Moved. Forwarding Address.
June 1st, 2009
It is official.
The blog has moved to
http://www.medscape.com/public/blogs
At least until they kick me off.
Oprah wants your children dead and I am moving
June 1st, 2009
Well, Oprah really doesn’t want your children to die. At least I do not think so. But one wonders. If you spend anytime at all in the antivax world then you are aware of Jenny McCarthy, who believes, despite all the evidence to the contrary, that vaccines are dangerous and cause autism. She has even go so far as staitng in her Time interview that
“I do believe sadly it’s going to take some diseases coming back to realize that we need to change and develop vaccines that are safe. If the vaccine companies are not listening to us, it’s their f___ing fault that the diseases are coming back. They’re making a product that’s s___. If you give us a safe vaccine, we’ll use it. It shouldn’t be polio versus autism (1).”
It isn’t. Holy False dichotomy, Batman. Vaccines are safe. The diseases they prevent are bad. Real bad. We do not want them back.
But the wise and powerful O has hired Ms McCarthy for, perhaps, a talk show where she can take her vaccine delusions to an even wider audience. And kids will die. And, in the end, Oprah will need to be added to the Jenny McCarthy body count.
When it comes to health care, and woo, Oprah is a goof; there is a nice review on Newsweek.
Go to oprah.com. Let her know that indirectly killing babies by supporting anivaccine nonsense is a bad idea. Let her know it will make her fat. But let her know.
So. This is my last entry at this site.
About a month ago I was contacted by the folks at Medscape asking if I would be interested in being their Infectious Disease blogger. Do the same thing I do here, but do it on Medcape, with a much bigger audience.
I said sure.
So starting this week I have sold my soul to the company store (my goal in life) and Rubor Dolor Calor Tumor will now be over at Medscape. I will post the official link after the first entry.
See you there.
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(1) http://www.time.com/time/health/article/0,8599,1888718,00.html
Kiss my Aspergillus
May 30th, 2009
Aspergillus is everywhere. It can be the mold on your bread, the mold on your cheese, and the mold on the cup of coffee that is left out for three or four weeks.
My wife, and most females, have curiously never seen mold on a cup of coffee left out for weeks. Most males have. Don’t know why, but when I was single I would let the dishes sit in the sink until the growth evolved into a life form that wanted to clean itself. I don’t do that anymore.
So when aspergillus is in a bronch culture, you have to ask if it as real or a contaminant, and Ella Fitzgerald can’t help you with that.
The patient has had Wegeners for 5 months and is on dialysis, prednisone, and just finished the Cytoxan that cleared up the pulmonary inflitrates on her CT.
Now back in the hospital, she has cavitating pulmonary nodules, the BAL from the bronchoscopy is growing aspergillus after only three days.
She is a touch short of breath, but no hemoptysis.
The gold standard for invasive aspergillus is biopsy showing invasion of the organisms, but the bronch biopsy did not show this.
Open lung? Treat?
The BAL had aspergillus on staining, so it must be a fairly high concentrations and she had no prior structural lung disease to predispose to heavy colonization. The chance that the aspergillus is the real deal is about 25%. Not good odds. But it’s a compatible CT and host and large amounts of aspergillus that grew rapidly. If the galactomannan assay is positive, then the diagnosis is clinched.
So she is on voriconazole and we shall see. Thats the royal we, not the multiple personality we.
=======
Mayo Clin Proc. 1992 Mar;67(3):221-7.L
Bronchoalveolar lavage (BAL) has been used extensively for assessment of immunocompromised hosts with pulmonary infiltrates. Reported estimates of the diagnostic utility of BAL have varied because of differences in patient populations, diagnostic criteria, and study methods. Herein we report on the use of BAL to determine at least one of the final diagnoses in 150 immunocompromised patients. Although the frequency with which BAL provided at least one of the final diagnoses (overall diagnostic yield) was seemingly low (39%), the yield increased substantially when only patients with pathologically proven diagnoses were considered. The sensitivity of BAL was 82%, and the specificity was 53%. The use of rigid diagnostic criteria enabled us to distinguish pathogens from colonizers. Pneumocystis was considered a pathogen whenever it was identified. It was the most common infectious pathogen identified (50%) despite the fact that our study population had relatively few patients (only 4%) with acquired immunodeficiency syndrome (AIDS). Organisms such as cytomegalovirus, Aspergillus, and Candida were frequently identified in BAL specimens but were eventually proved to be pathogens in only 24%, 25%, and 0% of cases, respectively. BAL detected pulmonary malignant lesions on the basis of positive cytologic results in four of six patients eventually found to have primary or metastatic lung cancer. Our results should enhance the understanding of the strengths and weaknesses of BAL and assist in the interpretation of associated microbiologic findings.
PMID: 1545588
The Secret
May 27th, 2009
Sometimes you suspect the diagnosis as soon as you walk in the room.
The patient was billed as chronic cough and elevated white count. Why?
He was thin and tanned, the latter odd for Oregon at this time of the year. What was striking was his clubbed fingers. Most impressive I have seen in years.
I take the history: slight non productive cough, 10 pound weight loss, his long bones have been aching for couple of months. 2 pack a day smoker for years.
Labs showed an elevated white count, 14 to 16, 000, but otherwise normal. His chest xray is ok.
His exam is negative except for the clubbing and muscle wasting. He says his hands have always been that way. There is congenital clubbing, but no way is this congenital, although I hope so. I go looking for the cancer that should be there.
CT scan shows a 4 cm mass, some sort of cancer, in his mediastinum, right behind his heart where it could not be seen on CXR. The clubbing was the hint.
“Of patients with idiopathic pulmonary fibrosis, 65% have clinical digital clubbing. In these patients, an increased occurrence has been shown in patients with higher grades of smooth muscle proliferation in the lungs.
Clubbing has been reported in 29% of patients with lung cancer and is observed more commonly in patients with non–small cell lung carcinoma (35%) than in patients with small cell lung carcinoma (4%).
Digital clubbing was reported in 38% of patients with Crohn disease, 15% of patients with ulcerative colitis, and 8% of patients with proctitis. Clubbing was observed in up to one third of Ugandan patients with pulmonary tuberculosis.).”
The long bone pain is probably pulmonary osteopathy, an unusual cause of bone pain. All his symptoms are from his cancer, which will be biopsied later in the week.
The reason I recognized this case is I compulsively go to noon report where the residents present interesting cases as unknowns and the Chief of Medicine, Dr. Jones, discusses the case, with input from the house-staff.
Not five days earlier they had presented a similar case and Dr. Jones finished by saying, “Some people say it is a waste of time teaching these rare diseases, but you never know when one will walk into clinic.”
And sure enough, there was a case.
I am disinclined towards the supernatural, but it is spooky how often you hear about a good case or read something new, and you see a similar case a week or two later. I always wonder how many similar cases I missed. It is why I say “I have never diagnosed a case” rather than “I have never seen a case.” I wonder how many I have seen and not known it.
The Secret is true. Just by knowing about a disease, the universe delivers it up to you. The secret doesn’t create health and wealth, it creates cancer, disease and death. A much more interesting, if awful, result.
+++++++
Why
May 26th, 2009
I sometimes get asked what: what does the patient have.
Sometimes I get asked how: how to treat the patient. That was todays patients. The patient had a fever the day after he has his laparoscopic mesenteric biopsy and three days later his blood cultures popped positive for Candida glabrata of all things.
They asked be about the best antibiotic to use (I picked caspofungin).
But the interesting question is why.
Preop, he had no symptoms.
Past medical history diabetes, pacemaker dependent, obesity with chronic ‘diaper rash’ in his skin folds. His pacer is three years old.
His exam is negative.
The classic risk factors for Candida in their blood are central lines, hyperal, broad spectrum antibiotics, neutropenia and a major surgery.
He had none of the above.
The only reason he could have positive blood cultures is if he had seeded his pacer system from his intermittently oozy groin Candida, and, unfortunately his TEE today showed infection on the wires.
Crap.
Can’t cure it medically and if the pacer system comes out, he has no rhythm. He has no rhythm, Who could ask for anything more? Me. It is why I am glad I am not a cardiologist.
There is exactly one case of C. glabrata pacer infection in the lit-tra-chure and a smattering of a handful of a smidgin of other Candida species on pacers. Like all infections of pacers, the system absolutely, positively has to be removed. Unlike prosthetic valve endocarditis, the literature suggests you are as likely to cure a pacer infection medically as you are to get an accounting of money spent to bail out Fanny Mae.
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J Infect. 2000 Sep;41(2):176-8. Medical treatment of a pacemaker endocarditis due to Candida albicans and to Candida glabrata.
We describe a case of pacemaker infection due to two fungal species: Candida albicans and C. glabrata. Transthoracic echocardiography showed a large vegetation on the intraventricular wires. Because of severe underlying diseases, surgery was believed to be contraindicated. The patient was treated using high dose of fluconazole, resulting in clinical improvement and negative blood cultures. However, 2 months later, the patient underwent a fatal stroke. At autopsy, a large vegetation was found only all along the wires. Postmortem culture of the infected material was positive for both C. albicans and C. glabrata. Copyright 2000 The British Infection Society.
PMID: 11023765
Onycomycosis gone bad
May 22nd, 2009
Patient rolls his car. It is always a bad idea to roll your own. Something, just what is not certain, maybe his dogs nail, punctured his palm. His hand, not the PDA.
Since then he has had ongoing pain and erythema on the palm of his hand and when he moves his middle finger.
I do not know about you, but I have trouble driving if I cannot fully extend my middle finger.
He received several courses of po antibiotics without resolution, and then to a hand surgeon and then to me.
The striking feature on exam is all his nails were heavily involved with a fungal infection.
It had cleared years ago after a course of terfinibine, but relapsed almost immediately after stopping the medication. At least as immediately as a nail can grow.
The surgeon opened it up and it s a low grade gooey mess, not typical of a bacterial infection.
I made sure that the cultures were sent for fungal cultures as well as for AFB, but now the cultures are growing a Trichophyton species.
I bet what ever penetrated his palm dragged in his nail mould and caused a tenosynovitis, since the most common pathogens for nail infections are the dermatophytes Trichophyton rubrum and Trichophyton mentagrophytes.
There are at best 18 references on Pubmed of soft tissue infections with these organisms, almost all in the profoundly immunoincompetant, and no cases of tenosynovitis.
The NEJM suggests the best therapy is itaconazole as the best rx.
In ID its all in your exposure history. You get infected with what you are exposed to. My wife, fortunately, has an infectious smile, so I am safe for the time being.
==
N Engl J Med. 2009 May 14;360(20):2108-16
Clinical practice. Fungal nail disease.
de Berker D.
PMID: 19439745
Cross Reaction
May 19th, 2009
Spent the day watching my son in the state golf tournament. He did ok. First time to state. No infections on the golf course.
My latest Cryptococcus case?
Doing great thanks to amphotericin B and flucytosine.
When the patient first came in he had nodules on his chest CT and was coughing up blood. In the differential is aspergillus infection and the pulmonologist sent of both cultures and a serum aspergillus galactomannan assay.
The galactomannan assay is a reasonable way to determine if a patient has invasive aspergillus. Galactomannan is one of the cell wall constituents and when the organisms gets in the blood, bits of the cell wall flake off into the blood, like dandruff, and can be measured.
His was positive at 0.56, just above the cut off of 0.5.
Does he have fleas and lice?
Nope.
The galactomannan assay can be false positive with, of all things, pipercillan/tazobactam.
And it turns out the cryptococcus makes Galactoxylomannan which cross reacts with the assay.
Since the patients titer of the serum cryptococcal antigen was >1:2048, I am not surprised the assay was positive, but a false positive.
More importantly, since the patient who is at risk for aspergillus is also at risk for cryptococcus, a positive galactomannan assay in the right host should probably result in a serum cryptococcal antigen as well.
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J Clin Microbiol. 2005 Jun;43(6):2929-31.
Cryptococcus neoformans Galactoxylomannan contains an epitope(s) that is cross-reactive with Aspergillus Galactomannan. We report a case of cryptococcosis in which a serum enzyme-linked immunosorbent assay (ELISA) for Aspergillus galactomannan was positive, with no evidence of aspergillosis. Soluble antigens from 19 Cryptococcus neoformans strains and purified carbohydrates of C. neoformans capsule were thus assayed in the Aspergillus galactomannan ELISA. Antigens from all C. neoformans strains, and purified galactoxylomannan, gave a positive reaction, suggesting that C. neoformans galactoxylomannan contains an epitope(s) that is cross-reactive with Aspergillus galactomannan.
N Engl J Med. 2003 Dec 11;349(24):2366-7.Links
False positive test for aspergillus antigenemia related to concomitant administration of piperacillin and tazobactam.
Sulahian A, Touratier S, Ribaud P.
PMID: 14668472
Saepius in Erroris, Nunquam in Nuto.
May 18th, 2009
Busy busy busy.
Sometimes life keeps me away from the computer. There are things to be done away from the interwebs, at least until I become one with matrix.
I spent a chunk of my day teaching residents as one of my hospitals has an internal medicine residency program. The problem is I often do not know here my ideas come from. Like today.
I was asked to see a patient with a hematologic malignancy and fevers for five days despite ceftriaxone and azithromycin for the not really there pneumonia.
I know from a quick chart review that is white cells have gone form 6 to 1.7, his platelets from 230k to 90, and his hgb has dropped 2 points. Rest of his labs are ok
So the patient tells me he has teeth chattering rigors (which he has during the interview), fevers, severe myalgias, and abdominal pain. Otherwise no localizing symptoms
Hmmmm.
PMH: Waldenstrom, but no treatment for a year.
Animals? Dogs.
Travel outside Portland?
We were at out cabin in Eastern Oregon, near Bend, at 4900 feet.
Why he mentioned the elevation, I do not know, but my ears perk up.
So, any ticks?
Yeah. 4 tick bites, and his wife volunteers that they are swarmed with ticks this time of years.
And like a bubble floating up out of the bath and popping, I could smell what he had. But I do not know where the thought came from. The diagnosis was made far below conscious thought, then I need to do a rapid song and dance to justify the diagnosis.
I should mention that I have yet to confirm the diagnosis, and like many great diagnoses I make, reality often contradicts me. Pesky labs.
My motto: Saepius in Erroris, Nunquam in Nuto.
Frequently in Error, Never in Doubt.
I will probably report in a few weeks I was wrong.
But for now I am calling it Colorado Tick Fever.
====
From http://www.oregon.gov/DHS/ph/acd/diseases/ctf/facts.shtml#more
What is Tick-borne Colorado Tick Fever (CTF)?
Colorado tick fever (CTF) is a tick-borne viral illness of humans in the United States. This disease is caused by infection with the Colorado tick fever virus, a member of the Coltivirus genera. In the past, it has been named Mountain fever or American mountain fever. CTF virus was first isolated from human blood in 1944.
How do people get CTF?
The organism that causes CTF is transmitted by the bite of an infected tick. The Rocky Mountain wood tick (Dermacentor andersoni) is the principal carrier of CTF in the United States. Some cases have been associated with exposures to the virus in laboratory settings and one case followed transfusion of blood from a person infected with CTF virus within 4 months of donation.
What are the symptoms of CTF?
Patients infected with CTF virus often develop a two-staged fever and illness following an average incubation period of 4 days (range of 1-19 days) after a tick bite. The early signs of CTF are often nonspecific and may resemble many other infectious and non-infectious diseases. Initial symptoms may include sudden onset of fever, chills, headache, pain behind the eyes, light sensitivity, muscle pain, and generalized malaise. Abdominal pain, nausea and vomiting may occur during the course of the illness in addition to a rash. Flat or pimply rashes may occur in 5% to 12% of cases. The acute illness lasts 5 to 10 days, and in half of the cases, a first phase, with fever lasting 2 to 3 days is followed by a period without fever of 24 to 72 hours with anorexia and malaise. A second phase consisting of a return of fever and an increase in symptoms lasts for about 48 hours. Two important symptoms are fever (two-staged in 50% of cases) and a recent tick bite. CTF can be a severe illness, especially in children under 10 and older adults. Hospitalization may occur in 20% of CTF cases.
(BTW: it leads to pancytopenia)
Where do the most cases of CTF occur in the United States?
CTF is a seasonal disease, and occurs in mountain forest habitats at altitudes from 4,000 to 10,000 feet in the Rocky Mountain region of the United States during the months of February through October. Approximately 90% of cases occur between April and July. Half of all cases are reported from Colorado and Idaho. An assessment of reported cases 1980 and 1988 revealed that of the 1,432 cases reported, the highest number (256) was from Colorado. Although no asymptomatic infections are known to occur, the disease is easily confused with other infections and is extensively underreported. Here in Oregon, 296 cases of CTF were reported from 1950 through 1983 with 82 (28%) residing in Harney County and 77 (26%) residing in Deschutes County (where Bend is).
Right again
May 13th, 2009
I no long remember why I became a doctor, it was too long ago and I barely remember yesterday anymore.
But I do remember why I remain one, and its because it is so cool.
It is nice to make people better and talk with them and help them, don’t get me wrong. But the fun, what really bakes my potato, is figuring out the diagnosis before the cultures pop positive.
Like the patient today. Old heart transplant, as an outpatient he has a new temporal headache, and, despite the negative biopsy (which are known to have a high false negative rate) he is put on high dose prednisone for temporal arteritis.
He declines, has hemoptysis, a nodular upper lobe infiltrate on CT and develops petechiae on his legs.
He is admitted, his blood cultures grow a yeast and he is transfered to my hospital.
I am far more often wrong than I am right, and it is always annoying how often reality gets in the way of a good diagnosis. I wish I were a CAM provider and did not have to worry about that.
I said that it will be Cryptococcus, that it is the ONLY diagnosis possible, and by golly his serum cryptococcal antigen is > 1:2048. CNS evaluation is in process.
It always impresses people when you hit one out the ballpark.
In my mind there are two take homes.
One. And I can’t prove this by any data that I can find, but my local rheumatologist agrees. If you are on transplant medications, you cannot develop a vasculitis. I wonder if the temporal arteritis was, in fact, early cryptococcal disease.
B. Disseminated cryptococcus causes petechiae. I didn’t know that. Red bumps and molluscum contagiosum are the most common manifestations. Ulcers and cellulitis less so, and while I cannot find it on pubmed, doing the google on the interwebs finds all sorts of references.
III. 3 out of 2 people do not understand arithmetic, but everyone seemed to worry it might be Candida. Candida does not get in the blood stream unless there is a intravascular catheter, which he does not have. Just because he has a heart transplant doesn’t mean he is equally at risk for all fungi. Candida just ain’t on the list.
Thats now four cases of cryptococcus, three in less than a month.
This will be the year of cryptococcus and west nile in Oregon.
Something wicked this way comes.
Cue up the music from Jaws.
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Arch Dermatol. 1996 May;132(5):545-8.
Cutaneous Cryptococcus infection and AIDS. Report of 12 cases and review of the literature.
BACKGROUND: Cryptococcal infections occur in 6% to 13% of patients with acquired immunodeficiency syndrome (AIDS), most commonly infecting the central nervous system. Cutaneous lesions have been described morphologically as umbilicated papules, nodules, and violaceous plaques and can mimic molluscum contagiosum and Kaposi’s sarcoma. Cutaneous lesions can present months prior to other signs of systemic infection.
OBSERVATIONS: Cases of infection with cutaneous Cryptococcus and AIDS were reviewed and compared with cases reported in the literature. Among patients with Cryptococcus infection and AIDS seen at our institutions, 5.9% had skin lesions. All patients with cutaneous lesions had systemic involvement. Women were less commonly infected than men. There was no apparent predisposition associated with age, race, or human immunodeficiency virus infection risk factors. The median CD4 helper T-cell count was 0.024 X 10(9)/L (24/microL), and 44% (16/36) of the patients had previous opportunistic infections. Lesions were most commonly seen on the head and neck (78% [36/46]) and often mimicked molluscum contagiosum (54% [25/46]). The median serum and cerebrospinal fluid cryptococcal antigen titers were 1:32,768 and 1:512, respectively. Patients in our group did well with therapy (one death at 6 weeks, compared with 38% [13/34] mortality in the literature). There was no correlation between onset of lesions, number of lesions, CD4 helper T-cell count, or histopathologic characteristics. CONCLUSIONS: Disseminated Cryptococcus infection in AIDS presents with cutaneous lesions in up to 6% of cases. Clinicians need to be aware of the varied morphologic characteristics, since cutaneous lesions may present well in advance of other signs of systemic infection.
PMID: 8624151
Potato Potatoe
May 12th, 2009
There is an ongoing ‘discussion’ in my family of what is better: rice or potatoes. I am a rice fan, my wife prefers potatoes. Mashed, fried, boiled or baked, she like her hot potatoes.
And that brings us to the clinical sign of the hot potato voice.
What is it about old time Doctors and their urge to descrbie everythung after one food or another? Makes eating less enjoyable.
Todays patient had fever, bad sore throat, was toxic appearing with a marked left shift. There was also a soft, deeper than usual, whispery voice, the hot potato voice, so called because it sounds as if the patient talks as if there is a hot potato in their mouth.
This is a sign of peritonsillar abscess or cellulitis.
And sure enough the CT showed two early tonsil abscesses and peritonsillar inflammation, and, though the magic of antibiotics, the patient is getting better.
However. Let’s see a show of hands: everyone who has listen to someone talk with their mouth full of hot potato. I thought so. Nobody.
And is the peculiar way of talking with a peritonsillar abscess really like talking with a hot potato in your mouth? There is no question in medicine that is not worth a study. Dr MF Bhutta compared the talking of people with tonsillitis to them what had a hot potato in their mouth and the sounds were different:
“The study, Hot Potato Voice in Peritonsillitis: A Misnomer, appeared in the Journal of Voice. “Voice changes are a well-recognised symptom in patients suffering from peritonsillitis,” it says. “The voice is said to be thick and muffled, and is described as a ‘hot potato voice’, because it is believed to resemble the voice of someone with a hot potato in [their] mouth. There have been few studies analysing … the voice changes in tonsillitis or peritonsillitis and none that have compared these changes with those that occur with a hot potato in the oral cavity.”
To remedy this lack of knowledge, the three doctors recruited two sets of volunteers. The first group comprised 10 hospital patients whose suffering related to their tonsils. Each volunteer pronounced three particular vowel sounds, which the doctors recorded and subsequently analysed using special software.
The second group were 10 healthy hospital staffers, “with each of these participants placing a British new potato of approximately 50 grams in their oral cavity, warmed by microwave to a ‘hot’, but not uncomfortable, temperature”.
The doctors detected unmistakable differences. The unique sound of someone burdened with an actual potato, they explain, “is related to interference with the anterior tongue function from the physical presence of the potato.”
There are obvious flaws in the study. The potato should have been an Idaho baker, not a new potato Wrong thermodynamics. Part of the reason people with tonsillitis talk that way is to decrease the pain they have when talking. The potato should have been HOT, not hot. It should hurt.
They need to repeat the study, or use hot pizza instead.
Baboon butts and hot potatoes, this blog has it all.
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http://www.guardian.co.uk/education/2009/jan/13/improbable-research-mahmood-bhutta
J Voice. 2006 Dec;20(4):616-22. Epub 2005 Dec 19.
“Hot potato voice” in peritonsillitis: a misnomer.
Bhutta MF, Worley GA, Harries ML.
Department of Ear Nose and Throat, The Royal Sussex County Hospital, Brighton, UK.
The “hot potato voice” is widely recognized as a symptom of peritonsillar cellulitis or abscess; yet there have been no studies assessing the resonance characteristics of the vocal tract in peritonsillitis. Analysis was undertaken of formant frequencies in the articulation of the vowels /i:/. /a:/ and /u:/ in six subjects with peritonsillitis and compared with articulation once the peritonsillitis had settled. Significant variation was found in F1 when articulating /i:/ and in F2 when articulating /a:/, which are explainable by dyskinesis of the peritonsillar musculature. These findings were compared with six subjects articulating the same vowels with and without a hot potato in their mouth. Variation was found in both F1 and F2 when articulating /i:/, which can be related to interference of the potato with movement of the anterior tongue. The changes in the vocal tract differ in these two cases and the title “hot potato voice” in peritonsillitis is a misnomer.
PMID: 16360301
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