Panton-Valentine Leukocidin and Staphyloccoccal Skin Infections in Schoolchildren 1

S aureus colonizes approximately 30% of the general population and up to 50% of persons who are intravenous drug users, diabetics, or healthcare workers. The organism is mainly transmitted between persons by close contact (1,2). In addition to its increasing ability to resist antimicrobial agents, S. aureus displays a wide array of virulence factors that render it capable of causing a larger spectrum of infections than any other bacteria (1). Exotoxins constitute essential components of the virulence mechanisms of S. aureus. Nearly all strains secrete hemolysins, nucleases, proteases, lipases, hyaluronidase, and collagenase, which convert host tissues into nutrients required for bacterial growth (3). Some strains produce additional exoproteins that may be responsible for particular clinical manifestations, including the staphylococcal enterotoxins, the toxic-shock syndrome toxin-1, the exfoliative toxins, and the Panton-Valentine leukocidin (PVL) (3). PVL, a bicomponent cytotoxin encoded by two contiguous and cotranscribed genes carried on a bacteriophage, causes leukocyte destruction and tissue necrosis. This cytotoxin is produced by <5% of S. aureus isolates and has been associated with necrotic lesions involving the skin and with severe necrotizing pneumonia (4,5). The Study From September 1999 to November 2000, 6 of the 22 students from a single third-grade classroom in a town of 12,000 in western Switzerland had 13 episodes of skin infections, including furuncles, abscesses, and cellulitis. The outbreak peaked in October and November 2000, with three new cases and four relapses (Figure 1). Two children were hospitalized. Most patients were treated with systemic antimicrobial agents. Some needed surgical incisions and drainage. Six cultures were performed and consistently grew S. aureus resistant to penicillin and amoxicillin (PRSA) and susceptible to flucloxacillin, amoxicillin/clavulanic acid, cephalosporins, erythromycin, doxycycline, clindamycin, trimethroprim/sulfamethoxazole, ciprofloxacin, and rifampin. At the end of November 2000, after health authorities were notified, nasal screening for carriage of S. aureus was performed first in the 22 classmates and their 2 teachers and next in the families of those who had had skin infections or who had been found to be carriers of PRSA. Nasal cultures were collected by using rayon swabs moistened with 5% NaCl, rotated five times in both anterior nares. The samples were carried within 2 hours to the laboratory and kept overnight at 35°C in an enrichment MuellerHinton broth with 5% NaCl. They were then plated onto mannitol-salt agar and sheep blood agar. The plates were incubated at 35°C with 5% CO2 for 24 hours. Persons with mannitol-fermenting, coagulase-positive colonies were considered carriers of S. aureus after species were confirmed and antimicrobial susceptibility was determined in an automated system (Vitek 2, bioMérieux, France). PRSA were saved and subsequently typed by pulsed-field gel electrophoresis (PFGE) after digestion by SmaI. Three isolates representative of the three clones were forwarded to the French Reference Center for Staphylococcal Toxemia, where polymerase chain reaction (PCR)-based methods were used to detect genetic sequences encoding enterotoxins, exfoliative toxins, toxic-shock syndrome toxin-1, βhemolysin, LukE-LukD leukotoxin, and PVL (4). Ten of the 22 classmates and 1 of the 2 teachers (46%) were colonized with S. aureus. None harbored methicillinresistant S. aureus (MRSA). Nine carried PRSA, including four of the six previously infected children (the other two had negative cultures). Two carried penicillin-susceptible isolates. The nine PRSA carriers and the two previously infected students with no nasal S. aureus had 36 family members, 3 of whom had recently also had skin infections. These three persons belonged to two families that included formerly infected classmates. Thirty-five family memDISPATCHES