DR. CORDOVER: Dr. Fox, what should we know about the genetic basis for MRSA resistance compared with sensitive-strain Staphylococcus? Are the characteristics of community-associated MRSA and hospital-associated methicillin-resistant Staph different?

DR. FOX: All methicillin-resistant Staphylococci contain a genetic element called the MEC-A gene. This gene encodes for the alteration in penicillin binding proteins which renders methicillin-resistant Staph resistant to all beta-lactam drugs including methicillin, oxycillin, and all cephalosporin-based antibiotics. We cling to the term methicillin although this particular antibiotic is no longer in production. But in the 1960’s and 1970’s, when this mechanism of resistance was first emerging, methicillin was the prototype drug and hence the term methicillin-resistant Staph aureus has stuck. Now, even though both community and hospital associated resistant Staph have this MEC-A genetic component, which encodes for alteration in penicillin binding proteins, there are still differences between the hospital- and community-associated strains of methicillin-resistant Staph.

Traditionally, until the last 5 years, we’ve thought of virtually all methicillin-resistant Staph as being hospital or healthcare associated. This epidemic began in the 1970’s and was with us in the 1970’s, 1980’s, and 1990’s. However, about half of all the resistant Staphylococcus that is in the hospital now is surprisingly community-associated methicillin-resistant Staphylococcus and only half of this is now the hospital-associated traditional strain of methicillin-resistant Staph. The following table will show you the differences between community-associated and hospital-associated Staph aureus.

Table 1. Comparison of HA-MRSA and CA-MRSA

The community-associated strain of Staph has a small genetic element with the MEC-A gene and hence it is not likely to be multiple drug resistant. When we traditionally think of hospital-associated resistant Staph, it used to be resistant to all anti-infective agents with the exception of vancomycin. The community-associated strain of Staph aureus is still susceptible, usually, to trimethoprimsulfa, doxycycline and its derivatives, and clindamycin. And fortunately, this gives us some oral alternatives for the treatment of these skin infections.

Similarly, the community-associated strain of resistant Staph possesses an additional genetic element known as Panton-Valentine leukocidin, or PVL. This PVL genetic component is probably important in the pathogenesis of the community-associated Staphylococcal skin infection. This genetic element encodes for a toxin which allows the Staph aureus to resist the body’s host defenses, especially with polymorphonuclear cells. It also allows the Staphylococcus to penetrate locally into the skin leading to abscess and skin infection.

The hospital-associated strains of resistant Staph only possess this PVL genetic component approximately 5% of the time. We can also do some more sophisticated genetic epidemiological studies between community- and hospital-associated resistant Staph and there are different types of genetic profiles or different clones that would be apparent even though they would phenotypically be methicillin-resistant.