Puswhisperer Year 8
Chapter One
I remain amazed that in the year 2015, I often cannot prove that a patient has syphilis or TB.
Lues has been in humans for at least 2000 years (and a similar disease in bears for at least 11,000; explaining Yogi’s somewhat odd behavior), yet I can often not say with certainty: yes, you have, or no you do not have, syphilis.
The most annoying variation is the discordant serology: a positive FTA and a negative RPR. I have seen a spate of these in the clinic, all from ophthalmology, all with some sort of eye problem: uveitis, scleritis or some such.
I have yet to get a history of a clinical syndrome, exposure, or inadvertent treatment of syphilis to account for the serologies and no reason for either a false positive FTA or a false negative RPR.
Discordant serologies are as interesting a problem as they are aggravating.
Persons with serodiscordant serologies (i.e. confirmed positive treponemal and persistently negative non treponemal tests) and no history of syphilis treatment present several important clinical and public health questions, particularly since they would likely be missed by the traditional algorithm: What is their risk of transmitting syphilis sexually? What is their risk of transmitting syphilis vertically? What is their risk of progression to tertiary syphilis? … A recent retrospective review suggests that it is low. The risk of progression to tertiary syphilis in serodiscordant patients in the modern antibiotic era is unknown and ethical and logistical challenges make it unlikely that a study to address this issue will be forthcoming. Two retrospective studies (Wohrl and Tuddenham) suggest that the risk of neurosyphilis at the time of discordant test results is low. The risk of ophthalmic syphilis may be higher, but the lack of objective measures for this diagnosis makes drawing conclusions difficult
That is the key problem: the lack of objective measures for the diagnosis of ocular syphilis. There are other serologic tests for syphilis, but they still do not tell me if there is or is not syphilis in the eye.
It is not like they can stick a needle in the eye for culture or PCR. Since I can’t prove a negative, what is a poor ID doc to do but treat?
Rationalization
History of Syphilis.
http://cid.oxfordjournals.org/content/40/10/1454.full
Emerging trends and persistent challenges in the management of adult syphilis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4545322/#CR46
Sex Transm Dis. 2015 Jun;42(6):347-9 Neurosyphilis and ophthalmic syphilis in persons with negative rapid plasma reagin and positive treponemal antibody test results.
http://www.ncbi.nlm.nih.gov/pubmed/25970316
Screening for Syphilis With the Treponemal Immunoassay: Analysis of Discordant Serology Results and Implications for Clinical Management.
http://www.ncbi.nlm.nih.gov/pubmed/21930610
POLL RESULTS
I hate discordant
- syphilis serologies 9%
- cultures 15%
- socks 52%
- twins 6%
- derpy (google it) 9%
- Other Answers 9%
- duets
- Bagpipe music. It's hell (http://bit.ly/1KV9lle)
Chapter Two
The patient long ago used up all her veins and is now muscling her heroin.
Three months ago, she was admitted for an arm abscess that grew MRSA. It was debrided, but the blood cultures grew B. cereus. It was ignored and probably rightly so.
Now she is admitted with another abscess; this one grew MSSA and S. anginosis from debridement. Oddly, it was in the arm she does not inject in (because of tattoos), and she also denies needle licking, a frequent source of oral streptococci in IVDA soft tissue infections. Her dentition is particularly bad, but there are no stigmata of endocarditis on exam. No murmur, no emboli, no nothing, and the TTE is negative.
They call me when the blood grows B. cereus on day three, just like last time.
Hmmm. B. cereus is found in heroin. I never say contaminated as that makes it sound like the producers are trying to make a sterile product.
Aerobic endospore-forming bacteria (Bacillus spp. and Paenibacillus macerans) were the predominant microflora isolated and at least one species was isolated from each sample. B. cereus was the most common species and was isolated from 95% of all samples, with B. licheniformis isolated from 40%. Between one and five samples yielded cultures of B. coagulans, B. laterosporus, B. pumilus, B. subtilis and P. macerans. Staphylococcus spp. were isolated from 23 (40%) samples; S. warneri and S. epidermidis were the most common and were cultured from 13 (22%) and 6 (10%) samples respectively. One or two samples yielded cultures of S. aureus, S. capitis and S. haemolyticus. The remainder of the flora detected comprised two samples contaminated with C. perfringens and two samples with either C. sordellii or C. tertium. Multiple bacterial species were isolated from 43 (74%) samples, a single species from the remaining 15.
I mean, euw.
Not unsurprisingly, B. cereus bacteremia is not uncommon in heroin users. But is it endocarditis? I really do not want to send a recalcitrant IVDA out with a PICC.
The data would
suggest that heroin addicts are at risk for developing Bacillus bacteremias, which may vary in severity from endocarditis to benign transient bacteremias.
So we got a TEE, and it was pristine. I cannot see three months of endocarditis with no vegetation or emboli. So we are going to treat it as transient.
For hoots and giggles, I sent both cultures off for pulse-field electrophoresis to see if there are the same. If they are...
Rationalization
J Med Microbiol. 2002 Nov;51(11):1001-8. An investigation into the microflora of heroin.
http://www.ncbi.nlm.nih.gov/pubmed/12448685
Can J Infect Dis Med Microbiol. 2015 Mar-Apr;26(2):103-4. A cluster of Bacillus cereus bacteremia cases among injection drug users.
http://www.ncbi.nlm.nih.gov/pubmed/26015795
Arch Intern Med. 1979 Mar;139(3):293-4. The spectrum of Bacillus bacteremias in heroin addicts.
http://www.ncbi.nlm.nih.gov/pubmed/106784
POLL RESULTS
The greatest Joker of all time
- Heath Ledger 19%
- Jack Nicholson 11%
- Cesar Romero 4%
- Mark Hamill 15%
- Donald Trump 47%
- Other Answers 4%
- Steve Miller Band
- Red Skelton
Chapter Three
As I have said before: your spouse, your parents, your children, your pastor and your government are among those will lie to you if the opportunity arises. Cultures will not lie. Assuming, of course, you understand the significance of the cultures. So often it seems that people cannot find their ID butt with both hands in a brightly lit room.
As one example, I really wish that people would no longer treat Candida in the sputum. There is virtually no such thing as Candida pneumonia. Stop giving micafungin. And quit treating Candida in the urine with micafungin. Less than 15% of the drug gets in the urine. It is homeopathy. Next time you get the urge to treat either, just stand at the bedside and burn a pile of 400 one dollar bills. At least you could make s’mores on the flames rather than throwing away medications because you paid no attention in class.
What fries my bacon is not so much that people are acting as if all there is to ID is throwing an antibiotic at whatever grows on a culture. Well, that does increasingly piss me off. It is how often in the era of the internet, when the entirety of human knowledge is at your fingertips, people lack the curiosity to look it up. It took me 15 seconds to find Candida Pneumonia in Intensive Care Unit?, the third hit on a google search of ‘Candida pneumonia.’ How hard is it? Evidently very.
The patient is admitted with an increasing headache, and a CT shows VP shunt malfunction. The CSF is not all that bad, a slight increase in PMN’s and protein, but the shunt is externalized, and the CSF cultures grow E. coli.
And that means one thing: somehow the shunt has come into contact with stool. In all the cases, I have seen the shunt has eroded into the colon, but his abdominal exam is negative, and he has zero abdominal complaints. Still, I ordered a CT, and the RLQ has extraluminal air and little pockets of fluid. The radiologist suggested it was either a contained diverticular abscess or the residua of a shunt perforation of the colon. Since the tip of the shunt also grew a K. pneumoniae, you know which I option I choose.
What I do not understand is how the E. coli gets into the ventricular fluid. Sure, it is a direct shot, but from a bacterial point of view, the distance from the colon to the brain is like the distance to Boston for me. And for an E. coli, it would be like swimming upstream in molasses. I also wonder just how E. coli gets from the bladder to the kidney to cause pyelonephritis, same issues.
Rationalization
Candida Pneumonia in Intensive Care Unit?.
http://ofid.oxfordjournals.org/content/1/1/ofu026.full
Neurosurg Rev. 1998;21(2-3):194-7. E. coli meningitis as an indicator of intestinal perforation by V-P shunt tube.
http://www.ncbi.nlm.nih.gov/pubmed/9795961
POLL RESULTS
I trust
- cultures 18%
- money 5%
- NPR 13%
- Fox 0%
- my ID consultant; they can find their butt with both hands. 55%
- Other Answers 8%
- Murphy. All others pay cash.
- My right eye... but only the right.
- mark crislip.
Chapter Four
The patient is an elderly female admitted with fever and mild abdominal pain. WBC was normal, but she was hovering at 101. She had been on levofloxacin for a UTI on admission, and a CT showed stranding and a ten-year-old abdominal aneurysm repair.
Work up was negative, and five days later, a repeat CT showed a collection around the graft with no gas, infection, or new dissection. Radiology said either, and if the latter we sure don't want to biopsy it.
Which is it? Got me. I bet on simple dissection, but who knows. Blood cultures are negative, but she is on antibiotics, and E. coli is not high on the list for late graft infections. Salmonella and Clostridia would be less uncommon.
There are, as is often the case, multiple other medical comorbidities, and psychosocial issues that mediate against a definitive diagnosis.
Dissecting aneurysms alone can cause fevers. Early in my practice, I had a patient admitted on a Friday afternoon with fevers, what looked to be a conjunctival hemorrhage and new AI murmur.
After blood cultures, antibiotics were started, and since it was late on a Friday and the patient was clinically stable, I did not order a stat ECHO.
On Monday, the fever had not resolved, and the blood cultures were negative. So I ordered an ECHO, and there was a dissection of the ascending aorta.
He went to the OR and did just fine, but arrggghhh, I sat on a dissecting aneurysm for 72 hours. Sometimes it is better to be lucky than to be good. I, of course, am both. Modest too.
I think of that case with every fever and AI I see and resist the urge to look for my second case. I refuse to let past missed weirdness guide my care.
Still, I did present the case as an unknown to a visiting professor who had published a similar case, and he totally missed it.
We never did get a diagnosis and she was sent home on hospice.
Rationalization
Vascular. 2013 Feb;21(1):10-3. doi: 10.1258/vasc.2011.cr0294. Epub 2012 May 22. Infection of endovascular abdominal aortic aneurysm stent graft after urosepsis: case report and review of the literature.
http://www.ncbi.nlm.nih.gov/pubmed/22619381
Rev Esp Cardiol. 2010 May;63(5):602-6. Fever due to inflammation in acute aortic dissection: Description and proposals for diagnostic and therapeutic management.
http://www.ncbi.nlm.nih.gov/pubmed/20450855
POLL RESULTS
In deciding on diagnostic and therapeutic interventions, I am most guided
by
- past failures 23%
- past successes 13%
- current insecurity 30%
- the Wall Street Journal 7%
- randomness 17%
- Other Answers 10%
- the phase of the moon.
- the kindness of others.
- the invisible hand of the Flying Spaghetti Monster.
Chapter Five
Some diseases can be difficult to diagnose either because standard tests are negative, or the patient does not have symptoms. The two diseases that give me the most conniptions are syphilis and TB. And of the two? TB is the biggest pain since you have to worry about exposures. At least syphilis is not (usually) a work-related infection. It depends, I suppose, on your job.
The patient is an elderly male, smoker, from SE Asia, with several months of cough and wasting. CT showed a lower lobe mass. Three smears were negative for AFB, and the bronchoscopy was negative for cancer but did have atypical cells. So off to remove the cancer and the day after resection, the bronchoscopy is growing M. tuberculosis. Crap.
Can TB present like cancer and vice versa? You bet. It was someone else's honest miss, but now the question is how many employees to screen. The patient has been in the system for a couple of months, being evaluated for his cough.
We say that TB is ruled out with three negative smears, or at least infectious TB. Is TB infectious if smear-negative? Again, you bet.
In The Netherlands, patients with smear-negative, culture-positive TB are responsible for 13% of TB transmission.
and
Recent studies in San Francisco and Vancouver that used molecular linkage estimated that, for 17%–20% of patients with TB, TB resulted from transmission by patients with smear-negative TB.
and to be even more aggravating
An intriguing finding is that, compared with index patients with smear-positive TB, index patients with smear-negative TB were associated with a disproportionate number of secondary cases with smear-negative TB
Although the study does mention the chest radiography findings. My patient does not have cavitary TB, which is chock-a-block full of AFB, but a solid mass, so I suspect he is less infectious. Still, I need to figure out how much contact tracing to do.
The other case? I missed. It was an elderly SE Asian female I was asked to see for a Klebsiella hip infection after a pinning of a fracture. A smoker, she had fevers and hip pain but no pulmonary symptoms. The CXR, done for PICC placement, had “chronic interstitial infiltrates, unchanged from prior examination from a year ago." I didn’t give the lung a second thought, setting the patient up for iv antibiotics to treat the hip osteomyelitis. For a variety of reasons, the surgical cure of her hip was delayed and to be done at another institution. Insurance and all that.
A month later, I get a call that she is admitted to the other hospital with miliary TB, and her sputum is AFB positive. Crap. Did she have active TB when I saw her, or did it reactivate after discharge? I do not know. But if a patient is not coughing, are they infectious for TB? You bet, but perhaps less so
We also found that cough severity in the index case is significantly associated with high transmission and that the presence of cavitation on chest radiograph is also associated, albeit marginally, with increased transmission…The importance of cough frequency as a surrogate for TB infectiousness is well recognized. Overnight cough frequency has been associated with the proportion of contacts with a positive TST.
My first case in practice was a patient who became neutropenic from tmp/sulfa, reactivated, and died of miliary TB. The diagnosis was made on post-mortem cultures and autopsy. I think if I knew then what I know now, I might have made the diagnosis pre-mortem, but it is because of that patient I know now what I now know. I may be channeling Rumsfeld.
Humans have been plagued by TB our entire time as a species, and the prompt and accurate diagnosis of the disease still eludes us. I have only a few years left in practice, I wonder how many more cases I will miss.
Rationalization
Am J Respir Crit Care Med. 2013 May 1; 187(9): 1007–1015. PMCID: PMC3707366 Cough Aerosols of Mycobacterium tuberculosis Predict New Infection. A Household Contact Study
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3707366/
Tuberculosis Transmission by Patients with Smear-Negative Pulmonary Tuberculosis in a Large Cohort in The Netherlands.
http://cid.oxfordjournals.org/content/47/9/1135.long
South Asian J Cancer. 2012 Jul-Sep; 1(1): 36–42. doi: 10.4103/2278-330X.96507 PMCID: PMC3876596 Pulmonary tuberculosis as differential diagnosis of lung cancer.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876596/
PLoS One. 2014 Jul 2;9(7):e100984. doi: 10.1371/journal.pone.0100984. eCollection 2014. Importance of cough and M. tuberculosis strain type as risks for increased transmission within households.
http://www.ncbi.nlm.nih.gov/pubmed/24988000
Chapter Six
The patient is admitted septic from cellulitis of the chest wall. MOSF, she has no signs of toxic shock, only septic shock, which is bad enough.
Within 12 hours blood cultures grow gram-positive cocci in chains and a CT, in anticipation of surgery, says
Chest: There is fairly extensive intravascular air identified. Gas is seen non-dependently within the left jugular and subclavian veins in a small amount. There is a much larger volume seen within the right external jugular, internal jugular, subclavian, cephalic, and the brachiocephalic veins. Small amount of air is seen within the main pulmonary outflow tract and the right ventricle. Typically this is not clinically relevant and related to contrast injection; however, the volume and location are atypical. There are inflammatory changes identified involving the fat of the right axilla and extending up into the thoracic outlet. No discrete abscess is identified. There is no definite subcutaneous air.
No gas in the tissues but gas in the vascular tree? What?
While most life makes gas, as my male children like to demonstrate loudly and proudly, I cannot find any cases of Group A Streptococcus making gas with necrotizing fasciitis nor causing a pyogenic vasculitis.
I have never seen gas reported in the vascular tree after CT, but it turns out it is not uncommon:
Iatrogenic vascular air emboli were seen in 14 patients (7% of total). The locations of air emboli were main pulmonary artery in 12 (6% of total), left brachiocephalic vein in 3 (1.5% of total), right atrial appendage in 4 (2% of total), and superior vena cava (SVC) in 1 (0.5%) patient.
Usually, the gas from CT is harmless, although there are a few bad outcomes reported.
The CT was repeated a few hours later, and gas was all gone. The cultures were identified S. pyogenes and, after debridement, she did as well as can be expected.
Gas is usually nothing or catastrophic and rarely in between. This time it was nothing. But gas always makes you nervous.
Rationalization
Lung India. 2015 May-Jun; 32(3): 216–219. doi: 10.4103/0970-2113.156216 PMCID: PMC4429381 Vascular air embolism after contrast administration on 64 row multiple detector computed tomography: A prospective analysis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429381/
Chapter Seven
I am off this weekend, although that will make little difference. Even when I turn my beeper off, I still feel the occasional phantom vibration on my right hip or a distant beep in the middle of the night. And I am not the only one.
Of the 169 participants who answered the question, 115 (68%, 95% confidence interval 61% to 75%) reported having experienced phantom vibrations. Most (68/112) who experienced phantom vibrations did so after carrying the device between 1 month and 1 year, and 13% experienced them daily. Four factors were independently associated with phantom vibrations: occupation (resident v attending physician, prevalence ratio 1.47, 95% confidence interval 1.10 to 1.97), device location (breast pocket v belt, prevalence ratio 1.66, 1.29 to 2.14), hours carried (per 6 hour increment, prevalence ratio 1.30, 1.07 to 1.58), and more frequent use in vibrate mode (per frequency category, prevalence ratio 1.18, 1.03 to 1.34). Of those who experienced phantom vibrations, 43 (39%, 30% to 48%) were able to stop them. Strategies for stopping phantom vibrations included taking the device off vibrate mode, changing the location of the device, and using a different device (success rates 75% v 63% v 50%, respectively, P=0.217). However, 39% (30% to 49%) of respondents did not attempt any strategies.
Oh well. At least I do not have phantom limb sensations.
The patient has an odd pattern. Six weeks ago, she had an isolated bone-chilling rigor. Could not hold a glass of water without spilling it.
Two weeks ago, the same thing and it was associated with a fever to 102.
And then a third, leading to admission.
Blood cultures grew S. intermedius.
ROS and evaluation for a reason are negative except for a sclerotic valve, but no endocarditis. The patient is on warfarin for endocarditis, and I have always wondered it warfarin leads to false-negative EHCO since vegetations are mostly clot. Some budding cardiologist get to work on this before I retire. But who has three rigors in 6 weeks with endocarditis? They should be febrile every day.
On the CT of the abdomen, there was thrombosis in the left portal vein. Septic thrombophlebitis? Again, she should be more febrile more often. And there was no liver pathology.
There is one case of septic portal vein with S. intermedius associated with diverticulitis.
There is the suggestion of a bone or some other radio-dense material poking into a mildly inflamed diverticulum. It is denser than a toothpick, which seems to lead the list with foreign body perforations, followed by chicken bones.
Probably all diverticular given the symptoms, but I am going to treat for septic clot in the portal vein. Safe >> sorry.
And I learned a new word today preparing this entry. Gossypiboma: a mass of cotton matrix left behind in a body cavity intraoperatively. I just do not see how I am going to use it in a sentence today.
Rationalization
BMJ. 2010 Dec 15;341:c6914. doi: 10.1136/bmj.c6914. Phantom vibration syndrome among medical staff: a cross sectional survey.
http://www.ncbi.nlm.nih.gov/pubmed/21159761
BMJ Case Rep. 2013 Feb 5;2013. pii: bcr2013008661. doi: 10.1136/bcr-2013-008661. Septic thrombophlebitis of the superior mesenteric vein with bacteraemia caused by Bacteroides fragilis and Streptococcus intermedius as a complication of diverculitis.
http://www.ncbi.nlm.nih.gov/pubmed/23389727
Cir Cir. 2015 Jun 30. pii: S0009-7411(15)00105-X. doi: 10.1016/j.circir.2015.05.029. [Pylephlebitis: a rare but possible complication of intra-abdominal infections].
http://www.ncbi.nlm.nih.gov/pubmed/26141109
World J Emerg Surg. 2014 Dec 19;9(1):63. doi: 10.1186/1749-7922-9-63. eCollection 2014. Toothpick ingestion complicated by cecal perforation: case report and literature review.
http://www.ncbi.nlm.nih.gov/pubmed/25584065
POLL RESULTS
I
- feel phantom beeper vibrations 22%
- hear phantom overhead pages. We call it hearing voices in the biz. 11%
- have acid flashbacks, man 2%
- have deja vu all over again 18%
- clearly remember events that never happened 44%
- Other Answers 2%
- remember too much, and too little, and neither helps.
Chapter Eight
Certain diagnoses annoy me. Atelectasis, as a cause of fevers, is one example. It doesn’t. Cause a fever that is.
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 medical students assure me that they are taught on their surgical rotation that yes, atelectasis is a cause of post-op fever. Atelectasis does, of course, give the team an excuse to do nothing, and most post-op fevers subsequently go away on their own.
The patient is a healthy 20-year-old, first pregnancy, s/p a C-section 14 days ago. She did well the first ten days, then had fevers, rigors, leukocytosis to 26 with a left shift, and was admitted.
CT showed the usual post-C-section uterus, but there were several rim enhancing collections that were called either blood or infection. After four days of fever, they called me.
I am primitive. Them thars abscesses, not blood. Abscess nicely accounts for the clinical picture. They need drainin’.
Ob-Gyn was worried this was a thrombophlebitis, septic or otherwise, that was causing the prolonged fever and started heparin.
Pelvic thrombophlebitis is another diagnosis that annoys me. So often over the years; there has been zero objective evidence for clot. None seen here. And if clot in the pelvis causes fevers, then how come none of the other clots I see cause fevers. DVT is as common as a lack of vaccine understanding by Presidential candidates, but unless they break loose (the clot, not the candidate), they do not cause fevers.
There is no clot, no positive cultures, so it is hard to credit either for the fevers from the vascular tree.
The history of the process suggests once upon a time infected clot may have been from Group A Streptococcus or Clostridia, but over time the syndrome has almost vanished as a clinical entity, with just 69 cases in 44,922 deliveries in one series.
A recent review suggests that much of the time the diagnosis is about as valid a cause of fever as atelectasis and
The absence of a definitive diagnostic technique made it difficult to corroborate a clinical suspicion and compare the effectiveness of treatment regimens proposed.
No kidding. And anticoagulation doesn’t seem to do much either.
And these veins are so piddly. The ovarian and pelvic veins are tiny and seem insignificant compared to the symptoms supposedly caused by the infected and uninfected clot I see in other places.
Now I am not Ob-Gyn by a long shot, but after reading over the literature, I agreed with one study that noted
Currently available imaging studies cannot diagnose the entity we now define as septic pelvic thrombophlebitis (once cases of ovarian vein thrombosis are excluded). Our findings do not support the time-honored rule that septic pelvic thrombophlebitis responds within 24-48 h to therapeutic anticoagulation with heparin. Therefore, criteria other than imaging studies or immediate defervescence following heparin therapy are necessary for diagnosis of septic pelvic thrombophlebitis. A more appropriate terminology for septic pelvic thrombophlebitis should be refractory postpartum fever of undetermined etiology.
If you are an OB doc reading this and respond with an anecdote rather than a robust reference, remember the plural of anecdote is anecdotes, not data. Thanks to motivated reasoning, I have yet to be dissuaded of the opinion that the three most dangerous words in medicine are ‘In my experience.’
Septic thrombophlebitis of pelvic veins does happen on occasion, albeit very rarely, but I think at a minimum it would have, oh, I don’t know, clot and positive cultures?
So color me unsatisfied.
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
Septic Pelvic Thrombophlebitis: Diagnosis and Management.
http://www.hindawi.com/journals/idog/2006/015614/abs/
J Matern Fetal Med. 1996 Nov-Dec;5(6):355-8.
Septic pelvic thrombophlebitis or refractory postpartum fever of undetermined etiology.
http://www.ncbi.nlm.nih.gov/pubmed/8972414
POLL RESULTS
I am most annoyed by
- the idea that atelectasis is a cause of fevers 4%
- antibiotics used as antipyretics 26%
- people calling for approval of antibiotics, and they cannot pronounce it. Ciprofloxacillin. Moron. 14%
- Dr. Oz combined with Google U. 44%
- a consult for endocarditis, and the patient has nail polish on all their nails. 7%
- Other Answers 4%
- changing ATBs before 48 hours when the patient is getting better.
- antibiotics and no S/S of infection
Chapter Nine
Just Another Day at the Hospital
The patient had the relatively sudden onset of right anterior chest pain. He has no fevers, chills or NS, but is uncertain as he has been intermittently short on his heroin supply and has had some withdrawal during this time. He is seen in the ER, and a CT reveals a mass in the chest wall where the first rib is connected to the sternum, eroding into bone, the chest wall, and pleural space.
CBC and blood cultures are normal and negative, respectively, and it is called a tumor. He is old enough and smokes enough for tumor be a reasonable presumptive diagnosis.
The pain worsens over the next week, and he is admitted since the mass has increased in size. Still no constitutional signs, and he goes for biopsy.
One of the hospitalists shows me the case, wondering what it might be given the lack of infection signs. I figure it was most likely a cold MSSA abscess or perhaps a fungus, but the rib is a distinctly odd place to get a hematogenous infection.
Call me if it is an infection.
And call me they did as it was MSSA.
The interesting thing is that he does have trauma to the rib. He says it goes out of joint all the time and has to be pushed back in. I did not know there was any such process, but I guess it is a form of the slipping rib syndrome.
Slipping rib syndrome is a condition that is often misdiagnosed or undiagnosed and can subsequently lead to months or years of unresolved abdominal and/or thoracic pain. Surgical findings suggest the condition arises from hypermobility of the anterior ends of the false rib costal cartilages, which often leads to slipping of the affected rib under the superior adjacent rib. This slippage or movement can lead to an irritation of the intercostal nerve, strain of the intercostal muscles, sprain of the lower costal cartilage, or general inflammation in the affected area.
The medical literature primarily refers to this condition as slipping rib syndrome. However, it has also been referred to as clicking rib, displaced ribs, interchondral subluxation, nerve nipping, painful rib syndrome, rib tip syndrome, slipping rib cartilage syndrome, traumatic intercostal neuritis, and 12th rib syndrome. Even though slipping rib syndrome was first described in 1919 and many cases have been described in the medical literature, this condition is rarely mentioned in present-day medical textbooks.
Although, as I roam the PubMeds I find all sorts of hypermobile rib syndromes, including dislocations and subluxations. The ribs can wander more than my attention at Grand Rounds. Squirrel! I suspect his intermittent rib dislocation, if that is what he had as the current CT shows shattered bone, was sufficient trauma to result in a place for the MSSA to land.
If there has ever been an infection in a rib dislocation/slip/subluxation, I can’t find one. So this is the first, and you know what that means don’t you? Going forward, you now have to, just have to, include this in your differential diagnosis of chest pain in the future.
Long time readers of the blog know how much I hate that conclusion in papers. Look at the third reference. It says
Although an uncommon disease, hematogenous osteomyelitis should be considered in the differential diagnosis of destructive lesions of the rib.
And I always think, screw you. I am not going to consider every weird disease manifestation ever reported. Common things are common. I bet those authors bore every physician that crosses their path with the weird case of rib osteomyelitis they saw back in the day. On second thought, isn’t that the raison d’etre of this blog? Perhaps I better tone it down.
The other thing is a beta d glucan was sent, and it was slightly positive at 97. Real? Maybe. This web page ()http://www.biocyc.org/SAUR158878/NEW-IMAGE?object=Beta-D-Glucans suggests that S. aureus can make beta D glucans, but I am not certain if it could react with the assay and biochemistry turns me into Mr. Gumby.
Staphylococcus bacteremia is a cause of a positive beta d glucan:
On day 7, 14 patients from group B (without fungal infections) had (1,3)-b-D-glucan levels 40 pg/ml: six patients had concurrent bacterial infections including pneumonia (n = 2; Streptococcus pneumoniae, Staphylococcus aureus), osteomyelitis (S. aureus), peritonitis, and catheter-associated bacteremia (n = 2; Staphylococcus epidermidis).
Another cold abscess, a new cause of infected chest walls and a potential reason for a true false positive (false true positive? You know what I mean) beta d glucan.
My son says ID is easy. All I ever say on the phone is check blood cultures and start vancomycin. It is not always quite that straight forward.
Rationalization
Slipping Rib Syndrome in a Collegiate Swimmer: A Case Report.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1150226/
Invasive fungal infections and (1,3)-β-d-glucan serum concentrations in long-term intensive care patients.
http://www.ijidonline.com/article/S1201-9712(08)01740-2/pdf
Acute hematogenous osteomyelitis of the rib.
http://www.ncbi.nlm.nih.gov/pubmed/6216594
Gumbys
https://montypython.fandom.com/wiki/Gumbys
Chapter Ten
The patient presents to the ER with hemoptysis and pleuritic chest pain. She had been well until the day of admission with no constitutional complaints. The CT done in the ER showed numerous fuzzy round lesions throughout both lung fields.
She was barely febrile, did not look toxic, had a minimally elevated WBC, and her blood cultures and ECHO were negative.
Her history is negative. No past medical history, she had been in jail for the three months prior to admission. As soon as she was released, she started using IV heroin and meth and, within 72 hours, was in the hospital.
She was clean in jail with no odd exposures while incarcerated and, with the exception of the drugs, no odd exposures since release.
So I couldn’t figure out an infection that would be culture-negative and cause so little symptoms outside of hemoptysis. The pattern on CT suggested a hematogenous etiology. So we started talking.
The heroin is standard issue mixed with tap water and filtered thought a cotton ball. I do not think this is cotton fever. Too extensive on CT.
The meth? She noted that it did not have the kick is was supposed to and wondered what it was. She tells me that meth is frequently adulterated with bath salts.
I think this is from the meth, or what passed for meth, a foreign body granulomatosis from the material being wedged in the microcirculation of the lung. She was bronched with no diagnosis (and no biopsy), the ANCA is negative. The only way we would be able to get the diagnosis is an open lung biopsy, which, as the patient improved, we did not do.
Back when I was an intern, we used to see a lot of pulmonary disease due to inorganic material in heroin, usually talc. Thanks to the power of capitalism, since I was an intern drugs have become both cheaper and purer, and I get the sense there is not as much heroin associated lung disease.
I cannot find a similar process as is seen from heroin reported from meth or bath salts, so my diagnosis is in the realm of hypothesis rather than reality. But that's my story, and I am sticking to it.
Rationalization
Forensic Sci Int. 2010 Apr 15;197(1-3):e27-30. doi: 10.1016/j.forsciint.2009.12.066.
Widespread pulmonary granulomatosis following long time intravenous drug abuse—a case report.
http://www.ncbi.nlm.nih.gov/pubmed/20137873.
One of multiple references.
The Toxicology of Bath Salts: A Review of Synthetic Cathinones
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550219/
Chapter Eleven
The patient had a surgical resection, a flap, and radiation of the chest wall six months prior to admission.
Two days prior to admit there was the abrupt onset of severe chest wall pain, fevers, and rigors.
The exam showed an exquisitely tender chest wall, but it was not red, hot, or focally swollen.
Blood cultures grow MSSA three days apart, and a small abscess was found on the CT that also grew MSSA.
The sine qua non of endocarditis is a sustained bacteremia, and positive blood cultures three days apart fits the bill.
Chest wall abscess is odd, and I had thought it most likely the chest wall was seeded from the bacteremia, the area of prior radiation being fertile soil for bacterial growth. I have seen a few infections over the years in areas of previous radiation. It may be a confirmation bias as there are not many references to suggest irradiated soft tissues have an increased risk for focal infection independent of prosthetic material.
The chance for implant infection was 4.88 times greater for implants that were exposed to radiation therapy compared with those that were not.
But, I am embarrassed to say, there was a key part of the history I missed. There was an ornate tattoo on the chest that I did not pay attention to as it looked fine. Tattoos are so common these days they have become part of the background noise if they do not look infected. It turned out, as the intern discovered, that the tat had been placed two weeks prior in an attempt to cover up the radiation dermatitis.
Is that the source of infection? A tat on radiation-damaged tissues seems a sufficient enough trauma, but at two weeks, the trauma was a bit distant in time from the clinical infection. I figure that S. aureus defines acute infection. The skin around the tattoo looked fine; the soft tissue involvement was deep.
There are a smattering of S aureus infections associated with tattooing, mostly in prisons and other areas with decreased hygiene like North Carolina, Ohio, Kentucky, and Vermont:
The situation is complicated by illegal tattoo artists offering less-expensive artwork, as their bargain prices often involve stinting on sterile technique.
and the
use of nonsterile equipment and suboptimal infection-control practices were identified as potential causes of the infections.
I wonder how the science education is in those states. It probably doesn't include germ theory. You get what you pay for; cheap is cheap. Although my patient got their tattoo from a reputable establishment.
References
Infectious complications following breast reconstruction with expanders and implants.
http://europepmc.org/abstract/med/12900604
Outbreak of Skin Infections Due to Panton-Valentine Leukocidin-Positive Methicillin-Susceptible Staphylococcus aureus in a French Prison in 20102011.
http://www.ncbi.nlm.nih.gov/pubmed/24619564
Illegal tattoos complicated by Staphylococcus infections: a north Carolina wound care and medical center experience.
http://www.ncbi.nlm.nih.gov/pubmed/25876168
Methicillin-resistant Staphylococcus aureus skin infections among tattoo recipientsOhio, Kentucky, and Vermont, 20042005.
http://www.ncbi.nlm.nih.gov/pubmed/16791134
Chapter Twelve
Out, out, brief candle! Life's but a walking shadow, a poor addict, That shoots his heroin upon the stage, And then is heard no more.
I feel sorry for IVDA. We have 13.8 billion years of the void behind us and an infinity of void in front of us, and they spend their brief existence with the monkey of addiction on their back. It is sad, and I think there but for the grace of evolution go I. Still, maybe heroin is no worse than compulsive blogging for dealing with the angst existence.
IVDA has shortened lives: murder, exposure, suicide, overdose, and infection are all potential causes of early mortality. And dead people can’t turn their lives around.
I have had a tonne of IVDA with infections this month. In talking with them, there seems to be a lack of awareness of proper technique as a way of avoiding infection and an early grave. It is a habit that people acquire without proper preparation and education.
So here is some advice for IVDA's and potential IVDA for avoiding some of the potential infections with your habit. Every one of these has been done by at least one patient I have seen.
Heroin is not sterile. It is a natural, organic material that is chock-a-block full of bacteria and yeast. Fortunately, most of the organisms are not particularly pathogenic, and if you cook the heroin, you may kill a good number of germs.
Do not use tap water, Culligan water, toilet water, puddle water spit, or old liquified clot. They are not sterile. Use sterile water or at least boil the water before using.
Don't lick your needle: the mouth contains vast quantities of bacteria, and, let's be honest, IVDA and good dental hygiene do not go hand in hand. And don’t lick your injection site either.
When you filter the drugs though cotton balls, know that not all cotton balls are sterile and can contain bacteria, including Pantoea from the cotton weevil colon.
Do not inject into the muscles or skin pop. The former can lead to an abscess and the latter to gas gangrene.
Don’t share needles and syringes. It is an excellent way to pass of hepatitis and HIV.
Wipe the injection site with alcohol and let the alcohol dry before injecting.
Simple things to prolong life by avoiding infections, but easier said than done. There are some interesting resources on the web that describe the ‘proper’ way to use heroin, but they might as well on display in the bottom of a locked filing cabinet stuck in a disused lavatory with a sign on the door saying ‘Beware of the Leopard. Most of my IVDA are homeless, with little education and no resources. How and where they are going to come across this information is beyond me.
So I suppose the needless death will continue.
Rationalization
Years of Potential Life Lost among Heroin Addicts 33 Years after Treatment.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2039886/
Causes of death in a cohort treated for opioid dependence between 1985 and 2005.
http://www.ncbi.nlm.nih.gov/pubmed/23961881
POLL RESULTS
I deal with existential angst with
alcohol 18%
SSRI's 7%
eating 11%
reading medical blogs 27%
denial 27%
Other Answers 11%
Playing video games
alcohol, eating, reading, listening to music
Gardening
sleep, perchance to dream.
spice melange
Herpetophobia
Chapter Thirteen
I get asked to see a patient because of a right lower lobe lung abscess.
The patient has an Oslerian presentation— the abrupt onset of fever, rigor, SOB, productive cough, and right-sided pleuritic chest pain. I say Oslerian as years ago, I ran across a book of disease descriptions by Osler, and one was pneumococcal pneumonia. It presents just like this patient.
The CXR had RLL consolidation, but the CT (Don’t ask. Who doesn’t get a CT these days?) had a cavity in the RLL with a nice meniscus of pus. The cavity was not seen on the CXR. A lung abscess/necrotizing pneumonia. So it could not be pneumococcal pneumonia, right?
Thing is, with the higher resolution of CTs we find all sorts of pathology we did not see back in the days of simple x-rays. CTs can result in articles in the NEJM, such as CT findings in the common cold. The mind-boggling aspect about the study was 14 patients had two, yes two, CTs.
As one critic noted
It is surprising that a journal of your reputation would publish a report on a small, uncontrolled study in which an expensive test, delivering a substantial dose of radiation to the eyes, demonstrates a well-known anatomical finding, with no appreciable benefit resulting from the exercise.
I still think that it is the dumbest study in the highest-rated journal ever.
The patient improved dramatically with 24 hours of ceftriaxone, so I suspect it was all pneumococcal pneumonia since that is about the only infection the usually gets better in 24 hours. Oh, and the pneumococcal urinary antigen was positive.
Like the common cold, if you CT patients with pneumonia, you will find more pathology:
In 351 cases of pneumococcal pneumonia, necrosis was reported in no (0%) original CXR readings and in 6 of 136 (4.4%) CTs. With rereading, 8 of 351 (2.3%) CXR and 15 of 136 (11.0%) CT had necrotizing changes. Overall, these changes were identified in 23 of 351 (6.6%) patients. The incidence of bacteremia and the admitting SMART-COP and PORT scores were similar in patients with and without necrosis (P = 1.00, P = .32, and P = .54, respectively). Type 3 pneumococcus was more commonly isolated from patients with necrosis than from patients without necrosis (P = .05), but 10 other serotypes were also implicated in 16 cases for which the organism was available for typing.
Although in the case of pneumonia, it might actually change therapy. In this case, there was a rapidly progressing empyema that needed a VATs.
Never did grow a Pneumococcus, but the patient did fine.
Rationalization
N Engl J Med. 1994 Jan 6;330(1):25–30. Computed tomographic study of the common cold.
http://www.ncbi.nlm.nih.gov/pubmed/8259141
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://www.ncbi.nlm.nih.gov/pubmed/22042878
South Med J. 2011 Aug;104(8):593-7. doi: 10.1097/SMJ.0b013e3182273b82. Incidence and impact of false-positive urine pneumococcal antigen testing in hospitalized patient.
http://www.ncbi.nlm.nih.gov/pubmed/21886070
Chapter Fourteen
The patient comes in with urosepsis and bacteremia with K. pneumoniae. Not that uncommon, she responds to ceftriaxone.
Klebsiella, with the expection of the serotypes K 1 & K2, has little propensity for causing metastatic focus. There are hundreds of thousands of Enterobacteriaceae bacteremias a year in the US and only a handful of metastatic complications.
And, as would be expected, she responded to the therapy and rapidly improved on ceftriaxone.
You know it is not going to end there.
Five days into the hospitalization, she develops abdominal pain, and a CT shows that her known abdominal aneurysm is leaking, and she is whisked off to the OR where it is bypassed and resected. The surgeon told me that the abdominal cavity did not look particularly inflamed.
I told the surgeon that it was unlikely for the K. pneumoniae to seed the graft or the aneurysm. But then the bulk of my practice is based on the unlikely occurrences.
In the OR, the surgeon sent off cultures of the aneurysm and a few days later all the clot from the aneurysm is growing K. pneumonaie. Infection is probably the reason it leaked.
There is one case I can find of K. pneumoniae infecting a pre-existing AAA, although there may be a few more buried in case series. It is safe to say that as a cause of infecting pre-existing aneurysms, K. pneumoniae is rare. I tend to think of Salmonella and Clostridia.
It is a good thing she went to the OR as antibiotics alone are not a good idea:
Treating an infected aortic aneurysm with antibiotics alone could not stop aneurysm expansion and eradicate the aortic infection before the aneurysm ruptures.
And I have to admit I was surprised that anyone even tried antibiotics alone.
Again, the patient did very well post-op and was discharged on lifetime antibiotics.
Rationalization
BMJ Case Rep. 2013 Apr 3;2013. pii: bcr2013008690. doi: 10.1136/bcr–2013–008690. Klebsiella pneumoniae liver abscess and endophthalmitis.
<https: data-preserve-html-node="true"//pubmed.ncbi.nlm.nih.gov/23559652/>
J Mt Sinai Hosp N Y. 1969 Jan-Feb;36(1):10–4. Aortic aneurysm infected with Klebsiella pneumoniae, serotype 1. Case report.
http://www.ncbi.nlm.nih.gov/pubmed/7240614
J Vasc Surg. 2012 Oct;56(4):943–50. doi: 10.1016/j.jvs.2012.03.018. Epub 2012 May 19. Treatment of primary infected aortic aneurysm without aortic resection.
http://www.ncbi.nlm.nih.gov/pubmed/22608792
Chapter Fifteen
I once counted up the number of bugs I need to know to be an ID doctor. About 1200. Not that many, but there are a few diseases I have yet to see. I have never seen a case of measles, although I may yet. I have yet to see Bubonic Plague or Rocky Mountain Spotted Fever. Maybe someday.
Some diseases I never expect to see more than once in a career.
Middle-aged patient is admitted with fevers and arterial embolic events. He needs to go to the OR to have clot removed from popliteal arteries.
His blood cultures grow MRSA, so it is going to be endocarditis. I have seen a tonne of these over the last 30 years. And the ECHO?
A left atrial myxoma.
So this is an infected left atrial myxoma.
I had a case maybe half a career ago where the myxoma was infected with an alpha Streptococcus. I figured, given the rarity of myxomas, I would never see a second.
There are a surprising number of hits (56) on the PubMeds for infected myxomas. I suppose their propensity to form clot leads to a fertile soil upon which bacteria can grow.
I have no great teaching points. This is a 'hey, look at the cool case.' Except.
I am always hesitant to get ECHOs on every patient who obviously has endocarditis to prove the diagnosis that is already made. I tend towards getting ECHOs when there is uncertainty, or I am concerned about a complication that will require surgical intervention.
So that is maybe three cases I can remember in 29 years of ID where an obvious case of endocarditis was something else: two myxomas and one dissecting ascending aortic aneurism.
I guess that is part of the medicine that is not cost-effective: every once in a while, you find a zebra when everything points to a horse.
And I suppose if you practice long enough, you will eventually see not only one of everything but two. But I still do not want to see a case of measles.
Rationalization
Infez Med. 2007 Dec;15(4):256–61. Infected atrial myxoma: case report and literature review.
http://www.ncbi.nlm.nih.gov/pubmed/18162737
Chapter Sixteen
“It is a far, far better thing that I do, than I have ever done; it is a far, far better test that I order than I have ever known.”
Two patients with identical issues:
Dialysis patients with pacemakers, both with sustained MRSA bacteremia for no reason. Both with negative exams. Both with negative TEEs. Both with fistulas. Both dependent on the pacemaker.
Pull the pacer? Revise the shunt? Treat and hope for the best?
I decided to order PET scans. There is an interesting literature using PET scans for a variety of ID issues. The problem in the US is they are usually only paid for if looking for cancer and they cost a pretty penny. But they are useful for FUO, and there are
promising results for patients presenting with infective endocarditis, especially for secondary infectious foci, or for patients presenting with suspected infection of pacemakers or implanted defibrillator; but results are still preliminary and must be confirmed.
There are intriguing case reports, and I would wager that the negative cases are not reported. The same issue with vascular graft infections. And I do not know the predictive value of a negative test. But I needed a compelling reason to pull the pacer.
So case 1 had a completely normal PET. But with no other explanation for the bacteremia, the pacer was pulled, and the wire culture was negative. We planned on treating for 4 weeks with vancomycin, but on week two, the blood cultures were still positive for MRSA. The blood cultures became negative on daptomycin, but we, and by we I mean I, do not know where the MRSA focus was. But he was cured.
Case 2, the PET scan glowed in the fistula but not the pacemaker. The fistula was explanted and was covered in pus that grew MRSA. The pacer was left in for cardiac reasons (patients don’t like a resting pulse of 20), and the patient has done fine.
The take-home? I don’t know. One helpful PET, one not so much.
It was the best of tests, it was the worst of tests?
Rationalization
Med Mal Infect. 2014 Jun;44(6):251–60. doi: 10.1016/j.medmal.2014.04.007. Epub 2014 May 18. Contribution of 18fluoro-deoxyglucose PET/CT for the diagnosis of infectious diseases.
http://www.ncbi.nlm.nih.gov/pubmed/24844599
Int J Infect Dis. 2014 Feb;19:87–90. doi: 10.1016/j.ijid.2013.10.011. Epub 2013 Nov 28. Pacemaker-related infection detected by (18)F-fluorodeoxyglucose positron emission tomography-computed tomography.
http://www.ncbi.nlm.nih.gov/pubmed/24291467
Int J Cardiol. 2013 Sep 1;167(5):1724–36. doi: 10.1016/j.ijcard.2012.12.005. Epub 2013 Jan 11. 18FDG-positron emission tomography (PET) has a role to play in the diagnosis and therapy of infective endocarditis and cardiac device infection.
http://www.ncbi.nlm.nih.gov/pubmed/23313465
Ann Vasc Surg. 2015 Aug;29(6):1321.e1–4. doi: 10.1016/j.avsg.2015.03.053. Epub 2015 Jun 14. Should white blood cell scan be replaced by (18)F-FDG PET-CT in the diagnosis of prosthetic vascular graft infection?
http://www.ncbi.nlm.nih.gov/pubmed/26080300
Chapter Seventeen
I am always amazed at what IVDAs will not do. I recently had a patient with classic right-sided endocarditis leave AMA after only three days of iv antibiotics. And another who was semi-paralyzed from a cervical spine epidural abscess who, while barely being able to walk post-op, also left AMA in the middle of the night. Both needed a fix. The siren call of heroin addiction is more powerful than the need to live. It is sad how often drug users ignore life-saving medical advice.
The patient was admitted three weeks ago with a week of back pain shortly after a fall. MRI showed a discitis in the lumbar spine, and the blood cultures and disc biopsy were positive for E. coli.
A long term heroin user, I figured she became infected with the E. coli from the water she uses to mix the heroin. E. coli is not found in heroin. Tap water is not sterile, and occasionally coliforms slip in at low levels. And sometimes at not so low levels. By EPA rules, in the US, 5.0% of sampled water can be coliform-positive in a month. Mmm. Tap water. Not that bottled is much better.
Where there are humans, there are coliforms. And worse.
She defervesced right away, and repeat blood cultures were negative. So we, and by we, I mean me, treated with 6 weeks of iv ceftriaxone.
She was back two weeks later with CHF, a vegetation on her mitral valve, and severe MR.
Huh. Last admit, I did not order an ECHO since E. coli bacteremia is common, but causing endocarditis is very rare.
We review the literature that summarizes a total of 41 cases, with a predominance of elderly women, diabetics, and patients with urinary tract infections and prosthetic heart valves.
Native valve cases in the literature are about a dozen. Ever. And that's with 100,000 plus cases of E. coli bacteremia a year just in the US.
That is the aggravating issue in clinical medicine. If you don’t do every test every time on every patient, you will occasionally miss or delay in making a diagnosis. But it is wrong to do studies when the yield is minuscule, and doing tests leads to false positives, further workup, and harm.
So annoying.
No harm was done, fortunately, but E coli endocarditis with progressive valve failure is a reason for surgery.
But.
The patient was clear on two issues: she fully intended to continue to use heroin, and she did not want surgery. And she too left AMA.
Progressive heart failure from endocarditis would not be my preferred way to die. But it will not be the first IVDA who chose that path.
Rationalization
J Infect Dis. 2005 May 1;191(9):1523–9. Epub 2005 Mar 22. Burden of community-onset Escherichia coli bacteremia in seniors.
http://www.ncbi.nlm.nih.gov/pubmed/15809912
Diagnosis of E.Coli Tricuspid Valve Endocarditis: A Case Report.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3071200/
Enferm Infecc Microbiol Clin. 2011 Apr;29(4):276–81. doi: 10.1016/j.eimc.2010.12.007. Epub 2011 Feb 22. [Left-sided endocarditis due to gram-negative bacilli: epidemiology and clinical characteristics]
http://www.ncbi.nlm.nih.gov/pubmed/21334783.
POLL RESULTS
To be on the safe side, I only drink
- filtered tap water 16%
- bottled water 7%
- whatever the 'in' fluid is. Coconut water at the moment. 2%
- beer 45%
- my own urine 14%
- Other Answers 16%
- well water
- Bourbon
- when I am not on call or driving
Chapter Eighteen
I graduated medical school in 1983, long before the current crop of housestaff was a failure of contraception. There was a lot we did not know back in the day, and what we did know was hard to find in the literature. Going through the Index Medicus and the stacks was a slow way to learn new information.
I remember the day I recycled a stack of papers as tall as me, realizing that with Pubmed and the Googles, I need never save a paper again. With the worlds information is at our fingertips, no question needs to go unanswered as long there is an internet connection. Last week on our daily constitutional, there were all these bugs in the air I had never seen before. Taking out my phone, I Googled (with speech recognition no less so did not even need to stop) “white bugs Portland” and found out all about the Ash whitefly infestation. It still amazes me I can learn anything at any time.
Which is why I do not understand why myths continue to be perpetuated in housestaff. It seems that people are still happy to take nonsense at face value.
Look it up. It isn’t hard.
I was asked to see a patient because of a complicated intra-abdominal infection that grew, among other organisms, Pseudomonas.
In the middle ages, they had demons to fear; in modernity, it is Pseudomonas. Despite the fact the patient was clinically stable, it was Pseudomonas, and they had to ‘double cover.’
With cefepime and pipercillin/tazobactam.
Eye roll at Dunning Kruger in action.
The Dunning-Kruger effect, named after David Dunning and Justin Kruger of Cornell University, occurs where people fail to adequately assess their level of competence — or specifically, their incompetence — at a task and thus consider themselves much more competent than everyone else. This lack of awareness is attributed to their lower level of competence robbing them of the ability to critically analyse their performance, leading to a significant overestimate of themselves.
Double coverage of Pseudomonas (with some exceptions) is an enduring medical myth, along with atelectasis causing fever and normal temperature being 98.6. These myths and there are others, appear immune to medical literature.
There are no clinical data that suggest that the combination of a β-lactam plus a fluoroquinolone results in improved patient outcomes compared with a β-lactam alone or a β-lactam plus an aminoglycoside. Results from studies that evaluate combination therapy versus monotherapy for gram-negative bacilli conflict with the common practice of use of double coverage. Strong evidence to support the administration of antimicrobials for double coverage of gram-negative organisms is lacking. Antimicrobial overuse may lead to antibiotic resistance, unnecessary adverse effects, and increased costs.
Remembering the concepts of evolution (and perhaps the resident who wrote that is from Kansas) would suggest the more intense the pressure, the more rapid the development of resistance, which is indeed true for bacteria:
We develop an automated assay for monitoring the parallel evolution of hundreds of Escherichia coli populations in a two-dimensional grid of drug gradients over many generations. We find a correlation between synergy and the rate of adaptation, whereby evolution in more synergistic drug combinations, typically preferred in clinical settings, is faster than evolution in antagonistic combinations. We also find that resistance to some synergistic combinations evolves faster than resistance to individual drugs. The accelerated evolution may be due to a larger selective advantage for resistance mutations in synergistic treatments.
Classically double coverage refers to a beta-lactam and an aminoglycoside or, more recently, a beta lactam-and a quinolone.
Cefepime and piperacillin work at the same site on the bacterial cell wall; double beta-lactams, while indeed two antibiotics, add nothing mechanistically for killing bacteria. Double beta-lactams became passé at the turn of the century in the approach to the neutropenic febrile, the only clinical scenario where it was extensively evaluated.
Although most combinations of new beta-lactam antibiotics (ureido-penicillins, third-generation cephalosporins, monobactams) appear to be indifferent, antagonism and possible selection of resistant mutants are the drawbacks of such combinations.
Physicians have to demonstrate competency before being allowed to deliver all kinds of services in the hospital. Sometimes I think we need to do the same with antibiotics.
Or better yet, don’t sit there like a brain dead medical zombie, Google it.
Rationalization
Am J Health Syst Pharm. 2011 Jan 15;68(2):119–24. doi: 10.2146/ajhp090360. Is double coverage of gram-negative organisms necessary?
http://www.ncbi.nlm.nih.gov/pubmed/21200057
Am J Med. 1986 May 30;80(5C):21–9.Synergism and antagonism in double beta-la ctam antibiotic combinations.
http://www.ncbi.nlm.nih.gov/pubmed/3487247
Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13977–81. doi: 10.1073/pnas.0805965105. Epub 2008 Sep 8. Accelerated evolution of resistance in multidrug environments.
http://www.ncbi.nlm.nih.gov/pubmed/18779569
POLL RESULTS
The most ridiculous myth in medicine is
- normal temperature in 98.6 10%
- gotta double cover Pseudomonas 2%
- 'in my experience' is a useful criteria for choosing a therapy 22%
- alternative medicine has something valid to offer to patient care 32%
- life is fair and we are born to be healthy 33%
- Other Answers 2%
- lab certification inspections are always fair and worthwhile and nobody ever gets away with anything.
Chapter Nineteen
Today I saw in a chart the 'diagnosis' of qi deficiency and blood stagnation as a reason for acupuncture. Don’t get me started. It was so very dispiriting to see ancient nonsense in an EMR as if it were actually meaningful. I knew that it was really a problem with too much phlegm, and the patient needed to be bled with leeches, but would they listen to me? No.
At least qi and blood stagnation don’t have ICD codes, even if acupuncture does.
Reality-based medicine, for all its flaws, has done so much to improve the human condition, but due to limitations, people still turn to nonsense.
I like to read history, and it is always striking as an ID doctor how people used to die from preventable infections. In Team of Rivals: The Political Genius of Abraham Lincoln people died left and right from infections, many of which I see at best once a decade or less. Safe water, flush toilets, vaccination, nutrition, and an understanding of disease epidemiology has made so many infections a rare curiosity.
Nothing brings it home like numbers. Today I came across the US mortality statistics from 1905.
46,788 deaths from epidemic diseases: 10,771 from typhoid (33/100,000), 10,729 from diphtheria, 17901 from malaria, 1180 from smallpox, 3,213 from measles, 3778 from scarlet fever, 6629 from influenza, and 1468 from erysipelas. Erysipelas! Group A streptococcal cellulitis killed almost 1500 people. Amazing.
62,162 from TB in all its forms (194/100,000), 1234 from syphilis, 10,551 from meningitis. 1214 from tetanus.
3374 people died of appendicitis.
And on and on and on, death after death from diseases that are rarely fatal today.
Heart disease was (relatively) nothing, having killed 38,510.
And that was in a population of 46,765,351.
I have seen one case of typhoid and a case of malaria or TB about once a year. I have never seen a case of measles. No diphtheria, and maybe one case of Scarlett fever.
1905 had a record number of football deaths with 19, resulting in reforms that led to the forward pass.
We had to wait until 1910 for the Flexner report to get medicine on a path a bit better than the forward pass.
All those improvements in human health and the marked decrease in infectious diseases have been made possible by the relentless research and efforts of all the natural and ancient healing modalities like, well, hmm.
None of them. The human condition has not been improved by any SCAM. Makes it all the sadder to see it in the medical record.
Chapter Twenty
Something Evil Must Be Going On
I like not working. I do have the best job in medicine, but somehow five days at Pacific Beach is just so much nicer than, say, the ICU and rush hour traffic. Fewer tats and less obesity as well. Ah well, bills must be paid, although I am not so certain the life of a beach bum is such a bad idea.
As I have mentioned in the past, the name of the bug will tell often tell you what the underlying problem is. While people can get infections for no damn good reason, often there is an underlying risk.
The patient is admitted with pneumonia. There is a right lower lobe somewhat round dense infiltrate and a mild leukocytosis. They call me as the blood is growing a gram-positive anaerobe. He is surprisingly non-toxic, and the cultures are C. perfringens.
C. perfringens is not exactly a common cause of pneumonia, with less than a dozen cases in the Pubmeds. It usually causes a necrotizing pneumonia and is from poor dentition.
He has no teeth, and no teeth means no anaerobes in the lung from aspiration.
Reported predisposing factors for systemic clostridial dissemination include intraoral pathology (carious teeth or gingival disease)…
Lung abscess is rare in those without teeth, and I would suppose this would apply to Clostridia as well. It isn't going to be pneumonia that led to the positive blood cultures.
Clostridia perfringens in the blood in someone who is not dying of MOSF from gas gangrene usually means a tumor as the reason.
The most frequently identified Clostridium species was Clostridium perfringens (in 10 [21.7%] of patients), followed by Clostridium septicum (in 9 [19.6%]). Thirty-one patients (67.4%) were aged ⩾65 years, 13 patients (28.3%) had diabetes mellitus, and underlying malignancy was present in 22 patients (47.8%).
and
An association between clostridial bacteremias and malignant disease has been described. Thirteen malignant diseases were identified in 12 of the 23 patients reported herein. Carcinoma of the colon and rectum was the most frequently associated malignant condition, but a wide variety of other malignant diseases were also identified.
That about 1 in 3 will have an underlying malignancy is reasonably consistent across studies. So we pan-scanned him. Tumor everywhere, including the area that was called a pneumonia. He decided, not unreasonably, for palliative care.
Rationalization
Cases J. 2009 Jan 14;2(1):50. doi: 10.1186/1757–1626–2–50. Necrotizing pneumonia and sepsis due to Clostridium perfringens: a case report.
http://www.ncbi.nlm.nih.gov/pubmed/19144160
Clin Infect Dis. 2001 Aug 1;33(3):349–53. Epub 2001 Jun 22. Clinical features of clostridial bacteremia: a review from a rural area.
http://www.ncbi.nlm.nih.gov/pubmed/11438901
Surg Gynecol Obstet. 1989 Nov;169(5):423–8. Clostridial sepsis and malignant disease.
http://www.ncbi.nlm.nih.gov/pubmed/2814753
Chapter Twenty-One
The patient has abrupt vision loss and a seizure. She is otherwise healthy with zero medical problems or risks.
An MRI suggests cerebritis, and a repeat two days later shows a ripening abscess in the occipital lobe. So they call me, and I say call a neurosurgeon: it is a brain abscess, and we need cultures.
She goes to surgery, pus is drained and, as I predicted, grows a S. intermedius. Not a hard prediction since the anginosis group of Streptococci are the most common organisms grown from brain abscesses.
Although what you can grow from an abscess markedly underestimates what can be found using magic, er, I mean 16S Ribosomal DNA Sequencing. Same thing. “Any sufficiently advanced technology is indistinguishable from magic.” - Arthur C. Clarke
But I think being an ID doctor is like being Hank in Camelot. I have to impress the savages by predicting an eclipse or a microbiology. It is how a reputation is made. What kind of reputation I will let you decide.
But why? Why the brain abscess? Most of the brain abscesses I see are due to trauma, either surgical or acute lead intoxication. Otherwise, brain abscesses occur when there is a right to left cardiac shunt, where bacteria bypass the filters of the lung and liver. The hospitalist had ordered an ECHO, and there was PFO. Bingo. The right to left shunt I was looking for.
The abscess cleared up nicely with antibiotics and drainage. Now, I suppose, the question of whether the PFO should be closed.
Rationalization
Clin Infect Dis. 2009 May 1;48(9):1169–78. doi: 10.1086/597578. The expansion of the microbiological spectrum of brain abscesses with use of multiple 16S ribosomal DNA sequencing.
http://www.ncbi.nlm.nih.gov/pubmed/19335164?dopt=Abstract
Undiagnosed patent foramen ovale presenting as a cryptogenic brain abscess: Case report and review of the literature.
http://www.sciencedirect.com/science/article/pii/S0147956305001482
Intern Med. 2012;51(9):1111–4. Epub 2012 Apr 29. Patent foramen ovale as a risk factor for cryptogenic brain abscess: case report and review of the literature.
http://www.ncbi.nlm.nih.gov/pubmed/22576398
POLL RESULTS
I want a reputation
- as a diagnostician. 19%
- as a nice guy. 17%
- of being hated and feared. Like Logan. 5%
- as the smartest person in the hospital. 24%
- as someone who can really hold their liquor. 26%
- Other Answers 10%
- As one who has fought the good fight, and made the world a better place.
- as one who is usually most completely misunderstood.
Chapter Twenty-Two
The most common infections have the acronym PUS: pneumonia, UTI, and soft tissue infection.
And the most common bugs for these infections? S. pneumoniae, E. coli and Group A Streptococcus aka S. pyogenes.
One would think, and that one would be me, that common things being common, people would know how to treat these infections. It ain’t brain surgery, and we are acutely aware of late how some brain surgeons think. They ain’t rocket scientists.
So I was asked by the residents about what oral therapy should be used at discharge for treating CAP due to S. pneumoniae, treating a pan susceptible E. coli urosepsis and a Group A Streptococcal cellulitis.
I often ask, “what do you want to do?”
And in all three cases, they said Augmentin.
Seriously.
S. pneumonaie and S. pyogenes never in the history of the universe make a beta-lactamase. And the E. coli? It was right there on the sensitivity report. Ampicillin ’S’. It is also not making a beta-lactamase.
So I asked why Augmentin. What are you going to get from the clavulanate?
Silence. They didn't know. I am increasingly of the opinion that a basic understanding of the most common ID problems is approaching zero. But they sure can use that EMR.
I have never been a beta-lactamase inhibitor kind of guy. There are too many beta-lactamases, and I fret about the stoichiometry of these drugs.
While the classic metaphor for antibiotics is a bullet, how many antibiotic molecules does it take to kill a bacteria? It depends on the antibiotic and the MIC, but the answer if you do the math, you know, the old grams to moles to molecules calculation, is in the hundreds. So I worry there is enough of the primary antibiotic getting through the beta-lactamases to kill the organism.
Most antibiotics work most of the time in most patients, and most of the time, Augmentin is being used, like the above examples, where amoxicillin could be used just as well i.e., when there is no worry about beta-lactamases.
And while we are on the topic, which is better for Pseudomonas, Piperacillin, or Zosin? Often beta-lactam resistance in Pseudomonas is due to permeability issues. Tazobactam inhibits the SHV–1 and TEM beta-lactamases, found in E. coli and their ilk. Pseudomonas beta-lactamases are often AmpC and are poorly inhibited by tazobactam. More often than not, tazobactam adds nothing to the ability of piperacillin to kill Pseudomonas. Tazobactam is there to kill the Enterobacteriaceae and anaerobes although the world of beta-lactamases is complex enough to make my head hurt and makes it impossible to make absolute statements.
Still, it flabbbers by gaster how often a beta-lactamase inhibitor combinations are given when there are no beta-lactamases present.
As I get older, the rank stupidity irritates me. Yet another sign I am an old geezer that needs to be put out to pasture.
I think there are two reasons to give Augmentin: prophylaxis for animal bites and if you do not like the patient, because Augmentin is expensive and will give them bad diarrhea. Most of the time, there are better/less expensive options.
Rationalization
AmpC β-Lactamases.
http://cmr.asm.org/content/22/1/161.full
Brain Surgeon
https://www.youtube.com/watch?v=THNPmhBl-8I
POLL RESULTS
I do not understand the allure of
- augmentin 7%
- light beer 28%
- the presidential debates 28%
- this blog 4%
- apple watch 30%
- Other Answers 4%
- New grad PAs as hospitalists
- unasyn
Chapter Twenty-Three
If I have an aesthetic, it tends towards the minimalist. I like Japanese and Mission Style and Degas and Rock with guitar, bass, drums, and vocal. Clean lines, right angles. That defines elegance. I was a physics major in college, and I was always attracted to the idea that understanding how the universe works result in equations that are 'simple'.
I apply that same aesthetic to the practice of medicine. At heart, I am an Occams kind of guy: Entities must not be multiplied beyond necessity.
Progress notes should be short, almost haiku in brevity, but if you choose your words correctly, 5–7–5 is often verbose.
You should be able to get the diagnosis with a minimum of steps since the core signs, and symptoms of any disease are few. The history and physical often takes time, being complete because we all know occasionally we will be blindsided by oddness unless we ask very specific questions.
Oh, your roommate has a cockatiel?
And you have to talk to the patient and the care team, which also takes time. There is more to medicine than making a diagnosis. But the core of seeing a consult, figuring out what is going on, usually takes very little time. It should be simple, and in simplicity, there is elegance.
Once you have a diagnosis, how may studies for diagnostic certainty do you need? How many tests to order? If I have a patient with a fever, emboli, murmur, and S. mitis in their blood, I do not need an ECHO to diagnose endocarditis. Someone will order one, but it serves no real purpose and violates my medical aesthetic. It adds unneeded information, although it might be good to know which valve is infected. Aortic vavle endocarditis makes me nervous.
What really violates my aesthetic is doing tests when the prior probability is zero. It is stupid and the stupid, to quote one of my favorite bloggers, it burns.
If a patient has fevers, but no positive blood cultures, no emboli, no murmur, no risks, and no reason in this Universe to suspect endocarditis, ordering an ECHO is a complete and utter waste of time and money. And people do it. All the time. ECHO just for fever. Don't.
We suspected that many TTEs in our hospital are obtained to “rule out” IE in patients with low pretest probability of IE. We conducted a prospective observational study of all patients referred for TTE to rule out IE in a large, urban, tertiary referral hospital (1) to determine the pretest likelihood of IE and (2) to test the impact of TTE results on clinical management and outcome.
And you cannot use an ECHO to "rule out" endocarditis. Writing such an order shows a profound lack of understanding and should probably be sufficient evidence to ignore the order. And the results?
Transthoracic echocardiography in low-risk patients does not add diagnostic information, and does not alter therapeutic strategies. Based on our findings, TTE is overused in the diagnosis of IE, primarily because it is obtained before all clinical information is available. Echocardiography in the diagnosis and management of IE should be reserved for patients with intermediate or high probability of IE, based on clinical findings and positive blood culture results.
It is not like there is a lack of literature that getting ECHOs is useless when there are no signs or symptoms of endocarditis. Or the idea that if there is a low pretest probability, a test is likely to be negative, and even a positive is likely to be a false positive.
Plus, it is ugly.
Patient with fever.
Work up to date yields nothing.
Does not need ECHO.
Rationalization
Overuse of Transthoracic Echocardiography in the Diagnosis of Native Valve Endocarditis.
http://archinte.jamanetwork.com/article.aspx?articleid=754054
The clinical implications (or lack thereof) of vegetations detected by echocardiography in patients not thought to have endocarditis.
http://onlinelibrary.wiley.com/doi/10.1002/clc.4960210311/abstract
Circulation. 1996 Feb 15;93(4):730–6. Diagnostic value of echocardiography in suspected endocarditis. An evaluation based on the pretest probability of disease
http://www.ncbi.nlm.nih.gov/pubmed/8641002
POLL RESULTS
My aesthetic is
- Minimalist 43%
- Louis 16 13%
- Hipster 10%
- Patrician 3%
- Walmart 10%
- Other Answers 20%
- Art Deco
- old
- cotton knits all the way down.
- Baroque
Chapter Twenty-Four
What Medicine Takes Away Medicine Gives Back
The patient was well one moment, then the next he was sicker than stink: fevers, rigors, right-sided pleuritic chest pain, delirium, and dyspnea.
He came to the ER, where he was admitted with pneumonia on CXR.
Sure sounds like Pneumococcus.
But.
He is a renal transplant patient, and he has a PICC through which he had been on antibiotics for an abdominal abscess treated at Outside Hospital. The ER obtained blood cultures and pulled the PICC.
He was septic, spending a couple of days in the ICU and improved with rapidity.
All the blood cultures grew P. aeruginosa, but the line and the BAL did not, and the panscan showed a multifocal pneumonia, but the abdomen was clean.
So where did the Pseudomonas come from? I am betting the line, despite negative cultures, and the pneumonia is a consequence of downstream seeding—no other reason I can find for this organism in the blood.
I have never seen a Pseudomonas pneumonia that wasn’t severe.
The clinical presentation is nonspecific, and although the pneumonia can be rapidly fatal, only 33% of the patients who were reported died.
and it is not high on my list for CAP. And ‘only’ 33%? That’s a lot. I hate the word only infection of death statistics. And the fever curve? It plummeted to normal right after the line was pulled and never budged upward again.
But maybe it was the transplant meds. Most of the Pseudomonas pneumonias in the literature are hospital and ventilator acquired. What kills people is often not the infection but the host response, the nefarious cytokine storm. The good thing about immunosuppression is while it increases the risk for infection, it decreases the risk of death.
The 28-day and 90-day mortality were significantly decreased for transplant recipients compared with nontransplant patients. These findings suggest that the immunosuppression associated with transplantation may provide a survival advantage to transplant recipients with sepsis through modulation of the inflammatory response.
I usually say in medicine, no good deed goes unpunished. In this case, not so much.
Rationalization
Pseudomonas aeruginosa Bacteremia: Risk Factors for Mortality and Influence of Delayed Receipt of Effective Antimicrobial Therapy on Clinical Outcome.
http://cid.oxfordjournals.org/content/37/6/745.long
Pseudomonas aeruginosa Community-Acquired Pneumonia in Previously Healthy Adults: Case Report and Review of the Literature.
http://cid.oxfordjournals.org/content/31/6/1349.full
Is bacteremic sepsis associated with higher mortality in transplant recipients than in nontransplant patients? A matched case-control propensity-adjusted study.
http://www.ncbi.nlm.nih.gov/pubmed/25301215
Chapter Twenty-Five
The patient is a young female with bad knees from a life of basketball. Kind of like Brandon Roy. She is getting her knees injected with abdominal fat. Really. As she tells it, an ND puts her under with nitrous, does a quick liposuction, spins down the fat cells, and injects them in the knees. Really.
There is an interesting, very preliminary, literature, on using stem cells derived from adipose to treat arthritis and other illnesses. They isolate stem cells from adipose, and inject them into joints. Lots of animal studies and no clinical trials, although they are in the process of doing studies. I tell my wife that my high cholesterol is just a testosterone precursor, and now I can tell her I am storing up stem cells.
It is a long way from current research to reinjecting adipose cells as “stem cell therapy.” But that is the nature of ND practice. Every time patients tell you what is being done by the ND you can’t believe what you are hearing. But anything goes in an ND practice since
There is no naturopathic-specific standard of care. Naturopathic doctors are taught and held to the same standards of care as conventional providers.
After the last injection, her knee became red, hot, and swollen. It was filled with pus in the OR with no cartilage and lots of bare bone. So much for stem cell regeneration.
It grew a S. salivarious. So how did a mouth Streptococcus get into the knee?
I have three possibilities.
First, bad luck. Bacteremia is common after routine brushing and flossing, and a knee full of fat would be a nice foreign body for inadvertent seeding.
The second is from the ND. He did not wear a mask, and at least in lumbar puncture associated meningitis, the source of the alpha Streptococcus in the spinal fluid is the person doing the LP. It is why masks are required for LP and perhaps for joint infections as well:
We consider a surgical mask to be a low-cost, simple addition to the aseptic technique that may assist in the prevention of nosocomial septic arthritis.
The only way I could determine that would be to type the Streptococcus in the wound, the patients mouth, and the NDs mouth. That is not going to happen.
Third is the injection itself. Turns out that before the knee was injected, an aliquot was injected into the patients gums for another reason. The needle was changed between injections, but it doesn’t seem like optimal infection control. It is odd enough that it doesn’t quite meet the letter of the CDC recommendations:
Do not administer medications from a syringe to multiple patients, even if the needle or cannula on the syringe is changed.
Which is it? I will never know. For now, it is a course of antibiotics for the septic joint.
Rationalization
Intra-Articular Injection of Mesenchymal Stem Cells for the Treatment of Osteoarthritis of the Knee: A Proof-of-Concept Clinical Trial.
http://onlinelibrary.wiley.com/doi/10.1002/stem.1634/full#stem1634-bib–0022
Iatrogenic Meningitis: The Case for Face Masks
http://cid.oxfordjournals.org/content/31/2/519.long
Med J Aust. 2013 Mar 18;198(5):285-6. The doctor and the mask: iatrogenic septic arthritis caused by Streptoccocus mitis.
2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings.
http://www.cdc.gov/hicpac/pdf/isolation/Isolation2007.pdf
Naturopathic White Paper: An Analysis
http://www.ore4sbm.com/naturopathy-white-paper/
Horrifying suffering caused by treating pertussis “naturally”
Naturopathic Diaries.
http://www.naturopathicdiaries.com/
Chapter Twenty-Six
The patient is an elderly male who is admitted with the somewhat abrupt of severe back pain and fevers.
He is found to have an alpha Streptococcus in the urine and was thought to have pyelonephritis as the cause of his symptoms.
Then his blood cultures were positive for Aerococcus urinae, and they called me with the question of how to treat the two infections.
It is not two infections, I said. Aerococcus is an alpha Streptococcus.
A. urinae is a gram-positive coccus that grows in pairs and clusters, produces alpha-hemolysis on blood agar, and is negative for catalase and pyrrolidonyl aminopeptidase.
But the patient probably has endocarditis. Get a TEE, and I will see the patient in the am.
In the meantime, I called the lab and asked them to check an e-test to penicillin.
Next day? The TEE showed a vegetation on the aortic valve, and the MIC was 0.04.
He is severely claustrophobic (fear of Santa), which delayed his spine MRI, which finally showed not only L4/L5 discitis/osteomyelitis and epidural inflammation, but bilateral iliopsoas abscesses.
While there are many cases of UTI due to Aerococcus, a bunch of cases of endocarditis, 4 cases of discitis, there are no cases of iliopsoas abscess or epidural involvement reported on the Pubmeds. So I am first. I, as I like to do, will blame Batson's plexus for the spine involvement:
The Batson venous plexus (Batson veins) is a network of valveless veins in the human body that connect the deep pelvic veins and thoracic veins (draining the inferior end of the urinary bladder, breast and prostate) to the internal vertebral venous plexuses.
Take home? Old people get UTI’s with alpha streptococci, and your lab needs to ID the organism, so you know if it is Aerococcus. And if you find Aerococcus in the blood, look at the valves and where ever there is pain. It may be more than urospepsis.
And if Larry the Lobster come in sick? Aerococcus viridans var. homari causes Gaffkaemia,
lethargy (typically seen as a drooping tail),[5] anorexia and a pink colour on the ventral side of the abdomen, which gives the disease its alternative common name of red tail disease. When lobsters are moribund, they may lie on their sides, and frequently lose appendages
Probably from steroid use.
Rationalization
Aerococcus urinae in Urinary Tract Infections.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC86536/
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
Clin Microbiol Infect. 2012 Jun;18(6):546–50. doi: 10.1111/j.1469–0691.2011.03609.x. Epub 2011 Sep 6. Clinical and microbiological features of bacteraemia with Aerococcus urinae.
http://www.ncbi.nlm.nih.gov/pubmed/21895858
Int J Cardiol. 2007 Feb 14;115(3):402–3. Infective endocarditis and spondylodiscitis in a patient due to Aerococcus urinae: first report.
http://www.ncbi.nlm.nih.gov/pubmed/16766062
Scand J Infect Dis. 2003;35(11–12):890–1. Spondylodiscitis due to Aerococcus urinae: a first report.
http://www.ncbi.nlm.nih.gov/pubmed/14723372
Neurosurgery. 2011 Nov;69(5):1007–14; discussion 1014. doi: 10.1227/NEU.0b013e3182274865. History of the vertebral venous plexus and the significant contributions of Breschet and Batson.
http://www.ncbi.nlm.nih.gov/pubmed/21654535
Larry the Lobster. For those of you who are unaware of the Spongebob Squarepants universe.
https://nickelodeon.fandom.com/wiki/Larry\_the\_Lobster
Chapter Twenty-Seven
The patient is a young male who has a discectomy for a herniated disc, a consequence of a fall. He is otherwise healthy and, after an uneventful stay, goes home.
Seventy-two hours after the surgery, he has a marked increase in his back pain, fever to 102, and teeth chattering rigors.
He is admitted, and the MRI shows a fluid collection, either hematoma or early infection, but the wound looks fine, and his WBC and differential are normal.
I put a lot of emphasis on rigors as increasing the odds of a bacterial infection in a patient, particularly bacteremia. In kids
It was demonstrated that 66% of the patients with rigor belonged to the bacterial infection group versus 50% in the non-rigor group.
And for adults look the OR:
In a multivariate analysis, several factors were independently associated with community-onset bacteremia, including an age of >65 years (odds ratio [OR], 2.81; 95% confidence interval [CI], 1.25–6.33), the presence of rigor (OR, 13.7; 95% CI, 4.47–42.0) or chills (OR, 6.04; 95% CI, 1.10–32.9), a body temperature >39.9 °C (OR, 2.68; 95% CI, 1.03–6.94), blood urea nitrogen >20 mg/dL (OR, 5.56; 95% CI, 2.03–15.7), a blood urea nitrogen/creatinine ratio >16 (OR, 2.29; 95% CI, 1.03–5.11), and thrombocytopenia (OR, 6.09; 95% CI, 1.84–20.0).
and
Elevated temperatures alone do not accurately predict bacteremia (for ≥38°C [>100.3°F], LR, 1.9 [95% CI, 1.4–2.4]; for ≥38.5°C [>101.2°F], LR, 1.4 [95% CI, 1.1–2.0]), nor does isolated leukocytosis (LR, <1.7). data-preserve-html-node="true" The severity of chills graded on an ordinal scale (shaking chills, LR, 4.7; 95% CI, 3.0–7.2) may be more useful.
So I told the surgeon the patient probably has an infection, and the only way to know is to open the wound.
And no infection, only a hematoma that extended to the epidural space. And the fever went away after the wound was opened.
There are a smattering of cases of hematoma as the putative cause of fevers. In a classic FUO paper, 3 patients out of 105 had a hematoma as the reason for fever, one subcapsular, one retroperitoneal, and one hemopericardium. And, unfortunately, the only way to know for sure is to open up the wound.
I have seen the odd hematoma over the years that I have credited as the reason for a fever. Unusual, but we see this.
But not a rigor. That annoys me.
Rationalization
Eur J Pediatr. 1997 Jun;156(6):457–9. The clinical significance of rigors in febrile children.
http://www.ncbi.nlm.nih.gov/pubmed/9208242
Diagn Microbiol Infect Dis. 2012 Jun;73(2):168–73. doi: 10.1016/j.diagmicrobio.2012.02.009. Epub 2012 Mar 29. Prediction of community-onset bacteremia among febrile adults visiting an emergency department: rigor matters.
http://www.ncbi.nlm.nih.gov/pubmed/22463870
JAMA. 2012 Aug 1;308(5):502–11. doi: 10.1001/jama.2012.8262. Does this adult patient with suspected bacteremia require blood cultures?
http://www.ncbi.nlm.nih.gov/pubmed/22851117
Diagn Microbiol Infect Dis. 1988 Dec;11(4):215–9. Soft tissue hematoma as a cause of fever in the adult.
http://www.ncbi.nlm.nih.gov/pubmed/3240663
Medicine (Baltimore). 1982 Sep;61(5):269–92. Fever of undetermined origin: diagnosis and follow-up of 105 patients.
https://pubmed.ncbi.nlm.nih.gov/6287162/
Chapter Twenty-Eight
Let us go out of our way to make patients anxious, shall we?
Rounds today took about 20 minutes longer than it should have.
I have a patient I think needs to be started on amphotericin B. I have a high index of suspicion of an invasive mold resistant to azoles. More on this case in the future if I do get an answer.
Several other doctors had rounded on the patient before me, and both had referred to the medication as ampho-terrible to the patient.
My my, aren’t you the clever one. But really? What purpose does that serve? None. For one, the current formulations of amphotericin B are not that bad in most patients. The old shake and bake is largely a thing of the past, and most patients tolerate the medication just fine. I have been giving amphotericin B for 30 years, and most of the time, it is tolerated with minimal side effects.
The only result of calling it ampho-terrible is to make the patient and family worried, a worry that is magnified by searching the internet.
And HCW’s do this all the time. Why go out of your way to repeat a not all that clever piece of medical slang whose sole purpose is to increase worry? I don’t badmouth your meds to patients with lame puns. I’ll be sure to refer to levophed as leavemdead. That will go over real well with families in the ICU.
And of course, it being all about me, it causes rounds to grind to a halt as I have to debunk the stupidity that is ampho-terrible.
And while we are on the topic of making patients unnecessarily anxious, why do those who place PICCs, and other central lines always have to mention that the catheter tip sits right above the heart? It is true but of almost zero clinical relevance and only wigs people out.
What and how we say things often has impact far out of proportion to reality.
The last thing I want the patient to think I am recommending is dripping ampho-terrible directly into the heart.
So stop it.
Chapter Twenty-Nine
The case begins like so many others: fevers and chest pain, and within 48 hours, the diagnosis is clear—right-sided MRSA endocarditis.
Unlike most cases, no apparent reason why except untreated HIV, but the patient has a decade of low viral loads and normal CD4 counts. But HIV is probably reason enough; since HIV patients are more likely to have a community-acquired bacteremia and, if due to S. aureus, more like to involve a valve.
So I can expect the patient not to respond quite well as a non-HIV pateint:
HIV–1 infection is associated with an increased risk of 30-day mortality after SAB and a very high rate of reinfection. Age, a foreign device, and Pitt score predicted outcome. For patients infected with HIV, neither CD4 T-lymphocyte counts nor plasma HIV RNA levels were associated with 30-day outcome.
Especially since the MIC to vancomycin is 1.0. And he doesn’t respond to antibiotics, remaining febrile. So on day 8, I declare a vancomycin failure after finding no drainable pus and change to ceftaroline.
Within 24 hours, the patient was afebrile and feeling great and was sent home to complete the course of antibiotics.
I don’t know. The fevers resolved before the vancomycin could be cleared or the ceftaroline could reach steady-state, much less penetrate a vegetation or septic pulmonary lesion, so probably true-true and unrelated, but it did not stop me from taking full credit.
Then the patient was back 10 days later with fevers, sweats, and a predominance of myalgias and arthralgias and now a lowish, but not neutropenic, WBC.
Again there was a workup for drainable pus, and none was found, so I declared it a serum sickness like reaction and changed to daptomycin and again within 24 hours all was normal. Daptomycin is not to be used for pneumonia, but septic emboli are not in the alveoli, and to date, I have had no daptomycin failures with septic pulmonary emboli, although there are reports in the PubMed. It does make me nervous.
And again, I don’t know. The patient improved too fast? Maybe not.
There are no case reports specifically of ceftaroline causing a serum sickness like illness, but there are with other cephalosporins. And although HIV patients, due to immune dysregulation, do get more adverse reactions to medications of all kinds, cephalosporins are not on the list. And it could have been the endocarditis, and the improvement was the natural history of the disease.
Again, it didn’t stop me from taking full credit. Got to get it when you can.
Rationalization
BMJ Open. 2014 Apr 23;4(4):e004075. doi: 10.1136/bmjopen–2013–004075. Outcome and reinfection after Staphylococcus aureus bacteraemia in individuals with and without HIV–1 infection: a case-control study.
http://www.ncbi.nlm.nih.gov/pubmed/24760348
BMC Infect Dis. 2011 Oct 31;11:298. doi: 10.1186/1471–2334–11–298. Community-associated methicillin-resistant Staphylococcus aureus bacteremia and endocarditis among HIV patients: a cohort study.
http://www.ncbi.nlm.nih.gov/pubmed/22040268
N Engl J Med. 1993 Jun 10;328(23):1670–4. Cutaneous disease and drug reactions in HIV infection.
http://www.ncbi.nlm.nih.gov/pubmed/8487826
POLL RESULTS
I
- take full credit when the patient gets better 11%
- blame others when patients do not improve 3%
- do the best I can and accept the outcome 42%
- am annoyed no end when all our hard work is credited to a higher power 39%
- never had treatment failure, what are you talking about? 5%
Chapter Thirty
The patient is admitted to an outside hospital with neurologic symptoms: abrupt numbness and tingling in the arms and legs with difficulty speaking.
LP is consistent with an inflammatory state (high protein and a paucity of cells). The presumptive diagnosis of Guillain-Barre Syndrome (GBS) was made as the symptoms started 17 days after receiving the flu vaccine. She was started on IVIG for 5 days and rapidly improved.
Three days into hospitalization, other serologies are ordered, and she was discharged.
Two weeks later, she is in my clinic, neurologically normal but with a positive Lyme Elisa and Western Blot.
By history, you would be hard-pressed to find someone with fewer risks for Lyme: no travel outside Oregon and, while an outdoors person, it is only winter sports. She has no history of tick bite or other signs of Lyme.
So I bet it is a false positive serology from all the IVIG. IVIG can have high titers against a variety of organisms, although it is usually the titers to viral pathogens that are measured.
I cannot find where anti-Borrelia titers have been measured in IVIG, but there is a case of Lyme seroconversion after IVIG. So maybe. I will have to repeat the Lyme serology after several months when all the IVIG has had a chance to be metabolized.
So was it the influenza vaccine that caused the neurologic symptoms? Could be. The timing is right, but her symptoms were more sensory than motor and occurred all at once rather than an ascending syndrome, so not really a GBS.
Neurology isn't my strong point. Once we get past right brain/left body, left brain/right body, I call a neurologist. But it was more of a distal acquired demyelinating symmetric neuropathy, even rarer but also reported after flu vaccination.
Whether due to the flu vaccine is another matter, I am always skeptical of causality without a better pathophysiologic explanation, but probably close enough for government work.
It would be good for the patient to have negative repeat Lyme serology, as not only as she would not need a course of therapy for Lyme, but she may be eligible for compensation from the National Vaccine Injury Compensation Program. It would help with the ginormous hospital bill.
Postscript
Repeat Lyme serology was negative.
Rationalization
Laboratory Serologic Problems Associated with Administration of Intravenous IgG.
http://www3.mdanderson.org/~citm/H–94–04.html
Clin Microbiol Infect. 2001 Dec;7(12):697–9. An unusual case of anti-Borrelia burgdorferi immunoglobulin G seroconversion caused by administration of intravenous gammaglobulins.
http://www.ncbi.nlm.nih.gov/pubmed/11843914
Guillain-Barré Syndrome, Influenza, and Influenza Vaccination: The Epidemiologic Evidence.
http://cid.oxfordjournals.org/content/58/8/1149.long
J Clin Neuromuscul Dis. 2013 Mar;14(3):117–22. doi: 10.1097/CND.0b013e318285256b.
Distal acquired demyelinating symmetric neuropathy after vaccination. http://www.ncbi.nlm.nih.gov/pubmed/23492464
Chapter Thirty-One
I am sure you have your clinical superstitions. I am not superstitious, knock on wood. The only medical superstition I have is that the less the indication for antibiotics, the greater the probability there will be an adverse reaction. And I know that it is not true.
I recently had two quasi-identical cases.
One male, one female. Both obese.
Both present with infection of the left lower pannus: fevers, erythema, leukocytosis.
Both have no reason infection: no trauma, no diabetes, no risks.
Both have a necrotizing panniculitis in the OR, with pus and organisms on gram stain.
One grows Peptostreptococcus (and a GNB that did not grow), the other Prevotella.
So two spontaneous anaerobic necrotizing panniculitises (actually Panniculitides, which is a constellation as well, I think.).
It is odd. Thirty years and I have never seen a similar case. Most of the infected pannuses I have seen have been after kidney transplants in the morbidly obese. Spontaneous infections, especially anaerobic infections, are uncommon. Probably my last cases as well as I do not believe that badness comes in threes.
There are other reasons for necrotizing panniculitis. It is associated with acinar cell carcinoma of the pancreas, but this isn’t that. Or that isn’t this.
No other diagnosis is evident, but the panniculitides have a broad differential diagnosis outside of infections, from Sweets to vasculitis.
But it is hard to argue with pus and a gram stain. And both improved on antibiotics after debridement.
But still. While I have a nagging feeling there might be more going on here, there wasn’t.
Rationalization
South Med J. 2008 May;101(5):554–5. doi: 10.1097/SMJ.0b013e31816bf5eb. Necrotizing panniculitis: a skin condition associated with acinar cell carcinoma of the pancreas.
https://pubmed.ncbi.nlm.nih.gov/18414166/
G Ital Dermatol Venereol. 2013 Aug;148(4):427–33. Infectious panniculitides: an update.
http://www.ncbi.nlm.nih.gov/pubmed/23900164
G Ital Dermatol Venereol. 2013 Aug;148(4):351–70. Panniculitides, an algorithmic approach.
http://www.ncbi.nlm.nih.gov/pubmed/23900158
Dermatol Ther. 2010 Jul-Aug;23(4):328–40. doi: 10.1111/j.1529–8019.2010.01333.x. Infection and panniculitis.
http://www.ncbi.nlm.nih.gov/pubmed/20666820
Chapter Thirty-Two
The patient is admitted with a bad case of cellulitis. Years ago, she had lymphoma treated with radiation, chemotherapy, and, ultimately, a bone marrow transplant.
What brought her to the ER was rigors and incapacitating back pain. Her entire leg had rubor, dolor, calor, and tumor.
Work up revealed S. equisimilis, a group G Streptococcus, in the blood. No surprise there. While perhaps the second cause of cellulitis, it is more likely than Group A Streptococcus to cause a bacteremic cellulitis.
When Streptococci was noted on the blood gram stain, she was changed to ampicillin and clindamycin.
I wondered. Does the Eagle effect apply to Streptococci other than S. pyogenes? Yep.
Treatment failure with high dose penicillin was observed despite in vitro sensitivity. The addition of clindamycin resulted in dramatic clinical improvement. This may indicate an Eagle-type effect (whereby antibiotics exhibit paradoxically reduced bactericidal activities at high drug concentrations), in group G beta-haemolytic infections.
Because of the severe back pain, she had an MRI, and there was an area in a vertebral body that was consistent with infection. But no disc involvement.
It is rare to see hematogenous osteomyelitis that does not originate in the adjacent tissues, such as joint or cartilage. Infections go to disc and spreads to adjacent bone, tumor goes to bone and spares the disc. So this should be tumor. It is one of the 3 or 4 rules in medicine, of which I have never seen an exception. Until now. Because 2 weeks ago, she had a negative PET scan, so the only explanation for the MRI changes would be a new infection.
So it will be a course of antibiotics for hematogenous osteomyelitis.
Rationalization
J Infect. 2005 Nov;51(4):e207–11. Clindamycin in the treatment of group G beta-haemolytic streptococcal infections.
http://www.ncbi.nlm.nih.gov/pubmed/16291271
Vertebral osteomyelitis without disc involvement.
http://www.clinicalradiologyonline.net/article/S0009–9260(04)00133–3/abstract
POLL RESULTS
Rules with no exceptions
- Infection goes to disc, tumor to bone. 4%
- Those who call antibiotics big, strong or powerful know nothing about antibiotics 30%
- Drs who routinely wear scrubs outside of the hospital are jerks 26%
- The nicer the patient, the more unusual and awful the diagnosis 22%
- Off hour pages always occur at the most inconvenient time 17%
Chapter Thirty-Three
The patient is a young female who is admitted first with fevers, then chills, then severe abdominal pain.
How severe? She cannot tolerate speed bumps or stop and go traffic.
It is the little things in medicine that I find, well, delightful. Like speed bumps. There was a paper that showed when there was pain as a car went over a speed bump the
sensitivity was 97% (95% confidence interval 85% to 100%), and the specificity was 30% (15% to 49%). The positive predictive value was 61% (47% to 74%), and the negative predictive value was 90% (56% to 100%).
for acute appendicitis. A nice pearl for peritonitis.
I remember, as an intern, I was called to evaluate an acute abdomen, in a young man writhing with RLQ pain. I called my attending, who noted that with real peritonitis, patients try and remain as still as possible. And while the patient complained of pain on palpation, when my attending surreptitiously jarred the bed, the patient made nary a peep. My attending said the patient was faking it (this was before CT by the way), and sure enough, it was discovered that the patient was going into the Marines the next day and was freaking out. He was fine.
As to the stop and go traffic, probably the same process, although the traffic in PDX has really sucked of late. The population of the area has doubled since I was in high school, but the roads are the same size, so it is more stop and stop. But both bumps and stops rattle the peritoneum nicely. I also remember going home after my total colectomy, and I can tell you, those speed bumps were the size of mountains. I really felt every bump and stop.
But her CT was negative so they watched her, and the next day her blood culture was growing group A Streptococcus. So I knew the diagnosis: spontaneous bacterial peritonitis. Group A Streptococcus does this in young women without ascites. Those who have been reading this blog for a while will remember my one other case in 2012. This time the diagnosis is presumptive asI did not have the exploratory laparotomy to prove it, but she improved rapidly after 48 hours of antibiotics and went home all better.
Rationalization
Pain over speed bumps in diagnosis of acute appendicitis: diagnostic accuracy study.
http://www.bmj.com/content/345/bmj.e8012
BMJ paper wins Ig Nobel award for speed bump diagnosis of appendicitis.
http://www.bmj.com/content/351/bmj.h5007.long
Overcoming the I/O bottleneck to the faulty RAM.
http://boards.medscape.com/forums/?128@@.2a2ee86a!comment=1
Chapter Thirty-Four
It is the holidays and work is slowing down. More importantly, I am slowing down. The dreary winter rains also drown ambition. All I really want to do is sit in front of the fire and watch the Blazers. So until the New Year, I may be writing in a more desultory manner.
I am asked to see a spontaneous S. aureus infection in a knee. The what is simple enough, but why?
He had trauma to his leg in 1966 and had multiple surgeries back last century to fix the trauma, including an artificial hip. But no infection. 2 months ago, he had a femur fracture associated with the hip plated. The surgeon tells me he could see the hardware when he washed out the knee.
It was an MSSA, but I called the lab. Is it penicillin-susceptible? Yep.
Seeing a penicillin-sensitive S. aureus in 2016 is like seeing a coelacanth. It makes me wonder if his Staph was acquired in 1966, although I would have to do some fancy-schmancy testing to prove it. My record for S. aureus reactivation is 60 years, and the literature is even longer.
So this may be a 50-year-old S. aureus. Almost as old as me. Although I like to say I am 406 in dog years. And S. aureus years? 1,016,160. The nice thing is I can kill a penicillin-susceptible Staph.
And that makes me wonder again. Given the doubling time of S. aureus and all the changes in the organism due to medical pressure, is the S. aureus today the same as 50 years ago? Or has it evolved into a new species: Staphylococcus aureus sapiens? Or Staphylococcus aureus interfectorem?
No one has ever been able to answer that question.
Rationalization
N Engl J Med. 2012 Feb 2;366(5):481-2. doi: 10.1056/NEJMc1111493.
Staphylococcus aureus reactivation osteomyelitis after 75 years
http://www.nejm.org/doi/full/10.1056/NEJMc1111493
POLL RESULTS
Winter. All I want to do is
- sleep 32%
- eat 4%
- drink 9%
- watch it rain 6%
- move to where the sun always shines 28%
- Other Answers 21%
- read
- Ski. And I'm older than Mark.
- Toboggin down a steep hill
- read some Jack London and burn daylight.
- Watch Netflix
- Die.
Chapter Thirty-Five
I can appreciate the smart ass comment and the glib response. In fact, I admire it except when I am taking a history. When I sit down to interview a new patient, the last thing I want to hear are the glib response to the questions I ask in order to try and figure out the illness. Please. I have work to do. I have to come up with a diagnosis and treatment for whatever it is you have. So just answer my questions.
The patient is a middle-aged insulin-dependent diabetic with a neurogenic bladder. She comes in febrile. The blood and urine grow MSSA. Urosepsis? Maybe. But.
The rule with S. aureus in the urine and blood is it is the one organism where you worry blood to urine rather than urine to blood, although both mechanisms are possible. If hematogenous, then what is the source?
Using needles is risk enough for bacteremia. From an ID perspective, there is little difference between a dialysis patient, an IDDM, and a heroin user. They all have the risk of direct injection of Staph with subsequent bacteremia.
And it turns out that for the last 2 months she has been getting twice a week acupuncture for her neurogenic bladder, multiple needles left in for 45 minutes, one of them right between the eyes where she has eczema.
Eczema skin is often colonized with S. aureus:
Bacteria were isolated from 70.2% of lesional and 32.7% of nonlesional skin samples from patients with eczema, of which S. aureus accounted for 47.3% and 27.9%, respectively.
So putting an acupuncture needle though eczema could be a good way to kickstart a Staph bacteremia.
Nineteen cases from 14 case reports concern staphylococcus infections associated with acupuncture. Of these, nine patients were infected by methicillin-resistant Staphylococcus aureus (MRSA): six from Australia, one from Korea, one from Taiwan, and one from Hong Kong.
In the Australian case, Murray et al. reported a 2008 outbreak of eight cases of invasive MRSA, six of them associated with acupuncture. After extensive investigation, the authors concluded that the outbreak most likely resulted from a breakdown in sterile technique during the acupuncture procedure and that the MRSA was probably transmitted from the medical practitioner to the patients.
But the acupuncturist evidently has good technique: he alcohols his hands and actually uses gloves. Amazing. My one Googlewhack has been a single picture of acupuncture using gloves (which is different than acupuncture gloves), and that was dry needling by a physical therapist. Although I can’t seem to find any such photo or video at present. But if you are going to do a useless intervention, at least use good technique.
So why the bacteremia? I don't have a smoking gun, so I blame bad luck from a needle—a common back explanation.
Rationalization
Eur J Clin Microbiol Infect Dis. 2010 Sep;29(9):1095–101. doi: 10.1007/s10096–010–0967–2. Epub 2010 May 30. Primary Staphylococcus aureus urinary tract infection: the role of undetected hematogenous seeding of the urinary tract.
http://www.ncbi.nlm.nih.gov/pubmed/20703891
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://www.ncbi.nlm.nih.gov/pubmed/19539997
Br J Dermatol. 2006 Oct;155(4):680–7. Skin colonization by Staphylococcus aureus in patients with eczema and atopic dermatitis and relevant combined topical therapy: a double-blind multicentre randomized controlled trial.
http://www.ncbi.nlm.nih.gov/pubmed/16965415
Adverse Events of Acupuncture: A Systematic Review of Case Reports.
http://www.hindawi.com/journals/ecam/2013/581203/
Chapter Thirty-Six
The patient had a renal transplant about a month ago. She develops cough and chest pain.
A CT shows a large mass in the right lung.
Two features about the mass. One: it is homogenous. No necrosis. If it were a mold, it would have some necrosis, the halo sign if Aspergillus and the reverse halo sign if a Mucor.
The halo sign is a CT finding of ground-glass opacity surrounding a pulmonary nodule or mass. The reversed halo sign is a rounded focal area of ground-glass opacity surrounded by a crescent or complete ring of consolidation.
So I bet on a yeast, Cryptococcus, or Nocardia. She is from SE Asia, so I suppose I would have to also worry about C. grubii and Talaromyces marneffei, the yeast formally known as Penicillium marneffei.
Taxonomy is a dynamic discipline, and name changes of fungi with biotechnological, industrial, or medical importance are often difficult to understand for researchers in the applied field.
Tell me about it. I am way to old a dog to learn the new tricks of taxonomy. Thank Brin for Google. However, a lung mass would be very odd for Talaromyces.
The other concerning feature is it crosses the fissure invading a second lobe. Cryptococcus and Nocardia do not do that, and it would be an odd presentation for an Actinomyces.
The bronchoscopy has nothing: no organisms, and the galactomannan and beta d glucan are negative. That makes many of the molds, and Nocardia, less likely. Mucor is the one common mold that makes neither.
So we moved on to a percutaneous biopsy, and it was Rhizopus. It was a big mass, so it was resected, and so far, the transplanted kidney is tolerating the lipid amphotericin.
Invasive molds are not common in renal transplants, occurring in .87% of patients in one series, but the most most common was Mucormycosis in 11 of 21 patients. That was in the cyclosporin era. In another series, Aspergillus predominated.
I plan to give a long course of lipid amphotericin or as long as her kidney tolerates it, then, as I have no way to prove a cure, lifetime posaconazole or as long as her finances tolerate it.
This is the second pulmonary mucor in a month. If catastrophes come in threes, then I am due to see another soon.
Rationalization
The Diagnostic Value of Halo and Reversed Halo Signs for Invasive Mold Infections in Compromised Hosts.
http://cid.oxfordjournals.org/content/52/9/1144.full
PLoS One. 2013 Sep 3;8(9):e72222. doi: 10.1371/journal.pone.0072222. eCollection 2013. Geographically structured populations of Cryptococcus neoformans Variety grubii in Asia correlate with HIV status and show a clonal population structure.
http://www.ncbi.nlm.nih.gov/pubmed/24019866
Thorax. 1998 Oct;53(10):905–6. Disseminated Penicillium marneffei infection presenting as a right upper lobe mass in an HIV positive patient
http://www.ncbi.nlm.nih.gov/pubmed/10193382
Adv Appl Microbiol. 2014;86:199–249. doi: 10.1016/B978–0–12–800262–9.00004–4. Modern taxonomy of biotechnologically important Aspergillus and Penicillium species.
http://www.ncbi.nlm.nih.gov/pubmed/24377856
Ann Transplant. 2008;13(4):55–8. Invasive fungal infections following renal transplantation: a review of 2410 recipients.
http://www.ncbi.nlm.nih.gov/pubmed/19034224
Transplant Proc. 2009 Jun;41(5):1654–6. doi: 10.1016/j.transproceed.2009.02.072. Pulmonary fungal infections in kidney transplant recipients: an 8-year study.
http://www.ncbi.nlm.nih.gov/pubmed/19545701
Scand J Infect Dis. 2007;39(8):703–6. Mucormycosis after kidney transplantations: report of seven cases.
http://www.ncbi.nlm.nih.gov/pubmed/17654347
Why Do We Believe That Catastrophes Come in Threes?
http://abcnews.go.com/Technology/WhosCounting/story?id=7988416&page=1
As we approach the Crislip, er, Christmas holiday, I want to wish everyone a nondenominational seasonal greeting, delivered in a bright red Starbucks cup.
POLL RESULTS
Everyone
- Merry Christmas 39%
- Happy Holidays 23%
- Bah Humbug 13%
- Talk like pirate. http://uncyclopedia.wikia.com/wiki/Pastafarian\_Ritual 23%
- Other Answers 2%
- go home, the hospital is now closed.
Chapter Thirty-Seven
How long to treat? Got me. The real answer is until the patient is cured, but that is often a gray area, so instead, we use 3, a magic number, 10, because we have 10 fingers, or some multiple of 7, as we have 7 days in a week.
It is a good thing we did not evolve to have 18 fingers or 19 day weeks. Antibiotic use would be crazy. I always make recommendations that are prime numbers. Keeps people on their toes. But really, would 5 weeks and 5 days be any worse than 6 weeks for endocarditis? Probably not.
Duration depends in part on the bug, the organ infected, and, most importantly, source control. One of my colleagues imitates me as an old, demented nursing home patient, banging on my thigh, shouting, "drain the pus, drain the pus.”
How long to give antibiotics for an S. intermedius empyema? Got me. The abscess was a ball the size of a grapefruit, and it was all drained by VATS. Repeat imaging 5 days later shows it mostly gone; just some inflamed pleura left behind. It is sensitive to penicillin. The patient looks great on paper and in person. He is probably cured. The literature is of little help. The best I can find suggests
The average duration of chest tube drainage was 8.4 days and that of antibiotic treatment was 14.0 days.
So 13 days it is.
More puzzling is why the empyema: teeth are fine, no loss of consciousness, no choking episodes, doesn’t snore. I have no multiple of seven to answer that question.
Rationalization
Tenn Med. 2006 Feb;99(2):37–9.Streptococcus intermedius: an unusual cause of a primary empyema.
http://www.ncbi.nlm.nih.gov/pubmed/16681236
Jpn J Infect Dis. 2008 Nov;61(6):484–6. Clinical analysis of cases of empyema due to Streptococcus milleri group.rimary empyema.
http://www.ncbi.nlm.nih.gov/pubmed/16681236 http://www.ncbi.nlm.nih.gov/pubmed/19050362
POLL RESULTS
I base duration on
- multiples of 7 32%
- prime numbers 9%
- social security number 3%
- numerology 11%
- a random number generator, then write it in Roman numerals 28%
- Other Answers 18%
- Whatever the insurance idiot with the HS diploma has pre-authed.
- common sense and some literature guidance
- evidence
- Treatment duration depends on the type of infection I am treating for. It could be 3/5/10/14 days
- 5-7days depending upon the severity and organism
- One of my mentors used to say "odd numbers if less than ten; even if above"
Chapter Thirty-Eight
Six years ago, the patient had significant lymphadenopathy. He had an extensive workup: biopsy, serologies, even had the node sent for molecular diagnostics, the 16S. Nothing came back but the pathology, which showed necrotizing granulomas.
Years pass and the lymph nodes did not resolve, and he had no other symptoms of note except for fatigue. Nothing to suggest an infection, and the while the nodes did not resolve, they did not advance.
He was sent to me for a second opinion, and after the usual H&P, I had nothing. No exposure history of note and the prior evaluation was complete.
So why the adenopathy? Got me.
But.
He does have SLE, on therapy, and so I Googled it.
Yep. Lupus can have granulomatous lymphadenitis.
And the culture of the node grew moderate P. acnes. Is that significant? I had forgotten about this whole literature, mostly out of Japan, linking sarcoidosis and P. acnes in lymph nodes.
I don’t know if I buy it, but it is an interesting literature. Outside of the sarcoid literature, there is very little on P. acnes as a cause of lymphadenitis. But I have to wonder. Given all the information this century on P. acnes as a cause of a wide variety of infections, it may be an under-appreciated cause of granulomatous lymphadenitis. Someone reading this get to work and prove me right.
My patient is doing fine and has nothing to suggest sarcoidosis, so for now, it is a curiosity. I am going to blame the lymphadenopathy on the SLE.
Rationalization
BMC Pediatr. 2013 Nov 5;13:179. doi: 10.1186/1471–2431–13–179. Systemic lupus erythematosus and granulomatous lymphadenopathy.
https://pubmed.ncbi.nlm.nih.gov/24192007/
Respir Investig. 2013 Jun;51(2):56–68. doi: 10.1016/j.resinv.2013.01.001. Epub 2013 Mar 17. Etiologic link between sarcoidosis and Propionibacterium acnes.
http://www.ncbi.nlm.nih.gov/pubmed/23790733
Presse Med. 2005 Aug 27;34(14):1005–6. Propionibacterium acnes adenitis.
http://www.ncbi.nlm.nih.gov/pubmed/16225253
Acta Otolaryngol. 1998 Jun;118(3):443–6. Microbiology of cervical lymphadenitis in adults.
http://www.ncbi.nlm.nih.gov/pubmed/9655225
Chapter Thirty-Nine
Work always slows down from Christmas to New Years. I guess bacteria know it is the holidays and take time off.
Plus, we had an ice storm, so the city was partly shut down today. The yearly ice storm is one of the reasons I bought a house on a hill. I got to sleep in today; us old geezers need our rest.
Back in 2013, I wrote about a case of Brucella suis in a patient who slaughtered swine for his pig roasts. I had assumed that the Brucella had gone from feral pig to farm pig to human.
Nope.
As I was reading for my Puscast this weekend (available on iTunes), I came across Identification of Source of Brucella suis Infection in Human by Whole-Genome Sequencing, United States and Tonga.
In August 2013, a man in his 20s from Tonga, Polynesia, who had moved to the United States in June 2010, was examined in a hospital in Portland, Oregon after experiencing 4 weeks of fever, night sweats, headache, productive cough, shortness of breath, and weight loss. He also reported pleuritic chest pain and abdominal pain radiating to his back. A computed tomography scan showed lung and liver abnormalities. Blood cultures grew Brucella suis biovar 1.
Hey. I know what case. Not often you get follow up in a journal.
Since Brucella is a big deal if it is in farm populations, they did whole-genome sequencing on my patients Brucella and found that it was related to Tonga Brucella, not NW Brucella.
Really? He had been in the US for 3 years. Seemed a bit long for a Brucella to incubate, and I did not buy it. Until Pubmed. I found a case of a farmer who was 20 years away from pig farming when he came down with B. suis, and there are a smattering of other cases of prolonged incubation.
Therefore, our patient had significant previous exposure to B. suis, but 20 years elapsed before she presented with brucellosis. In contrast, the incubation period of brucellosis usually is only of several weeks’ duration. The case report that we present adds to the handful of reported cases of prolonged latency of brucellosis, most of which have been associated with B. suis infection.
That is S. aureus level dormancy.
Rationalization
This Little Piggie.
http://boards.medscape.com/forums/?128@@.2a5946ef!comment=1
Puscast
https://itunes.apple.com/us/podcast/persiflagers-infectious-disease/id79930757?mt=2
Identification of Source of Brucella suis Infection in Human by Whole-Genome Sequencing, United States and Tonga.
http://wwwnc.cdc.gov/eid/article/22/1/15–0843\_article
Visceral Abscesses Due to Brucella suis Infection in a Retired Pig Farmer
http://cid.oxfordjournals.org/content/32/8/e129.full.pdf
Brucellosis Reactivation after 28 Years.
http://wwwnc.cdc.gov/eid/article/16/12/10–0678\_article
Chapter Forty
I usually do this post Monday/Wednesday, but Wednesday, I took the evening off to see Patti Smith. Amazing. I hope I have half the energy and passion at 69 that she does. It is hard to believe that Horses is 40 years old. I was 18 when that album came out—one of the great albums by one of the great rockers.
The patient had the sudden onset of dysphagia, then fevers and chills. After three days of inability to take anything oral, she comes to the hospital and is admitted.
Blood cultures grow MRSA, and as part of the workup of the dysphagia, a CT was done showing a retropharyngeal abscess at the level of C3 with gas in it.
Is the gas from staph? Maybe. Gas is not common with S. aureus, but the worst gas I have ever seen was from an MSSA infection. The end result of metabolism is the production of gas, which my boys like to demonstrate loudly and proudly.
But gas next to the esophagus also suggests a perforation. She denied any specific injury but on direct questioning had been eating stale tortilla chips the day before.
Tortilla chips are like shuriken, and I have seen other esophageal tears that were temporally related to chips.
No perforation has been found, but it could have self-sealed.
For now, antibiotics and see if she gets better.
Rationalization
Subacute Necrotizing Fasciitis Caused by Gas-Producing Staphylococcus aureus.
http://link.springer.com/article/10.1007/s10096–003–1023–2
Am J Gastroenterol. 1992 Jan;87(1):128–31. Tortilla corn chip-associated esophageal perforation: an unusual presentation of achalasia.
http://www.ncbi.nlm.nih.gov/pubmed/1728109
N Engl J Med. 1990 May 10;322(19):1399–400. Esophageal tear caused by a tortilla chip.
http://www.ncbi.nlm.nih.gov/pubmed/2325744
Not Quite an Explanation
http://boards.medscape.com/forums/?128@@.2a05951d!comment=1
POLL RESULTS
Best Rocker Ever
- Patti Smith 6%
- Bruce Springsteen 30%
- Pete Townsend 15%
- Jimmy Plant 12%
- Joe Strummer 0%
- Other Answers 36%
- Joe Cocker
- mick jagger
- Rolling Stones
- Reuben and the Jets.
- carlos santana
- Nickelback! (jk)
- Grateful dead
- Brian May
Chapter Forty-One
Let The Chips Fall Where They May
I usually do this post Monday/Wednesday, but Wednesday, I took the evening off to see Patti Smith. Amazing. I hope I have half the energy and passion at 69 that she does. It is hard to believe that Horses is 40 years old. I was 18 when that album came out—one of the great albums by one of the great rockers.
The patient had the sudden onset of dysphagia, then fevers and chills. After three days of inability to take anything oral, she comes to the hospital and is admitted.
Blood cultures grow MRSA, and as part of the workup of the dysphagia, a CT was done showing a retropharyngeal abscess at the level of C3 with gas in it.
Is the gas from Staph? Maybe. Gas is not common with S. aureus infections, but the most extensive gas I have ever seen was from an MSSA infection. The end result of metabolism is the production of gas, which my boys like to demonstrate loudly and proudly.
But gas next to the esophagus also suggests a perforation. She denied any specific injury but on direct questioning had been eating stale tortilla chips the day before.
Tortilla chips are like shuriken, and I have seen other esophageal tears that were temporally related to tortilla chips.
No perforation has been found, but it could have self-sealed.
For now, antibiotics and see if she gets better.
She did.
Rationalization
Subacute Necrotizing Fasciitis Caused by Gas-Producing Staphylococcus aureus.
http://link.springer.com/article/10.1007/s10096–003–1023–2
Am J Gastroenterol. 1992 Jan;87(1):128–31. Tortilla corn chip-associated esophageal perforation: an unusual presentation of achalasia.
http://www.ncbi.nlm.nih.gov/pubmed/1728109
N Engl J Med. 1990 May 10;322(19):1399–400. Esophageal tear caused by a tortilla chip.
http://www.ncbi.nlm.nih.gov/pubmed/2325744
Not Quite an Explanation
http://boards.medscape.com/forums/?128@@.2a05951d!comment=1
POLL RESULTS
Best Rocker Ever
- Patti Smith 6%
- Bruce Springsteen 30%
- Pete Townsend 15%
- Jimmy Plant 12%
- Joe Strummer 0%
- Other Answers 36%
- Joe Cocker
- mick jagger
- Rolling Stones
- Reuben and the Jets.
- carlos santana
- Nickelback! (jk)
- Grateful dead
- Brian May
Chapter Forty-Two
Cellulitis is not an uncommon cause of consultation, usually because the patient does not get better immediately.
The usual reason patients do not get better immediately is that cellulitis sometimes takes time to get better. Patience is often all that is needed.
My totally unvalidated by the literature rules of thumb are that once antibiotics are started, the cellulitis gets worse for a day, then stabilizes, then, perhaps, recedes. Sometimes the cellulitis evolves from cherry-red to meat red to bruise red to better, especially if there is extensive disease and a lot of subcutaneous bleeding. And for every 50 pounds over ideal body weight, add a day to respond, although the last has some quasi-support
Hence, obese patients with erysipelas are prone to complications and should be carefully evaluated because of the potential severity of disease and the increased risk of failure of empirical antimicrobial therapy.
Bullous erysipelas, which is what I tend to see, is less common than I would have thought and is a more severe form of the disease:
Bulla formation is a complication of erysipelas, seen in our series in 5.2% of the patients (26 of 498 admissions for erysipelas and cellulitis). The course of the disease is protracted, requiring longer medical attention.
I had two patients with classic bullous erysipelas transferred in from out of state. One even had Crislip sign, the hallmark of Group A Streptococcus. I think. Neither had a microbiologic diagnosis, although one had an elevated ASO. I tend not to think of testing for streptococcal antigens to make the diagnosis. Perhaps I should.
Slow to respond and extensive cellulitis tends to lead to creative antibiotic choices. One had been on vancomycin and piperacillin-tazobactam, and who isn’t? I still have yet to order Zosyn, but that is the most popular decerebrate antibiotics du jour. The other had been on daptomycin, ceftaroline, and ciprofloxacin.
Both by ID doctors, by the way. Really? Well, bullous cellulitis does have a broader differential than Staph and Strep. I suppose if my patient had been doing poorly, I would have opted for adding clindamycin to my cefazolin, what with the Eagle effect, and my love of messing with toxin production. I would not have tried the therapy from 1932: milk injections.
Bullous impetigo is usually due to S. aureus making exfoliative toxin but in bullous erysipelas? I can’t find much as to the pathophysiology, only the suggestion that bullae may mean a mixed infection.
Our findings suggest that S. aureus is frequently involved in and probably contributes to synergy with beta-hemolytic streptococci to the complicated course of bullous erysipelas.
The literature also suggests you should fret re: MRSA. Perhaps. All my patients to date have responded to cefazolin. Which means I am about to get burned by an MRSA.
Rationalization
Crislip's Sign
http://boards.medscape.com/forums/?128@@.2a32c105!comment=1
A blistering disease: bullous erysipelas.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513413/
J Am Acad Dermatol. 1999 Nov;41(5 Pt 1):733–7. Bullous erysipelas: A retrospective study of 26 patients.
http://www.ncbi.nlm.nih.gov/pubmed/?term=10534636
Dermatology. 2006;212(1):31–5. Bullous erysipelas: clinical presentation, staphylococcal involvement and methicillin resistance.
http://www.ncbi.nlm.nih.gov/pubmed/16319471
TREATMENT OF ERYSIPELAS BY INJECTIONS OF MILK.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2520119/
Br Med J. 1932 Jun 18;1(3728):1124. FOUR CASES OF ERYSIPELAS TREATED BY MILK INJECTIONS.
http://www.ncbi.nlm.nih.gov/pubmed/20776908
Clin Exp Dermatol. 2011 Jun;36(4):351–4. doi: 10.1111/j.1365–2230.2010.03978.x. Epub 2010 Dec 24. Local complications of erysipelas: a study of associated risk factors.
http://www.ncbi.nlm.nih.gov/pubmed/21198795
Br J Dermatol. 1985 May;112(5):559–67. The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas.
http://www.ncbi.nlm.nih.gov/pubmed/4005155
Chapter Forty-Three
The patient presents with a stroke. And a fever. And all his blood cultures are positive for an alpha Streptococcus. Been there done that. Another case of endocarditis.
Well, not so much been there done that as the cultures grew Aerococcus urinae.
That is a bug that usually causes urinary tract infections in the elderly. For years the lab only reported alpha Streptococci, never speciating it further, but I would get the call from the geriatric service asking how to treat a UTI with the alpha strep. And I would ramble on about Aerococcus urinae.
There are about a dozen cases in the literature of this organism causing endocarditis, just enough that I can count them on both hands. They call me Count Rugen.
And this is my second case. So I have now reported 14% of the world's cases. Whoa.
I have no idea how to treat this organism based on the literature: people have used a variety of beta-lactams with and without aminoglycosides. Twelve cases is a collection of anecdotes, and the plural of anecdote is anecdotes, not data. And the pleural of infection is empyema. Yes, I know I have used that ‘joke’ before.
The MIC to penicillin is 0.023, so I am disinclined towards killing this elderly patients few remaining nephrons.
So a course of penicillin it is. And a cure.
Rationalization
Odd bacteria in bad places.
http://boards.medscape.com/forums/?128@@.2a5c5bfe!comment=1
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
Aerococcus urinae Endocarditis: A Report of Two Cases and Review of Literature.
http://www.pcp.org.ph/documents/PJIM/Volume%2048%20(2010)/Number%201%20(January-June)/Aeroccus.pdf
Chapter Forty-Four
The patient is an elderly diabetic who had periorbital cellulitis.
She was treated with a course of antibiotics and improved, but after stopping the Augmentin, the symptoms recurred, and a CT showed not only an abscess in the lateral muscle of the eye but the infection had eroded through the lateral bones of the orbit.
No trauma or other reasons for an infection.
The infection was debrided, the gram stain showed no organisms, and was, unfortunately, culture negative. Probably from the prior antibiotics.
There are certain areas of the body that give me old Frog and Toad shivers when operated on, and one of them is the eye. Your mileage will vary.
The bones of the orbit are not a place I have seen osteomyelitis. Like never.
Osteo is osteo, I suppose, but there are not a lot of cases I can find of osteomyelitis of the orbit when there is no associated sinusitis. Extension from the eye is odd.
There is one case of cat scratch disease in a kid, and she does have a cat, but that is about it.
With no MRSA isolated, I figure no MRSA present. MRSA will not get better on Augmentin. Maybe.
We further demonstrate that mecC-MRSA strains are susceptible to the combination of penicillin and the ²-lactam inhibitor clavulanic acid in vitro and that the same combination is effective in vivo for the treatment of experimental mecC-MRSA infection in wax moth larvae.
As far as I know, we dont have any mecC strains around, and the patients wax moth larvae appear fine.
So I guess it will be a course of ceftriaxone.
Rationalization
Laryngoscope. 2015 Aug 26. doi: 10.1002/lary.25529. Characteristics of patients treated for orbital cellulitis: An analysis of inpatient data.
http://www.ncbi.nlm.nih.gov/pubmed/26307941
Cat Scratch Disease Presenting as Orbital Abscess and Osteomyelitis.
http://jcm.asm.org/content/41/8/3991.short
Antimicrob Agents Chemother. 2015 Dec;59(12):7396404. doi: 10.1128/AAC.0146915. Epub 2015 Sep 21. Old Drugs To Treat Resistant Bugs: Methicillin-Resistant Staphylococcus aureus Isolates with mecC Are Susceptible to a Combination of Penicillin and Clavulanic Acid.
http://www.ncbi.nlm.nih.gov/pubmed/26392513
POLL RESULTS
I get the Frog and Toad shivers thinking about
- eye operations 11%
- a foley coming out with the balloon up 23%
- a Trump Presidency 50%
- Sammy Hagar fronting Van Halen 5%
- more books about Lisbeth Salander not written by Stieg Larsson 7%
- Other Answers 5%
- any of the Gopers as POTUS. I mean, really.
Chapter Forty-Five
I am not a fan of failure. But it happens. Antibiotics work more often than not, but for some infections, I expect a relapse. But not 4 years later. On antibiotics.
I saw the patient 4 years ago for an MSSA prosthetic knee infection. She had it debrided, poly exchanged, and a long course of combination antibiotics.
At the end of the treatment, I told her she had two choices. Stop antibiotics and see if the infection comes back or stay on chronic antibiotics. Most people do not want to risk another I&D and 6 weeks plus in a nursing home after removing their knee. For some patients, (and Tommy Chong) to be jointless for 3 months could be a death sentence.
I have been suggesting chronic suppressive antibiotics for years on the basis of clinical wisdom, i.e., making stuff up. I hate making stuff up, so it was nice to see a study to support me this year:
Chronic suppression with oral antibiotics increased the infection-free prosthetic survival rate following surgical treatment for periprosthetic joint infection. Patients who underwent irrigation and debridement with polyethylene exchange and those who had a Staphylococcus aureus infection had the greatest benefit.
I had seen her every year for an antibiotic refill, and the knee had been doing fine.
And then.
She twisted her knee in a pothole, the knee became red, hot, swollen, and tender, and a tap grew the same MSSA as before. On antibiotics. So annoying after four years.
Was it the trauma? I had vague memories of a literature where trauma caused reactivation of infection. I couldn’t find it, just a pair of case reports concerning tuberculosis. Anything that rare is likely true-true and unrelated.
So I am left with great annoyance at the relapse, and I feel sorry for the patient, who is now knee-less for 6 weeks and more.
Rationalization
J Bone Joint Surg Am. 2015 Aug 5;97(15):1220–32. doi: 10.2106/JBJS.N.00999. Chronic Suppression of Periprosthetic Joint Infections with Oral Antibiotics Increases Infection-Free Survivorship.
http://www.ncbi.nlm.nih.gov/pubmed/26246256
Neth J Med. 2008 Sep;66(8):363–4. Reactivation of dormant microorganisms following a trauma. Pneumonia, sternal abscess and calcaneus osteomyelitis due to Mycobacterium tuberculosis.
http://www.ncbi.nlm.nih.gov/pubmed/18809990
Chest. 1975 Oct;68(4):596–8. Reactivation of pulmonary tuberculosis due to trauma.
http://www.ncbi.nlm.nih.gov/pubmed/1175423
Chapter Forty-Six
Windows. Mac. iOs. Android. PowerChart. McKesson. Epic.
Today, thanks to Corporate (you know, Corporate, the people who never do the actual patient care) decided we needed a new interface on the EMR. Now my workflow has gone to crap, I can’t find anything, and no, we can’t give you the old interface back, thanks for asking.
My first computer was a TRS–80, and I have used dozens of computer operating systems, and I cannot learn another damn interface. Oh, it is supposed to make my life easier? I guess that is why the “Infectious Disease View” has a growth chart. So helpful.
I am increasingly glad I see the light at the end of the ID career tunnel. I just hope it is not an oncoming train.
As long as I am manifesting my EOG (Early Onset Grumpiness), what the hell is it about Augmentin?
I had a patient with a colonic perforation abscess. The cultures grew S. anginosis, and I suggested they finish up with a course of amoxicillin.
Of course, they wanted to send the patient out on Augmentin. They always want to use Augmentin instead of amoxicillin for Streptococci.
Streptococci do not make a beta-lactamase. Ever. So what does a beta-lactamase add? Nothing. So using Augmentin instead would be, well, stupid.
Not that Augmentin is totally without effect. It does add cost and increases the risk of diarrhea.
Besides prophylaxis after an animal bite, the only reason I can see to prescribe Augmentin is you don’t like the patient. Which is not a reason I would recommend.
I would bet dollars to donuts (what a weird idiom) that most people who prescribe Augmentin (or Zosin for that matter) have no idea why these drugs have sulbactam and tazobactam and for which organisms it is appropriate.
There is a lot of worry about inappropriate antibiotic prescribing and its effects on resistance. I wonder how much is due to many physicians not knowing the difference between a burro and a burrow when it comes to antibiotics. Unfortunately, education is not the answer:
The educational intervention studied demonstrated no substantial change to overall adherence. Given the frequent failure of such interventions, stronger and more directly mandated adoption of prescribing guidelines is recommended for surgical services. Future consideration should be given to focused computer-based solutions, integrated with electronic medical records where possible.
Really? Focused computer-based solutions, integrated with electronic medical records where possible? I am sure no one will be able to use the interface.
Rationalization
Educational Antimicrobial Stewardship Intervention Ineffective in Changing Surgical Prophylactic Antibiotic Prescribing.
http://online.liebertpub.com/doi/abs/10.1089/sur.2015.194
POLL RESULTS
The best interface is/was
- OS X 11%
- Windows 3.11 11%
- DOS 8%
- Pen and Paper 43%
- Analog am transistor radios 11%
- Other Answers 16%
- Win10
- Linux
- rotary dial telephone, weighing at least five pounds, black.
- carrier pigeon
- My old Palm pilot. It is still the best for scheduling.
- personal conversation
Chapter Forty-Seven
There are some antibiotics I wish I did not have to use—too many side effects.
Quinolones. Drives C. difficile, MRSA, sudden death, tendon rupture, AAA rupture, and retinal detachment.
Linezolid. Neuropathy, thrombocytopenia, and costs a mint.
Vancomycin. It is most notable for clinical failure, the archetype antibiotic with poor pharmacokinetics, too much toxicity, and a lack of efficacy, especially as the MIC in S. aureus keeps creeping up.
And others.
The patient comes in with fevers to 104, diffuse erythroderma of the head and chest with some periorbital sparing, no PMN’s and transaminases 5 x normal.
Extensive and expensive workup and history reveal nothing expect she had been started on TMP/Sulfa 5 days before the onset for a UTI.
The working diagnosis is TMP/Bactrim adverse reaction, a modified DRESS, perhaps DRSS since there is no eosinophilia.
My first consult, all those years ago, was a TMP/Sulfa induced neutropenia that died of reactivation military TB, so this case makes me nervous. When patients have a reaction to TMP/Sulfa, it always seems to be a log or 2 worse than reactions to other antibiotics.
It lasted for 7 days after stopping the TMP/Sulfa when her WBC popped up, and she got all better.
What was the mechanism for the neutropenia? I can’t find it. Trimethoprim has a high affinity for bacterial dihydrofolate reductase that is thousands of times greater than for human dihydrofolate reductase. Sulfamethoxazole inhibits dihydropteroate synthetase, which humans do not make.
So are there people whose dihydrofolate reductase is more bacterial than human? Don’t know. I can’t find any study of human polymorphism’s in dihydrofolate reductase as it relates to trimethoprim, only in pathogens.
And try as I might, I can’t find the original study (my google-fu is off, so I had to request the 1982 article from the library) that demonstrates the decreased affinity of trimethoprim for human dihydrofolate reductase. As best I can tell, the data dates from the late ’ the 70s/early 80’s long before it was ‘easy’ to check for polymorphisms. So just how good is the data behind that oft-repeated phrase “Trimethoprim’s affinity for bacterial dihydrofolate reductase is several thousand times greater than its affinity for human dihydrofolate reductase”?
Everyone points to the same 1982 Drugs reference. It makes me suspicious as I have seen other erroneous quotes perpetuated in the medical literature. Sometimes trying to find the answer to a simple question leads to so many dead ends looking for the data behind the dogma. If anyone knows better, let me know. And when I get the article from 1982, I'll see where it leads me and get back to you.
Rationalization
Pharmacotherapy. 2010 May;30(5):539. doi: 10.1592/phco.30.5.539. Trimethoprim-sulfamethoxazole-induced hepatotoxicity in a pediatric patient.
http://www.ncbi.nlm.nih.gov/pubmed/20412003
Am J Med. 2011 Jul;124(7):588–97. doi: 10.1016/j.amjmed.2011.01.017. Epub 2011 May 17. The DRESS syndrome: a literature review.http://www.ncbi.nlm.nih.gov/pubmed/21592453
J Infect. 2006 Feb;52(2):e49–52. Epub 2005 Jul 5. Trimethoprim-sulfamethoxazole induced rash and fatal hematologic disorders.
http://www.ncbi.nlm.nih.gov/pubmed/15996741
Dihydrofolate Reductase Gene Variations in Susceptibility to Disease and Treatment Outcomes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078682/
Drugs June 1982, Volume 23, Issue 6, pp 405-430 Trimethoprim: A Review of its Antibacterial Activity, Pharmacokinetics and Therapeutic Use in Urinary Tract Infections
Chapter Forty-Eight
The patient was admitted with rigors, fevers, RUQ, and a jump in her transaminases.
She was in a clinic during a rigor, blood cultures were obtained, and the patient was admitted. The diagnosis was an obstructed biliary drain, present due to hepatobiliary cancer.
Within a day, the cultures were positive for yeast, gram-positive cocci, and gram-negative rods.
Polymicrobial bacteremia is a bad thing.
The overall 30-day mortality rate of the polymicrobial group was significantly higher than those with monomicrobial BSIs (30.3 and 11.6%, respectively; p < 0.001).
And patients with polymicrobial are more likely to receive inappropriate antibiotics. And choosing the wrong antibiotic in serious infections increases mortality:
In meta-analyses of adjusted data, AAT was associated with lower risk of mortality (adjusted summary OR 0.43, 95 % CI 0.23–0.83; 6 studies, 1409 patients). Conversely, IAT increased risk of mortality (adjusted summary OR 3.30, 95 % CI 2.42–4.49; 16 studies, 2493 patients). A limited number of studies suggested higher cost and longer hospital stay with IAT.
So I rarely quibble with the initial antibiotics in ill patients as long as it kills the bugs that could kill the patient. But best guess, especially in patients with a lot of contact with the medical-industrial complex like mine, can be wrong, so you like to know the culture and sensitivity ASAP.
Where was the culture sent? I asked the resident.
I always call for the culture results myself. I often have an odd question or two, depending on what is growing. It is never an issue, and I call labs and hospitals every day for cultures. And they are always helpful and give the results. Always. Except.
Quest, they replied, and I swore.
A quest is “a long or arduous search for something.” Frodo went on a quest to Mt Doom to destroy the One Ring. I worried, from prior experience, that tomorrow I would undertake a quest to get the needed information.
The next morning I called for labs and, after identifying myself as a treating doctor calling from the ICU looking for the identification of the gram-positives and gram-negatives in the blood cultures, they game me nothing.
Zip. I had no information, account number or otherwise, to prove I could receive the information. As if some random person is calling from the ICU (everyone has caller ID these days) looking for very specific culture information.
So I called the clinic, who called the nurse who talked with the ordering doctor who called the lab who faxed it to the clinic who faxed it to the hospital who called me, then I walked back to the unit and read the report. You know, a quest.
It turns out the patient didn’t need the extra doses of vancomycin and meropenem she received while I waited the hour and a half it took to get the potentially critical and life-saving information that I should have received in three minutes on the initial phone call.
Yes, I know, blah blah blah HIPPA blah blah rules blah blah. Not impressed. I get my critical culture data from everyone else I call.
Such is the power of the fear of HIPPA, but it is not what I would call good care.
Rationalization
Acad Emerg Med. 2010 Oct;17(10):1072–9. doi: 10.1111/j.1553–2712.2010.00871.x. Characteristics and outcomes of polymicrobial bloodstream infections in the emergency department: A matched case-control study.
http://www.ncbi.nlm.nih.gov/pubmed/21040108
BMC Infect Dis. 2015 Sep 30;15:395. doi: 10.1186/s12879–015–1123–5. Appropriate initial antibiotic therapy in hospitalized patients with gram-negative infections: systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/26423743
Chapter Forty-Nine
I'm back. Five days hiking in the Palm Springs area. Miss me? I thought not.
I started with vinyl, then cassettes. My best friend had an 8 track, and it changed tracks with a loud clunk. Right in the middle of the guitar solo on Black Magic Women. Not the best technology. I remember the first time I heard a CD, Even in the Quietest Moments, and I was blown away. No hiss, no pop, no skip. I never looked back. But I miss all those mixtapes despite the crappy sound.
The patient comes in with all the usual signs and symptoms of tricuspid valve endocarditis. The preliminary PCR on the blood cultures is MRSA. Fine. The patient is on vancomycin, so fine.
The next day I check the cultures. At the top of the report, it says methicillin-resistant Staphylococcus aureus, so my eye goes straight to the vancomycin susceptibility.
MIC of 2. Expletive deleted. We have had plenty of MICs of 1, but only one case of late with an MIC of 2. I hope this is not a harbinger of further Staphylococcal evolution. And MICs of 2 have a higher failure rate.
Vancomycin MIC was significantly associated with mortality for MRSA infection irrespective of the source of infection or MIC methodology (odds ratio [OR], 1.64; 95% confidence interval [CI], 1.142.37; P < .01). This mortality association was predominantly driven by bloodstream infections (BSIs; OR, 1.58; 95% CI, 1.062.37; P = .03) and isolates with a vancomycin MIC of 2 ¼g/mL by Etest (OR, 1.72; 95% CI, 1.342.21; P < .01). Vancomycin MIC was significantly associated with treatment failure irrespective of source of infection or MIC methodology (OR, 2.69; 95% CI, 1.604.51; P < .01).
The patient has one of the worst embolic chest CTs I have seen, the lungs looking like swiss cheese, so I am even less enthusiastic about continuing the vancomycin. But what else? So I look at the other susceptibilities.
MIC to oxacillin is 0.25. What the? That is an MSSA. But all three blood cultures are the same. MecA positive, oxacillin sensitive. It's an MRSA MSSA?
I do a Pubmed and cannot find much, so I call the head of micro, and she tells me it is likely an empty cassette. See. I was going somewhere with that opening paragraph. I suppose to make it understandable to the youngsters, it should be called an empty thumb drive.
I had not heard of an empty cassette. It turns out
This phenomenon results from the fact that the currently FDA-approved assay doesn't detect the mecA gene itself (the one that encodes resistance), but rather a sequence that includes part of the staphylococcal chromosomal cassette mec element (SCCmec) and the S. aureus orfX gene. Since the SCCmec element is the cassette that carries the mecA complex, the assay should be goodthat is, unless the mecA complex has dropped out, resulting in an empty cassette, leaving a methicillin-susceptible S. aureus that tests positive by the Xpert assay.
The other possibility, not in this case, is there are also coagulase-negative Staphylococcus with the mecA in the blood culture that the assay detects.
The problem is it could revert to the real deal,
Approximately 3% of Staphylococcus aureus strains that, according to results of conventional phenotypic methods, are highly susceptible to methicillin-like antibiotics also have polymerase chain reaction (PCR) results positive for mecA. The genetic nature of these mecA-positive methicillin-susceptible S. aureus (MSSA) strains has not been investigated. We report the first clearly defined case of reversion from methicillin susceptibility to methicillin resistance among mecA-positive MSSA within a patient during antibiotic therapy.
So I am chicken to give nafcillin given how little room I have to maneuver given the severity of her disease. So ceftaroline it is, even with the suggestion that higher MIC to vancomycin may have increased beta-lactam failure.
With S. aureus, it is damned if you do, damned if you do. And it is getting just too complicated.
Rationalization
Clin Infect Dis. 2012 Mar;54(6):75571. doi: 10.1093/cid/cir935. Epub 2012 Feb 2. The clinical significance of vancomycin minimum inhibitory concentration in Staphylococcus aureus infections: a systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed?term=22302374
Prevalence and Genetic Relatedness of Methicillin-Susceptible Staphylococcus aureus Isolates Detected by the Xpert MRSA Nasal Assay.
http://jcm.asm.org/content/49/8/2996.full
Watch out for the drop outs!
http://haicontroversies.blogspot.com/2009/08/watch-out-for-drop-outs.html
J Infect Dis. 2015 Oct 26. pii: jiv512. Reversion From Methicillin Susceptibility to Methicillin Resistance in Staphylococcus aureus During Treatment of Bacteremia.
http://www.ncbi.nlm.nih.gov/pubmed/26503983
POLL RESULTS
It should be called an empty
- cassette
- 27%
- CD 0%
- thumb drive 18%
- iPhone 9%
- internet stream 27%
- Other Answers 18
- shell of a man, sucked dry by the system and pitched into the gutter to be gnawed by a stray cat, then ants, and taken by the wind.
Chapter Fifty
The patient has fevers, disorientation, and what appears to be numerous septic embolic lesions in his lung. She has a pacemaker.
So it is a pacer infection, right? Seems simple.
But.
Blood cultures are 1/2 S. mutans, an oral Streptococcus.
How often do oral Streptococci cause pacer wire endocarditis? Never. Well, never say never in medicine, but I can’t find a case on the Pubmeds. One series out of France had zero cases due to oral Streptococci causing pacer wire infections. Other Streptococci yes, but no viridans strep.
And.
She has no teeth.
The supposed pathogenesis of endocarditis from Streptococci strep is they gain access to the bloodstream by brushing and flossing, neither needed if you lack teeth. To get a viridans Streptococcal endocarditis in an edentulous patient is curious enough to warrant a case report. So if this is indeed due to S. mutans, how did it get there?
And.
The TEE showed no vegetations on either the valve or the wires.
But.
The patient is on warfarin for atrial fibrillation, so I would not expect to see large vegetations. Antiplatelet therapy may lead to smaller vegetations, and I suspect warfarin would as well, but no one has yet to do the study. Get to work people.
But.
How is she going to get numerous large septic pulmonary emboli if the warfarin is preventing vegetation formation?
And.
We have worked up every other cause of these lung lesions, including a biopsy, with no alternative diagnosis.
If.
I dont treat for endocarditis, and it is present the disease will only progress, and cardiology is understandably wary about pulling the leads.
And.
She has improved on antibiotics. While I usually say pacemaker wire infections can't be cured, is that true of very sensitive oral Streptococci? No one knows, but we are going to try.
Sometimes these cases are like light beer. They look like they might have all the right ingredients, but somehow they just do not satisfy.
Rationalization
Clin Infect Dis. 2004 Jul 1;39(1):6874. Epub 2004 Jun 14. Endocarditis in patients with a permanent pacemaker: a 1-year epidemiological survey on infective endocarditis due to valvular and/or pacemaker infection.
http://www.ncbi.nlm.nih.gov/pubmed/15206055
Int J Cardiol. 2009 Sep 11;137(1):e134. doi: 10.1016/j.ijcard.2008.05.040. Epub 2008 Aug 5. Streptococcus oralis endocarditis presenting as infective discitis in an edentulous patient.
http://www.ncbi.nlm.nih.gov/pubmed/18684532
Clin Infect Dis. 2007 May 1;44(9):11806. Epub 2007 Mar 14. Impact of prior antiplatelet therapy on risk of embolism in infective endocarditis.
http://www.ncbi.nlm.nih.gov/pubmed/17407036?dopt=Abstract
Int J Antimicrob Agents. 1999 Feb;11(2):15961. Beneficial effect of combination antiplatelet therapy on the development of experimental Staphylococcus aureus endocarditis.
http://www.ncbi.nlm.nih.gov/pubmed/10221420
POLL RESULTS
Some cases are like
- light beer 18%
- a box of chocolates 18%
- a Christmas present containing horse manure. How a neurosurgeon once described me. He meant it as a compliment. I think. 14%
- a fever-induced hallucination 25%
- a presidential candidate position statement 18%
- Other Answers 7%
- little traps designed to make you feel stupid!
- tasteless garbage. No nutritional value. Not filling. Leave a bad taste in the mouth. Flatulogenic in the extreme.
Chapter Fifty-One
I am starting to think that this blog is devolving into constant whinging. But it is certainly a feature (or perhaps a bug) of age and experience that issues that in the past would not annoy me Now. Piss. Me. Off.
The patient had grown up in the Central Valley of California and, in his youth, had acquired both HIV and Coccidioides meningitis. His course had been complicated, and he still has an Ommaya reservoir in his head.
Another feature of my advanced age is I remember a time before fluconazole when all the Coccidioides meningitis patients received amphotericin B through an Ommaya to keep the infection in remission. Most eventually died of complications of the shunt. Fluconazole suppression is one of the satisfying advances in medicine.
But his last decade has been uneventful. His viral load has been suppressed, and he has been on chronic fluconazole.
He presents to my hospital with a headache and confusion that has been progressing for several weeks. The LP shows 150 PMN's and a protein in the 600's. Imaging is negative.
It turns out his AIDS doc suggested the patient stop his fluconazole 6 months ago. The chart note, available thanks to EPIC, says something to the effect that since the patient has normal CD4 and has done well for a decade and has no problems, let's stop the fluconazole and see what happens.
As best I can tell, she did not call ID, nor did she try and look up the answer. If you did do a quick google search, a process that took me less than 30 seconds, you would come across the third hit on Google Scholar, Is It Ever Safe To Stop Azole Therapy for Coccidioides immitis Meningitis? And the answer?
No.
Sorry I shouted. Unlike love, Coccidioides is forever. The fluconazole should never have been stopped.
And Coccidioides has too many vowels to pronounce easily.
It really fries my bacon when people make decisions when they have no idea what they are doing, especially in an era when it is so easy to get an answer.
One other interesting pearl for me from the case, yet another example of the Baader-Meinhof Phenomenon in action. Just this November was Role of Coccidioides Antigen Testing in the Cerebrospinal Fluid for the Diagnosis of Coccidioidal Meningitis. I filed it away in memory, thinking I would never see a case of Coccidioides meningitis in my remaining years in practice. But it looks to be a great test:
Thirty-six patients with 42 episode of CM were studied. The sensitivity and specificity of CAg were 93% and 100%, respectively. Cultures of CSF were positive in 7%, antibodies were demonstrated by immunodiffusion in 67% and complement fixation in 70%, and immunoglobulin M and G antibodies were demonstrated by enzyme immunoassay in 8% and 85%, respectively.
So we sent the test off. Cultures are still negative, but the assay came back whopping positive. And back on fluconazole, the patient is feeling much better.
Rationalization
Is It Ever Safe To Stop Azole Therapy for Coccidioides immitis Meningitis?
http://annals.org/article.aspx?articleid=709422
Role of Coccidioides Antigen Testing in the Cerebrospinal Fluid for the Diagnosis of Coccidioidal Meningitis.
http://www.ncbi.nlm.nih.gov/pubmed/26209683
Chapter Fifty-Two
It is the little factoids that make ID interesting, and it is the interwebs that allow me to discover them. I wonder if ID would be half as interesting if I could not answer almost every question, scratch every brain itch, almost instantly.
The patient is admitted with fevers to 104, rigors and vomiting one hour after accessing his port. I have seen that pattern before. It takes about an hour from exposure to endotoxin to rigors and fevers. About 20 years ago, I had a patient who had her Groshong flushed once a month, and about an hour later, after getting home, she had fevers and rigors. This went on for 6 months or so as she thought it was part of the Groshong maintenance until she mentioned it in passing to a nurse. Her line cultures grow Enterobacter. The bacteria were in the lumen and pushed into the bloodstream once a month.
In this case, the cultures grew Serratia marcescens. Fine. But why?
My first thought was contamination from the compounding pharmacy from which she received some of her therapies, so I called them. Nope. They 'quarantine' all their IV's and wait for cultures from the specimens to be negative before shipping.
First dead end.
My second thought was tap water as Serratia can be found in tap, and other, water. He is on the water supply of a local suburb and has no pink stains in the shower, which may be due to Serratia. Serratia makes a distinctive pink/red pigment. If you have never read Serratia marcescens: historical perspective and clinical review from the NEJM, do so. One of those classics in ID that reviews some of the curious manifestations of Serratia and its pigments.
So maybe, maybe not. I have no way to easily test the water.
I asked about hot tubs, swimming pools, and the like. It turns out he uses mud baths to 'detox'. He takes the needle out of the port, lets it heal for a day or so, then visits the mud bath.
Could that be the source? Do mud baths have a microbiology? Depends on the mud. In a Roman thermae aquae iasae archaeological site
We found well-preserved, rocky artefacts that had been buried in the healing mud (fango) for more than 1,500 years at the Roman archaeological site at Varaždinske Toplice. This Roman pool with fango sediments and artefacts is fed from hot sulphidic springs. The fango exhibited nearly neutral pH, a high level of organic C, an elevated concentration of heavy metals and a high total microbial biomass, greater than 10(8) cells per gram of dry weight. The dominant microbes, assessed by molecular profiling (denaturing gradient gel electrophoresis), were affiliated with Thiobacillus, Sulfuricurvum, Polaromonas, and Bdellovibrio. Polymerase chain reaction screening for microbial functional guilds revealed the presence of sulphur oxidizers and methanogens but no sulphate reducers. The dominance of four Proteobacterial classes (α-, β-, δ- and ε-Proteobacteria) was confirmed by fluorescence in situ hybridisation; Actinobacteria were less abundant. Cultivable bacteria represented up to 23.4 % of the total bacterial counts when cultivation media was enriched with fango. These bacteria represented the genera Acinetobacter, Aeromonas, Arthrobacter, Comamonas, Ewingella, Flavobacterium, Pseudomonas, Rahnella and Staphylococcus.
Ick. In Germany
To estimate the danger of infection by a mud bath, especially in group baths, 51 mud samples were analysed before and 80 after application for faecal and total coliforms (FC, GC), Pseudomonas aeruginosa. Staphylococcus aureus and Candida albicans. The latter two germs were not identified in any of the samples. Pseudomonas aeruginosa was found in about 11% of the samples of both groups.
But no Serratia in mud on the Pubmeds. I did find it in the Proceedings of the Estonian Academy of Sciences, Geology 1992, where they cultured mud baths and found Serratia in addition to many other pathogenic gram-negative rods. Maybe the muds are not so much detoxifying as toxifying.
So the tap water? Colonization from the mud bath? Both or neither? No idea. But I love me the serendipity of what can be discovered with Google and a bit of curiosity.
Rationalization
Clin Infect Dis. 2014 Jul 1;59(1):1-8. doi: 10.1093/cid/ciu218. Epub 2014 Apr 11. Outbreak of Serratia marcescens bloodstream infections in patients receiving parenteral nutrition prepared by a compounding pharmacy.
http://www.ncbi.nlm.nih.gov/pubmed/24729502
Ann Agric Environ Med. 2006;13(2):323-35. Legionella and other gram-negative bacteria in potable water from various rural and urban sources.
http://www.ncbi.nlm.nih.gov/pubmed/17196009
N Engl J Med. 1979 Apr 19;300(16):887-93. Serratia marcescens: historical perspective and clinical review.
http://www.ncbi.nlm.nih.gov/pubmed/370597
Microb Ecol. 2015 Feb;69(2):293-306. doi: 10.1007/s00248-014-0491-5. Epub 2014 Sep 21. Microbiology of healing mud (fango) from Roman thermae aquae iasae archaeological site (Varaždinske Toplice, Croatia).
http://www.ncbi.nlm.nih.gov/pubmed/25241172
Offentl Gesundheitswes. 1991 Jul;53(7):338-43. Microbiologic studies of mud for human pathogenic bacteria before and after balneologic use.
Proceedings of the Estonian Academy of Sciences, Geology 1992
Chapter Fifty-Three
Making the correct diagnosis is all about pattern recognition. The problem is that humans are prone to faulty pattern recognition. The time I spend in the SCAM world (Supplement, Complementary and Alternative Medicine) has made me aware of the TNTC ways (well, I could count them, but I don’t want to bother) humans think poorly. I hope it has made me a better diagnostician. Especially since patients do not bother to read the textbooks before they come in and don't know what their signs and symptoms are supposed to be.
I am also biased to focus on the outliers, the signs, and symptoms that do not fit since I am often called when the standard diagnosis and treatment fails. Do you let the signs and symptoms make the diagnosis or the diagnosis determine the significance of the symptoms? I find a common mistake is to interpret the case through the lens of the diagnosis, focusing on those that support the diagnosis and ignoring those that do not: the confirmation bias. The best example of this is Fox News.
The patient is admitted with urosepsis: fevers, rigors, back pain, and E. coli in the blood and urine. Not uncommon for an elderly female. She receives standard treatment for a complicated UTI and, within a week, is back with the same E. coli in her blood and urine. So they call me.
Everything looks like a standard urosepsis except the back pain. It has never been flank, but midline and she complains of weakness in her legs and back spasms when she moves. The exam doesn’t help. There is neither tenderness over the kidneys, nor the LS spine where she hurts and her muscle strength is normal as best I can tell. It hurts too much to abduct her leg. But the pattern suggests the problem is in and around her LS spine, an area with multiple surgeries.
So I decided to go with the back as the source for the infection rather than a look at the kidneys for a perinephric abscess.
And the MRI showed a large paraspinal abscess and lumbar discitis.
I suspect the initial physicians credited the initial back pain to pyelonephritis. It is the path of least resistance, and I do not know that I wouldn't have done the same first time around. Common things are common after all.
Why the back infection? Yet again, I like to blame Batson's plexus, although this is the first time I can remember blaming Dr. Batson for a bladder infection going to the back in a female. All the cases I have seen in the past have been in males with a large prostate.
Listen to the history and the pattern it suggests. Works more often than not.
Now we can drain the pus and treat the patient.
Rationalization
Neurosurgery. 2011 Nov;69(5):1007-14; discussion 1014. doi: 10.1227/NEU.0b013e3182274865. History of the vertebral venous plexus and the significant contributions of Breschet and Batson.
http://www.ncbi.nlm.nih.gov/pubmed/21654535
Chapter Fifty-Four
Recently at one of my hospitals, they were nice kind enough to give an Infectious Disease View on PowerChart, and my workflow has gone to crap. It does offer a pediatric growth chart, and while I get a BUN and BUN/Creat ratio, I do not get the actual creatinine. How nice.
I guess it is a sign of age, but I just can’t take anymore interface changes. There is Powerchart, all the iterations of EPIC, Windows, Mac, iOS, Android, and every year for the last 30 years, they have changed. I can’t learn any more interfaces.
Stop it. Especially with the EMR, the interface changes have never, ever made life better. Ever. Only more confusing and more obtuse. I hate to say it, but I miss MS-DOS.
It occurred to me today that for the last month or so, I have seen a lot of invasive Group A Streptococcal infections. Bacteremias, soft tissue infections, even a community-acquired pneumonia.
Usually, I see a Group A Streptococcus every month or two, and I have seen at least a half dozen this year. This weekend on-call, there were several S. pyogenes infections on the sign-out list as well.
Is it real? I called the State, and they did not know but will look into it. Evidently, I am not the only one to have called and asked.
So maybe. Maybe not. Humans have a terrible habit of seeing patterns in random data, and we do not like randomness. I always suggest The Drunkard’s Walk: How Randomness Rules Our Lives as a good read that may change how you look at the world.
There have been nationwide outbreaks of Group A Streptococcus. It happened in New Zealand although the CDC says
Worldwide, rates of severe invasive disease (STSS and NF) increased from the mid–1980s to early 1990s. Increases in the severity of disease were associated with increases in prevalence of M–1 and M–3 serotypes (emm types 1 and 3). Rates of invasive disease have been stable over the last 15 years in the United States.
Who knows, maybe it is just the clustering illusion. But perhaps this is the beginning of another evolutionary change in Group A Streptococcus, aka, another damn interface change.
I hate interface changes.
Rationalization
J Infect. 2015 Feb;70(2):127–34. doi: 10.1016/j.jinf.2014.09.001. Epub 2014 Sep 20. Increasing incidence of invasive group A streptococcus disease in New Zealand, 2002–2012: a national population-based study.
http://www.ncbi.nlm.nih.gov/pubmed/25246363
Evolutionary pathway to increased virulence and epidemic group A Streptococcus disease derived from 3,615 genome sequences.
http://www.pnas.org/content/111/17/E1768
POLL RESULTS
The best interface is
- text 15%
- folders and mouse 4%
- speech 37%
- the Matrix. I want me that ethernet jack in the back of my skull 30%
- predictive ESP 11%
- Other Answers 4%
- The magic 8 ball
Chapter Fifty-Five
The patient is a young female, as an outpatient had an infection requiring a course of antibiotics which were completed. Then she disappeared to answer the siren call of heroin. A month ago, she was arrested and has been in jail. For a day or three before admission, she had fevers, and it was noted that she still had her PICC, unused, in the arm. She went to the ER, cultures were done, the PICC pulled, and antibiotics started.
Twelve hours later, she developed pleuritic chest pain and wheezes.
At that point, a CT was done, and there were three, peripheral, fluffy balls abutting the chest wall, one of which had cavitated.
Both blood cultures were negative, as was the TTE, but the catheter tip grew MSSA.
Hmmm. How to put it together?
I suspect a catheter infection and pulling out the catheter stripped off the clot, embolizing to the lung.
xw on a catheter is not a good thing:
Patients with Staphylococcus aureus colonization of an intravascular catheter but without demonstrated bacteremia within 24 h after intravascular catheter removal had a 24% (12 of 49 patients) chance of subsequent S. aureus bacteremia if they did not receive immediate antistaphylococcal antibiotics.
and
Staphylococcus aureus colonization of intravascular (IV) catheters as a strong predictor of subsequent S. aureus bacteremia (SAB), even in the absence of clinical signs of systemic infection. Bacteremia was effectively prevented by timely antibiotic therapy.
But one of the lesions had a cavity. So how long does it take a cavity to form in the lung after an embolic event? The best I can find is for sterile infarcts:
The greater the size of the infarct, the more likely its centre will be hypoxic and necrotic. Pulmonary infarct larger than 4 x 4 cm in size have a great tendency for cavitation (12). The median time from the first detection of consolidation to cavity formation is 14 days
So for an aseptic thrombosis, it is a late finding.
For septic emboli?
Chest radiograph showed the appearance of multiple cavitating nodules in both lung fields within a few days after admission.
So a "few days." Meh. Hard to know if the cavity could form in about 12 hours, although by history, that is the case for my patient. Maybe academic, since she will need a long course of antibiotics either way, but enquiring minds want to know.
Rationalization
Clin Infect Dis. 2008 Jan 1;46(1):114-8. doi: 10.1086/524077. Bacteremic complications of intravascular catheters colonized with Staphylococcus aureus.
http://www.ncbi.nlm.nih.gov/pubmed/18171225?dopt=Abstract
Medicine (Baltimore). 2011 Jul;90(4):284-8. doi: 10.1097/MD.0b013e31822403e9. Preventing Staphylococcus aureus bacteremia and sepsis in patients with Staphylococcus aureus colonization of intravascular catheters: a retrospective multicenter study and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/21694650?dopt=Abstract
Clin Microbiol Rev. 2008 Apr; 21(2): 305–333. Cavitary Pulmonary Disease.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292573/
Cavitary Pulmonary Infarct: The Differential Diagnostic Dilemma – A Case Report.
http://cdn.intechopen.com/pdfs-wm/25540.pdf
Nihon Kokyuki Gakkai Zasshi. 2006 Nov;44(11):879-84. [A case of septic pulmonary embolism showing the rapid appearance of multiple cavities in both lung fields induced by urinary tract infection].
http://www.ncbi.nlm.nih.gov/pubmed/17144591
Septic Pulmonary Embolism: Analysis of Twenty-Eight Cases.
http://www.tsim.org.tw/journal/jour24-1/07.PDF
Chapter Fifty-Six
The patient had an episode about two weeks prior to admission, where she could not speak for 24 hours. It passed. Then a week later it returned and persisted for five days: confusion with speech that was mostly random words.
The patient was admitted to the hospital.
The exam was negative except for the inability to produce coherent speech.
Screening labs were normal as was the exam: specifically, no cerebellar, posterior column, or pupillary abnormalities.
It was known at the time of admission that the peripheral RPR was 1:2048, and the CD4 was 140. The presumptive admitting diagnosis was tertiary syphilis.
But there were none of the classic physical findings of syphilis, and the problem with HIV is Occam is of no help.
With a focal speech problem, we were concerned there may be a secondary diagnosis: some mass lesions in the brain. I was worried more about toxoplasmosis than anything else, so before the LP, there was an MRI.
It looked textbook for HSV encephalitis. And the LP?
250 WBC, slightly elevated protein, and slightly decreased glucose. No red cells.
More like syphilis than HSV. And the HSV PCR was eventually negative.
But can syphilis present like ‘x’ where ‘x’ equals HSV. Of course, it can. It’s syphilis. Virtually any disease can be substituted for ‘x’. But I looked in PubMed to make sure. Yep.
We report a case of neurosyphilis with magnetic resonance imaging (MRI) brain scan findings compatible with a diagnosis of herpes simplex encephalitis with negative testing for herpes simplex virus in the cerebral spinal fluid. An extensive review of the literature has been undertaken revealing 24 cases worldwide where there are mesiotemporal changes on MRI concurrent with a diagnosis of neurosyphilis. Therefore, it is now well established that neurosyphilis, ‘the great imitator’, should be considered in the differential diagnosis in all patients demonstrating mesiotemporal changes on MRI, changes usually seen in herpes simplex encephalitis.
I have to admit that if the patient presented with the above clinical signs and symptoms and the MRI but no pre-existing RPR, I doubt I would have made the diagnosis of syphilis with alacrity. I would have called it HSV encephalitis and puzzled over the negative PCR and worried it was a tumor or some other process. The patient probably would have gone on to brain biopsy—good thing someone had already ordered the RPR.
The above abstract says it all: consider the ‘the great imitator.’
Rationalization
J S C Med Assoc. 1998 Jul;94(7):315–7. Neurosyphilis mimicking herpes simplex encephalitis.
http://www.ncbi.nlm.nih.gov/pubmed/9689783
Intern Med J. 2012 Sep;42(9):1057–63. doi: 10.1111/j.1445–5994.2012.02829.x. Mesiotemporal changes on magnetic resonance imaging in neurosyphilis.
http://www.ncbi.nlm.nih.gov/pubmed/24020346
For you youngsters, Rich Little: https://www.youtube.com/watch?v=78sSn3E\_Vvc
Chapter Fifty-Seven
The patient is admitted with acute community-acquired pneumonia. She has a right lower lobe consolidation with a complex pleural effusion. As an outpatient, she had been on a course of levofloxacin with perhaps had a wee bit of improvement.
All the cultures were negative, CBC and LFT’s normal, and a CT showed the aforementioned pneumonia, a lot of adenopathy in the chest, which was odd, and a big spleen. She is from SE Asia, TB status is unknown, and she has perhaps had a month of failure to thrive.
So TB? I don’t think. Safe is better than sorry, so airborne isolation and a bronchoscopy. All her smears, including two from a bronchoscopy, are negative.
Smear negative x 3 is how we exclude TB, although the prior quinolone use gives me pause. The use of quinolones, being active against MTb, can delay the diagnosis:
Previous treatment with any antibiotic, and not only a FQ, is associated with a delay in TB diagnosis.
and
14.4% of our patients with tuberculosis received a fluoroquinolone before the diagnosis. With a 34 day delay in antituberculous treatment and more frequent coexistence of underlying disease and hypoalbuminaemia, empirical fluoroquinolone treatment was associated with a poor outcome. Mycobacterium tuberculosis isolates could obtain ofloxacin resistance within 1 week.
But isolation is also associated with more complications, so we, and by we I mean I, took the patient out of isolation. The smears were negative, after all. Why get tests if you are not going to act on them? And then she was off to the OR for a biopsy of the lymph nodes as we were most worried about lymphoma.
Nope.
Necrotizing granuloma with AFB. Gosh Golly Gee Wilikers. Not what I really want to say, of course, but this is a PG-rated blog, and what I really said is usually limited to my response to a Trump speech. Well, not that bad. But safe to say, I was not happy.
So back into isolation after 24 hours. But how infectious is a non-coughing patient with smear-negative TB (assuming TB, as of 3 weeks, the cultures are still negative)? In the real world,
patients with smear-negative, culture-positive TB are responsible for 13% of TB transmission.
but in the hospital, probably not so much:
TB transmission seems unlikely and contact tracing not generally warranted after cumulative exposure <40 data-preserve-html-node="true" hours.
So I do not think I put my colleagues at any risk by taking the patient out of isolation. Still, I would not recommend hotboxing with a smear-negative, culture-positive TB patients.
Rationalization
Int J Tuberc Lung Dis. 2011 Aug;15(8):1062–8. doi: 10.5588/ijtld.10.0734. Is the delay in diagnosis of pulmonary tuberculosis related to exposure to fluoroquinolones or any antibiotic?
http://www.ncbi.nlm.nih.gov/pubmed/21740669
Thorax. 2006 Oct; 61(10): 903–908. Empirical treatment with a fluoroquinolone delays the treatment for tuberculosis and is associated with a poor prognosis in endemic areas.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2104756/
Tuberculosis Transmission by Patients with Smear-Negative Pulmonary Tuberculosis in a Large Cohort in The Netherlands.
http://cid.oxfordjournals.org/content/47/9/1135.full
J Occup Med Toxicol. 2009 Jun 8;4:11. doi: 10.1186/1745–6673–4–11. In-hospital contact investigation among health care workers after exposure to smear-negative tuberculosis.
http://www.ncbi.nlm.nih.gov/pubmed/19505310
Tuberculosis Outbreak in Marijuana Users, Seattle, Washington, 2004.
http://wwwnc.cdc.gov/eid/article/12/7/05–1436\_article
POLL RESULTS
I hate being wrong about
- Tb 33%
- basketball games 4%
- my spouse's mood 27%
- candidates 10%
- tax forms 15%
- Other Answers 12%
- the on call schedule
- Anything
- everything, all the time. But I'm a guy, and I can't change that.
- anything
Chapter Fifty-Eight
The patient is admitted with fungemia, Candida parapsilosis, from a central line. The central line is for short bowel syndrome and is used for TPN.
What to do?
Well, pull the line for starters. The odds are against salvage. People always want to try and save the line. Don’t. Wouldn’t be prudent.
In contrast, treatment of catheter-associated fungemia without removal of the catheter has a low success rate and is associated with higher mortality. Recent reports involving children with Candida CRBSI found that the addition of antifungal lock therapy led to a high cure rate without catheter removal, but there are insufficient data to recommend routine catheter salvage using this approach for this infection unless there are unusual extenuating circumstances (e.g., no alternative catheter insertion site).
And treat for, hmm, how long? The name of the reference used by the housestaff is UpToDate. I think it should be called TryingToCatchUp, since I am never, ever, up do date. There is just too much information and too little time.
But the IDSA just released the updated Candida guidelines, just in time, as my Ambien prescription has expired.
So is the recommendation still to treat for two weeks?
Recommended duration of therapy for candidemia without obvious metastatic complications is for 2 weeks after documented clearance of Candida species from the bloodstream and resolution of symptoms attributable to candidemia (strong recommendation; moderate-quality evidence).
Yep. So not behind on that issue. But the amazing thing is that 18 of 140, a mere 13%, of recommendations are based on high-quality evidence and most of those for mucocutaneous diseases. 85 of 140, a whopping 61%, were based on either low or very low-quality evidence, and that was for the more serious manifestation of Candida. It is almost as bad as the ILADS guidelines. Not quite, since the Candida guidelines are at least grounded in reality. But close.
The expert panel “believes,” which is what you do in the absence of data, 4 times and
It is intuitive that each patient with candidemia must be managed individually…
Sometimes it reads more like an alternative medicine review than a paper grounded in science. Isn’t a strong opinion based on low-quality evidence, so common in the guidelines, what presidential aspirants do? Are the guidelines the medical equivalent of a presidential debate? Without the hand size insinuations? I suppose calling it the Summary Opinion of Just A Bunch of Guys would not cut it.
I am glad to have the guidelines, they are nice summaries, but it shows how much work we, and by we I mean not me, have to do.
Rationalization
Clinical Practice Guidelines for the Diagnosis and Management of Intravascular Catheter-Related Infection: 2009 Update by the Infectious Diseases Society of America.
http://cid.oxfordjournals.org/content/49/1/1.full
Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America.
http://cid.oxfordjournals.org/content/62/4/e1.full
Lyme: Two Worlds Compared and Contrasted.
https://www.sciencebasedmedicine.org/lyme-two-worlds-compared-and-contrasted/
POLL RESULTS
I
- prefer high-quality evidence 60%
- make stuff up as I go along 14%
- defer to the opinions of my betters 9%
- have no betters; my opinion reigns supreme 2%
- don't let evidence interfere with my opinions. Too painful. 14%
Chapter Fifty-Nine
Fevers. Pancreatitis or Infection? Yes
There are questions with no good answers. One is whether the cause of fevers in a patient with pancreatitis is due to ‘just’ the pancreatitis, or is there a superinfection.
I don’t know. I ain’t psychic, and I can't tell the difference on clinical grounds. It is one of those consults that makes you, and by you, I mean me, feel like an intern again.
The problem is that often there is nothing to drain, the pancreas is surrounded by a phleg, mon. A phleg, as I understand it, is Jamaican slang for goop. So nothing to tap.
And the blood cultures are negative as if that means anything. If, instead of cultures, you use magic, aka 16s ribosome, you find the blood is full of pathogens.
Bacterial DNA was detected in peripheral blood from 68.8% of patients with acute pancreatitis, and more than half (60.4%) of the patients encountered polymicrobial flora. Translocated bacteria in patients with acute pancreatitis were primarily constituted of opportunistic pathogens derived from the gut, including Escherichia coli, Shigella flexneri, Enterobacteriaceae bacterium, Acinetobacter lwoffii, Bacillus coagulans, and Enterococcus faecium.
So is the fever from infection or pancreatitis? Yep. Probably the same thing.
So it is hard to not give antibiotics for fevers and an elevated WBC with a marked left shift, at least for a while, even when the blood cultures are negative, and there is no abscess, only phleg. And the benefit of antibiotics?
to date there is no evidence that supports the routine use of antibiotic prophylaxis in patients with SAP.
or is it
We concluded that prophylactic antibiotics may reduce mortality and length of hospitalization in patients with acute pancreatitis, but the quality of the evidence is low.
or is it
Prophylactic antibiotic treatment reduced occurrence of IPN, but did not affect mortality, NPN, or surgical intervention in patients with ANP.
or is it
The highest quality, currently available data fail to support prophylactic use of antibiotics, which should be added to treatment regimens only where infection has been proven.
or is it
Antibiotic prophylaxis of SAP does not reduce mortality or protect against infected necrosis, or frequency of surgical intervention.
or is it
Prophylactic antibiotic treatment is associated with a significant reduction of pancreatic or peripancreatic infection, non-pancreatic infection, and length of hospital stay, but cannot prevent death and surgical intervention in acute necrotizing pancreatitis.
or is it
Despite variations in drug agent, case mix, duration of treatment and methodological quality (especially the lack of double blinded studies), there was strong evidence that intravenous antibiotic prophylactic therapy for 10 to 14 days decreased the risk of superinfection of necrotic tissue and mortality in patients with severe acute pancreatitis with proven pancreatic necrosis at CT.
And on and on.
Newton's Law holds true. For every study, there is an equal and opposite study.
Rationalization
Crit Care Med. 2013 Aug;41(8):1938–50. doi: 10.1097/CCM.0b013e31828a3dba. Bacteremia in patients with acute pancreatitis as revealed by 16S ribosomal RNA gene-based techniques*.
http://www.ncbi.nlm.nih.gov/pubmed/23863226
Curr Gastroenterol Rep. 2011 Aug;13(4):336–43. doi: 10.1007/s11894–011–0198–4. Acute pancreatitis: should we use antibiotics?
http://www.ncbi.nlm.nih.gov/pubmed/21607652
Medwave. 2014 Aug 6;14(7):e6004. doi: 10.5867/medwave.2014.07.6004. Is antibiotic prophylaxis in acute pancreatitis beneficial?
(http://www.ncbi.nlm.nih.gov/pubmed/25333686).
Dig Surg. 2010;27(6):442–9. doi: 10.1159/000318780. Epub 2010 Nov 11. Prophylactic antibiotics reduce pancreatic necrosis in acute necrotizing pancreatitis: a meta-analysis of randomized trials.
http://www.ncbi.nlm.nih.gov/pubmed/21071945
Am J Surg. 2009 Jun;197(6):806–13. doi: 10.1016/j.amjsurg.2008.08.016. Epub 2009 Feb 13. Antibiotic prophylaxis is not protective in severe acute pancreatitis: a systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/19217608
Scand J Gastroenterol. 2008;43(10):1249–58. doi: 10.1080/00365520802130175. Prophylactic antibiotic treatment in acute necrotizing pancreatitis: results from a meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/18609129
Cochrane Database Syst Rev. 2003;(4):CD002941. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis.
http://www.ncbi.nlm.nih.gov/pubmed/14583957
Chapter Sixty
That awful feeling of your heart in your throat when anxiety hits, like when the return address on the mail is from the IRS or an attorney. Ick.
Worse, though, maybe when your throat is in your heart. Yeah. I’m going somewhere with this.
The patient is admitted with fevers and a severe sore throat. The CT shows diffuse inflammation along one side on the neck, and he is started in antibiotics. He never needs surgery as he never formed an abscess, and he improved without a microbial diagnosis. After a week of iv, he was sent home on Augmentin. Who isn’t?
Five days after stopping the antibiotics, he returns with pleuritic chest pain, shortness of breath, and hypotension.
An ECHO shows tamponade and off to the OR for a window. The fluid is mostly hemorrhagic and grows a Peptostreptococcus.
Huh?
He has horrible dentition but is otherwise without medical problems. CT of the chest shows no contiguous infection.
Anaerobes are not that uncommon as a cause of purulent pericarditis, especially in those with poor dentition:
Anaerobic bacteria predominated in patients with pericarditis who also had mediastinitis that followed esophageal perforation and in patients whose pericarditis was associated with orofacial and dental infections. The predominant aerobic bacteria were Staphylococcus aureus (3 isolates) and Klebsiella pneumoniae (2 isolates), and the predominant anaerobic bacteria were Prevotella species (4 isolates), Peptostreptococcus species (3 isolates), and Propionibacterium acnes (2 isolates).
and
Microbiology cultures isolated anaerobic agents of Fusobacterium spp., Corynebacterium spp. and Peptostreptococcus.
Although it is my first anaerobe. To date, all my percarditi (that should be the plural) have been S. aureus and Pneumococcus. So how did the bug get to the pericardium? From the teeth or the neck infection? And by the bloodstream or perhaps by way of the lymphatics?
... recent (recent for 1973, no so recent for us) Russian literature shows, some impressive connections between the tonsils and the heart have been demonstrated by injection of lymphatic channels in cadavers.
I like the photo that shows the neck and heart directly connected by the lymphatics. A nice route for bacteria. Anyway, that's my explanation, and I am sticking with it.
With a pericardial window and antibiotics, and the patient has done just fine.
Rationalization
Arch Intern Med. 1996 Sep 9;156(16):1857–60. Microbiology of acute purulent pericarditis. A 12-year experience in a military hospital.
https://www.ncbi.nlm.nih.gov/pubmed/8790081
Rev Port Cardiol. 2008 Jul-Aug;27(7–8):959–64. Purulent pericarditis with cardiac tamponade caused by anaerobic agents.
https://www.ncbi.nlm.nih.gov/pubmed/18959092
Circulation. 1973 Jul;48(1):9–18. The chain that links the heart to the throat.
http://circ.ahajournals.org/content/48/1/9.long
ANDRUISHIN IN: Data towards the anatomic substantiation of the spread of infection from the tonsils and pharynx to the heart. Arkh Anat 56: 45, 1969
POLL
The quickest way to a man's heart is
- through his stomach
- through a sternotomy
- by the neck lymphatics
- chest wall with an ax
- inappropriate answer here
- hormonally mediated intervention followed by something traditional from Joy of Cooking.
Chapter Sixty-One
The More Things Change, The More Things Are Different
Jean-Baptiste Alphonse Karr I’m not.
The patient is admitted with leukemia, neutropenic fevers, and an acute soft tissue infection with bacteremia.
Cultures of the blood grow group G Streptococcus, S. equilsimilis, not a surprise. But she does form a large thigh abscess, which is odd. While there are a smattering of monomicrobial abscesses with Group G streptococci, it is not high on my list of causes of soft tissue abscesses.
We drained the pus (it grew S. equilsimilis), put her on antibiotics, and waited. She did well. After a month, the WBC returned, kind of, as the chemotherapy was not effective for induction. Her ANC is barely over 1000.
While never febrile, her alkaline phosphatase shot up. Odd. Maybe antibiotics, but under the circumstances, I fretted about hepatosplenic Candida.
Definitely not typical as no fever or leukocytosis, but she is at risk. So we ordered a CT of the liver.
Nope. Negative.
She as so few PMN’s perhaps she can’t generate the CT lesions and fever, which are the (usual) hallmark of the disease. I have seen two cases in my career that had negative CT’s, but the diagnosis was made on liver biopsy. We see this:
In two cases, pathologic proof of candidiasis was established even when all imaging studies were normal. For maximum imaging sensitivity, patients should be studied with US and nonenhanced and enhanced CT. Even when both US and CT scans are negative, if there is a strong clinical suggestion of candidiasis, open biopsy is recommended.
That was then. This is now. We also sent off a beta-d-glucan, and it was off the wall positive. While not specific for Candida, there is no other indication of an alternative fungus.
If the proof is in the treatment, and it often is not, she did improve on fluconazole. So close enough for blogging.
Rationalization
Medicine (Baltimore). 1985 Mar;64(2):75–88. Infections due to Lancefield group G streptococci.
http://www.ncbi.nlm.nih.gov/pubmed/3974442
Hepatosplenic Candidiasis.
http://www.nejm.org/doi/full/10.1056/NEJMicm040112
Hepatic Lesions of Chronic Disseminated Candidiasis May Become Invisible During Neutropenia.
http://www.bloodjournal.org/content/90/10/3858?sso-checked=true
Hepatosplenic candidiasis: wheels within wheels.
http://pubs.rsna.org/doi/abs/10.1148/radiology.166.2.3275982
Chapter Sixty-Two
That was then.
Years ago, when I was an intern, I was called to see an admit with horrible abdominal pain. Yes, they called the internal medicine team for a surgical case. Still happens. Where does the Lone Ranger take his garbage? To the dump da da dump da da dump dump dump.
It was a young male, thrashing about on the gurney with horrible abdominal pain. I was impressed. He looked to be in 11/10 pain.
My attending? He noted that patients with peritonitis lie still. They do not thrash. And while the patient said the abdominal palpation resulted in horrible pain, when distracted, his exam was fine. When my attending knocked gurney with his thighs? Nothing.
Turns out, the kid was due to go into the Marines the next day and was freaking out.
This is now.
The patient had abdominal surgery five days prior to admission and was admitted with MOSF. The CT showed free air but could have been due the surgery. The abdominal exam was not that impressive, but he was on pain medications.
But I asked the patient: did the speed bumps hurt?
The husband replied that every speed bump and pothole caused excruciating pain. There was a fun study that received, I think, an undeserved Ig Noble, on speed bumps and abdominal pain:
The analysis included 64 participants who had travelled over speed bumps on their journey to hospital. Of these, 34 had a confirmed histological diagnosis of appendicitis, 33 of whom reported increased pain over speed bumps. The sensitivity was 97% (95% confidence interval 85% to 100%), and the specificity was 30% (15% to 49%). The positive predictive value was 61% (47% to 74%), and the negative predictive value was 90% (56% to 100%). The likelihood ratios were 1.4 (1.1 to 1.8) for a positive test result and 0.1 (0.0 to 0.7) for a negative result. Speed bumps had a better sensitivity and negative likelihood ratio than did other clinical features assessed, including migration of pain and rebound tenderness.
While the study was in appendicitis, I suspect it is a nice historical hint of peritonitis, the modern equivalent of jiggling the bed.
In the OR there was a hole in the bowel and peritonitis.
I like the question and ask it of all my abdominal pain patients, like the patient today.
CT is negative for an explanation of his severe abdominal pain, but he, too, noted that speed bumps were pure misery. Work up is in process. I'll let you know, as I am suspecting cholesterol emboli, which would be a first for me.
It is often the little things that are not only fun but can be a hint at bigger issues.
Now how to apply the information that all mammals empty their bladder in 21 +/- 13 seconds.
Rationalization
Pain over speed bumps in diagnosis of acute appendicitis: diagnostic accuracy study. BMJ 2012; 345.
http://www.bmj.com/content/345/bmj.e8012
Chapter Sixty-Three
Back from 5 days in SoCal, complete with a brand new head cold. Probably from all that sun exposure and the resultant vitamin D toxicity.
Ever have a 737 slam on its breaks halfway down the runway on takeoff? We did. Those planes can stop very fast if need be. Evidently, another plane was crossing the runway when it shouldn't. The pilot apologized, and we all had a free drink. As far as I was concerned, no apologies were necessary. I was just glad not to die in a fiery crash in LAX so I can continue to write this blog.
The patient is admitted with flank pain and fevers. The CT showed a small stone in the left ureter with partial obstruction, so probably pyelonephritis.
He is otherwise healthy except for multiple sclerosis.
Blood and urine cultures are done, and after 48 hours, the cultures are growing a yeast from two separate days.
Didn’t expect that.
A sustained fungemia makes me worry about an endovascular infection. Like S. aureus, but less so, I worry that it is a bloodstream infection seeding the kidney, not urosepsis. Although there is no reason for yeast endocarditis and the ECHO is negative.
Initially, I had the patient on micafungin due to worries about an endovascular infection, and he responded clinically and microbiologically despite the poor penetration of micafungin in the urine.
The lab could not ID the organism and had to send it out. After five days, we had an ID: Saccharomyces cerevisiae, the yeast for baking and brewing. The patient did neither.
Why did this occur? I have no answer. No risks, no immunosuppression, and no probiotics.
So bad luck it is.
I can remember less than a handful of Saccharomyces cerevisiae fungemias, my last case in 2011 associated with drinking Pruno.
When I was a fellow, I had an AIDS patient who was a homebrewer who had Saccharomyces cerevisiae in his blood. I guess you say I knew what aled him. Long time readers have seen this feeble attempt at humor before, but I never tire of it.
I changed the patient to fluconazole, to which it was sensitive, and he did fine.
Rationalization
J Mycol Med. 2015 Dec;25(4):303 5. doi: 10.1016/j.mycmed.2015.09.004. Epub 2015 Oct 27. [Urinary infection by Saccharomyces cerevisiae: Emerging yeast?].
http://www.ncbi.nlm.nih.gov/pubmed/26522963
Clin Infect Dis. 2005 Jun 1;40(11):1625 34. Epub 2005 Apr 25. Saccharomyces cerevisiae fungemia: an emerging infectious disease.
http://www.ncbi.nlm.nih.gov/pubmed/15889360
An Evening Drink.
http://boards.medscape.com/forums/?128@@.2a06bdbb!comment=1
POLL RESULTS
When flying I worry most about
- burning to death in a crash on take off or landing. 15%
- sitting near the toilet in the back 22%
- slow internet speeds 1%
- getting sucked out a window during decompression. The movie Airport traumatized me for life. 4%
- getting bird flu or XDRTB from that coughing idjet in the seat behind me 49%
- Other Answers 9%
- Being able to ever walk again after the lower-extremity ischemic necrosis.
- boredom
- Nothing, I'd enjoy sitting near the toilet in the bath for a quickie with the GF :D
- getting a blood clot in my leg
- waking up from the nightmare. I don't fly, but I do dream of flying often, as a human with the power to levitate at will. It's really pretty cool.
- enough legroom and general comfort during the journey
Chapter Sixty-Four
The good names always come too late. My wife gave me a diagnosis last week. Witzelsucht: “a morbid tendency to pun, make poor jokes, and tell pointless stories.” Such a perfect name for the blog. Does anyone want to buy me the domain? At $2495, it would make an ideal birthday present.
The patient and her family all come down with gastroenteritis: pure diarrhea. A week into the illness, the family improved, but she developed fevers and rigors. Seen in the ER, work-up was negative, including a CT, and she was sent home.
Less than a day later, the blood cultures were positive for Enterococcus. She is called back in, and repeat blood cultures are positive with Enterococcus as well.
The sine qua non of endocarditis is a sustained bacteremia, but with no other reason for bacteremia and an ECHO with moderate MR but no vegetation, I feel that I need to treat for endocarditis.
Most of the enterococcal endocarditis I see is a complication of a UTI, often in men with large prostates. Or is it large prostrates? I think it is former, but many of my patients suffer from the latter.
Can the gastroenteritis be the reason for the endocarditis?
Well, there is the well known association between S. bovis endocarditis and colon cancer.
There is the lesser-known association between ulcerative colitis, and, to a lesser extent Crohn’s, and endocarditis
On the basis of these data, a 44-fold overrepresentation of inflammatory bowel diseases among the 213 patients with endocarditis was calculated…
But there are only a smattering of cases of endocarditis following a GI infection.
It kind of surprises me upon reflection that we do not see more endocarditis after various forms of colitis. There are 48 million GI infections a year in the US. One would think that this much GI upset would lead to more bacterial endocarditis as a complication of bacterial translocation than is reported.
Or maybe no one looked.
Or maybe they all get antibiotics, aborting any endocarditis.
Or maybe it isn’t a thing.
But with a GI organism on a valve after a GI disease, I am inclined to blame the gastroenteritis.
Rationalization
Ulster Med J. 1991 Apr; 60(1): 114–116. PMCID: PMC2448624 Infective endocarditis due to ulcerative colitis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2448624/
Am J Med. 1992 Apr;92(4):391–5. Increased risk of bacterial endocarditis in inflammatory bowel disease.
https://www.ncbi.nlm.nih.gov/pubmed/1307218
POLL RESULTS
My favorite foreign word we need to use in English is
- Witzelsucht 9%
- Schadenfreude: pleasure derived from the misfortunes of others. 38%
- Backpfeifengesicht: A face badly in need of a fist. 32%
- Sgiomlaireachd (Scottish Gaelic): When people interrupt you at meal time. 3%
- Tatemae and Honne (Japanese): What you pretend to believe and what you actually believe, respectively. 15%
Chapter Sixty-Five
Yesterday was grilled cheese sandwich day. I hope you celebrated; I did. Darigold white cheddar grilled cheese. MMmmmmmm.
Today? It evidently was diabetic foot infection day. All my consults were variations on that theme.
One was a bit curious. The patient had an ulcer of the heel for three years that slowly healed using a variety of modalities, and for 3 months, the foot had been doing fine.
One month ago she had an angioplasty of the leg, and last week the heel became red, hot and tender.
The plain films revealed nothing. I was quite surprised. One would think that sitting above an ulcer for several years, there would be some sort of change in the bone, but the cortex looks pristine.
An MRI was not done due to an ICD, an overrated contraindication. Maybe. I can’t ever talk a radiologist into doing one. And there is the whole induction of current in a wire by a changing magnetic field that gives me pause.
So she gets a bone scan, and it glowed in the heel in a manner consistent with osteomyelitis.
I presume a true positive, but is this acute osteomyelitis? Or a relapse of a chronic infection. If acute, why? The bone has been covered for months. If chronic, where are the bone changes?
So here is my idle speculation. Is this kind of, sort of, maybe, perhaps a boney immune reconstitution inflammatory syndrome?
With the revascularization of the leg, she was now able to deliver WBC and all the other constituents of an inflammatory response to the bone and is now symptomatic for an infection that had been sitting there for months, doing nothing.
IRIS and osteomyelitis is reported in AIDS with a variety of fungi and AFB, but no cases in normalish people.
Revascularization IRIS would be an excellent explanation for the clinical findings, but there ain’t no such thing.
Until today.
Rationalization
Heart. 2015 Dec;101(24):1950–3. doi: 10.1136 heartjnl–2015–308495. Epub 2015 Sep 29. Safe use of MRI in people with cardiac implantable electronic devices.
http://www.ncbi.nlm.nih.gov/pubmed/26420818
Chapter Sixty-Six
Everyone is going to die. Sorry. That includes you. I suspect that I will die of an infectious disease; I have the nagging suspicion that doctors die of their specialty. I am glad I am not an Ob doc.
The younger the death, the more tragic the death. A 99-year-old succumbs to pneumonia, it is sad, but at least they had a good run.
I particularly hate influenza. I remember the 2009 H1N1 pandemic, where we had around 15 deaths in our hospital system, mostly young people. Some anti-flu vaccine dumb asses say the flu is not such a bad illness. I would like them to say that to the grieving parents.
Besides the increase in mortality from flu that year, the other oddity was 3 of the deaths were from encephalitis, a complication I had not seen before or since, at least until this year.
The patient is a middle-aged female with a transplant. She had PCR proven influenza B. Odd this year. As of last week, my lab has identified slightly more influenza B than A, rather than the usual 5–10%. This pattern is seen in the rest of the state, but not nationally. She was treated with oseltamivir, and her pulmonary symptoms were improving.
Eight days into her disease, she became confused, unresponsive, with increased muscle tone and tremors. Work up revealed nothing but an LP and MRI consistent with encephalitis. All the usual tests were negative.
The presumptive diagnosis was influenza B encephalitis.
Most of the cases of influenza B encephalitis are in children and associated with mutism, which this patient had. It can be both an acute process and a post-influenza process. It is rare in the adult, and I wonder how much her immunosuppression resulted in this manifestation of influenza b.
While oseltamivir may be less effective in influenza B, her pulmonary status and fevers were getting better. It was a bit too early to think it was more autoimmune than direct invasion. So infectious or post-infectious? Don’t know.
I never did find out if she had been vaccinated; her care was at Outside Hospital.
The other aspect that occurred to me with this case is all I know about influenza concerns A. The information on B? As one review notes
Following a comprehensive search of peer-reviewed and gray literature sources, we found that published data on influenza B epidemiology and burden are scarce. Surveillance data show frequent co-circulation of both influenza B lineages during influenza seasons, but little is known about its impact, especially in adults, and the clinical burden of influenza B remains unknown.
What data there is suggests B is every bit as bad as A, contrary to popular belief. We just do not see B as often.
Rationalization
Encephalitis Associated with Influenza B Virus Infection in 2 Children and a Review of the Literature.
http://cid.oxfordjournals.org/content/36/7/e87.full
Clin Infect Dis. 2014 Mar;58(6):775–84. doi: 10.1093/cid/cit922. Epub 2013 Dec 18. Neurological manifestations of influenza infection in children and adults: results of a National British Surveillance Study.
https://www.ncbi.nlm.nih.gov/pubmed/24352349
Lower Clinical Effectiveness of Oseltamivir against Influenza B Contrasted with Influenza A Infection in Children.
http://cid.oxfordjournals.org/content/44/2/197.abstract?sid=9b255f75-e122–4857-b401–868a30ce36af
Hum Vaccin Immunother. 2016 Feb 18:1–10. A comprehensive review of the epidemiology and disease burden of Influenza B in 9 European countries.
https://www.ncbi.nlm.nih.gov/pubmed/26890005
Chapter Sixty-Seven
I always treat the aich eee double toothpicks out of S. aureus bacteremia.
Even when coming from a boil, MRSA in the bloodstream usually gets at least 4 weeks of IV therapy, usually vancomycin.
The plural of anecdote is anecdotes, not data, but this year I have had a flurry of relapses after a month of vancomycin.
All the cases have three commonalities. The MIC to vancomycin was 1, the relapses were in bone, and the patients had no initial symptoms of a bone infection.
Given the high MIC and the poor penetration vancomycin into bone, I likely did little with the antibiotics.
...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).
I suspect those concentrations may be an overestimate. I really want to give up on vancomycin now and forever.
There is an old mistype from 1988, Vancomycin: Renewed interest in an old drag that I am no longer so sure is a typo. Vancomycin is such a drag. But are the options any better?
The most recent patient had bacteremia with MRSA from a boil, MIC 1, who received four weeks of 8 mg/kg/d daptomycin due to the need for a once a day antibiotic. Two months after finishing antibiotics, she presents with a septic joint.
Evaluation eventually finds a Brodie s abscess in the femoral neck, and on CT, you can see a defect in the femoral head that could be where the abscess ruptured into the joint. This is perhaps the third Brodie s I have seen and the first in the femoral neck.
It is an odd place for a Brodies, not unheard of, although I could have a horrible garbage disposal accident and still count the reported cases.
While there was no clinical suspicion initially of a bone infection, daptomycin should have been sufficient to eradicate the Staph:
After a single-dose intravenous infusion, bone daptomycin concentrations were above the MIC of daptomycin for Staphylococcus aureus in all subjects, and the median bone penetration percentage was 9.0%
Now? Probably ceftaroline. It had bone levels of 2.83 ± 1.50 in a study were vancomycin levels were 0.52 ± 0.69.
Although I am not so sure any antibiotic really treats MRSA except cold steel.
Rationalization
Antimicrob Agents Chemother. 1988 Sep; 32(9): 1320 1322. PMCID: PMC175859 Vancomycin concentrations in infected and noninfected human bone.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC175859/
Efficacy of the new cephalosporin ceftaroline in the treatment of experimental methicillin-resistant Staphylococcus aureus acute osteomyelitis.
http://jac.oxfordjournals.org/content/65/8/1749.full
POLL RESULTS
The best way to kill MRSA is
- daptomycin 6%
- ceftaroline 4%
- autoclave 37%
- thermonuclear bomb 24%
- you kidding? you can't kill a staph 22%
- Other Answers 6%
- Depends how sick the patient is, but cotrim is good for most.
- 10% sodium hypochlorite. Try developing resistance to THAT stuff. Stupid germs....
- make them watch the Republican debates
Chapter Sixty-Eight
Everything is Going to Hell in a Hand Basket
In dog years, I turned 413 today. Where did the time fly? I can still put on my socks in the morning standing on one foot, but that is about the last vestige of my youth that remains. Gone are hair, vision, and sanity.
Years ago, I remember reading (I think it was in the History of Civilization) that there are some Sumerian clay tablets from 2000 BC complaining about the decline in standards, that kids don’t respect their elders and don’t have any work ethic. I keep that in mind when I want to complain that everything is going to hell in a handbasket.
Because it is. Well some things are.
What would you do if you had people with no education in science-based medicine, but instead having an education mostly grounded in pseudo-sciences like homeopathy, acupuncture, and hydrotherapy? People with little or no postgraduate training. Have you ever known a new medical school graduate who was even barely competent to diagnose and treat any disease? Not me.
In Oregon, the legislature has made these under-educated, untrained pseudo-science practicing primary care providers. And I am starting to see the results.
The patient had traveled to Asia a few years ago and came back with a bump on his abdomen. It had waxed and waned over the years, and he is concerned it may be a parasite of some sort.
Maybe. I have seen a few odd subcutaneous parasites over the years, those that have wandered into an organ where it did not belong. I have seen a gnathostomiasis and a cysticercosis that caused a chronic subcutaneous nodule. There are a variety of others that can do the same:
Nematodes are roundworms that cause diseases with cutaneous manifestations, such as cutaneous larval migrans, onchocerciasis, filariasis, gnathostomiasis, loiasis, dracunculiasis, strongyloidiasis, ascariasis, streptocerciasis, dirofilariasis, and trichinosis. Tremadotes, also known as flukes, cause schistosomiasis, paragonimiasis, and fascioliasis. Cestodes (tapeworms) are flat, hermaphroditic parasites that cause diseases such as sparganosis, cysticercosis, and echinococcus.
So maybe it is a parasite, although the exposure history is not impressive. I will try to get it biopsied, which he has been hesitant to do.
He has been seen by an ND, and by the patients report had a negative saliva test for parasites (!) but did have a positive test whereby the ND held a variety of glass vials against the bump and had a positive test (!!).
“That is how she diagnoses parasites,” my patient said.
What? Sounds like a version of the wackaloon SCAM (Supplements, Complementary and Alternative Medicine) known as applied kinesiology. And since the test was positive, the patient was given a prescription for metronidazole (!!!). Look at the list above, see much there treatable by metronidazole? Of course not. But standard ND practice.
But it’s a parasite, don’t you know. I sometimes get the impression that SCAM providers do not understand that parasites have life cycles, exposure risks, and specific treatments. Like toxins, parasites are a nonspecific evil humor treated with antibiotics, again with antibiotics being a generic idea, not a specific drug with a specific activity.
Thanks to EPIC, I could look at the ND notes, but they were unrevealing. The only documentation I could find suggested the patient had congestion of liver and kidney relieved by acupuncture. As if that is any better.
I have seen a slight uptick in these kinds of consults as people with travel exposures are seeing ND’s first rather than reality-based providers. And I expect to see more.
See. Some things really are going to hell in a handbasket.
Rationalization
Naturopathic Diaries.
http://www.naturopathicdiaries.com/
The truth ND's do not want you to know.
Disingenuous: Deconstruction of a naturopathic white paper.
https://www.sciencebasedmedicine.org/disingenuous-deconstruction-of-a-naturopathic-white-paper/
Am Acad Dermatol. 2015 Dec;73(6):947–57; quiz 957–8. doi: 10.1016/j.jaad.2014.11.035. Mucocutaneous manifestations of helminth infections: Trematodes and cestodes.
https://www.ncbi.nlm.nih.gov/pubmed/26568338
Parasite Testing Through Kinesiology
https://rhrplus.com/b2evolution/blogs/index.php/Jane/parasite-testing-through-kinesiology
Chapter Sixty-Nine
The patient is admitted with fevers, emboli in the conjunctiva, and a vegetation of the mitral valve.
The blood cultures grow S. gordonii. I do believe that is the first S. gordonii endocarditis I have seen. My prior, and first, case of S. gordonii was a discitis back in 2010; I know as I wrote about it at the time. Have I been doing this blog that long? Man.
S. gordonii is one of the oral Streptococci, and the patient does have bad dentition, so I have a reasonable source for the infection as well.
S. gordonii is a relatively rare cause of reported endocarditis (one hit on PubMed), perhaps as most labs do not bother to go beyond calling it a “viridins Streptococcus.” With the MALDI-TOV, I get the suspicion more bugs are getting named, and like in fantasy novels, when you know a creature's true name, you can control and kill it.
The MIC is 0.1. Again. It seems like that is all my oral Streptococci. I also suspect that there is MIC creep to penicillin among the oral Streptococci, with more and more being intermediate to penicillin, but I can find no reviews to support that observation.
He also had a cluster of non-itching, non-painful blisters on his forehead. It didn’t quite look like Zoster. He had no history of prior cold sores nor any exposure, but I assumed this is a fever blister in an odd place.
So I sent a viral culture, and it came back Herpes Simpex Virus–1. I have seen HSV just about everywhere at one time or another. Where fingers go, so follows HSV, so the forehead was not that odd. The most curious place was right between the shoulder blades, the place I cannot reach on my own. Never did figure out just how it got there.
The classic infection to cause HSV 1 to reactivate is bacterial meningitis, although there are numerous other factors associated with fever blisters:
Reactivation of the virus and re-initiation of the productive cycle may sometimes occur spontaneously, but this is more often secondary to infection with human immunodeficiency virus, cancer, exposure to UV light, organ transplantation, pregnancy or menstruation, fever, cold, X-ray irradiation, chemotherapy, fractures, tooth extraction, sideropenia, gastrointestinal upset, surgery or other stress-inducing states.
It occurred to me that while HSV is common, and almost all my patients have a fever, I rarely see fever blisters. So why does fever lead to a fever blister? Evil humors, i.e., cytokines.
These results suggest that TNF-alpha and IFN-gamma play a protective role in acute infection with HSV–1. We also examined the rate of reactivation induced by ultraviolet (UV) light in latently infected mice over 60 days postinoculation… The rates of reactivation in IFN-gamma(-/-) mice and TNF-alpha(-/-) mice were significantly higher than that in B6 mice; 16% (4 of 25) showed reactivation in B6 mice, 47% (9 of 19) in IFN-gamma(-/-) mice, and 48% (10 of 21) in TNF-alpha(-/-) mice. These results suggest that IFN-gamma and TNF-alpha play an important role in acute infection and reactivation from latency.
Endocarditis, and other infections, should be a nice inducer of cytokines, so why I don’t see more fever blisters eludes me.
Rationalization
A Strep I had not heard of. Which one? I am not telling in the title. Call it a strep tease.
Enferm Infecc Microbiol Clin. 1994 Jan;12(1):41–2. [Endocarditis caused by Streptococcus gordonii].
https://www.ncbi.nlm.nih.gov/pubmed/8155757
J Infect. 2008 Dec;57(6):493–4. doi: 10.1016/j.jinf.2008.10.001. Epub 2008 Nov 21. Herpes reactivation in patients with bacterial meningitis.
http://www.ncbi.nlm.nih.gov/pubmed/19027168
J Interferon Cytokine Res. 2002 Jun;22(6):671–6. Role of IFN-gamma and tumor necrosis factor-alpha in herpes simplex virus type 1 infection.
http://www.ncbi.nlm.nih.gov/pubmed/12162877
Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis.
http://www.clinicalmicrobiologyandinfection.com/article/S1198–743X(14)63911–2/fulltext
Chapter Seventy
I remember years ago, a neurosurgeon told me, Crislip, you are like getting a Christmas present, and when you unwrap it, there is horseshit.
I always assumed it was meant as a compliment, that he enjoyed my consultation, but didn't always like my conclusions. But then, my ego is such I would interpret such a statement with a positive spin. Zaphod Beeblebrox has nothing on me.
But I did spend a lot of my day today telling doctors things they did not want to hear: a TEE here, a needed surgery there, a prolonged course of antibiotics there.
But I always tell the house-staff -- if your day is not a total pain in the neck, you are not paying proper attention.
The patient is an elderly male who is admitted with urinary symptoms: fevers, frequency, hematuria.
UA has pyuria. And the culture grows Actinomyces. Say what?
Or a better, say why?
Shooting from the hip, I figured the only way you would get Actinomyces in the bladder would be abdominal Actinomyces eroding into the bladder. But I went to Pubmed just in case.
There are not a lot of hits. There are a few cases from the organism eroding into the bladder, but there are more cases of primary disease-causing a mass in the bladder like a tumor. And a few cases are from infections in urachal remnants. With men always consider the prostrate as it is often pronounced, but only 2 cases in the Pubmeds.
So I told the team we had to go looking. CT? Normal. Cystoscopy? Normal.
So I found bupkis, i.e., nothing at all.
Bupkis, by the way, literally means small round fecal pellets, referring to the shape of goat droppings.
Maybe my neurosurgeon was off by an animal. But at least I learned a bit about Actinomyces.
Rationalization
Int J Urol. 2007 Oct;14(10):96971. Primary vesical actinomycosis: a case report and literature review.
https://pubmed.ncbi.nlm.nih.gov/17880305/
Can Urol Assoc J. 2013 Jul-Aug;7(78):E5024. doi: 10.5489/cuaj.405. Actinomycosis of the urinary bladder.
https://pubmed.ncbi.nlm.nih.gov/23914269/
Korean J Urol. 2010 Jun;51(6):43840. doi: 10.4111/kju.2010.51.6.438. Epub 2010 Jun 21. Urachal actinomycosis mimicking a urachal tumor.
https://pubmed.ncbi.nlm.nih.gov/20577614/
POLL RESULTS
I least want to be considered
- horse 6%
- chicken 17%
- bull 5%
- goat 13%
- dumb 50%
- Other Answers 9%
- mostly harmless.
- heartless
- the elephant in the room...
- zebra
Chapter Seventy-One
The colon is not a pleasant place, being filled with, among other things, a tremendous number of bacteria.
I am always amazed these bacteria do not escape to wreak havoc more often.
Inflammation, from infection or ischemia or toxin or IBD, should result in bacteremia. Who would want to stick an open wound into stool? Not me.
But bacteremia, at least clinically significant bacteremia, is rare from most bowel problems that do not result in perforation.
The patient had C. difficile diarrhea for no apparent reason. No prior antibiotics or GI issues. It happens.
…that as many as 45.7% of patients with CDI had no prior exposure to antibiotics in the 90-day period before the onset of CDI. In another case-control study, 52% of patients had no antibiotic exposure in the 4-week time period prior to CDI onset.
Probably as C. difficile is often like any other food-borne diarrhea.
… there is mounting concern over food-borne and zoonotic spread of C. difficile in the community.
It responded to metronidazole then relapsed, and around the time of the relapse he started to have progressive neck pain and fevers.
Because of diabetes and renal insufficiency, the MRI of the neck without contrast was done and negative.
The next day both blood cultures grew a gram-negative rod, identified as an Enterobacter, and an MRI with contrast showed a cervical epidural abscess that was subsequently drained.
Most of the spontaneous epidural abscesses (no discitis or trauma) I see are S. aureus. Gram-negative? Not so much. But it also happens:
The following causative G(-) pathogens were detected: Klebsiella pneumoniae (three patients), Salmonella spp. (three), Escherichia coli (two), Enterobacter spp. (two), Aeromonas hydrophila (one), and Prevotella melaninogenica (one). Both Enterobacter strains were resistant to multiple antibiotics. Of the 12 patients, eight (66.7%) had spontaneous SEA, whereas the remaining four had postneurosurgical SEA. Thoracic, lumbar, and thoracolumbar spine segments were the most commonly affected.
I presume the source was translocation from the pseudomembranous colitis. There is but one similar case I can find on PubMed, also with Enterobacter. Probably a coincidence. All the other reports concern bacteremia with C. difficile or fungemia from probiotics.
I wonder, though, what 16S testing on the blood of a pseudomembranous colitis patient would show. I would bet on lots of organisms.
Rationalization
Community-acquired Clostridium difficile infection: an increasing public health threat.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962320/
J Clin Neurosci. 2011 Feb;18(2):213–7. doi: 10.1016/j.jocn.2010.05.015. Epub 2010 Dec 24. Clinical characteristics and therapeutic outcome of Gram-negative bacterial spinal epidural abscess in adults.
https://www.ncbi.nlm.nih.gov/pubmed/21185728
J Clin Pathol. 1985 Nov;38(11):1314–5. Bacteraemia secondary to pseudomembranous colitis.
https://www.ncbi.nlm.nih.gov/pubmed/4066992
Chapter Seventy-Two
Last week I walked into a patient room to do a consult. She looked up at me, put her hands together in prayer, and said in a thick Russian accent, “Thank you, Jesus Christ and God for sending me an old doctor, someone with experience.”
Finally, I get some credit for age.
It was quite a contrast to the other event that day. ID in Portland has never been economically viable, and we have always needed institutional support. Hopefully, we make up for the cost with decreased morbidity, mortality, cost, and length of stay from consultations, as well as the benefits of infection control, P&T, and antibiotic stewardship. Oh, and the estimated $90,000 a year in free curbsides.
ID is a value-added specialty. However, not everyone thinks so. It was suggested that rather than the $1.25 I was earning at one hospital that a 0.3 FTE was more appropriate. At about 1/30 the 1.8 million a year the last CEO received, it was felt to be exorbitant, so we ended our 26-year relationship. I may be an old doctor with experience, but evidently not even worth the price of a small coffee at Starbucks to some. Me bitter much?
Oh well. At least it is a point in my career where I no longer need to worry. I am of an age where fewer meetings are appealing, but I will miss the fun of the clinical cases.
The patient had the abrupt onset of first nausea and vomiting, then high fevers. She went to the ER and was markedly hypotensive, so was admitted for sepsis. I saw her 24 hours later for the question of tampon related toxic shock syndrome (TSS). At that time, her only complaint was an almost cholera level diarrhea.
Looking at the case definition, the answer was no. She had no rash and no organ involvement. A low calcium and red conjunctiva were it. And in 24 hours, she was all better.
I thought it was probably a GI illness, but if it was TSS, it was a forme fruste of the syndrome, which this old, experienced doctor has seen before.
Vaginal cultures grew MSSA, and on day three, she had a splotchy rash on the trunk and legs, but not the palms or soles. This would be the second time I have seen the rash of TSS occur late after the patient is off pressors. I wonder if the vascular constriction of pressors prevents the rash from being seen. No skin perfusion, no redness?
So TSS-ish. But from what. TSST is a super-antigen and
TSST–1 was the first marker toxin identified for TSS, and this toxin is currently accepted as the cause of 100% of menstruation-associated TSS cases. TSST–1 is the only PTSAg known to cause TSS from intravaginal sources; this is presumably due to its unique capacity to cross mucosal surfaces.
100% is a pretty specific number, as in all.
Staphylococci also make enterotoxins that can cause non-menstrual TSS, and her predominant symptom was profuse diarrhea. So maybe it was due to an enterotoxin, and TSST–1 causes 99.9999999999999999999999999999999% of menstruation-associated TSS? Seems unlikely.
Or maybe she had some protective antibody to modify the course of the disease.
I don’t know.
S. aureus makes a jaw-dropping number of toxins as they try their very best to kill us, and I have no way to find out which one. Like much of clinical ID, it is fun to think about but with no practical application.
Rationalization
The Complexity, Relative Value, and Financial Worth of Curbside Consultations in an Academic Infectious Diseases Unit.
http://cid.oxfordjournals.org/content/51/6/651.full
Toxic shock syndrome (other than Streptococcal) (TSS) 2011 Case Definition.
Exotoxins of Staphylococcus aureus.
http://cmr.asm.org/content/13/1/16.full
Food Poisoning and Staphylococcus aureus Enterotoxins.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153270/
POLL RESULTS
In the US the best way to recognize value is to
- give money 58%
- offer complements 3%
- offer a laural and hardy handshake 6%
- give chocolates and flowers 3%
- hold the screen door open as they leave so it doesn't hit them in the ass 28%
- Other Answers 3%
- look around for that which is grossly undervalued by the most people. There's your best stuff.
Chapter Seventy-Three
Sometimes Catastrophic, Sometimes Mostly Harmless
There are those processes that strike fear in the hearts of ID docs everywhere. Gas gangrene is high on that list.
I think I was traumatized as a child from the scene in Gone with the Wind where they amputate a gangrenous leg without anesthesia. THE most horrific scene in a movie ever.
The few gas gangrenes I have seen in my career have been rapidly fatal in a particularly horrifying way. The only infection I have seen that can be worse is Meningococcus.
So when I get called about a C. perfringens, it always grabs my attention.
The patient is a healthy young female who has the abrupt onset of severe abdominal pain.
At first, it was thought to be an acute appendicitis, but a CT showed a 6 cm tubo-ovarian abscess (TOA).
A percutaneous drain was placed, and all it grew was C. perfringens. The patient looked just fine and, except for quiescent inflammatory bowel disease, no issues.
It is the weird thing about C. perfringins; sometimes it causes the most overwhelming infection imaginable, and sometimes it is remarkably benign. It will grow from the blood or a gallbladder or an abscess, and the patient will be just fine, smoking a cigarette and watching Sesame Street. Well, that was actually a 16-year old I saw on my OB rotation as a student who I was tasked with informing about postpartum birth control options. But you get the idea.
So I went looking. C. perfringens associated with TOA? Nope. C. perfringens associated with IBD and TOA? Nope.
TOA a rarely result in ID involvement, and while they can contain
Escherichia coli, Bacteroides fragilis, Bacteroides species, Peptostreptococcus, Peptococcus, and aerobic streptococci.
as well as a hodgepodge of case reports of odd bugs, Clostridia are not on the list.
You know the ID motto: find pus, drain pus, find bug, kill bug. Go home.
And so I did.
The patient did just fine.
Rationalization
Rev Infect Dis. 1983 Sep-Oct;5(5):876 84. Tubo-ovarian abscess: contemporary approach to management.
http://www.ncbi.nlm.nih.gov/pubmed/6635426
1983? The year I graduated medical school. Maybe historical rather than contemporary, although the approach to TOA has not really changed.
POLL RESULTS
I most fear
- gas gangrene 0%
- meningococcus 8%
- a letter from the IRS 2%
- the 2016 Presidential election results 70%
- being buried alive. 11%
- Other Answers 10%
- My mother in law
- ..fear itself.
- other people. Because Sartre, you know.
- cigarette-smoking Sesame Street watchers
- Being attached by meat-eating dinosaurs.
- mama
Chapter Seventy-Four
The patient awoke from sleep with abrupt onset chest pain. The pain was over the sternum, crossed the midline, 9/10, worse with breathing and sitting up. Several days later, fevers started, and he came to the ER and was admitted.
Six months ago, the patient had a second kidney transplant for polycystic kidney disease and had been doing well with no issues.
The exam was negative, except he had severe chest pain when I pushed on the sternum and thumped on his back.
He had a mild leukopenia and transaminitis. CK normal.
Work up? ECHO normal. Chest CT with some hazy infiltrates and bilateral pleural effusions. EGD was normal.
I could not quite figure out the source of pain. I wondered if maybe an epidural abscess that was causing referred pain, but I really couldn’t fit this severe pain into a pattern I recognized.
I suggested maybe an MRI of the spine, but I was flummoxed and left for the weekend.
My coverage saw the patient and sent a quantitative CMV PCR, and it came back over 2 million. He had a CMV positive donor but had been CMV positive as well.
And there was this shift in perspective. I had focused entirely on the pain, it was the hinge-point of my differential diagnosis, and it was the wrong hinge-point.
I didn’t have a single neuron fire for CMV, but once the CMV came back, I suddenly saw the skull rather than the lady looking in the mirror. Of course, it was CMV. Duh.
The diagnosis was staring me in the face, and I did not see it. That happens now and then, where I walk down the wrong path, focusing on the wrong symptom.
The pain? Still not certain, but I suspect a CMV neuropathy. I have seen a few cases over the years in AIDS patients.
12 AIDS patients with a clinically, electrophysiologically, and pathologically homogeneous painful peripheral neuropathy had a significantly higher rate of any or active clinical cytomegalovirus (CMV) infection than did a group of 30 AIDS controls. In 9 patients this syndrome began in close temporal association with clinical infection with CMV. Painful peripheral neuropathy in AIDS may be caused by a CMV dorsal root ganglionitis.
So why not a transplant patient as well? It is what it is. I am still not satisfied I understand the pain.
For now, it is a course of ganciclovir and see how he does.
And some days, I wish I was half as smart as I like to think I am.
Rationalization
Rinsho Shinkeigaku. 2001 Jan;41(1):31–5. [A case of acute sensory neuropathy associated with cytomegalovirus infection].
http://www.ncbi.nlm.nih.gov/pubmed/11433764
Multiple etiologies of axonal sensory motor polyneuropathy in a renal transplant recipient: a case report.
http://jmedicalcasereports.biomedcentral.com/articles/10.1186/1752–1947–5–530
Lancet. 1989 Oct 21;2(8669):937–41. Association of painful peripheral neuropathy in AIDS with cytomegalovirus infection.
https://pubmed.ncbi.nlm.nih.gov/2571861/
Chapter Seventy-Five
What is worse: Candida on a valve or in the esophagus?
Last night we saw The Who for what is likely their last show in PDX. Tremendous. I have mentioned in the past that The Who is the best band of all time. It is one of few statements on this blog that is absolutely true. I thought as I watched Pete Townsend play at age 70, amazing for such an old geezer. And then I realized I am only 11 years younger. Damn. I’m not going to die before I get old, and neither is Pete or Roger.
The patient has short bowel syndrome and is TPN dependent. At outside hospital, she had Candidemia, presumptively line related, that was treated with a course of high dose fluconazole.
Several weeks after the end of the treatment, she is again febrile, and blood cultures again grow Candida albicans. The line is pulled. No Candida on the catheter. TTE shows nothing, but the 1–3 beta D glucan rises after pulling the line, and four days later, blood cultures are still growing Candida.
That would be a sustained fungemia, the sine qua non of an endovascular infection. There is no clot in the subclavian, and the TEE shows a vegetation on the aortic valve.
Crap.
This is perhaps the fourth or 5th case of Candida endocarditis in my career. I always worry about endocarditis in presumptive line-related infections, but rarely see it. It would appear that endocarditis occurs in maybe 5% of those with Candidemia.
The results of transthoracic echocardiography (TTE) suggested infective endocarditis (IE) in 5/172 patients (2.9 %), and the result of transesophageal echocardiography (TEE) was positive in 10/87 (11.5 %). Among 11 confirmed cases of CIE, the disease was clinically unsuspected in three patients. At least 4.2 % of all candidemic patients have CIE. CIE is frequently clinically unsuspected and echocardiography is required to demonstrate a high proportion of cases.
I have cured at least one case of right-sided Candida endocarditis with medical therapy, although it is not the preferred option. The patient is actively bleeding (long story) and so not a candidate at the moment for valve replacement and anti-coagulation.
So for now, it is temporizing with antibiotics. I went with micafungin as the patient has renal issues and
Mortality was not affected by use of surgical therapy or choice of antifungal agent. A subgroup analysis was performed on 33 patients for whom specific antifungal therapy information was available. In this subgroup, 11 patients received amphotericin B-based therapy and 14 received echinocandin-based therapy. Despite a higher percentage of older patients and nosocomial infection in the echinocandin group, mortality rates were similar between the two group.
And it seems to be working, at least for now. But long term po fluconazole is not going to be an option with short bowel. No bowel, no absorption, although it may be interesting to have her on a 5-day course of fluconazole while on the micafungin and see if there are measurable fluconazole blood levels.
Here is the weird thing in the guidelines. They suggest 150 mg micafungin a day for endocarditis. Fine. For Candidemia, they recommend 100 mg a day for both neutropenic and non-neutropenic. Fine. And esophagitis? 150 a day! That must be one wicked illness.
The guidelines say
Thus, higher doses of echinocandins are recommended for use for esophageal disease than are used for candidemia to decrease relapses.
But the studies referenced were in HIV, often compared to relatively low dose fluconazole (100–200 a day), and the differences were not close to statistical significance.
Four weeks after stopping study drug, symptoms had recurred in 18 (28%) of 64 patients given caspofungin and in 12 (17%) of 72 patients given fluconazole (P = 0.19).
And that in mostly HIV patients with a CD of 30. What? They relapsed? Color me shocked.
Sometimes when you go back to the original material, it appears that the recommendations are based on BS (bad studies) and only adds cost without added efficacy.
In this study, we realized a reduction in drug-acquisition costs, which were decreased by $300 per patient with micafungin 100 mg daily versus 150 mg daily. For a 14-day course of candidemia treatment, there was a potential savings of $600 per patient in drug-acquisition costs when 100 mg daily was ordered instead of 150 mg daily
Just what we need. More money spent on unneeded antibiotics.
It took over a year, but with po fluconazole and checking blood levels, here beta-D-glucan fell, I stopped the fluconazole, and no replapse.
Rationalization
Eur J Clin Microbiol Infect Dis. 2015 Aug;34(8):1543–9. doi: 10.1007/s10096–015–2384-z. Epub 2015 May 13. The search for endocarditis in patients with candidemia: a systematic recommendation for echocardiography? A prospective cohort.
https://www.ncbi.nlm.nih.gov/pubmed/25966975
Antimicrob Agents Chemother. 2015 Apr;59(4):2365–73. doi: 10.1128/AAC.04867–14. Epub 2015 Feb 2. Candida infective endocarditis: an observational cohort study with a focus on therapy.
https://pubmed.ncbi.nlm.nih.gov/25645855/
Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America.
http://cid.oxfordjournals.org/content/62/4/e1.full#ref–24
POLL RESULTS
The Greatest Band of All Time
- The Who 11%
- The Who 3%
- The Who 6%
- The Who 0%
- Go ahead and give a different answer. It's wrong. The right answer is The Who. 39%
- Other Answers 42%
- Benny Goodman's
- The Guess Who
- The Archies. They look exactly the same after almost 50 years.
- Rush
- Mountain
- Jethro Tull
- Spinal Tap
- Zappa. Go ahead. Try to argue it. Zappa.
- The Beatles
- Simon & Garsparkle
- The Bangles
Chapter Seventy-Six
The patient has a hematologic malignancy and is on dialysis. She had a potential exposure to hepatitis B and is non-immune, so HBIG was ordered.
75 minutes after the im injection, the patient had tachypnea, then a rigor, then fevers, then dropped her blood pressure.
Perfect timing and response to a bolus from endotoxin, but I thought perhaps it was an allergic reaction to the HBIG.
She had the usual resuscitation and did fine. The hospitalist asked me if the patient needed antibiotics, and I was uncertain, but when the BP tanked, I agreed it was a good idea.
Forty-eight hours later, the blood cultures were growing a gram-negative rod that was identified as Cupriavidus pauculus.
Never heard of that before. If it helps, it used to be Ralstonia paucula, formerly classified as CDC group IVc–2. Yes. I know. Does not help.
A whopping 15 hits on the Pubmeds, with 6 clinical cases. The entire Wikipedia entry says
Cupriavidus pauculus is a Gram-negative, nonfermentative, motile bacterium of the genus Cupriavidus and family Burkholderiaceae isolated from water from ultrafiltration systems and bottled mineral water. C. pauculus is associated with human infections.
and one report says
Cupriavidus spp. are ubiquitous environmental organisms that are mostly found in soil, in water, and on plants.
There are a pair of reported pseudo-outbreaks with the organism as well.
So is it real? It is hard to argue with the timing and the delayed time to positivity of the blood cultures suggests it was not a line infection. Subsequent blood cultures were negative. We have had no other similar cases, and two others had received HBIG the same day.
Is it from the HBIG? There are no reported cases of contaminated HBIG associated infections the IC practitioner or I could find, although we are reporting it as such.
Close enough for me to call it.
The patient? Did fine.
Rationalization
Pseudo-Outbreak of Cupriavidus pauculus Infection at an Outpatient Clinic Related to Rinsing Culturette Swabs in Tap Water.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2897476/
Chapter Seventy-Seven
I had a pair of cases this week, one with a diagnosis I never considered, the other I considered and dismissed. More on those cases in the future. I was bitching that I wish I were half as smart as I like to think I am, and one of the hospitalists commented, “medicine makes you humble.”
And I said, “No. Nothing makes me humble. Feel stupid? Yes. Humble? Never." What's the point in false humility? Frequently in error, never in doubt is my motto.
The patient is a young female, no past medical history of note, who comes in with classic purpura fulminans.
I figured it was going to be Meningococcus. The other usual suspects, Pneumococcus and Capnocytophagia, usually occur in the asplenic, and she has her spleen. There are a hodgepodge of other organisms causing purpura fulminans with case reports, but I put my money on Meningococcus.
Nope.
MSSA. S. aureus is also on the purpura fulminans list, although it would be my first case.
The CID article suggests that S. aureus purpura fulminans may, in part, be a superantigen disease, like toxic shock, so then would it be clindamycin and IVIG?
The accompanying editorial, from 2005, notes
The rationale for intravenous immune globulin (IVIG) in the treatment of this condition is weak. This treatment approach assumes that toxin production is the culprit in triggering purpura fulminans, which, for reasons discussed above, is far from established. Moreover, IVIG therapy has not been shown to benefit persons with septic or toxic shock syndromes in any prospective, randomized trial, and although it is generally safe, the treatment is not without risk. Until there is better evidence in support of this therapy, it cannot be recommended, nor can other nostrums, such medicinal leeches, which, believe it or not, also have been suggested for treatment of purpura fulminans.
I think the subsequent data for IVIG is perhaps a bit better for (Streptococcal) TSS, so we opted for treatment.
A chest CT had thin-walled cavities, not typical of right-sided endocarditis, so we got an ECHO. There was a vegetation on the pulmonic valve. Isolated pulmonic valve endocarditis is very unusual, 1.5% to 2% of endocarditis, and the second in my career that I can remember.
And there are no reported cases of S. aureus endocarditis causing purpura fulminans, so the first for me and the world.
No end of oddities in this disease.
Rationalization
Clin Infect Dis. 2005 Apr 1;40(7):941–7. Epub 2005 Mar 2. Purpura fulminans due to Staphylococcus aureus.
http://www.ncbi.nlm.nih.gov/pubmed/15824983
Am J Cardiol. 2015 Dec 15;116(12):1928–31. doi: 10.1016/j.amjcard.2015.09.038. Epub 2015 Oct 9. Infective Endocarditis Involving the Pulmonary Valve.
http://www.ncbi.nlm.nih.gov/pubmed/26611123
Proc R Soc Med. 1910; 3(Sect Study Dis Child): 75–78. PMCID: PMC1961228 Purpura Fulminans.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1961228/?page=1
Note the year.
Crit Care. 2015 Feb 26;19:90. doi: 10.1186/s13054–015–0793–0. The original sins of clinical trials with intravenous immunoglobulins in sepsis.
http://www.ncbi.nlm.nih.gov/pubmed/25882822
Clin Infect Dis. 2014 Sep 15;59(6):851–7. doi: 10.1093/cid/ciu449. Epub 2014 Jun 13. Clinical efficacy of polyspecific intravenous immunoglobulin therapy in patients with streptococcal toxic shock syndrome: a comparative observational study.
http://www.ncbi.nlm.nih.gov/pubmed/24928291
POLL RESULTS
I am never
- humble 23%
- uncertain 6%
- meek 23%
- in doubt 14%
- in error 14%
- Other Answers 20%
- Right answer, wrong question
- fully confident of other people's certainty
- 100% sure of myself
- humbly uncertain, meekly in doubt, or ever in error concerning my lack of certainty and/or expertise vis-a-vis the subject at hand. Or some such thing
- Able to comfortably say never.
Chapter Seventy-Eight
None for a decade. Two in a week.
I am not one for superstitions, knock on wood. The closest I have to a superstition is I always put a tracheostomy kit in the room of a patient with a retropharyngeal abscess. It will never need to be used. It has worked 100% of the time.
I am not inclined to think most clusters are real. For example, we may have a four-month stretch where surgical infections apparently have a spike. Most of the time, it is an artifact; if we had picked a different four-month interval, the spike would vanish. Yet another example of the clustering illusion, although try telling that to anyone.
But it is always odd when you have a streak of unusual cases.
The first was an elderly patient with a prosthetic valve and month of low-grade fevers. Work up is negative, including an ECHO, but for the positive blood cultures, 1/4 on day 5.
The other has dental work, then malaise for a couple of weeks, the hurts his back lifting. Mild at first, the pain progressives, and he develops fevers and rigors. An MRI shows discitis, and he too has 1/4 blood cultures positive on day five but a negative TTE.
Both have Haemophilus parainfuenza, both probable endocarditis.
Late positive blood cultures are often the case for this organism; my record was 1/9 positive cultures on day 5 for an otherwise classic case of endocarditis. It is one fastidious beastie.
I have seen at least one each of HACEK (Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species) endocarditis last century, but this century has been quiet. Only the Haemophili, nary a ACEK. It would appear that in the group, H. parainfluenza is the most common of the HACEK group of cause endocarditis, which explains my experience.
As a cause of spine infections, Haemophilus parainfuenza is even odder: one epidural and two vertebral osteomyelitis’s on the Pubmeds. Both are doing well on ceftriaxone.
Celebrities die in threes. So will I see a third HACEK? Somehow I don’t think so
Rationalization
HACEK Infective Endocarditis: Characteristics and Outcomes from a Large, Multi-National Cohort.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0063181
Rev Infect Dis. 1991 Jul-Aug;13(4):609–12. Haemophilus parainfluenzae as a rare cause of epidural abscess: case report and review.
https://www.ncbi.nlm.nih.gov/pubmed/1925278
J Rheumatol. 1992 Mar;19(3):491–3. Early diagnosis of vertebral osteomyelitis due to a rare pathogen: Haemophilus parainfluenzae.
https://pubmed.ncbi.nlm.nih.gov/1578470/
No, Celebrities Don’t Die in Threes.
http://factually.gizmodo.com/no-celebrities-dont-die-in-threes–1622278656
POLL RESULTS
My superstition is
- mention it is quiet, get slammed with admits 45%
- full moons bring out the crazies 28%
- antibiotics are antipyretics 3%
- vancomycin is a big gun, powerful antibiotic 3%
- a rabbit's foot brings good luck, except for the rabbit 16%
- Other Answers 5%
- whatever Murphy's law dictates
- red tennis shoes keep you safe from most every sort of misfortune, if you wear them.
Chapter Seventy-Nine
I love getting a call from the ER about a disease I have never heard of and, of course, I have never seen.
Yes, let us call the ID doc for advice about a topic about which he knows nothing. Of course, the ER doesn't that.
You now get the opportunity to feel superior because you have seen the disease and can roll your eyes at the so-called ‘expert.’
“This is Crislip. Someone page me?”
“Hey Mark, we have a case of Eczema herpeticum that we need to admit.”
“What’s that?”
“Widely disseminated herpes in a patient with eczema.”
“Really. Never heard of it.”
“We are admitting her for IV acyclovir.”
“Is that the treatment?”
“Yep."
“News to me.
"And they want an ID consult.”
"Well, a fat lot of good I will do.”
It is an interesting disease, usually seen in kids. It is also known as Kaposi varicelliform eruption. Not fair. Moritz has two diseases named after him, and I have none. But then he had to go through as a Moritz. A childhood of suffering from cracker jokes.
She has had a lifetime of eczema and has had a few episodes of cold sores. Now? It almost looks like smallpox. A swab of the skin grew HSV–1, as it should. She did fine, and the lesions melted away on acyclovir. It was a very superficial infection, and it doesn’t look like it will leave any scarring.
Eczema herpeticum can mimic smallpox in that the lesions look similar, the patient can be very ill, and the pox comes on at once rather than in waves.
What I wonder about is if there is any relationship between Eczema herpeticum and Eczema vaccinatum, where patients with eczema get smallpox after the vaccine. Maybe
Kaposi described a disseminated vesiculopustular eruption in children with eczema but did not associate it with vaccination. It was eventually found that “Kaposi’s varicelliform eruption” can be caused by either vaccinia or HSV; severe HSV infections in AD patients are now designated eczema herpeticum.
But if they have the same pathophysiology, I can’t find it.
Rationalization
Eczema herpeticum.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520662/
Eczema Herpeticum: Would You Know It If You Saw It?
https://www.ncbi.nlm.nih.gov/pubmed/26241712. Me? No.
Emerg Infect Dis. 2009 Jul;15(7):1102–4. doi: 10.3201/eid1507.090093. Eczema herpeticum and clinical criteria for investigating smallpox.
https://www.ncbi.nlm.nih.gov/pubmed/19624930
Clin Infect Dis. 2012 Mar;54(6):832–40. doi: 10.1093/cid/cir952. Epub 2012 Jan 30. Eczema vaccinatum.
https://pubmed.ncbi.nlm.nih.gov/22291103/
POLL RESULTS
I
- knew all about this disease. 12%
- knew nothing about this disease. 22%
- avoid derm. I hate making rash decisions. 47%
- vaguely remember it but my attention fades concerning anything in latin. 15%
- Other Answers 3%
- once had to dig a "herpes" culture out of the bin to prove it was VZV, after the other MT pitched it on my day off. Pediatric case. No followup to me.
- ED implemented bio-terrorism protocol because they were sure it was smallpox...it was dermis-take they didn't contact ID first.
Chapter Eighty
The patient had chemo for cancer about 10 days prior to admission. Now she is in with MOSF, severe hypotension, hypothermia, abdominal pain, and a CT that is consistent with typhlitis, aka neutropenic enterocolitis.
She has a colectomy for a dead colon and gets the usual ICU care.
The next day the blood cultures are growing a gram-positive rod. They call me.
Usually, typhlitis is due to a mixed bacteriual infection, the colonic flora invading the bowel, an intestinal mixed synergistic necrotizing infection. And usually, it is seen in leukemics or lymphomics, and this patient has a solid tumor. So odd for typhlitis, although she was neutropenic at admit.
There were three Clostridia I considered. C. perfringens, but does not have the hemolytic anemia often seen with this organism. C. sordellii, but this is not associated with GI disease. And C. septicum, although most of these are associated with solid tumors. But I put my money on C. septicum.
And then? I googled. And found two cases of C. septicum typhlitis associated with docetaxel, the chemotherapeutic drug she had received. Or maybe C. chauvoei.
C. chauvoei has a close phylogenetic relationship with C. septicum, making the two species difficult to differentiate using conventional microbiologic methods.
The lab told me the MALDI-TOF gave it 99.9% C. septicum, which looks to be a valid identification.
It was even possible to identify species that are generally difficult to differentiate by traditional methods, such as C. chauvoei and C. septicum.
So this is the second or third case of typhlitis after docetaxel, and I asked the pharmacy to report it. We treated with penicillin and clindamycin.
She actually survived, and given the severe and prolonged hypothermia and hypotension (4 days), I did not expect it. And she developed an impressive leukemoid reaction of 65K that we, and by we I mean I, attributed to both widespread infection combined with reperfusion leukocytosis.
Rationalization
J Infect. 2012 Feb;64(2):225–7. doi: 10.1016/j.jinf.2011.09.004. Epub 2011 Sep 16. Lethal human neutropenic entercolitis caused by Clostridium chauvoei in the United States: tip of the iceberg?
https://www.ncbi.nlm.nih.gov/pubmed/21945880
Challenging the problem of clostridial identification with matrix-assisted laser desorption and ionization–time-of-flight mass spectrometry (MALDI–TOF MS).
http://www.sciencedirect.com/science/article/pii/S1075996408000759
Typhlitis Associated With Docetaxel Treatment.
http://jnci.oxfordjournals.org/content/88/15/1078.full.pdf
Chapter Eighty-One
The patient had a renal transplant for polycystic kidney disease with removal of the native kidneys. He has been doing well for years when he has fevers, chills, and malaise. Work up suggests a kidney infection, and he gets a course of antibiotics with resolution.
The symptoms abate, then return. He gets another negative workup and responds to another course of antibiotics.
I see him in the clinic, and I got nothing. There is no focality, and he had a CT of the abdomen that shows nothing besides a transplanted kidney and multiple liver cysts. He is, by the way, the rare patient that has a type 1 reaction to ciprofloxacin with his throat closing off. That is an unusual reaction to a quinolone that I have never seen before.
Well, I say, let's finish up the cephalosporin and see what happens. And what happens is the symptoms come back with a vengeance.
Severe rigors and a temperature to 102, and this time the blood cultures grow K. pneumoniae.
I figure one the liver cysts is infected, but which one? Time for a PET scan, which glowed nicely in one of the cysts.
This is the first polycystic kidney disease I have seen with an infected liver cyst, and they do occur.
In patients with infected renal cysts, aspiration or renal transcatheter arterial embolization after appropriate antibiotic therapy was effective. Although aspiration was often effective in patients with infected hepatic cysts, a good outcome was less likely than in those with renal cysts.
The PET is the way to make the diagnosis:
Sensitivities of CT, magnetic resonance imaging, and PET/CT were 25.0, 71.4, and 95.0%.
IR drained it dry. Now the big questions are
\1) Are liver cysts like renal cysts with poor penetration of antibiotics. Not certain, but I suspect so.
\2) And how do you prove cure? Another PET seems a bit excessive.
Given the vagaries of 1 and 2, the TMP resistance, and the reaction to Cipro, I opted for a looooooooooooooooooooog course of a po cephalosporin.
It worked.
Rationalization
Clin Ther. 2010 Mar;32(3):515–26. doi: 10.1016/j.clinthera.2010.03.002. Anaphylactoid reaction considered ciprofloxacin related: a case report and literature review.
http://www.ncbi.nlm.nih.gov/pubmed/20399988
Nephron Clin Pract. 2009;112(3):c157–63. doi: 10.1159/000214211. Epub 2009 Apr 24. Infected hepatic and renal cysts: differential impact on outcome in autosomal dominant polycystic kidney disease.
https://www.ncbi.nlm.nih.gov/pubmed/19390216
Braz J Med Biol Res. 2014 Jul;47(7):584–93. Epub 2014 Jun 13. Cyst infection in hospital-admitted autosomal dominant polycystic kidney disease patients is predominantly multifocal and associated with kidney and liver volume.
https://www.ncbi.nlm.nih.gov/pubmed/24919173
Chapter Eighty-Two
It was so weird. I was walking by a parking meter near the hospital when it made the kerchunk sound of a dropping coin. I stopped and looked at the machine. There was no one else around, so on a whim, I put a finger in the coin return. A dime! I now have a superpower that I need to get to work around ATMs.
Yes, I know, the dime was probably there all along, but I like to have just a wee bit of magic in my life. Medicine and magic don't mix unless you are an alternative medicine provider. Medicine always has the hard reality of failure.
The patient has a port infection with MSSA. The port is pulled, the repeat blood cultures and ECHO are negative, and she defervesces in less than 48 hours.
Looks like an uncomplicated MSSA line infection. She has several co-morbidities that lead to a 4-week course of cefazolin.
She has no peripheral access and needs a line. So after 5 days, the port is put back in.
One week after stopping the antibiotics, she is back with fevers and sustained positive blood cultures with the same MSSA.
Crap. I am not a fan of failure, and I can count on one hand, even after losing a couple of fingers, the number of patients who have relapsed after treating a line related MSSA bacteremia. It really pissed me off, and yes, it is all about me. Not really. But I still take failure personally.
So we started over: work up was again negative, including port cultures.
Where did the staph come from? This time we got an ultrasound of the subclavian and found it lined non-obstructing clot. So that was the probable source of the recurrent infection, septic thrombophlebitis of the subclavian, and we put the line right back in the clot. Never had that happen before.
I wonder it was more a fibrin sheath as in:
A fibrin sheath is a circumferential sleeve of endothelium that forms around the surface of implanted central venous catheters and frequently remains intact within the lumen of the vein after removal of the catheters. We describe a new entity of infective endovascular fibrin sheath vegetations.
Although this was in the subclavian, not the vena cava, it is probably the moral equivalent.
Now a longer course of antibiotics and some anticoagulation to avoid a second relapse. That would really fry my bacon.
Rationalization
Infective Endovascular Fibrin Sheath VegetationsA New Cause of Bacteremia Detected by Transesophageal Echocardiogram.
https://www.ncbi.nlm.nih.gov/pubmed/?term=25865922
POLL RESULTS
In my life, I need more
- magic 21%
- beer 18%
- money 10%
- respect 4%
- time. So little left, so much to do. 41%
- Other Answers 6%
- Disrespect, to keep me humble.
- All of the above
- Devices: https://reflectionandfood.files.wordpress.com/2014/08/leunig-devices.jpg
- reason to live.
Chapter Eighty-Three
The patient is admitted septic and is started on vancomycin and cefepime.
No problem there.
The blood grows MSSA. The central line is pulled. The cefepime is stopped, and the vancomycin continued.
Wrong.
Never. Ever. Treat MSSA with vancomycin unless there is a compelling allergic reaction to a beta-lactam. For example
Those receiving nafcillin or cefazolin had 79% lower mortality hazards compared with those who received vancomycin alone (adjusted hazard ratio (HR): 0.21; 95% confidence interval (CI): 0.09, 0.47). Among the 122 patients who initially received vancomycin empirically, those who were switched to nafcillin or cefazolin (66/122) had 69% lower mortality hazards (adjusted HR: 0.31; 95% CI: 0.10, 0.95) compared to those who remained on vancomycin.
and
Nafcillin was superior to vancomycin in preventing bacteriologic failure (persistent bacteremia or relapse) for methicillin-susceptible S. aureus (MSSA) bacteremia. Failure to remove infected intravascular devices/catheters and vancomycin therapy were common factors in patients experiencing multiple (greater than 2) relapses. However, by multivariate analysis, only endocarditis and therapy with vancomycin (versus nafcillin) were significantly associated with relapse.
Although there are those who would call vancomycin a big gun (and I call those people idjets) when compared to anti-staphylococcal beta-lactams, vancomycin is always inferior; it stinks on ice.
The patient slowly deferveses, and the treatment is de-escalated to cephalexin.
Wrong.
At least it wasn’t oral clindamycin, the goto wrong choice of surgery residents everywhere for S. aureus bacteremia.
Never. Ever. Treat S. aureus bacteremia with oral therapy. And the bare minimum for IV therapy for uncomplicated S. aureus bacteremia is 14 days.
Therefore, in the treatment of uncomplicated SAB, it seems reasonable to consider at least 14 days of antibiotic therapy to prevent relapse, as practice guidelines recommend. Because of its poor prognosis, primary bacteremia, even with a low risk of complication, should not be treated with short-course therapy.
But was this uncomplicated? No. Fevers persisted for 4 days with positive blood cultures on day 3 to vancomycin. That’s an endovascular infection, in this case, clot in the subclavian rather than a valve.
There is a reason why ID consultation should be mandated for all S. aureus bacteremias:
Infectious diseases consultation was independently associated with a reduction in 28-day mortality.
Although I have to admit I have half a mind (yeah, I wrote that) to not allow anyone to give any antibiotic without ID approval.
I have to admit I am getting grumpier about these kinds of cases as I get older. It not as if it is hard to find the answer to the simplest of clinical questions if you take the required 22 seconds. If my 12-year-old son could do it, so can you.
Rationalization
Comparative effectiveness of nafcillin or cefazolin versus vancomycin in methicillin-susceptible Staphylococcus aureus bacteremia.
http://bmcinfectdis.biomedcentral.com/articles/10.1186/1471–2334–11–279
Treatment Duration for Uncomplicated Staphylococcus aureus Bacteremia To Prevent Relapse: Analysis of a Prospective Observational Cohort Study.
http://aac.asm.org/content/57/3/1150.full
The Value of Infectious Diseases Consultation in Staphylococcus aureus Bacteremia.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3606273/
Staphylococcus aureus Bacteremia: Recurrence and the Impact of Antibiotic Treatment in a Prospective Multicenter Study.
Nine Questions, Nine Answers.
https://www.sciencebasedmedicine.org/nine-questions-nine-answers/
Chapter Eighty-Four
The patient has a dialysis-related MRSA bacteremia. Not an uncommon problem. He gets a month of vancomycin and relapses with a metastatic infection.
That is unusual, but it happens. S. aureus has a nasty propensity for coming back after treatment. Where the relapse occurred was most odd: mid rib. The last time I wrote about a rib osteomyelitis was 2010, so this makes the second hematogenous rib osteomyelitis I have seen.
It was debrided and treated with another course of vancomycin. And now, 6 months later, it’s back.
Kind of no surprise, but the MIC to vancomycin has changed, going from < 0.5 to 1.
Natural selection in action.
It may be hVISA
Heterogeneous VISA (hVISA) appears to be the stage that precedes the development of intermediate-level resistance in S. aureus or VISA. These are strains of S. aureus containing subpopulations of vancomycin-intermediate daughter cells; the MICs for the parent strains of these daughter cells fall within the susceptible range of 1 to 4 μg/ml (Fig. (Fig.1).1). Vancomycin creates a selective pressure that favors the outgrowth of rare, vancomycin-resistant clones leading to hVISA clones, and eventually, with continued exposure, to a uniform population of VISA clones.
and dialysis, with intermittent vancomycin dosing in an immunoincompetent host is is the best way I can think of to select for VISA. Many of the reports of increasing MIC’s to vancomycin are in dialysis patients and,
The evolution of vancomycin and oxacillin MICs of this strain was striking.
Understanding infectious diseases is understanding evolution.
I have mentioned this before, but I still wonder if the S. aureus of today is the same species of S. aureus of 50 years ago. 50 years of doubling time for bacteria is about 3 million years for humans, and 3 million years ago, we were Lucy, wandering Ethiopia. In 3 million years, Australopithecus afarensis became Homo sapiens sapiens. Has S. aureus become S. aureus imgonnakillu? Microbiologists always look at me like I’m nuts when I ask the question. But I still wonder.
Sometimes at work, they put up a map, and you are supposed to put a pin in the country of your ancestors. I always stick my pin on Hadar.
Now it is more debridement and a course of daptomycin. And likely daptomycin resistance.
Rationalization
Scand J Infect Dis. 2000;32(3):223–7. Osteomyelitis of the ribs in the antibiotic era.
http://www.ncbi.nlm.nih.gov/pubmed/10879590
Antimicrob Agents Chemother. 2003 Oct; 47(10): 3040–3045. Staphylococcus aureus with Heterogeneous Resistance to Vancomycin: Epidemiology, Clinical Significance, and Critical Assessment of Diagnostic Methods.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC201119/
Vancomycin-Intermediate Staphylococcus aureus with Phenotypic Susceptibility to Methicillin in a Patient with Recurrent Bacteremia
https://pubmed.ncbi.nlm.nih.gov/12802763/
POLL RESULTS
My ancestors came from
- Ethiopia 5%
- Europe 33%
- Asia 8%
- Alpha Draconis. Bow down to your lizard overlords 31%
- Atlantis 15%
- Other Answers 8%
- Pangaea
- Primordial soup?
- Earth
Chapter Eighty-Five
Silly me.
I remember when “upgrade” had something to do with improving a product.
I came to work to find the new Epic upgrade. It’s slower (Maybe. Now they pop an hourglass on the screen and I am conditioned by Windows to know that an hourglass means a long wait), my workflow has vanished, the amount of screen clutter has increased, so I can’t find the data for the cruft, more white space, so more scrolling, it is totally non-intuitive (one would think placing an order would be obvious and not require three clicks to get get to the order screen), the icons meaningless (fortunately they can be removed) and the color options have been generated by the Psychedelic Vomit Machine (tm). Every iteration of Epic is worse than the one before for what I want to do.
Remember in the HHGTTG that the Earth is actually a computer program designed to find the ultimate question to life, the universe, and everything? I think one of the subroutines is to evaluate frustration and anger by continually messing with user interfaces: Epics, Windows, OS X, Android, and all the different websites and apps have to change their user interface at least once a year. Drives me nuts.
The patient is a young female with no medical problems who comes in with fevers and petechiae/purpura.
Purpura scares me. When my kids had fevers, I was always nervously looked for purpura. Over the years, I have seen too many people dead in less than a day from Meningococcus.
She was also hypotensive and neutropenic, but no CNS symptoms, and the LP was normal. With 48 hours, she was back to normal, and the blood cultures had Meningococcus.
So how long does she need treatment?
More often than not, a positive blood culture makes the diagnosis but matters little in the duration of antibiotics.
The recommendations for Meningococcus is for a week, based on no data I can find. I am increasingly of a mind that bacteremia is usually not important in deciding the length of therapy (with the big exceptions of S. aureus and Candida).
Once the patient gets a slug of antibiotics, the blood is probably sterile for most bugs, and most organisms have little or no predilection for causing a metastatic infections (again, with the big exceptions of S. aureus and Candida).
The only real question is the adequacy of source control, and for Meningococcemia, there is no source to control.
Three days of 12 million units a day of penicillin is enough to cure ALL patients:
The dose of benzyl penicillin we used is lower than the usual recommended dose, but this dose has been used at Auckland Hospital and many other New Zealand hospitals for >40 years. We assume that dosages much lower even than our routine 12 MU (7.2 g) per day in the earliest study drove this initial, now historical local decision, which has been perpetuated by successive generations of New Zealand infectious diseases physicians.
Regardless of the form of meningococcal disease.
Four days of ceftriaxone is just as effective as penicillin or even as little as 2 days of daily ceftriaxone.
How low can you go?
Rationalization
Three Days of Intravenous Benzyl Penicillin Treatment of Meningococcal Disease in Adults
http://cid.oxfordjournals.org/content/37/5/658.full.pdf
Pediatr Infect Dis J. 1988 Oct;7(10):711–3.Once daily ceftriaxone for meningococcemia and meningococcal meningitis.
http://www.ncbi.nlm.nih.gov/pubmed/3054778
Eur J Clin Microbiol Infect Dis. 1993 Oct;12(10):766–8. Ceftriaxone versus penicillin G in the short-term treatment of meningococcal meningitis in adults.
http://www.ncbi.nlm.nih.gov/pubmed/8307046
POLL RESULTS
Epic upgrades
- should come with Zoloft 6%
- should come with Zofran 3%
- should come with valium 28%
- should come with LSD to make the colors appear normal 34%
- should come every 42 years 28%
Chapter Eighty-Six
The Return of the Bad Old Days
The patient, a newly diagnosed HIV, CD counts < 50, was admitted with fever and rigors.
After 24 hours, the blood and urine are growing a gram-negative rod.
I like to swing for the fence, calling the bug before the lab identifies it. It is fun and it does make an impression. As I have said before, no one remembers that Babe Ruth also led the league for strikeouts.
I said it should be Salmonella.
And it was.
The benefits of being old, my career in medicine coincided with the AIDS epidemic. In the early part of my practice was in the middle of the worst of the AIDS years. We didn’t have a clue as to what caused the disease, much less any way to treat it.
Recurrent Salmonella bacteremia was a problem back in the bad old days that required chronic quinolone suppression but has mostly disappeared in the era of HAART:
Compared with patients enrolled in the pre-HAART era, patients who received HAART had an incidence of recurrent NTS bacteremia that was significantly reduced by 96%; the incidence of recurrent NTS bacteremia was 2.56 cases per 100 person-years in the HAART era, compared with 70.56 cases per 100 person-years in the pre-HAART era.
But it still happens.
The disappearance was probably in large part due to immune reconstitution, but some decrease may have also been to the use of AZT, which can inhibit Salmonella.
The use of zidovudine was associated with the lowest rate of recurrences compared with cotrimoxazole or amoxicillin as suppressive therapy. In the microbiologic assay, zidovudine showed bactericidal effect on Salmonella species at current dosages, and resistance to zidovudine was uncommon (2 cases, 4%). Due to its direct effect on Salmonella species, a zidovudine-containing regimen may protect against the recurrence of the disease.
AZT has become passé this century, so it will be interesting to see what happens with invasive Salmonella in HIV.
Also of interest is the patient is from rural SE Asia, so a co-infection with Schistosomiasis is being evaluated.
We suggest that prolonged salmonellosis in schistosome-infected patients is due to an association of Salmonella sp. with the schistosome worms themselves and further that the schistosome worms provide a multiplication focus for these bacteria in the mesenteric portal system, with a persisting bacteremia following.
I’ll let you know.
But I wish the Bad Old Days did not keep returning.
Rationalization
Risk of Recurrent Nontyphoid Salmonella Bacteremia in HIV-Infected Patients in the Era of Highly Active Antiretroviral Therapy and an Increasing Trend of Fluoroquinolone Resistance Acta Microbiol Immunol Hung. 1997;44(2):165–71. In vitro antimicrobial properties of azidothymidine (AZT).
http://www.ncbi.nlm.nih.gov/pubmed/9330665
J Infect Dis. 1999 Jun;179(6):1553–6. Zidovudine therapy protects against Salmonella bacteremia recurrence in human immunodeficiency virus-infected patients.
http://www.ncbi.nlm.nih.gov/pubmed/10228081
Infect Immun. 1984 May; 44(2): 274–281. PMCID: PMC263513 Mechanism of interaction of Salmonella and Schistosoma species.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC263513/
POLL RESULTS
Things were
- better back in the day. 8%
- worse back in the day. 13%
- I was too drunk/high at the time to remember 14%
- Some things were better, some things were worse. I hate to commit 52%
- I live in the present, who wants to learn from the past? 5%
- Other Answers 8%
- These are the good old days. (And I'm older than you are. So enjoy!)
- I wasn't born
- better because I was too drunk/high all the time
- Depends on which day.
- Mostly the same in many ways, but our perception changes. Imagine the filthy bathrooms you lived with in college rentals, and what you tolerate now.
Chapter Eighty-Seven
I am getting progressively grumpy in my old age. Twice this week I was asked about starting antibiotics in patients because of fevers.
Antibiotics.
Are.
NOT.
Antipyretics.
Duh.
NSAIDs and acetaminophen are antipyretics. Antibiotics are used to kill bacteria. You would think people would have been taught that distinction back in medical school. Nope.
And bacterial infections are usually infections of something: lung or liver or brain, and if all the somethings are uninfected based on negative cultures and the donut of truth, they do not have a process amenable to vancomycin and Zosin, thank you very much.
Sigh. Yep. Grumpy.
The patient is admitted with fevers, untreated HIV with a CD4 count under 100, and a rash that looks like widely disseminated molluscum.
There is a list of infections that looks like disseminated molluscum in AIDS. Molluscum, Cryptococcus, Penicillium (now renamed Talaromyces), and Histoplasmosis.
Coming from SE Asia, I was betting on Penicillium, but that just shows the parochial nature of my knowledge base. I thought of Histoplasmosis as a US/Caribbean/African disease, but it is also in Asia.
Unbeknownst to me, but known to google, Histoplasma is more common than Talaromyces in Thailand, the patients birthplace.
Histoplasmosis and penicilliosis are fungal infections with similar clinical presentation and laboratory findings that were reported mainly in the era prior to highly active antiretroviral therapy. We conducted a retrospective review at two hospitals in Central Thailand of the medical records of HIV-positive patients with microbiologic evidence of histoplasmosis or penicilliosis between January 2003 to September 2007 when antiretrovirals became widely available in Thailand. Fifty patients met inclusion criteria; 36 had histoplasmosis, and 14 had penicilliosis. Symptoms and laboratory findings on presentation were similar between the two infections except for a greater incidence of tachypnea and neutropenia among patients with histoplasmosis (both p < 0.05). For histoplasmosis, blood culture had a significantly lower yield for detecting infection compared to tissue microscopic examination highlighting the importance of obtaining tissue for diagnosis (p < 0.05).
And the biopsy of the skin shows Histoplasmosis. It has been over 15 years since she was in an endemic area, so a late reactivation.
I checked a beta D glucan, and it was only 177. Not as high as I would expect for a widely disseminated fungus.
I was also curious as to whether the Asian Histoplasma is the same as the North American strain. I bet not; it must have diverged and should be a different spp, much like Histoplasma duboisii, but how much it may have diverged the literature is silent.
The guidelines suggest lipid amphotericin as
the mortality rate was lower (2% vs. 13%) among recipients of liposomal amphotericin B (3 mg/kg daily for 1–2 weeks) than among recipients of the deoxycholate formulation
But if you look at the original reference, it says
Three patients (of 22) treated with amphotericin B and one (of 51) treated with liposomal amphotericin B died during induction (P = 0.04).
Meaning there was no notable difference with that p-value. The text does suggest that regular amphotericin is inferior if you find a series of anecdotes compelling:
One of 53 patients (2%) treated with liposomal amphotericin B died of bacteremia caused by Staphylococcus aureus compared with 3 of 24 patients (13%) in the amphotericin B treatment group who died of progression of disseminated histoplasmosis (difference, 11 percentage points [CI, 6 to 37 percentage points]) (P = 0.04 [log-rank test]). Of the 57 patients who completed itraconazole consolidation therapy, 5 additional patients died (P = 0.11). In the amphotericin B treatment group, one patient died of histoplasmosis at day 17 and another died suddenly, possibly of hypokalemia that occurred at day 38. In the liposomal amphotericin B treatment group, one patient died at day 29 of progression of histoplasmosis, one nonadherent patient died of progression of disseminated histoplasmosis at day 120, and one patient died of opportunistic infections.
And other parameters were no difference between the two groups. So color me unimpressed.
But I still gave the lipid amphotericin as in the study it was less toxic and the fevers resolved faster. But not because it was an antipyretic.
Rationalization
Southeast Asian J Trop Med Public Health. 2012 Mar;43(2):436–41. Histoplasmosis and penicilliosis among HIV-infected Thai patients: a retrospective review.
http://www.ncbi.nlm.nih.gov/pubmed/23082594
Am J Trop Med Hyg. 2014 Jun 4; 90(6): 982–983. doi: 10.4269/ajtmh.14–0175 PMCID: PMC4047757 Histoplasma capsulatum: More Widespread than Previously Thought.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047757/
Med Mycol. 2008 Feb;46(1):93–5. doi: 10.1080/13693780701642235. Histoplasmosis as a cause for a positive Fungitell (1 –> 3)-beta-D-glucan test.
http://www.ncbi.nlm.nih.gov/pubmed/18297546
Ann Intern Med. 2002 Jul 16;137(2):105–9. Safety and efficacy of liposomal amphotericin B compared with conventional amphotericin B for induction therapy of histoplasmosis in patients with AIDS.
http://www.ncbi.nlm.nih.gov/pubmed/12118965
Chapter Eighty-Eight
Stinky Feet, Cheese, and Sepsis
Fever and chills on dialysis are a common enough problem. I am not prone to the naturalistic fallacy, but having a dialysis catheter in your subclavian is not natural. But it is often better than death.
All catheters eventually either break or get infected, and with the fever and chills, it looked like the second option. Usually, it is some sort of Staphylococcus, but this time it was gram-positive rods in all the blood cultures.
That is curious, probably some sort of Corynebacterium or even a P. acnes, although we do not often look for that beast:
Propionibacterium acnes was detected in significant counts in the vascular catheters of 39 patients. This represents 14.7% (95% CI, 12.5-16.9) of all positive catheters. Propionibacterium is the second most frequent genus-colonizing catheter tips after Staphylococcus spp. Methodological shortcomings impair the detection and proper adscription of P. acnes as a potential cause of catheter-related infections.
and Listeria in the elderly. So he was put on ampicillin, and he got better while we waited for the name of the beast. After two days, nothing, so I called the lab. The microbiologist tells me the MALDI says it is Brevibacterium.
And that is? Never heard of that bug.
There are at least 26 Brevibacterium, the most famous being
Brevibacterium linens is ubiquitously present on the human skin, where it causes foot odor. The familiar odor is due to sulphur containing compounds known as S-methyl thioesters. The same bacterium is also employed to ferment several cheeses such as Munster, Limburger, Port-du-Salut, Raclette, Livarot, Pont l'Eveque and Năsal. Its aroma also attracts mosquitoes
According to the Microbe Wiki
B.linens plays a big role in the metabolism of cheeses. The ripening of the cheese goes from a yeast and mold flora to a bacterial flora. The yeast uses the lactate in the curd for energy, increasing the pH, allowing growth of B.linens. These cheeses are high in salt concentration with allows only halotolerant microorganisms to grow on the surface of the cheese.
Maybe these cheeses came from our less fastidious forebears, and one author asks,
And is tday's concern for scrupulous cleanliness in the dairy depriving future gourmets of delicious aromas still confined to the crevices of the human body?
Ick. Toe cheese is bad enough, but belly button cheese? I’ll pass.
I asked the tech if the plates smelled like cheese. She said she is not in the habit of sniffing unusual organisms. Words to live by from a wise microbiologist. The patient? No cheese consumption, and it was likely B. casei anyway.
There are 13 hits for this organism causing bacteremia, mostly catheter related infections but not a lot of information as to whether catheters can be salvaged. Vancomycin had the best MIC’s, so we went for a course of therapy to see if we can save the catheter as the patient is short on further access.
I know ID is not a popular specialty, but what other area of medicine can offer human body cheese? Kids today just do not know a good thing when they see it.
Rationalization
J Infect. 2008 Apr;56(4):257-60. doi: 10.1016/j.jinf.2008.01.012. Epub 2008 Mar 12. Propionibacterium acnes is a common colonizer of intravascular catheters.
http://www.ncbi.nlm.nih.gov/pubmed/18336916
Infection. 2006 Apr;34(2):103-6. Central venous catheter infection with Brevibacterium sp. in an immunocompetent woman: case report and review of the literature.
http://www.ncbi.nlm.nih.gov/pubmed/16703303
Cheese, toes, and mosquitoes. BMJ 1996; 312 doi: http://dx.doi.org/10.1136/bmj.312.7038.1105
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350886/pdf/bmj00539-0061.pdf
Scientists create toe, belly button cheese from human bacteria.
http://www.cbsnews.com/news/scientists-create-toe-belly-button-cheese-from-human-bacteria/
The 2015 ID Fellowship Match “Historic Bad”: Part 1, Debating the Cause.
POLL RESULTS
I would avoid ID as
- it is filled with too many people enamored of their ideas 10%
- the first name in the title is infectious, and I am a germaphobe 5%
- evolution is true. Sorry. Wrong ID. 34%
- thinking makes my brain hurt like Mr. Gumby 27%
- I prefer surgery, and with increasing resistance, ID will go back to be being a surgical specialty 20%
- Other Answer 5%
- fry cooks make more money and are less likely to be sued.
Chapter Eighty-Nine
"Nothing is unnatural - just untried."
The title is a quote from Rita Mae Brown.
Consults come in a variety of flavors, and I am definitely speaking metaphorically here. I still am of the opinion that every consult request can be boiled down to five or less words.
Why fever?
What antibiotics?
How long?
No idea what is wrong.
Etc.
I think most of my colleagues like to hear extended presentations before seeing a patient, but I am not that interested in what you have to say, and all I really need is a name and a room number.
Because I am going to read the chart and do and an aich and pea, so when you tell me the age and gender, etc., you are just wasting your time, and more importantly, my time.
Many of my referring physicians are aware of this and comply:
“Multiple infected joints”
I can do that.
The patient is an elderly female who became ill with fevers and back pain. By the end of three days, she had red hot, swollen wrists, knees, and back.
Blood and all the joints grow Group C, S. equisimilis, not a common cause of joint infection.
Two new cases of acute bacterial arthritis due to group C streptococci are reported, and a MEDLINE search was performed, which located 22 additional cases.
But a polyarticular infection is common.
The infection was polyarticular in a third of cases.
My record with this organism is both shoulders, wrists, hips, and ankles, 8 joints. Reported cases of back infections are even rarer.
I will be damned if I can remember the classification of the Streptococci; every time I get a case, I review the topic, and I forget each paragraph as soon as I read it.
Why did the patient have this disease? No clue. He hasn’t been horsing around. Or skunking around, for that matter. Or been around any other pestilential vector.
So it is I&D and antibiotics. She did fine
The odd question is the use of steroids. In children, the use of dexamethasone leads to more rapid improvement; can I extrapolate that to adults? I don’t know. Probably. It is my age; I can’t bring my self to give steroids for acute infection even as the data trickles in on the benefits for a variety of acute bacterial diseases from cellulitis to pneumonia to septic arthritis. It feels unnatural. Yet another sign I am approaching the end of my career.
Rationalization
Semin Arthritis Rheum. 2001 Aug;31(1):43-51. Acute bacterial arthritis caused by group C streptococci.
http://www.ncbi.nlm.nih.gov/pubmed/11503138
Streptococcus species (Group G and Group C Streptococci, Viridans Group, Nutritionally Variant Streptococci).
http://www.antimicrobe.org/b241.asp
Beta-hemolytic Streptococcus spp. from horses a retrospective study (2000–2010).
http://vdi.sagepub.com/content/24/1/142.full
Streptococcus equisimilis Infection in Striped Skunks (Mephitis mephitis) in Saskatchewan.
http://www.bioone.org/doi/pdf/10.7589/0090-3558-38.3.641
PREVALENCE OF STREPTOCOCCUS DYSGALACTIAE SUBSP. EQUISIMILIS AND S. EQUI SUBSP. ZOOEPIDEMICUS IN A SAMPLE OF HEALTHY DOGS, CATS AND HORSES.
Pediatrics. 2015 Oct;136(4):e776-82. doi: 10.1542/peds.2014-4025. Epub 2015 Sep 7. Dexamethasone Therapy for Septic Arthritis in Children.
http://www.ncbi.nlm.nih.gov/pubmed/26347429
Poll Results
Unnatural is
- steroids for infected joints 12%
- giving piperacillin-tazobactam (I have yet to order it) 6%
- ABIM MOC 14%
- light beer 52%
- as unnatural does. What does Forrest Gump mean by that? 9%
- Other Answers 8%
- Blue raspberry flavoured drinks.
- Trump's hair
- Nothing. The antonym of natural is supernatural.
- not necessarily so.
- Eating cooked meat and not sleeping in a cave.
Chapter Ninety
The patient has had a ventriculo-peritoneal shunt for years with no problems. She is admitted with fevers, headache, and an altered sensorium. 700 PMNS, protein of 300 and a glucose <10, data-preserve-html-node="true" meningitis is diagnosed, she is started on iv antibiotics, and the shunt is pulled.
The CSF and the blood grow E. coli.
UA is negative, and the CT of the abdomen, after the shunt is removed, has a few non-abscess looking fluid collections. So they call me to comment on the reason for the E. coli.
As I have said in the past, parents, children, spouses, government officials, and Presidential candidates will lie. Oh, how the candidates will lie. But the cultures? They never lie. You just have to understand what they are saying as the cultures sometimes speak the language of ID.
Not a romance language exactly, although there are some infections you get from romance. But I digress.
E. coli in a shunt infection, means the catheter eroded into the bowel.
E. Coli in the CSF of a V-P shunted patient is found, bowel perforation should be assumed. Four cases developed such a complication among 643 hydrocephalic patients of various etiology over a period of ten years.
I have seen this three other times in my career, although in the prior cases, I had the CT before the shunt came out to prove the diagnosis.
Now? Her abdominal exam is negative, and there was no abscess, but I added a 5-day course of metronidazole just to clean things up.
Bowel is remarkably tough, as anyone who eats sausage knows. I wonder how self-sealing the bowel is. We eat all sorts of sharp things by mistake (or deliberately) yet we see only the occasional toothpick or other odd foreign body perforation. But bowel integrity must get violated on occasion. If so, I can find nothing in the PubMeds or the Googles to confirm or deny the supposition that bowel is self-sealing.
So I am guessing/hoping that whatever hole the VP shunt poked in the gut sealed on its own.
Rationalization
Neurosurg Rev. 1998;21(2-3):194-7. E. coli meningitis as an indicator of intestinal perforation by V-P shunt tube.
http://www.ncbi.nlm.nih.gov/pubmed/9795961
World J Gastroenterol. 2013 Oct 14; 19(38): 6447–6452. Published online 2013 Oct 14. doi: 10.3748/wjg.v19.i38.6447 PMCID: PMC3801315 Emergency admissions due to swallowed foreign bodies in adults.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3801315/
Clin Med Insights Case Rep. 2013; 6: 131–135. Published online 2013 Jul 7. doi: 10.4137/CCRep.S11486 PMCID: PMC3712003 Toothpick Perforation of the Intestines Presenting as Recurrent Abdominal Pain: Possible Roles of Abdominal Ultrasound and MRI.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712003/
POLL RESULTS
You always get the truth from
- cultures 43%
- Aes Sedai, but the truth she tells you isn't the one you think you hear. 8%
- George Washington 5%
- Cassandra 15%
- my conscience. But I choose to do otherwise 18%
- Other Answers 13%
- Aslan
- the puppy of the house
- Bathroom mirror
- those who have no unexpressed self-interest in telling you something other than the truth.
- Drunk people, children, and leggings.
Chapter Ninety-One
Simultaneously Adequate and Inadequate
When I walk the halls of the hospital, and people ask how are you, I often reply, only partly as a joke, I'm adequate.
The great thing about ID is on any given day, you get the chance to feel simultaneously inadequate and a genius.
I have an FUO I have not been able to figure out going on 2 weeks now, which does occur frequently and the lack of a diagnosis may be a good thing.
It included 54 men and 49 women (mean age: 57 years) in 52 of whom the final diagnosis could not be established …As observed in the most recent case series, the rate of undiagnosed patients is increasing. The prognosis was good for undiagnosed FUO.
But it still annoys me. It is my job to come up with an answer.
On the other hand, on the same day, I can feel like the smartest person in the room. An elderly female has a migratory arthralgias, first one shoulder, then the other shoulder before settling in the knee.
All the blood cultures and the knee were growing gram-positive cocci in pairs and chains.
After two days, the lab still did not have an identification of the organism, so I gave them a call, and they told me they were thinking some sort of Enterococcus. Hmmm.
I have never seen a case of Enterococcus native joint infection. That would be an odd bug. But if not Enterococcus, then what? Chains and pairs is an Enterococcus, but a standard Enterococcus would be identified in less than 48 hours and usually has a GU source, which this patient did not have. I thought it over and predicted in writing it would be S. gallolyticus, what used to be a non-enterococcal Group D Streptococcus formally known as S. bovis.
S. gallolyticus is not a common cause of septic joints, but this organism tends to cause septic joints when it causes endocarditis.
Osteoarticular infections was a presenting symptom in 63% of the cases of IE.
due to S. bovis.
And the next day, the lab called it S. gallolyticus, and the ECHO had a mitral vegetation. The colonoscopy looking for a cancer will be done as an outpatient. And I was temporarily adequate again.
I have mentioned before that while everyone remembers that Babe Ruth called a home run, no one remembers he also led the league in strikeouts. Predict a zebra diagnosis, and you will apperat to be House-like genius, and no one will ever remember the cases you missed or did not diagnose.
You can perseverate over your FUO failures late at night when there is nobody around.
Rationalization
Presse Med. 2014 Sep;43(9):e233–40. doi: 10.1016/j.lpm.2014.02.026. Epub 2014 Jun 28. Fever of unknown origin in the 2000s: evaluation of 103 cases over eleven years.
http://www.ncbi.nlm.nih.gov/pubmed/24985921
Clin Infect Dis. 1995 Sep;21(3):516–22. Enterococcal arthritis: case report and review.
http://www.ncbi.nlm.nih.gov/pubmed/8527536
Semin Arthritis Rheum. 2016 Jun;45(6):738–46. doi: 10.1016/j.semarthrit.2016.02.001. Epub 2016 Feb 8. Streptococcus bovis septic arthritis and osteomyelitis: A report of 21 cases and a literature review.
http://www.ncbi.nlm.nih.gov/pubmed/26992635
POLL RESULTS
I am usually
- adequate 16%
- the smartest person in the room 5%
- a fraud 9%
- doing the best I can with what I have 52%
- suffering from this terrible pain down the diodes of my left side 16%
- Other Answers 3%
- justifiably cranky. And don't get me started on whatever, as it's too late now, and you have no valid base from which to argue. OK?
- Skipping to the beat. Or skipping a beat.
Chapter Ninety-Two
It is the little things that annoy the hell out of me.
There are three journals I feel I should subscribe to: The NEJM, CID, and JID. None of them have electronic-only versions. I have asked. They have said no. I download all the pdfs to read since electronic versions allow me to make the print bigger. Every time I get a dead tree copy, they go straight from the mailbox to the recycling bin—what a waste. I am sure the paper version is required so they can continue to sell ad space.
Attention journal print advertisers: you are wasting your money.
But the NEJM adds insult to injury. Two years ago, they sent me a NEJM logo mouse pad as a gift for subscribing. This year I wrote on my renewal card in big block letters DO NOT SEND ME YOUR STUPID MOUSE PAD.
They sent it anyway.
In this era of trackpads and laser mice, who needs a trackpad? I am surprised they did not offer me all their podcasts on 8 track tape.
Not only is the mouse pad as useless as a book in Trump's library, it annoys me because it is a waste. It was a waste of hydrocarbons to make it, to put it in the bubble lined mailer (more unneeded plastic. As if a rubber mouse pad is going to break in transit) and a waste of the hydrocarbons burned to deliver it to across the county.
We are at 400 ppm and rising fast. Making and delivering useless plastic doodads only adds insult to injury. I bet they have a warehouse full of these mouse pads, next to piles of NEJM floppy discs and NEJM 1200 baud modems, the NEJM equivalent of the Island of Misfit Toys.
Next time? As a 'gift', use my part of that $118,549,282 for something actually useful, like planting a tree for all the CO2 needlessly produced by each of those dumbass mouse pads.
But I grump, and you are really here for a bit of ID.
For years I have not really known what to do at the end of therapy for patients with prosthetic joints we are trying to salvage.
They finish a course of iv then po antibiotics, and then what? They only way to know if there is a cure is to stop and see if they relapse, and if they do, it is back to square one, often needing a joint explant. Knee-less or hip-less is not the best way to spend your golden years.
So I have told patients there are two choices: stop and see what happens, and if it comes back, you lose the knee OR chronic suppression, assuming an inexpensive, nontoxic, and effective po antibiotic.
Neither option is good, but often in medicine, it is deciding on the least bad option, and most choose suppression. I see them once a year, have a nice chat, admire the functioning knee, and send off with another year's supply of whatever.
Recently one patient, on chronic cephalexin for two years for MSSA, was advised by his MD in Another Hospital (tm) to stop. In two weeks, she was back in the hospital, the same MSSA in the knee. She is currently jointless, awaiting a new knee, and none too happy.
But now there is data, albeit not great data, to support chronic suppression.
Early, small studies suggested little efficacy and a lot of toxicity, but that was from the 1980s. Ew.
A recent study suggests otherwise:
Chronic suppression with oral antibiotics increased the infection-free prosthetic survival rate following surgical treatment for periprosthetic joint infection. Patients who underwent irrigation and debridement with polyethylene exchange and those who had a Staphylococcus aureus infection had the greatest benefit.
Combine that study with the always misleading bias of bad outcome from stopping suppression, and I think I will continue with suppression when I can.
Rationalization
Orthopedics. 1991 Aug;14(8):841 4. Suppressive antibiotic therapy in chronic prosthetic joint infections.
http://www.ncbi.nlm.nih.gov/pubmed/1923965
J Bone Joint Surg Am. 2015 Aug 5;97(15):1220 32. doi: 10.2106/JBJS.N.00999. Chronic Suppression of Periprosthetic Joint Infections with Oral Antibiotics Increases Infection-Free Survivorship.
https://pubmed.ncbi.nlm.nih.gov/26246256/
Chapter Ninety-Three
The patient is a healthy middle-aged male who has a month of cough, fevers, chills, and weight loss.
CXR shows a bilateral lower lobe pneumonia, and he receives a variety of oral antibiotics with no improvement. He is non-toxic, and the cough is non-productive.
A chest CT is done and shows dense, confluent round infiltrates. Work up shows a serum cryptococcal antigen of > 1: a very large number. The CSF cryptococcal antigen is 1:2.
So it is a case of cryptococcal pneumonia with dissemination and early meningitis. Work-up reveals no immunocompromise, and I can find no risks. Yesterday the lab let me know it is C. gattii.
I have seen a bunch (is that the collective noun for pneumonias? Maybe a cough of pneumonias or a sputum of pneumonias?) of cryptococcal pneumonias, and they have all had exposure to fir trees, the ecological niche in the NW: a horse trainer where the barn had fir bark dust on the ground, a transplant patient who lived downwind of a tree grinding facility and a young female who worked at a nursery that specialized in Canadian firs.
This patient? Nothing.
Cryptococcus has been increasing year after year in Oregon, from a couple of cases a year in 2006 to 60 cases in 2014. It comes from Vancouver Island, which became an epicenter for C. gattii around the turn of the century. Anther failure of the border patrol. We really need to build a wall to keep Cryptococcus out and make the Canadians pay for it. And we need to send all the Cryptococcus back to Canada. Believe me when I tell you that.
Unfortunately, C. gattii is less responsive to antifungals, and for now, he is on amphotericin B and 5 FC, despite the current price gouging with the medication:
Due to generic drug manufacturer monopolization, flucytosine currently costs approximately $2000 per day in the United States, with a 2-week flucytosine treatment course costing approximately $28 000. The daily flucytosine treatment cost in the United Kingdom is approximately $22.
And the reason this disease is increasing in the Great Pacific NW may be due to climate change, changing the environment in the favor of Cryptococcus.
Rationalization
Characterization of Environmental Sources of the Human and Animal Pathogen Cryptococcus gattii in British Columbia, Canada, and the Pacific Northwest of the United States.
http://aem.asm.org/content/73/5/1433.short
Spread of Cryptococcus gattii into Pacific Northwest Region of the United States.
http://wwwnc.cdc.gov/eid/article/15/8/08-1384\_article
A rare genotype of Cryptococcus gattii caused the cryptococcosis outbreak on Vancouver Island (British Columbia, Canada).
http://www.pnas.org/content/101/49/17258.short
Treatment and Outcomes among Patients with Cryptococcus gattii Infections in the United States Pacific Northwest.
http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0088875
Cryptococcal Meningitis Treatment Strategies Affected by the Explosive Cost of Flucytosine in the United States: A Cost-effectiveness Analysis.
http://www.ncbi.nlm.nih.gov/pubmed/27009249
Spread of Deadly Cryptococcal Disease in U.S. Northwest Linked to Global Warming.
Climate Change and Infectious Disease: Is the Future Here?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230419/
POLL RESULTS
We need a wall to keep out
- cryptococcus 5%
- dengue 2%
- zika 9%
- mosquitos 33%
- Pink Floyd 30%
- Other Answers 21%
- drug manufacturer monopolies
- Donald Trump
- The unDead
- Donald Trump
- Trump
- Donald Drumpf
- the wall-builders.
- The Donald
- politicians
Chapter Ninety-Four
The patient presents with SIRS with no particular focus. Some chronic stasis changes in the lower extremities from CHF is about it.
He is hypotensive, has a WBC of 33, and altered mental status, so he gets the usual ICU care in addition to ceftazidime and vancomycin. We have no cefepime. We have run out. So ceftazidime instead.
It seems anymore we are being price gouged for old antibiotics like 5-FC and doxycycline and or we have a shortage of products like a third world county. It is nuts. Either no one can afford an antibiotic, or no one can get it. I guess that’s market forces at work: screw you or screw you.
Maybe someday I will get to use moxalactam and lincomycin again as we run out of modern antibiotics. It will be like getting to drive an Edsel because they have run out of Volts. And yes, I recently got a Volt. I love it. So far, I have gone 3500 miles and burned 4/5 of a tank of gas, about 7 gallons.
The next day the patient is markedly better and complains of thigh pain. On exam, the thigh is unremarkable for 3 of 4: no rubor, calor, or tumor, but there is a fair amount of dolor when you squeeze it.
CK is normal, so off to CT, which shows phlegmon around the thigh muscles.
Surgery doesn’t think it is an operative problem, and they call me.
Blood cultures are negative, and I think this is a case of (non)tropical pyomyositis, although as the Great Pacific NW warms a tad, maybe we are heading towards tropical. Tropical pyomyositis is
suppuration within skeletal muscles, manifesting as single or multiple abscesses. The most common organism implicated is Staphylococcus aureus. In 20%–50% of cases there is a history of trauma to the affected muscles. Commonly involved muscles are quadriceps, glutei, pectoralis major, serratus anterior, biceps, iliopsoas, gastrocnemius, abdominal and spinal muscles.
The number two bug is S. pyogenes.
There is a key clinical pearl with pyomyositis. Ready?
Serum creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) levels were not elevated in any of the 12 patients
because it is an infection mostly between and among the muscle fibers, not of muscle. Muscle is tough to infect without preexisting trauma, and with trauma, it is probably hematoma that is infected. Think how many times your tongue gets bit with that filthy mouth of yours (you kiss your spouse with that mouth?) and how rare tongue infections are.
As best I can tell, the 'tropical' part of the disease name occurs because the first cases were described in J Trop Med Hyg in 1947. The better term is spontaneous bacterial myositis or just bacteria myositis.
But. If you make a diagnosis of bacterial myositis, everyone yawns. If you call it tropical, add a pyo, and suddenly you have made a rare and exotic diagnosis, eliciting an appreciate murmur from the audience. Believe me.
The patient did fine with just antibiotics, so I suspect is was a Streptococcus.
Rationalization
Tropical pyomyositis (myositis tropicans): current perspective.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1743005/
N Am J Med Sci. 2013 Oct; 5(10): 600–603. doi: 10.4103/1947–2714.120796 PMCID: PMC3842701 Tropical Pyomyositis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842701/
Traquair RN. Pyomyositis. J Trop Med Hyg. 1947;50:81–9.
POLL RESULTS
To impress people I
- always add tropical and pyo. Tropical pyo COPD 11%
- only use Latin terms. I'm a dermatologist 6%
- make up diseases. You have chronic tropical pyo Candida 11%
- make up words. You have tropical pyo fadupin 11%
- quote made up references no one will check. As it said in 1947 J Trop Med Hyg 50%
- Other Answers 11%
- Never try to impress people
- Tropical pyo believemeface
- keep my damn mouth shut.
Chapter Ninety-Five
I wish when I had started out in medicine all those years ago, I had kept a record of all the outliers I have seen—lowest sodium, highest WBC, etc. I have seen a lot of amazing pathology over the years but just try and remember it. I have easily consulted on 15,000 patients and ten times that number of curbsides and phone calls. But I no longer remember the cases from last week, much less from a decade or two ago.
This blog has been a record of the amazing diseases I have seen over the last nine years, but try finding anything on a blog, much less using it as a reference source. And when I read an old post, I’ll be damned if I can remember actually writing it.
There is no doubt that Google and PubMed are great support for the aging brain.
The patient was successfully treated for MSSA endocarditis two months ago, and then, unfortunately, relapsed his iv drug habit. I have enough trouble resisting donuts and ice cream; I can’t imagine the siren call of heroin or cigarettes.
He presented to the ER with fevers, and blood cultures were positive.
For 4 organisms.
S. mitis, S. sanguis, S. gordonnii and Gamella haemolysans.
That is a personal record for polymicrobial endocarditis, my prior being three (S. viridins, S. aureus, and coagulase-negative Staphylococcus) in all the blood cultures. Or so I remember it.
In the prior case, there was a vegetation on the MV, AV and TV; in this case, just the TV.
Not only polymicrobial, but it is also a post-endocarditis endocarditis. Most of the cases I have taken care of have seeded when an IVDA continues to use their line, a non-nosocomial healthcare-associated infective endocarditis.
…vascular manipulation was the leading source of bacteraemia causing HAIE.
Heron users often can’t leave that line alone. The literature suggests S. aureus as the most common cause, although my unreliable memory suggests I have seen, or at least remember, more cases due to Candida.
A vegetation is fertile soil for bacterial growth, so it is no surprise the clot will become infected with new organisms, especially if the needle is licked. I am surprised it is as rare as it is.
I could also swear there is an article on post-endocarditis endocarditis with fresh, as opposed to old, clot, but my Google-Fu must be off as I can't find it.
Penicillin G is the treatment for all 4, gotta kill them all.
Rationalization
Medicine (Baltimore). 2015 Dec;94(49):e2000. doi: 10.1097/MD.0000000000002000. Polymicrobial Infective Endocarditis: Clinical Features and Prognosis.
http://www.ncbi.nlm.nih.gov/pubmed/26656328
Non-nosocomial healthcare-associated infective endocarditis in Taiwan: an underrecognized disease with poor outcome.
http://bmcinfectdis.biomedcentral.com/articles/10.1186/1471–2334–11–221
Healthcare-associated infective endocarditis: an undesirable effect of healthcare universalization.
https://pubmed.ncbi.nlm.nih.gov/19732086/
Chapter Ninety-Six
The patient has had HIV for 25 years, mostly well controlled. She has been ill for a month or so with a febrile illness and has had an extensive workup.
There has been a pericardial effusion/thickening that was tapped: no infection, no malignancy.
Bone marrow biopsy was negative. No infection, no malignancy.
FNA (that just sounds rude as it is pronounced effin A) of an enlarged lymph node was negative: no malignancy, no infection, although as an FNA, there was no node architecture seen.
Plus, the whole FUO workup for CD4s of 68 was negative.
So they called me. Besides some minimal time in Histoplasma territory in the past, I had nothing.
My only suggestion was to get a whole lymph node. Effin A's are worthless with no architecture, you do not really know what was in the node. Since she had a prior history of KS and a negative workup for lymphoma, I wondered about multicentric Castleman’s diseases.
Seemed a diagnosis of last resort. I have yet to see a case of multicentric Castleman's, so getting to be about time. Except for the pericardial involvement. That is very rare with Castleman's with about three cases on the Pubmeds.
So we took out a whole node and tapped a new pleural effusion, and it came back?
Body cavity lymphoma, which is known to cause effusions
Serous effusions are a common complication of lymphomas. Although the frequency of pleural effusion is 20–30% in non-Hodgkin’s lymphoma (NHL) and Hodgkin’s disease (HD), the involvement of peritoneal and pericardial cavities is uncommon.
Just like Castlemans, I had heard of serous body cavity lymphoma in the past, but I had never seen a case.
Like Casteman’s, it is also an HHV–8 disease.
Primary effusion lymphoma (PEL) is a human herpes virus–8 (HHV8)-associated large-cell non-Hodgkin lymphoma localized in body cavities and presenting as pleural, peritoneal, or pericardial lymphomatous effusions.
and
PEL is considered to be always associated with human herpes virus–8 (HHV8) infection; therefore, this term is restricted to those lymphomatous effusions that are associated with HHV8. It has been shown that the presence of the virus in the neoplastic cells can be demonstrated either by immunohistochemical methods using the HHV8 LNA–1 latent protein antibody, or by molecular techniques such as PCR amplification or Southern blot analysis[4–12] PEL typically involves only one body site, the most common being the pleural cavity; however, involvement of two body cavity sites has been reported in some series
At least we have the diagnosis. Now it’s up to the oncologist.
And the take-home? In FUO workups, don't get an effin A. Take out the whole node, put half in saline for culture and half, only half, just half, in formalin for histopathology.
Rationalization
Curr Opin Oncol. 2011 Sep;23(5):475–81. doi: 10.1097/CCO.0b013e328349c233. HIV-associated multicentric Castleman disease.
http://www.ncbi.nlm.nih.gov/pubmed/21760504
Curr Opin HIV AIDS. 2009 Jan;4(1):16–21. HIV-associated multicentric Castleman disease.
http://www.ncbi.nlm.nih.gov/pubmed/19343828
Diagn Cytopathol. 2006 May;34(5):335–47. Serous effusions in malignant lymphomas: a review.
http://www.ncbi.nlm.nih.gov/pubmed/16604559
Cytojournal. 2009; 6: 21. Published online 2009 Oct 9. doi: 10.4103/1742–6413.56361 PMCID: PMC2762694 Primary effusion lymphoma involving three body cavities.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762694/
The Joker - Why So Serious?
https://www.youtube.com/watch?v=4Vxu2VNWneg
Chapter Ninety-Seven
The patient, a young male, had 10 days of non-focal fevers except for a persistent headache that was right behind the eyes.
Four weeks prior to the onset of illness, he had been in Central America, where he had minimal infectious disease exposures. Two weeks before, he had been in Maui again with minimal ID exposure.
The exam was negative, he looked tired but not toxic, and labs showed a low WBC with a lymphocyte predominance (no atypical lymphocytes) and a mild transaminitis.
When I saw him, he had a negative EBV and CMV serology, negative monospot, negative Hepatitis ABC serologies, and a negative malaria smear, albeit when he was not febrile.
So work up continued: I sent off serologies for typhoid fever and Brucella, the former was positive, but he had the typhoid vaccine. As best I can tell, I cannot order acute and convalescent typhoid serology anymore, just an all or nothing test, like a pregnancy test.
Dengue serology, because of the Hawaii trip, was eventually negative, as was leptospirosis.
And the fevers went on for another two weeks. A pan scan was not impressive for pathology. Then just before the fevers resolved, he developed not an exudative pharyngitis but a swollen throat and mild cervical lymphadenopathy, with the emphasis on mild.
Repeated the EBV and CMV serologies, and the EBV serology, which had been stone-cold negative, was now whopping positive.
So this was a rare manifestation of EBV, the typhoidal form.
Her history of travel and exposures to food and water did not make typhoid fever a likely diagnostic possibility. Because she presented with prolonged fevers, fatigue, anorexia, weight loss, and night sweats with hepatosplenomegaly, lymphoma was possible. Initially, Epstein-Barr virus (EBV) was not considered because of her age, the absence of pharyngitis and cervical adenopathy, and the higher likelihood of another diagnosis, i.e., lymphoma. Eventually, her FUO was diagnosed as EBV, presenting as “typhoidal mononucleosis.” Typhoidal mononucleosis is an extremely rare presentation of EBV as a cause of FUO in an adult.
I am uncertain if I have seen a case, perhaps so, as when the serology came back, I said, oh, expletive deleted, I missed a case of typhoidal mono. Although I do not think the diagnosis could have been made any faster, I prefer to at least consider a diagnosis before the tests return, rather than after.
This was not, by the way, mono complicating typhoid fever.
There is a real paucity of reports on this form of EBV, one Pubmed reference, and short asides in EBV reviews. There are also a smattering of cases of EBV being initially mistaken for lymphoma in the older population.
As is the case with EBV, time is the best therapy, and he slowly improved.
And you know the rule of case reports: no matter how odd the disease, you are now obligated to consider the diagnosis in all your future patients.
Rationalization
Dengue Fever – Hawaii Island Outbreak.
http://health.hawaii.gov/docd/dengue-outbreak–2015/
Hawaii J Med Public Health. 2014 Nov;73(11 Suppl 2):21–3. Leptospirosis: the microscopic danger in paradise
http://www.ncbi.nlm.nih.gov/pubmed/25478298).
Heart Lung. 2013 Jan-Feb;42(1):79–81. doi: 10.1016/j.hrtlng.2012.06.004. Epub 2012 Jul 19. Fever of unknown origin (FUO) in an elderly adult due to Epstein-Barr virus (EBV) presenting as “typhoidal mononucleosis,” mimicking a lymphoma.
http://www.ncbi.nlm.nih.gov/pubmed/22818119
INFECTIOUS MONONUCLEOSIS COMPLICATING TYPHOID FEVER. From 1939. I love old reports.
http://annals.org/article.aspx?articleid=671908
Chapter Ninety-Eight
Back from a humid, sweating vacation, first in Boston, then Minnesota, visiting family.
Corn sweat. In rural Minnesota, out in the infinite fields of corn, you can feel the result. Perspiration just does not evaporate.
It is nice to be back in the great Pacific NW where the corn doesn’t sweat, thanks to the application of corn antiperspirants.
When I had left last week, I had a patient with a sustained community-acquired MSSA bacteremia without a focus. That usually means endocarditis, or, more broadly, an endovascular infection.
In this case, the patient had some abdominal pain and was getting a CT as I was heading out to the airport.
It turned out the CT showed that a known AAA was now surrounded by edema/phlegmon and a leak, which subsequently completely ruptured with fatal results.
Hematogenously infected AAA’s are rare; I have seen less than a handful, and I wonder if it is due to the lack of AAA’s in the population.
An aneurysm was present in 263 (8.9%) men and 74 (2.2%) women
And while S. aureus loves to go to clot, S. aureus bacteremia is also uncommon.
The annual incidence of S. aureus bacteremia in the United States is 4 to 38 per 100,000 person-year.
To have both bacteremia and AAA at the same time would the rare and probably why I see one such infection only once a decade or so. Which, given the usually fatal outcome, is just as well.
Rationalization
IDCases. 2016 Jul 30;5:60–2. doi: 10.1016/j.idcr.2016.07.010. eCollection 2016. Staphylococcus aureus aortitis and retroperitoneal fibrosis: A case report and literature review.
http://www.ncbi.nlm.nih.gov/pubmed/27516965
Am J Epidemiol. 2001 Aug 1;154(3):236–44. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study : The Tromsø Study.
http://www.ncbi.nlm.nih.gov/pubmed/11479188
Epidemiology of Staphylococcus aureus bacteremia in adults.
http://www.uptodate.com/contents/epidemiology-of-staphylococcus-aureus-bacteremia-in-adults
Chapter Ninety-Nine
My practice is almost entirely hospital-based. At one time, I was the only ID doc at 4 widely separated hospitals and was never able or interested in building an outpatient clinic.
And hospitals get slow, at least for infections, in August. I had one August, back with the last recession, where I had one consult for the entire month.
Partly, I suppose, due to doctors and patients taking August off, countering the increase in surgical site infections that comes with the summer:
The rate of SSI following commonly performed surgical procedures was higher during the summer compared with the remainder of the year. Summer SSI rates remained elevated after stratification by organism and spinal versus nonspinal surgery, and rates did not change after controlling for other known SSI risk factors.
Bacteria probably love a hot, sweaty wound. It is like putting me in a Baskin Robbins with an ‘all you can eat’ sign.
But given our relentless suppression of hospital-acquired infection, it has been a long time since I paid my mortgage from seeing nosocomial infections.
I mostly rely on outpatient bad luck and bad habits for my consults, and August must be the time of good luck. Summer modifies
human activity, seasonal variability in human immune system function, seasonal variations in vitamin D levels, seasonality of melatonin, and pathogen infectivity.
to make my practice light.
I have always been intrigued by the association of vitamin D levels and infection:
epidemiologic studies have demonstrated strong associations between seasonal variations in vitamin D levels and the incidence of various infectious diseases.
But I suspect it is overrated as a risk.
Infections are usually multifactorial in origin, and I cannot credit any one factor for the summer doldrums. I have plenty of non-clinical work to get caught up on, but it is dull.
I want to see infectious diseases and come to work geared up for a day of bugs and drugs. Having a slow day is like putting the car in neutral and flooring the gas pedal: lots of energy expended with no result.
It never lasts. One way to get a consult or three is to leave early. The other, I hope, is to publish this. The Universe will then try and show me just how wrong I am.
Rationalization
Seasonal Patterns of Infectious Diseases.
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020005
Int J Prev Med. 2013 Feb;4(2):128–32. Factors influencing the seasonal patterns of infectious diseases.
http://www.ncbi.nlm.nih.gov/pubmed/23543865
VITAMIN D FOR TREATMENT AND PREVENTION Of INFECTIOUS DISEASES: A SYSTEMATIC REVIEW OF RANDOMIZED CONTROLLED TRIALS.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855046/
Infect Control Hosp Epidemiol. 2015 Sep;36(9):1011–6. doi: 10.1017/ice.2015.121. Epub 2015 May 26. Seasonal Variation of Common Surgical Site Infections: Does Season Matter?
https://pubmed.ncbi.nlm.nih.gov/26008876/
POLL RESULTS
- The cure for the doldrums is
- a good wind 22%
- mosquitos 10%
- thunderstorms 32%
- a full moon 17%
- winter 10%
- Other Answers 10%
- a vacation
- sacrificing a few horses to Neptune.
- sporting event
Chapter One Hundred
Phone calls can be the coolest cases.
ID weekend call covers a lot of territory—six hospitals in 2 states. I couldn’t do it without the support of tremendous hospitalists and the ability to review the chart on EPIC. I do not offer procedures but answers to odd questions, and on the weekend, those questions can be fielded without seeing the patients, temporizing until Monday.
Saturday, I get a phone call. Some of the best cases are cubsides.
The patient had some trauma at the coast and now is in with a cellulitis of the arm.
The weird thing is gram negatives are in the blood. Could it be a Vibrio? Sure.
Although in the great Pacific Northwest, it has been mostly Vibrio parahaemolyticus, thanks to global warming.
This report documents a large outbreak of V. parahaemolyticus serotype O6:K18 in the United States, and it expands the range of epidemiologically confirmed V. parahaemolyticus illness to a latitude higher than 60 degrees — more than 1000 km north of British Columbia, previously the northernmost area reported to have locally acquired illness.14 Furthermore, our findings provide evidence to support the hypothesis that a water temperature above 15.0°C at the time of oyster harvest is an appropriate threshold indicator of increased risk of V. parahaemolyticus infection from the consumption of raw oysters.15–17 Although water temperatures have reached 15.0°C at Farm A each year since 1997, 2004 was unusual because mean temperatures were above 15.0°C for a much longer period and were almost 2°C warmer than during any of the previous years.
A problem seen outside of the great Pacific NW.
But Vibrio parahaemolyticus is not that Vibrio that usually causes soft tissue infections. That would be V. vulnificans and Vibrio alginolyticus.
And it was a cellulitis, not a necrotizing infection that was responding to ceftriaxone, so I was not too worried about Aeromonas. The patient is also normal, with no other medical problems. So I said keep the antibiotics going and call me tomorrow with the name of the beast.
Shewanella algae.
OK.
Yet another emerging pathogen. It says so in the title.
Shewanella skin and soft tissue infections are more commonly seen in immunocompromised patients with a pre-existing cutaneous ulcer and most often associated with exposure to marine environments…Peripheral vascular diseases were the predominant risk factors with comorbidities like diabetes, hypertension and hepatobiliary diseases. Third generation cephalosporins, meropenem and gentamicin were the most effective antibiotics.
And this organism may also be increasing with warming ocean temperatures. An interesting and diverse species, others have been used to make omega–3 fatty acids, fuel cells and to reduce heavy metals. Ozzy beware.
And it is used as a fish probiotic.
The common probiotics that are used for aquaculture practices include Lactobacillus, Lactococcus, Leuconostoc, Enterococcus, Carnobacterium, Shewanella, Bacillus, Aeromonas, Vibrio, Enterobacter, Pseudomonas, Clostridium, and Saccharomyces species.
Whoa. What a list. I’ll stick with yogurt, thank you very much.
The patient continued to improve on ceftriaxone, and I left it to my partner to do the final follow up.
But as the world warms, I doubt I have seen the last of Shewanella.
Rationalization
Outbreak of Vibrio parahaemolyticus Gastroenteritis Associated with Alaskan Oysters.
http://www.nejm.org/doi/full/10.1056/NEJMoa051594#t=article
Emerging Vibrio risk at high latitudes in response to ocean warming.
http://www.nature.com/nclimate/journal/v3/n1/full/nclimate1628.html
J Clin Diagn Res. 2015 Feb;9(2):DC16–20. doi: 10.7860/JCDR/2015/12152.5585. Epub 2015 Feb 1. Skin and Soft Tissue Infections due to Shewanella algae - An Emerging Pathogen.
http://www.ncbi.nlm.nih.gov/pubmed/25859455
Sun, surf and septicaemia.
http://www.abc.net.au/science/articles/2004/10/08/1213608.htm
Fish Shellfish Immunol. 2010 Jul;29(1):2–14. doi: 10.1016/j.fsi.2010.02.017. Epub 2010 Feb 26. Probiotics and immunity: a fish perspective
http://www.ncbi.nlm.nih.gov/pubmed/2021968.
Appl Environ Microbiol. 2015 Oct 23;82(1):218–31. doi: 10.1128/AEM.02266–15. The Microbiota of Freshwater Fish and Freshwater Niches Contain Omega–3 Fatty Acid-Producing Shewanella Species.
http://www.ncbi.nlm.nih.gov/pubmed/26497452
Chapter One Hundred One
I am getting old (I will turn 60 this spring), and with age comes refractory grumpiness.
I have been doing ID about 31 years if you include fellowship, and here is how I see others doing ID.
They do a history, physical, labs, x-rays, and cultures. Then they ignore all of it and treat every organism that pops into their mind, regardless of probability, cultures, or disconfirming studies. God forbid an antibiotic should ever be stopped when the cultures are negative. So often, I see a patient who was started on vancomycin/zosin for sepsis, and while S. aureus or E. coli is in the blood, the unneeded antibiotic is not stopped.
Infections have patterns and risks, not that anyone seems to pay them any mind. Grump grump grump.
The patient is an elderly diabetic/renal transplant patient who fell, breaking several ribs.
She noted a fever (100.3, not my definition of a fever), but it persisted, and a CXR showed a pleural effusion and patchy infiltrates.
Over the next two months, she had negative diagnostic tests that eventually lead to VATS.
At no time did the patient feel ill—no constitutional or other signs of infection.
The pleural fluid had a significantly elevated LDH, depending on the tap 200-2000 WBC (lymphocytes and monocytes) and a negative gram stain and culture. The sputum was equally unrevealing.
Yet somehow, when I was consulted after the VATs, she was on cefepime, metronidazole, vancomycin, and micafungin for no other reason than they wanted to cover gram-negative rods, anaerobes, mursa, and fungus.
It wasn’t that there was any clinical or laboratory reason for any of the above. It is like they are playing an expensive version of Pokemon Go with antibiotics and microorganisms. Gotta get them all. I suspect many consider bacteria like demons, a vague, poorly understood evil that must be combatted with equally vague and poorly understood antibiotics.
So I took a history. She travels to the Washington/Canada border and through eastern Washington to Montana regularly.
So I figured it was either Cryptococcus or Coccidiomycosis.
There is a curious literature of trauma causing the reactivation of TB, but I do not really buy it. I suspect it is more coincidence than causal.
I suggested stopping all the unneeded antibiotics and sent off a serum CRAG that was positive. Unfortunately did not ever get pleural fluid to test.
Ah, nothing like a history combined with an understanding of infectious diseases to make a diagnosis. Not a common problem, and there are only a handful of pleural effusions from Cryptococcus, but you must, must I tell you, think about it.
Cryptococcal infection must be considered in the differential diagnosis of patients with pleural effusion, especially patients with serious underlying diseases treated with corticosteroids. The cryptococcal antigen test appears to be a useful adjunct in diagnosis, and serial determinations may be helpful in assessing response to treatment.
Yes. MUST.
Pleural effusion is an unusual manifestation of cryptococcosis. Cryptococcal infection must be considered in the case of patients on immunosuppressives, especially solid-organ transplant recipients, who present with pleural effusion, even if pleural fluid culture is negative.
Every weird infection MUST.BE.CONSIDERED.
The CSF was negative.
Probably the reason she did so well was her immunosuppression. Calcineurin-inhibitors such as tacrolimus result in a kinder, gentler infection:
In multivariate analysis, the receipt of a calcineurin-inhibitor agent was independently associated with a lower mortality.
Probably acting as an antifungal.
Importantly, we demonstrate that C. gattii calcineurin is essential for virulence in a murine inhalation model, supporting C. gattii calcineurin as an attractive antifungal drug target.
and
Synergistic interactions were observed between CIs and antifungal agents against 53 (90%) of 59 Cryptococcus neoformans isolates from solid organ transplant recipients with cryptococcosis and may account for better outcomes in patients with cryptococcosis receiving these immunosuppressive agents.
Rationalization
Am Rev Respir Dis. 1980 Apr;121(4):7437. Pleural effusions due to Cryptococcus neoformans: a review of the literature and report of two cases with cryptococcal antigen determinations.
http://www.ncbi.nlm.nih.gov/pubmed/6992663
BMC Infect Dis. 2015 Sep 22;15:385. doi: 10.1186/s1287901511324. Pleural effusion as the initial clinical presentation in disseminated cryptococcosis and fungaemia: an unusual manifestation and a literature review.
http://www.ncbi.nlm.nih.gov/pubmed/26395579
Reactivation of dormant microorganisms following a trauma.
http://njmonline.nl/getpdf.php?id=706
G3 (Bethesda). 2013 Mar;3(3):52739. doi: 10.1534/g3.112.004242. Epub 2013 Mar 1. Calcineurin governs thermotolerance and virulence of Cryptococcus gattii.
http://www.ncbi.nlm.nih.gov/pubmed/23450261
Antimicrob Agents Chemother. 2008 Feb;52(2):7358. Epub 2007 Dec 10. Calcineurin inhibitor agents interact synergistically with antifungal agents in vitro against Cryptococcus neoformans isolates: correlation with outcome in solid organ transplant recipients with cryptococcosis.
http://www.ncbi.nlm.nih.gov/pubmed/18070977
A Critical Appraisal of 98.6°F, the Upper Limit of the Normal Body Temperature, and Other Legacies of Carl Reinhold August Wunderlich.
http://jama.jamanetwork.com/article.aspx?articleid=400116.
It should be required reading for all medical students. Judging from experience asking them about what is a fever, I suspect it isn't. So much for understanding a vital sign. There is no end to my grumpiness. And get off my lawn.
POLL RESULTS
- ID is
- like Pokeman Go 5%
- from Revelations 10%
- part of chaos theory 45%
- easy. If you think of a bug, treat it. 12%
- as fantastical as Wheel of Time 19%
- Other Answers
10%- a daily confirmation that, indeed, you can't fix stupid. In that way, it's a lot like politics.
- the lottery
Chapter One Hundred Two