An ongoing dialogue on HIV/AIDS, infectious diseases,
November 22nd, 2015
Just Wondering: Quick ID Questions to Consider
Several quick ID queries, some of them answerable on the Google machine — but I’m not going there. Too busy laundering my white coat!
- What ever happened to amphotericin A?
- What’s the difference between a “serovar” and a “serotype”?
- Do dogs feel bad that Pasteurella multocida is more famous than Capnocytophaga canimorsus?
- Colistin resistance is bad — but how often does colistin actually work anyway?
- No one asks you to share a room with a stranger in a hotel — why do we ask sick people in hospitals to do this? Even sick people with infections?
- Why is there group A, B, C, D, F, and G, but no group E beta strep? At least I don’t think there is. Is it like Windows 9?
- Why do all the abbreviations for “integrase inhibitor” — InI, INSTI, II — sound and look so silly? Just say “integrase.”
- Why do we say trimethoprim-sulfamethoxazole with the trimethoprim part first, but the pharmacy usually writes it for our patients the opposite way?
- Don’t you think that if probiotics really prevented or helped some condition, we’d know it by now?
- Even though the name has changed, is anyone ever going to stop saying Strep bovis?
- Why are the guidelines for meningococcal immunization so complicated? Have to look them up every time.
- Why do C diff precautions start the moment we send the diagnostic test, but MRSA precautions await the results of staph susceptibility testing?
- Why was optochin never developed into an antibiotic? Is it because it doesn’t end in “-mycin” or “-cillin” or “-floxin”?
- Does anyone really know the best dosing option for strep throat?
- What proportion of doctors immediately think Aeromonas hydrophila when they hear about medicinal leeches? And what proportion who read this blog?
- Who decided it should be MRSA — and not ORSA or NRSA?
- What percentage of hospital-based ID consults recommend additional blood cultures — even when there are numerous negatives already done on that patient?
- Why did the new endocarditis guidelines advise against using penicillin for penicillin-sensitive Staph aureus? (In Boston, we call it PSSA — say it, you’ll get the joke.) In vitro, it’s the most active drug, after all.
- MALDI-TOF or MALDI-TOF MS? Seems the former should be sufficient.
- Endocarditis cases in Britain rise since they stopped using antibiotic prophylaxis for dental work — evidence that this is in fact an important preventive strategy? Or just that the British have, ahem, dental issues?
- Why do doctors always use the term “germ” in non-medical communications, but never do otherwise? And why does it mean a virus or bacteria or fungus, but never a parasite?
- When the inactivated zoster vaccine is approved, what happens to all those zoster vaccine curbside consults?
- Dogma is that you don’t need antibiotics after I and D of uncomplicated skin abscess. So why is 10 days of TMP-SMX better than 3?
- Why are certain toxic and little-used HIV drugs (ddI, d4T in particular) still on the market? Is there anyone who wouldn’t benefit from switching to something different?
- When we will stop using antibiotics to treat C diff?
- Could this white coat poll be any closer? Memories of Bush vs Gore.
Answers, opinions, speculations welcome!
Seems probiotics helped this guy (listen/watch through 1:50).
[youtube http://www.youtube.com/watch?v=3xJWxPE8G2c]
20 Responses to “Just Wondering: Quick ID Questions to Consider”
Paul E. Sax, MD
Contributing Editor
NEJM Journal Watch
Infectious Diseases
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“•Why do we say trimethoprim-sulfamethoxazole with the trimethoprim part first, but the pharmacy usually writes it for our patients the opposite way?”
Because every formulation (tablets, ped. suspension, IV) of sulfamethoxazole/trimethoprim lists the components in that order.
But, pharmacists just refer to it as “Bactrim,” “Septra,” or “sulfatrim.”
“•Why do we say trimethoprim-sulfamethoxazole with the trimethoprim part first, but the pharmacy usually writes it for our patients the opposite way?”
In the UK and Eire we’d just call it Co-trimoxazole and probably write it as trimethoprim/sulfamethoxazole were we asked to explain the components. The use of brand names is frowned except in specifically defined cases. Occasionally doctors might write “Septrin”, the only brand available.
Hi Patrick, brand names are frowned upon here too, but some are really sticky. TMP-SMX discussed here; others here.
So this doesn’t answer any of your questions (sorry!) but I had another one in the same vein, so to speak…
What happened to the penicillins other than G and V? I would absolutely love to be able to prescribe penicillin X (http://aac.asm.org/content/12/1/31.full.pdf).
Oh well.
I don’t think that will work out, but I’d still like to know what happened to them.
Re PSSA: testing for PSSA is not straight forward. We have at least one false negative result (using more sophisticated tests than the cefinase test) once in a year in invasive S. aureus infection. Just last week, we had a S. aureus endocarditis with a PSSA (tested negative in an outside lab) which was clearly positive in our lab.
We have always used penicillin for PSSA in the past (trusting our lab), but we are currently discussing to stop testing for PSSA and treating everyone with flucloxacillin.
Interesting — is this true even when the K-B disk diameter to penicillin is huge? Is that a false call also?
Paul
I always thought the most appropriate abbreviation was BLRSA: beta-lactam resistant staph aureus.
Pronounced, no doubt, as “BLERSA”. Love it!
Paul
In Brazil we say sulfametoxazol first…
Why is there group A, B, C, D, F, and G, but no group E beta strep? At least I don’t think there is. Is it like Windows 9?
Answer: groups C,E,F; G; H, and K-U streptococci, infrequently causes human disease. Source: Levinson W, Jawetz E. Medical Microbiology and Immunology Examination & Board Review. 7th ed, Mc Graw Hill.
Do dogs feel bad that Pasteurella multocida is more famous than Capnocytophaga canimorsus?
Answer: Maybe/Maybe not.
Why do all the abbreviations for “integrase inhibitor” — InI, INSTI, II — sound and look so silly? Just say “integrase.”
INSTI is a quick test for HIV 1/2. The test is intended for use by trained personnel in medical facilities, clinical laboratories, emergency care situations, and physicians’ offices as a screening assay capable of providing test results in as little as 60 seconds. The assay is packaged as a kit containing INSTI™ Membrane Units, Sample Diluent, Color Developer and Clarifying Solution, and is available in point-of-care use packaging. Source: http://www.biolytical.com/products/instiHIV
Dogma is that you don’t need antibiotics after I and D of uncomplicated skin abscess. So why is 10 days of TMP-SMX better than 3?
Answer: Maybe to increase marketing in TMP-SMZ (which is the form that both active principles appear on the box of that medicine).
Hiram, thanks for those breat answers! But there’s plenty of C, F, and G disease out there — look for an interesting upcoming publication in OFID on causes of cellulitis.
Paul
* Does anyone really know the best dosing option for strep throat?
Penicillin is still considered the best choice to treat streptococcal pharyngitis, a single intramuscular dose of penicillin G benzathine 1.200.000 U will be sufficient.
van Driel ML, De Sutter AI, Keber N, Habraken H, Christiaens T. Different antibiotic treatments for group A streptococcal pharyngitis. Cochrane Database Syst Rev. 2013 Apr 30;4: PubMed
Great reference, Federico, but the pediatricians will not be fans of this conclusion!
Paul
re: Probiotics- I just found probiotic tea, sold in standard tea bags, at the grocery store. Since then i’ve been wondering (even if probiotics worked in the first place) how this Bacillus species they tout survives after being soaked in BOILING water before it’s consumed? Just wondering….
Hello happy end of year and wishes of happiness for next one.
Serovars and serotypes? These are terms essentially interchangeable.
But, since pathogens exhibiting a specific serotype (with same specific serovars based on the cell surface observed antigens) will encounter specific cells owned by different individuals in multiple species. Question of the organization , the sequence of these antigens based on cell surface antigens pathogens will be of great interest. If a virus Serotype exhibits A, B and C Serovars is in contact with HLAXXX cell, and that “A serovar” is initiating “B serovar” activation leading to phagocytosis activated by “C serovar”.If B serovar is the first to enter in contact with cell receptor and through steric overcrowding blocks “A serovar” activation and do not permit Activation of “C serovar” than there is no phagocytosis. Conformation of targeted cells surfaces may be in such hypothesis of great importance too. So such as in “homozygotes twins” epigenetic makes the difference. So serotypes depends of serovars but are not expressing same things. Just for laugh.
Michel Vandevelde MD, PhD and talking with HIV from so many years.
1. AmA (as opposed to AmB): My understanding is that back in the olden days, both were derived from Streptomyces, but AmB was much more active than AmA, so the latter was scrapped. Curiously, nystatin (another polyene) was also available intravenously eons ago, but it was deemed too toxic and was thus scrapped. I wonder what their threshold of defining toxicity was, given that AmB-d lingered for decades.
2. Ah, colistin. Terrible drug as monotherapy. Prior to ceftazidime/avibactam, we routinely used it in combination with doripenem to treat KPC+ enterics, with less than terrible outcomes (Qureshi ZA et al. Antimicrob Agents Chemother. 2012 Apr;56(4):2108-13). Alas ceftaz/avi is inactive against CR-Acinetobacter, probably because it cowers in the face of OXA-23–we still use it there, always in combination (Shields RK et al PLoS One. 2012;7(12):e52349). Maybe plazomicin will be better…or maybe the era of antibiotics is spiraling to an end, and the only way we can cure these patients is with “phage therapy” and stool transplants to decolonize their guts.
http://aac.asm.org/content/56/4/2108
http://www.ncbi.nlm.nih.gov/pubmed/23285002
3. *Why do we ask sick patients in hospitals to do this? Oh, infection control. What I’ve always found curious is how they tend to lump different patients with the same contact precautions in the same room without giving any consideration to the susceptibility pattern of the offending pathogen. Eg: two MRSA-colonized patients can inhabit the same space, but what if someone’s MRSA is uber-resistant (let’s say to TMP/SMX and clindamycin) while the other’s MRSA is relatively friendly. This doesn’t seem like a good idea, but our “flagging” system doesn’t capture these nuances.
4. S. bovis: I think with the advent of MALDI-TOF (MS?), “gallolyticus” is going to become more mainstream. I have had to do a lot of google-related “lookups” after we adopted the MALDI, and I have noticed an increase in consults for things like CoNS pseudobacteremia because our MALDI will call it “S. hominis,” which no one has heard of. However, there are some nuances about what the MALDI can actually do, as not all S. gallolyticus are associated with colon adenocarcinoma. S. bovis is most accurately S. gallolyticus subsp. gallolyticus. Here is a more erudite explanation that I totally stole from one of my attendings, Dr. Curry: “MALDI databases and commercial biochemical IDs lump S. gallolyticus together in a group that includes S. gallolyticus subsp. pasteurianus, S. infantarius subsp. coli, and S. infantarius subsp infantarius, none of which is associated with colonic adenocarcinoma. Only mannitol fermentation is known to distinguish S. gallolyticus subsp. gallolyticus from the others.”
5. Meningococcal vaccines: I have the same qualm with pneumococcus–we have a flowchart in our HIV clinic, otherwise I would never remember.
6. C. diff precautions: I have always thought about this and secretly hoped no one else would. According to one of our infection control folks, we have a new committee to investigate the need for empiric CDI precautions. She couldn’t tell me specifically why, but she thinks the 2001 outbreak we had may have had something to do with it (Muto CA et al. Infect Control Hosp Epidemiol. 2005 Mar;26(3):273-80).
http://www.ncbi.nlm.nih.gov/pubmed/15796280
7. Aeromonas and leeches: I only know this from the George Washington ID board review course…
8. MRSA vs ORSA: Actually, the 2005 AHA endocarditis guidelines do call it ORSA. Was it really commonly referred to as ORSA back then? The 2015 AHA endocarditis guidelines refer to it as MRSA. BLERSA is hilarious but alas, we have ceftaroline now…
9. My question: How on earth are we going to start abbreviating ceftazidime/avibactam and ceftolozane/tazobactam, without having to resort to trade names? Cefavi? Cef/tazo? Sounds too much like ceftaz and pip/tazo. One of our pharmacists coined “tol/taz,” but that seems a bit much.
-Ghady
Ghady,
What a treasure trove of information! Thanks for the great answers.
Paul
Re: “Why do C diff precautions start the moment we send the diagnostic test, but MRSA precautions await the results of staph susceptibility testing?” If someone has active diarrhea and there is concern for C dif, then I’m concerned for spread to visitors, healthcare workers and throughout the hospital. If someone has MRSA bacteremia from osteomyelitis or an abscess, though, I’m much less concerned about it being spread to hospital contacts. At our hospital, we isolated people who grow colonizing MRSA out of their posterior nares. The cost/benefit ratio of this seems unfavorable to me, but maybe there is some data out there to suggest that the practice is in fact justified?
Tim, I see what you’re saying. But both are spread from person-to-person and require contact precautions, and the likelihood of a Staph aureus (from any site) being MRSA once identified in culture is around 30-60% (depends on the patient) — at least as high as the likelihood of a positive C diff test in a patient with diarrhea.
I’m not saying we should do it, just that there’s a double standard!
Paul
This question popped into my head as I clicked on the links in this article:
1) Has anyone ever paid the ~$30 for 24 hour access to a single journal article when they don’t have institutional access?
2) Is there a nice way to tell people it’s “vancomycin” NOT “vancomy-uh-sin”? I’ve even heard similar pronunciations from an ID doctor