Truth be told, other staphylococcus species are more common on human skin. These almost never cause disease. S. Aureus is a little more frequently pathogenic.
The key point here is that staph can cause disease in some people and not in others. The other factor in its virulence is the severity of the disease it has the potential to cause. One may wonder why it lives causing no harm in one person and causes a life-threatening disease in another, you have put your finger on the great unknowns in medicine, although much progress has been made. It still looks random to me.
I once had a friend who got nasty skin infection as she was failing out of premed. The stress of not doing well in school and seeing a relationship break-up along with the usual parental pressures, weakened her in ways that sound cheezy if spoken in medical circles. Shaving her legs provided the gateway to the bacteria (some would call the skin the most important component of the immune system.)
Some staph causes invasive disease, getting well past skin structures and being potentially lethal. In general that would be a function of a gene carried by the invasive bacteria. We always had effective antibiotics, but now the bacteria is becoming more and more resistant. Penicillin once worked, but that drug became ineffective early in the antibiotic era and methicillin was developed to counter the bacteria's first attempt at inactivating our drugs. Now Staph has evolved resistance to methicillin and many other anitbiotics. Although not a formal characterization of staph, physicians have been known to refer to "multiply drug resistant staph."
It turns out the genes for invasiveness and resistance now co-exist in a new strain of staph.
Antibiotics become resistant to the antibiotics that are used to kill it. The more the use of a given antibiotic, the greater the resistance. Some of that resistance wears off when an antibiotic falls into disuse from ineffectiveness.
Basic cleanliness is critically important for the spread of pathogens in hospitals. Since antibiotics are most frequently used for the critically ill in hospitals, it is no surprise that resistance first appeared in hospitals and is increasingly spilling into the community. Anywhere people live, work and play in close proximity to each other will be the first areas of concern. The same pattern will follow with skin infections with other skin bacteria as they become more resistant.
Genetic change in bacteria occurs faster than people, given a generation time measured in minutes to hours. Doubling time for E. Coli is usually about 20 minutes. The question everyone should ask is "has the bacteria changed?"
To date, most MRSA strains isolated from patients with [community-acquired-MRSA] infections have been microbiologically distinct from those endemic in healthcare settings, suggesting that some of these strains may have arisin de novo in the community via acquisition of methicillin resistance genes by established methicillin-susceptible S. aureus strains.
Basic hygiene, using antibiotics only when necessary (which means getting them out of the food supply) and a lot of bench research is what will get us out of this mess. Physicians can be a little more firm in saying no for conditions (like simple bronchitis associated with colds) that should get better without antibiotics and patients should not regard drugs as panaceas. Drug companies should also be careful how they market, lest a few marginal physicians exacerbate an already spreading problem.
The alternative is returning to pre-antibiotic rates of infection mortality. And that's really scary.
The good news is that reducing the use of antibiotics is slowly followed by a decline in resistance as the strategies of treating infections with cycling antibiotics or multi-drug regimens has been shown to reduce resistance rates .
TB is an even scarier problem, but the subject of another blog post, some other day. Maybe.