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Mercy, mercy, what is MRSA? The initials stand for methicillin resistant Staphylococcus aureus. MRSA has become a watchword or marker for antibiotic resistance among bacteria in hospital and nursing home environments, and for the same bacterial resistance creeping into community settings. It is far from the whole story, however.
First, we need a few definitions. Staphylococcus (staff-low-COCK-us) comes from Greek staphyle, bunch of grapes, and kokkus, a berry. Aureus means golden. When any Staphylococcus aureus grows on a culture plate, it can look vaguely like a blob of grapes/berries with a golden tint. There are many Staphylococcus aureus strains, not just one. They are now classified by their genetic codes. Some cause minor infections, like impetigo, and some cause serious to lethal ones.
Penicillin G was introduced in 1941 as a miracle antibiotic. Within 4 years, drug resistance to it was found in some Staphylococcus aureus strains. So-called semisynthetic penicillins were created in the 1950’s and ’60’s to overcome it. The first was methicillin in 1960, then came cloxacillin, oxacillin, and dicloxacillin. They can bind to a different bacterial wall protein than penicillin to prevent replication. One year later in 1961, a methicillin resistant Staphylococcus aureus strain was isolated. Methicillin became the model drug in this group. Hence the label MRSA. It is not even made anymore. Testing to oxacillin is used to identify what is still labeled MRSA.
Staphylococcus aureus has long been the stereotypic bad bug that developed antibiotic defenses, even though hundreds of other bacteria have developed resistance to their antibiotics which were never useful against Staphylococcus aureus. The presence of MRSA strains symbolizes the level of bacterial drug resistance in general, since MRSA resist many other antibiotics, leaving very few to treat it.
Most MRSA have somehow been confined to hospitals and nursing homes until more recently when they have been found increasingly in community settings, sending shivers down the infectious disease experts’ spines. So much appears to be spread by hands. And so many people carry bacteria in their nostrils, some persistently. And, we must “face” the fact that all of us pick our noses — just our own, that is.
A Feb. 3, 2005, New England Journal of Medicine article highlighted a clustered occurrence in 2003 of 8 MRSA infections in 5 of the 58 St. Louis Rams football team, all from abrasion wounds. The Center for Disease Control and Prevention was invited to investigate. It found the MRSA in all infections was identical, compared to their genetic bank of 3,241(!) strains of staphylococcus aureus. Infections in a competing team, called “team A” (?), found after a game were the same. Curiously, only methicillin sensitive Staphylococcus aureus were cultured from team whirlpools, taping gels, and from 35 of 84 nasal cultures of players and staff (42 percent of noses with bugs. See, I told you).
The points to pick from the study (not noses) are: better hygiene measures in the locker room helped; where the MRSA came from is not clear, but it signifies more community infiltration of MRSA; lots of noses were “bugged”; and MRSA is spread playing football but not golf (my take on it).
Bacterial drug resistance has increased over the years, but has been long a fact of medical life. Thankfully, the drugs are still a couple of steps ahead of the bacterial retaliation. We also may be in a period of medical paranoia and antibiotic undertreatment. Yielding to a philosophical concept at the cost of misery doesn’t make sense if you’re the miserable one. In any event, make sure you wash your hands, especially after your digits do intranasal duty, to mercifully prevent MRSA spread.
