Now an army of six bacteria called “ESKAPE bacteria“ (Enterococcus faecium, Staphylococcus aureus, Klebsiella species, Acinetobacter baumannii, Pseudomonas aeruginosa, Enterobacter species) are among the biggest threats of infectious diseases physicians face today. These bacteria are now resistant to most antibiotics, antibacterial wash and antiseptics used in hospitals.

Recently published data about hand washing makes it more difficult to recommend this to prevent spreading infections. Healthcare workers washing hands for more than ten times develop dermatitis and have higher bacterial count than the ones who wash less. Using antibacterial wash is making infection control more difficult.

We must first reduce routine invasive procedures and blood tests performed in hospitals to help reduce contaminated hospital waste that spread infections. People who consult doctors must also learn not to demand blood tests and antibiotics, if not this are likely to be a major war, which we will not win.

Please visit my website medifix.co.uk and keep posting. I’ve linked this page to help educate people.

C.diff does not release spores. It becomes a spore when it encounters adverse conditions and can live for long periods of time on surfaces. It is hard to kill but not impossible. As I said before wash your hands with soap and water.

C.diff is common enough and well known. Like MRSA a large percentage of the population is colonised with it and have no symptoms. it lives in the gut and in normal conditions is pretty harmless. The problem occurs when someone is on antibiotics that wipe out of damage the natural flora of the gut allowing C.diff to take over and become the predominant bacteria. Then it can be deadly and is much much harder to treat than MRSA.

Clearly, though, many if not most people who contract MRSA in a hospital are probably very ill to begin with, so ascribing a true cause of death is debatable. But that it’s even 20k per year, officially, as it was in 2005,is too many. I don’t think you will argue that it’s actually less than that…

A secondary problem is the fact that once infected, a person can continue to carry it, in essence to be colonized by it, and be reinfected. I am one such person. After a 3.5 month ear infection which spread to my eye and some more sensitive mucosa, I found a doctor who was familiar with MRSA and its treatment. I now know to tell any physician treating me that I’m prone to MRSA and what to prescribe. Very few question me, but none refuse.

As for resistance due to antibiotic use, SciAm published an article showing that far more resistance occurs due to natural swapping of RNA between micro-organisms, and from their interactions with natural resistance compounds in various organisms. Resistance due to antibiotic overuse does occur, but it’s the minority case. Figure: ‘new’ diseases, including more virulent forms of existing ones, have been occurring far longer than antibiotics have been used, even if one includes “natural” antibiotics as studied in ethnobotany.

20% to 30% death rate? You’re running around with your hair on fire. For real data on things medical, always go to PubMed http://www.ncbi.nlm.nih.gov/sites/entrez … but pack a lunch and reading glasses. People who contract MRSA are twice as likely to be dead a year later than those who contract MSSA (methicillin susceptible staph, the normal kind), and staph contracted in a health care setting is twice as likely to be MRSA (but due to invasive procedures not found outside such settings, rather than setting-dependent prevalence). The mortality difference is due to the previously mentioned identification problem. SA infections altogether remain a very small minority of mortality causes.

The most promising news with respect to MRSA is that the staph proteome has been fully sequenced. New identification procedures, drugs and delivery methods are in the works.

http://www.scopus.com/scopus/record/display.url?eid=2-s2.0-0032951278&view=basic&origin=inward&txGid=ZIrL8ux6WjbaBFaK00fMIxq%3a2

It would seem to imply that the use antibiotics does have an effect on resistance. I’m not sure how closely related vanc and avoparcin are, but it’s interesting that they aren’t necessarily using the same drug the resistance was seen in. Of course this is gut bacteria.

If you are in a hospital it is worth putting a 10 foot sign beside your bed that says “don’t even think about touching me, if you haven’t just washed your hands”

http://www.sciencedaily.com/releases/2008/12/081204160602.htm

In WW1 soldiers in the trenches could kill lice and their eggs hiding in the seams of clothes just by rubbing a bar of soap down them. I bet that wouldn’t work with today’s soaps, which are little more than lumps of perfumed lard by comparison, and doubtless weekened so the manufacturers can also sell deodorants.

I guess the problem is that, weak as modern soap is (or *because* it is so weak), people simply use it so often. Maybe some enterprising biologist could make a fortune by breeding genetically modified skin bacteria that make body odour smell of roses – Then we wouldn’t need to wash so much

You may be right. What is obvious from our conversation is the value of ICPs or Infection Control Practitioners in healthcare settings, who review the susceptibilities of isolates and develop specialized plans for reducing antimicrobial resistance in nosocomial infections.

From my state health department, of 136 CA-MRSA isolates in 2001:
75% susceptible to ciprofloxacin
82% susceptible to clindamycin
42% susceptible to erythromycin
99% susceptible to gentamycin
100% susceptible to TMP-SMX
100% susceptible to rifampin
94% susceptible to tetracycline
and 100% susceptible to vancomycin.

Those numbers have almost certainly decreased since 2001.

So I suppose the argument as to whether to use drugs in sequence or to mix them up depends largely upon where the particular bacteria that develop resistance develop said resistance. If the primary location is within patients, then it seems to me that using a variety of drugs is best. If the primary location is outside of patients in places of the hospital that have sub-therapeutic amounts of the drugs (e.g. sheets, door knobs), then I suppose the response would be to use one at a time.

While there is no universal protocol for treating an MRSA infection (as all strains present different susceptibilities to different drugs), Vancomycin is predominantly used to treat infections. Now I’m not a clinician, but I am quite sure of this. The problem with randomly selecting one of 5 drugs is that you’re exposing a nosocomial staph population to all 5 different drugs at varying pressures, and there is inherently a greater risk for resistance to develop resistance against all 5 at the same time. Some drugs like Rifampin just don’t get used a lot because clinicians need to preserve a “last-line” defense.

Resistance can take decades to develop or it can occur upon the first application of an antibiotic. By using one antibiotic at a time, you are leaving a greater hope that if a strain develops resistance to one drug (ie vancomycin), it will not have even been exposed and will be 90-100% susceptible to the other drugs until new treatments are approved.

There just might be one or two more drugs out there, but the only drugs I can name off the top of my head for MRSA are Vancomycin, Daptomycin, and Rifampin. MRSAs are increasingly becoming VISA (Vancomycin-Intermediate), and will become VRSA. These are usually treated with Daptomycin. I have heard of incident cases from state hospitals during my time at the health department of patients who are treated in house for an MRSA infection, get discharged, and return 2 weeks later with strains that are somehow resistant to two of the three aforementioned drugs. While they are rare, they are out there, and if selection favors those strains (which it does upon being exposed to ABs), they will slowly spread throughout the community.

So as I understand it, it’s not so much an even use of the last remaining drugs we have as it is a strategic deployment.

I am not of course that familiar with this subject. Yet it does seem to me that bovine ABs can end up heavily in the environment, such as when they wash out feedlots etc. I agree that AB use in humans has been over the top, and this is clearly a sort of unintended selection experiment at work. ABs, hormones and other drugs and compounds are showing up in detectable levels in rivers.

L. C.

Something really needs to be done.

And the problem is there is no “random” treatment. MRSA is resistant to most drugs we have against S. aureus. There are ~5 other drugs we know of that might kill off systemic MRSA. As we use them, resistance will develop, there is absolutely no question about that. The solution is to develop new antibiotics to stay one step ahead of the evolution of bacteria. Sadly, there is no market to develop new drugs, they simply are not profitable like viagra or xanax.

I don’t understand why this is an argument against a randomized strategy. Consider, for a moment, if hospital X prefers drug A of those five or so drugs that still work. That virtually guarantees that the germs that are hanging out around hospital X will gain resistance to that particular drug. More explicitly, it guarantees that those variants of the bug that are resistant to drug A are the ones that will survive more and more. If the hospital moves on to drug B, then it will just develop resistance to drug B in addition to drug A, and we will have fewer and fewer drugs.

If, on the other hand, the hospital tries to make use of all five drugs as evenly as possible, then no particular variant of the beastie that is resistant to any one of these drugs will be allowed to succeed. Instead, for evolution to favor the bacteria, they will have to develop resistance to all five antibacterials simultaneously. And that is a [i]drastically[/i] more difficult task than to just develop resistance to one of them. So it seems to me that we should be using a randomized strategy [i]in conjunction[/i] with the development of new antibacterials.