‘Superbug’s’ killer cousin
If you’ve been reading the papers these last weeks, you probably know about the deadly form of antibiotic-resistant Staphylococcus aureus called MRSA, which, in 2005, killed 19,000 people in the United States -- more people than died of AIDS that year. And you probably also know -- or think you know -- that this “superbug” is out there among us, killing children, killing young athletes and closing schools, and that none of us is safe.
If that’s what you think, you’re wrong. What most of the news stories have done is compare apples and oranges -- and then mix them in a blender. To put it simply, there’s more than one kind of MRSA, which stands for methicillin-resistant Staphylococcus aureus. There are two very different antibiotic-resistant forms of the same bacterium, and they spread, and sometimes kill, in very different ways. All MRSAs are resistant, but some are much more resistant than others.
The staph that kills large numbers of people is hospital-acquired staph. That’s where the 19,000 deaths come in. Also, those 19,000 people died with staph, not necessarily because of it. There is no breakdown offered in the recent report on the subject by the Centers for Disease Control and Prevention, so we don’t know what proportion of people infected with hospital-acquired MRSA actually died of cancer or stroke. Nonetheless, it is safe to say that hospital staph is a serious, and sometimes lethal, problem.
But here’s the conundrum: Another kind of staph infection, this one acquired out in the community, is much more “virulent” -- by which I mean invasive and quick to replicate in the host -- than hospital-acquired staph. This is the notorious “USA 300” strain, the one that has been dubbed the “superbug.” This is the one that has been causing panic in the community at large, closing schools and killing a number (but not a terribly large number) of people.
USA 300, and a few other community-acquired strains, contain in their genetic makeup many more virulence factors than hospital strains have. These traits make them more invasive and better at causing infection in healthy people. But even though they’re more virulent, they lack many of the resistance genes that characterize MRSA in hospitals. That means they’re more treatable.
In our fears about the new, invasive superbug, we should not lose track of the fact that hospital-acquired, extensively antibiotic-resistant infections are the greater problem.
Staphylococcus aureus is an ancient germ that’s caused serious human disease for thousands of years, as can be seen from ancient skeletons with bone lesions typical of osteomyelitis, a staph infection. According to Gordon Archer, a staph expert at the Medical College of Virginia, all forms of staph have the ability, under the right circumstances, to cause a range of conditions, from abscesses to necrotizing pneumonia and endocarditis, an often fatal heart infection. Still, despite its high infectivity, USA 300 only rarely progresses to the point at which it becomes life-threatening. USA 300 terrifies because it’s becoming ubiquitous, its spread is silent and its outbreaks, mostly among young people, seem ominously random.
That randomness comes from the way staph germs colonize the body. According to Henry Chambers, chief of the infectious diseases division at San Francisco General Hospital, 100 million Americans carry colonies of staph germs in their nasal passages, armpits and groins. Of those carriers, about one-third, or 30 million, may carry resistant strains. A small percentage of those carriers get sick: Chambers, doing a back-of-the-envelope calculation, thinks that up to half a million people come down with active infections a year. The vast majority of those infections aren’t invasive, and when they are, Chambers says, there’s often some predisposing factor, like recent antibiotic use.
Staph germs have to penetrate skin or mucus membranes through a cut or abrasion to cause infection. Community-acquired staph invades mostly skin and soft tissue, producing skin infections, abscesses and boils. According to Archer, many abscesses need only to be cut, drained and covered, though one larger than 5 centimeters, or beginning to spread or enter the bloodstream, needs antibiotic treatment as well. Fortunately, even community MRSA strains, including USA 300, are still sensitive to many antibiotics.
No one knows which genetic factors make USA 300 so invasive. It typically breaks out in settings where people share towels or razors, or where, as among football linemen, skin is likely to be scraped. The best way to block its transmission is to stop sharing personal items, as young athletes often do in locker rooms, and to wash hands frequently. Hygiene is the most effective weapon in the struggle to stop staph of any strain in the community.
Hygiene is the best -- and only -- barrier for staph in hospitals too, but there the problem is more complicated. Hospital patients are awash in a sea of antibiotics; the constant use and overuse of these drugs in hospitals allows the evolution of extensive antibiotic resistance. Some staph infections caught in hospitals are resistant to almost every antibiotic except for a handful of new drugs and the powerful vancomycin, held in reserve for the most severe cases. Unfortunately, even vancomycin doesn’t always work very well, and vancomycin-resistant strains have already begun to pop up in several places.
There seems to be a trade-off between resistance and virulence: The more drugs a germ can withstand, the more crippled it may be in other ways. It may not grow as rapidly as nonresistant staph or be as directly transmissible. Still, in a hospital environment, staph doesn’t need to be as invasive as community strains do. Hospital strains prey on a sicker population. So even strains whose virulence is hobbled by their many genes for antibiotic resistance may still be strong enough to infect hospital patients.
What’s more, hospital strains don’t need to jump directly from person to person. They have help. Physicians, nurses and orderlies spread the strains among patients. A touch of a hand or the brush of a hospital gown against a bed can spread staph infection. Any break in hygiene, no matter how slight, may propel germs from patient to patient.
Hospital equipment and procedures can also introduce staph infections. The strains can enter through surgical wounds, intravenous lines or catheters. Ventilators can enable germs to slip deep into patients’ lungs, sometimes producing lethal pneumonia. “People in hospitals are set up for infection,” Chambers said. “If you have predisposing factors, it’s easier to get a less virulent strain.” And the infections, being heavily resistant, are hard to treat.
Here’s another twist: USA 300, which until now has generally been found out in the community, has begun to be found in hospitals as well, where it’s causing some proportion of infections. What will happen as it continues its journey along hospital corridors? It surely will pick up more resistance, and perhaps lose some of its virulence. It may out-compete earlier forms of hospital antibiotic-resistant infections. It may not matter much. In hospitals, all resistant staph strains can kill.
Some hospitals are working hard to improve hygiene and push down infection rates -- but not all hospitals. Some doctors do their utmost to prevent infection; others shove the problem, and the blame, away. But closing our eyes won’t help. Hospital antibiotic-resistant staph strains take thousands of lives annually, and cause thousands more painful, lingering infections. They are not less dangerous because they strike surgical patients, diabetics and the elderly, offstage, behind hospital curtains, out of our sight.
