E-Letter responses to:

reports: Maria Labandeira-Rey, Florence Couzon, Sandrine Boisset, Eric L. Brown, Michele Bes, Yvonne Benito, Elena M. Barbu, Vanessa Vazquez, Magnus Höök, Jerome Etienne, François Vandenesch, and M. Gabriela Bowden Staphylococcus aureus Panton-Valentine Leukocidin Causes Necrotizing Pneumonia Science 2007; 315: 1130-1133 [Abstract] [Full text] [PDF]

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Published E-Letter responses:

Response to S. J. Seligman's E-Letter

M. Gabriela Bowden, Francois Vandenesch   (24 May 2007)

Does Panton-Valentine Leukocidin Itself Cause Necrotizing Pneumonia?

Stephen J. Seligman   (24 May 2007)

Response to S. J. Seligman's E-Letter 24 May 2007
M. Gabriela Bowden The Texas A&M University System Health Science Center, Houston, TX 77030, USA, Francois Vandenesch Respond to this E-Letter: Re: Response to S. J. Seligman's E-Letter	We are grateful for the opportunity to address the issues introduced by S. J. Seligman. The data presented in our Report (1) may seem contradictory to the results shown by Voyich et al. (2). However, there are fundamental differences in technical aspects of their analysis and in the infection models used in both reports. Our Report clearly shows that Panton-Valentine leukocidin (PVL) is an important S. aureus virulence factor using a Balb/c pneumonia model (1). In contrast, most of the data shown by Voyich et al. were generated using a sepsis model, infecting mice intravenously (2). We agree that PVL may not be a major virulence factor when S. aureus is introduced using this route. These authors also tested the role of PVL using a skin infection model developed in hairless mice, but did not detect differences whether the infecting strains were PVL-positive or -negative. We have obtained the bacterial strains used in the Voyich et al. report and tested them in our Balb/C pneumonia and skin infection models. Using their strains, we show that PVL is a major virulence factor both in pneumonia and in deep-seated skin infections. In our Balb/C infection models, when PVL is expressed, we observe dramatic differences in morbidity (weight loss) and tissue (skin and lung) necrosis. In summary, CA-MRSA expresses many virulence factors that play relevant roles according to the route and site of infection studied. Factors that interfere with thrombosis and hemostasis may play a preponderant role in sepsis. Our data show that PVL plays a crucial role in necrotizing pneumonia and deep skin and soft tissue infections. In the last sentence of the abstract, Voyich et al. wrote "[W]e conclude that PVL is not the major virulence determinant of CA-MRSA." It is possible that they reached this conclusion by overinterpreting the negative results obtained with their models. Scientists should always remember that lacking proof for an activity in a given model does not absolutely prove that the activity does not exist. M. Gabriela Bowden Center for Extracellular Matrix Biology, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX 77030, USA. Francois Vandenesch Faculté de Médecine RTH Laennec, INSERM U851, équipe Pathogénie des Staphylocoques, Rue Guillaume Paradin, 69372 Lyon cedex 08, France. References 1. M. Labandeira et al., Science 315, 1130 (2007) (published online 18 Jan 2007; 10.1126/science.1137165). 2. J. Voyich et al., J. Infect. Dis. D 194, 1761 (2006).
Does Panton-Valentine Leukocidin Itself Cause Necrotizing Pneumonia? 24 May 2007
Stephen J. Seligman Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595, USA Respond to this E-Letter: Re: Does Panton-Valentine Leukocidin Itself Cause Necrotizing Pneumonia?	The article by M. Labandeira-Rey et al. (Reports, 23 Feb., p. 1130; published Science Express, 18 Jan.) presents significant evidence implicating Panton-Valentine leukocidin (PVL) in the virulence of methicillin-resistant Staphylococcus aureus. However, the data are in apparent contradiction with the results recently reported by Voyich et al., who found that virulence was not associated with PVL (1). What could be the cause of the discrepancy? In both papers, the lukS and lukF genes (the genes that mediate PVL synthesis) were knocked out through allelic replacement. In the first paper, the result was loss of virulence, whereas in the second, virulence persisted with the PVL-deleted strains. However, the virulence manifestations studied were different. In the Labandeira-Rey article, necrotizing pneumonia was studied in mice. In the Voyich piece, the virulence manifestations were mouse sepsis and skin abscess formation. Accordingly, the data suggest that other genes, most likely in the same genomic island as the lukS-lukF genes, are implicated in mouse sepsis and skin abscesses, but functioning lukS-lukF genes are crucial in the pathogenesis of necrotizing pneumonia. Stephen J. Seligman Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595, USA. Reference 1. J. Voyich et al., J. Infect. Dis. D 194, 1761 (2006).