Journal Article

Involvement of Panton-Valentine Leukocidin—Producing <i>Staphylococcus aureus</i> in Primary Skin Infections and Pneumonia

Gerard Lina, Yves Piémont, Florence Godail-Gamot, Michèle Bes, Marie-Odile Peter, Valérie Gauduchon, François Vandenesch and Jerome Etienne

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 29, issue 5, pages 1128-1132
Published in print November 1999 | ISSN: 1058-4838
Published online November 1999 | e-ISSN: 1537-6591 | DOI:
Involvement of Panton-Valentine Leukocidin—Producing Staphylococcus aureus in Primary Skin Infections and Pneumonia

More Like This

Show all results sharing these subjects:

  • Infectious Diseases
  • Immunology
  • Public Health and Epidemiology
  • Microbiology


Show Summary Details


Panton-Valentine leukocidin (PVL) is a cytotoxin that causes leukocyte destruction and tissue necrosis. It is produced by fewer than 5% of Staphylococcus aureus strains. A collection of 172 S. aureus strains were screened for PVL genes by polymerase chain reaction amplification. PVL genes were detected in 93% of strains associated with furunculosis and in 85% of those associated with severe necrotic hemorrhagic pneumonia (all community-acquired). They were detected in 55% of cellulitis strains, 50% of cutaneous abscess strains, 23% of osteomyelitis strains, and 13% of finger-pulp-infection strains. PVL genes were not detected in strains responsible for other infections, such as infective endocarditis, mediastinitis, hospital-acquired pneumonia, urinary tract infection, and enterocolitis, or in those associated with toxic-shock syndrome. It thus appears that PVL is mainly associated with necrotic lesions involving the skin or mucosa.

Journal Article.  3351 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.