…then what we think makes community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) so infectious might be wrong. A to-be published article in the Journal of Infectious Diseases (Dec. 15) asks “Is Panton-Valentine Leukocidin the major virulence determinant in community-associated methicillin-resistant Staphylococcus aureus disease?” Before everyone wanders off due to boredom, let me translate: we don’t really understand how CA-MRSA can kill you.
The study, conducted by Jovanka Voyich and colleagues, examined the assumption that the Panton-Valentine Leukocidin toxin (‘PVL’) is what causes CA-MRSA infection. Epidemiological studies have found that PVL is strongly correlated with disease. However, the authors engineered identical CA-MRSA that can not produce PVL, and found that in mice, there is no effect of the presence or absence of PVL to cause disease in either bloodstream infections or skin infections (in the case of bloodstream infections, ‘disease’ means the mousey dies).
What’s particularly interesting is that the function of PVL, which is to lyse human neutrophils when the neutrophils engulf the bacteria, does not appear to be affected by the presence or absence of PVL. While there are some caveats (for example, necrophilizing pneumonia wasn’t examined), it seems pretty solid. The authors suggest that a gene (or genes) linked to PVL are responsible for causing disease; PVL might just be along for the ride with the actual cause of disease.
This study highlights the importance of follow-up functional studies. While epidemiology can reveal plausible hypotheses, many of them must be, when possible, tested with good experiments. Also, it’s interesting to note that even though PVL might not do anything, it’s still an excellent marker for diagnosing the potential to cause disease.