
Frequent Carriage of Panton-Valentine Leucocidin Genes by Staphylococcus aureus Isolates from Surgically Drained Abscesses
Author(s) -
B. Issartel,
Anne Tristan,
Sylvain Lechevallier,
F. Bruyère,
Gérard Lina,
Benoît Garin,
F. Lacassin,
Michèle Bes,
François Vandenesch,
Jérôme Étienne
Publication year - 2005
Publication title -
journal of clinical microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.349
H-Index - 255
eISSN - 1070-633X
pISSN - 0095-1137
DOI - 10.1128/jcm.43.7.3203-3207.2005
Subject(s) - staphylococcus aureus , carriage , panton–valentine leukocidin , microbiology and biotechnology , medicine , virulence , leukocidin , micrococcaceae , toxin , staphylococcal infections , biology , methicillin resistant staphylococcus aureus , gene , bacteria , pathology , biochemistry , genetics
Between 1 February and 15 April 2002, 95 patients were admitted to Gaston Bourret Territorial Hospital (New Caledonia, France) for drainage of community-acquired soft tissue abscesses. Staphylococcus aureus was detected in 68 cases (72%). Two-thirds of the patients with S. aureus infection had furuncles, which were located on the limbs in 82% of cases. The median interval between symptom onset and hospital admission was 5.7 days. Three-quarters of the patients were Melanesians living in tribes. Fifty-four S. aureus isolates were screened for toxin genes. Panton-Valentine leucocidin (PVL) genes were detected in 48 isolates (89%), the exfoliative toxin A gene was detected in 1 isolate, and no toxin genes were detected in 4 isolates. S. aureus nasal carriage was detected in 39.7% of patients with S. aureus infections. Two infecting S. aureus strains and two nasal carriage strains were resistant to methicillin. Comparative pulsed-field gel electrophoresis, performed in 16 cases, showed that five of six patients with PVL-positive nasal carriage strains were infected by the same strains. In contrast, 8 of 10 patients with PVL-negative nasal carriage strains were infected by PVL-positive strains. PVL genes thus appear to be a major virulence factor in both primary and secondary S. aureus skin infections.