MRSA Research Center

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For Laboratory Researchers – FAQs

How does Staphylococcus aureus become resistant to methicillin?

MRSA strains carry an extra gene (mecA) that encodes a penicillin binding protein (called PBP2a) that replaces the wildtype penicillin binding proteins when any drug related to penicillin is present.

What is SCCmec?

SCCmec stands for staphylococcal cassette chromosome mec, a family of mobile genetic elements that carry a copy of the methicillin resistance gene, mecA, into the chromosome along with the genes (ccr) required for the integration and excision of the element.  All MRSA strains carry at least one SCCmec element in the chromosome.  They are stratified into types I-VIII based on which combination of ccr gene allotype and mec class are present together in the same element.

What is SCCmec IV?

SCCmec type IV, containing ccr allotype 2 and mec class A, is the type of SCCmec  that has become a genetic marker for community-associated MRSA in a variety of ancestral lineages around the globe.  In contrast to the healthcare associated SCCmec types, mecIV does not usually contain any other antibiotic resistance genes besides mecA.

What is the MRSA strain USA300?

The designation of USA300 refers to the SmaI restriction fragment pattern of the strain resolved by pulsed field gel electrophoresis.  The significance of USA300 is that it is currently highly prevalent as a cause of skin and soft tissue infection, necrotizing pneumonia, and sepsis in individuals with little or no risk factors for healthcare- associated MRSA infection.

Why is Panton Valentine Leukocidin (PVL) important for the virulence of community–associated MRSA?

PVL is a leukocidin, which means it targets and destroys neutrophils, the first line of the human innate immune defense against bacterial infection.  Although PVL has an extraordinary epidemiologic link with CA-MRSA infection, studies in rodents have not conclusively shown that PVL accounts for the elevated virulence phenotype.  USA300 CA-MRSA strains are highly virulent in rodent models of infection whether or not the PVL gene is present.  This has been shown using isogenic knockout strains of PVL+ and PVL- MRSA as well as with many clinical isolates that are naturally PVL positive and negative.  However, such studies do not rule out the possibility that PVL plays a role in the ability of S. aureus to persist and disseminate among healthy human hosts.  It is also possible that PVL does play a role in virulence but animal models of infection do not mimic the situation in humans.