Antibiotic Resistant Staph Infections

oliphaunt writes "This! morning! at! Yahoo! there! is! a! story! about! drug-resistant! bacteria! This is interesting because, as of July 5 of this year, "It was the first case of vancomycin-resistant Staphylococcus aureus in the United States." Nobody can PROVE it of course, but this is probably a result of overprescription of antibiotics, and people not following doctor's directions, combined with stuff like antibiotic hand soap available over the counter. So what do we do when the bugs are resistant to everything we have? The answer is we die."

Comments

Re:vancomycin resistance does not come from hand s

[tid242]

well although i agree with your spirit, i do not agree with your facts...

vancomycin (an extremely rare antibiotic, used only in cases of desperation)

this is what vanco is supposed to be, but in fact it is used quite frequently, and is actually gaining popularity given that virtually every major medical centre in the US is now seeing the prevalence of MRSA going through the roof (as MRSA is resistant to pretty much everything except for vanco, linezolid (Zyvox) and dalfopristin/quinupristin (Synercid)). vanco is now the drug of choice in many institituitions until lab sensitivities come back, at which time a patient with a staph infection may be switched to something else or remain on vanco. with infectious disease health care providers simply cannot afford to prescribe nafcillin and wait a day for labs to come back and tell them whether or not the organism is resistant, so they prescribe vanco first and modify later (and you would too if you were on the east coast and 1 in 3 staph infections were nafcillin resistant)...

furthermore:
vancomycin resistance can come from serendipity, from vancomycin exposure, or from a mechanism which creates a much broader resistance to a class of antibiotics which includes vancomycin, subsequent to exposure to other antibiotics in that class

there are currently no antibiotics on the market in use with the same mechanism of action (MOA) of vanco (which is a glycopeptide cell wall inhibitor). the Penicillins/cephalosporins are cell wall inhibitors of a different nature, and do not promote resistance to vancomycin directly, although ceftazidime (Fortaz) independently causes an increased incidence of VRE (Vancomycin-Resistant Enterococcus (not the same as staph a)) for reasons unbeknownst to the medical/research community. Likewise aminoglycosides, flouroquinolones, macrolides, et al. also do not increase the incidence of vancomycin resistance in and of themselves. however all of these compounds increase the selective pressure on organisms, thus favoring strains that more easily acquire resistance than their counterparts... But contrary to your point most of the time when you hear about cross-resistance they're talking about resistances to drugs in the same class or with the same mechanism of action such as all beta-lactams (pens & cephs), all aminiglycocydes (gent, tobra, amikacin), all flouroquinolones (levofloxacin, ciprofloxacin, gatifloxacin, etc) and the like, but this isn't something that normally happens with outliers such as vanco, zyvox, synercid, rifampin, etc.

just as an aside (but of interest), the CDC labels VISA/GISA as staph a with a minimum inhibitory concentration (MIC) of vanco to be greater than 8mcg/mL, and VRSA to be greater than 32mcg/mL. When one does pharmacokinetic dosing for vanco, by the book one looks for a peak serum vanco concentration of 20-40mcg/mL, and a trough of 5-15mcg/mL (usually broken down to 5-10 for normal infections and 10-15 for serious concentrations.) But in real life people don't even look at the peaks (it doesn't improve outcomes and costs too much to do if it doesn't help), just the troughs, and as you probably know vancomycin is a time-dependent killer (like the beta-lactams (with the exception of the carbapenems of course) and macrolides) so a range of 8-32mcg/mL for an intermediate strain won't necessarily tell you if it will work in a clinic, especially since many infections are in areas with poor circulation (necrosed tissue etc) in which the drug levels won't be anything near what they are in the plasma (due to poor tissue perfusion). And thus the distinction between VRSA and VISA/GISA are more of scientific/epidemiological significance than of actual clinical significance (especially if you've only got a vanco peak of 20mcg/mL and your MIC is 25 for the strain). And if you're just looking for hard-to-treat cases of Staph a, then this news is nothing new...

-tid242