Maryn McKenna

Journalist and Author

Pigs, antibiotics, and staph where it shouldn't be

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The “third epidemic” of MRSA (drug-resistant staph) — the one that started in farm animals given antibiotics, and subsequently spread to humans — has been contentious since its emergence. This week there are several pieces of new news about it. They’re not likely to solve any of the disagreements, but they’re certainly interesting.

Very quick recap for those coming in late: MRSA, short for methicillin-resistant Staphylococcus aureus, describes strains of staph that have become resistant to most common antibiotics. It’s been gaining ground on us for about 50 years, first in hospitals, then in the everyday world and now in farm animals and farm-workers. Surveillance for it is not excellent, but in various studies, it kills 19,000 Americans, puts about 370,000 in the hospital, and sends possibly 7 million to a primary care visit or ER, and causes billions of additional dollars in health care spending — all in a year. For the most serious infections, there are only a few drugs that still work. It’s the leading organism in the under-appreciated international epidemic of antibiotic resistance. (If you’d like to know more, I wrote a book about it.)

Livestock-associated MRSA — many researchers just call it “pig MRSA,” which makes swine agriculture very unhappy, but the more technical term is MRSA ST398 — was first noted in 2004 in a Dutch toddler being prepped for surgery; then identified in her family and their social circle, all of whom were pig farmers; and then was found in their pigs. Along with the standard suite of MRSA resistance factors — all the beta-lactam antibiotics, which means anything ending in “-illin,” most cephalosporins, the monobactams and carbepenems, and also erythromycin — this new strain was resistant to tetracycline. That was odd, because the Netherlands’ rate of MRSA was so low that they were not bothering to give humans tetracycline for MRSA; but tetracycline was the most common drug given to pigs in large-scale agriculture there. It was proof the organism had been resident in pigs, become resistant as a result of ag antibiotic use, and then crossed to humans. (Yeah, this is all told in the book. OK, no more shilling.)

Since that first finding, ST398 has spread throughout the European Union, into Canada, and in one state in the US, Iowa. (Veterinarians assume it has spread more widely than that, but Iowa happens to be the only state where researchers have looked for it.) It is less common than other strains of MRSA, but it has been identified as the cause of mild skin infections among farm workers, serious hospital infections such as ventilator-associated pneumonia, and life-threatening community infections such as flesh-eating disease. It’s also been found in retail meat in several different countries. (We haven’t yet managed to move my archives over, but there’s a 2-year history of ST398 coverage at my old blog.)

Despite the low number of known cases, MRSA ST398 is important, for several reasons: First, because as those death and illness numbers demonstrate, any additional MRSA is bad news. Second, because MRSA ST398 bridges the human and animal worlds, demonstrating how easily an organism that is resident in animals can cause illness to humans, and also can move across the world with agricultural trade. And third, because its occurrence underlines the consequences of antibiotic overuse in agriculture: If they hadn’t been giving tetracycline to pigs in the Netherlands — a country that, within about a decade, went from small family farms to the largest user of ag antibiotics in the EU — “pig MRSA” might not exist.

So, this week’s update, courtesy again of the Interscience Conference on Antimicrobial Agents and Chemotherapy, or ICAAC: two findings that are somewhat contradictory.

First, a team in the Netherlands wanted to know how much of an infection risk ST398 truly poses. That’s an especially important question in the country where the strain got going. In the Netherlands, which exerts very close control over MRSA overall, certain categories of hospital patients are checked to see whether they are carrying the resistant bug, and if so, put into isolation and treated until they are clear. But some people are considered to be such high infection risks that they are put into isolation presumptively — and since 2007, those categories have included farm workers and veterinarians.

That’s a lot of tests, which means a lot of expense. So the team who presented this week tried to assess whether that isolation and testing are necessary, by measuring how often carriage of MRSA ST398 converts to an active infection. They looked at every MRSA isolate identified in 2009 at two hospitals in the southeast, where pig-raising is most dense, and identified a huge reservoir of carriage of ST398: 61% of the MRSA-positive patients, or 298 out of 486. But of those 298, only 7 developed an infection, and none of them passed the infection to a second patient. The 188 patients carrying hospital MRSA, on the other hand, caused 83 secondary cases — enough to force closure of a department in one of the hospitals. (van de Sande et al., ICAAC 2010)

So while pig MRSA’s easy to acquire, given the right exposure, it may not often cause illness. Problem is, according to a second piece of research discussed this week, when it does, it can be unexpected and devastating.

A coalition of 21 hospitals in Spain wanted to know how many of the MRSA bloodstream infections occurring in their institutions were caused by the community strain of MRSA instead of the hospital strain — something that would signal a change in the epidemiology of what can be a devastating illness. They checked every MRSA bacteremia case from June 2008 through December 2009. They found 324, overall, with 10 of them caused by community strains. But they also found something they didn’t expect: Almost as many, eight of 324, were caused by ST398. (Camoez et al., ICAAC 2010)

This isn’t the first time that MRSA ST398 — an organism linked to agriculture and to spread through farm workers and veterinarians — has been found to cause hospital infections or serious infection. It has caused ventilator-associated pneumonia in Germany and post-surgical infections in Canada.

One of the ways that epidemiology measures the seriousness of an outbreak is to compare it to the expected background occurrence of a disease. In the case of MRSA ST398, that background rate is zero. The strain’s an artifact of the overuse of antibiotics in agriculture. It’s really worth thinking about how many more such organisms we want to produce.

Image: photographer unknown.

Update: The French case — not MRSA but so interesting

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I’m flattered to have as a regular reader Dr. Peter Davies, a professor of swine health and production in the University of Minnesota’s Department of Veterinary Population Medicine. (Disclosure: I worked part-time at U Minn from mid-2006 to mid-2010, but in a different school.) In a comment on my previous post, he points out — perils of reading on a smartphone — an important point where I erred: The staph strain involved in the death of the French 14-year-old was not MRSA, but MSSA, drug-sensitive staph, that had picked up a resistance factor.

Unpacking that a bit: At a minimum, MRSA is resistant to all beta-lactam antibiotics — penicillin, the semi-synthetic penicillins (including methicillin, what the M in MRSA stands for), several generations of cephalosporins, monobactams, and carbapenems. It is also separately, but variably, resistant to macrolides (such as erythromycin), lincosamides (clindamycin), aminoglycosides (gentamicin), fluoroquinolones (ciprofloxacin) and tetracycline.

Livestock-associated MRSA, known as ST398 for its performance on a particular test (multi-locus sequence typing) was first identified as having a tie to pig-farming because it was also resistant to tetracycline, which was being given to the pigs on the farms where the first human carriers worked. (Hence its jocular name, “pig MRSA,” though it’s since been found in other animals.)

The ST398 strain involved in the French girl’s death does not have that broad array of resistance. Chiefly, it was not resistant to beta-lactams, and so can’t be considered MRSA. On analysis, it was resistant to the macrolides, of which the best-known are erythromycin and azithromycin (Zithromax or Z-Pak). Here’s something else intriguing: On another test (spa typing), the ST398 strain in the French girl was one known as t571; the ST398 that has spread from pigs to humans in the European Union, and subsequently to Canada and the United States, is usually t034.

Here’s why this is all so interesting: MSSA ST398 t571 was reported just a few years ago in New York City, in a Bronx community that has close ties to the Dominican Republic, and also in the towns in the Dominican Republic where those Bronx residents come from and visit. (Here’s my initial post on that finding from a medical meeting, and subsequent post when the paper was published.) In that case, the ST398 was fully drug-sensitive — and there was no visible link to pigs, though the authors speculated that livestock, perhaps poultry, might be playing a role on either side of the “air bridge” connecting the two communities.

In the paper (Bhat, Dumortier, Taylor et al., EID 2009, DOI: 10.3201/eid1502.080609), the authors expressed concern that, given staph’s promiscuous ability to acquire resistance — and the fact that ST398 is not regularly surveilled for —  the ST398 in New York could become an undetected resistant strain:

Given ST398’s history of rapid dissemination in the Netherlands, its potential for the acquisition of methicillin resistance, and its ability to cause infections in both community and hospital settings, monitoring the prevalence of this strain in northern Manhattan and the Dominican Republic will be important to understand more about its virulence and its ability to spread in these communities.

And now it appears it has become resistant — but in France, not New York City or the Dominican Republic, and to macrolides, not  beta-lactams. It’s one more reminder of staph’s genius at acquiring genetic defenses, and of how our lack of attention to its mutability and spread continues to allow it to take us by surprise.

News break: "Pig MRSA" ST398 involved in the death of a child?

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The latest postings to the website of the CDC journal Emerging Infectious Diseases include a sad and very troubling letter from physicians in Lyon and Paris, reporting the death from necrotizing pneumonia of a previously healthy 14-year-old girl. That would be sad under any conditions, but here’s what makes the death so troubling: It appears to have been caused by MRSA — but not by the community strain, USA300, that has been implicated in a number of deaths from necrotizing pneumonia. (Several such stories are told in SUPERBUG the book.)

Instead, her death appears to have been caused by infection with MRSA ST398 — the livestock-associated strain that was first noted in pigs raised with antibiotics, and the pig-farm workers caring for them, in the Netherlands 6 years ago, and that has since spread across the European Union, Canada and into the United States. (My 3-year archive of ST398 posts is here.)

This may be the first death associated with ST398, though I can’t say that for sure as I am away from my big computer and working without my database. I’ll update later today and confirm or knock that down.

The physicians say that the girl came in with flu-like symptoms and abdominal pain, was put on IV antibiotics (cefotaxime and amikacin), underwent an exploratory laparotomy that showed nothing, and shortly afterward developed acute respiratory distress and was put on a vent. A chest X-ray was shadowy on both sides. She went rapidly downhill and died 6 days later.

On analysis, the staph strain infecting her was ST398; there was no indication where she had picked it up. The strain had an unusual characteristic: It possessed the ability to make the cell-destroying toxin Panton-Valentine leukocidin, PVL for short, a genetic trick that until now has been a property only of community MRSA strains such as USA300. Though its role is disputed, PVL has been linked to community MRSA’s ability to start infections on intact skin, and to the cellular damage that destroys children’s lungs in cases of pneumonia caused by USA300. Until now, ST398 has been PVL-negative.

The physicians’ letter is short and there’s much more to find out about this case. But if the report and analysis are correct, this is bad news. One of the repeated themes in the 50-year evolution of MRSA has been its ability — all staph’s ability — to promiscuously swap and share the bits of DNA that confer resistance and enhance virulence. Another, since the emergence of ST398, has been the potential peril of a staph strain adapting and mutating in the millions of farm animals around the world that are routinely given antibiotics — and that for the most part are not checked to see whether they harbor resistant organisms. If this report (and my interpretation) are correct, then those two trends are converging in a way that cannot bode well.

Antibiotic use in animals: The feds move, a little

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(You leave the country for a few days — I spoke at a conference in Brussels, which was was lovely, thanks for asking — and all kinds of news breaks out. So, sorry to be late on this, but it’s an important issue.)

Last week, the Food and Drug Adminstration took the first (baby, mincing, tentative) steps to address the problem of antibiotics being used in animal agriculture, not to treat disease, but to make animals grow up to market weight faster. This practice — variously called subtherapeutic dosing, growth promotion, and “for production purposes” in the FDA’s exceedingly careful language — has been fully banned in the European Union for 4 years, and some aspects of the practice have been banned longer.

The simple reason for the ban: There’s decades of good science and real-world experience showing that it contributes to the development of drug-resistant organisms in farm animals and the farm environment, organisms that leave farms in the animals and in their manure, and also contaminate the environment beyond farm borders via leakage into groundwater and dust blowing off manure lagoons.That movement off the farm is critical because many of the drugs used in agriculture are the same, or close analogs, of drugs used in human medicine; so resistance that develops on the farm endangers human health as well. (MRSA ST398, livestock-associated MRSA, is the latest example of this. Find a long archive of posts on ST398 here.)

Just to be clear, growth-promoters don’t treat disease; they’re given to healthy animals solely for the purpose of getting them up to sale weight and to market faster. The ways in which antibiotics are given to livestock to treat or prevent disease have their own issues, but those are not part of the FDA effort. (Historical note: The growth-promoting effect of trace amounts of antibiotics was first recognized in 1947, when scientists at Lederle were looking for something to do with the leftover fermentation mash from the manufacture of chlortetracycline, fed it to chickens, and discovered they thrived on it. Stuart Levy’s The Antibiotic Paradox tells this story in detail.)

In human medicine, when we give antibiotics to people who are not sick with a bacterial illness, we call it inappropriate use — and aim massive education campaigns at the practice in an attempt to dial it down. In contract, the animal side has had a free pass for a long time, to the extent that it remains unclear how many antibiotics are used in farming in the US (best estimate: about 70% of all antibiotic use in the US per year), and there is no organized surveillance that would look at what organisms are emerging in animals from that use.

The FDA has been trying to put curbs on growth promoters since the 1970s, always without success; the lobbying against it, by agriculture and also by pharmaceutical interests, is reliably intense. There’s been a parallel effort in Congress to limit the use in animals of drugs that have close analogs in human medicine, via the Preservation of Antibiotics for Medical Treatment Act, or PAMTA, authored by Rep. Louise Slaughter (D-NY), Congress’s only microbiologist. PAMTA has been introduced in several Congresses but this year finally gained some traction. Last year, the Obama administration signaled, in testimony by then-new assistant FDA commissioner Joshua Sharfstein, that it might be friendly to the idea of dialing back on growth-promoter antibiotic use, and it looked as though the long logjam might finally be broken.

Well, OK: Not broken, exactly. Just shifted a little, and maybe showing a tiny bit of light.

On Tuesday, the FDA released a “draft guidance” that proposes animal ag do two things: stop using growth-promoting subtherapeutic dosing, and administer antibiotics to animals under the supervision of a veterinarian. That’s the good news.

The bad news: It’s only a guidance, not a regulation. In other words, it has no force in law. It’s more like a request — though in a press conference last week, Sharfstein suggested it might also be a shot across agriculture’s collective bow:

We have the regulatory mechanisms and the industry knows that. But we are also interested in what things can be done just voluntarily that they would do them. And I think it’ll be interesting to see how the industry responds to this and how – what direction their comments take. …We’re not handcuffed to the steering wheel of a particular strategy at this point. We really want to understand what people think. And but we’re also – I’m not ruling out anything that we could do to accomplish these important public health goals. (Transcript)

Reactions to the FDA announcement were predictable — effectively “No science, more research needed”: Here’s the National Cattlemen’s Beef Association, the National Pork Producers Council, and a standing statement by the Animal Health Institute. (Supporting the FDA move: the Pew Charitable Trusts, the New York Times.)

The draft guidance stays open for public comment for 60 days, until Aug. 30. The required Federal Register posting is here, with the mailing address. Electronic comments can be left at Regulations.gov; the docket number for the guidance is FDA-2010-D-0094; 33 comments have been posted already.

Antibiotic resistance in food — some governments pay attention

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Folks, I told you Tuesday about a Congressional hearing on antibiotic resistance, featuring NIAID Director Dr. Anthony Fauci and CDC Director Dr. Thomas Frieden. Not much new was said, but it’s encouraging that the hearing was held at all. (Fauci testimony here, Frieden here.)

Coincidentally, constant reader Pat Gardiner of the UK alerted me to a gathering being held on the same day in Ireland, by the quasi-government agency SafeFood—which reports to the North-South Ministerial Council of Ireland, which deals with whole-island issues under the Good Friday agreement, which is more about the Irish political structure than you probably ever wanted to know.

The conference was titled Antimicrobial resistance and food safety and featured government officials and academic researchers from across Ireland. Here’s the agenda, and here’s the press release with the names of key speakers. Even more important, here are links to a report on antibiotic resistance in food that Safefood released in advance of this conference: executive summary and whole thing.  I especially recommend from p.25 in the big report for an accessible discussion of the connections between ag antibiotic use and human health. Key quote among many:

The majority of the evidence acquired through outbreak and epidemiological investigations of sporadic infections, field studies, case reports, ecological and temporal associations and molecular sub-typing studies support the causal link between the use of antimicrobial agents in food animals and human illness. A few papers have questioned this but these have not survived detailed scrutiny.

It’s refreshing to see a government body engage seriously with this emerging issue, which we’ve been talking about for, well, years now, on this blog (sometime this month we passed our 3-year anniversary). I wish, wistfully, that the government doing the discussing was ours.

A blog reaction so perfect I want to print the whole thing…

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(…but I won’t, because it’s not fair use or good blogger behavior. But I want to!)

Melissa Graham of Chicago had a great corporate life — and then she re-evaluated, became a chef and caterer, and began organizing in Chicago for sustainable local food, farmers’ markets, and a family-friendly food system. She blogs at the food and food-policy blog The Local Beet. And she’s written a reaction to SUPERBUG that not only completely gets the book, but is emotional and thoughtful and moving besides.

She says, in part:

Before reading Superbug, the question of confinement raised animals was an ethical one for me – whether the misery inflicted upon animals and, for that matter, the humans working in those facilities by the putrid conditions outweighed the need to eat cheap meat. Even the environmental degradation resulting from the inevitable careless management of CAFOs seemed a distant and intangible casualty. For me, Superbug has changed the argument from one of ethics to a moral imperative. In every hamburger of unknown origin, I see Tony Love’s face or even worse that of Carlos Don IV.

Carlos was another healthy kid who left on a school trip to the mountain and returned with a 104°F fever. The first doctor diagnosed Carlos with walking pneumonia so his mother kept him home bundled and hydrated until she realized that he was beginning to hallucinate. She rushed Carlos to the hospital and the doctor’s ultimately diagnosed his condition as MRSA. A long slow death march ensued during which Carlos’s lungs dissolved and clotting choked off the blood to his lower intestines, legs and arms. In two weeks, he was dead.

After reading Carlos’s story late in the evening, I woke a bewildered little locavore from a dead sleep to scrub his hands clean. I hugged him as tightly as I could.

…[recently] I had the pleasure to hear Ruth Reichl speak and she implored the audience to stop eating confinement raised animals. As she put it, if everyone stopped buying them and eating them, the practice would be history. Knowing what I now know, I think it’s our moral duty.

To give the post the traffic it deserves, please go here.

Catching up to MRSA news (not about me)

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Constant readers: I’m looking forward to having the breathing space to get back to in-depth blogging. Meanwhile, though, news is zipping by — so here’s a quick list of recent things worth reading.

“Cows on Drugs” — a superb history of the 30-year-old fight to get unnecessary antibiotics out of food animals. Note, written by a former commissioner of the Food and Drug Administration, not exactly a wild-eyed radical:

More than 30 years ago, when I was commissioner of the United States Food and Drug Administration, we proposed eliminating the use of penicillin and two other antibiotics to promote growth in animals raised for food. When agribusiness interests persuaded Congress not to approve that regulation, we saw firsthand how strong politics can trump wise policy and good science.Even back then, this nontherapeutic use of antibiotics was being linked to the evolution of antibiotic resistance in bacteria that infect humans. To the leading microbiologists on the F.D.A.’s advisory committee, it was clearly a very bad idea to fatten animals with the same antibiotics used to treat people. But the American Meat Institute and its lobbyists in Washington blocked the F.D.A. proposal.

Antibiotic resistance in your kitchen, playroom, car... — After years of begging from health advocates, the FDA and EPA are taking a second look at the chemical compound triclosan, an antibacterial that is put into, well, almost anything you can name: soaps, hand sanitizers, cutting boards, toys. Triclosan is suspected of interfering with hormone regulation in the body, and also increases resistance in organisms in our environment. (When I ask you to use hand sanitizers that contain only alcohol or salts, not antibacterials, triclosan is one of the things I’m thinking of.) The FDA will report its findings in a year. I’d rather see it happen sooner, but it’s a great move.

No progress on hospital-acquired infections — The Agency for Healthcare Research and Quality, part of the Department of Health and Human Services, has published its 2009 National Healthcare Quality Report. The news is not good. To quote the agency’s own language: “Very little progress has been made on eliminating health care-associated infections.” This is all hospital-acquired infections, not just MRSA, but MRSA is a leading organism. The ugly details:

  • Post-operative bloodstream infections up 8%
  • Post-operative catheter-associated urinary-tract infections up 3.6%
  • “Selected infections due to medical care” up by 1.6%
  • Bloodstream infections as a result of central lines unchanged.

(NB, three professional organizations — the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, and the Association for Professionals in Infection Control — put out a statement in response to this report saying it “presents an outdated and incomplete picture on healthcare-associated infections (HAIs) in our healthcare system.” The gist of the statement seems to be that they’ve got better numbers coming… soon. When there’s actual data, I’ll let you know.)

SUPERBUG on Capitol Hill

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Constant readers, I’ve been shamefully absent from the blog, but with reason, since I’ve been traveling promoting the book. There was a pretty interesting opportunity this week that I wanted to tell you about: I was asked to be part of two Congressional briefings in Washington, DC Wednesday, addressing the overuse of antibiotics in agriculture and the contribution that makes to the emergence of resistant organisms such as MRSA. I went specifically to tell the story of the emergence of MRSA ST398, which we’ve been talking about for years here.

The briefings (FYI, “hearings” are for Congresspersons, “briefings” are for their staff) were cosponsored by the Pew Charitable Trusts, Union of Concerned Scientists, American Public Health Association, Infectious Diseases Society of America, and the nonprofit Keep Antibiotics Working.

Here’s Pew’s announcement, here’s the UCS version, here’s a write-up from the Washington Examiner, and here’s a longer one from the site Spectrum Science.

"Pig MRSA" causing human infections

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Hi, everyone. Apologies for dropping out of sight! As SUPERBUG’s publication draws closer (and it’s very close now), I keep finding new tasks that I have do to. Last week’s was to go to New York to shoot a video for the Simon & Schuster website — and while there, I got caught in Snowpocalypse, got delayed coming home, and picked up a nasty cold. So I’m a bit behind.

But there’s exciting news tonight to start us up again: “pig MRSA,” ST398, causing human infections in Canada and Denmark.

“Infections” is important, because up til now, most evidence for  the spread of MRSA ST398 in humans has been through detection of colonization, the symptomless carriage of MRSA on the skin and in the nostrils. The first finding of ST398 in the Netherlands was via colonization; so was its first identification in humans in Canada, and also in the United States just about a year ago.

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Farming and antibiotics – and voices from the ag side

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The whole issue of how antibiotics get used in agriculture — as growth promoters, as prophylatic treatment to prevent spread of infection within a farm, or as true treatment — is intensely controversial. For a sense of how farmers feel embattled, read the comments to this entry at FairFoodFight on whether there is a distinction between “Big Ag” and “small ag.” and consider that the PAMTA legislation I posted about in December, which would require veterinarian oversight of farm use of antibiotics,  has been strongly opposed by agricultural interests every time it has been introduced. (Large-farm use of antibiotics, let me remind you, has been concluded to be the driver behind the emergence of “pig MRSA” ST398.)

But I recently ran across two pieces online that I want to draw your attention to, because they demonstrate that thinking in agriculture about antibiotic use is not monolithic, and may be changing. Both were posted on the same site, the Illinois-based Agri-News Online.

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