Everything you wanted to know about community acquired MRSA---

can be found in the March 7 2006 issue of Annals of Internal Medicine. A study from Atlanta found that 63% of staphylococcal skin and soft tissue infections were due to CA-MRSA, underscoring the need to direct empiric therapy of such infections toward CA-MRSA. Empiric antibiotic selection in 2/3 of these cases was inadequate. (Kidney Notes cited this paper).

Despite the vast increase in CA-MRSA infections this nation wide survey of colonization rates revealed that in noninstitutionalized persons the prevalence of any Staph aureus nasal colonization was 31.6% but only 0.84% for MRSA. There is no clear explanation for this seemingly discordant finding. Perhaps transmission and invasion of CA-MRSA does not correlate with nasal carriage, reflecting differences in transmissibility and pathogenesis compared to “old” MRSA strains.

An editorial in the same issue offers these pearls about CA-MRSA, some of which I’ve mentioned before:

1) CA-MRSA is a distinct form of MRSA. It is not a spread of the old nosocomial strain to the community---it’s a new bug which is distinguished by its genome, its pathogenicity and its antimicrobial sensitivity pattern. Indeed the distinction between hospital and community is becoming blurred, as the new strain is showing up increasingly in hospitals.

2) Almost all CA-MRSA (and virtually none of the traditional MRSA) produce the Panton-Valentine leukocidin (PVL). This toxin causes tissue necrosis, possibly explaining the association of CA-MRSA with necrotizing fasciitis and severe necrotizing pneumonia. The fact that such severe necrotizing sequelae are seen only in a small minority of CA-MRSA infections suggests the necessity of variable co-factors conspiring with PVL to produce severe infections. The presence of PVL may be responsible for the necrotic center characteristic of the much more common skin infections leading to the frequent mistaken impression of spider bite.

3) CA-MRSA isolates are sensitive to tetracyclines, trimethoprim-sulfamethoxazole and clindamycin. Although the use of such agents is popular the author cautions that they have not been studied in clinical trials. Clindamycin has the added problem of frequent acquired resistance which can be anticipated if the isolate is resistant to erythromycin and predicted in the micro lab with the “D” test. For severe infections vancomycin or linezolid should be used. Daptomycin is acceptable if there is no pulmonary involvement.