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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."
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-
Just like individual freedom is every man's responcibility, so is health.
Do you know how much antibiotics are put into your milk and meat? Those hormones and antibiotics put into your food are also one of the reasons of obesity in the USA.
It's just like fighting McDonalds- remember how we got them to switch from those nasty poly boxes?
Well, it's time to let those dairy and milk producers know that we refuse to eat antibiotic and hormone contaminated food!
It's only a matter of time untill a super-bug evolves. Aids is going to seem like kids' poo.
You can help- call for not using antibiotics except when they are needed.
Don't buy meat and dairy unless they are antibiotic and hormone-additives clear.
Don't use antibacterial soap.
And don't ask your doctor for an antibiotic pill to cure your cold or flu!It won't help anyway.
Another thing to remember, is that you have to take the full one or two week course on treatment if you're ever prescribed antibiotics! Othervise, your bacteria become resistant.Even skipping one day is enough to let that hundred semi-resistant bacteria multiply into thousands,then millions. If you go for treatment, stick to it.
Triclosan is the active ingredient in the antibacterial hand soaps.
From the Soap and Detergent Association:
http://www.sdahq.org/health/faq.html
One statement they make is "Washing with plain soap and water removes many germs from the hands. Antibacterial soaps contain an active ingredient that keeps the number of germs at a reduced level for an extended period of time, providing improved germ control."
So don't let the advertising con you into thinking that plain soap has suddenly stopped working. Triclosan just makes your hands temporarily unsurvivable for germs. Everything is an issue of degrees, and this seems like using a scorched earth policy on your hands.
Take it for what it's worth.
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.
If this guy caught the infection in the hospital, how could antibiotic soaps or failing to follow doctor's directions have been contributing factors, especially given the rarity and strength of vancomycin?
What happens is first- and second-line antibiotics, like penicillin, get overused. This creates many different strains of bacteria all over that are antibiotic resistant. If you get sick with one of these superbugs and can't shake it off on your own then you go to the hospital and get vancomycin. Since so much vancomycin has to be used in hositals it stands to reason that eventually one strain of bacteria will evolve that's immune to it. If there weren't so many strains of bacteria that were immune to penicillin there wouldn't be as much of a need to use vancomycin as much, resulting in fewer strains of vancomycin.
BTW, hospitals of full of antibiotic resistant strains of bacteria, due both to all the antibiotics used there and to all the people that go there with antibiotic resistant strains ofbacteria already in them.
Mr. Spey
Cover your butt. Bernard is watching.
More information is appropriate here.
What WolfWithoutAClause was talking about is called bacteriophage therapy. A bacteriophage is a type of virus that attacks bacteria. ("Bacteriophage" literally means bacterium eater.) Bacteriophages were discovered in 1917. In the 1920's and 1930's, bacteriophages were used to treat bacterial infections like typhus and cholera. The results were very mixed.
In the 1940's, bacteriophage therapy fell out of favor as penicillin became more and more popular.
Recent studies of bacteriophage therapy in Eastern Europe and in Asia have tentatively concluded that it can, when properly employed, approach the effectiveness of antibiotic therapy.
But there is a problem. Bacteriophages and antibiotics work in pretty much the same way, albeit through different mechanisms: the agent in use attacks the bacteria population present in the patient, killing all those that are susceptible. Neither antibiotics nor bacteriophages kill 100% of the bacterial infection, because bacteria mutate and evolve quite rapidly. If bacteriophage therapy were in as widespread use as antibiotic therapy is today, we'd see the same basic problems: resistant strains appearing thanks to therapeutic culling of the susceptible populations.
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
The problem is that resistance is not limited to one strain. Bacteria have the ability to swap genetic "cartridges" that confer antibiotic resistance to completely different types of bacteria. One strain we can deal with, widespread resistance to known antibiotics is another matter. There's a very real probability that the human race could be severely deciminated, if not completely wiped out. I'm not saying that such a doomsday scenario is unavoidable, but efforts should be made to reduce its likelihood.