contribution of genetically restricted, methicillin-susceptible strains to the ongoing epidemic of community-acquired Staphylococcus aureus infections.
BACKGROUND
Within the current worldwide epidemic of community-acquired Staphylococcus aureus infections, attention has focused on the role of methicillin-resistant strains. We characterize methicillin-susceptible strains that also contribute to this epidemic.


METHODS
We tracked cultures from abscess specimens submitted to the microbiology laboratory at St. Louis Children's Hospital and examined Panton-Valentine leukocidin (PVL) genes in methicillin-susceptible S. aureus (MSSA) isolates. We further characterized some isolates by multilocus sequence typing, pulsed-field gel electrophoresis, antibiotic susceptibility, accessory gene regulator (agr) allele, and presence of the arcA gene of the arginine catabolic mobile element.


RESULTS
From 1999 to 2007, we detected a 250-fold increase in cultures of abscesses yielding methicillin-resistant S. aureus (MRSA) and a 5-fold increase in abscess cultures yielding MSSA. MSSA isolates from abscesses and wounds were more likely to encode PVL than isolates from other sources. In contrast to PVL-negative isolates of MSSA, which were genetically diverse, PVL-positive isolates were predominantly multilocus sequence typing type 8 and agr type 1. More than half of PVL-positive MSSA isolates were resistant to erythromycin and susceptible to clindamycin with the absence of inducible resistance, a pattern uncommon in PVL-negative MSSA but frequent in the USA300 clone of MRSA. In addition, pulsed-field gel electrophoresis of PVL-positive MSSA strains revealed the USA300 pattern.


CONCLUSIONS
In addition to methicillin-resistant strains, the current epidemic of S. aureus infections includes infections caused by methicillin-susceptible strains that are closely related genetically and share phenotypic characteristics other than susceptibility to methicillin. These findings suggest that factors other than methicillin resistance are driving the epidemic.
Orscheln
Rachel C
RC
Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Hunstad
David A
DA
Fritz
Stephanie A
SA
Loughman
Jennifer A
JA
Mitchell
Kimberly
K
Storch
Emily K
EK
Gaudreault
Monique
M
Sellenriek
Patricia L
PL
Armstrong
Jon R
JR
Mardis
Elaine R
ER
Storch
Gregory A
GA
D000038:Abscess / Q000453:epidemiology / Q000382:microbiology; D000293:Adolescent; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics; D001427:Bacterial Toxins / Q000235:genetics; D015373:Bacterial Typing Techniques / Q000379:methods; D002648:Child; D002675:Child, Preschool; D002981:Clindamycin / Q000494:pharmacology; D016000:Cluster Analysis; D017714:Community-Acquired Infections / Q000453:epidemiology* / Q000382:microbiology*; D016172:DNA Fingerprinting / Q000379:methods; D004269:DNA, Bacterial / Q000235:genetics; D016521:Electrophoresis, Gel, Pulsed-Field; D004917:Erythromycin / Q000494:pharmacology; D005098:Exotoxins / Q000235:genetics; D005260:Female; D005838:Genotype; D006801:Humans; D007956:Leukocidins / Q000235:genetics; D008297:Male; D008712:Methicillin / Q000494:pharmacology; D017422:Sequence Analysis, DNA / Q000379:methods; D013203:Staphylococcal Infections / Q000453:epidemiology* / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification*
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004269:DNA, Bacterial; D005098:Exotoxins; D007956:Leukocidins; C078284:Panton-Valentine leukocidin; D002981:Clindamycin; D004917:Erythromycin; D008712:Methicillin