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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."
Now we know what killed the dinosaurs, antibiotic soap!
The patient, a 40-year-old Michigan man with diabetes, seems to have caught the bug off an infected catheter inserted while he was in the hospital for the amputation of a gangrenous toe
Suddenly I realize that I am not having such a bad day after all.
there is zero evidence to link resistance to
vancomycin (an extremely rare antibiotic, used only
in cases of desperation) to the use of hand soap.
in my opinion the body of this article is
sensationalistic hogwash.
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.
hand soap is not in any structurally related class.
-I like my women like I like my tea: green-
Anyway, there are other things we can do. Phage is always there in our armoury, and unlike antibiotics, bacteria have little chance of out evolving it...
(For those not in the know, Phage is the name given to viruses that have coevolved with bacteria. The idea is that you hunt around for a virus that kills the bacteria and spray the viruses around and the bacteria is killed. It seems to work... the Russians use it sometimes, it's cheaper than antibiotics.Viruses mutate faster than bacteria can.)
-WolfWithoutAClause
"Gravity is only a theory, not a fact!"Anyone else think the poster has had a little too much caffeine?
I had a staph infection two years ago, and it really was a bummer. Happily it was just at the skin level or I would probably not be here now. We have known for quite a while that staph would eventually beat vancomycin, it was just a matter of time. That's why it was only used in the most dire cases, in the hope of extending the time before it became resistant. It didn't occur because of not following doctor's orders, since it would probably only be used under intensive care like conditions, with either IV or daily distributions of pills.
Incidentally, new research has focused on interrupting the communication that Staph does to announce its population is large enough to attack. It doesn't attack right away but waits for numbers to be large enough to overwhelm the immune system. If it can either be triggered to attack before numbers are large enough, or never recieve the attack signal, staph infections would likely be dealt with by the immune system.
Degaussing scares the bad magnetism out of the monitor and fills it with good karma.
See my previous post, since I don't want to repeat myself too much.
... I guess I just repeated myself a bunch. Oh well.
The short version is antibiotic hand soap breeds bacteria that are immune to that type of antibiotic. Since there are only three or four different types of antibiotics out there, breeding a resistant strain from hand soap means the strain is also immune to an entire type of antibiotic, so if you have a staph infection and use the soap you could get a strain of staph resistant to whatever particular antibiotic is in the soap. If someone else living in the same household gets infected with this new resistant strain of staph, they can't be helped by an entire type of antibiotic, focing the use of second- or third-line antibiotics. And the only way to breed a resistant strain is to use an antibiotic on it.
Hmmm
Mr. Spey
Cover your butt. Bernard is watching.
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
With a few exceptions, secrecy is deeply incompatible with democracy and with science. --Carl Sagan
There are lots of things that are 'antibacterial' without being an 'antibiotic'. Chlorox is certainly antibacterial, but it's not an antibiotic in the sense that a doctor prescribes.
The compound used in most soaps, triclosan, isn't related to penecillin, erythromycin, etc. I certainly wouldn't recommend you eat Dial.
So washing your hands with antibacterial Dial isn't going to doom you to death by vancomycin resistant staph.
There are good reasons to avoid antibacterial soap, like killing of beneficial organisms, but don't confuse that with antibiotic resistant organisms caused by misuse of prescribed antibiotics.
The strongest things survive
No, the fittest things survive. In evolutionary biology, fitness is defined as the ability to pass on your genes. This may be related to strength. It may not.
nature is developing a new device
Nature is developing nothing. There is no consciousness guiding the development of these organisms.
The number of bacteria on the planet is unimaginably huge. Bacteria are capable of passing genes between each other horizontally. As a result, you can effectively treat the entire bacterial population of the planet as a single gene pool. Given enough time, any beneficial mutation will pass from one end of the population to the other.
.
Now, this is obviously a problem in terms of antibiotics. Many antibiotics are still generated from natural sources, and some fairly harmless bacterial species has probably developed immunity to that (by virtue of happening to live in the soil around the ferns that secrete it, for example). The genes providing that immunity can pass to pretty much ever other bacterial species on the planet. This isn't a rapid process, but it will be sped up by imposing additional selection pressure - for instance, treating bacteria with that antibiotic.
Overuse or inappropriate use of antibiotics isn't really the trigger here. Imposing any degree of selection pressure will result in the same thing happening - it's only a matter of timing. More careful use of antibiotics may give us a few hundred years more if we're lucky, ten years more if we're not. The point to remember is that no matter how clever your antibiotic, there will be a gene in some bacterium somewhere that provides immunity to it. And, if you wait long enough, that will end up in the bacteria you're trying to kill.
It's not an intractable problem. There's likely to (somewhere) be an enzyme that will digest your antibiotic, but if you develop something that degrades that enzyme you're back in business. The chances of a random bacterium having both the resistance and an unrelated gene that protects the resistance mechanism is the square root of the probability of it having the resistance alone (probably less - having the resistance is likely to have proven useful in nature, and so will be more popular. The probability of having both genes will therefore be corespondingly less), which gives us a fighting chance. New techniques in drug development are likely to mean that we can design new drgs that can defeat any resistance mechanism that turns up.
Remember though, antibiotics have only been around for a hundred years or so. Humanity survived before then. Antibiotics increase average life expectency, but they're not required for continued human survival.
My final year dissertation was on this topic. You can find a copy at www-jcsu.jesus.cam.ac.uk/~mjg59/resistance.pdf