PT  - JOURNAL ARTICLE
AU  - Susan E. Crawford
AU  - Michael Z. David
AU  - Daniel Glikman
AU  - Kimberly J. King
AU  - Susan Boyle-Vavra
AU  - Robert S. Daum
TI  - Clinical Importance of Purulence in Methicillin-Resistant <em>Staphylococcus aureus</em> Skin and Soft Tissue Infections
AID  - 10.3122/jabfm.2009.06.090025
DP  - 2009 Nov 01
TA  - The Journal of the American Board of Family Medicine
PG  - 647--654
VI  - 22
IP  - 6
4099  - http://www.jabfm.org/content/22/6/647.short
4100  - http://www.jabfm.org/content/22/6/647.full
SO  - J Am Board Fam Med2009 Nov 01; 22
AB  - Background: The so-called community-associated methicillin-resistant Staphylococcus aureus (MRSA) strains are more frequently susceptible to non–ß-lactam antibiotics (including clindamycin) than health care-associated MRSA strains. We assessed whether predictive clinical characteristics of presumptive MRSA infections can be identified to guide choice of empiric antibiotic therapy.Methods: A clinical syndrome was assigned to each inpatient and outpatient at the University of Chicago Medical Center with an MRSA infection in 2004 to 2005. Antimicrobial susceptibilities and molecular characteristics of MRSA isolates were assessed. Patients were stratified by lesion characteristics.Results: Of MRSA isolates from 262 patients with purulent skin and soft tissue infections (SSTIs), 231 (88%) were susceptible to clindamycin, 253 (97%) contained staphylococcal chromosomal cassette mec (SCCmec) IV, and 245 (94%) contained Panton-Valentine leukocidin (pvl) genes, characteristics associated with community-associated MRSA strains. The presence of a purulent SSTI had a positive predictive value of 88% for a clindamycin-susceptible MRSA isolate. Among 87 isolates from a nonpurulent SSTI, 44% were susceptible to clindamycin and 34% contained pvl genes. In 179 invasive MRSA disease isolates, 33% were clindamycin-susceptible and 26% carried pvl genes.Conclusions: A purulent MRSA SSTI strongly predicted the presence of a clindamycin-susceptible MRSA isolate. Presence of the pvl genes was almost universal among MRSA isolates causing purulent SSTIs; this was less common in nonpurulent SSTIs and other clinical syndromes.