be too picky as it looked like tumor) and put in a new hip.

Pathology: acute and chronic osteomyelitis, and they call me. She has no reason for the hip infection that I can discern.

So, I have a just-so story.

It is difficult to infect long bones without trauma. There is the occasional Brodies abscess, but this is not an abscess. I hypothesize she had a relatively minor fracture of her hip, since the pain started low grade and progressed, and then seeded the fracture site due to the bacteremia that is part of life. Probably a mouth bug as she had no constitutional symptoms. Overtime, like ice in cement, it eroded away, and the fracture extended until structural failure. It had to have been there a while to result in new bone formation.

Now what? I don’t have a bug, and the whole infected bone is now in pathology, so she should be a cure. I suppose it is better to treat an infection that isn't present rather than not treat an infection that is present, so I am going to give her a course of antibiotics, something with rifampin in the mix.

Rationalization

Clin Orthop Relat Res. 1976 Jun;(117):296302. Acute hematogenous osteomyelitis complicating closed fractures.

http://www.ncbi.nlm.nih.gov/pubmed/1277679

Clin Orthop Relat Res. 1996 Apr;(325):23944. Acute hematogenous osteomyelitis of a closed fracture with chronic superinfection.

http://www.ncbi.nlm.nih.gov/pubmed/8998882

An Med Interna. 2006 Dec;23(12):58890. [osteomyelitis due to Escherichia coli complicating a closed humeral fracture].

http://www.ncbi.nlm.nih.gov/pubmed/17371148

Rev Chir Orthop Reparatrice Appar Mot. 1990;76(8):5917. [Infection by the hematogenic route of closed vertebral fracture: apropos of a case and review of the literature].

http://www.ncbi.nlm.nih.gov/pubmed/2151482

And to my readers.

My first blog post was September 7, 2008 and I have been putting out two or three of these a week since. Short a tragic early death, I see no end in sight. ID remains that varied and interesting.

Thank you for taking the time to read my posts, and I hope the next year is as fun and interesting for you as I know it will be for me.

POLL RESULTS

I celebrate New Years

• with an excess of alcohol. 7%
• with growing angst that I am another year closer to death 19%
• by going to bed early. 38%
• Twilight Zone Marathon. I really like the one with Shatner on the plane with the wing monster covered in bad carpet. 12%
• not at all since the world ended in 2012. This is all a prolonged Occurrence at Owl Creek Bridge. 17%
• Other Answers 7%
  • I walked in the First Walk & Run at midnight in downtown Portland

Another Infection Without A Good Solution

Jan 3, 2014

The patient is an elderly diabetic with E. coli in the blood from a urinary tract infection. It is treated, and the patient gets better with no complaints.

A month later, he presents with back pain and this time with a Pseudomonal UTI. An MRI showed mid-thoracic discitis and osteomyelitis.

As an aside, there are only two things that are 100% in ID. One is that if a HCW uses the terms big gun, strong, or powerful as descriptors of antibiotics, they are idiots who know knowing about the treatment of infectious diseases. The other is that infection always goes to the disc and then to the adjacent bone. Tumor goes to bone and spares the disc. I have yet to see an exception to either.

They did a CT biopsy of the lesion, and it grew nothing, so he received 6 weeks of cefepime with no improvement. Repeat studies showed a slight progression of the osteomyelitis and a surrounding phlegmon. Phlegmon. A word that always sounds like some sort of Jamaican patois, although referring to what I do not know. English always sounds so much better when others speak it. I think for newscasts, the anchors should be Indian, the sportscasters Scottish, and the weathermen Jamaican. It would sound so much better. But I digress. Squirrel.

So, the CT guided biopsy is repeated, and this time grows coagulase-negative Staphylococcus. I don't believe it, so we get the friendly neighborhood neurosurgeon to do an open biopsy.

The same E. coli grew as before. The neurosurgeon tells me debridement is not a good option as most people do not do well without a spine (Congress the main exception).

There is not a lot of published experience with hematogenous gram-negative vertebral osteomyelitis, but what little is there suggests quinolones are key to cure. And generally, debridement is important for all forms of osteomyelitis. This case is quinolone-resistant and not amenable to debridement. Not good. This time I suggested ceftriaxone at maximum dose for 8 weeks.

And he did ok.

Rationalization

Eur Spine J. 2013 Aug;22(8):1845 53. doi: 10.1007/s00586 013 2750 4. Epub 2013 Apr 1. The management gram-negative bacterial haematogenous vertebral osteomyelitis: a case series of diagnosis, treatment and therapeutic outcomes.

http://www.ncbi.nlm.nih.gov/pubmed/23543389

Squirrel.

https://www.youtube.com/watch?v=fy-CBs0XNlM

POLL RESULTS

English sounds best spoken with

• an Indian accent 9%

• an English accent 30%

• a Jamaican accent 9%

• an Irish accent 17%

• a Scottish accent 23%

• Other Answers 12%

• American accent

• by The Chipmunks

• some intelligence

• English accents are much better for villains.

• ...the experience of a good education in the English language. Otherwise, it can be a painful listening experience.

Influenza is in the house

Jan 6, 2014

I had a hectic call weekend. Flu season is kicking in like gangbusters, and I saw 9 patients in the ICU with influenza and its complications. One of the hospitals in our system is a level one trauma center, and they offer advanced life support like ECMO, so we are a tertiary referral center for all the flu patients that could not otherwise be ventilated. There have been four deaths scattered across the 6 hospitals in our system, all young, i.e., less than 65.

The rest of the hospitals are certainly busy with influenza, 40 admits, and 40% of testing for flu-like illness is positive for influenza, almost all H1N1. Not as bad as 2009 when all the ICUs were at capacity. But still bad, especially for those with the flu.

I am kind of surprised that H1N has come back with such a vengeance. The last two years were relatively quiet, and I would have thought that everyone would either be immune from the vaccine or the disease.

Is it a wee bit of genetic drift, so the organism has mutated away from the immune response? It may be changing for the worst:

"In our study, the rate of severely diseased patients with influenza A(H1N1)pdm09 virus infection increased 3-fold in the first postpandemic season, resulting in an in-hospital mortality rate of 12% compared with 5% in the pandemic season. "

And we have had a number of nasal PCR negatives that were BAL positive, so I wonder if the virus has evolved a greater affinity for lower respiratory receptors?

Who knows. Smarter people than I will let us know in a year or so.

In the meantime, get the vaccine. Overall, it is about 50% effective for preventing influenza. I look at the flu vaccine like a seatbelt. It is not 100% at preventing death, but I would rather have a header with a texting driver wearing seat belts than without. That would be me wearing the seat belt. I would rather be exposed to influenza after the vaccine than without.

And if you are one of those healthcare workers who have not been vaccinated (i.e., a dumb ass), I refer you to the recent CID that the data suggests the HCW flu vaccination prevents deaths in patients.

“The cohort and case-control studies indicated significant protective associations for influenza-like illness and laboratory-confirmed influenza. No studies reported harms to patients. Using GRADE, the quality of the evidence for the effect of HCP vaccination on mortality and influenza cases in patients was moderate and low, respectively. The evidence quality for the effect of HCP vaccination on patient hospitalization was low. The overall evidence quality was moderate. Conclusions. The quality of evidence is higher for mortality than for other outcomes. HCP influenza vaccination can enhance patient safety.”

Rationalization

Clin Infect Dis. 2014 Jan;58(1):50–7. doi: 10.1093/cid/cit580. Epub 2013 Sep 17. Effect of influenza vaccination of healthcare personnel on morbidity and mortality among patients: systematic review and grading of evidence.

http://www.ncbi.nlm.nih.gov/pubmed/?term=24046301

Emerg Infect Dis. 2013 May;19(5):748-55. doi: 10.3201/eid1905.130034.Changes in severity of influenza A(H1N1)pdm09 infection from pandemic to first postpandemic season, Germany.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647517/

Interv Med Appl Sci. 2013 Dec;5(4):186–92. doi: 10.1556/IMAS.5.2013.4.7. Epub 2013 Dec 20. Atypical clinic presentation of pandemic influenza A successfully rescued by extracorporeal membrane oxygenation - Our experience and review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/24381738

Can't Exclude

Jan 8, 2019

The patient is admitted with acute fever, rigors, and hypotension to the ICU. He rapidly improves on antibiotics, and within 24 hours, both sets of blood cultures, drawn 5 minutes apart, grow S. pneumoniae with a penicillin MIC of 0.12.

They call me, and there is evidently no source for the bacteremia: no pneumonia, etc.

Pneumococcal bacteremia should have a reason, either something wonky with antibodies (a deficiency or, as is more common in my population, myeloma) or HIV.

“Fifteen patients (2.8%) had 31 episodes of pneumococcal bacteremia. Except for multiple myeloma (P < .02), the underlying disease was remarkably similar among patients with single and recurrent episodes of pneumococcal bacteremia. However, among patients positive for human immunodeficiency virus infection, those who had recurrences were at a more advanced stage of their disease than those who did not. The presence of an ultimately fatal underlying condition was more frequent in case patients (P < .001). Overall, 47% of the patients with recurrences died during their second episode of pneumococcal bacteremia…. Our data suggest that recurrence is more than anecdotal in patients with bacteremic infections caused by S pneumoniae (2.8%). We believe that recurrence is a warning sign of immunodeficiency. Patients with multiple myeloma, human immunodeficiency virus infection, solid organ tumors, and chronic liver disease with bacteremic pneumococcal infections should be offered antipneumococcal vaccine and other potentially preventive measures, despite doubts about their efficacy. This is justified by the high mortality rate associated with recurrent episodes (47%).”

I check immunoglobulin levels and an SPEP on everyone with Pneumococcal bacteremia and catch maybe a gammaglobulinopathy a year.

But this evaluation was negative for a reason.

But did he have a complication of bacteremia? He has a pacer and the loudest aortic stenosis murmur I have heard in years. TEE was not diagnostic for either a pacer wire infection or a vegetation, but the valve was so ratty the cardiologist said they could not rule out endocarditis. Of course, you can't. ECHO's, as far as I am concerned, only rule in endocarditis.

So I feel I need to treat for endocarditis. Pneumococcal endocarditis is relatively rare, I bet I have not seen more than a half dozen in my time, and none resistant to penicillin. If the wires are infected, I will not cure it. Fortunately, it would appear from the IDSA guidelines that MIC ceftriaxone alone at high dose should suffice. I would hate to add gentamicin given the age and kidney function of the patient.

“In one multi- center study with a relatively large (n 24) number of patients with IE caused by S pneumoniae resistant to penicillin (MIC 0.1 to 4 g/mL), patients were evaluated and compared with 39 patients who were infected with penicillin- susceptible strains. Several observations were made. Infection by penicillin-resistant strains did not worsen prognosis. High-dose penicillin or a third-generation cephalosporin can be used in patients with penicillin-resistant infection and without meningitis.”

Sometimes treating an infection that may not be there is the safer option, but never the satisfying option.

Rationalization

Int J Infect Dis. 2013 Dec 8. pii: S1201–9712(13)00350–0. doi: 10.1016/j.ijid.2013.10.020. [Epub ahead of print] Immunoglobulin deficiency in patients with Streptococcus pneumoniae or Haemophilus influenzae invasive infections.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/?term=24326288>

Clin Infect Dis. 2014 Jan;58(1):79–92. doi: 10.1093/cid/cit596. Epub 2013 Sep 17. Community-Acquired Bacterial Bloodstream Infections in HIV-Infected Patients: A Systematic Review.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/24046307>

Arch Intern Med. 1996 Jul 8;156(13):1429–34. Recurrent pneumococcal bacteremia. A warning of immunodeficiency.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/?term=8678711>

Quick Questions

Jan 10, 2014

I get all these odd questions over the phone, for which I often have no answer. Well, I sometimes have answers, but I pull them out of my nether regions. Part of being a specialist is ignorance with style.

The one question that gives me the screaming meemies is the how and if to treat a neurogenic bladder with a chronic catheter and maybe/maybe not symptoms of a UTI, some bacteriuria, and pyuria. Got me. And is there anything to do to prevent infections? Not in this reality.

Another question is it OK to put an artificial hip in this patient with bacteriuria? Probably. And I am happy to say there is actually a little data, so quit waking me up from my nap:

Arthroplasty infection after 3 months occurred in one of 228 patients undergoing THAs and 12 of 243 patients undergoing HAs (six of 117 in Group A and six of 126 in Group B); bacteria cultured from the wound were dissimilar to those cultured in urine samples in any case. No patient presented signs of PJI by 1 year after the index surgery&. We identified no case of PJI from a urinary origin in patients with asymptomatic bacteriuria whether or not they had been treated with specific antibiotics.

This week was an odd one. A patient with an elective aortic valve replacement and CABG for left main disease is scheduled the next day had a big scratch from his cat. Should I operate? I said no.

I don't worry that much about Streptococci, Staphylococci, or Pasteurella, but what about Bartonella?

Serum and blood samples from 192 patients, who reported animal exposure (100.0%) and recent animal bites or scratches (88.0%), were screened for antibodies by indirect immunofluorescence assays and for bacteremia using the BAPGM (Bartonella alpha Proteobacteria growth medium) platform. Predominant symptoms included fatigue (79.2%), sleeplessness (64.1%), joint pain (64.1%), and muscle pain (63.0%). Bartonella spp. seroreactivity or bacteremia was documented in 49.5% (n = 95) and 23.9% (n = 46) of the patients, respectively; however, indirect immunofluorescence antibodies were not detected in 30.4% (n = 14) of bacteremic patients. Regarding components of the BAPGM platform, Bartonella DNA was amplified from 7.5% of blood (n = 21), 8.7% of serum (n = 25), and 10.3% of enrichment culture samples (n = 29). Polymerase chain reaction (PCR) on only extracted blood would not have detected Bartonella infection in 34.7% (16/46) of bacteremic patients. Serology, in conjunction with blood, serum, and BAPGM enrichment culture PCR, facilitates the diagnosis of Bartonella spp. bacteremia in immunocompetent patients.

And

Using PCR in conjunction with pre-enrichment culture, we detected Bartonella henselae and B. vinsonii subspecies berkhoffii in the blood of 14 immunocompetent persons who had frequent animal contact and arthropod exposure.

Makes me nervous sticking in a prosthetic valve non-urgently; although the odds of seeding the valve are low, the results would be catastrophic. At some point, superstition kicks in for very low probability events. But there is this primitive reptilian part of my brain that whispers in my ear, "If I said go ahead, I just know the patient would get prosthetic valve endocarditis." I hate listening to it, but it seemed the safer option.

I also suggested a course of doxycycline or levofloxacin to play it safe.

Rationalization

Clin Orthop Relat Res. 2013 Dec;471(12):3822 9. doi: 10.1007/s11999 013 2868-z. Are antibiotics necessary in hip arthroplasty with asymptomatic bacteriuria? Seeding risk with/without treatment.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/?term=23430723>

Diagn Microbiol Infect Dis. 2011 Dec;71(4):430 7. doi: 10.1016/j.diagmicrobio.2011.09.001. Epub 2011 Oct 13. Bartonella spp. bacteremia in high-risk immunocompetent patients.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/21996096?dopt=Abstract>

Emerg Infect Dis. 2007 Jun;13(6):938 41. Bartonella species in blood of immunocompetent persons with animal and arthropod contact.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/17553243>

POLL RESULTS

I make

• rational decisions 7%
• decisions that I rationalize as rational 74%
• decisions based on gut feelings. 5%
• decisions to minimize fear, uncertainty and doubt 5%
• decisions only after putting a penny in the mystic seer machine in the Busy Bee Diner in Ridgeview, Ohio 7%
• Other Answers 3%
  • rational decisions for irrational times
  • I never make decisions. They're so ... final.

Close Enough

Jan 16, 2014

The patient is admitted with two days of rigors and fevers. He hurts all over, especially in the thigh and low back. It is a pain and leg weakness that gets him to go to the ER. No other signs and symptoms, although he has hemochromatosis and, as a result, diabetes. Regular readers of the blog know I dreaded writing that last sentence.

He is septic in the ICU, and as he wakes up, he has markedly decreased muscle strength in both of his thighs. He has to use a walker to get to the toilet and cannot lift either leg more than a foot off the bed. No back pain. His blood and urine are growing MRSA.

The muscle weakness makes me nervous, especially with S. aureus in the urine. I had some thought in my brain that S. aureus in the urine should make one worry about an epidural abscess? Discitis? Something with the spine.

As you know, I love the Googles, and in a few minutes I had the reference. It is nice not to have to remember facts exactly, just well enough to Google it. And here it is.

“In septic conditions, especially without IDUC, SABU may indicate SAB with foci of infection in the urinary tract or the vertebral column.”

So off to the MRI and close but no cigar:

"NO DISCRETE EPIDURAL ABSCESS IS NOTED. ENHANCING AREAS IN THE EPIDURAL SPACE AT L5-S1, LIKELY PROMINENT VENOUS STRUCTURES. PHLEGMONOUS TISSUE IS THOUGHT LESS LIKELY. RECOMMEND CLINICAL CORRELATION.

DEGENERATIVE DISC DISEASE AS DESCRIBED WITH A ANNULAR TEAR AND SMALL CENTRAL EXTRUSION AT L5-S1 RESULTING IN MILD NARROWING OF THE CANAL AND NEURAL FORAMINAL STENOSIS."

Radiologists love to shout.

The level that innervates the thigh is abby normal, but not textbook for infection. There does not appear to be enough anatomical changes to account for the weakness. But I have had a couple of MRIs that were false negatives for discitis early in SAB, so he is heading for a 6-week course of vancomycin. Maybe I will get an MRI again in a few weeks but spending money for curiosity's sake is so last century.

Rationalization

J Infect. 2009 Jul;59(1):37–41. doi: 10.1016/j.jinf.2009.05.002. Epub 2009 May 23. The clinical significance of concurrent Staphylococcus aureus bacteriuria in patients with S. aureus bacteremia.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/19539997>

Unexpected Twice

Jan 20, 2014

An unexpected pair of pathogens this week. The first was due to a positive MRI. The patient had a car accident and had an MRI for persisting back pain. The spine was fine, but a pulmonary nodule was found that did not change over the next few months. That led to the PET scan that glowed like Chernobyl. That led to the OR where it was removed as suspected cancer, and they referred the patient to me. Kind of like a bug sneezing. He had no symptoms.

The other was a case of H1N1 that was intubated for respiratory failure. CT had the usual diffuse infiltrates but also had two round nodules. The bronchoscopy cultures were positive, and they called me. As best as can be determined, before the abrupt onset of influenza, he too was asymptomatic.

Both had Cryptococcus. Neither had a positive antigen in the blood or CSF.

Cryptococcus is a problem in the great Pacific Northwest, having entered from Canada, where it has been endemic since the turn of the century. A failure of Homeland Security, I suppose, the yeast has been sweeping south like a fungal Schlieffen Plan.

I have seen a half dozen of cancers on PET over the years that turned out to be an infection, the majority having been Cryptococcus. The big question is whether or not to treat now that it has been cut out. I decided yes since there was other pathology in the lung that could have been residual disease.

The serendipitous finding in the influenza patient was a little more of an easy decision. He may not be immunodeficient at admit, but influenza may not be beneficial for immune function, and an ARDS lung would be fertile soil for Cryptococcus to grow.

So, both are going to get a course of fluconazole. Celebrity deaths come in threes. I hope that is not as true for Cryptococcus as well.

Rationalization

Einstein (Sao Paulo). 2012 Oct-Dec;10(4):502 4. Not all that shines is cancer: pulmonary cryptococcosis mimicking lymphoma in [(18)] F fluoro 2-deoxy-D-glucose positron emission tomography.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/23386093>

BMJ Case Rep. 2012 Jan 10;2012. pii: bcr1120115224. doi: 10.1136/bcr.11.2011.5224. Cryptococcal meningoencephalitis after H1N1 influenza.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/22665712>

J Immunol. 1986 Dec 15;137(12):3777 81. Influenza virus infection induces functional alterations in peripheral blood lymphocytes.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/?term=2431043>

Schlieffen Plan.

<https: data-preserve-html-node="true"//en.wikipedia.org/wiki/Schlieffen_Plan>

Because a Little Bug Went Ka-Choo

<https: data-preserve-html-node="true"//seuss.fandom.com/wiki/Because_a_Little_Bug_Went_Ka-choo>

POLL RESULTS

My Favorite Seuss Book:

• Horten Hears a Who 7%
• How the Grinch Stole Christmas 12%
• The Cat in the Hat 23%
• The Lorax 21%
• Hop on Pop 14%
• Other Answers 23%
  • Wacky Wednesday
  • fox in socks
  • circus Mcgurkus
  • Green Eggs and Ham.
  • green eggs and ham
  • One Fish, Two Fish, Red Rish, Blue Fish
  • One Fish, Two Fish
  • Given my age group, do you wonder that I can't recall the Seuss books?

Wrong. Thank Goodness

Jan 25, 2014

I saw a patient in follow up as an outpatient for MRSA pneumonia and bacteremia. He had been hospitalized at another hospital and had had a complicated course with an empyema and several days on the ventilator. He had been discharged on a course of ceftaroline and was doing ok, except...

When I saw him in clinic, one eye was red, closed, and photophobic. On exam, the pupil was open, and he could only see my hand vaguely.

He said that when he came off the ventilator, his eye had been red and tender, and the discharge diagnosis had called it conjunctivitis. No mention was made of decreased vision.

OMG, as the kids say. My heart sank. I thought for sure it was hematogenous seeding of the eye with the MRSA. I had one patient who seeded both his eyes and became blind from MRSA endophthalmitis.

It is a well-described manifestation of endocarditis and bacteremia, but rare. What really worried me is that he was now 10 days in with no treatment. I was sure the vision was as good as gone.

But I called the ophthalmologists, and they saw him an hour later.

It was closed-angle glaucoma. I would not have recognized that if it had walked up and bit me on the butt. At least I know if the eye is red, fixed, and sightless, I should call an eye doctor, even if I don't really know what is going on.

They did some sort of laser therapy, and when I saw him a week later, the vision had mostly returned, the eye was no longer red, and the pupil was normal. Whew.

There are a few cases of various infections associated with closed-angle glaucoma, mostly those that involve the retina (CMV, syphilis, histoplasmosis) but none with S. aureus. True, true, and unrelated in this case.

I think a lot of his symptoms were masked by being on the ventilator and then the recovery. He was too ill to note that his eye was an issue, especially since the pain was minimal, and it was passed off as dry eye from being on the ventilator.

Rationalization

Ugeskr Laeger. 2012 Nov 26;174(48):30178. [Endophthalmitis as the first clinical manifestation of infectious endocarditis].

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/23195356>

BMJ. 2006 Dec 2;333(7579):11578. Misdiagnosis of angle closure glaucoma.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/17138997>

POLL RESULTS

The organ I least understand is

• the eye. 10%
• the gallbladder. 1%
• the brain. 25%
• the mind. Specifically, that of my spouse. 40%
• the kidney. The loop of Henle never seemed reasonable. 21%
• Other Answers 3%
  • The harmonica
  • The skin. It does weird things.

Yeast is Yeast

Jan 28, 2014

Sometimes a consult is about what to make of an odd bug in an unusual place.

The patient is an otherwise healthy young female who has a recurrent vaginal yeast infection that does not respond to fluconazole. She has pain, itching, and dryness, so she is symptomatic.

After several failed courses of increasing fluconazole doses and duration, the primary sends off a culture. It is yeast. But not Candida. It is Rhodotorula mucilaginosa. The last odd yeast I was called about was a Cryptococcus laurentii. I had not heard of that Cryptococcus, although I had heard of Rhodotorula. I do not think I had ever seen a case, and if I had it was so long ago, and I have forgotten about it.

My first thought was an immunodeficiency. But everything checked out. No cancer or diabetes or other medical problems.

So, where did it come from? A review says

R. mucilaginosa is commonly isolated from foods and beverages. Several studies have reported the presence of R. mucilaginosa in peanuts, apple cider, cherries, fresh fruits, fruit juice, cheese, sausages, edible molluscs, and crustaceans. Although the consumption of food contaminated with yeast may not have a direct role in causing opportunistic infections, there is growing concern that food may be an underestimated source of environmental pathogens.

Most reports have it causing fungemia in the immunocompetent and focal, often prosthetic, infections in otherwise normal hosts. The organism evidently has a predilection for plastic. There is not a lot on the Pubmeds that I can find with the yeast causing symptomatic vaginitis, although it can be part of normal flora.

And, according to the ever-helpful Doctor Fungus, Rhodotorula is usually resistant to fluconazole (hence the clinical failure) but it susceptible to the hellaciously expensive voriconazole. So, I gave it a try to good effect. Cure.

Rationalization

Interdisciplinary Perspectives on Infectious Diseases Volume 2012 (2012), Article ID 465717, 7 pages http://dx.doi.org/10.1155/2012/465717 Epidemiology of Rhodotorula: An Emerging Pathogen

http://www.hindawi.com/journals/ipid/2012/465717/

Mycoses. 1989 Mar;32(3):131–5. Incidence of yeasts in pregnant and non-pregnant women in Nigeria.

http://www.ncbi.nlm.nih.gov/pubmed/2733724

Long Term Care

Jan 30, 2014

One of the allures of ID, at least for me, is that I cure most of the diseases I see. One of the downsides is that there is little continuity of care. I see most patients for no more than half a year at most, then usually never again. Except for HIV, which is now a mostly a chronic illness, I see few patients over time. That can also be a good thing, as there are some people who you really dread when you see their name on the day's clinic list. They are few and far between, so it is unusual to have patients on the schedule that make me cringe.

One patient I have probably written about before whom I look forward to seeing. She developed Cryptococcal meningitis and fungemia about 6 years ago, probably from all the Canadian bark dust at her workplace. Canada, to the North of the great Pacific NW, is rife with Cryptococcus gattii, which grows in the firs and pines that were made into bark dust. Maybe not, but that is my story, and I am sticking with it. If I ever get to go to Vancouver and Victoria BC again, I am not going to inhale.

And I am waiting for the first case or outbreak from a Christmas tree. It is only a matter of time before someone drags a Cryptococcal laden pine into the house some December and someone gets really unlucky. You heard it here first.

What has been amazing is the slow response to disease. After a very poorly tolerated course of amphotericin and 5-FC she has been 600 mg a day of fluconazole. 6 years ago, the titer was 1:512, and every year it falls by about a dilution. 128, 64, 32, 16, and now 1:8.

She has no diagnosable immunologic problem and feels well except for a bit of increased irritability and ringing in the ear since the meningitis. It is not uncommon to have either symptom after an inflammatory meningitis.

C. gattii tends to respond more poorly to fluconazole, but at least she is responding. I started the fluconazole in the era before voriconazole and posaconazole. There is some data to suggest these azoles may be of use in patients not responding to fluconazole, but there is not the clinical data I would like. Wiser cryptococcal experts than I have suggested staying the course, and the newer azoles are so damn expensive.

What to do when the titer reaches zero? Decrease the dose? Stop? Hope voriconazole is generic? At the rate the titer is falling, it may be some other doc who makes the decision since by then, I may be retired.

The nice thing is I get to see the patient and her spouse over time and chat. I occasionally miss the long-term contact with the patient.

Rationalization

Antimicrob Agents Chemother. 2013 Nov;57(11):5478–85. doi: 10.1128/AAC.02287–12. Epub 2013 Aug 26. Azole resistance in Cryptococcus gattii from the Pacific Northwest: Investigation of the role of ERG11.

http://www.ncbi.nlm.nih.gov/pubmed/23979758

Antimicrob Agents Chemother. 2012 Nov;56(11):5898–906. doi: 10.1128/AAC.01115–12. Epub 2012 Sep 4. Cryptococcus neoformans-Cryptococcus gattii species complex: an international study of wild-type susceptibility endpoint distributions and epidemiological cutoff values for fluconazole, itraconazole, posaconazole, and voriconazole.

http://www.ncbi.nlm.nih.gov/pubmed/22948877

Acta Neurol Taiwan. 2012 Mar;21(1):8–17. Neuro-psychological sequelae in HIV-negative cryptococcal meningitis after complete anti-fungal treatment.

http://www.ncbi.nlm.nih.gov/pubmed/22879084

Otolaryngol Head Neck Surg. 1997 Apr;116(4):536–40. Vestibular dysfunction due to cryptococcal meningitis.

http://www.ncbi.nlm.nih.gov/pubmed/9141406

Laryngoscope. 1991 Aug;101(8):876–82. Otologic sequelae after pneumococcal meningitis: a survey of 164 consecutive cases with a follow-up of 94 survivors.

http://www.ncbi.nlm.nih.gov/pubmed/1865737

I Have Returned

Oct 30, 2017

Back from vacation. And that terrible emptiness of being without rubor, dolor, calor, and tumor can be filled.

16 days off in a row. The most ever, not counting various surgeries in my career. No EMR, no journals, no calls, no pages and barely any email. No internet for most of the trip. I was surprised I did not miss it. At all. But hiking every day in the canyon country of Utah and Arizona is so mind-boggling amazing who has time to consider ID? I highly recommend it before the west burns. My only complaint is Utah is no good at making, or even offering, cocktails and beer. Can't have everything.

Time and tides wait for no man. Or perhaps I should say And te tide and te time þat tu iboren were, schal beon iblescet. The pus, it keeps on a flowing.

The patient survives Fournier's gangrene but is readmitted two months later with pelvic pain. The CT shows gas in the PS, pubic symphysis, joint and osteomyelitis around the symphysis pubis.

The symphysis pubis is a weird joint, or, like the sacroiliac, a weird pseudo-joint. Like oregano.

There is this whole unsatisfying literature on inflammation of the PS joint, called osteitis pubis, that occurs in athletes and postpartum. It is thought to be an overuse syndrome and not an infection, but I have always wondered. Perhaps it is more akin to the (admittedly controversial) idea that some herniated discs get secondarily infected with organisms of low pathogenic potential. These infections likely get better on their own. Some bacterial infections do resolve without antibiotics, sad to say. But there has never been a systematic prospective evaluation of osteitis pubis that I can find. It is too rare, so all there is are case series, aka an unhelpful hodgepodge.

The few PS infections I have seen have been complications of GU procedures and so obvious. E. coli is not subtle, even in a PS. In this case one of the organisms from the Fournier's has managed to get into the PS joint and adjacent bone. But which one?

My definition of futile is treating chronic osteomyelitis in a smoking diabetic with no debridement and empiric antibiotics. I have submitted the definition to the OED for their consideration. I am the professor in this metaphor btw. But, like the SI joint, try and find a surgeon to operate on it. No one has experience with the joint in smaller hospitals, so I have to transfer him for definitive diagnosis and treatment.

Rationalization

Acta Chir Orthop Traumatol Cech. 2016;83(6):411-417. [Infectious Inflammation of Pubic Symphysis (Symphysitis Pubis Purulenta): Five Case Reports and Literature View].

https://www.ncbi.nlm.nih.gov/pubmed/28026738

World J Orthop. 2015 Oct 18;6(9):672-9. doi: 10.5312/wjo.v6.i9.672. eCollection 2015 Oct 18. Osteitis pubis in elite athletes: Diagnostic and therapeutic approach.

https://www.ncbi.nlm.nih.gov/pubmed/26495244

Acta Orthop Belg. 2006 Oct;72(5):541-8. Osteitis or osteomyelitis of the pubis? A diagnostic and therapeutic challenge: report of 9 cases and review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/17152416

South Med J. 1985 Feb;78(2):213-4. Postpartum osteitis pubis

https://www.ncbi.nlm.nih.gov/pubmed/3975721

BMC Med. 2015 Jan 22;13:13. doi: 10.1186/s12916-015-0267-x. Could low grade bacterial infection contribute to low back pain? A systematic review.

https://www.ncbi.nlm.nih.gov/pubmed/25609421

There is a mold growing in what !?!

Jan 31, 2014

There is something you do not often see in blood cultures: hyphae and mold.

The last time, and I think the only time, I saw a patient with mold in blood cultures was a couple of years ago. A patient bought some meth, and his dealer tossed in a vial of brown water to use for shooting up. The brown water was chock-a-block full of mucormycosis, and he became transiently very sick.

This time it is a non-compliant dialysis patient. She comes in for dialysis, almost prn, acidic and hyperkalemic, gets dialyzed, then leaves, often AMA, for days at a time. She has been doing this for years.

This time she comes in volume long, hyperkalemic, febrile, and the blood is growing a mold; "fungal elements," at 48 hours. I called the lab and, yep, it's a mold of some kind, but they cannot tell me what.

The exam has lots of pathology: murmur, a non-infected looking catheter, a two-month right-sided non-cavitary pneumonia, a red dialysis fistula.

I figure this is going to be mucor of some sort (a slangish term for the family Zygomycetes, which consists of the molds Absidia, Apophysomyces, Cokeromyces, Cunninghamella, Mucormycosis, Rhizomucor, Rhizopus, Saksenaea, and Syncephalastrum. Those names are like supercalifragilisticexpialidocious).

These organisms occasionally cause disease in patients who have acidosis, in part because low pH increases available iron for the mold:

As mentioned earlier, patients in ketoacidosis, or indeed any systemic acidosis, have increased available iron in serum due to dissociation of iron from sequestering proteins in acidic conditions.

And she is certainly acidotic all the time. And it was a Zygomycetes. Repeat cultures are negative.

What is odd is there is no focal necrotic infection. I can’t find anything to debride, and her fevers and WBC are down. She was well on her way to improvement before the cultures became positive. Is this a transient Zygomyces like my meth user? My bet. From the catheter (pulled)? I can’t think it is a contaminant.

For now, she is on posaconazole and doing just fine. I am aware amphotericin B is considered the treatment of choice, but there are both social and access issues that make that amphotericin problematic. In the old, amphotericin B days, I never had a mucor survive. In the posaconazole era, I have yet to have a patient die of mucor.

I remain nervous that I am missing a source somewhere, but so far, I can't find it.

And she left AMA. Never saw her again.

Rationalization

Clin Microbiol Rev. 2005 Jul;18(3):556–69. Novel perspectives on mucormycosis: pathophysiology, presentation, and management.

http://www.ncbi.nlm.nih.gov/pubmed/?term=16020690

Crit Rev Microbiol. 2013 Aug;39(3):310–24. doi: 10.3109/1040841X.2012.711741. Epub 2012 Aug 24. Mucormycosis treated with posaconazole: review of 96 case reports.

http://www.ncbi.nlm.nih.gov/pubmed/22917084

Mercury Poisoning

Feb 3, 2014

No, not the Graham Parker song. Man, Squeezing Out Sparks was a great album. I have not listened to it in years. It is some of the music I lost in the transition from analog to digital. I still remember hearing my first CD, Even in the Quietest Moment by Supertramp at Fred’s Sound of Music all those years ago. No pop, no hiss, no scratch. I abandoned all my vinyl for digital and never looked, or listened, back.

I digress.

I saw the patient for Pneumococcal bacteremia with a septic joint. While taking the history, I discovered that he had had a tattoo that had been bothering him. It was red and itching and had been for months.

Looking at the tattoo, the dye was reds and blues, and it was indeed red, mostly in the areas of red dye. It was excoriated, and the edges of some of the ink were disrupted. I figured it was a mycobacterial infection, probably M. chelonae. There are no shortage of cases of atypical mycobacteria complicating tattoos.

When he followed up as an outpatient, I suggested he see a dermatologist before embarking on therapy because it would be nice to get a biopsy with cultures.

The dermatologist had a different diagnosis. Did you know inks have mercury for the color? From Wikipedia:

Heavy metals used for colors include mercury (red); lead (yellow, green, white); cadmium (red, orange, yellow); nickel (black); zinc (yellow, white); chromium (green); cobalt (blue); aluminium (green, violet); titanium (white); copper (blue, green); iron (brown, red, black); and barium (white). Metal oxides used include ferrocyanide and ferricyanide (yellow, red, green, blue). Organic chemicals used include azo-chemicals (orange, brown, yellow, green, violet) and naptha-derived chemicals (red). Carbon (soot or ash) is also used for black. Other compounds used as pigments include antimony, arsenic, beryllium, calcium, lithium, selenium, and sulphur.

And here I thought vaccines were full of toxins .

Hypersensitivity to red pigments is common, especially those containing mercuric sulfide (cinnabar).

It looked not unlike the picture in the NEJM link below. The dermatologist noted the skin redness improved in the hospital probably from the short course of steroids the patient received and prescribed some topical steroids.

Live and learn. This is yet another endless example of why ID, and medicine, is so fun.

Rationalization

Euro Surveill. 2013 Aug 8;18(32):20553. Systematic review of tattoo-associated skin infection with rapidly growing mycobacteria and public health investigation of a cluster in Scotland, 2010.

http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20553

Tattoo Allergy Joel Cook, M.D., and John Metcalf, M.D. N Engl J Med 2009; 361:e1July 2, 2009DOI: 10.1056/NEJMicm0706441.

http://www.nejm.org/doi/full/10.1056/NEJMicm0706441

POLL RESULTS

From 1979 I prefer

• Elvis Costello 21%
• Graham Parker 3%
• The Clash 9%
• Neil Young & Crazy Horse 26%
• Supertramp 29%
• Other Answers 12%
  • Queen, of course. After all, the topic today is ... Mercury.
  • Scooby-Doo...i was only 5 yrs old at the time.
  • Poco
  • I was 2 years old at the time

Wicked

Feb 5, 2014

You cursed MRSA! Look what you’ve done! I’m melting! Melting! Oh, what a world! What a world!

~The Wicked Witch of the West. Sort of.

The patient is an elderly female who develops cellulitis on the chest wall with a remarkable amount of pain. She slides into sepsis and is transferred to one of my hospitals for ICU care and debridement.

She is in septic, not toxic, shock, and is taken to the OR where extensive necrotizing fasciitis was found.

After 24 hours, all the cultures are growing MRSA. She has no good risk factors for this infection. No diabetes, no trauma, no nothing except some obesity with skin fold yeast causing a little maceration. Maybe that was all the anatomical problem needed to give the MRSA a toe hold.

If I were a superhero, my arch enemy would be S. aureus. Like in the comics, I never definitively defeat my nemesis, just win the battle only to have the villain return the next time stronger and better prepared.

MRSA is an increasing cause of necrotizing fasciitis, perhaps in part because so many strains make the Panton-Valentine leucocidin, which to human tissues is like water on Elphaba Thropp. Although S. aureus makes more than enough virulence factors to kill us without the PVL, I doubt the PVL is a good thing.

PVL strains are strongly associated with skin and soft-tissue infections, but are comparatively rare in pneumonia (OR 0·37, 95% CI 0·22–0·63), musculoskeletal infections (0·44, 0·19–0·99), bacteraemias (0·10, 0·06–0·18), and colonizing strains (0·07, 0·01–0·31). PVL-positive skin and soft-tissue infections are more likely to be treated surgically than are PVL-negative infections… Although strains carrying PVL genes are commonly identified in invasive staphylococcal disease, direct evidence increasingly suggests that PVL is not the main determinant of severity or outcome. Clinical studies from Australia have directly compared outcome for PVL-positive and PVL-negative strains for a range of invasive infections, consistently reporting outcome to be independent of PVL, with the exception of increased surgical treatment for skin and soft-tissue infections…In-vitro studies have failed to correlate the amount of PVL toxin produced by different S aureus strains with the severity of clinical disease and experimental studies of animal models of skin and soft-tissue infection and pneumonia have not convincingly shown PVL to have an effect on the development of disease independent of bacterial strain.

Fortunately for the patient, she is allergic to vancomycin. I say fortunately as the MIC was 1.0, and I increasingly suspect that vancomycin should be the fourth- or fifth-line drug against MRSA, especially as the MIC creeps up. Although what the ‘right’ order for treatment (ceftaroline, vancomycin, tigecycline, daptomycin, linezolid) should be/cannot be definitely determined at present from clinical trials, I have a bias against vancomycin. It sure would be nice to have comparative trials of all five. And it would be nice to have an end to global warming and universal health care. Probably not in my lifetime.

I opted for linezolid as it

offers by far the greatest number of patients included in controlled trials with a strong tendency of superiority over vancomycin in terms of eradication and clinical success.

Strong tendency probably means bias in the trial to favor the studied drug, but linezolid also messes with protein (i.e., virulence factor) synthesis, which may be a good thing. I will take what I can get. At least for necrotizing fasciitis, the real treatment of choice is cold steel in the hands of a good surgeon, and I do not need to rely only on antibiotics to cure the patient.

Rationalization

Lancet Infect Dis. 2013 Jan;13(1):43–54. doi: 10.1016/S1473–3099(12)70238–4. Epub 2012 Oct 26. The role of the Panton-Valentine leucocidin toxin in staphylococcal disease: a systematic review and meta-analysis.

http://www.ncbi.nlm.nih.gov/pubmed/23103172

Eur J Med Res. 2010; 15(12): 554–563. Treatment of complicated skin and soft-tissue infections caused by resistant bacteria: value of linezolid, tigecycline, daptomycin and vancomycin.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352104/

POLL RESULTS

My favorite superhero is

• Stealth. The Peter Cline version. 0%
• St. George, the Mighty Dragon 13%
• Batman 20%
• Spiderman 10%
• The Tick 33%
• Other Answers 23%
  • Captain America
  • Batwoman
  • mighty mouse
  • Peds Infc doc Mike Muszynsky... pardon the spelling... it's been a while. He cared about us techs in the Virology lab... once upon a time.

Worst case

Feb 7, 2014

The patient comes to the ER with 48 hours of fevers and weakness. He has no specific complaints but is not mentally clear due to his age and underlying medical problems, both acute and chronic.

In the ER, he is found to have a cellulitis and an acute coronary syndrome, whatever that is.

Are the two related? Those who listen to my podcasts are well aware of the bee in my bonnet. Infections are inflammatory, inflammation is pro-thrombotic, and that leads to clots in all the wrong places. UTI, influenza, bacterial pneumonia, and zoster are a few of the infections associated with TIA, stroke, pulmonary embolism, or myocardial infarction. Heck, even dental work is bad for you:

The rate of vascular events significantly increased in the first 4 weeks after invasive dental treatment (incidence ratio, 1.50 [95% CI, 1.09 to 2.06]) and gradually returned to the baseline rate within 6 months. The positive association remained after exclusion of persons with diabetes, hypertension, or coronary artery disease or persons with prescriptions for antiplatelet or salicylate drugs before treatment.

Inflammation is bad. It is why I would worry if any SCAM really could boost the immune system, it would also boost the risk of vascular events. Fortunately for patients, boosting of the immune system is a crock. While there are no studies (yet) to associate cellulitis with vascular events, I am never surprised to see a vascular event following an infection. It is my favorite confirmation bias.

So, he gets cefazolin in the ER, they take him directly to the cath lab, and place a few stents. The next day his blood cultures are growing S. aureus. Great. Staph bacteremia in a diabetic while a coronary stent is being placed.

Infected stents are rare. I have seen, and cured, one MSSA AAA stent. Most occur as a complication at the time of placement, and I could find no reports of stents going in while the patient was bacteremic. His is probably not involved, but I am not keen on the idea of being proved wrong by not treating and having him present with a coronary artery aneurysm or worse. Medical therapy can be effective, and surgery is not without its risks.

Intravenous antibiotics are the mainstay of therapy in patients with coronary stent infections. However, given that foreign body infections are extremely resistant to antibiotics and host defense mechanisms, surgery with debridement and/or stent removal may be required. Indeed, six of the ten patients with documented coronary stent infection underwent a surgical procedure, whereby the infected stent was removed completely in three subjects and partially in one patient. However, it is noteworthy that half of the surgical patients died, suggesting only a limited benefit of surgery in this population. Based on the currently available data, mortality may be as high as 40% despite antibiotic and/or surgical treatment.

I opted for a 6-week course of nafcillin, and I hope it nips the infection in the bud, which I gather has nothing to do with beer.

And he was either a cure or never needed the antibiotics in the first place. No way to know.

Rationalization

Ann Intern Med. 2010 Oct 19;153(8):499–506. doi: 10.7326/0003–4819–153–8–201010190–00006. Invasive dental treatment and risk for vascular events: a self-controlled case series.

http://www.ncbi.nlm.nih.gov/pubmed/20956706

Swiss Med Wkly. 2005 Aug 20;135(33–34):483–7. Coronary stent infection: a rare but severe complication of percutaneous coronary intervention.

http://www.smw.ch/docs/pdf200x/2005/33/smw–11142.pdf

Tough Job

Feb 10, 2014

The patient is a young female admitted with a routine pneumonia that cavitates. We do not have positive cultures, but she has no risks for unusual infections, so I bet the GPC seen on the gram stain was a pneumococcus that didn’t grow. Cavitating pneumococcal pneumonia is seen from time to time:

Necrotizing changes in the lungs were seen in 6.6% of a large series of adults with pneumococcal pneumonia but were often overlooked on initial readings. Patients with necrosis were not more likely to have bacteremia or more severe disease. Type 3 pneumococcus was the most commonly identified serotype.

I was asked to see the patient because it was not her first cavitary pneumonia, the other occurring 8 years ago.

Admitting history did not suggest an apparent immunodeficiency, and there was no microbiology to suggest an opportunistic infection.

CF and immotile cilia seemed unlikely by the fact she has a child.

No opportunistic infection makes HIV, CD4, and anti-cytokine antibodies lower on the list.

I suspected some version common variable immunodeficiency or CGD in that order. Respiratory infections point to antibody problems more than white cell problems.

The house staff had already sent off quantitative immunoglobulins, which came back while my resident was seeing the consult, so he did some reading and asked some pointed questions to explain the lab abnormalities.

Ever had a bad skin problem? Oh yeah. Years ago, a psoriasis-like rash on my neck and in high school a month where I had small pimples all over my body.

Any problems with your teeth? Oh yeah. My baby teeth did not come out and had to be pulled.

Textbook presentation of Job’s (hyperimmunoglobulin E) syndrome and her IgE’s were off the wall, 19 x the upper limit of normal.

Mutations in the STAT3 gene cause Job syndrome. This gene provides instructions for making a protein that plays an important role in several body systems. The STAT3 protein is involved in many cellular functions, including cell growth and division, cell movement, and the self-destruction of cells (apoptosis). To carry out these roles, the STAT3 protein attaches to DNA and helps control the activity of particular genes. Little is known about the effects of STAT3 mutations on the body’s cells and tissues. Changes in this gene alter the structure and function of the STAT3 protein, impairing its ability to control the activity of other genes. The defective protein disrupts cellular functions such as immune system regulation. The resulting immune system abnormalities make people with Job syndrome highly susceptible to infections. The STAT3 protein is also involved in the formation of cells that build and break down bone tissue, which could help explain why STAT3 mutations lead to the skeletal and dental abnormalities characteristic of this condition.

They also get fractures, sinusitis, cold S. aureus abscesses, and pneumatoceles, which may be developing instead of what was initially called a lung abscess. Nothing to do for it but treat the infections when they occur. Thirty years of sending off immunoglobulins, and I have diagnosed several myelomas and antibody deficiencies. This is the first Job's I have seen.

Rationalization

Clin Infect Dis. 2012 Jan 1;54(1):10–6. doi: 10.1093/cid/cir749. Epub 2011 Oct 31. The incidence of necrotizing changes in adults with pneumococcal pneumonia. <http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/22042878>

Jobs Syndrome

http://ghr.nlm.nih.gov/condition/job-syndrome

Scand Cardiovasc J. 1997;31(3):177–9. Pneumatocele complicated by fungal lung abscess in Job’s syndrome. Successful lobectomy with the aid of videothoracoscopy.

http://www.ncbi.nlm.nih.gov/pubmed/9264169

What is Worse than Drunk Driving?

Feb 12, 2014

How do you respond when you see a failure of policies and procedures?

For hand hygiene in my institutions if it is noticed that someone has not washed their hands the expected interaction is

“Foam, please.”

Then the expected response is to say, “Thank you.”

As a system, we recognize that during a busy multi-tasking day foaming can be forgotten and it is everyone's job to nicely remind each other to do the right thing. It is an approach that appears to work at my hospitals, although it took a lot of groundwork. I talked to every physician group in our hospital in advance so that we could nip in the bud any butt head doctor who wanted to throw a hissy fit when reminded to foam. And yes, there are those doctors.

Sometimes, though, I witness a more egregious failure of infection control, with HCW’s ignoring the isolation signs on the door. Over the years I have seen some interesting failures of adherence with isolation practices at the 7 hospitals I can cover. Since we are supposed to be nice and respectful to each other, I usually point out the failure to comply and gently re-enforce our policies. I am deliberately being vague as to what, when, and where, as the specifics are not important. I bet every ID doc and IC practitioner can come up with some horror story of people failing to follow isolation guidelines.

This got me thinking.

We have known about the efficacy of hand hygiene for 150 years.

We are 15 years into the MRSA/MDRO era, sliding slowing into the post-antibiotic era.

We know that we can spread resistant organisms in the hospital.

We know that when patients acquire resistant organisms, they are more like to get an infection from that MDRO and die. Let me repeat that.

People die from the bacteria we give them.

We know that proper adherence to infection control practices results in a decrease in the spread of organisms, a decrease in infections, and a decrease in death. Let me repeat that.

Proper infection control prevents death.

We know that the above information is widely and consistently disseminated and available. Everyone knows it.

Similarly.

We know that drinking makes for bad motor skills.

We know that drinking and driving increases the rates of car accidents and death.

We know if you do not drink and drive, it decreases accidents and deaths.

And we know that the above information is widely and consistently disseminated and available. Everyone knows it.

So, is there a difference in fundamental behavior between someone who does not follow infection control procedures and a drunk driver? Not really.

I can think of two differences. When a drunk driver kills someone, you know exactly when it happens. You never know when and which HCW passes on a fatal infectious disease.

And compared to hospital acquired infections, drunk drivers are amateurs. Drunk drivers kill 10,000 a year in the US and alcohol is involved in 700,000 accidents.

Hospital-acquired infections? 1,700,000 a year with 98,000 deaths.

Poor infection control helps kill ten times the number of people that drunk drivers do.

At least you can argue that alcohol ruins people's judgment; what is the excuse for the HCW who ignores the isolation sign for an MRDO? In the year 2014 I cannot think of a legitimate reason.

I think that may be my new rant (or as my kids call it, a meme) for infection control: failure to comply is worse than drunk driving. It is more like drinking and driving. While texting. At night. On a curving road. Going 75. In the sleet.

If you are a patient, a family member, or a HCW and you witness a failure of infection control, remember you are seeing behavior far more dangerous to you, your loved one, and your patient than drunk driving. You might mention it to someone.

Wild Ideas

Feb 14, 2014

I love wild speculation. I do not take it seriously, especially when the source is me, but off the wall ideas are fun. I especially like off the wall speculation that explains why a patient has a particular presentation.

The patient was admitted to another hospital several weeks ago for fevers and sepsis after shooing up heroin. One of his blood cultures grew Cryptococcus laurentii. Work up for immunodeficiency and meningitis was negative and he left AMA, preferring to answer the siren call of heroin.

I am not sure where the Cryptococcus came from in this patient. It is not noted to found in heroin but is found in soil and birds. Homeless, I suppose he picked it up from the environment, and there are no shortage of feral pigeons in downtown Portland.

Fast forward 2 weeks. He is back in with fevers, hypotension, and a touch of ARDS right after injecting heroin.

Heroin, as I have mentioned in the past, is not sterile. It is a rich microbiologic stew of multiple organisms. I can’t say the heroin is contaminated since it is not as if they are trying to produce a sterile product. Heroin, and the bacteria that come with it, are a natural product.

Here is where I am going to speculate wildly. Yesterday a colleague mentioned that she had watched a TV show on the Science network that suggested rain was due to bacteria. That was news to me. I knew vaguely that the air had, like heroin, a rich ecosystem, but other than as a distribution mechanism for fungal spores, I didn’t give it much thought. Turns out it is true:

That means that Pseudomonas syringae and the other living microbes in the clouds might just be perpetuating themselves—and spreading—when it snows or rains.

And

He analysed the hailstones’ multi-layer structure, finding that while their outer layers had relatively few bacteria, the cores contained high concentrations. “You have a high concentration of ‘culturable’ bacteria in the centres, on the order of thousands per millilitre of meltwater…

...that the bacteria’s rise into clouds, stimulation of precipitation, and return to ground level may have evolved as a dispersal mechanism

I only mention this because the patient uses rainwater to mix the heroin and, with it, perhaps a bolus of Pseudomonal endotoxin to explain the culture-negative sepsis.

Or not. Even for my overactive imagination, it is a stretch, but fun to consider. I always like to say that everything of interest in the world has an infection at its center. Guess that is true of rain as well.

Rationalization

Feral pigeons as carriers of Cryptococcus laurentii, Cryptococcus uniguttulatus and Debaryomyces hansenii. Medical Mycology Volume 37, Issue 5, pages 367–369, October 1999

<https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/10520162>

From Trees and Grass, Bacteria That Cause Snow and Rain.

http://www.nytimes.com/2010/05/25/science/25snow.html?\_r=0

Do Microbes Make Snow?

http://www.scientificamerican.com/article/do-microbes-make-snow/

Bacteria in the sky, making it rain, snow, and hail.

http://all-geo.org/highlyallochthonous/2011/05/bacteria-in-the-sky-making-it-rain-snow-and-hail/

POLL RESULTS

Rain is due to

• bacteria 13%
• being unloved. 10%
• washing the car 49%
• bad thoughts 13%
• tears 5%
• Other Answers 10%
  • when Laura, the Light of Zartha, is sad
  • Marriage equality.
  • Physics, hydrology and thermodynamics.

Not Cancer

Feb 17, 2014

The patient is being seen for routine health care, and the primary has a listen to the lungs. She hears consolidation in one area. The patient has no symptoms of pneumonia. A chest CXR shows a lung mass, that leads to a hot pet scan that leads to a partial lung resection (too deep for a biopsy) that shows not cancer.

The patient is a diabetic renal transplant patient with a cough but no other symptoms. She has a chest X-ray that shows a peripheral mass that has a CT guided biopsy that shows not cancer.

The patient is an AIDS patient with the new diagnosis of cryptococcal meningitis. After a course of amphotericin and 5 FC, he is changed to high dose fluconazole. He is admitted a month later with altered mental status, and a CT of the chest shows that he now has several large lung masses that are biopsied and show not cancer.

All three cases are in the last few months, and all are Cryptococcus. In none of the cases did we grow the bug, but all had a positive antigen and/or consistent pathology. I suspect, but do not know, that all were C. gattii. I am seeing quite the surge of cases this winter.

I am surprised. C. gattii grows on firs and pines in the great Pacific Northwest and has slowly been invading south from BC. I would have thought that I would see the organisms come summer when the dry air and dirt would aerosolize the yeast, not the cold, dank winter. I expect in the years to come that we will see a seasonal outbreak in January that will be traced to Christmas trees. Not yet. But it will happen.

Where did they get their Cryptococcus? Not certain in two, but one lives downwind of a company that chips and shreds trees.

Airborne concentrations increased during felling of the red alder, but no substantial change was observed for the Douglas fir. However, for both trees, air samples taken during branch chipping indicated much greater (10- to 140-fold) airborne C. gattii concentrations than were observed during quiescence. Aerosolization of C. gattii through such activities is likely to increase the risk of exposure and the dispersal of cryptococci through wind.

And I have mentioned the case I think was acquired from bark dust in the horse training arena, and another who worked in a tree nursery with lots of firs and pines trucked in from the North. Part of the endless fun of ID is trying to discover the source of the infection.

It may be getting to the point where any patient in the great Pacific NW who has a lung mass should probably get a cryptococcal antigen before resection. And if you are visiting the great Pacific NW, might I advise against inhaling?

Rationalization

Cryptococcus gattii Dispersal Mechanisms, British Columbia, Canada.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725814/

Ancient Dispersal of the Human Fungal Pathogen Cryptococcus gattii from the Amazon Rainforest.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0071148

Belly Pain

Feb 19, 2014

The patient has the abrupt onset of abdominal pain about 6 days prior to admission. The pain is mostly RUQ but does pass the midline. She gets a work-up as an outpatient: CT, routine labs, and nothing is unusual. The pain continues, and she is admitted. Afebrile, her abdominal exam is benign, maybe maybe some RUQ tenderness to deep palpation. UGI shows nothing, and she remains afebrile. She does have CLL for which she has been receiving rituximab, but besides the abdominal pain, there is nothing abnormal.

Then, on day 9, she gets waves of dewdrops on a rose petal. Chickenpox, or in this case, since she had the disease as a child, disseminated zoster.

Is that the cause of the pain?

My first thought was that the pain was rashless shingles. It is not unheard being first suggested as far back as 1907, although hard to diagnose.

But the abdominal pain was not as dermatomal as I would have liked, so I turned to the consultants' best friend, PubMed.

It turns out that visceral zoster occurs, presenting as abdominal pain most often in patients with hematologic malignancies or transplants. But the interesting thing is there can be a delay between the onset of pain and the rash.

We report a 54-year-old man who developed visceral varicella-zoster virus (VZV) infection after autologous peripheral blood stem cell transplantation (auto-PBSCT) without using immunosuppressive agents for multiple myeloma. He suffered from severe abdominal pain 2 months after auto-PBSCT, and morphine chloride was needed to control it. Since the characteristic skin rash of VZV infection appeared over his entire body on the seventh hospital day, aciclovir was immediately started with favorable results. It is extremely difficult to diagnose the VZV infection when severe abdominal pain proceeds and the eruptions characteristic of VZV infections are absent.

Once the rash started, he received iv acyclovir and did quite well. I suspect more because his hematologic problem was relatively mild, at least compared to a bone marrow transplant.

I have been misled in the past by zoster pain that preceded the rash. I remember a case as intern of a 90-year-old who we worried was dissecting a thoracic aneurysm or having some equally catastrophic cause of his severe chest pain. He got the state-of-the-art workup (for 1984, as I remember we did not have a CT scanner at the time) with no results. Then on day three, the zoster rash blossomed. I had a similar case of belly pain presenting a few days before the rash back in the days when I would function as a general medicine attending i.e., a long time ago.

It is hard to make a diagnosis of zoster quickly when the rash isn't there.

Rationalization

J Infect Dis. 1992 Aug;166 Suppl 1:S30-4. Varicella-zoster virus reactivation without rash.

http://www.ncbi.nlm.nih.gov/pubmed/1320648

Curr Top Microbiol Immunol. 2010;342:243-53. doi: 10.1007/82_2009_3. Neurological disease produced by varicella zoster virus reactivation without rash.

http://www.ncbi.nlm.nih.gov/pubmed/20186614

Nihon Shokakibyo Gakkai Zasshi. 2010 Dec;107(12):1947-55. [Case of visceral varicella-zoster virus infection after autologous peripheral blood stem cell transplantation in which severe abdominal pain preceded the skin rash].

http://www.ncbi.nlm.nih.gov/pubmed/21139364

POLL RESULTS

I am most often fooled by

• the history 20%
• the physical 3%
• the ER 13%
• the EMR 23%
• Pete Townsend 35%
• Other Answers 8%
  • People who have issues with veracity.

Harm

Feb 21, 2014

I was consulted recently for a patient with advanced HIV disease who was admitted with pneumonia. Her disease is stable, but her immune system is suboptimal. The CD4s, for those of you in the know, are hovering around 100. Her father and husband developed an upper respiratory infection, and she had to take care of them both

She knew that she needed to protect herself from acquiring their illness, so she took Airborne.

And, surprise, surprise, she went on to develop first fevers, then a cough, then shortness of breath, then an admission to the ICU for pneumonia with a touch of sepsis.

I have written about Airborne in the past. There is no reason, besides the fact it was invented by a schoolteacher, that it would have any effect what-so-ever in preventing infection. We are all aware that schoolteachers are the acknowledged masters at infection prevention.

As the Medical Letter mentioned

There are some concerns. First, there is no conclusive evidence that this product or any of its ingredients prevents colds or shortens their duration. Second, the adult tablet contains 1 g of vitamin C, and the directions for use advise taking 1 tablet at the first sign of a cold and repeating the dose every 3 hours as necessary. Vitamin C in doses higher than 1 g increases oxalate and urate excretion and may cause kidney stones (EN Taylor et al, J Am Soc Nephrol 2004; 15:3225). Third, the safety of this herbal extraction combination has not been established. And with herbs and dietary supplements in general, we only have the manufacturers' word on the label for what's in them.

and why they paid a 30 million dollar fine to the FTC:

"there is no competent and reliable scientific evidence to support the claims made by the defendants that Airborne tablets can prevent or reduce the risk of colds, sickness, or infection; protect against or help fight germs; reduce the severity or duration of a cold; and protect against colds, sickness, or infection in crowded places such as airplanes, offices, or schools."

But as long as these products contain the quack Miranda and are unregulated, they can and will be sold to people who think they have efficacy even if the label says, "This product is not intended to diagnose, treat, cure, or prevent disease”. It does support the immune system, as if the immune system needs a bra or jock strap. That is a phase that always inspires confidence.

I suspect that she would have acquired the infection no matter what she did. My specialty is called Infectious diseases for a reason. But she may have been better off spending her money on a mask and good handwashing rather than on the false sense of security evident in the use of Airborne. And a false sense of security tends to cause people to be less fastidious with effective infection prevention.

One of the many ways pseudo-medicines can harm.

POLL RESULTS

• to prevent a cold, I
• take airborne 0%
• take a z-pack 2%
• don't inhale 29%
• 1 oz of single malt scotch q 2 h until it passes 33%
• take vitamin C, D, echinacea, honey, and garlic. 11%
• Other Answers 24%
  • Avoid all human contact
  • take zinc supplements
  • avoid others with a cold and wash my hands.
  • undergo a state of hibernation until the respiratory virus season ends.
  • Wash my hands
  • ...trust to luck and try to avoid people. To treat, elderberry capsules at the first symptoms seem to work well. YMMV
  • Wash my hands and stay wear a mask.

I guess it does, doesn't it

Feb 24, 2014

The patient is admitted with fevers and low blood pressure. She has a mid-thoracic spinal injury from a motor vehicle accident several years ago. She also likes to use intramuscular heroin, not having to worry about any discomfort in her legs from injecting.

Review of systems and exam are non-focal on admission, but she is clinically ill with SIRS and, after cultures and antibiotics, is off to the ICU.

The next day there are two new pieces of information: the blood is growing Group A Streptococcus and the CT, obtained looking for a source of infection, finds a huge iliopsoas abscess. Really big, the size of a very large grapefruit. Biggest iliopsoas I have ever seen, and I have seen a few.

So, they call me, and I say that’s odd. Group A Streptococcus doesn’t cause iliopsoas abscesses. It is more likely S. aureus and part of a mixed infection, but it is large (did I mention that?) and needs draining.

The patient was taken to the OR, and the abscess was drained. It grew nothing but Group A Streptococcus.

I guess Group A Streptococcus does cause iliopsoas abscesses after all.

Pubmed (or for me, Pusmed) suggests I was almost right. There are three cases reported in adults and 4 in children, so it is not high on the list of microbiologic etiologies. Two cases were from a cutaneous site, one an IVDA. The third was a sore throat gone very very bad.

But still, I should know better after all these years to not make a pronouncement that bug x does not cause disease y. Any bug can infect any organ at any time. It is, after all, the lifeblood of this blog.

As I have mentioned, I hate when a one-of-a-kind case is described, and the authors suggest the organism should be considered in future cases. Forgetaboutit. If you see an iliopsoas abscess, it is going to be S. aureus or a mixed infection. Don’t even consider a Group A Streptococcus. It almost never happens.

Rationalization

Ann Dermatol Venereol. 2010 May;137(5):369–72. doi: 10.1016/j.annder.2010.02.020. Epub 2010 Apr 2. [Two cases of psoas abscesses caused by group A beta-haemolytic streptococcal infection with a cutaneous portal of entry].

http://www.ncbi.nlm.nih.gov/pubmed/20470918

J Clin Microbiol. 2003 Oct;41(10):4888–91. Molecular characterization of a strain of group a streptococcus isolated from a patient with a psoas abscess.

http://www.ncbi.nlm.nih.gov/pubmed/14532252

POLL RESULTS

I follow the rule

• Common things are common 46%
• Common things not common in ID 2%
• Uncommon things are common. Huh? 2%
• Tautologies are tautological.
• 30%
• Who cares what grows, I can kill damn never everything with Vancomycin and Piperacillin-Tazobactam 15%
• Other Answers 4%
  • the bugs are smarter than we are.
  • Having faith in the basic goodness of mankind and trusting people to do the right thing is the most certain way to get screwed that you will ever discover.

Sir Osis of Liver

Feb 26, 2014

A middle-aged male with end-stage liver disease from a combination of alcohol use and hepatitis C is admitted with an altered mental status and MOSF. He grows E. coli out of his ascites and blood and MSSA out of his blood and urine. The prior doc had directed most of the antibiotic thought against the SBP and bacteremia, first with iv ceftriaxone and now po ciprofloxacin for the E. coli.

During this time, the patient only kind of sort of improved. I often get called on change of service when a doc is picking up a new patient, evaluates their clinical course, and wonders if the patient has the right plan for their infection. So, the new doc comes on and is concerned about the slow improvement in the patient. The WBC is not coming down, and clinically the patient is not much better.

It’s the economy stupid. That was the motto coined by James Carville back in the day. My equivalent might be, It’s the Staph, stupid. Except for the folks with whom I work are many things, but stupid is not on the list. Still, people just do not give S. aureus enough thought on occasion.

I do not find much on the patient but a murmur and all the stigmata of a Childs class C liver disease. They want to put a shunt in to help with the encephalopathy. I figure that may not be an optimal idea until we make sure he does not have an ongoing endovascular infection, i.e., I.E.

The patient has a double hit. Polymicrobial bacteremia with S. aureus is bad:

Polymicrobial SAB is associated with more severe illness than monomicrobial SAB, with neutropenia, biliary tract catheters and intra-abdominal infection being significant risk factors for polymicrobial SAB.

as is S. aureus bacteremia in the cirrhotic

The 30-day mortality rate of LC patients was significantly higher than that of patients with other diseases (32 % vs. 22 %, respectively; P = 0.047).

He is now on an anti-staph antibiotic and will be getting a TEE in the near future.

And what do Crohn's, cirrhosis, and ophthalmology all have in common? A vestigial ‘h’ that serves no purpose except to make words hard to spell. We need to get the ‘h’ out of there.

Rationalization

Knight-Mare Hare

https://www.facebook.com/video/video.php?v=2185154024396

Eur J Clin Microbiol Infect Dis. 2012 Dec;31(12):3309–16. doi: 10.1007/s10096–012–1697–4. Epub 2012 Jul 26. Clinical significance of Staphylococcus aureus bacteremia in patients with liver cirrhosis.

http://www.ncbi.nlm.nih.gov/pubmed/22833245

J Infect. 2012 Aug;65(2):119–27. doi: 10.1016/j.jinf.2012.02.015. Epub 2012 Mar 9. Clinical significance and outcome of polymicrobial Staphylococcus aureus bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/22410381

No one has EVER seen this before. And maybe not me.

Feb 28, 2014

The patient has unresponsive C. difficile, community acquired. They have tried vancomycin and metronidazole in various permutations with a worsening white count and differential and diarrhea.

She has modest abdominal pain and at one point, passes something that looks like a colonic sausage casing. I did not see it, but what the hospitalist describes sounds like the patient passed bowel lining.

There are psychosocial issues that are limiting care: she is refusing most of the offered medical care. She refuses a stool transplant (not an easy sell under the best of times) and colonoscopy but will take oral medication. Psychiatry is consulted and thinks she has hypoactive delirium a process that mimics depression and prevents her from making good decisions. I had not heard of hypoactive delirium before.

We add fidaxomicin. It is the first time I have given that medication. It looks great in clinical trials, perhaps superior to the standard therapies, but most of my patients can’t afford a medication that costs about as much as a high-end MacBook Pro.

We are worried about perforation, so we get a CT. Very thickened colon and two, count them two, colo-colo fistulas. I didn’t expect that.

There are no cases of colo-colo fistula from C. difficile, just one colocutaneous fistula. It makes me wonder if there is some other process, like Crohn's, that more commonly causes bowel fistulas. Without a colonoscopy to look for another cause, I can't say for sure the fistulas are from the C. difficile.

The patient is responding to the fidaxomicin with improving parameters, but there are still those fistulas to worry about and their real etiology; do I have the first case ever or a true-true and unrelated? I may never know.

There is the perfect world, and then there is the one in which I practice where it is rarely smooth and often filled with the unexpected. It gives me something to blog about.

Postscript

One follow-up. The patient with the C. difficile and the two fistulas finally had a colonoscopy and did indeed have Crohn’s.

Rationalization

COLOCUTANEOUS FISTULA COMPLICATING CLOSTRIDIUM DIFFICILE (CD) COLITIS AJ Al Alwan, MJ Beyak, KN Jeejeebhoy

http://www.pulsus.com/cddw2002/abs/abs131.htm

Palliat Med. 2006 Jan;20(1):17–23. Hypoactive delirium: assessing the extent of the problem for inpatient specialist palliative care.

http://www.ncbi.nlm.nih.gov/pubmed/16482754

Expletive Deleted

Mar 3, 2014

There has been catching up on the part of the hospitals in my fair city to make sure physicians, who have a long history of being slackers, are up to date on vaccinations and ppd status.

Having to document their ppd TB has been the big pain for many MD’s. Many of us, like me, converted years ago and did our INH. Try finding those records, in another state in a more primitive medical era. Not easy.

And then there are the childhood diseases: chickenpox, mumps, measles. I had the first two. I have 8mm film that my parents shot of me with both illnesses. I have no idea why. But I am adorable. I had V1 shingles as a fellow, so my chickenpox status is reasonably assured. And I was in the measles trials to prove efficacy, although I do not know if it was in the treatment or placebo group. I have been assured by my father that I eventually was vaccinated.

For us old geezers, children of the pre-vaccine era, all we had to say was yep, we had the disease as kids, and all was good.

Currently, one of our ICUs has a cluster of chickenpox. Three patients turned positive with a rash all within 4 days of each other. It seems unlikely they would all have reactivation disease in the same period. Given the incubation period, they must have all had the same exposure 10 to 21 days ago, but we know of no index case in the staff of the unit, although the investigation is ongoing. It could have been a visitor. It would not have been the first time an infected family member wandered through the ICU. We are big on giving families access to the ICU, but families are not always big on paying attention to the rules, like to stay out if you are sick. Years ago, we had a kid with pertussis in the NICU, coughing all over the kids for 30 minutes before the nurse noticed. There were no secondary cases, but if I had my way, there would be no visitors in the hospital.

It was my partner who diagnosed the illness in all three patients, and in two there was a delay of a day or two before they were put in proper isolation. He had chickenpox as a kid, or so his parents told him. He never had the vaccine or a titer. Until today. Zip. Nil. Nada. He was puzzled as he has taken care of many patients with zoster over the years, but I figure no MD is ever in a room long enough to get an infectious disease.

Expletive deleted.

I had to send him home for 21 days after his last exposure, and I so did not want to. But I can’t give him a pass just because it would make my life easier. So I just doubled my work for 11 days, and I get to take call this weekend.

Double expletive deleted.

I hope he is genuinely immune and, since he had the vaccine yesterday, he will get a rapid anamnestic response and have a titer in a week.

Otherwise? I hope he comes down with chickenpox tomorrow. That will be the fastest way for him to get back to work. In the meantime, while I cover his service, I am going to tell everyone he is out with secondary syphilis. Serves him right.

Rationalization

Chickenpox (Varicella).

http://www.cdc.gov/chickenpox/index.html

Infestation

Mar 5, 2014

I itch just writing this. The patient is a homeless alcoholic who is admitted with altered mental status. He is covered with lice and scabies. It is impressive. There is more damaged/excoriated skin than normal skin, although not the hyperkeratotic lesions of what we used to call Norwegian scabies, now called crusted scabies.

Crusted scabies (also called Norwegian scabies) is a very contagious variant of scabies in which there are thousands or even millions of mites, but very little itch. The patient presents with a generalized scaly rash. It is frequently misdiagnosed as psoriasis. Unlike the usual form of scabies, crusted scabies may affect the scalp.

Evidently, the International Norwegian Cabal objected, so crusted scabies it is. If anyone wants to call it Crislip Scabies, it is OK with me. The nurses said that when they put the ointment in the hair, they saw waves of parasites rundown the forehead and neck trying to escape certain death, like Orcs fleeing a tidal wave.

Pardon me. I must scratch again, and I did not even see the patient until after he was treated

He was also febrile, and 48 hours later, one of his blood cultures became positive for MSSA. Certainly, his skin was damaged enough to be colonized with S. aureus, and S. aureus is part of the human condition. But could it be the lice or scabies as a vector for the S. aureus?

We isolated bacteria from ticks, lice, and fleas. These bacteria were mostly Gram-positive (Firmicutes), although representatives from the Proteobacteria (alpha, beta, gamma subdivisions) and CFB group were also isolated. Most of the isolates we found were from genera that were present in most of the ectoparasites studied, but a few genera were restricted to one species of ectoparasite. The most commonly isolated genera were Stenotrophomonas, Staphylococcus, Pseudomonas, Acinetobacter and Bacillus.

and having scabies is a risk for Staphylococcus aureus bacteremia (SAB) in some populations.

A total of 125 patients (indigenous, 111; non-indigenous, 14) presented with SAB during the study period Indigenous adults were more likely to present with an infective focus (indigenous, 75; non-indigenous, 6) (P = 0.004). These were most often skin infections (skin abscesses, 31; scabies, 4).

But it looks more than the trauma to the skin is more important as a risk than the bugs as a vector:

Aerobic and anaerobic bacteria were grown from specimens obtained from 30 children with secondarily infected scabies lesions. Aerobic or facultative bacteria only were present in 14 (47%) patients, anaerobic bacteria only were present in 6 (20%) patients, and a mixed anaerobic-aerobic flora was present in 10 (33%) patients. Fifty isolates were recovered (1.7 per specimen); 27 were aerobic or facultative bacteria and 23 were strict anaerobes. The predominant aerobic and facultative bacteria were Staphylococcus aureus (nine isolates), group A streptococci (five isolates), and Pseudomonas aeruginosa (three isolates).

The scabies burrow looks to be an excellent place for S. aureus to set up shop before invading the bloodstream.

Scanning electron microscopy demonstrated extensive bacterial colonization of scabies burrows honeycombing the stratum corneum of an elderly woman with erythroderma. Cultures of scybala revealed hemolytic Staphylococcus aureus

So it appears scabies and lice are better than bedbugs for promoting S. aureus.

The bedbugs were homogenized and streaked onto standard microbiological media, including 5% sheep blood agar. ..For 2 patients, VRE was isolated from 1 bedbug each. For 1 other patient, MRSA was isolated from 3 bedbugs.

Although if anyone has homogenized lice or scabies and looked for S. aureus, I cannot find the reference.

I am now going to take a shower.

Rationalization

Parasitol Res. 2003 Mar;89(4):32634. Epub 2002 Dec 11. A survey of bacterial diversity in ticks, lice and fleas from Australia.

http://www.ncbi.nlm.nih.gov/pubmed/12632173

J Am Geriatr Soc. 2009 Sep;57(9):17134. doi: 10.1111/j.15325415.2009.02412.x. A case report of crusted scabies with methicillin-resistant Staphylococcus aureus bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/19895437

Actas Dermosifiliogr. 2008 Jun;99(5):4256. [Staphylococcus aureus sepsis as a complication of scabies].

http://www.ncbi.nlm.nih.gov/pubmed/18501183

J Clin Microbiol. 1995 Aug;33(8):213940. Microbiology of secondary bacterial infection in scabies lesions.

http://www.ncbi.nlm.nih.gov/pubmed/7559963

J Am Acad Dermatol. 1988 Oct;19(4):6738. Staphylococcus aureus colonization of burrows in erythrodermic Norwegian scabies. A case study of iatrogenic contagion.

http://www.ncbi.nlm.nih.gov/pubmed/2972758

Volume 17, Number 6June 2011 Bedbugs as Vectors for Drug-Resistant Bacteria

http://wwwnc.cdc.gov/eid/article/17/6/101978\_article.htm

POLL RESULTS

I itch when

• I see fleas 2%
• I see lice 12%
• I see scabies 6%
• I see the words fleas, lice or scabies 60%
• I see Norwegians. 15%
• Other Answers 5%
  • cold and dry weather
  • I don't itch.

What are the odds?

Mar 10, 2014

As I mentioned a week ago, my partner was exposed to chicken pox but is not immune to VZV, having slipped through the screening cracks on his way up the medical-industrial complex. So, he is out for the incubation period, and I have twice the amount of work to do. Unfortunately, my multiple personality disorder does not allow me to be at two hospitals at the same time, so the days are longer. Fortunately, it's ID. I have seen so many cool cases the last week, and I have grist for the ID mill for several weeks. Double the work is double the fun, although at my age, double the fatigue.

All three patients with VZV are on the ECMO service, a uniquely ill and physiologically stressed population. Being partially responsible for these patients makes me feel like an intern, trying to grasp the physiology, the technology, and the consequences of ECMO. I am not certain that my 30 years of knowledge and experience apply to these patients, and when I make recommendations, it is not with the usual arrogant authority of someone who thinks he really knows his stuff. I guess it is good to be a newbie every once and awhile.

The VZV is interesting. The three cases all occurred within about 4 days of each other, suggesting a common exposure around 14 days ago. As best we can tell, there is no index case, unless it was a family member with chickenpox that went unnoticed.

But even more curious is the serologies all came back with very high IgGs and negative IgMs to VZV. I think we have a pseudo-cluster, and all three cases are reactivation VZV.

Also, all three are middle-aged. It has been suggested that one of the consequences of the VZV vaccine will be to lower the age of the first case of shingles since people are not being boosted by re-exposure to wild type VZV from their children and grandchildren. The epidemiology to support this variable, but it is an interesting hypothesis.

I have looked, and there is nothing on the PubMeds to suggest those on ECMO are more likely to get reactivation VZV, although some of our nurses have indicated they have seen a number of these rashes in the past, but no one thought of VZV.

So, what is more likely? Three patients all getting a second case of VZV or three patients reactivating VZV roughly simultaneously? I bet the latter. The risk of shingles is 4 per 1000 each year. Getting three at once would be rare, but not that rare. Weirder things happen every day. Like an ID doc not being immune to chickenpox.

Rationalization

J Infect. 2002 May;44(4):211-9. The effect of vaccination on the epidemiology of varicella zoster virus.

http://www.ncbi.nlm.nih.gov/pubmed/12099726

Poll Results

Rare is

• a VZV seronegative doctor 19%
• having twice the fun with twice the work 19%
• a good steak 15%
• hens teeth 17%
• an easy EMR 27%
• Other Answers
• 4%
  • a truly compassionate conservative.
  • Not always a horse.

Infections Change. Infections Stay the Same.

Mar 12, 2014

The patent, an otherwise healthy male, has the removal of a ventricular ependymal cyst and did well for the first few weeks, but then had a bleed into the surgical site. This required evacuation, and again the patient did well. For a while.

A month after the second surgery, he had the relatively abrupt onset of new headaches and then a seizure. CT showed a mass in the brain, and he was off for a third craniotomy. This time it was an abscess, and they called ID.

Gram stain was negative for organisms, and the patient had no risks for any unusual infections. So, I tried to kill all the usual suspects while I waited for the cultures. I suspected something indolent, given the lack of symptoms prior to the admission, as he had no fevers or suggestions of infection. But in 2014, you have to kill MRSA even if you do not see it on the gram stain.

My professional life has been one of change. When I started in 1990, there was AIDS and neutropenic fevers and diabetic foot infections and ICU infections and surgical wound infections galore. Then there was HAART and G-CSF and better diabetic control and ICU bundles and SKIP, and so many of the infections I used to take care of have gone the way of the Mensheviks.

They are pitiful, isolated infections! They are bankrupts. Their role is played out. Go where you belong from now on—into the dustbin of history.

At least it feels that way sometimes. S. aureus remains my bête noire, but not like the old days, at least as a cause of inpatient infections. In the old days, there would have been a Staphylococcus in the abscess or some other common and destructive bacteria. Not anymore.

On day 5, all the cultures were growing P. acnes.

When it comes to surgical infections, and perhaps it is because I am looking for it, I have been seeing more P. acnes, although I suspect that it is more that since we have mostly eradicated all the other causes, this is what is left.

A month's delay in clinical presentation is nothing. Years ago, I had a post-craniotomy infection that presented 8 years after surgery, and that is not even the record.

There are a couple of dozen references of P. acnes causing brain abscess in the PubMeds, and I suspect it causes more infections than we know since it is slow to grow, and people do not look for it.

Debridement is done and now a long course of penicillin G. At least I can still use penicillin for some infections.

Rationalization

Arch Neurol. 2009 Jun;66(6):793-5. doi: 10.1001/archneurol.2009.75. Propionibacterium acnes brain abscess appearing 10 years after neurosurgery.

http://www.ncbi.nlm.nih.gov/pubmed/19506144

Korean J Lab Med. 2011 Apr;31(2):122-6. doi: 10.3343/kjlm.2011.31.2.122. A case of brain abscess caused by Propionibacterium acnes 13 months after neurosurgery and confirmed by 16S rRNA gene sequencing.

http://www.ncbi.nlm.nih.gov/pubmed/21474989

Ash heap of history

https://en.wikipedia.org/wiki/Ash\_heap\_of\_history

POLL RESULTS

My bête noire is

• S. aureus. 26%
• Lex Luthor. 14%
• French. 10%
• the human condition. 34%
• Stalin. 9%
• Other Answers 7%
  • Grizzly
  • the voice in my head that keeps me up at 3 AM and wins all the arguments it should lose.

AAA Infection

Mar 19, 2014

Back from a long weekend in Las Vegas. For Oregonian hippies at heart, we sure enjoy Vegas, although as an ID doc, I remember the Vegas motto: "What happens in Vegas goes home to your significant other."

I may have told this story before. My old attending was in Vegas for the national ID meeting and, while having a drink in the bar, was approached for a 'date', which he declined. She replied, “What kind of meeting is this? Business is never this slow."

I bear in mind that the first word of my specialty is 'infectious'.

Every day gone from work puts you behind three days, so I wonder when I get back if it was worth it. Yes. But it is amazing how fast work piles up while I am gone.

The patient has diabetes and is admitted with fevers to Outside hospital. Blood cultures grow Bacteroides fragilis, so he has a CT looking for a source. No reason for the bacteremia is found, but he has an AAA that is too small to repair. He is given a short course of Augmentin (what else?) and is sent home.

He returns a month later with abdominal pain and leukocytosis. The CT is repeated, and the AAA is bigger and angry looking. He is taken to the OR and found to have a markedly inflamed aorta with pus around it, but the bowel looks fine.

He has an exciting operative course and reading the op report reinforces how glad I am not a surgeon. However, the patient makes it through.

The gram stain of the aorta shows pus, but no organisms and the AAA and blood cultures are negative. Pathology shows infected AAA but no organisms.

Infected AAAs are rare, and I tend to think of Salmonella and S. aureus as the leading causes, but as is always the case in ID, there are a hodgepodge of reported organisms:

Cultures of aortic wall specimens and blood were positive in 10 patients and included Salmonella in 2, Streptococcus in 2, Campylobacter fetus in 2, and Listeria, Haemophilus influenzae, Serratia marcescens, Bacteroides thetaiotaomicron, and an unknown organism in 1 patient each.

and B. fragilis is rare:

Although mycotic aneurysms have been well described in the literature, an aneurysm infected solely with Bacteroides fragilis is unusual, with only eight similar cases in the literature.

It would have been nice if the graft had grown the organism as well, but I suspect the prior antibiotics were enough to mess up the cultures.

Given the risk of graft infection, I will suggest lifetime metronidazole.

Rationalization

Surg Today. 2011 Mar;41(3):346-51. doi: 10.1007/s00595-010-4279-z. Epub 2011 Mar 2. Primary infected abdominal aortic aneurysm: surgical procedures, early mortality rates, and a survey of the prevalence of infectious organisms over a 30-year period.

http://www.ncbi.nlm.nih.gov/pubmed/21365414

J Cardiothorac Surg. 2008 May 20;3:29. doi: 10.1186/1749-8090-3-29. Bacteroides fragilis aortic arch pseudoaneurysm: case report with review.

http://www.ncbi.nlm.nih.gov/pubmed/18492250

POLL RESULTS

What happens in Vegas

• stays in Vegas 4%
• is cured with ceftriaxone 30%
• is against the law at home 14%
• costs too much 25%
• is not winning at gambling. I never see anyone win. 23%
• Other Answers 4%
  • is illegal in most other states.
  • is confusing when views through the lens of two bags of grass, seventy-five pellets of mescaline, five sheets of high powered blotter acid, ...

Odd bacteria in bad places.

Mar 21, 2014

Odd bacteria in bad places. That may the definition of an ID consult, although I still say the job boils down to me find bug, me kill bug, me go home.

The first is an elderly male who presents with fevers and painful vision loss in the left eye and blurry vision in the right eye. He goes to the ER and has endophthalmitis. He has an ECHO that shows a large vegetation on this aortic valve, and the blood cultures all grow Kingella kingae.

Kingella is part of the HACEK (Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, Kingella) group of bacteria, an occasional cause of endocarditis. Emphasis on occasional. It took me 15 years to see one each in the acronym, and the Kingella was the first, a native valve I successfully treated with a course of aztreonam due to allergies.

The data, such as it is, suggests a reasonable chance of cure without surgery, which, due to comorbidities, they want to avoid:

Of those with PVE 8 (30%) required surgical treatment and 19 (70%) were treated with medical therapy alone. There were no in-hospital deaths in either treatment group. Of the 24 PVE patients with 1 year follow-up data, there was one death (cause unknown) and three who required cardiac surgery in the medically treated group, but no deaths, relapses or further surgery requirement in the surgically treated group.

Even rarer is endophthalmitis, with one case in the Pubmeds from Kingella and only a smattering from the HACEK group. He beat the odds twice for odd infections, I suppose he should try Powerball next.

The other, equally unfortunate patient, is a middle-aged female who had a second, technically very difficult, aortic valve replacement two months ago. Now she presents with a month of fevers and malaise, and the blood cultures grow Aerococcus urinae.

Every once and a while, you will see a patient with a UTI that grows an alpha strep. If you ask the lab to look further, they may find Aerococcus. On valves, it is less common than HACEK, and as best I can tell has never been reported on a prosthetic valve.

A third valve replacement and the second in two months is, according to the surgeons, very high risk, so for the short term, it is iv antibiotics.

Both represent difficult decisions as to which is the least bad option: to the OR sooner rather than later or medical therapy when both options have a high probability of bad outcomes. When my father retired from cardiology, he told me the best thing about not working, and what allowed him to sleep again, was no longer being responsible for complicated cases. I sympathize.

Rationalization

PLoS One. 2013 May 17;8(5):e63181. doi: 10.1371/journal.pone.0063181. Print 2013. HACEK infective endocarditis: characteristics and outcomes from a large, multi-national cohort.

http://www.ncbi.nlm.nih.gov/pubmed/23690995

Am J Ophthalmol. 2002 Jan;133(1):144–5. Bilateral endogenous endophthalmitis caused by HACEK microorganism.

https://www.ncbi.nlm.nih.gov/pubmed/11755854

Scand J Infect Dis. 2010 Oct;42(10):775–80. doi: 10.3109/00365548.2010.485576. Aerococcus urinae and Aerococcus sanguinicola, two frequently misidentified uropathogens.

http://www.ncbi.nlm.nih.gov/pubmed/20482457

Rev Med Brux. 2008 Nov-Dec;29(6):568–71. [Aerococcus urinae endocarditis: first case report in Belgium and review of the literature].

http://www.ncbi.nlm.nih.gov/pubmed/19202713

What to do?

Mar 24, 2014

I am a little under the weather, some kind of viral URI that has taken away my legs and my brain. I can't go up steps without feeling like I am 56. No, wait. I am 56. That's 372 in dog years. And my thought processes are slow as a NW slug but without the slime. Yet. I am not a fan of being infected since infections are for other people. I feel I have had my share of medical problems in my 372 years and can do without viruses.

Viri, especially in the Herpes family, can be problematic since they are common, often in a constant state of reproduction or reactivation and easy to isolate. I see, and ignore, HSV and CMV all the time, although what to do about CMV in the ICU is problematic.

These preliminary findings suggest that reactivation of CMV frequently occurs in critically ill immunocompetent patients and is associated with prolonged hospitalization or death. A controlled trial of CMV prophylaxis in this setting is warranted.

Although there are no treatment studies yet and it may be those with the higher viral loads who at risk for adverse outcomes.

Diarrhea is common, and more often than not, there is no microbiologic diagnosis. In the outpatient setting, it goes away. In the inpatient setting, it also goes away. There are a variety of reasons, especially not missing C. difficile, that make inpatient evaluations of diarrhea more comprehensive. And once you are in the hospital, watching and waiting just isn't an option. It should be. But it isn’t. So, I would suspect that those with diarrhea in the hospital are much more likely to get a colonoscopy, which is why over the years, I have seen the occasional case of CMV colitis in normal people.

I suspect that CMV is more common in a wide variety of patients than we suspect, but most young people with no co-morbidities do not end up with a colonoscopy to make the diagnosis.

The patient is a young male with ulcerative colitis on immunosuppression (low dose prednisone, biologics, azathioprine) who, because of his diarrhea and cramps, has a colonoscopy and the biopsy show UC and a smattering of CMV. After the colonoscopy, the prednisone was increased, and now he is better. What to do?

His CMV viral load was low, the involvement was minimal, he was better, and he had no medication coverage. So, after discussion, we opted to do nothing. And he is doing fine.

CMV and UC can be a bad combination and

interferes strongly with the natural progression of ulcerative colitis. While immune treatments have a clear influence on the occurrence of cytomegalovirus colitis in ulcerative colitis (favorable for steroids and cyclosporin and rather inhibitory for infliximab), the role of cytomegalovirus infection on ulcerative colitis is more debated with roles ranging from innocent bystander to key pathogen suggested.

The literature is all over the map, but it looks like it should be more of a concern in severe disease and steroid-refractory disease, and my patient was neither. Whether and in whom treatment is effective is not known, at least based on controlled trials. So, for now, we will watch carefully.

So far, so good.

Rationalization

JAMA. 2008 Jul 23;300(4):413-22. doi: 10.1001/jama.300.4.413. Cytomegalovirus reactivation in critically ill immunocompetent patients.

http://www.ncbi.nlm.nih.gov/pubmed/18647984

Crit Care. 2011;15(2):R77. doi: 10.1186/cc10069. Epub 2011 Mar 1. Cytomegalovirus reactivation and associated outcome of critically ill patients with severe sepsis.

http://www.ncbi.nlm.nih.gov/pubmed/21362193

Hepatogastroenterology. 2012 Oct;59(119):2137-41. doi: 10.5754/hge10825. Cytomegalovirus colitis in immunocompetent patients: a clinical and endoscopic study.

http://www.ncbi.nlm.nih.gov/pubmed/23435132

Dig Liver Dis. 2012 Jul;44(7):541-8. doi: 10.1016/j.dld.2012.03.018. Epub 2012 Apr 25. Management of cytomegalovirus infection in inflammatory bowel diseases.

http://www.ncbi.nlm.nih.gov/pubmed/22538204

Am J Gastroenterol. 2001 Mar;96(3):773-5. Prevalence of cytomegalovirus infection in severe refractory ulcerative and Crohn's colitis.

http://www.ncbi.nlm.nih.gov/pubmed/11280549

Rogue Plastic

Mar 26, 2014

The patient is admitted for fevers and confusion. He has been on a prednisone taper for myositis and is currently on 10 mg a day. He gets the usual antibiotics, and after 48 hours, all the cultures are growing Group B Streptococcus.

That is not a surprise. It happens:

Primary bacteremia was the most frequent clinical diagnosis, occurring in 7 (22%) of 32 patients. Nonhematologic cancer was the most frequently associated condition (25%). Nineteen percent of the patients had diabetes mellitus.

As part of the fever work up, it is discovered that the patient has several inch pieces of plastic in the pulmonary artery that appears to be a piece of a PICC or similar catheter.

He has had several admissions in the past two years for sepsis and orthopedic infections and has had both CVP's and PICCs but was unaware that there was a piece still in his vascular tree.

Interventional radiology was unable to remove it. He said he could grab it, but it would not budge. I guess the radiologist is not the rightful King of England. Cardiovascular surgery was asked; they are not interested in taking it out. Wimps.

But the big question: Is the rogue catheter infected and what to do about it?

Got me. There are no cases of infected rogue catheters in the Pubmeds that I can find. Group B Streptococcus is an unusual cause of endovascular infections, especially prosthetic valve endocarditis, of which there are but a handful reported. It has little predilection for metastatic complications. The catheter has been there at least four months, so it is likely partly or completely endothelialized.

So, the odds it is infected are low, but if it has been seeded, it could erode through the pulmonary artery. So, after discussing the pros and cons with the patient, we decided on a long course of ceftriaxone. And another PICC.

Sometimes it is my job to come up with a therapeutic course when there is zero data to support my decisions. As my partner noted, when we were discussing the case, whatever decision you make, make sure you feel bad about it.

She did fine.

Rationalization

Medicine (Baltimore). 1995 Jul;74(4):176-90. Group B streptococcal bacteremia in adults. Five years' experience and a review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/7623653

Late Encephalopathy

Mar 31, 2014

The brain is not very forgiving. Emotionally, spiritually, intellectually, or medically. It is part of why CNS infections make me nervous. Patients often do not return to normal, although the deficits and changes can be subtle and obvious only to those who know the patient well. So often it is depression and irritability, that is so unlike the patient. It is best not to get the brain infected.

The patient is healthy, with no medical problems but in his mid 60's. He had the abrupt onset of a blistering rash on his left buttock that was only noticed after wiping. Over the next few days is progressed to a mild, burning/itching pain.

Then, five days in, the patient developed a headache, started talking gibberish, and was unaware of where he was. Off to the ER where LP was consistent with viral meningitis (500 lymphocytes, protein 170, normal glucose), and the MRI showed temporal/parietal encephalitis. The HSV PCR was negative, so it is likely VZV encephalitis1.

An abnormal spinal tap is probably the norm in shingles, although most patients with no CNS complaints do not get an LP.

So, we start IV acyclovir, and I worried.

Will it be

The outcome was favorable in 108 of 176 patients (61%) (71 with complete resolution), 31 (18%) were mildly impaired, 25 (14%) were severely impaired, and 3 (1%) were in a vegetative state. The most frequent symptoms were difficulty concentrating (42%), behavioral disorders (27%), speech disorders (20%), and memory loss (19%). Fifteen of 63 patients (24%) previously employed were still unable to resume work. Long-term outcome was significantly associated with comorbid conditions, age, level of education, and the causative agent of encephalitis.

Or

The four patients with encephalitis had a less favorable prognosis: one patient recovered without residual neurological sequelae; two had a chronic neuropsychological handicap, speech difficulties, facial nerve palsy, and focal seizures; one patient died.

Follow up 14 days later. Mental status is completely back to normal according to the patient and, more importantly, according to the spouse. Whew. Oddly, there is now an S1 S2 neuropathy, numbness, extending down the back of the leg to the foot that was not present during admission, and the rash never left the buttock.

Rationalization

J Med Virol. 2014 Feb 14. doi: 10.1002/jmv.23902. [Epub ahead of print] Clinical features, outcomes, and cerebrospinal fluid findings in adult patients with central nervous system (CNS) infections caused by varicella-zoster virus: Comparison with enterovirus CNS infections.

http://www.ncbi.nlm.nih.gov/pubmed/24532558

BMJ Case Rep. 2012 May 30;2012. pii: bcr0320126041. doi: 10.1136/bcr.03.2012.6041. Shingles with secondary asymptomatic CNS involvement!

http://www.ncbi.nlm.nih.gov/pubmed/22669873

Clin Infect Dis. 2012 May;54(10):1455-64. doi: 10.1093/cid/cis226. Epub 2012 Mar 28. Long-term outcome of patients presenting with acute infectious encephalitis of various causes in France.

http://www.ncbi.nlm.nih.gov/pubmed/22460967

Int J Infect Dis. 2013 Jul;17(7):e529-34. doi: 10.1016/j.ijid.2013.01.031. Epub 2013 Apr 6. Infection of the central nervous system caused by varicella zoster virus reactivation: a retrospective case series study.

http://www.ncbi.nlm.nih.gov/pubmed/23566589

Somewhere Endovascular

Apr 2, 2014

The patient is admitted with failure to thrive in large part due to dementia. He had a midline catheter, and at some point, during the hospitalization, there was a fever, which lead to blood cultures, which grew a yeast, which was identified as Candida tropicalis.

Pull the line and start fluconazole I commanded, and so it came to pass.

The patient responded clinically with normalization of infection parameters. Tip of the catheter also grew C. tropicalis, tying it all together nicely as a CLABSI. For those of you who do not have to deal with awkward eponyms, it is short for Central Line-associated Blood Stream Infection.

Repeat the cultures I commanded, and so it came to pass that on day 3 and day 7, the C. tropicalis was still in the blood cultures.

The sine qua non of endocarditis is a sustained bacteremia, or fungemia, and nosocomial endocarditis is one of those infections of modernity, a complication of central lines:

There were 13 external lines, 9 tunneled lines, and 2 implantable ports. Responsible microorganisms included Staphylococcus aureus in 54.6%, coagulase-negative staphylococci in 37.5%, Candida species (spp.) in 16.6%, and enterococci in 12.5%. Five cases were polymicrobial. The line tip was within the right atrium (RA) in 37.5%, the superior vena cava (SVC)-RA junction in 20.8%, the SVC in 33.3%, and the pulmonary artery in 4.2% of patients. Sites of endocardial involvement were the aortic valve in 6 patients, mitral valve in 7 patients, tricuspid valve in 6 patients, right atrial wall in 11 patients, and pacemaker wire in 2 patients. Isolated right-sided involvement occurred in 50% of cases, isolated left-sided in 33.4%, and bilateral involvement in 16.6%.

Get an ECHO I commanded, and so it came to pass. I fully expected the ECHO to show a vegetation the size of my ego, Candida often making exceptionally large vegetations. It didn't. Clean.

Hmmm. Then it occurred to me that it was a midline catheter. Midlines end in the subclavian. I suppose an alternative explanation would be infected clot of the subclavian, since to be picky, the sine qua non of an endovascular infection is sustained bacteremia.

Ultrasound the subclavian I commanded, and so it came to pass. And bingo was his name-o. Clot.

Suppurative thrombophlebitis of the subclavian is not common and usually bacterial. Candida as a cause is rare but reported with

24 additional cases of Candida induced central veins thrombophlebitis reported since 1978... Literature data suggest that Candida caused central veins thrombophlebitis is a rare and probably underdiagnosed infectious complication of the critically ill patient. Despite the dramatic presentation with persistent candidemia, mortality is low even with a conservative medical approach...

But no reported cases from C. tropicalis.

So, antifungals and anticoagulation it is. When you think endocarditis, also think somewhere endovascular.

Rationalization

Clin Cardiol. 2009 Dec;32(12):E48-54. doi: 10.1002/clc.20498. Endocarditis complicating central venous catheter bloodstream infections: a unique form of health care associated endocarditis.

http://www.ncbi.nlm.nih.gov/pubmed/20014189

Med Mycol. 2012 Apr;50(3):299-304. doi: 10.3109/13693786.2011.604046. Epub 2011 Sep 12. Candidal thrombophlebitis of central veins: case report and review.

http://www.ncbi.nlm.nih.gov/pubmed/21905947

It was Greek to me

Apr 4, 2014

The patient is newly diagnosed with aplastic anemia when she has an episode of hematuria and is admitted. She also has fevers and neutropenia (WBC of 0.1), so cultures are done, and she is admitted. For the next several days, she has fevers in the 38.2 range despite antibiotics, and they call me.

BTW. I dislike the term 'low-grade fever.’ Fever, to my mind, is binary, like pregnancy. Either your temperature is abby normal, or it isn't.

Review of systems and exam are negative, as are the blood cultures in my system. She is clinically doing quite well on antibiotics and looks fine. But.

The morning of her admission, and before the hematuria, she had been at the University where they did blood cultures, and it is growing Lactobacillus in the anaerobe bottles of both sets of blood cultures. What's that doing there? So, I start asking.

It turns out that she has been feeling a bit under the weather and has been eating a lot of Greek yogurt, containing Lactobacillus bulgaricus and Streptococcus thermophilus, Lactobacillus acidophilus, Bifidus and Lactobacillus casei.

Is the yogurt the source? Maybe. The Lactobacilli in yogurt are not the same strains as found in the stool, he is newly neutropenic, and he has been consuming lots of Lactobacilli. Still, it is unusual with

Eight cases of bacteremia associated with Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus GG, and Bacillus subtilis were reported in six publications.

And the epidemiology also suggests it is odd. The 2 times I have seen Saccharomyces boulardii in the blood were patients with severe colitis placed on probiotics, and it is why severe colitis or neutropenia is a contraindication for the use of probiotics in our institution. So, I am going to call the yogurt the source.

Now, if someone would just do a study that demonstrates Hefeweizen can prevent antibiotic-associated diarrhea, life would be good indeed.

Rationalization

Praxis (Bern 1994). 2009 May 13;98(10):547-50. doi: 10.1024/1661-8157.98.10.547. [Does yoghurt gnaw at cardiac valves?].

http://www.ncbi.nlm.nih.gov/pubmed/19424951

Med Mal Infect. 2013 Apr;43(4):171-3. doi: 10.1016/j.medmal.2013.01.007. Epub 2013 Apr 23. Lactobacillus paracasei endocarditis in a consumer of probiotics.

http://www.ncbi.nlm.nih.gov/pubmed/23622954

Safety of Probiotics to Reduce Risk and Prevent or Treat Disease Evidence Reports/Technology Assessments, No. 200

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0015579/

Scand J Infect Dis. 2006;38(5):327-31. Probiotic lactobacilli and bacteraemia in Stockholm.

http://www.ncbi.nlm.nih.gov/pubmed/16709533

Myocardial What?

Apr 16, 2014

I'm back from a 12-day trip to the Land of the Angles. Did you miss me? Or even notice that I was gone? Either way, I have returned.

Whenever I leave work for an extended period of time, infections come out, although I hurry to remind everyone that association is not causation.

H1N1 started while I was on spring break all those years ago. And this time, we appear to be having a bit of an adenovirus problem in Portland while I was gone. We have had a small flurry of cases, and typing is still pending, but several have had reasonably severe pneumonia, one ending up on ECMO. I wonder how much of the increased number of cases is easier diagnostics since we now have the ability to screen for multiple viral pulmonary pathogens with PCR.

The patient is a 23-year-old female with no medical problems except a smoker who has progressive shortness of breath and ends up on a ventilator in the ICU for 2 days. PCR is positive of adenovirus, and she slowly improves, is extubated, and is moved to the floor.

On day 10, she has the abrupt onset of heavy substernal chest pain radiating to the left shoulder, increased shortness of breath, and new ST elevations. Troponin bumps to 19. They tell me that this is significant. I'll take their word for it. In my day, we diagnosed myocardial infarctions with CK and LDH isoenzymes. She gets better rapidly with morphine and nitroglycerine. The ECHO normal EF and diffuse wall motion abnormalities.

So, what is it? Cardiology called it myocarditis based on the ECHO and the diffuse changes on the EKG.

But.

It occurred late (myocarditis usually occurs with the primary illness), the history suggests an MI (my dad always says if the labs contradict the history, then it is the labs that are wrong) and adenovirus is extremely rare as a cause of myocarditis:

From our data, it seems doubtful that adenoviruses are major pathogens of myocarditis or DCM, whereas enterovirus genome was identified in a significant number of patients with both diseases.

although there are case reports.

I think it was an acute vascular event. Those of you lucky enough to listen to my podcasts know I harp on the issue that infections are inflammatory, inflammation is pro-thrombotic, and thrombosis leads to vascular clot.

Every infection that has been looked at, UTI, pneumonia, zoster, influenza, peritonitis, routine childhood infections, heck, even a dental cleaning, has been shown to be associated with increased risk for one vascular event or another, stroke, TIA, MI, or pulmonary embolism, in the weeks following the infection.

Also, being hospitalized for infection is associated with increased risk of death after discharge compared to similar patients admitted for non-infectious reasons, although the cause of death is not known. I bet it is due to vascular events.

It is why if some pseudo-medical intervention really could boost your immune system, and it is fortunate they can't, it would likely lead to a vascular event.

There is a career to be made in an intervention study. I bet that all infected patients would benefit from being sent home on some sort of anticoagulation, probably aspirin. I just wish there was a study to prove it.

Someone get to work on that study before I retire, OK?

Rationalization

Acta Cardiol. 1999 Apr;54(2):83-8. Adenoviruses and enteroviruses as pathogens in myocarditis and dilated cardiomyopathy.

http://www.ncbi.nlm.nih.gov/pubmed/10378019

Boost Your Immune System?

http://www.sciencebasedmedicine.org/boost-your-immune-system/

More Speculation

Apr 18, 2014

I have been chair of Infection Control at multiple hospitals going on 24 years, and it allows me to compare and contrast practice and infections.

One hospital has fewer hospital-acquired C. difficile infections than another of about the same size, but as best I can tell, there is another difference in practice.

So here is some wild speculation.

C. difficile is in part a foodborne illness:

Data on the presence and prevalence of C. difficile in food products are newly available, and there are limited epidemiologic data to connect C. difficile found in the food supply to human illness.

It is more commonly isolated in meats than vegetables:

In a study of more varied retail meat products conducted in the United States, C. difficile was isolated from 42% of retail beef, pork, and turkey samples purchased at grocery stores in Tucson, Arizona, over 3 months.

As compared to

...another study, C. difficile was isolated from 3 (7.5%) of 40 ready-to-eat retail salads by researchers in Scotland.

And we know that hospital-onset C. difficile is often not hospital-acquired:

Of the 333 patients with no more than 2 SNVs (consistent with transmission), 126 patients (38%) had close hospital contact with another patient, and 120 patients (36%) had no hospital or community contact with another patient.

It suggests that while we till the soil in the hospital, we do not provide the seed of C. difficile. Or do we? Where is the C difficile in the hospital coming from?

The hospital with the lower C. difficile rate is an Adventist hospital, and they have a mostly vegetarian kitchen that supplies food to patients. Hmmm. I wonder. Could the fact that a vegetarian cafeteria is probably less likely to have C. difficile in the food account for less disease in patients? And are vegetarians less prone to C. difficile? I would suspect yes, but I do not know. The PubMeds are silent on the issue.

So, there is some wild speculation for someone else to do the work to prove or disprove my hypothesis. Yet another great idea, like urine transplants for recurrent UTI’s, that I will leave for others to get the glory. How nice of me.

Rationalization

Clin Infect Dis. 2010 Sep 1;51(5):577–82. doi: 10.1086/655692. Clostridium difficile in food and domestic animals: a new foodborne pathogen?

http://www.ncbi.nlm.nih.gov/pubmed/?term=20642351

N Engl J Med. 2013 Sep 26;369(13):1195–205. doi: 10.1056/NEJMoa1216064. Diverse sources of C. difficile infection identified on whole-genome sequencing.

http://www.ncbi.nlm.nih.gov/pubmed/?term=24066741

More Questions than Answers.

Apr 21, 2014

Three weeks ago, the patient had a fusion with a bone graft and initially did well.

Then she had the abrupt onset of ‘flu,’ and the surgical site becomes red, hot, and painful. Off to the OR, where the wound is debrided, and there is pus into the ankle joint.

Another late MRSA infection I would have thought, but the cultures are growing E. coli, P. mirabilis, and A. hydrophilia.

One, one being me, would think she had been walking in sewage given that microbiology, but I grilled her on her exposure, and she has been fastidious about wound care. So, where did these bugs come from?

Is it from the bone graft? We are looking into that possibility, and there have been infections associated with tissue transplants of all kinds, and musculoskeletal products are occasionally contaminated:

Explanted tissues: these were positive to culture in 292 out of 3117 (9.4%) allografts from living donors; the bacteria isolated showed low pathogenicity. Out of 897 allografts 117 cadaver donors bacteria with low pathogenicity were isolated in 68 (7.6%) and high pathogenicity in 12 (1.3%). Implants: cultures were positive in 116/2191 (5.3%) implants with allografts from living donors and in 55/1288 (4.3%) implants with allografts from cadavers. The bacteria isolated are the same as those shown in the explants.

But with these bugs, I would have thought she would have been symptomatic much earlier than three weeks. It will take some time to see if this is due contamination.

The curiosity was the Aeromonas. It was only resistant to meropenem, which was a surprise. Unbeknownst to me, Aeromonas often has a cphA-encoded metallo-beta-lactamase and is carbapenem-resistant. But why? It is not like the waters are saturated with carbapenem antibiotics. Maybe it is from hospitals:

Unexpected resistance to imipenem, an antibiotic of clinical usage, was also detected, which suggests that resistance may have been transferred to the Aeromonas population from the environment.

but I do not think so. Reports of carbapenem resistance in Aeromonas almost predates the clinical use of the antibiotic class.

Here is a bit of history. The first carbapenem discovered was thienamycin and was isolated in 1976 from the soil bacteria Streptomyces cattleya. I cannot find any suggestion that Streptomyces cattleya and Aeromonas share a common habitat, although that is not to say there may not be other organisms in the water that also make a carbapenem to which Aeromonas may want a defense. It appears that these carbapenemases are natural in Aeromonas species:

We speculate that many environmental strains have the potential to code for a carbapenemase even though they have probably never been exposed to a carbapenem or possibly to any other antibiotic apart from naturally occurring penicillins and cephalosporins.

So, what is driving the carbapenem resistance in the wild by Aeromonas? I can’t find an answer. But these are the kind of questions that intrigue me. Medicine always generates more questions than answers.

Rationalization

Chir Organi Mov. 2003 Oct-Dec;88(4):345–50. Bacterial contamination of musculoskeletal allografts.

http://www.ncbi.nlm.nih.gov/pubmed/15259549

J Hosp Infect. 2002 Apr;50(4):293–7. Experience with a bone bank operation and allograft bone infection in recipients at a medical centre in southern Taiwan.

http://www.ncbi.nlm.nih.gov/pubmed/12014903

Antimicrob Agents Chemother. 1993 Jun;37(6):1324–8. High specificity of cphA-encoded metallo-beta-lactamase from Aeromonas hydrophila AE036 for carbapenems and its contribution to beta-lactam resistance.

http://www.ncbi.nlm.nih.gov/pubmed/8328781

Int Microbiol. 2004 Sep;7(3):207–11. Resistance to beta-lactam antibiotics in Aeromonas hydrophila isolated from rainbow trout (Oncorhynchus mykiss).

http://www.ncbi.nlm.nih.gov/pubmed/15492935

Journal of Antimicrobial Chemotherapy (1996) 37, 33–44 The ‘hidden’ carbapenemase of Aeromonas hydrophila

http://jac.oxfordjournals.org/content/37/1/33.full.pdf

More Yeast

Apr 23, 2014

The patient is an otherwise healthy female who has had a month of a slow decline. She has been mostly weak and unsteady on her feet, but no headache, fevers, chills, or any symptom to suggest an infection.

It is a near syncopal event that gets her to the hospital where they find a multi-lobar pneumonia for which she has no symptomatology.

She gets blood cultures and is started on CAP therapy, and with 48 hours, the blood cultures are growing a yeast. They call me.

She has been nowhere, done nothing, so I suspect Cryptococcus, which is endemic in the great Pacific NW. And indeed, the cryptococcal antigen in the blood is greater than 1:1024. I have had a flurry of Cryptococcus this year and not the DQ kind.

A spinal tap shows lots of yeast, but few WBC, and the glucose is normal. The CSF titer is also greater than 1:1024.

She is started on amphotericin B and 5-FC, and after a week, the yeast is identified as C. gattii.

It is quite remarkable just how little inflammatory reaction she is having to the yeast. It is like the old, awful days of AIDS when patients would be devoured by infections with remarkably little inflammatory response.

As best I can tell, she does not have an immunodeficiency. Her CD4s are fine, the HIV is negative and no anti-interferon-γ antibodies. But I suspect something is stopping her from mounting an inflammatory response.

Then she has all the adverse reactions to lipid amphotericin you could ask for, and I wanted to change to an azole. What to do? The MIC’s to voriconazole (0.5) are much lower than fluconazole (8), but who knows if this would translate to a better outcome. There is no clinical data. Not that it matters. One of the joys of practicing medicine in the US is trying to give optimal care that insurance will not pay for, and the company will not help with the cost. She cannot afford a course of voriconazole, so really high dose fluconazole it is.

At least she doesn’t need treatment for hepatitis C.

Rationalization

N Engl J Med. 2012 Aug 23;367(8):725–34. doi: 10.1056/NEJMoa1111160. Adult-onset immunodeficiency in Thailand and Taiwan.

http://www.ncbi.nlm.nih.gov/pubmed/22913682

Sympathetic

Apr 25, 2014

Every patient is the same, and every patient is different. The first allows me to know how to treat patients with a given illness. The latter is the variability in disease that makes medicine interesting.

The patient is a mid-thirties male who comes in with a GI bleed. While being evaluated, he has a fever, which leads to blood cultures, which are positive for alpha Streptococcus.

The call me. Exam has a mitral murmur (he has a history of mitral valve prolapse) and very nice conjunctival hemorrhages, a classic sign for endocarditis. It turns out he has been ill for at least a month, maybe more, with a low-grade grunge. Like many a young endocarditis patient, he has habits (heroin) that make paying close attention to his health problematic.

So, we get a TTE, and the mitral valve is trashed, multiple vegetations, and severe MR. That also makes me suspect that he has had his disease longer than a month. Emboli and that much destruction tend to occur after months of S. viridans endocarditis.

He also has a pericardial effusion with borderline tamponade physiology (as fluid in the pericardium increases, it compresses the heart, decreasing cardiac output), which I did not find on exam — no rubs, jugular venous distension, or pulsus paradoxus (“an exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg”).

It is weird how I read an article, and shortly thereafter, it becomes relevant. Just a couple of weeks ago, I read Risk factors for pericardial effusion in native valve infective endocarditis and its influence on outcome. They note

Patients with large-to-very large PE had a higher rate of systemic emboli (22% vs 18%) and periannular abscess (22% vs 6%) than patients without PE.

It is the words ‘periannular abscess’ that make me nervous. While no abscess was noted on TTE, I am never assuaged by a negative TTE, and his troponins were 3 on admit. Where is that coming from? Damaged myocardium.

TEE is in order, and it came back…

No abscess. Just a sympathetic pericardial effusion.

Good. I like being wrong.

Rationalization

Am J Cardiol. 2013 Nov 15;112(10):1646–51. doi: 10.1016/j.amjcard.2013.07.024. Epub 2013 Sep 19. Risk factors for pericardial effusion in native valve infective endocarditis and its influence on outcome.

http://www.ncbi.nlm.nih.gov/pubmed/24055065

Pulsus Paradoxus

https://www.ncbi.nlm.nih.gov/books/NBK482292/

How Long Is It?

Apr 28, 2014

I often get duration questions. How long to treat is the most common, but there are variations on the question of how long, and I always think of the Lifeboat sketch. Probably just me. I like to tell them: "Top hole. Bally Jerry pranged his kite right in the how’s your father. Hairy blighter, dicky-birdied, feathered back on his Sammy, took a waspy, flipped over on his Betty Harper’s, and caught his can in the Bertie."

Hmm. Come to think of it, I suspect I might know why I am getting fewer consults.

The patient is diabetic, alcoholic with months of fevers, night sweats, weight loss, and a productive cough. He is admitted, and the CXR and CT show multi-lobar pneumonia with cavities. The sputum is 4+ for AFB, and the PCR is positive for M. tuberculosis.

He is started on 4 drug therapy. At some point, without my permission, it acquired the acronym RIPE, even though the first word in any TB treatment regimen is always isoniazid. Really, by tradition, it should be IRPE, even if it can't be pronounced as easily. People just have no respect for tradition.

Unfortunately, he gets hepatitis on the therapy, and his meds are held, then restarted one at a time a couple of days apart. No recurrence of the hepatitis, but the fevers persist. Each day they reach 40, and no other source can be found.

So how long will the fevers last with Tb on therapy? Assuming the meds are appropriate (sensitivities are pending) and absorbed. As an aside, I suspect we should be checking drug levels TB patients as low levels may predict failure and resistance:

Low drug AUCs are predictive of clinical outcomes in tuberculosis patients.

And I am always leery of absorption in ill patients.

Fevers are of variable duration during TB therapy:

Most patients were treated with isoniazid, rifampicin and pyrazinamide. Of 83 individuals who became afebrile while in hospital, 74 (89%) did so within a week and 77 (93%) in 2 weeks. Prolonged fever was associated with alcoholism, anaemia, hyponatraemia and hypoalbuminaemia.

He has all the above. And note the regimen goes in order of isoniazid, rifampicin and pyrazinamide. And

Resolution of fever was variable (mean, 16 days; median, 10 days; range, 1 to 109 days). Thirty-eight patients (64%) became afebrile within 2 wk (group 1); 21 (36%) had fever for longer than 2 wk (group 2). Far advanced disease and high temperature (> 38.8 degrees C) on admission were more frequent in group 2 (p < 0.05 and p < 0.01, respectively). However, the groups did not differ in demographic features or in the frequency of symptoms on admission, alcoholism, lung cavitation, numerous acid-fast bacilli on sputum smears, or coexisting bacterial respiratory infection. Antimicrobial drug treatment of presumed coexistent bacterial infection in 19 febrile patients did not influence the course of fever.

So, patience with the fevers while awaiting the sensitivities and continue IRPE, pronounced as if a newborn is about to puke. As it should be.

And the fevers dribbled slowly off the court.

Rationalization

J Infect Dis. 2013 Nov 1;208(9):1464 73. doi: 10.1093/infdis/jit352. Epub 2013 Jul 29. Serum drug concentrations predictive of pulmonary tuberculosis outcomes.

http://www.ncbi.nlm.nih.gov/pubmed/23901086

Tubercle. 1987 Dec;68(4):255 60. The course of fever during treatment of pulmonary tuberculosis.

http://www.ncbi.nlm.nih.gov/pubmed/3455566

Am Rev Respir Dis. 1981 Jan;123(1):20 4. Fever response of patients on therapy for pulmonary tuberculosis.

http://www.ncbi.nlm.nih.gov/pubmed/7458082

The Lifeboat Sketch

http://www.montypython.net/scripts/lifeboat.php

The Banter Sketch

http://www.montypython.net/scripts/RAFbanter.php

POLL RESULTS

People today don't respect

• tradition 27%
• their elders 31%
• consultants 15%
• Otis Redding 8%
• the Portland Trailblazers. Kickin' some Houston butt. Go Blazers. 8%
• Other Answers 12%
  • Rodney Dangerfield
  • reality, or the close approximation thereof that most of us live with on a daily basis.
  • all of the above

African Roulette

May 1, 2014

People who live in the industrialized West lose track of diseases that are important in the rest of the world. People are surprised when I mention that I am treating a case of Tuberculosis. To most, TB is one of those diseases of another time and place. But even in Portland, Oregon, I see a half dozen cases of TB a year.

The patient has been going to Africa every year for the last 20 years. In the beginning, he took prophylaxis, but after a while, he gave up because of the bother, and year after year, he had no problems.

Ten days after returning from central Africa, he gets malaise, then severe rigors, a temperature to 104, and mild confusion. He toughs it out for a day but becomes too ill and ends up in the ER. His WBC is 2, his platelets are 20K, and 2% of his red cells have P. falciparum. And he looked ill, totally wasted, sweaty and prostrate with fever. I see lots of infected patients, and he looked much sicker than the average bacterial infection.

There is an internal subjective ill-o-meter that most docs develop. It is not as accurate as a blood gas or CBC, but you have a sense from looking at patients how ill they are. He was 11 on the non-septic scale.

We started him on Malarone, and within 3 days, the malaria was gone, and he was walking the halls, legs a bit wobbly, but otherwise better.

Malaria is bad, and P. falciparum is the worst:

From 1963 to 2001, 185 malaria-related deaths were reported to the CDC: 123 (66.5%) occurred among U.S. travelers, 31 (16.8%) occurred among refugees and visitors, 17 (9.2%) occurred among military personnel, and 14 (7.6%) occurred among unknown or other groups (percentages add to 100.1% because of rounding) (Figure 1). The number of deaths among U.S. travelers has remained relatively constant over time, varying between 0 and 10 deaths (median, 3). Among the 123 U.S. travelers, 49 (39.8%) were women and the median age was 51 years (mean, 48.7 years [range, 12 to 91 years]). Most deaths (114 [92.7%]) were attributed to P. falciparum, 4 (3.3%) were attributed to P. vivax, 2 (1.6%) were attributed to P. malariae, and 1 (0.8%) was attributed to P. ovale. In 2 (1.6%) cases, the species was not determined or not reported.

But the more sobering statistic is

The estimated case-fatality rate for U.S. travelers with reported cases of imported malaria (all species) was 0.9% (range, 0% to 4.4% by year).

But 1.3% death rate for P. falciparum.

While the low WBC and platelets are probably from the malaria, mosquitos can carry more than one pathogen, but the dengue serology was negative as well.

And next time? He is going to take malaria prophylaxis.

Rationalization

Ann Intern Med. 2004 Oct 5;141(7):547–55. Malaria-related deaths among U.S. travelers, 1963–2001.

http://www.ncbi.nlm.nih.gov/pubmed/15466772

I can't vent the spleen

May 2, 2014

The patient had a high thoracic spine injury from an MVA 8 years ago.

Over the last 6 months, she has had multiple admissions for sepsis: she spikes a fever, gets hypotensive, the WBC gets in the high 20s, low 30’s and the blood cultures are always negative. She gets better very rapidly on antibiotics and is sent home.

Various processes are blamed for recurrent septoid presentations: UTI, a large ongoing sacral decubitus, maybe pneumonia.

When I saw her last admission, it was C. difficile, and again she improved rapidly on therapy. Last admit, when I saw her for the first time, there was also a CT that showed something in the upper pole of the spleen, maybe an abscess, maybe not. I noted it, but she responded to the metronidazole. At no time have there been any positive blood cultures, although lots of urine and wound cultures with various typical organisms.

I talked to IR (shouldn’t it be I am? IR sounds ungrammatical except for Baboons), and being in the upper pole of the spleen, they would have to go through lung to drain it. It is take it out or watch it. Since she got better and it was too big (4.5 cm) for medical cure, we watched it. You do not remove a spleen willy-nilly. The last one I suggested removal years ago almost died from bleeding complications. Bad outcomes always give one pause.

With this episode of sepsis, the lesion in the spleen had grown. So, we tanked her up with all the vaccines, and she had her spleen out.

Yep. Abscess. Pus. But all the cultures and stains are negative.

I do not have a good why for a splenic abscess, and I do not have an organism. No host risks, no reason for an odd organism (like TB or Brucella), no nothing. Playing the odds, I would expect.

Streptococcus viridans was the most common pathogen (27.8%), follow by Klebsiella pneumoniae (22.2%). The mortality rate during the inpatient period and the previous 90 days was 16.6%. Three of four patients with Klebsiella pneumoniae showed a single abscess pocket. Four patients (22.2%) underwent percutaneous drainage, eight (44.5%) received antibiotic treatment only and six (33.3%) underwent splenectomy.

At least there is now a cure. And one of the few splenic abscesses I have seen.

Rationalization

Yonsei Med J. 2011 Mar;52(2):288–92. doi: 10.3349/ymj.2011.52.2.288. Splenic abscess: a single institution study and review of the literature.

<http: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/21319348>

I.R. Baboon

https://villains.fandom.com/wiki/I.R.\_Baboon

POLL RESULTS

the organ I am most hesitant to biopsy is

• brain 41%
• heart 15%
• spleen 15%
• Hammond 17%
• pipe 11%

Didn’t See That Coming. Yet Again.

May 5, 2014

The problem with ID, and empiric therapy, is that you cannot always predict what will grow in the cultures. Most of the time, empiric antibiotics have a broad enough spectrum to kill the patient's infection, but not always. Over the years, I have been surprised by what has grown in patients, and I hate being surprised as it can mean there was a hole in the initial therapy.

The patient is an elderly female with myelodysplastic syndrome (MDS) and progressive renal failure who come in for the initiation of peritoneal dialysis. Besides a well-documented anaphylaxis to penicillin, she has multiple chronic medical problems, the most relevant being CHF.

The CHF has been refractory to medical therapy, and she now has moderate anasarca and ascites, hence the need for dialysis. The peritoneal dialysis catheter is placed without problems, but three days later, she has fevers, altered mental status, and abdominal pain.

The CAPD fluid has 800 WBC (but she is nearly neutropenic from MDS) and gram-positive rods. They call me.

I figure it is going to be an inadvertent bowel perforation from the CAPD catheter. Gram-positive rods include a variety of species, but in the CAPD fluid culture, I would worry most about be Clostridia. The patient had been placed on vancomycin, metronidazole, and cefepime, which seemed reasonable.

The next day the blood and peritoneal fluid were growing a gram-positive rod. And the next day is identified as Listeria monocytogenes.

The two organisms that are rarely covered with most empiric antibiotic combinations, especially the penicillin-allergic patients, are maybe Listeria and Stenotrophomonas. Certainly, my flawed memory suggests that is the case in my practice.

Is this hospital-acquired peritonitis with bacteremia? Bacteremia seeding the peritoneum? I quizzed the family about her risks and found none.

There are many examples of hospital-acquired Listeria, although mostly outbreaks, and we have had no other isolates in the lab. Of course, it would be difficult to identify the source of a sporadic case, and the patient's illness made her functionally NPO.

The organism can be on most meats, vegetables, and the environment:

The aim of this study was to determine the prevalence of Listeria spp. and Listeria monocytogenes (L. monocytogenes) in urban public lavatories and on shoe soles of facility patrons in a European capital city. More than 91% of all municipal public lavatories in Vienna close to public hubs were included in this study. Overall, 373 swab samples of public lavatories and shoes of facility patrons were enriched, according to ISO 11290–1. Listeria monocytogenes isolates were subtyped using pulsed-field gel electrophoresis. A total of 24 samples were positive for Listeria spp., yielding an overall prevalence of 6.4% (24/373). Listeria monocytogenes was found in 2.1% (8/373) of all samples. Swabs from lavatories in parks, container lavatories and lavatories at markets had the highest prevalences of 20.7% (6/29), 20% (2/10) and 12.5% (1/8) Listeria spp., respectively. These detection rates were statistically significantly higher than those associated with lavatories in shopping centres (P = 0.003, P = 0.002, P = 0.02) and at public transport locations (P = 0.0004, P = 0.005, P = 0.02). Shoes sampled at Christmas markets showed the highest Listeria spp. and L. monocytogenes prevalences of 80% (4/5) and 40% (2/5), respectively. With regard to shoe type, Listeria spp. detection rates were 14.3% (3/21; winter boots), 13.3% (2/15; hiking boots), sport shoes (5.9%; 2/34) and brogues (5.1%; 4/79). No Listeria spp. were found on shoe soles that had smooth treads (0/76), while Listeria spp. were detected on 19.5% (8/41) of medium depth tread shoe types and on 9.4% (3/32) of deep tread shoes. These data suggest that soil environment is still one of the most important reservoirs for the foodborne pathogen L. monocytogenes.

and her age and MDS was certainly enough to get the disease from minimal exposure.

Compared with persons <65 data-preserve-html-node="true" years with no underlying conditions, those with chronic lymphocytic leukemia had a >1000-fold increased risk of acquiring listeriosis, and those with liver cancer; myeoloproliferative disorder; multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pancreas, lung, and brain cancer; cirrhosis; organ transplantation; and pregnancy had a 100–1000-fold increased risk of listeriosis.

While there are reports of SBP from Listeria, there are only about 13 reported in CAPD patients. Rare indeed.

Rationalization

Clin Infect Dis. 2013 Jan;56(1):20–6. doi: 10.1093/cid/cis817. Epub 2012 Sep 20. Hospital-acquired listeriosis outbreak caused by contaminated diced celery–Texas, 2010.

http://www.ncbi.nlm.nih.gov/pubmed/22997210

Clin Infect Dis. 2012 Mar 1;54(5):652–60. doi: 10.1093/cid/cir902. Epub 2011 Dec 9. Incidence of listeriosis and related mortality among groups at risk of acquiring listeriosis.

http://www.ncbi.nlm.nih.gov/pubmed/22157172

Zoonoses Public Health. 2014 Apr 21. doi: 10.1111/zph.12121. [Epub ahead of print] Urban Prevalence of Listeria spp. and Listeria monocytogenes in Public Lavatories and on Shoe Soles of Facility Patrons in the European Capital City Vienna.

http://www.ncbi.nlm.nih.gov/pubmed/24751465

Neth J Med. 2011 Oct;69(10):461–4. Listeria peritonitis in patients on peritoneal dialysis: two cases and a review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/22058269

Clot

May 7, 2014

I remember, as an intern, one of the other house staff (honest, it was someone other than me) had an IV drug user admitted with fevers. I trained in a county hospital, and often we had to draw our own blood and start our own iv’s. The patient had exhausted all her superficial veins and had been using the femoral vein. My colleague could not get any blood peripherally and, it being the first month of internship, could not hit the femoral vein either. In disgust, the patient commandeered the syringe, stuck her own femoral vein, and filled the syringe. He mentioned this in rounds, and I thought it quite handy at the time, but did he ever get chewed out by the attending.

The patient from several months ago had a similar problem. He has been using his femoral veins for heroin and now has S. aureus in the blood and clot in the iliofemoral vein.

I like to remind the house staff that the other name for S. aureus is coagulase-positive Staphylococcus. It loves to solidify blood. To quote the Wikipedia:

Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood.

It is quite the enzyme and can turn a tube of rabbit serum solid. While S. aureus is the usual organism that makes a coagulase, I found out today that

There are 7 coagulase positive species of Staphylococcus, most other than S. aureus have an animal host but may not be wholly restricted to that host. They are listed below with their predominant hosts: S. pseudintermedius - mostly found in dogs and cats. S. intermedius - feral pigeons S. schleiferi ss coagulans - dogs S. delphini - dolphins, seals, horses S. hyicus - pigs and cattle. Not always coagulase positive S. lutrae - otters S. pseudintermedius, intermedius and delphini are closely related and are difficult to separate phenotypically. Further studies are required to establish the host associations of each of these, other than S. pseudintermedius which predominates in dogs and cats.

A hodgepodge of other organisms makes a coagulase including Yersinia pestis, explaining in part its presentation of DIC/purpura fulminans.

I am never surprised to see clot/thrombosis with S. aureus infections. I am more surprised when I do not.

Using the femoral vein for drug injection is not uncommon and not safe. In Seattle

One hundred respondents (40%) had injected into the femoral vein, 55% of whom were actively doing so, and 58% of whom reported medical complications that they attributed to the practice. Most (66%) used the femoral vein due to difficulty accessing other veins, although 61% reported other veins they could access and 67% reporting using other sites since initiating femoral injection. While injecting into muscle was more frequent among older IDUs with longer injection careers, the prevalence of femoral injection was highest among respondents in their late twenties with 2.5–6 years of injecting drugs.

Of course, being in Portland, my first thought is, what do you expect from Seattle? There is a pdf online so you can learn to shoot in the femoral vein the right way as well as all sorts of handy hints for safe IVDU.

Antibiotics and anticoagulation (under the care of a health care provider, one hopes. Evidently, some IVDU who use the femoral vein are getting warfarin on the street) usually takes care of the problem without surgery.

The things you can learn in this job with a little curiosity and the Googles.

Rationalization

Mol Microbiol. 1989 Jun;3(6):767–75. A Yersinia pestis-specific DNA fragment encodes temperature-dependent coagulase and fibrinolysin-associated phenotypes.

http://www.ncbi.nlm.nih.gov/pubmed/2526282

J Bacteriol. Jan 1965; 89(1): 101–105. PMCID: PMC315554 Plasma Coagulation by Organisms Other Than Staphylococcus aureus.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC315554/

J Urban Health. Apr 2012; 89(2): 365–372. Published online Mar 6, 2012. doi: 10.1007/s11524–011–9664–4 PMCID: PMC3324607 Prevalence and Characteristics of Femoral Injection among Seattle-Area Injection Drug Users

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324607/

Swiss Med Wkly. 2002 Jul 13;132(27–28):386–92. Septic deep venous thrombosis in intravenous drug users.

http://www.ncbi.nlm.nih.gov/pubmed/12428193

“Street” supplies of the anticoagulant drug warfarin: a worrying new trend.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564363/

Using Magic

May 9, 2014

The last decade has seen progress that has been to the detriment of the inpatient ID consultive service. HAART, GCSF, infection prevention bundles, hospitalists, and more have led to either a decrease in hospitalized infections or better management. My inpatient service has slowly declined over the last decade, which is OK as I am on the tail end of my career and no longer wish to work as hard as I did when I was young.

Fortunately for ID, there is still prednisone, methotrexate, and the biologics generating the occasional odd infection.

The patient is an elderly male on prednisone and methotrexate for a collagen vascular disease. In the late fall, he developed fevers and a general malaise. Work up found bilateral masses in the kidneys, which were thought to be lymphoma.

Two biopsies later, no malignancy is found, only inflammation, so they send the patient to me.

ID history yields no exposure except perhaps for Brucella, and that is a stretch. And as a rule, infections of the kidney are not bilateral, so I figure this is going to be something odd.

Since I have nothing to culture, I decide to use magic, er, I mean, molecular diagnostics and send the kidney biopsy for broad-spectrum PCR.

And it comes back Eurotium sp. Say what? Isn't that what Wolverine's skeleton is made of?

Eurotium species are the sexual states of Aspergillus species, notably the Aspergillus glaucus group among others. Eurotium is common and is most closely related to Emericella, another genus with Aspergillus anamorphs. Eurotium is likely to be present along with related Aspergilli if growth has been long term and the nutrients of the substrate are conducive for the conversion to sexual phase.

Who knew Aspergillus had sex? These life cycles, while important, have little clinical utility, and I will not remember any of this once I am doing reading it.

Browsing the Pubmeds finds two infections, a pneumonia and a brain abscess due to Eurotium and/or A. glaucus. Most of the literature concerns the production of mycotoxins and their environmental effects. For example, Eurotium is common in damaged flue-cured tobacco, found on barley kernels, and on Portuguese dry-smoked sausages amongst others. It looks like a major part of my diet is Eurotium.

So, while common in the environment, it is not so common in the kidneys. I’ll blame the prednisone and methotrexate, but I have no real clue where it came from.

The patient has made a marked clinical improvement of voriconazole with the resolution of the fevers and a return of a sense of well-being. Repeat imaging of the kidneys is several weeks away; I figure it will take 6 weeks or so before there would be any radiographic change, and he doesn’t need the radiation.

I wish we had more accessible access to magic. I send my specimens to U of W, and each PCR is $500, so for AFB, bacteria, and fungal, it is $1500. Well worth it if you can make a diagnosis, but so much of ID diagnostics is still trying to grow bugs on variations of agar and is so last century.

Rationalization

Mycologia. 2013 Jul-Aug;105(4):912–37. doi: 10.3852/12–151. Epub 2013 Feb 8. Taxonomic revision of Eurotium and transfer of species to Aspergillus.

http://www.ncbi.nlm.nih.gov/pubmed/23396159

Eur J Clin Microbiol Infect Dis. 2007 Oct;26(10):747–50. Fatal brain infection caused by Aspergillus glaucus in an immunocompetent patient identified by sequencing of the ribosomal 18S–28S internal transcribed spacer.

http://www.ncbi.nlm.nih.gov/pubmed/17665232

The Flux

May 12, 2014

There are so many causes of diarrhea. Causing the flux is a method by which many organisms spread. It is a ‘smart’ way to be contagious as it often gets the bacteria back to water when it can spread further.

Keeping drinking water separate from wastewater was one of the important advances in health, right up there with vaccines and good nutrition. We take safe water for granted, but I often marvel at a cup of cold water right out the tap. It is a luxury many do not have.

The patient is admitted with severe diarrhea, neutropenia, and fevers after chemotherapy for pancreatic cancer. She receives broad-spectrum antibiotics, and while the WBC improves, the fevers persist as does the diarrhea.

Fever is often associated with diarrhea, so cause and effect are suspect. My just-so story to explain the association is that back in the day before plumbing and refrigerators, a common source of bacterial infection was food and drink. Given that the best way to treat an infection is source control, having endotoxin lead to diarrhea and vomiting would be an efficient, if an unpleasant way, to remove infection.

However, on day three, the stool cultures grew Aeromonas hydrophilia. It has been a long time since I have seen that organism in a stool culture. The first was early in my practice when I saw a patient with bloody diarrhea. Aeromonas is a waterborne organism, so I went looking for a source. It turned out she had a jug of holy water from Mexico that, when cultured, grew Aeromonas. One of the several bacteria associated with holy water infections.

In this case, I could find no obvious water exposure, but Aeromonas happens.

A. hydrophila was found in 1.1% of patients with diarrhea and in none of 533 control patients (P less than 0.02). Cases were detected 1.5 times more often during the summer months than the winter months, and most occurred in children less than 2 years of age. Clinical features included fever greater than 38 degrees C (55%), abdominal cramps (35%), vomiting (25%), and duration of illness greater than 10 days (50%).

Aeromonas does cause infections in those with hepatobiliary disease, including pancreatic cancer, but as best as can be determined, the infections is limited to her GI tract.

She slowly improved on a po quinolone.

Rationalization

J Hosp Infect. 1996 Jan;32(1):51–5. Holy water–a risk factor for hospital-acquired infection.

http://www.ncbi.nlm.nih.gov/pubmed/8904372

J Clin Microbiol. 1985 Jun;21(6):909–13. Clinical and microbiological features of Aeromonas hydrophila-associated diarrhea.

http://www.ncbi.nlm.nih.gov/pubmed/4008621

Clin Infect Dis. 2003 Aug 15;37(4):506–13. Epub 2003 Jul 30. Aeromonas infection of the hepatobiliary system: report of 15 cases and review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/12905134

Supportive Care in Cancer November 1995, Volume 3, Issue 6, pp 414–417 Nature and outcome of febrile episodes in patients with pancreatic and hepatobiliary cancer

http://link.springer.com/article/10.1007/BF00364982

Pulling the Plug

May 14, 2014

The patient had lymphoma a decade ago and was considered a cure. She has 5 days of fevers and abdominal pain and comes in with SIRS and tumor lysis syndrome.

I did not know there was such a thing as spontaneous tumor lysis syndrome, I thought it only occurred with chemotherapy. But it can occur with a variety of tumors:

Although it is more commonly seen after treatment, the spontaneous form of this syndrome has been reported mostly among patients with hematologic malignant diseases. The prevalence of spontaneous tumour lysis in patients with solid tumours is harder to ascertain because it is based primarily on case reports.

Blood cultures grow a gram-positive rod, so they call me.

As an outpatient, she had a CT that demonstrated a mass in the RLQ, presumptive for recurrence of lymphoma, but had not yet had a biopsy. Her exam had moderate abdominal pain and distension, and she required pressors, but her labs were not that bad.

I thought it should be Clostridia, more specifically C. septicum, which has a predilection for being associated with cancer, as I discussed back in 2010 in Classical Gas Gangrene. Clostridia likes devitalized tissue to get a toe hold for subsequent dissemination, so a spontaneously lysing tumor seemed good soil in which the Clostridia could grow.

The repeat CT was curious, showing the RLQ mass was gone. It really lysed. There was ascites, which was tapped, but did not appear purulent.

I called the lab, who said yep, it was shaped like a Clostridia (square gram-positive rods), so I maximized the killing of Clostridia. The patient continued to worsen, and the next day the lab could only tell me it was 50% probability a C. argentinense. I love it when bacteria are reported like quantum probability functions. I wonder if you could use Clostridia in a double-slit experiment.

Still, Clostridia in the blood can be bad, no matter what the species.

Patients with Clostridium bacteriemia were older, had a higher frequency of gastrointestinal disease (especially colorectal tumours), were associated more frequently with polymicrobial bacteraemia, and had a higher mortality rate. In the second part of the study, each of the 80 cases of Clostridium bacteraemia was evaluated individually for clinical relevance by an infectious diseases expert. In two-thirds of the cases, isolates of Clostridium from blood were considered to be of clinical relevance, whereas in one-third of cases, the clinical significance of this finding was doubtful. It was concluded that growth of Clostridium spp. in blood cultures, even in the absence of one of the histotoxic syndromes, is often of clinical significance, and that such findings should be properly evaluated and not ignored.

Because of a worsening clinical course, she was taken for an exploratory lap. The abdomen was filled with stool secondary to a perforation.

I bet the tumor had eroded through the bowel wall and was acting as a plug to keep bowel contents out of the peritoneal cavity. When it lysed, the plug was pulled and that is why she went on to develop worsening sepsis, not due to the Clostridia. I have seen this occur a couple of times with chemotherapy, and there are other reports with lymphoma and other cancers involving bowel wall:

Primary intestinal lymphoma with spontaneous perforation and after systemic chemotherapy is rare. The present study summarizes retrospectively the outcome of eight free intestinal perforated patients diagnosed with intestinal non-Hodgkin’s lymphoma. Two patients had a history of systemic chemotherapy before perforation. The most common symptoms of the patients were abdominal pain, nausea, vomiting, weight loss, and fever. Sites of perforation were ileum in four, jejunum in two, cecum in one, and sigmoid colon in one patient. Synchronous lymphoma was present in three patients.

An unusual and catastrophic complication.

Rationalization

Clin Microbiol Infect. 2006 Oct;12(10):1006–12. The possible significance of Clostridium spp. in blood cultures.

http://www.ncbi.nlm.nih.gov/pubmed/16961638

CMAJ. May 15, 2012; 184(8): 913–916. Spontaneous tumour lysis syndrome

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348194/

Dig Dis Sci. 2007 Aug;52(8):1752–6. Epub 2007 Apr 10. Spontaneous intestinal perforation due to non-Hodgkin’s lymphoma: evaluation of eight cases.

http://www.ncbi.nlm.nih.gov/pubmed/17420936

The Mitis Touch

May 16, 2014

One of the many medical problems that have faded in the last decade is the neutropenic fever. With kinder, gentler chemotherapy, colony-stimulating factors, and prophylactic antibiotics, patients do not get the infectious complications at rates as they did back in the day. And fortunately, leukemia is a relatively uncommon malignancy.

Two patients this week, at different hospitals, with prolonged neutropenia, and both had a rigor followed by a temperature to 102. They both were admitted, and both had one of two sets of blood cultures positive for gram-positive cocci in chains.

Contaminant? I am asked.

No such thing in this patent population. It is a real bacteremia; the question is whether it is a significant or complicated bacteremia. Neither patient had a significant mucositis but given that Streptococcal (and other organisms) will often get in the bloodstream as part of life, I figure all Streptococci in the blood are real.

So, wait on the identification of the organism.

Both grew a S. mitis, one with an MIC to penicillin of 0.38, the other 0.01. Well, probably S. mitis. As is so often the case with bacterial identification, S. mitis was as close as they could get. Some bacteria are more diverse than we can tell from standard testing.

Compared with patients infected with non-S. mitis strains, patients infected with S. mitis strains were more likely to have a moderate or severe clinical disease (e.g., VGS shock syndrome). Combined with the sequence data, whole-genome analyses showed that S. mitis strains may more precisely be considered as >2 species.

Careful evaluation did not suggest any focal infection, and both responded rapidly to antibiotics with no signs of sepsis or toxic shock syndrome.

Both probably had antibiotic pressure selecting for the S. mitis; one was on ciprofloxacin, the other tmp/sulfa.

Risk factors in this patient population include severe neutropenia, oral mucositis, administration of high-dose cytosine arabinoside, and antimicrobial prophylaxis with either trimethoprim-sulfamethoxazole or a fluoroquinolone… Streptococcus mitis has been the causative species in most cases.

Prophylactic antibiotics have helped decrease gram-negative infections in neutropenics, but with the result of infections with resistant S. mitis. Try and prevent S. mitis, and no doubt, some other pathogen will slip through. No good deed ever goes unpunished, and the bacteria will always find a way.

Rationalization

Clin Infect Dis. 2002 Jun 1;34(11):1524–9. Epub 2002 May 6. Infections caused by viridans streptococci in patients with neutropenia.

http://www.ncbi.nlm.nih.gov/pubmed/12015700

Emerg Infect Dis. 2014 May;20(5):762–71. doi: 10.3201/eid2005.130953. Streptococcus mitis Strains Causing Severe Clinical Disease in Cancer Patients.

http://www.ncbi.nlm.nih.gov/pubmed/24750901

You Can Wait. Really. You Can.

May 19, 2014

An adult was admitted to one of my hospitals with bacterial meningitis. The patient was in the system for several hours before the diagnosis was considered and placed in proper isolation. So, as is often the case, everyone freaked and wanted ciprofloxacin prophylaxis.

It is an adult, so it is unlikely Meningococcus, there is no Meningococcus in the community, and above all, you have time, the time it takes to grow the cultures, which, as would be expected in an adult, have S. pneumoniae after 24 hours.

There is apparently some misunderstanding about the necessity of post-exposure prophylaxis for health care providers exposed to real or potential cases of Meningococcus.

Family members exposed to an index case are transiently at increased risk for disease with an attack rate of .3 to 1%. This is probably due to genetic/hereditary variations in the immune system that predispose the patient and their family to invasive disease. It is probably more the patient and less the organism that leads to infection.

For family members, greater than 4 hours of exposure or contact with respiratory secretions, antibiotic prophylaxis is recommended.

How about health care providers? It would be rare indeed for an HCW to have spent more than four hours in a room with a patient, much less have been exposed to respiratory secretions. I once had a doc in who intubated a patient in full PPE (the doc, not the patient) and still wanted ciprofloxacin.

There are at best a half dozen cases of secondary infection in HCWs ever reported, and they all had one factor in common: exposure to respiratory secretions without proper PPE:

Transmission of N. meningitidis to health-care personnel has occurred after unprotected exposure to infected patients during endotracheal intubation, airway suctioning, and oxygen administration (68), but more than one occupationally acquired infection from the same index patient has not been reported. Findings from this investigation indicate that breaches in infection control and likely contributed to secondary cases of meningococcal disease.

Unless exposed to direct secretions, no antibiotic prophylaxis is warranted, only driving cost, toxicity, and resistance without benefit.

To be on the safe side, any person directly exposed to the cases nasopharyngeal secretions (e.g., through kissing or mouth-to-mouth resuscitation) is also advised to take prophylaxis. On the other hand, health care workers who havent had contact with secretions are not at risk and do not benefit from prophylaxis.

So, stop asking for the ciprofloxacin.

Here is a suggested approach:

\1) Meningitis is suspected. Droplet Isolation i.e., surgical masks. Viola. Everyone is safe.

\2) LP shows meningitis by cell count, protein, glucose. Wait. No hurry for prophylactic antibiotics, Meningococcus is not like lice, jumping off the patient on to you. And I would be shocked if you were really exposed.

\3) Gram stain is negative or gram-positive cocci. Meningococcus is gram-negative diplococci. Wait. It isn't Meningococcus; prophylactic antibiotics will not be needed.

\4) Gram stain has gram-negative diplococci. Wait. No hurry.

\5) Cultures grow N. meningitis. Prophylaxis for those who were directly exposed to respiratory secretions: mouth to mouth, suctioning, intubation, or other respiratory procedures without PPE.

Other health care providers do not need prophylaxis, and to do so would be let us say ill-advised. Or stupid.

Rationalization

\1) Occupational Transmission of Neisseria meningitidis California, 2009 Weekly November 19, 2010 / 59(45);14801483.

https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5945a2.htm

\2) Oregon CD Summary February 14, 2012 Vol. 61, No. 4.

https://www.oregon.gov/OHA/PH/DISEASESCONDITIONS/COMMUNICABLEDISEASE/CDSUMMARYNEWSLETTER/Documents/2012/ohd6104.pdf

POLL RESULTS

I always take a prophylactic when I may have been exposed to

• meningococcus 10%
• syphilis 0%
• gonorrhea 0%
• a new idea 30%
• a contradictory idea 50%
• Other Answers 10%
  • the wife's brother's right-wing nut-job spouse.

Stones Not Grass?

May 23, 2014

I have always been a fan of language and obscure words and phrases. It is probably to my detriment, as communication is not as efficient if people do not share a common vocabulary. Still, I now wish I had called the blog something like Reflections of a Nimgimmer or An ID Mumpsimus. Ah well. Rubor, Dolor, Calor, Tumor it is.

It has been an amazingly busy week. I have not had this kind of volume in years and had a personal one-day record 14 consults. So, I missed my usual Wednesday post. But lots of great ID cases. But then, aren't they all? I say it is the great docs who make the great cases. Yeah, it should have been mumpsimus.

One consult was an elderly female who for the past two years has had a mass growing in the RUQ, between the liver and the chest wall. I am not certain why they sat on it, but it was eventually biopsied, and she was sent to me.

She had some mild constitutional symptoms, mostly fatigue, but was otherwise healthy. Besides diverticulosis (but never -itis), the patient had an uneventful gallbladder removal four years ago.

And the biopsy had ‘sulfur’ granules and thin gram-positive branching rods. Unfortunately, cultures were not done, but the pathology is consistent, or more exactly classic, for actinomycosis.

So where did that come from? There are no cases of actinomycosis from diverticular disease and a smattering from cholecystectomies, usually associated with loss of stones into the abdomen at the time of surgery.

There are no lost stones on the current CT, and the abscess is subphrenic space, not in the gallbladder fossa, but crediting the cholecystectomy and lost stones is the most likely explanation. I was always taught that the pressure in the abdomen is lowest in the RUQ, so pus and debris tend to be sucked up there. That, I suspect, is nonsense. The sucking part, not the lower pressure.

Infection is a better diagnosis than a tumor. Now for a year or so of penicillin. And it was cured.

And I did not know this:

In 1890, Eugen Bostroem isolated the causative organism from a culture of grain, grasses, and soil. After Bostroem’s discovery there was a general misconception that actinomycosis was a mycosis that affected individuals who chewed grass or straw.

Rationalization

Clin Infect Dis. 2007 Jan 15;44(2):e1–4. Epub 2006 Dec 6. Abdominal abscesses due to actinomycosis after laparoscopic cholecystectomy: case reports and review.

http://www.ncbi.nlm.nih.gov/pubmed/17173208

South Med J. 2009 Jul;102(7):725–7. doi: 10.1097/SMJ.0b013e3181abddc5. Subphrenic abscess secondary to Actinomycosis meyeri and Klebsiella ozaenae following laparoscopic cholecystectomy.

http://www.ncbi.nlm.nih.gov/pubmed/19487988

Acta Radiol Short Rep. 2014 Feb 21;3(2):2047981614524570. doi: 10.1177/2047981614524570. eCollection 2014. Abdominopelvic actinomycosis: spectrum of imaging findings and common mimickers.

http://www.ncbi.nlm.nih.gov/pubmed/24778807

Nimgimmer (Grose 1811 Dictionary). Nimgimmer. A physician or surgeon, particularly those who cure the venereal disease

A mumpsimus is a "traditional custom obstinately adhered to however unreasonable it may be", or "someone who obstinately clings to an error, bad habit or prejudice, even after the foible has been exposed and the person humiliated; also, any error, bad habit, or prejudice clung to in this fashion".

Lick

May 28, 2014

I mostly feel sorry for IVDA. I know a lot of people have more contempt than pity, but I suspect they deny whatever alternative monkey they have on their backs. Mine comes in the form of a rectangle of fried dough with maple frosting, so who am I to judge?

I see a lot of IVDAs; it is a lifestyle prone to infections. I just hope they don’t die of their disease and eventually kick the habit. Dead people never get to turn their life around.

The patient is a young female who, after a period of abstinence, relapses her habit and goes back to heroin. Injecting in her legs, she has fevers, rigors, and unilateral leg pain. The ER does an ultrasound, and she has extensive deep venous thrombosis, so she is started on anticoagulation.

The leg gets worse, redder and tender, and she is admitted, and the next day all three blood cultures are growing S. Intermedius, an oral streptococcus. Sustained bacteremia. Endocarditis, right? I don’t know. No murmur or emboli, but those would take time to develop. No vegetation on ECHO, but that also takes time to develop, and I have always wondered if anticoagulation makes vegetations less likely to been seen on echo. It is a study for a budding cardiologist.

And then there is that clot. Is this a septic thrombophlebitis of the leg? Could be. There are only 11 cases of septic thrombophlebitis due to S. viridans group and none in an extremity. There are few cases that occurred in the internal jugular and a few in the abdomen. So not a common cause of a septic vein.

And how did that organism get in the leg/blood?

“Do you lick your needles?” I asked.

“Yes.”

“Well, that’s probably how that bug got in your blood.”

“Expletive deleted.”

Needle licking is common; I usually ask IVDA and often get an affirmative:

Thirteen (32.5%, 95% CI, 18.6–49.1) of 40 subjects reported licking their needles prior to injecting. Reasons included ritualistic practices, cleaning the needle, enjoying the taste of the drug, checking the “quality” of the drug, and checking that the needle was in usable condition.

And here I always thought it was because it makes the dull needle slide in easier.

I suppose, either way, she gets four weeks or so of iv antibiotics. And she improved rapidly with ceftriaxone and continued anticoagulation.

Rationalization

Int J Drug Policy. 2008 Aug;19(4):342–5. doi: 10.1016/j.drugpo.2007.06.006. Epub 2007 Jul 26. Why some injection drug users lick their needles: a preliminary survey.

http://www.ncbi.nlm.nih.gov/pubmed/18638706

Fox Den Variant?

May 30, 2014

Draining fistulas are good you. Really. As long as the pus and bacteria have egress to the outside world, the patients will do fine. When I was young and inexperienced, I would see patients who had years of draining chronic osteomyelitis, a sequela of trauma in the pre-antibiotic era. And I would treat it. And the fistula would close. And, with no egress to the outside world, the pus and bacteria would back up into an abscess, then the bloodstream, then the patient would get sick. So I learned. If you cannot do definite source control and the patient is not clinically infected, let the fistula drain. It gives the evil humors someplace to go.

The patient has had years of Crohn’s bowel disease refractory to most medications. He has several chronic fistulas for years that have been draining until recently when one spontaneously stopped. And he got sick, with fevers, chills, and a red, tender mass on his backside where the fistula used to drain. CT was interesting as you could see a fistula from the colon to an abscess, and there was an area of new fibrotic tissue acting like a dam right where the fistula used to drain. A month ago, he had been placed on oral antibiotics, and I wonder if they were too successful.

He had the dam removed, pus was drained, and he is now feeling a lot better.

Here is a curious finding. One of the cultures from as admission is growing both an anaerobe and Actinomyces urogenitalis. There are only a handful of cases where Actinomyces urogenitalis has been associated with the disease; it is mostly a commensal.

But. I wonder if this is a version of Fox Den disease, aka Pyoderma Fistulans Sinifica. I have written about Fox Den before.

PFS, which has not been previously described in the English-language literature, must be differentiated from hidradenitis suppurativa, pilonidal sinus, and perianal fistula. The fistulous tracts of PFS are always lined by stratified squamous-cell epithelium but, unlike those of hidradenitis, reach deep into the subcutaneous fat, run epifascially for long distances, and have no relation to skin appendices.

And

Obligate anaerobes are the predominant bacteria in PFS. Among the most striking bacteriologic findings in our study were the absence of fecal obligate anaerobes (such as Bacteroides fragilis) in all but one case and the predominance in all cases of Fusobacterium, Prevotella, and Peptostreptococcus species. Although Actinomyces was isolated from four patients, in no case were mycelium-type colonies seen in histologic cross-section. None of our patients had systemic disease. Moreover, the discharge of sulfur granules that is characteristic of actinomycosis has not been documented in PFS. Actinomycotic infections cross anatomic barriers; PFS does not.

Probably not Fox Den since the fistula are coming from bowel on CT, although it has similar microbiology and clinical presentation. And this time, there are also gram-positive rods in the abscess, final ID pending. So maybe a variant?

For now, I need to treat the abscess, but what to do about the ongoing fistulas is problematic. Antibiotics may make things worse again.

Rationalization

Characterization of Actinomyces isolates from samples from the human urogenital tract: description of Actinomyces urogenitalis sp. nov.

http://ijs.sgmjournals.org/content/50/4/1649.full.pdf

Genus Actinomyces.

http://www.bacterio.net/actinomyces.html

Clin Infect Dis. 1995 Jul;21(1):162–70. Pyoderma fistulans sinifica (fox den disease): a distinctive soft-tissue infection.

http://www.ncbi.nlm.nih.gov/pubmed/7578725

Two Problems

Jun 2, 2014

I once added up all the organisms in the index of Mandel to see how many I needed to know to do my job. I included only those I recognized, and I was a splitter, for example, each Klebsiella spp. was counted separately. There are, for example, a lot of Salmonella. There were maybe 1200 potential pathogens I know or need to know. Not that many, and it makes my job conceptually simple: Me find bug, me kill bug, me go home.

Of the three parts of the job, me go home is the only reliable and simple aspect. Finding, then killing, is not so simple.

The patient has two problems: one is a chronically infected shoulder from multiple failed repairs of a rotator cuff tear. It is I&D’d and grows P. acnes with a few colonies of a resistant coagulase-negative Staphylococcus. No surprise.

P. acnes is the most frequent bacteria found in postoperative infections of the shoulder. Cases typically involved either a male patient who underwent RCR and complained (after a short symptom-free interval) of pain, mild fever, and inflammation of the scar or a male patient who underwent a prosthetic implant, complained of symptoms indicative of chronic infection, such as chronic pain and mild local signs, and had previously had negative culture results. The shoulder seems to have a propensity for developing P. acnes infection. The pathophysiology is difficult to understand.

So, he grew what he should have. But the patient's other problem is Medicare. There should really be an ICD 9 code for having Medicare because it can be a problem. I have seen V62.6, Refusal of treatment because of the reason of conscience or religion, accorded to Jehovah’s witnesses for refusal to accept blood transfusions. Refusing transfusions can have serious complications; I have seen two patients bleed to death as a result of being a JW.

The problem is Medicare does not pay for home antibiotics. I have to come up with a once-a-day antibiotic so the patient, who is otherwise vigorous and active, doesn't have to go to a nursing home. Nursing homes, or as we call them, Skilled Nursing Facilities (SNF), can have their issues, he says with a certain understatement.

How do I kill both bugs with one drug once a day? I laid out the options to the patient: the tried and true (which would mean a SNF) vs the it should work but not a lot of clinical data (which could be given once a day in the infusion clinic and paid for).

He opted for the latter. No way was he going to a nursing home. So daptomycin it is. Based on what literature there is, I do not think I am going to compromise care with the choice, although I sometimes feel more like the Magic 8 Ball than an evidenced-based practitioner: Signs point to yes. I sure do hate having to consider reimbursement when I make clinical decisions.

I have no idea what the solution is to the mess that is the US health care system. I assume any practicing doc who thinks she knows the answer is pulling a Dunning-Kruger and talking out of their, er, well, you know. So, feel free to pontificate in the comments. Whatever it ends up being will be suboptimal. But it must be better than what we have today.

Addendum

It worked.

Rationalization

Clin Infect Dis. 2008 Jun 15;46(12):1884 6. doi: 10.1086/588477. Propionibacterium acnes postoperative shoulder arthritis: an emerging clinical entity.

http://www.ncbi.nlm.nih.gov/pubmed/18462110

Clin Neurol Neurosurg. 2009 Sep;111(7):610 2. doi: 10.1016/j.clineuro.2009.04.003. Epub 2009 May 17. Propionibacterium skull osteomyelitis treated with daptomycin.

http://www.ncbi.nlm.nih.gov/pubmed/19450922

POLL RESULTS

What US health care needs is

• a single payer 59%
• free market 7%
• survival of the fittest 4%
• screw them, I got mine 0%
• got me, I am just a cork in the ocean of medicine 26%
• Other Answers 4%
  • For the government to stay out of it!
  • A redo

Stupid

Jun 4, 2014

Work is oddly slow the last several days, more like August than spring with the volume of work. While I have a couple of potential fascinomas pending, I do not have the final confirmatory tests to demonstrate either my clinical brilliance or my clinical cluelessness. Such is medicine.

So rather than talk about clinical infectious diseases, I will winge about definitions. The nice thing about blogging, at least my conception of blogging, is I can do what I want. And since I am only speaking for me, not any of my hospitals, I can also say what I want.

In infection control we spend a lot of time on surgical site infections (SSI) and are quite proud of the marked reduction at all my hospitals.

This year, 2014, the CDC/NHSN changed some of the SSI definitions, and now they make no allowance for pre-existing infections in operative sites.

if a patient has an infection in the organ/space being operated on, a subsequent continuation of this infection type during the remainder of the surveillance period is considered an organ/space SSI.

So what does that mean in the real world?

For example, an appendectomy with subsequent subdiaphragmatic abscess would be reported as an organ/space SSI at the intraabdominal specific site (SSI-IAB) when both organ/space SSI and IAB criteria are met.

Basically, if there is a pre-existing infection and we operate on it and do not cure it the first time around, we take credit for the infection. That is one of the stupidest definitions I can imagine, completely divorced from the reality of medicine. I suppose the CDC has good reason for such a ridiculous change, but I cannot find it or think of what it might be.

The whole point of surveillance for SSI's is not only to find infections but to look for issues that can be changed to prevent future infections.

So, we have to report, and do all the work on drilldowns, for infections for which we are not responsible. It is galling to have to eat these infections and put them on the IC report. I refer to these, informally, as the stupid CDC infections. And that leads to a decline in the credibility of the CDC.

I would be hard-pressed to find another example more out of touch with the practice of medicine. Perhaps the ABIM recert/MOC process, which may be the most pointless waste of time ever. Although perhaps that will change. I hope the CDC does as well.

POLL RESULTS

The stupidest thing in medicine is

• NHSN definition of Organ/Space SSI 5%
• ABIM MOC process 15%
• 1000 dollars a pill for Sovaldi. No wait, that's greed, not stupidity 20%
• forced charting in the EMR 7%
• Medicare paying for SNF but not home antibiotics 48%
• Other Answers 5%
  • Telling Hospital Administration in advance exactly when the Inspectors are coming to visit. Lab becomes a circus of catchup and fill-in-the-blanks.
  • Insurance bimbettes dictating care
  • Insurance companies dictating care

Sympathetic Heart Ache

Jun 9, 2014

The patient is homeless, admitted with the inability to walk, and confused. He said he had fallen off a park bench and injured his leg a week before admission. At the time denied any other trauma or substance abuse, but his mental status was unreliable due to the severity of this illness.

His leg had a large abscess in the thigh, in the OR it was an infected hematoma. It grew MSSA.

Above his clavicle, he also had a large abscess that on CT went into his mediastinum. That was drained, and it too grew MSSA.

The abscess abutted the pericardium, and there was pericardial fluid on the CT. An ECHO demonstrated a large pericardial effusion that was called chronic due to the appearance. There was early tamponade, and the fluid was thick, with strands and septations. The fluid was tapped, it was pus, gram stain negative, but it also grew MSSA, and then was definitively treated with a pericardial window.

I generally think of bacterial pericarditis as a rapidly fatal disease as pus quickly fills up the pericardial space, but that is when it occurs from direct seeding of the pericardial space.

I suspect what happened here was more like what we see in the lung. There is a pneumonia that leads to a complex, but sterile, sympathetic pleural effusion. Then, if the fluid goes undrained too long, the bacteria eventually wander from the pneumonia into the pleural space and empyema results.

I suspect the mediastinal abscess caused the same physiology: contiguous pericardial 'irritation' from the abscess first resulted in the slow accumulation of a large, complex fluid collection around the heart, a sympathetic effusion that was seeded about the time it was tapped. It would explain the negative gram stain, the large amount of fluid around the heart, and the fact he did not acutely die of tamponade.

When his mental status cleared, I asked him how he got an infection in his chest. He said he awoke in the night because someone stabbed him the neck three quick times the week before admission. I am skeptical as I would doubt that such an injury would be survivable, but he had some form of trauma that led to the infection.

Rationalization

Br J Oral Maxillofac Surg. 1989 Oct;27(5):423-8. Mediastinitis and pericarditis caused by dental infection.

http://www.ncbi.nlm.nih.gov/pubmed/2804046

Med J Malaysia. 1989 Dec;44(4):348-50. Mediastinal abscess and pericarditis complicating retropharyngeal abscess--a case report.

http://www.ncbi.nlm.nih.gov/pubmed/2520047

Chirurg. 1983 Sep;54(9):617-20. [Suppurative mediastinitis following tooth extraction in sympathetic pericardial effusion].

http://www.ncbi.nlm.nih.gov/pubmed/6628064

Hit by Lightning Twice. And a Genius Idea

Jun 11, 2014

Hit by Lightning Twice

The patient is a young female who has the abrupt onset of fevers, nausea, then vomiting, then diarrhea, and then moderately severe abdominal pain.

After 24 hours without improvement, she was off to the ER. Of note was an elevated WBC, left shift, and a CT that showed enteritis and free fluid in the abdomen.

She was cultured and started on antibiotics, and the next day one of the blood cultures was growing gram-positive cocci in chains in the anaerobic bottle. They called me.

I had a few ideas after a review of risk factors. She had done nothing to put her at risk for unusual diseases. The stool for WBC is negative, as is the stool culture.

Of interest is she had an identical presentation a decade ago at another hospital that was due to a Streptococcus of some sort, although that episode was cellulitis.

Hmm. I was not certain how to put it together. I mentioned a few things (including the eventual diagnosis, just to brag) but was not enamored of any diagnosis. The cultures, I figured, would help define the diagnosis. And it did. Kind of.

The blood cultures grow Group A Streptococcus. What she had was spontaneous bacterial peritonitis (SBP), which I have discussed before. We would have to do an exploratory lap to confirm the diagnosis, and as she is getting better on beta-lactams with nothing to suggest a toxic shock or necrotizing fasciitis, an e-lap seems excessive.

SBP is a rare manifestation of S. pyogenes, akin to getting hit by lightning. We got the records from the outside hospital, and what is odd is that it is the same organism and presentation as a decade ago. Hit by lightning twice, although the record is seven.

Recurrent SBP from S. pyogenes is not reported, and recurrent bacteremia/sepsis is also rarely reported. Immunologic work-up is pending (it was negative), but history does not suggest a prior problem with infections.

A Genius Idea

If you read this blog regularly, you should be amazed at the variety of infections that one ID doctor can see in the middle of nowhere. Imagine the great cases being seen across the world.

I do not have the time or the inclination to write these up as a formal case report. Every couple of years, I suggest the following: what the ID world needs in an online database of cool and unusual cases that any clinician can search or add too. Just the basics of the case: age, gender, bug, organ, treatment, outcome, co-morbidities, source of infection, contact information. Two pages of data at most. KISS would be critical. Over time it could be an invaluable resource for research and treatment of patients.

I have suggested this several times to various administrations at the IDSA and have never received a reply. If not the IDSA, then some up and coming informatics ID doc or other hungry young academic. It is a brilliant idea (as are all my ideas); someone with institutional backing needs to make it a reality. If Project Tycho can get funded, perhaps this idea could as well. Get to work.

Rationalization

Br J Surg. 2010 Jan;97(1):104-8. doi: 10.1002/bjs.6822. Diagnosis and treatment of spontaneous group A streptococcal peritonitis.

http://www.ncbi.nlm.nih.gov/pubmed/20013929

J Clin Microbiol. 2011 Apr;49(4):1671-3. doi: 10.1128/JCM.02378-10. Epub 2011 Feb 23. Recurrent sepsis caused by Streptococcus pyogenes.

http://www.ncbi.nlm.nih.gov/pubmed/21346045

Project Tycho

https://www.tycho.pitt.edu/

Most lightning strikes survived

https://www.guinnessworldrecords.com/world-records/most-lightning-strikes-survived?

Belize Boil

Jun 13, 2014

No, it is not a variation on Cajun cuisine.

The patient is a young female who has spent the last six months in Belize. Part of her trip involved hikes into the jungle, and she remembers numerous bug bites.

Some of them did not heal; they became red bumps that then became small chronic ulcers with surrounding erythema. After several rounds of unsuccessful antibiotics, she sought care at a local hospital, and a touch prep showed Leishmania, and she returned to the US for therapy.

Which Leishmania? L. brasiliensis and L. mexicana are endemic in the county, and I have a call out to the CDC to aid in diagnosis. They have the ability to culture the organism which will guide therapy since

Whereas ketoconazole had a higher cure rate for L. mexicana (8/9 versus 4/7), the response rate in L. brasiliensis was much lower (7/23 versus 24/25).

And the species also make a difference for the potential for spread beyond the skin.

Leishmania, like Histoplasmosis and Trypanosomiasis, I find interesting since they occur both in the Old and New World. Africa and S. America started to pull apart about 145 million years ago, leaving pathogens on each side of the Atlantic to evolve down different paths resulting in disease presentations. Or so I had always assumed.

Always wrong to assume:

Visceral leishmaniasis in the New World is of unknown origin. Current studies cannot confirm the human disease prior to the European invasion of South America. These findings suggest that Leishmania chagasi arrived from Europe and that this species is very similar to L. infantum.

And

The first Leishmania fossil occurs in the Cretaceous Paleoartic. Given this origin, Leishmania may have been brought to the Neortic by primitive mammals through the Bering Straits. Recent studies by Kerr et al. have suggested that the most acceptable theory for the entrance of Leishmania into America is through the Bering Straits. During the Miocene, a primitive mammal, probably an infected rodent, brought the parasite into the New World.

There are fossil Leishmania? Yep. In amber. How cool. What other subspecialty has its diseases preserved in prehistoric sap?

Rationalization

Treatment of cutaneous leishmaniasis among travellers. J. Antimicrob. Chemother. (2004) 53 (2): 158-166.

http://jac.oxfordjournals.org/content/53/2/158.long

Leishmania : origin, evolution and future since the Precambrian.

http://onlinelibrary.wiley.com/store/10.1111/j.1574-695X.2008.00455.x/asset/j.1574-695X.2008.00455.x.pdf

Molecular trees of trypanosomes incongruent with fossil records of hosts.

http://www.scielo.br/scielo.php?script=sci\_arttext&pid=S0074-02762006000100006

Paleoleishmania

https://en.wikipedia.org/wiki/Paleoleishmania

Real World, Perfect World

Jun 16, 2014

I have to practice medicine in the real world, not always my favorite place since the real world often conspires to prevent perfect care.

It is bad enough to be a homeless, uninsured heroin user. Add to that an unwillingness to stick with the plan, and reality becomes one crazy honey badger.

The patient is admitted with a red, hot, swollen, tender leg. Ultrasound shows the femoral vein filled with clot, and one blood culture is positive at 48 hours for MSSA, but she is afebrile. Repeat blood cultures are negative, as is the TTE. After four days of cefazolin and she skips out, only to return three days later with the leg worse, but afebrile and negative blood cultures. After three days, she again skips out, only to return two days later with the leg worse, but still afebrile and negative blood cultures.

Safe to say she is not an optimal candidate for outpatient iv antibiotics. So, what to do? No fever, no-repeat positive blood cultures, negative TTE, and nine days of iv antibiotics, albeit spread out over two weeks. And the blood culture was positive late.

Logistic regression analyses revealed that a time to positivity of < or = 14 h was an independent predictor of an endovascular source of infection (P < .0005), extended bacteremia (P < .0005), metastatic infection (P < .0005), and attributable mortality (P = .017).

So, can I get away with oral antibiotics at this point? Perhaps. Everything points against a complicated S. aureus infection as if any S. aureus in the blood can be considered uncomplicated. But

Data about the required duration of intravenous therapy for suppurative thrombophlebitis is lacking. Among 36 episodes of proven suppurative thrombophlebitis requiring hospital admission, no relapses occurred when treatment was given for >7 days intravenously and followed by oral therapy. A <4 data-preserve-html-node="true"-week course of intravenous antibiotics may be sufficient.

The perfect, they say, is the enemy of the good. I suppose. But in medicine I prefer to strive for the perfect despite whatever honey badger reality sends my way.

She left AMA again, this time to not return.

Rationalization

Clin Infect Dis. 2008 Mar 1;46(5):741-4. doi: 10.1086/527445. Less than 28 days of intravenous antibiotic treatment is sufficient for suppurative thrombophlebitis in injection drug users.

http://www.ncbi.nlm.nih.gov/pubmed/18233950

Clin Infect Dis. 2005 Sep 1;41(5):594-8. Epub 2005 Jul 22. Time to positivity in Staphylococcus aureus bacteremia: possible correlation with the source and outcome of infection.

http://www.ncbi.nlm.nih.gov/pubmed/16080079

Honey Badger

https://en.wikipedia.org/wiki/The\_Crazy\_Nastyass\_Honey\_Badger

POLL RESULTS

I practice in

• the real world 14%
• a virtual world. I'll take the blue pill. 5%
• a virtual world. I'll take the red pill. 3%
• the rose colored past 14%
• a world of my imagination where I deny your reality and substitute my own 57%
• Other Answers 8%
  • 221 B Baker St, to foil Prof. Honey Badger
  • WAYNE'S WORLD
  • A small room lined with tinfoil and Polaroid photos of ducks.

Occam and Fallacies

Jun 19, 2014

The patient is a middle-aged male with diabetes who is admitted with diabetic ketoacidosis (DKA) and sepsis.

Exam shows a dead toe, all black, perhaps, it is reported, from trauma.

CT of the abdomen shows what looks to be a splenic infarct, although TTE is negative.

And all the blood cultures grow MSSA.

I put the patient on nafcillin for probable endocarditis. While, the toe is black, and the spleen has an infarct, there no emboli anywhere else on exam. So, are these findings a manifestation of endocarditis? I’m not sure. Pulmonary status is currently tenuous, so no TEE as it would probably lead to intubation.

Which came first, the DKA or the infection? I can’t tell. Infection and Infarction are the gruesome twosomes that lead to DKA, so maybe the infection set it off.

The next day I round, and the nafcillin has been stopped, and he is now on cefepime and vancomycin. Sigh. Why is that? She got clinically worse, and they wanted to broaden coverage. Double sigh. You did it, I pointed out, at the expense of optimally killing the organism that is causing the infection.

There is no need to worry about other organisms when everything can be accounted for by MSSA sepsis. Hickam may have his dictum, but I remain an Occam's kind of guy most of the time: Numquam ponenda est pluralitas sine necessitate [Plurality must never be posited without necessity].

I do have the advantage of 30 years of knowledge and experience and know it takes time for patients with MSSA endocarditis to get better. One of the many reasons ID consultations leads to better outcomes with S. aureus bacteremia. Patients often get worse before they get better, in part because it takes time for antibiotics to reach steady-state and ‘kick in’ and in part because the initial kill off may release more bacterial body parts into the bloodstream, exacerbating the sepsis.

In polymicrobial sepsis, bactericidal antibiotics resulted in more inflammation and more severe acute kidney injury. However, the resolution of inflammation and acute kidney injury was faster with antibiotics and correlated best with survival. These results suggest that transient worsening of renal function may be an expected consequence of sepsis therapy.

But the change in antibiotics probably had more to do with the logical fallacies of antibiotic therapy that every generation needs to learn. From the classic Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy, these are the

Fallacies in Antibiotic Therapy

• Broader is better.
• Failure to respond is failure to cover.
• When in doubt, change or add another.
• Sickness requires immediate treatment.
• Response implies diagnosis.
• Bigger disease, bigger drugs.
• Bigger disease, newer drugs.
• Antibiotics are non-toxic.

I add my own.

• Once started, an antibiotic cannot be stopped.
• Once a class of antibiotic is started, you need to stay in class.
• Gotta double cover (i.e., give two antibiotics) a particular organism.
• The primary reason a particular antibiotic is given is “I like it.”

When I was an intern, I carried around the NEJM article on the physiology of the Swan-Ganz catheter, and every time I had a patient with a Swan, I would read the article and compare it to my patient. There is a blast from the past. I haven’t seen a Swan in years. One day I no longer needed the reference; I understood the Swan. Nowadays, I think the house staff should carry around Observations on spiraling empiricism and read it before giving any antibiotic. It might improve care.

Rationalization

Clin Infect Dis. 2006 Jul 1;43(1):e6-8. Epub 2006 May 23. Diabetic ketoacidosis precipitated by Staphylococcus aureus abscess and bacteremia due to acupuncture: case report and review of the literature.

http://www.ncbi.nlm.nih.gov/pubmed/?term=16758409

Crit Care Med. 2012 Feb;40(2):538-43. doi: 10.1097/CCM.0b013e31822f0d2e. Bactericidal antibiotics temporarily increase inflammation and worsen acute kidney injury in experimental sepsis.

http://www.ncbi.nlm.nih.gov/pubmed/21926582

Medicine (Baltimore). 2009 Sep;88(5):263-7. doi: 10.1097/MD.0b013e3181b8fccb. Infectious diseases consultation lowers mortality from Staphylococcus aureus bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/19745684

Am J Med. 1989 Aug;87(2):201-6. Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy.

http://www.ncbi.nlm.nih.gov/pubmed/?term=2667357

Right. Wrong. Then right, kind of.

Jun 20, 2014

I like to call the bug based on history before the lab can identify it by biochemicals. It is fun and impresses others no end.

I get a call to see a middle-aged male for some sort of Streptococcus in the blood.

I tend to be a minimalist for information when I get a call from residents. I want as little bias going in, so I often make them give me a five-word question. They can sometimes do it. But it is very hard. They can't resist the urge to provide gender and age and use up their five-word allotment.

Strep in the blood of lymphoma patient. Seven words. Not bad.

Oh, I said. It will be S. mitis. It is the most common Streptococcus in cancer patients. I'll be there shortly.

The resident thought it would be S. pneumoniae.

I recently wrote about two other S. mitis cases, so I was feeling a little self-assured. Not so much after the history. He had lymphoma a decade ago and has been in remission due to an autologous bone marrow transplant (BMT) with no chemotherapy for years but a touch of chronic neutropenia (1200-1500). Not risks I would expect for S. mitis.

The gram stain said pairs and chains. So, I told the resident they were likely right. Pneumococcus. My note said Pneumococcus and group B Streptococcus lead the list, less like viridans Streptococcus.

And it was two sets with S. mitis, one set with Group B Streptococcus. His teeth are fine, the ECHO is negative for vegetation, and he never had mediastinal radiation. So, with no good reason for the S. mitis, I feel I should treat for endocarditis.

S. mitis does occur in bone marrow transplant patients, but around the time of the transplant, not a decade out.

And the Group B Streptococcus? No idea. Nothing on BMT and Group B Streptococcus on the Googles or the PubMed. BMT patients get more S. pneumoniae infections due to defective antibody production; perhaps the same would apply to Group B Streptococcus as well, although

The role of antibodies in protection against GBS disease in nonpregnant adults is unresolved&Although groups of adults at high risk for invasive GBS disease have been identified, the role of capsular polysaccharide antibodies in the prevention of either localized or invasive GBS disease in nonpregnant adults has not been adequately evaluated. Older adults and those with significant underlying diseases may have other defects (e.g., phagocyte or complement dysfunction or impaired macrophage Fc³-receptor function) that contribute to an increased risk of GBS infection.

So partial credit? Bah. I want it all, not just a piece.

Rationalization

Bone Marrow Transplant. 1998 Mar;21(6):591-5. Streptococcus viridans bacteremia following autologous peripheral blood stem cell transplantation.

http://www.ncbi.nlm.nih.gov/pubmed/9543063

Early and late invasive pneumococcal infection following stem cell transplantation: a European Bone Marrow Transplantation survey.

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.2002.03457.x/full

Group B Streptococcal Disease in Nonpregnant Adults.

http://cid.oxfordjournals.org/content/33/4/556.full

POLL RESULTS

I

• like being right 24%
• like not being wrong 41%
• never commit so I am never in error 0%
• frequently in error but never in doubt 24%
• let my my spouse decide, let them take the credit or blame 3%
• Other Answers 7%
  • let my spouse decide, she is never wrong
  • Am always right regardless of facts in evidence.

Compost

]Jun 24, 2014

The patient is an older male on methotrexate and 5 mg a day prednisone for rheumatoid arthritis. He comes in with fevers and a non-productive cough for several days. CXR shows an upper lobe consolidated infiltrate with some question of hazy nodules.

Usual workup for a community-acquired pneumonia is negative: gram stain has WBCs and no organisms, blood and sputum cultures are negative, and urine Legionella is negative.

I am asked to see him and find that he is a gardener and just had a large load on compost delivered that he spread around the garden. Hmmm.

I have had a few infections I think were related to composting: a Nocardia sternal wound infection and an extensive inhalational Aspergillus pneumonia.

My wife is an obsessive gardener and loves to run all the yard debris through a chipper-shredder into her compost pile. For some reason, she always looks longingly at me at the end of the movie Fargo.

I wondered about Legionella, but it was peat moss, not compost, that I remembered as a risk.

According to Steele et al., potting soils are made from different products. In Australia, they tend to consist of composted waste products such as sawdust and hammer milled bark while in Europe, peat moss is a significant component. It is indicated that the use of different products emanating from wood could facilitate the occurrence of different Legionella bacteria in potting soil. In some parts of Europe, potting soils have bark soil as a component. However, studies from Switzerland have shown that Legionella spp. could also be present in potting soil containing peat moss.

But the PCR on the bronchoscopy was positive for Legionella.

My memory was faulty: compost and potting soils are a source of Legionella, mostly Legionella longbeachae and

Infection with this species will not be detected by current urinary antigen tests and will be missed by laboratories that perform serological assays only for L. pneumophila.

Most of the cases are reported in the land down under. The PCR does not identify which Legionella it is, but I bet Legionella longbeachae, especially as there was no good water source for an exposure. He improved rapidly in a quinolone.

And as the first reports of Legionella from 1984 noted, Legionella can cause nodules.

Infiltrates were typically segmental to lobar; nodular infiltrates were noted in three cases.

Spring is here, and with it will come Legionella, not only from thundershowers but in gardeners.

Rationalization

J Infect Chemother. 2001 Dec;7(4):224-7. Distribution of Legionella longbeachae and other legionellae in Japanese potting soils.

http://www.ncbi.nlm.nih.gov/pubmed/11810588

Clin Microbiol Infect. 2009 Jun;15(6):571-5. doi: 10.1111/j.1469-0691.2009.02742.x. Epub 2009 Apr 21. Commercial potting soils as an alternative infection source of Legionella pneumophila and other Legionella species in Switzerland.

http://www.ncbi.nlm.nih.gov/pubmed/19392903

Legionella longbeachae and Legionellosis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377390/

Eurosurveillance, Volume 15, Issue 8, 25 February 2010 LEGIONELLA, SPRINGTIME AND POTTING SOILS

http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19497

Clin Microbiol Infect. 2007 Jan;13(1):88-91. Legionnaires' disease and gardening.

http://www.ncbi.nlm.nih.gov/pubmed/17184293

Diagnosis of Legionella Infection. Clin Infect Dis. (2003) 36 (1): 64-69.

http://cid.oxfordjournals.org/content/36/1/64.full

Radiology. 1984 Mar;150(3):633-7. Pneumonia caused by Pittsburgh pneumonia agent: radiologic manifestations.

http://www.ncbi.nlm.nih.gov/pubmed/6695060

Working with minimal data

Jun 25, 2014

Physicians are given wide latitude in deciding on what diagnostic and therapeutic interventions to offer patients.

That can be good and bad. I try and avoid flowery language when I have only the slimmest of data to support a therapy. Treatments in medicine can fade from the proven and true into the grey and then into the wackaloon. So much of my practice is in the grey, although I like to think it is in the science-based grey.

The patient is an elderly male, several months out of a knee replacement when the joint becomes red, hot, and tender. In the OR, the joint is filled with pus. I never say frank pus, as that implies there is such a thing as occult pus. The gram stain is negative, and the cultures eventually grow C. albicans.

So, what to do? There is little data on the approach to Candida infections of a prosthesis, a couple of dozen reports at most, and they predate the echinocandin era.

Take out the joint? It would probably be best, but the patient does not want it, and there are multiple co-morbidities and social factors that make a two-stage replacement medically and socially problematic. There are a few cases I could find where salvage was tried with Candida.

So, debridement and antibiotics. Amphotericin is toxic, and azoles are more static. Echinocandins do have the advantage of killing yeast, working in biofilms, and there are cases of iv catheters being salvaged with these agents. Nothing, though, about the efficacy in patients with prosthetic joint infections.

So, I am going to try a course of micafungin and then a long course of fluconazole. I told the patient there is little experience with Candida prosthetic oint infections, that the antibiotics will probably not work, and he will probably end up with the joint removed, but the approach is a reasonable extrapolation given the literature.

He specifically thanked me for being honest and straight with him, although he was a little bummed out as a result of our conversation.

Maybe I should have said it was a miracle treatment that will burn through the yeast or a revolutionary Candida buster.

Sign. Somehow, I do not think I will ever get a syndicated TV show.

Rationalization

Acta Orthop. 2013 Dec;84(6):517-23. doi: 10.3109/17453674.2013.859422. Epub 2013 Oct 31. 2-stage revision recommended for treatment of fungal hip and knee prosthetic joint infections.

http://www.ncbi.nlm.nih.gov/pubmed/24171675

Int J Antimicrob Agents. 2014 Feb;43(2):114-20. doi: 10.1016/j.ijantimicag.2013.10.023. Epub 2013 Nov 25. Strength in numbers: antifungal strategies against fungal biofilms.

http://www.ncbi.nlm.nih.gov/pubmed/24359842

J Antibiot (Tokyo). 2013 Dec;66(12):701-4. doi: 10.1038/ja.2013.83. Epub 2013 Sep 11. In vitro effectiveness of anidulafungin against Candida sp. biofilms.

http://www.ncbi.nlm.nih.gov/pubmed/24022607

Pediatr Infect Dis J. 2013 Mar;32(3):289-91. doi: 10.1097/INF.0b013e3182784867. Echinocandin and ethanol lock therapy treatment of fungal catheter infections.

http://www.ncbi.nlm.nih.gov/pubmed/23076381

POLL RESULTS

When using treatments with little supporting data, I like to

• be vaguely upbeat 33%
• lie 2%
• use flowery language 2%
• have plausible deniability 22%
• snow them with medical terminology 26%
• Other Answers 15%
• When all else fails, tell the truth straight up.
• Tell them that I am flying blind
• be honest that I don't know what I am doing
• Be paid in advance.

With Great Power

Jun 27, 2014

Over the past several years, it has become de rigueur to mention in the chart that the recommendations of the consultant are appreciated. Not. Sometimes the phrase is in the chart before I even do the consultation. The phase has all the sincerity of phone help centers who mention they are sorry about whatever issue you are calling about. No. You are not sorry. You don t really care. So, stop saying it, wasting time, and let's get my problem fixed.

Sometimes my input is appreciated and sometimes not so much. I preferred the note from one of our intensivists when he first started: ID recommendations noted. Will consider. That's how it should be, although he too now uses the appreciated gambit.

The patient is a normal young female with no medical problems. A month ago, she had a spider bite that became red, hot, swollen, tender, and expressed copious pus. It was a brown recluse I am told, although no spider was ever seen.

It is amazing how often the Brown recluse is blamed, given that given that

the brown recluse, Loxosceles reclusa, does not occur in Oregon, despite reports to the contrary.

Go to the Wikipedia page if you want to see its range. It is not West of the Rockies; or found on the West coast, best coast.

We do have the Hobo Spider,

Tegenaria agrestis is a non-native species in the United States, where it was introduced to the Pacific Northwest from Western Europe. It is believed to have first appeared in the port city of Seattle sometime before the 1930s.

and the Hobo spider bite is probably not that bad:

The CDC and other U.S. government agencies have also used this same study as the basis for a report claiming that the hobo spider bite causes necrosis in humans, despite the absence of any confirmed cases. Subsequent attempts to replicate the study by injecting sufficient venom to ensure envenomation have failed to produce necrotic lesions, and there is even question as to whether the lesions observed in the original study were necrotic. In Canada, there are scientists who claim that no hobo spider bites lead to dermal necrosis. Hobo spiders are common in Europe, though bites are relatively uncommon, and there are no confirmed reports of them causing necrosis despite hundreds of years of coexistence there.

which is also true of the other biting spider in Oregon, the yellow sac spider.

Besides probably having relatively non-toxic bites, the other characteristic of these spiders is Romulan cloaking devices, as they have never been seen or captured at a bite site. Things may be different in Texas (understatement), but MRSA from spider bites is almost always just MRSA, not a spider bite. The patient always blames a spider but never sees one:

Often, people first think the area is a spider bite; however, unless a spider is actually seen, the irritation is likely not a spider bite. Most staph skin infections, including MRSA, appear as a bump or infected area on the skin.

If Peter Parker had been bitten in Portland, his power would be invisibility.

Now, a month after the bite, she has fevers, pleuritic chest pain, and multiple peripheral cavitary lesions on the chest CT. Blood is growing MRSA. So right-sided endocarditis is the presumptive diagnosis despite a negative TTE. The alleged bite is still infected but improving. MRSA can cause skin necrosis with the best of them, perhaps due to toxin production:

Other distinguishing features of community-associated MRSA isolates include a high prevalence of genes encoding the two-component Panton Valentine leukocidin; this exotoxin is associated with necrosis of the skin, severe necrotizing pneumonia, and abscess formation, although its role in the pathogenesis of community-associated MRSA infections remains controversial.

Although I usually say that if you can see it without a microscope, it is not an ID problem but a job for Bug Girl. Bug Girl knows her spiders, but do you really want to know the horrible truth about Spiderman?

Rationalization

Surg Infect (Larchmt). 2003 Winter;4(4):311 5. Spider Bites Presenting with Methicillin-Resistant Staphylococcus aureus Soft Tissue Infection Require Early Aggressive Treatment.

http://www.ncbi.nlm.nih.gov/pubmed/15012857

Skin and Soft-Tissue Infections Caused by Methicillin-Resistant Staphylococcus aureus. N Engl J Med 2007;357:380 90.

http://www.nejm.org/doi/pdf/10.1056/NEJMcp070747

The horrible truth about Spiderman’s Anatomy

https://membracid.wordpress.com/2012/07/25/the-horrible-truth-about-spidermans-anatomy/

POLL RESULTS

I want to be

• appreciated 15%
• understood 10%
• sedated 22%
• anonymous 20%
• worshiped 22%
• Other Answers 12%
  • high
  • a soccer star
  • right more often than not.
  • adored (Stone Roses)
  • Highly compensated

Go West Young Vector

Jun 30, 2014

There are many great things about the Pacific NW. Unrivaled natural beauty (and that is just my wife, you should see the mountains, oceans and high desert), great beer, great food, nice people.

The downside to the Pacific NW is that from an ID perspective, it is kind of dull. We have a touch of relapsing fever in Eastern Oregon, C. gattii invading from Canada, and a bit of Brucella suis in the wild pigs. Not much else. All the good diseases need to be imported.

A young male had a tick bite on the back while in Connecticut. It had been about 48 hours since he had been in a tick-infested field. As an Oregonian, he thought nothing about it, but about a week later, he developed fevers to 103, headache, myalgias, and a bull's eye rash at the bite site.

Lyme disease. I do not get to see much Lyme in the West. In California, part of the reason there is not a lot of Lyme may be the fence lizard, whose blood is Borrelia-cidal. What I do not understand there is so much Lyme is the Washinton, DC area, where there is an endless supply of fence-sitting lizards.

Cell phones are great as patients take pictures of their rashes, and I can see them evolve. Unfortunately, the rash looked more confluent than bull's eye, so I would have called it a group A streptococcal cellulitis if the tick bite had not occurred in the NE. He had already been placed on a course of doxycycline, and I had little to add to the care.

Lyme is one of many diseases that may increase with global warming since warmer weather means more ticks:

Climate warming may have co-driven the emergence of Lyme disease in northeastern North America, and in the future, may drive substantial disease spread into new geographic regions and increase tick-borne disease risk where the climate is currently suitable. Our findings highlight the potential for climate change to have profound effects on vectors and vector-borne diseases, and the need to refocus efforts to understand these effects.

Best I can tell, Oregon is not included in the potential spread of Lyme carrying ticks. But who knows how vectors, hosts, and inadvertent human transport of pathogens may spread disease. I always remember that Bubonic plague entered San Francisco in 1900 and then

plague outbreaks were first detected in Oregon in 1934, in Montana in 1935, and in Utah, Idaho, and Nevada in 1936.

moving more than 1400 miles in about 40 years. West Nile crossed the US in less than a decade. So, I am not so sanguine we will be protected from Lyme or, currently, Chikungunya, should the right circumstances exist.

Rationalization

Estimated Effects of Projected Climate Change on the Basic Reproductive Number of the Lyme Disease Vector Ixodes scapularis.

http://ehp.niehs.nih.gov/1307799/

Effect of Climate Change on Lyme Disease Risk in North America.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2582486/

INITIATION AND SPREAD OF TRAVELING WAVES OF PLAGUE, YERSINIA PESTIS, IN THE WESTERN UNITED STATES.

http://www.ajtmh.org/content/76/2/365.long

Better than Expected

Jul 2, 2014

The patient has the abrupt onset of fever, rigors, confusion, and a rapid decline into unresponsiveness. Not good when in the 8th decade of life.

She is brought into the ER, and an LP is consistent with bacterial meningitis, although no organisms are seen on the gram stain. Both sets of blood cultures were growing, gram-positive cocci in chains.

All clinical signs were pointing to an adverse outcome:

On admission, 14 percent of patients were comatose and 33 percent had focal neurologic abnormalities. The overall mortality rate was 21 percent. The mortality rate was higher among patients with pneumococcal meningitis than among those with meningococcal meningitis (30 percent vs. 7 percent, P<0.001). data-preserve-html-node="true" The outcome was unfavorable in 34 percent of episodes. Risk factors for an unfavorable outcome were advanced age, presence of otitis or sinusitis, absence of rash, a low score on the Glasgow Coma Scale on admission, tachycardia, a positive blood culture, an elevated erythrocyte sedimentation rate, thrombocytopenia, and a low cerebrospinal fluid white-cell count.

The patient received the usual hodgepodge of antibiotics, and within 24 hours was clinically back to normal, much to my surprise.

And the cultures grew S. mitis.

Didn't see that coming. All the viridans Streptococcal meningitis I have seen have been a complication of myelograms, often from the mouth of the health care provider, so wear a mask if you do the procedure:

a-Hemolytic streptococcal meningitis has been reported as a rare complication of LP performed for various reasons—diagnostic and therapeutic taps, pneumoencephalography, spinal anesthesia (including obstetrical epidurals), and myelography. At least 75 cases of meningitis occurring as the result of LP have been reported in the English literature, but the paucity of these reports may not reflect the actual incidence of this infection, which can be expected to rise with the increasing popularity of obstetrical epidurals.

Viridans Streptococcal meningitis patients often do very poorly, probably due to the direct inoculation of bacteria into the CSF, bypassing any immune response. What the normal clinical course for hematogenous S. mitis meningitis is unknown.

S. mitis as a cause of spontaneous community meningitis is rare, with only a couple of cases reported, although as best I can tell, patients with spontaneous viridans Streptococcal meningitis do reasonably well.

Meningitis caused by streptococci other than S. pneumoniae are often related to a distant focus of infection or to neurosurgical procedures, and, in our experience, they seem to have a good outcome.

Her ECHO was without vegetations, but with an old, sclerotic valve I have to worry this is early endocarditis since that is the far more typical reason S. mitis is in the blood.

She had an uneventful recovery.

Rationalization

Clinical Features and Prognostic Factors in Adults with Bacterial Meningitis N Engl J Med 2004; 351:1849-1859 October 28, 2004

http://www.nejm.org/doi/full/10.1056/NEJMoa040845

Iatrogenic Meningitis: The Case for Face Masks

http://cid.oxfordjournals.org/content/31/2/519.full.pdf

Int J Infect Dis. 2008 Nov;12(6):e107-9. doi: 10.1016/j.ijid.2008.01.003. Epub 2008 Apr 2. Community-acquired Streptococcus mitis meningitis: a case report.

http://www.ncbi.nlm.nih.gov/pubmed/18378176

Med Clin (Barc). 2003 May 24;120(19):739-41. [Meningitis caused by streptococci other than S. pneumoniae: clinical and microbiological features of 13 cases].

http://www.ncbi.nlm.nih.gov/pubmed/12781084

Tell Me About the Rabbits George

Jul 14, 2014

Summertime and the living can be easy. I returned today from a week in Sunriver, Oregon. If there is a better place for hiking, biking, golf, beer, and food in the world, I would be surprised. The problem with vacation is that for every day you are gone, the work to do when you return doubles. So, when I start the day, I think, why did I come back from vacation?

And then, I start to see patients and remember how much fun doing infectious diseases in a hospital can be.

The patient is a middle-aged male who had a first kidney transplant ten days prior to re-admission. Then he developed fevers, rigors, myalgias, and polyarticular arthralgias, including bilateral jaw pain.

Fever work-up was unimpressive except for an increase in the creatinine from 0.8 at discharge to 1.8 and a mild leukocytosis.

The rest of the labs, cultures, and x-rays were unrevealing.

When I see polyarticular arthralgias, where all the joints hurt, I think of immune-complex disease.

The worst case I ever saw was an IVDA with acute hepatitis B, and literally, every joint (yes, all 360; I counted) in her body had rubor, dolor, calor, and tumor from immune complexes. When every joint is inflamed, it is a particularly painful experience.

So, I asked the patient: ever had a rabbit? Yes, was the answer, many years ago.

He had anti-thymocyte globulin with the transplant; a rabbit derived antibody. Now I am not sure I believe the prior rabbit exposure as a risk, but for your consideration I offer

Serum sickness after rabbit anti-thymocyte globulin (ATG) has a reported incidence of 7–27% in kidney transplant patients. We describe four patients with previous exposure to rabbits who developed serum sickness after primary rabbit ATG induction — all patients presented with jaw pain. Three of four patients treated with plasmapheresis and steroids had prompt recovery, and one patient treated with steroids had a slower recovery. We performed a telephone interview of 214 patients contemporaneously transplanted between November 2006 and July 2008 regarding rabbit exposure. More than half of the patients had some type of previous rabbit exposure. There was a suggestion that patients with serum sickness were more frequently exposed to rabbits than those without. Jaw pain appears to be a hallmark symptom and treatment with plasmapheresis and steroids relieves symptoms more rapidly than steroids alone.

The timing is right (more than a week after infusion) as is the clinical picture:

Diagnostic Criteria for Serum Sickness

Major criteria

• more than 7 days since initial thymoglobulin administration
• Persistent high fevers (>101°F)
• Persistent arthritis/arthralgias
• Positive heterologous antibodies on ELISA

Minor criteria

• +/- Acute renal failure
• +/- Rash
• +/- Trismus
• +/- Low serum complement (C3, C4)

So ATG serum sickness it is, although it is a diagnosis of exclusion. He was improving on his own with no specific intervention, although for severe cases, treatment is high dose steroids and plasmapheresis.

Rationalization

Am J Kidney Dis. Jan 2010; 55(1): 141–143. Serum Sickness After Treatment With Rabbit Antithymocyte Globulin in Kidney Transplant Recipients With Previous Rabbit Exposure

http://www.ncbi.nlm.nih.gov/pubmed/19628314

Serum sickness following rabbit antithymocyte-globulin induction in a liver transplant recipient: Case report and literature review

http://onlinelibrary.wiley.com/doi/10.1002/lt.21098/full

Summertime and the Living is Infected.

Jul 16, 2014

It is hot and muggy here in the Great Pacific NW. Unusual weather. We have had thunderstorms every summer for the last several years, something I do not remember from my childhood. But given that I have two children and cannot remember their names accurately, my thoughts as to how the weather was back in the day, or how anything was for that matter, is suspect.

However, most homes in Portland do not have central air unless you have a heat pump. Cold and rain are more an issue than hot and muggy.

Changes in weather bring with it infectious diseases. Of course, regular readers of this blog know that I see anything and everything as a vector for infection. It is one of the many reasons I am not invited to parties.

Thunderstorms mean Legionella.

Cases occurred with striking summertime seasonality. Occurrence of cases was associated with monthly average temperature (incidence rate ratio [IRR] per degree Celsius, 1.07 [95% confidence interval [CI], 1.05-1.09]) and relative humidity (IRR per 1% increase in relative humidity, 1.09 [95% CI, 1.06-1.12]) by Poisson regression analysis. However, case-crossover analysis identified an acute association with precipitation (odds ratio [OR], 2.48 [95% CI, 1.30-3.12]) and increased humidity (OR per 1% increase in relative humidity, 1.08 [95% CI, 1.05-1.11]) 6-10 days before occurrence of cases.

Probably why we never saw much Legionella in the great Pacific NW before. Wrong weather. We have at least two Legionella pneumonias in my hospital system, so confirmation bias is at its strongest.

Summertime is also surgical wound season, probably because it is also S. aureus season.

Nevertheless, several investigators have demonstrated seasonal variation in S. aureus infections, particularly skin infections, with a preponderance of infections during the summer and autumn.

I am not surprised, with people are stewing in their sweat with a fresh wound. It must be an all you can eat buffet for the bacteria.

I have seen a slight bolus of post-op infections in the last few weeks, all with S. aureus and all but one does not have central air. Several were in pannuses (panni?), an excellent place for bacteria to prosper on a hot, muggy day. More confirmation bias, I suppose. We are trying to give patients reminders to keep as clean, dry, and cool as possible.

I wonder why summer is S. aureus time. Better growth media? Skin makes

Dermcidin, an antimicrobial peptide which is constitutively expressed in eccrine sweat glands

and dermcidin kills S. aureus.

As best I can tell, no one has measured dermcidin levels in summer vs winter. If the protein is constitutively produced, maybe the outpouring of summertime sweats dilutes dermcidin to the point it is no longer active. Unlike homeopathy, in reality-based medicine, the more dilute a medication, the less effective it is.

There is yet another great study idea for someone. If only my blog suggestions would become automatically become a reality.

Rationalization

J Infect Dis. 2005 Dec 15;192(12):2066-73. Epub 2005 Nov 11. 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

BMJ Open. 2013 Mar 5;3(3). pii: e002428. doi: 10.1136/bmjopen-2012-002428. Meteorological factors and risk of community-acquired Legionnaires' disease in Switzerland: an epidemiological study.

http://www.ncbi.nlm.nih.gov/pubmed/23468470

Orthopedics. 2014 Feb;37(2):e182-6. doi: 10.3928/01477447-20140124-23. Seasonality of infection rates after total joint arthroplasty.

http://www.ncbi.nlm.nih.gov/pubmed/24679206

J Neurosurg Spine. 2013 Jan;18(1):57-62. doi: 10.3171/2012.10.SPINE12572. Epub 2012 Nov 2. The seasonality of postoperative infection in spine surgery.

http://www.ncbi.nlm.nih.gov/pubmed/23121653

PLoS One. 2011 Mar 23;6(3):e17925. doi: 10.1371/journal.pone.0017925. Seasonality of MRSA infections.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017925

Antimicrob Agents Chemother. 2009 Jun;53(6):2499-509. doi: 10.1128/AAC.01679-08. Epub 2009 Apr 13. Dermcidin-derived peptides show a different mode of action than the cathelicidin LL-37 against Staphylococcus aureus.

http://www.ncbi.nlm.nih.gov/pubmed/19364862

Is it the 'n' in TNF?

Jul 18, 2014

The patient is admitted with progressive back pain over a month and a half. As part of the evaluation, a CXR shows there is free air in the abdomen.

He is admitted to the hospital, and a CT confirms the free air but no good reason. PET several days later shows a widely metastatic something with marked resolution of the free air. There is no reason seen on the PET for the free air, and he has remarkably little abdominal pain.

Surgery says it is a micro-perforation, give antibiotics and see if he declares a reason for the free air. The patient doesn’t ever develop abdominal complaints, but the WBC keeps ticking along at 40K.

Finally, a biopsy shows an adenocarcinoma, but the samples have extensive necrosis.

With the widely metastatic cancer with necrosis, I think I have what is driving the leukocytoses as the patient looks clinically well.

But why is the tumor so necrotic? Just outgrew its blood supply? Or could the inflammatory process of the perforation have something to do with it?

Infections have been used therapeutically. You may be aware that the 1927 Nobel for medicine was given to Julius Wagner-Jauregg for successful treating neurosyphilis with malaria.

A review of the literature during the time revealed that out of 35 studies conducted by 1926 researchers, the results were as follows: 27.5 percent full remission, 26.5 percent partial remission, and 46 percent deaths or no change.

Although he had to wait for his prize until one of the Nobel committee members retired:

Despite the impact of Wagner-Jauregg’s treatment, he had to wait 10 years until the retirement of B. Gadelius, a Swedish professor of psychiatry on the Nobel Prize Committee who refused to award the prize to “a physician who injected malaria into a paralytic, because he was in his eyes a criminal.”

How about infections to treat cancer? It had been noticed 100 years ago that tumors could regress after infections. Infections do lead to the release of tumor necrosis factor. So maybe.

Clostridium novyi and Salmonella typhimurium have the most experience, although Salmonella choleraesuis, Vibrio cholerae, Listeria monocytogenes, and Escherichia coli have been investigated.

I can't find the reference, my Google-Fu must be off, but I remember there is a report of a lab tech who tried to cure his lymphoma by injecting himself with Salmonella. He added to Koch's postulate that bacteria cause sepsis, although I do not think it helped his lymphoma.

So maybe the inflammatory response to the micro-perforation is what led to the extensive tumor necrosis. Or not. I just enjoy exploring these digressions.

While it is an interesting idea, it is also a dangerous one, and it would be inadvisable to try it without IRB support:

Two neurosurgeons at the University of California, Davis have stepped down from their positions after intentionally infecting three brain-cancer patients with a bowel bacteria they thought would save their lives. While one patient lived a year after the treatment, the other two died soon after the procedure prompting a university investigation that concluded that Dr J Paul Muizelaar and Dr Rudolph J Schrot had violated the school's code of conduct.

Even as a last-ditch therapy, IV Enterobacter aerogenes could not but be seen by an ID doctor as way stupid and certain to kill, the literature suggests up to a 29% mortality rate.

Rationalization

Yale J Biol Med. Jun 2013; 86(2): 245–254. Julius Wagner-Jauregg and the Legacy of Malarial Therapy for the Treatment of General Paresis of the Insane

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670443/

Bacteria in cancer therapy: a novel experimental strategy

http://www.jbiomedsci.com/content/17/1/21

Two doctors resign after they inject brain cancer sufferers with bowel bacteria without permission - killing two patients.

https://www.dailymail.co.uk/news/article-2402204/Two-doctors-resign-injecting-brain-cancer-patients-bacteria.html

Int J Antimicrob Agents. 2013 Mar;41(3):236-49. doi: 10.1016/j.ijantimicag.2012.10.022. Epub 2013 Jan 10. Characterisation and clinical features of Enterobacter cloacae bloodstream infections occurring at a tertiary care university hospital in Switzerland: is cefepime adequate therapy?

http://www.ncbi.nlm.nih.gov/pubmed/23313399

Allergic? I do not think so.

Jul 21, 2014

A history of allergies to antibiotics are often a source of consternation. Penicillin is a common cause of a fatal allergic reaction, and if you have seen one anaphylactic reaction, you do not want to see a second. Often the allergy isn't. Nausea and vomiting. Penicillin stopped working, so I couldn't take it anymore. Diarrhea. Those are not 'allergies’.

Other histories are more difficult to interpret. My mother said I almost died from penicillin, but the exact reaction is lost in the mists of time. But if you search the medical record, you can find receipt of a penicillin and the patient tolerated it just fine.

Or the patient this week. 75-year-old female with enterococcal endocarditis. As a teenager she had a penicillin with swelling and a rash.

Hives? I ask.

I think so is the reply. But no throat swelling or trying to die.

Now the last thing I want to do is give an elderly person vancomycin and gentamicin for six weeks. Ampicillin and ceftriaxone are the best choice, but can I give it without killing the patient? Probably. Most patients who think they are allergic to penicillin are not:

Only 10% to 20% of patients reporting a history of penicillin allergy are truly allergic when assessed by skin testing. Taking a detailed history of a patient's reaction to penicillin may allow clinicians to exclude true penicillin allergy, allowing these patients to receive penicillin. Patients with a concerning history of type I penicillin allergy who have a compelling need for a drug containing penicillin should undergo skin testing. Virtually all patients with a negative skin test result can take penicillin without serious sequelae.

And in the old days, it was product contamination as well as penicillin break down products that led to the allergic reactions. I cannot find data to suggest if Type 1 antibiotic allergies fade with time. How often does penicillin allergy cross-react with ampicillin? Reasonably often, but not always:

Thirty subjects with a history of allergic reactions to penicillins were studied. In vivo and in vitro specific IgE antibodies were determined to different penicillin determinants. Fifteen subjects developed anaphylactic responses and the remainder urticaria and angioedema. The drug most frequently involved in the patients' allergic reactions was ampicillin (AMP). The benzylpenicilloyl (BPO) skin test was positive in 16 (53.3%) patients, whereas 23 (76.6%) patients were positive to minor determinant mixture (MDM), benzylpenicillin (PG), AMP, or amoxicillin. (AX).

And as best I can tell, there are (understandably) no clinical trials giving ampicillin to penicillin Type 1 allergic patients.

So, it didn't sound like a true death-dealing reaction, it was long ago, so the reaction might not have been to penicillin, and the odds of cross-reaction are not 100%.

I told the patient that there were two options, but as long as you are in the hospital, we can desensitize you and monitor you carefully.

I also put the code cart in the room. My only superstition: put the emergency equipment in the patient's room, and you will never have to use it. And she tolerated escalating doses of ampicillin just fine, so I will not have to destroy her 8th nerve and/or nephrons to cure her infection. I do not like using Ben Tre as my model for curing infections.

BTW: in the era of home antibiotic infusion, be aware of the spouse's allergy history:

We present a case of an immediate allergic reaction in a penicillin-sensitive spouse of a patient receiving parenteral mezlocillin sodium therapy. A seminal level of 42 μg/mL of mezlocillin was documented by bioassay.

Rationalization

Salkind AR, Cuddy PG, Foxworth JW. Is this patient allergic to penicillin? An evidence-based analysis of the likelihood of penicillin allergy. JAMA. 2001;285:2498-2505.

http://jama.jamanetwork.com/article.aspx?articleid=193846

The Role of Penicilloylated Protein Impurities, Penicillin Polymers and Dimers in Penicillin Allergy (Part 1 of 2)

http://www.karger.com/Article/Abstract/230070

Allergy. 1997 Jan;52(1):89-93. Immediate hypersensitivity to penicillins. Studies on Italian subjects.

http://www.ncbi.nlm.nih.gov/pubmed/9062634

Cross Reactivity Between Ampicillin and Penicillin G Roger H. Stewart, MD; Stephen B. Webster, MD JAMA. 1970;213(1):131. doi:10.1001/jama.1970.03170270071029.

http://jama.jamanetwork.com/article.aspx?articleid=355377

Arch Intern Med. 1989 Jul;149(7):1603-4. An unforeseen complication of home parenteral antibiotic therapy.

http://www.ncbi.nlm.nih.gov/pubmed/2742434

Ben Tre

http://www.sunday-guardian.com/analysis/we-had-to-destroy-village-in-order-to-save-it

Total Recall

Jul 27, 2014

I started this post on Wednesday but was so busy I did not get to finish it until today, so a very special Saturday evening post. I wonder if Norman Rockwell ever painted pus.

I often see premature closure. Most often, it is in patients who are returning from abroad with a fever. The differential starts and ends with malaria, and often physicians fail to consider more mundane, non-travel related infections.

This week there was a recall of peaches, plums, nectarines, and pluots over concerns of possible Listeria contamination.

My first thought was: what is a pluot? Evidently some weird fruit hybrid:

Pluots, apriums, apriplums, or plumcots, are some of the hybrids between different Prunus species that are also called interspecific (or IS) plums.

Everyone who bought these fruits received a warning letter: you have eaten a weird fruit hybrid and you may have been exposed to Listeria. Finally, an ID use for those grocery store cards.

And after eating some of the nectarines 48 hours before, a patient present to the ER with headache, fevers, and myalgias.

The LP has 800 WBC, 50:50 neutrophils and lymphocytes, normal glucose, and slight elevation of protein.

Listeria, right? Seemed a bit too fast, although.

The median incubation period is 3-4 days.

The patient is young with no medical problems. Listeria is a disease of the old and immunoincompetent.

Compared with persons <65 data-preserve-html-node="true" years with no underlying conditions, those with chronic lymphocytic leukemia had a >1000-fold increased risk of acquiring listeriosis, and those with liver cancer; myeoloproliferative disorder; multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pancreas, lung, and brain cancer; cirrhosis; organ transplantation; and pregnancy had a 100-1000-fold increased risk of listeriosis.

So, I suggested the usual evaluation for aseptic meningitis (VDRL, HSV, HIV, Enterovirus, West Nile, (still not in Oregon)), and the enteroviral PCR was positive. No Listeria.

The next was an ER call about a 95-year-old with watery diarrhea after eating an implicated fruit. Incubation for this disease is 24 hours, and given his age, I suggested amoxicillin after sending of stool cultures. If an alternative diagnosis was made, I do not know. And the high-risk OB service is evidently getting lots of calls.

I made it this far, so I just have to say it, Listeria hysteria. Somehow, I feel no better.

Rationalization

Clin Infect Dis. 2012 Mar 1;54(5):652-60. doi: 10.1093/cid/cir902. Epub 2011 Dec 9. Incidence of listeriosis and related mortality among groups at risk of acquiring listeriosis.

http://www.ncbi.nlm.nih.gov/pubmed/22157172

Clin Infect Dis. 2006 Nov 15;43(10):1233-8. Epub 2006 Oct 10. Community-acquired Listeria monocytogenes meningitis in adults.

http://www.ncbi.nlm.nih.gov/pubmed/17051485?dopt=Abstract

J Infect. 2010 Dec;61(6):465-70. doi: 10.1016/j.jinf.2010.08.007. Epub 2010 Sep 24. A large outbreak of Listeria monocytogenes infection with short incubation period in a tertiary care hospital.

http://www.ncbi.nlm.nih.gov/pubmed/20813130

Clin Infect Dis. 2005 May 1;40(9):1327-32. Epub 2005 Mar 31. Gastroenteritis due to Listeria monocytogenes.

http://www.ncbi.nlm.nih.gov/pubmed/15825036

Total Recall

http://www.imdb.com/title/tt0100802

Old Dog, New Tricks

Jul 28, 2014

This is my 24th year in ID practice. They say that half of everything you learn in medical school is not true; the problem is that you do not know which half. But more than faulty information that is subsequently found to be suspect, it is the torrent of new information and technology that is mind-numbing.

Since I was a medical student, there have been 3rd generation cephalosporins, quinolones, MRSA, hepatitis C, H. pylori, MRIs, HIV, SARS, and on and on and on. My father was a cardiologist, and he said when he was a resident, there were EKG's, morphine and digoxin. The rest of his practice, from cardiac catheterization to CABG to ECHO's and all the medications for the treatment of cardiovascular disease, he had to learn after he went into practice. As I have said before, it must be nice to be an alternative medicine practitioner. Learn one (of 67) true cause of all disease and never have to learn anything again.

My current intellectual nemesis is Extracorporeal membrane oxygenation or ECMO. One of the hospitals in our system offers ECMO, and they get referrals from across the great Pacific NW for patients who are unable to be oxygenated from a variety, usually infectious, of diseases. My partners are the usual ID consultants, but on weekends and vacation, I get to cover. And the service makes me feel like an intern.

The patients can be profoundly ill, some with MOSF, and on ECMO for weeks. We certainly have patients who would otherwise have died but trying to determine if these patients are infected and what to make of positive cultures remains a challenge.

For example, Candida in a bronchoscopy. Usually, this can be ignored. I take that back. It can always be ignored. Candida in the sputum never represents deep disease. Candida pneumonia is not a clinical entity. But how about the profoundly damaged lungs of ECMO patients? I am not so certain. Several have had Candida only in the sputum but a very positive 1-3 beta-D-glucan and improved on antifungals, for whatever that is worth.

Or coagulase-negative Staphylococcus in the blood of someone who is has been on vascular support for weeks. Hard to ignore even one of 4 positive cultures in a patient whose blood is always going through plastic, especially as they are never febrile. And as best I can tell their CBCs are always deranged with a left shift and a leukocytosis:

Besides thrombocytopenia, there were lowered circulating levels of factors VII and XII, which may be related to changes in the pulmonary endothelium. ECMO was associated with relative leukopenia and a marked shift to immature circulating leukocytes.

But from the underlying infection, a new infection or the ECMO? Got me.

This weekend I saw a patient who ended up on ECMO after 13 days or so of viral pneumonia, and after all that time, still had a positive PCR for adenovirus.

Treat? I don't know. The data for cidofovir is mostly in transplants and not impressive for efficacy, although great for toxicity.

The mainstay of treatment for patients with severe adenovirus pneumonia is still supportive, with the use of antivirals not apparently effective.

But small numbers of patients make risk vs benefit calculus uncertain. At two weeks, her immune response should be kicking in to take care of the infections without the need for added renal toxicity of cidofovir.

ECMO is a service that makes me feel like an intern, uncertain and questioning all my ICU rules of thumb. I'm too old for this crap; the problem with medicine is you never get to coast on experience.

Rationalization

Pediatr Crit Care Med. 2011 May;12(3):277-81. doi: 10.1097/PCC.0b013e3181e28894. Infections acquired during extracorporeal membrane oxygenation in neonates, children, and adults.

http://www.ncbi.nlm.nih.gov/pubmed/20495508

J Heart Lung Transplant. 2007 Sep;26(9):883-9. Treatment of adenovirus pneumonia with cidofovir in pediatric lung transplant recipients.

http://www.ncbi.nlm.nih.gov/pubmed/17845926

Respir Med. 2013 Nov;107(11):1810-3. doi: 10.1016/j.rmed.2013.09.008. Epub 2013 Sep 19. Severe adenovirus pneumonia requiring extracorporeal membrane oxygenation support--Serotype 7 revisited.

http://www.ncbi.nlm.nih.gov/pubmed/24070567

Hematologic Observations Made in Patients With Acute Respiratory Distress Syndrome in the Cooperative ECMO Project

http://onlinelibrary.wiley.com/doi/10.1111/j.1525-1594.1978.tb00998.x/abstract

POLL RESULTS

The trick I have most trouble learning is

• new diagnostics 10%
• new therapeutics 26%
• the EMR 18%
• ICD-10 10%
• none. I just do what I am told and count the days to retirement 28%
• Other Answers 8%
  • keeping my mouth shut when it's likely I have nothing rational or constructive to contribute to the conversation.
  • Which are the safest sushi offerings.
  • I *am* retired, you insensitive clod!

Failure

Jul 31, 2014

When S. aureus gets in the bloodstream, it loves to go places to cause metastatic infections.

The problem is that infections are not always symptomatic:

The incidence of metastatic infection was similar in patients with Streptococcus species and patients with S. aureus bacteremia. Signs and symptoms guiding the attending physician in the diagnostic workup were present in only a minority of cases (41%).

Annoying. In the above study, out of Europe, everyone got a TEE and a PET/CT. PET scans, while excellent for finding infections, are costly and not practical in the US. But you wonder what may be brewing in patients with gram-positive bacteremia and part of the reason I always treat the hell out of S. aureus bacteremia.

The patient was admitted to 8 weeks ago with S. aureus bacteremia (SAB). Work up, which did not include a PET scan, found a paraspinal abscess, and he received a six-week course of iv antibiotics. At the end of therapy, his paraspinal infection was gone, but he complained of hip pain in a native hip, but no pain in his artificial hip.

He had both hips tapped, and the normal, painful hip had no fluid, and the cultures were negative. His artificial, painless, hip, grew the same S. aureus as six weeks ago.

Expletive deleted.

The literature would suggest that S. aureus seeds joints about a third of the time. That seems excessive, but it has been the case in more than one study. This is the first patient I can remember to have had a relapse in an infected prosthetic joint after bacteremia was treated.

So I wonder. He never had symptoms of infection in his prosthetic joint, so no clinical indication to tap the joint or debride it. Should all S. aureus bacteraemias with prosthetic joints get empiric rifampin? It may help

Estimated across all of these studies, adjunctive rifampicin was associated with trends towards reduced all-cause mortality and reduced clinical or bacteriological failure.

and it may harm:

Limited data suggest that rifampicin-induced hepatitis is not clinically significant, but that drug interactions are.

Should they all get a joint aspiration? A PET, at six grand a pop plus? Got me. While I know what to do for SAB, there are always variations that demonstrate I do not know what to do for SAB.

Now he gets a debridement and another course of antibiotics, this time with rifampin. And if he has infection elsewhere, he has no symptoms. I am not reassured. S. aureus, after all these years, tasks me. Staph tasks me, and I shall have it. I'll chase Staph round the Moons of Nibia and round the Antares Maelstrom and round Perdition's flames before I give up!

Rationalization

Medicine (Baltimore). 2012 Mar;91(2):86-94. doi: 10.1097/MD.0b013e31824d7ed2. Metastatic infectious disease and clinical outcome in Staphylococcus aureus and Streptococcus species bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/22391470

J Infect. 2011 Jul;63(1):17-22. doi: 10.1016/j.jinf.2011.05.005. Epub 2011 May 14. Periprosthetic joint infection following Staphylococcus aureus bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/21663971

Clin Infect Dis. 2001 Feb 15;32(4):647-9. Epub 2001 Feb 7. Infection of orthopedic prostheses after Staphylococcus aureus bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/11181131

J Med Microbiol. 2014 Jun;63(Pt 6):841-8. doi: 10.1099/jmm.0.072280-0. Epub 2014 Mar 12. Adjunctive rifampicin may improve outcomes in Staphylococcus aureus bacteriemia: a systematic review.

https://doi.org/10.1099/jmm.0.072280-0

Once, Twice, Three Times a Toxin

Aug 1, 2014

The patient has the onset of fevers, nausea, vomiting, and red palms with her period. She is seen in the outpatient setting, and labs are OK, so she is sent home.

Her palms peel a couple of weeks later.

A month later, the same thing except this time it is noted she has a strawberry tongue. Labs are fine, and she is sent home.

Her palms peel again.

A month later, it occurs again, but this time her blood pressure is down, and she is admitted.

She has red palms, not soles, normal tongue and conjunctiva, and labs were fine. She gets better with TSS therapy, including IVIG.

After several days the vaginal cultures grow MSSA.

It looks like three episodes of toxic almost-shock syndrome. She never had the full syndrome with renal failure, low calcium, and refractory hypotension. Besides TSS, Kawasaki's is the only disease that can look like this, and the PubMeds have no hits for recurrent Kawasaki's.

Why the recurrent TSS is an interesting question, I presume that for whatever reason, she is unable to make antibody against toxic shock toxin; that seems to be the case in the few reports where antibody levels were measured. There is no indication that this represents a prior immunodeficiency, and with the dose of IVIG, it will be a while before immunoglobulin levels will be useful.

I presume she is colonized with a TSST producing S. aureus. Given the one case of recurrent disease of menstrual TSS with no tampon use, it is probably worth an attempt at decolonization.

TSS has been very rare since its initial description last century, and I had only heard of a case of recurrent disease from many years ago.

Rationalization

Clin Infect Dis. 2001 May 15;32(10):1470-9. Epub 2001 Apr 18. Recurrent nonmenstrual toxic shock syndrome: clinical manifestations, diagnosis, and treatment.

http://www.ncbi.nlm.nih.gov/pubmed/11317249

Australas J Dermatol. 2013 Nov;54(4):283-6. doi: 10.1111/j.1440-0960.2012.00938.x. Epub 2012 Aug 17. Recurrent menstrual toxic shock syndrome despite discontinuation of tampon use: is menstrual toxic shock syndrome really caused by tampons?

http://www.ncbi.nlm.nih.gov/pubmed/22897229

Obstet Gynecol. 1984 Nov;64(5):666-71. Toxic shock syndrome Staphylococcus aureus: effect of tampons on toxic shock syndrome toxin 1 production.

http://www.ncbi.nlm.nih.gov/pubmed/6436761

Zentralbl Bakteriol. 1996 Jul;284(2-3):164-9. T-cell activation and proliferation in a case of recurrent menstrual toxic shock syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/8837379

Infect Immun. Feb 1997; 65(2): 366–372. PMCID: PMC174604 Intravenous immunoglobulin inhibits staphylococcal toxin-induced human mononuclear phagocyte tumor necrosis factor alpha production.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC174604/

Avoiding a foolish consistency

Aug 5, 2014

"A foolish consistency is the hobgoblin of little minds, adored by little statesmen and philosophers and divines. With consistency a great soul has simply nothing to do. He may as well concern himself with his shadow on the wall. Speak what you think now in hard words, and to-morrow speak what to-morrow thinks in hard words again, though it contradict every thing you said to-day." ~Ralph Waldo Emerson

I have always liked that quote, even though the author has both a Ralph and a Waldo as part of his name, neither of which inspires confidence. But then again, there is Waldo Butters, so it is only half an uninspiring name. Are there any Ralph's who suggest greatness? I can't think of one. There is a Ralph the Timid, so I may be right.

Still, you have to keep up in medicine and change your mind as the data comes in, and new information is endless. There are over 10,000 PubMed articles a year published that are tagged as 'Infection', and at best, you can read just a fraction of the literature.

And there is this ebb and flow of studies, alternatively suggesting that a therapy is effective and then it is not. And all of them are probably wrong (from an essay everyone should read and re-read):

There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings might often be simply accurate measures of the prevailing bias.

So, in areas of uncertainly (pretty much most of medicine), there is this changing internal assessment as to what the preponderance of the literature suggests about the best treatment of a disease.

Part of the problem in ID is we act as if all the patients and all organisms are the same. However, there are variations in a given host's immune system and a given organism's virulence that we are unable to quantitate.

So, what is a poor ID doc to do?

The patient was admitted with MSSA right-sided endocarditis, and hemodynamically he is not doing great. His kidney function is marginal (Cr 2.2), and he is on a ventilator. ECHO show vegetations on all tricuspid leaflets and wide-open TR with moderate pulmonary hypertension. Surgeons are considering taking him to the OR to fix his valve. He had a rash to ampicillin that is allegedly severe.

So, what antibiotics should he be on? If he goes to the OR, I want the valve as close to sterile as I can get it.

Well, Nafcillin. Still the best for MSSA, right? I can almost certainly give it safely, but he is so hemodynamically tenuous I would hate to wrong. I was always taught that cefazolin was slightly inferior to nafcillin for the treatment of MSSA.

But I am not so certain that is clinically relevant:

The CIE might be associated with persistent bacteremia if cefazolin is used for MSSA bacteremia with a high burden of infections. However, the sites of infections are more important factors for the clinical outcome than the CIE.

and it is less toxic and equally efficacious in bacteremia

Cefazolin appears similar to oxacillin in the treatment of complicated MSSA bacteremia but with significantly improved safety.

And what about combination therapy? Aminoglycosides are a bad idea with the increased creatinine, but rifampin? Over the years, I have wandered away from rifampin for infections that did not involve prosthetic material as it only added toxicity. But maybe not.

Estimated across all of these studies, adjunctive rifampicin was associated with trends towards reduced all-cause mortality and reduced clinical or bacteriological failure. The fifth study indicated that adjunctive rifampicin accelerates the resolution of persistent SAB in neonates.

I am always suspicious of meta-analyses as their basic idea is that by heaping all the cow pies into one pile, you get clinical gold. Methodologically flawed studies are not improved with a meta-analysis, and the more you know about the totality of a literature, the less enthusiastic you will be about meta-analyses.

So, what to do? It is the job of a consultant to make the best decisions based on the information at hand. Or to be uncertain with style and panache. For now, it is cefazolin and rifampin.

He survived.

Rationalization

Why Most Published Research Findings Are False John P. A. Ioannidis

https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124

Microb Drug Resist. 2014 Jul 7. [Epub ahead of print] Clinical Implications of Cefazolin Inoculum Effect and β-Lactamase Type on Methicillin-Susceptible Staphylococcus aureus Bacteremia.

http://www.ncbi.nlm.nih.gov/pubmed/25000230

Antimicrob Agents Chemother. 2014 Jun 16. pii: AAC.02800-14. [Epub ahead of print] Comparison of cefazolin versus oxacillin for the treatment of complicated bacteremia caused by methicillin-susceptible Staphylococcus aureus.

http://www.ncbi.nlm.nih.gov/pubmed/24936596

J Med Microbiol. 2014 Jun;63(Pt 6):841-8. doi: 10.1099/jmm.0.072280-0. Epub 2014 Mar 12. Adjunctive rifampicin may improve outcomes in Staphylococcus aureus bacteraemia: a systematic review.

http://www.ncbi.nlm.nih.gov/pubmed/24623637

J Med Microbiol. 2014 Jun;63(Pt 6):841-8. doi: 10.1099/jmm.0.072280-0. Epub 2014 Mar 12. Adjunctive rifampicin may improve outcomes in Staphylococcus aureus bacteraemia: a systematic review.

http://www.ncbi.nlm.nih.gov/pubmed/24623637

Meta-analysis: Its strengths and limitations

http://www.ccjm.org/content/75/6/431.full

Waldo Butters

https://dresdenfiles.fandom.com/wiki/Waldo\_Butters

Ralph the Timid

https://en.wikipedia.org/wiki/Ralph\_the\_Timid

POLL RESULTS

I

• keep up and change my practice accordingly 17%
• think that what was good when I was an intern is just fine toda 3%
• get consultants to tell me what to do 0%
• am frozen by indecision 21%
• am but a cork bobbing in a sea of change with no control and go where the wind and tides of medicine push me 41%
• Other Answers 17%
  • would like to keep up and change my practice accordingly
  • know the answers - am just waiting for the research to catch up
  • am decisively indecisive.

Wine Matures with Age. Doctors get Grumpy.

Aug 6, 2014

I keep wondering what they are teaching kids in medical schools these days. I lecture to students all the time, and they still are taught the same ole same ole.

Atelectasis causes fevers, right? Most medical students fresh off their surgical rotation were told that.

Nope.

The available evidence regarding the association of atelectasis and fever is scarce. We found no clinical evidence supporting the concept that atelectasis is associated with EPF. More so, there is no clear evidence that atelectasis causes fever at all.

And that is not new information; the lecture slide I use is over a decade old. Of course, saying the fever is due to atelectasis means you do not have to work up the fever and can ignore it, but it is so disingenuous.

And speaking of fever, the mean temperature is 98.6. Right? Most medical students think it is.

Nope.

36.8°C (98.2°F) rather than 37.0°C (98.6°F) was the mean oral temperature of our subjects;

And that information is from 1992, so not exactly breaking news. I know. I am quibbling over 0.4 degrees, but for a so-called vital sign, it sure doesn't seem vital for medical students to be taught accurate information.

But if there is one ID issue that continually gripes my cookies year after year is the way S. aureus bacteremia is treated. People keep wanting to treat community-acquired bacteriemia with oral antibiotics, often clindamycin, for crying out loud.

We have known this since 1976: Community-acquired S. aureus bacteremia without a focus is probably endocarditis.

One hundred and five cases of bacteremia due to Staphylococcus aureus were reviewed to assess the current clinical spectrum of serious staphylococcal disease. Mortality was 21 percent, lower than previously reported. Patients could be separated into two groups according to the presence of identifiable primary staphylococcal infections; 63 bacteremic patients had such lesions, the remaining 42 lacked them. The latter group contained 24 of 26 cases of endocarditis.

I have quoted this article so many times I plan on having it on my tombstone.

And

Community-acquired S. aureus bacteremia frequently develops in the absence of a primary focus of infection and is more likely to result in endocarditis.

I suspect that many think they all that is required to treat infections is do a culture and sensitivity. Pick an antibiotic and give it. They certainly do not seem to teach students the significance of positive blood cultures of what is arguably the most common and serious pathogen in the hospital.

Or maybe it is just information overload, and students have had to stuff their heads with other information leaving no room for facts like normal temperature and the significance of S. aureus bacteremia. Instead, they have to learn how to use the EMR.

I am probably a grouchy old fart, but issues like this annoy me no end.

Rationalization

Chest. 2011 Aug;140(2):418-24. doi: 10.1378/chest.11-0127. Epub 2011 Apr 28. Atelectasis as a cause of postoperative fever: where is the clinical evidence?

http://www.ncbi.nlm.nih.gov/pubmed/21527508

A Critical Appraisal of 98.6°F, the Upper Limit of the Normal Body Temperature, and Other Legacies of Carl Reinhold August Wunderlich. JAMA. 1992;268(12):1578-1580. doi:10.1001/jama.1992.03490120092034

http://jama.jamanetwork.com/article.aspx?articleid=400116

Am J Med. 1976 Apr;60(4):495-500. Staphylococcus aureus bacteremia. Current clinical patterns.

http://www.ncbi.nlm.nih.gov/pubmed/1274983

J Med. 1984;15(3):193-211. Staphylococcus aureus bacteremia and endocarditis: comparison of nosocomial and community-acquired infection.

http://www.ncbi.nlm.nih.gov/pubmed/6597254

I want a good reason

Aug 8, 2014

The patient is a young IV heroin user who has the fairly abrupt onset of left flank pain. He toughs it out for several days, but then has a fever and a rigor, so off to the ER.

CBC, UA, BC, and UC are all normal, but the CT shows an area of necrosis in the middle of the kidney and a perinephric fluid collection.

It is an odd CT, at least for an infection.

Usually, when there is a kidney infection, there is also either a cyclitis or at least an abnormal UA. Nothing. So, he has a CT guided biopsy, it is pus, and it grows MSSA.

So, a primary renal abscess it is. But why? I would have thought this a common enough problem, but the PubMeds were surprisingly unrevealing. Abscess from cystitis and pyelonephritis, yes. But a spontaneous renal/perinephric bacterial abscess is rarely reported.

The patient does not have endocarditis for an embolic etiology (and the kidney does not look embolic) and no right to left shunt for this to be a paradoxical embolus. So, I do not have an apparent reason for the abscess.

I suppose he could have seeded a renal cyst. Infected solitary renal cysts are reported, and it could have then ruptured into the perinephric space.

Two cases of suppuration in solitary renal cysts are reported. The clinical history of acute pyelonephritis, avascular mass lesion of the kidney with ipsilateral pleural effusion (triad) seen in a female patient of child-bearing age is characteristic of this condition. Surgical management is satisfactory. Our Case 1 is the first reported case of solitary infected cyst that ruptured retroperitoneally, clinically mimicking a subphrenic abscess.

I kind of like that idea because it at least explains what is a rare phenomenon. IVDA seems an insufficient explanation, despite the propensity of S. aureus to cause distant infections. S. aureus usually seeds areas with pathology of some sort. The kidney is too necrotic to tell if there was/is a cyst there. As is often the case, I am not going to let the lack of confirming data get in the way of a good explanation.

Rationalization

Urology. 1978 Feb;11(2):164-7. Solitary infected renal cyst: report of 2 cases and review of literature.

https://www.ncbi.nlm.nih.gov/pubmed/343345

I Wonder

Aug 11, 2014

Sometimes I ask questions for which there are no answers. And sometimes I wonder if I should be asking the questions in the first place. It would sure take less time if I quit wondering about issues that may have zero relevance to anything.

A case in point.

The patient has an MSSA empyema and has had his VATS and is getting better. He has good reason for the pneumonia and diabetes but is doing well on therapy except for a new drug rash on vancomycin.

What is curious is his chest CT. His entire pleural space is calcified, presumptively from a distant exposure to asbestos. His op report mentioned a thick peel, the calcium, and pus.

He has numerous well-documented allergies to antibiotics, including type I reactions to beta-lactams.

The question I wondered about? Should I treat him for osteomyelitis? His pleural space is a calcium pitcher that had been filled with S. aureus.

I cannot find anything even remotely like this on the interwebs. Pleural plaques have a variety of etiologies, and there is the occasional pleural space that has mesothelioma that gets infected.

I can't find cases of soft tissue calcifications acting like a foreign body for recurrent infections. The closest I can get is calciphylaxis, and that is not even close. I spent at least 45 minutes using every search term I could think of. Nothing.

Given the allergies, linezolid is the only reasonable long-term solution, but toxicities and cost mount quickly with that drug.

So maybe I should not have wondered. Now I have uncertainly with no solutions, not even a solution I can make up.

Rationalization

Clin J Am Soc Nephrol. 2008 Jul;3(4):1139-43. doi: 10.2215/CJN.00530108. Epub 2008 Apr 16. Calciphylaxis from nonuremic causes: a systematic review.

http://www.ncbi.nlm.nih.gov/pubmed/18417747

Born Under a Bad Sign

Aug 13, 2014

The patient had a small mass on the inner chest wall six years ago on CT and for reasons about which I am unsure it was not followed up.

It grew.

This year the CT showed a lemon-sized mass between the liver and the chest wall, and 1.5 months ago, it was biopsied.

It was not sent for culture but was classic: gram-positive branching rods and sulfur granules. So the patient was sent to me.

Zero reasons for Actinomycosis. No trauma, no nothing in his abdomen except a lap cholecystectomy 8 years ago. I double-checked, but there were no spilled gallstones from the procedure on CT, which would make for nice nidus of infection.

Intra-abdominal abscess formation can present as a delayed complication dropped stones during LC, but these cases usually presents within a few years of the procedure. In this case, however, an intra-abdominal abscess formed 11 years after the LC. This extended duration from surgical manipulation to symptom onset is likely secondary to the indolent nature of the infecting organism, A. israelii.

But as I just learned or had forgotten, there are radiolucent gallstones, which are rare and made of cholesterol. So maybe.

So, I treated presumptive Actinomycosis, and he not only failed to get better, he worsened with fevers, pain, malaise, and weight loss. He looks sick. Not the clinical response that I am used to. Repeat CT shows the mass is not only bigger, and the center is more liquid.

Well, we need to get a culture I tell the patient, to make sure I am treating the right infection. So, we drain it under CT within an hour; he has intractable rigors that last for an hour.

That is odd since that is what is seen after draining more classical bacterial abscesses. They can get a surge of endotoxin at the time of drainage and get quite ill; I think of it as the bacterial equivalent of a Jarisch-Herxheimer reaction.

But the gram stain has gram-negative rods, and today it was identified at K. pneumoniae. Again, a review of the CT has no reason for this organism, either. I can't believe a Klebsiella has been there for six years, although it kinda sorta happened before

A case is reported of a subphrenic abscess 12 months post-laparoscopic cholecystectomy in a 72-year-old male with identification of Actinomyces meyeri and the oropharyngeal commensal Klebsiella ozaenae.

Was it a complication of the first biopsy? Again, a Klebsiella would not be high on my list of pathogens. Or is it the random seeding of the Actinomycosis for no reason what-so-ever?

He is living the blues song Born Under a Bad Sign:

Born under a bad sign, been down since I began to crawl

If it wasn't for bad luck, I wouldn't have no luck at all

So now, I need to kill two infections: Actinomycosis and Klebsiella, but I have no goof explanation for either.

Unsatisfying. Of course, it is not the job of the universe to make me happy, although it should be.

Rationalization

Surg Laparosc Endosc Percutan Tech. 2007 Dec;17(6):542-4. Intra-abdominal actinomycosis 11 years after spilled gallstones at the time of laparoscopic cholecystectomy.

http://www.ncbi.nlm.nih.gov/pubmed/18097319

South Med J. 2009 Jul;102(7):725-7. doi: 10.1097/SMJ.0b013e3181abddc5. Subphrenic abscess secondary to Actinomycosis meyeri and Klebsiella ozaenae following laparoscopic cholecystectomy.

https://doi.org/10.1097/smj.0b013e3181abddc5

POLL RESULTS

The job of the Universe is to

• make me happy 17%
• make me wealthy 0%
• make me feel insignificant 15%
• give me total perspective, like that of Zaphod Beeblebrox. Another Pan Galactic Gargle Blaster if you please 32%
• grind me down till I die alone and forgotten 33%
• Other Answers 3%
  • sweep up after itself

The Lure of Berries

Aug 18, 2014

There are many nice things about living in the great Pacific NW. I probably should not mention it in the blog as readers will only feel bad that they have to live in whatever inferior part of the world they are stuck in.

It has been a long berry season. The strawberries are still being picked and, with it, Leptospirosis, Escherichia coli O157:H7, and Norovirus.

Raspberry season is over, so will have to rely on imported berries, and with it Cyclospora.

When one bathroom door closes, another one opens.

Infection risk never stops, but I never let it get in the way of a good meal. But the pursuit of berries can have other downsides.

The patient presents with hip pain several months after a hip replacement. CT shows an iliopsoas abscess, and a tap of both the hip and abscess grew MSSA.

Talking to her, it was not hard to miss two features. The first is psoriasis. Psoriasis plaques are usually colonized with S. aureus. So, there is a good source for the infection.

The second was the numerous scabbed-over and inflamed scratches on her arm.

A particularly aggressive cat? I asked, pointing at her trauma.

Nope. Picking blackberries. And the pain in her hip began shortly after picking the blackberries. Wild, warm Oregon blackberries are heaven, so much better than the farm-raised ones. But it is virtually impossible to get them without trauma. There is a patch I graze on this time of year during my daily constitutional, and I have the skin injuries to prove it.

If you ever run across Cascade Berry (a cross between the blackberry and the loganberry) Jam, do NOT pass it up. Oh man, so good on homemade warm biscuits or croissants.

I wonder if drool will short out my keyboard.

The only infection associated with blackberry scratches I can find is a case of sporotrichosis. I could not find any published information that blackberry scratches are any worse than any other plant trauma, but they sure seem so to me. They are always deep and seem to be more inflamed than other environmental trauma.

That is now three severe infections I have seen over the years following blackberry picking, the others being a group A Streptococcus necrotizing fasciitis and a cellulitis with endocarditis, also a Streptococcus pyogenes.

It is not going to stop me from getting those last few berries tonight.

Rationalization

Clin Infect Dis. 2009 Mar 15;48(6):691-7. doi: 10.1086/597036. Resurgence of field fever in a temperate country: an epidemic of leptospirosis among seasonal strawberry harvesters in Germany in 2007.

http://www.ncbi.nlm.nih.gov/pubmed/19193108

Food Environ Virol. 2013 Jul 26. [Epub ahead of print] Detection and Typing of Norovirus from Frozen Strawberries Involved in a Large-Scale Gastroenteritis Outbreak in Germany.

http://www.ncbi.nlm.nih.gov/pubmed/23888384

Clin Infect Dis. 2013 Oct;57(8):1129-34. doi: 10.1093/cid/cit468. Epub 2013 Jul 21. Escherichia coli O157:H7 infections associated with consumption of locally grown strawberries contaminated by deer.

http://www.ncbi.nlm.nih.gov/pubmed/23876397

Emerg Infect Dis. 1999 Nov-Dec;5(6):766-74. Epidemiologic studies of Cyclospora cayetanensis in Guatemala.

http://www.ncbi.nlm.nih.gov/pubmed/10603209

Int J Dermatol. 2006 Apr;45(4):450-3. Disseminated sporotrichosis mimicking sarcoidosis.

http://www.ncbi.nlm.nih.gov/pubmed/16650176

POLL RESULTS

For my last meal before the lethal infection, let me die with the taste on my lips of fresh Oregon

• strawberries 21%
• raspberries 23%
• blueberries 8%
• blackberries 27%
• marionberries 10%
• Other Answers 10%
  • Dingleberries
  • Mirror pond pale ale.
  • always been a fan of halleberries.
  • smoked salmon on toasted, garlic-buttered French bread.
  • Perhaps best I don't get that explicit.

Who is that Masked Man?

Aug 21, 2014

Those who read this blog regularly know that I think that every health care worker has an obligation to maximally protect their patients and that part of that obligation includes getting the influenza vaccine.

In the hospital, we take care of the most vulnerable patients, and health care acquired influenza has significant morbidity:

A total of 570 (17.3%) of 3,299 influenza cases were healthcare associated; 345 (60.5%) were acquired in a long-term care facility (LTCF), and 225 (39.5%) were acquired in an acute care facility (ACF).

and mortality rates of 13% to 27% depending on the population studied.

It is why I have zero respect for health care workers who are not vaccinated, suggesting in the past that they are a dumb ass if they use any of the reasons enumerated for avoiding the flu vaccine. I stick by that assessment. I do not want the unvaccinated taking care of me and mine any more than I would an HCW who refused to do hand hygiene.

Unfortunately

Oregon is the only state that has language in the statutes that prevents the vaccination from being a condition of employment.

So, we cannot mandate the flu vaccine. The Oregon Nursing Association has been helpful in making sure that we keep the option open for your parents or children to get influenza in the hospital and die.

The Oregon Nurses Association (ONA) believes that all nurses and healthcare workers should get an influenza vaccination, but not as a condition of employment. Currently, Oregon law (ORS 433.407) says that facilities that employ healthcare workers must offer vaccines, but cannot require people to get vaccinated as a condition of employment.

And how is that working out?

69 percent of employees in Oregon’s hospitals and 52 percent of employees in long-term care facilities were vaccinated during that same time period.

Or think of it this way: 31 percent of employees in Oregon’s hospitals and 48 percent of employees in long-term care facilities are allowed to potentially pass on a preventable fatal infection to their patients.

There once was a poster in the ICU that declared Nursing "The Caring Profession." No longer, in Oregon, at least when it comes to caring about the spread of influenza. But I am old school. I think HCW's have a higher responsibility to patients, not a common approach in this century.

The preponderance of data demonstrates that HCW influenza vaccination benefits patients:

Pooled risk ratios across trials for all-cause mortality and influenza-like illness were 0.71 (95% confidence interval [CI]: 0.59, 0.85) and 0.58 (95% CI: 0.46, 0.73), respectively; pooled estimates for all-cause hospitalization and laboratory-confirmed influenza were not statistically significant. The cohort and case-control studies indicated significant protective associations for influenza-like illness and laboratory-confirmed influenza. Conclusions. The quality of evidence is higher for mortality than for other outcomes. HCP influenza vaccination can enhance patient safety.

and the community:

For every 15 healthcare providers who receive the influenza vaccination, one fewer person in the community will contract an influenza-like illness, according to a study using California public health data from 2009 – 2012.

Actions have consequences, and the result of the Oregon Legislature preventing flu vaccination mandates may well be to kill people. To my mind, it is like preventing airbags in cars or hand hygiene, denying hospitals a proven weapon to safely reduce the morbidity and mortality from influenza in their patients.

I have watched nosocomial morbidity and mortality fall each year as a result of applying best practices to patient care. One of the take-home messages of the book about the early AIDS epidemic, And the Band Played On, was how many needless deaths occurred because basic infection control was ignored due to political considerations. On a smaller scale, history repeats itself in Oregon with flu vaccinations. Sad.

PS To be clear, I am not speaking for any hospital or hospital system. It is all my opinion, and I often get my opinions voted down.

Rationalization

Infect Control Hosp Epidemiol. 2014 Feb;35(2):169-75. doi: 10.1086/674858. Epub 2014 Jan 8. Healthcare-associated influenza in Canadian hospitals from 2006 to 2012.

http://www.ncbi.nlm.nih.gov/pubmed/24442080

BMC Infect Dis. 2013 Mar 7;13:127. doi: 10.1186/1471-2334-13-127. Nosocomial outbreak of the pandemic Influenza A (H1N1) 2009 in critical hematologic patients during seasonal influenza 2010-2011: detection of oseltamivir resistant variant viruses.

http://www.ncbi.nlm.nih.gov/pubmed/23496867

Emerg Infect Dis. 2011 Apr;17(4):592-8. doi: 10.3201/eid1704.101679. Nosocomial pandemic (H1N1) 2009, United Kingdom, 2009-2010.

http://www.ncbi.nlm.nih.gov/pubmed/21470446

Oregon Nurses Association Attempts to Change Oregon’s Vaccination Law.

https://www.thelundreport.org/content/oregon-nurses-association-attempts-change-oregon%E2%80%99s-vaccination-law

Nursing is no longer the caring profession.

http://www.telegraph.co.uk/health/8728849/Nursing-is-no-longer-the-caring-profession.html

Effect of Influenza Vaccination of Health Care Personnel on Morbidity and Mortality among Patients: Systematic Review and Grading of Evidence.

http://cid.oxfordjournals.org/content/early/2013/09/17/cid.cit580.abstract

Study: When hospital workers get vaccines, community flu rates fall.

http://www.apic.org/For-Media/News-Releases/Article?id=e0b94274-5340-47ca-b86f-fdb64c90e79e

POLL RESULTS

I support

• mandatory flu vaccination of HCW 80%
• voluntary flu vaccinations since my fears trump your safety 0%
• vitamin C and D is all you need, but THEY do not want you to know 3%
• no vaccinations but masks for everyone in the country during flu season. If nothing else, an aesthetic improvement. 6%
• no inhaling for the flu season 10%
• Other Answers 1%
  • Non-vaccinated HCWs have the option of enclosing their heads in an airtight bag on arrival at work.

Quick questions, slow answers

Aug 25, 2014

I really enjoy working at my hospitals. I work with mostly smart, kind people, and a supportive administration. But.

So much of being a consultant is asking questions and then looking for answers.

The patient is an elderly female with radiation cystitis after treatment of uterine cancer. Since the bleeding didn't stop on its own, they tried formalin in the bladder, which is evidently an effective therapy.

However, soon after the installation, she went 'septic' and had to be moved to the ICU. She had the usual workup for sepsis and was placed on a course of antibiotics.

All cultures were negative, and they called me for advice on the type and duration of antibiotics.

She had cystitis in the past, so I figured they stirred up some endotoxin with the formalin therapy. And it should sterilize the bladder, rendering cultures negative. But would it? Formalin should inactive endotoxin, right? I can't find much as I type this, but formalin inactivation of various microbial toxins is common.

We have an attending who always puts medications at the top of the list at noon report when discussing a case, and appropriately so. While I like to presume all diseases are due to infection, occasionally, there are other, albeit less interesting, causes for a patient's symptoms.

Perhaps the formalin is the cause. So, I went to the web. At work, most of the computers have IE 7 whose sole purpose is to freeze mid-search so that everything takes twice as long. There is also the random infinite page load, which perhaps is the network, but I doubt it as changing computers fixes it. Man, it is frustrating. I am just using PubMed and Google Scholar. All the knowledge of the world at my fingertips, hidden behind the modern symbol of eternity, the windows hourglass, and a hypothyroid progress bar.

It could be the formalin, although acute reactions are rare:

A case of shock following intravesical formalin instillation for massive bladder hemorrhage owing to post-radiation cystitis is reported.

It could be an allergic reaction. Also, formalin is metabolized to formic acid (ant venom) with causes hypotension and MOSF in overdoses. I suspect if there is a lot of bladder wall inflammation, systemic absorption of the formalin would be possible. It would have been interesting to get a formic acid level on admit to ICU.

Whether it was time or the antibiotics, the patient slowly improved. Now if I could just get the browser at work to improve as well.

Rationalization

J Bacteriol. May 1969; 98(2): 437–442. PMCID: PMC284835 Effect of Formaldehyde on the Immunochemical and Biological Activity of Staphylococcal Endotoxin B

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC284835/

[A case of shock following intravesical formalin instillation].

http://www.ncbi.nlm.nih.gov/pubmed/1524012

Postgrad Med J. Jan 1985; 61(711): 35–36. PMCID: PMC2418107 Formic acid poisoning with suicidal intent: a report of 53 cases.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2418107/?page=1

Urology. 1978 Jun;11(6):588-90. Fatal complication of intravesical formalin during control of intractable hemorrhage from radiation cystitis.

http://www.ncbi.nlm.nih.gov/pubmed/566977

SBP? SFP? SCP? LSMFT?

Aug 27, 2014

The patient has end-stage liver disease with all the metabolic complications: elevated bilirubin, low albumin, coagulopathy, and ascites.

She is on a quinolone for SBP prophylaxis and comes in with fevers, diarrhea, and abdominal pain. C. difficile toxin is positive. Not too much of a surprise since few antibiotics drive superinfections like quinolones. They are great for killing bugs and almost as great at selecting a variety of resistant organisms. They are often the best choice for an infection, but I am never surprised when there are downstream complications from their use, and I avoid them when I can.

Because of the abdominal pain and ascites, a tap was done. 5000 WBC. So SBP as well. Is this from the colitis with translocation? I do not know. SBP is common enough in those with ascites, but I cannot find where anyone has looked to see if C. difficile increases the risk. Someone get to work and do the study.

But then all the cultures grow a fungus, subsequently identified as C. albicans.

SFP? The few cases of Candida peritonitis I have seen have been a complication of peritoneal dialysis.

It happens, although not often.

Spontaneous fungal peritonitis was attributed to Candida species, while fungemia was caused by Aspergillus species.

My first consult all those years ago was an end-stage liver disease patient with fevers and leukocytosis. Despite an extensive work-up and increasingly desperate antibiotics, the patient progressed with MOSF and died. An autopsy found cardiac infection with Aspergillus. So I tend to fret about fungi in ESLD, a failure to diagnose makes an impression.

As an aside, my second consult in practice died of miliary TB, also diagnosed at autopsy. Not an auspicious start to an ID career. I might make the Aspergillus diagnosis today with a beta-D-glucan or a galactomannan, but I would still would not diagnose TB case in time. Rapid death from miliary TB usually is a diagnosis of luck if there are no risk factors.

Ten patients were infected with Candida spp. (C. albicans, 8; C. tropicalis, 1; C. glabrata, 1), and 5 with Cryptococcus neoformans. Eleven patients were co-infected with bacteria that were susceptible to the antibiotics administered. Only 5 patients were treated using appropriate anti-fungal agents. The 1-month mortality rate for SFP patients was 73.3 % (11 out of 15; median time to death, 2 days [range, 0-22]), which was significantly higher than patients with SBP alone (28.7 %, P = 0.0007). SFP is severe complication related to high mortality in cirrhotic patients.

We looked for a bowel perforation and found none, and she improved nicely on fluconazole.

There is perhaps a dozen reported cases of SFP/SCP, and this is not only my first but likely the last I will see. I am not going to be doing this another 24 years.

PS

As I review this entry in 2020, I will note that it has been subsequently shown that during C. difficile infections there is often fungal translocation as determined by beta-D-glucan levels and C. difficile is a risk from Candida in the blood stream. So not such a surprise.

Rationalization

Int J Infect Dis. 2014 Jun;23:69-74. doi: 10.1016/j.ijid.2013.12.014. Epub 2014 Apr 12. Fungal infection in patients with end-stage liver disease: low frequency or low index of suspicion.

http://www.ncbi.nlm.nih.gov/pubmed/24726663

Scand J Infect Dis. 2004;36(9):649-55. Clinical significance of untreated Candida species isolated from ascites in cirrhotic patients.

http://www.ncbi.nlm.nih.gov/pubmed/15370651

Eur J Clin Microbiol Infect Dis. 2014 Feb;33(2):259-64. doi: 10.1007/s10096-013-1953-2. Epub 2013 Sep 2. Spontaneous fungal peritonitis: a severe complication in patients with advanced liver cirrhosis.

http://www.ncbi.nlm.nih.gov/pubmed/23996048

Man Oh Man

Aug 29, 2014

The patient is an elderly female with the usual medical problems of age: diabetes, obesity, hypertension, chronic renal insufficiency, and a pacemaker.

She has chronic, severe, lymphedema and comes in with fever and chills to another hospital. Cellulitis is the diagnosis, and she rapidly improves on cefepime. The blood cultures grow Acinetobacter baumannii. Not high on the list of causative organisms, and the Pubmeds would agree.

While well described as a cause of necrotizing fasciitis and a complication of war trauma, straight up cellulitis, inflammation of the cellu, is rare, although this would be my second case.

Because the patient clinically responded and the only antibiotic to which the organism was quasi-sensitive that is not an aminoglycoside was cefepime (organism is ‘I’), she was sent out on the antibiotic. Ten days later, she is back in one of my hospitals, and the blood cultures are growing the same organism.

Recurrent bacteremia from cellulitis? The legs are red and swollen but cool to the touch. It would be nice to have some dolor and calor to point to the soft tissue as a source.

Every time I see a wire in the chest, I fret. The rabbit model of endocarditis is to put a wire across a valve and give the bunny a bolus of bacteria. They all get endocarditis as a result. Although I see my fair share of pacemaker infections, we probably do not see more as humans have less intense bacteremia than a lab rabbit.

A quick PubMed finds one Acinetobacter pacer infection. So not common. But a sustained bacteremia is the sine qua non of an endovascular infection.

So, we get a TEE: tricuspid and wire vegetations and maybe a vegetation on the aortic valve.

Not good. She is now on tobramycin and ampicillin-sulbactam. Pearl for you non-ID docs: it's the sulbactam that has the activity.

Of the ²-lactamase inhibitors, sulbactam possesses the greatest intrinsic bactericidal activity against A. baumannii isolates. Results of clinical investigations have documented the efficacy of sulbactam (commercially available in the United States in combination with ampicillin) in mild-to severe A. baumannii infections.

Now what? At a minimum, the pacer needs to come out, which we can probably do safely. But I can't cure an Acinetobacter endocarditis medically, and her comorbidities and metabolic derangements make valve surgery extremely risky. No good solution to this problem.

A couple of years ago, I came across the antibiogram of my hospital from 1990, the year I started in practice. I could kill everything back in the day. No MRSA, no VRE, no MRDO.

Now? Increasingly I see infections I can neither kill nor cut out. Resistant infections in inaccessible places in compromised patients. Three this week alone. I used to think ID was going to become a surgical specialty again, now I think its heading to be the next [insert futile profession here].

Rationalization

J Formos Med Assoc. 2003 Sep;102(9):650-2. Community-acquired bacteremic cellulitis caused by Acinetobacter baumannii

http://www.ncbi.nlm.nih.gov/pubmed/14625612

Any Bug in Any Place

http://boards.medscape.com/forums?128@@.2a59972f!comment=1

Arch Mal Coeur Vaiss. 1986 Apr;79(4):483-8. [Endocarditis on cardiac pacemaker endocavitary electrodes. Apropos of 7 cases].

http://www.ncbi.nlm.nih.gov/pubmed/3090966

Treatment of Acinetobacter Infections Clinical Infectious Diseases Volume 51, Issue 1Pp. 79-84.

http://cid.oxfordjournals.org/content/51/1/79.full

Clin Infect Dis. 1992 May;14(5):1145-8. Infective endocarditis of a native valve due to Acinetobacter: case report and review.

http://www.ncbi.nlm.nih.gov/pubmed/1600019

POLL RESULTS

The most futile profession is

• ID 2%
• Parent 11%
• UN Peacekeeper 40%
• Skeptic 4%
• Trick Question. They all are. 29%
• Other Answers 13%
  • cop and preacher
  • Teacher. All of the others fail on the refusal of people to learn.
  • Conservationist.
  • customer complaints department
  • voter