Everyone’s up in arms about historian James McWilliams’ New York Times op-ed last week, misleadingly headlined “Free-Range Trichinosis,” about how a study found more pathogens in pastured pigs than factory ones. Many bloggers have taken McWilliams to task for omitting the industry funding source for the research and misrepresenting its findings. (Update: McWilliams has responded to both allegations here.) However, I think he also erred in presenting pastured-pork fans as primarily motivated by flavor and the naive idea of “happy” pigs. I’d argue that most of us seek out small, local hog farmers because our consciences won’t let us support the industrial meat system, which is titanically destructive to any nearby land, water, and air; to the people with the misfortune to work in it; and to the sentient animals it turns into protein widgets.
We can add public health to that list of victims. Forget trichinosis: CAFOs’ antibiotic abuse has incubated far, far nastier little bugs, such as methicillin-resistant Staphylococcus aureus (MRSA).
Journalist Maryn McKenna is just now putting the finishing touches on the first book about MRSA. “Superbug: The Rise of Drug-Resistant Staph and the Danger of a World Without Antibiotics” will be published by Free Press, a division of Simon & Schuster, in 2010. (Follow its progress on her Superbug blog.) The book, she tells us, is both a biography of the bug — charting the hidden history of how MRSA arose first in hospitals and then in the outside world, how it wasn’t taken seriously for decades, and the recent recognition of the importance of MRSA in pets and food animals — as well as a detective story.
McKenna has the chops to cover this tricky tale. She has long written about infectious disease, global health, and health policy for national magazines and newspapers, and is also the author of “Beating Back the Devil: On the Front Lines with the Disease Detectives of the Epidemic Intelligence Service,” about the Centers for Disease Control. She was kind enough to answer some in-depth questions for the Ethicurean team about MRSA in general as well as its presence in farming and potentially, in the pork on your fork.
The Ethicurean: What is MRSA, exactly?
McKenna: MRSA stands for methicillin-resistant S. aureus. To unpack that a little bit: The staphylococci are a broad family of bacteria that live on and in humans and animals. S. aureus is a strain that is adapted to humans. It’s probably one of mankind’s oldest companions, evolutionarily speaking, because it does such a good job of living in, on, with us. It’s estimated that up to one-third of the population has S. aureus living in their nostrils or elsewhere on their bodies without causing disease. However, when it does cause disease, it does a very good job of it: S. aureus has a really wide array of ways to make us sick, from starting skin boils to creating bloodstream infections to producing toxins that do everything from causing food poisoning to destroying lung tissue.
“Methicillin” was the first of a class of drugs, the semi-synthetic penicillins, that were produced in the early 1960s after staph worldwide became resistant to natural penicillin. Methicillin actually isn’t sold anymore, so “methicillin resistance” is really shorthand for S. aureus’s current array of resistance factors. S. aureus that is resistant to the semi-synthetic penicillins is also resistant to several other classes of drugs — all the workhorse antibiotics of everyday medicine, and in many cases additional classes of drugs as well.
It’s important to realize that there are (at least) three main subsets of MRSA:
How serious is MRSA for those who contract it?
Hospital infections can be gruesome, because the patients are in such a debilitated state to begin with, and also tragic because it is usually the health care institution caring for them that is responsible for their infection. About 90% of community cases fall into a category that medicine calls “skin and soft tissue infections.” That sounds benign, and sometimes they are — but sometimes people end up on drugs for weeks, they have to have surgery to carve away dead tissue, and they often have recurrences.
The cases that really stick with me are the necrotizing pneumonia cases, which are community MRSA infections that tend to follow on a case of flu. They blow up out of nowhere and can kill a child in, literally, hours. I’ve interviewed a number of parents of such children — most died, a few survived — and I was very shaken. And I’ve covered epidemics and disasters all my life, so I am pretty hard to shake.
Yikes. OK, so how did MSRA get into farms from hospitals?
It didn’t, or at least not directly. MRSA emerged first in hospitals. Which makes sense when you think about it: Hospitals are a place where many people are immune-impaired in various ways, and getting very large amounts of antibiotics. It’s an almost perfect Darwinian battleground for the emergence of resistant organisms.
But it’s a misconception to say that hospitals are responsible for the expansion of MRSA. There is this persistent idea that dirty hospitals leaked MRSA into the rest of society; the corollary is that if we just cleaned up the hospitals and solved the problem of nosocomial infection, MRSA would go away. I disagree. To me it seems clear that the community strains surfaced independently, reaching a sort of tipping point in the mid-1990s, and there have been parallel epidemics that are now converging.
How this all relates to ST398, which has only been around for a few years, is still being explored. The Netherlands, where it emerged, has very stringent national policies on hospital infection control, so there are very low rates of hospital MRSA; and it never had the kind of community MRSA epidemic that the US has experienced. So there was an open ecological niche for ST398 to fill. And the country also has a fairly recent conversion of small-scale agriculture to intensive industrial farming, especially in pigs, especially in the southeast.
The way that strain was identified was, there was a baby girl who lived in the southeast who needed heart surgery. Anyone being admitted to hospital in the Netherlands is checked for MRSA colonization, the symptomless carriage of the bug on the skin or in the nostrils, because they could be an unwitting transporter of the bug into the hospital. So they checked her, and found she was carrying a strain; and when they analyzed the strain, it wasn’t recognized by any of the standard tests. In fact, in the earliest papers, it is called NT-MRSA, for “not typeable.” They checked her parents, and they had it. The parents were pig farmers. They checked the pigs, and the pigs were carrying it — and then they checked friends of the family, who were also pig farmers, and some of them had it too.
Mind you, that was all colonization; none of these people were sick. But it was still a new strain of MRSA in a place where no MRSA should be, so it was intriguing and alarming. And then it did start causing illnesses, some very serious, and some in people with no contact to farming.
But isn’t the industry saying that there’s no definitive evidence linking MRSA in pigs to MRSA in humans?
It depends on your standards of evidence. MRSA ST398 has been found colonizing pig farms and pig farmers in the US, Canada, and in the European Union. You can argue about how prevalent it is — it’s easy to cast doubt on whether it is common, because not very many studies have been done. But you can’t argue that it is there.
The argument over whether ST398 in pigs is causing MRSA disease in humans is more subtle. It definitely has in the Netherlands, though not often so far. Has it done so in the US? No one has done the microbiology to tell. We know there is a lot of community-strain MRSA everywhere in the country, much more than most people realize. It is so common that many physicians essentially now diagnose it by sight; if they order tests, the tests will be for drug sensitivity, because that helps the patient, not for strain identification, because that is primarily useful to public health authorities. If there were ST398 cases hiding within that larger epidemic of USA300, it would take a fair amount of science to find out, and someone has to pay for that science to be done.
A related argument is, Well, MRSA colonization may be widespread, but as long as it doesn’t cause illness, that’s not a problem. Again, I disagree. The presence of any resistant organism is a concern, because bacteria are promiscuous: They swap genetic information, including resistance factors, through an array of strategies evolved over millions of generations. It is not sensible to dismiss a resistant organism to which both animals and humans are vulnerable, and which is already present in animals with which humans share space, because humans are not being made obviously sick by it today.
Does any agency know how much antibiotics are used in livestock operations? Or what kinds?
Hardly. The Government Accountability Office says we don’t even know how many CAFOs [confined animal feeding operations] there are, let alone what they are using. In a 2008 report, they estimated there were 12,000 such farms.
The most detailed calculation of antibiotic use on farms is still the Union of Concerned Scientists’ 2001 report “Hogging It” — that’s the one that estimated that 70 percent of antibiotic use in the US is in agriculture rather than human medicine.
Which types of farms use the most?
Generally speaking, farms where the natural protections of an animal’s immune system are going to be undermined, such as when they are confined or overly crowded. That pretty much translates to a CAFO.
Just to note, the issue that gets the most press with CAFOs is using sub-therapeutic doses of antibiotics as growth promoters, to make animals put on weight quickly. I have had livestock veterinarians tell me that growth promotion is passing out of use. But no one argues that animals still get dosed prophylactically: that is, if a certain percentage of a herd/flock shows symptoms of illness, the entire herd/flock gets dosed just in case. If you have thousands of animals, it’s simply not economically efficient, maybe not even logistically possible, to diagnose and treat them individually.
When we do that to humans — give them antibiotics that they don’t need, such as taking them for a cold — it is called inappropriate antibiotic use. Inappropriate use is a known trigger for the development of resistance.
Suppose I’m your average urbanite who doesn’t live on or go near farms. Do I need to worry about MRSA? Can I get MRSA from handling pork?
If MRSA ST398 is in pork — it’s been found in Canada and Europe, but not here yet — then the issue is not eating the pork (as long as you cook it), but rather handling it. It is possible that you could handle raw pork, unthinkingly touch your eyes or nose, and colonize yourself. The strain might continue to live on you, and it might cause disease down the road. If that sounds hypothetical, it’s because there is little research so far to confirm it. Basically, treat raw pork like raw chicken: Consider it a possible source of foodborne illness, don’t let it cross-contaminate other foods, and wash your hands.
Why isn’t the government tracking the spread of the different strains of MRSA more systematically?
It’s an excellent question. Right now, every estimate of MRSA prevalence in the community or in hospitals is an extrapolation from some smaller data set. Human MRSA is not a reportable disease nationally. A few states have made it so, thanks to efforts by citizen activists. But those registries are new and they are not going to match up, because some count only hospital infections, and some also count invasive or fatal community cases. No one is systematically checking food animals for the bug, and no one is checking retail meat. If I had only one recommendation to make after working on this, it would be that it is essential to pay for improved surveillance — because until we know how big the problem is, we will not be able to understand the dimension of the threat or develop strategies to counteract it.
Further recommended reading about MRSA, food animals, and antibiotic use: