An ongoing dialogue on HIV/AIDS, infectious diseases,
August 22nd, 2008
We have met the enemy … and it is MRSA
In Jerry Groopman’s recent New Yorker piece on antibiotic-resistant bacteria, he quotes Dr. Louis Rice from the Cleveland VA, who uses the term “ESKAPE” bacteria: an acronym for Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumanni, Pseudomonas aeruginosa, and Enterobacter.
Nothing against the mostly gram-negative nasties in this list (and the focus of the New Yorker article), but in my opinion there is one bacterial King of Pain, and it is MRSA — methcillin-resistant Staph aureus. Already a hospital-based problem when I began medical school in the 1980s, MRSA is now absolutely everywhere, and I’ll go out on a limb and state that it is the most common and worrisome source of serious infectious suffering we have out there right now.
In this past week alone, I have seen or heard about the following patients (some details slightly changed due to HIPAA, and even more importantly, this list isn’t even all-inclusive):
- A 54 year old anaesthesiologist has had 4 episodes of soft-tissue infection due to MRSA, the two most recent involving his hands — both required incision and drainage, with subsequent prolonged absence from work. Needless to say, he’s terrified of transmitting MRSA to one of his patients — a justifiable fear. Another detail — both his wife and one of his kids have had MRSA abscesses as well, with one of them severe enough to require hospitalization.
- A 25 year old woman developed mastitis two weeks after delivery of her first child. The diagnosis was entertained only after cephalexin and clindamycin didn’t work; the culture obtained by the OB confirmed MRSA, resistant to erythromycin (and hence clindamycin too). I’ve now seen several cases of MRSA mastitis, and whatever hormonal changes cause post-partum blues, they certainly are not helped by this infection. Her baby boy so far is infection-free, but of course she is consumed with fear that he will get it — and no one can provide reassurance that it won’t happen.
- A 60 year old woman with bronchiectasis and low-grade pulmonary M. avium infection, who several months ago developed a new terrible cough, one with increased sputum production and — of course — MRSA in abundance on culture. Usual courses of antibiotcs have been of transient help only; she’s now on daily trimethoprim-sulfamethoxazole to keep this in check.
- A 41 year old HIV + man — otherwise stable on antiretroviral therapy — with another MRSA abscess on his abdomen. I write “another” because he’s now had so many episodes (conservative estimate: twenty) that I’ve given him a standing prescription for doxycycline, which he fills at the first inkling that he’s starting to have a problem.
- A 39 year old woman who, after caring for her mother at home who died of MRSA-related infection (among other problems), is absolutely convinced that she has it herself, and has been to her primary care doctor multiple times for various cultures — all negative so far. But what should her PCP tell her?
One thing that has amazed me about this “new” MRSA (and is there any doubt the USA300 strain is more virulent than the hospital one from the old days?) is that no one is spared — it’s striking the immunocompetent as well as the immunocompromised, the old and the young (my wife’s pediatric practice has had numerous cases; some of the most difficult outbreaks have been on athletic teams), those in the hospital and those who’ve been nowhere near it. The kids who died in Massachusetts last year from MRSA pneumonia following influenza are tragic examples of how bad this thing is. Empiric antibiotic regimens for critically-ill persons these days must include something for MRSA, regardless of the host.
Another remarkable thing is that despite how common MRSA has become, we often don’t know what to do about it. Numerous questions: What are the most effective preventive measures? Why do some people rapidly become colonized, and others escape? Why does colonization become disease in some people and not others? What are the most effective antibiotics among the many we currently use? (A partial list, depending on sensitivities: doxycycline, minocycline, levofloxacin, moxifloxacin, trimethoprim-sulfa, clindamycin, rifampin, linezolid, vancomycin, daptomycin … soon ceftibiprole?) Do local measures (frequent laundering sheets and towels, mupirocin ointment, alcohol-based hand sanitizers, covering all cuts) do anything to reduce relapses? When is surgery required? How about systemic decontamination procedures? How often are household pets vectors? And on and on.
I wish I had the answer to these questions — certainly I’ve tried and recommended all of the above. But it’s time to bring out a favored cliche of academic medicine, because rarely has it been so true: “More research is needed.” Indeed.
A table requires 3 legs to stand. Lets cut one off…
Staphylococcus aureus (and most GNR’s) has been demonstrated to survive in inanimate objects and surfaces for up to 2 months. A recent study from Rush demonstrates the hazard ratio for environmental VRE transmission (colonization) to a non-colonized patient occupying a room that previously, within 2 weeks, of roughly 4. These organisms do not care if they are transmitted from patient or surface to a HCW to a new patient. Its not much of a leap to make this connection with SA. We have been promoting and enforcing hand hygene and antibiotic stewardship for years and the problem is getting worse.
Patient rooms must be cleaned and disinfected. Most institutions do not follow the two step process as outlined by the CDC. Wiping with a disinfecting wipe is not disinfecting. Disinfectants require a wet dwell time to achieve their label claims. Environmental service workers are pressed for time, especially in the surgery environment. I have never seen anyone standing around with a stop watch or timer. Its my opinion that we must look to the environment of care as a fomite. A controversial subject, but lets use our common sense. How many of us use a paper towel to open the bathroom door ? If your answer is yes, you believe that the environment is a fomit.
I am all in favor of studying, but lets look to what we may have been missing right under our nose. If we can stop the exponential cycle of colonization, then maybe we can prevent MDRO’s from taking advantage of us when the time is right.
I would like to second the last comment regarding environmental transmission. As a nurse, I have seen institutional environments that are truly not conducive to proper decontamination procedures. Nurses and other direct patient care providers are faced with higher patient loads and sicker patients requiring more complex care. As an attorney, I have reviewed medical records that tell the story of patients with awful nosocomial infections–although I can see how overtaxed providers were in most cases, the ultimate result is that patients suffer. I think to truly address MRSA, VRE, and these other emerging threats, we would have to revamp the American healthcare model.
Yes, good points about the nosocomial transmission — and another article in today’s (Sept 3) WSJ about resistant bacteria and antibiotic stewardship programs, worth a read.
Might I suggest that the “elephant in the room” is what happens outside the hospital? What infection control practices are suitable for MRSA in the community? After all, more than half of community-acquired soft-tissue infections are now due to MRSA. This is a very challenging era we’re in.
Staphylococcus aureus is undoubtedly one of the most versatile and successful of human parasites. With an array of genes coding for a number of pathogenic enzymes and toxins, it can not only distribute these genes among its phage type, but also acquire new genes from transducing phages and shuffle them to produce new successful strains.
The introduction of antibiotics generated a novel environment in which the the ac
Staphylococcus aureus is undoubtedly one of the most versatile and successful of human parasites. With an array of genes coding for a number of pathogenic enzymes and toxins, it can not only distribute these genes among its phage type, but also acquire new genes from transducing phages and shuffle them to produce new successful strains.
The introduction of antibiotics generated a novel environment in which the the acqisition of resistance genes became vital for the survival of pathogenic bacteria. However the acquisition and operation of a new gene also meant the appropriation of vital resources e.g. ATP , which the bacterium needs for its propagation.
Ali (M.Sc. thesis, 1979, Manchester University,) showed that the competetive survival of the resistant bacteria required a nutritious medium and a reasonably high concentration of the relevant antibiotic in the environment. An infected patient under treatment will provide these factors. In the inanimate environment hygeine will play a central role. Infected pus, secretions, discharge, seepage, etc. from the patient provides the niche for the survival of these bacteria.
An antibiotic which would selectively kill MRSA will be ideal. When this is not available, sound infection control practice in the hospital: hygeine and choice of antibiotic should help us to reduce the incidence of this infection.
Staphylococcus aureus had probably an evolutionary coexistence with humans ever since their arrival on our planet and I doubt this would become a problem in the community. The defence mechanisms of the indindividual ,both innate and adaptive immunity will play the usual roles in the presence of these strains.
The antibiotics made an immense contribution to human health. We cannot escape the side effects. All our ingenuity will be reqired to tackle them.