A group led by Dr. James M. Musser at the Center for Molecular and Translational Human Infectious Diseases Research of The Methodist Hospital Research Institute in Houston, Texas has demonstrated that the cytotoxin Paton-Valentine leukocidin (PVL) does not affect methicillin-resistant Staphlococcus aureus (MRSA)-induced pneumonia.
Their report can be found in the March 2010 issue of The American Journal of Pathology.
Community-associated-MRSA causes a wide spectrum of infections, ranging from mild skin problems to fatal invasive diseases. MRSA spreads rapidly from initial topical symptoms to affect vital organs, often resulting in widespread infection, toxic shock, and 'flesh eating' pneumonia. MRSA is resistant to traditional anti-staphylococcal beta-lactam antibiotics and is therefore much more difficult to treat.
The cytolytic toxin PVL is a CA-MRSA virulence factor that has been epidemiologically associated with the development of invasive, and sometimes fatal, pneumonia in affected patients and has therefore become a target for new therapeutics. To explore the role of PVL in invasive MRSA, Olsen et al examined both wild-type and PVL-deficient MRSA in a model of CA-MRSA pneumonia. They found no effect of PVL on virulence in MRSA-associated pneumonia, as a PVL-mutated strain caused similar lower respiratory tract pathology as a wild-type strain. These data highlight the importance of context in the pathogenesis of MRSA-associated pneumonia.
Addition studies are underway by Dr. Musser and colleagues "to test the hypothesis that PVL enhances pathogenesis during influenza virus co-infection. These studies are especially important in the context of the recent global spread of a H1N1 influenza strain and widespread concerns about a detrimental effect on human health."
Materials provided by American Journal of Pathology. Note: Content may be edited for style and length.
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