Maryn McKenna

Journalist and Author

ST398 found again — in Italy

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There’s a letter in the upcoming issue of Emerging Infectious Diseases (hat tip Pat Gardiner) alerting the medical community that “pig MRSA” ST398 has been found in Italy, adding t the steadily enlarging list of countries where this strain has been identified.

(NB: Because most of these surveys are one-offs, we don’t yet know whether ST398 is truly expanding its range, or has always been there, but no one looked until now.)

Angelo Pan and colleagues of the Cremona Hospital and other institutions report that a pig-farm worker was discovered to have a severe pyomyositis (abscess buried in muscle):

The case-patient was a 58-year-old man admitted to a surgical department in Cremona, Italy, on July 30, 2007, because of a 1-week history of fever and intense pain in his right buttock. He worked on a pig farm, was obese, consumed high volumes of wine (1.5 L/day), was taking medication for hypertension, and had not had recent (Based on clinical and magnetic resonance imaging data, the diagnosis was cellulitis, pyomyositis, and pelvic multiloculated abscess of the buttock. A needle aspiration of the abscess, guided by computed tomography, was performed. Because of persistent fever (38.5°C), oral ciprofloxacin was added to the patient’s treatment regimen on day 3. Blood and abscess cultures yielded MRSA that was sensitive to glycopeptides, rifampin, linezolid, gentamicin, and mupirocin and resistant to co-trimoxazole, macrolides, clindamycin, and fluoroquinolones. After treatment was switched to vancomycin plus rifampin, the patient’s general condition improved; he was discharged from the hospital after 24 days.

An investigation was launched, and the results were intriguing:

Two fellow workers were colonized with S. aureus, 1 with methicillin-sensitive S. aureus (MSSA) and the other with MRSA. The pig farm, a farrow-to-finish production farm with 3,500 pigs, was screened for MRSA … Dust swabs were taken from 5 areas of the farm; 7 MRSA isolates were detected.
The isolate from the patient belonged to spa type t899, was ST398, carried an SCCmec type IVa cassette, and was PVL negative. The isolate from the MRSA-colonized worker was a t108 strain carrying SCCmec type V. The isolate from the MSSA-colonized worker was identified as t899. The dust swabs yielded 7 isolates: 2 belonged to t899 and carried SCCmec IVa; 5 belonged to t108 and carryied SCCmec V. The isolates obtained from the patient, farrowing area 7, and gestation area 1 were indistinguishable (i.e., same spa type, SCCmec type, and ST profile; Table), thus confirming the animal origin of transmission.

So, we have:

  • A high rate of carriage on the farm (3 of 4 workers with ST398, either MR or MS)
  • A strain-type that is both MRSA and MSSA, suggesting that in its drug-sensitive state it can acquire resistance factors rather easily
  • A PVL-negative strain that nevertheless causes invasive disease requiring more than 3 weeks hospitalization

None of these are good news.

The authors very sensibly call for more public-health attention to this strain, which — we have contended before — is long overdue:

…attention should be given to the emergence of MRSA strains among animals, and continuous surveillance in humans should monitor the extent of disease from MRSA ST398, especially in areas of intensive animal farming. Collaboration between infectious disease specialists, microbiologists, and epidemiologists, on both the human and the veterinary sides, should be strengthened and readied for appropriate action whenever complex, zoonotic, public health issues occur.

The cite is: Pan A, Battisti A, Zoncada A, Bernieri F, Boldini M, Franco A, et al. Community-acquired methicillin-resistant Staphylococcus aureus ST398 infection, Italy [letter]. Emerg Infect Dis [serial on the Internet]. 2009 May. DOI: 10.3201/eid1505.081417

Does ethanol production produce resistant bacteria too?

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One of the challenges of disappearing down the rabbit hole of a gnarly chapter — gee, it’s dark down here — is that I get behind on my RSS feeds, and suddenly every entry in my Google Reader is at 1000+ and it’s all just too daunting.

So, trying to catch up a bit, I found two related, interesting and troubling stories from the Associated Press (4 April) and the online magazine Grist (7 April — yes, I said I was behind…).

Synopsis/synthesis: Corn-based ethanol, former darling of the energy and large-scale agriculture industries, suddenly doesn’t look like such a good idea – and not just because the market for it is crashing. Turns out that ethanol is made by adding yeast and sugar to corn mash; the yeast convert the carbohydrates to the alcohol that is the basis of the fuel. (Yes, just like making beer.) However, the mash is particularly attractive to Lactobacillus and other bacteria that produce lactic acid as a waste product rather than alcohol, and a tank full of lactic acid doesn’t make very good fuel. So, to keep the bacteria under control, ethanol producers add antibiotics. Specifically, penicillin and erythromycin — you’ll recognize those — and tylosin and virginiamycin, two macrolides, related to erythromycin, that are approved in the US for veterinary use.

Now, the problem with this practice, as you might predict, is that if the mash is not appropriately dosed, the presence of antibiotics within it can prompt some of the bacteria to develop resistance. (Here’s an article from the trade magazine Ethanol Producer discussing just that possibility.)

And the further complication of this is that the leftover mash, now called “distillers’ grains,” is sold as animal feed. Ask yourself: Where in animal production are animals most likely to eat grains? Answer: At finishing, in feedlots. In other words, fermented grains that may contain antibiotic residue, and may contain resistant bacteria, are being sold as feed to animals that are already being raised in conditions that have been shown to foster the development of resistant bacteria through subtherapeutic and prophylactic antibiotic use. In fact, some research has drawn an explicit link: Kansas State University scientists have found higher levels of E. coli O157 in the guts of cattle that were fed distillers’ grains.

All of this was new to me, but there’s an additional facet to the story that the AP and Grist pieces don’t highlight, and that just makes my head hurt: the use of virginiamycin. For those new to the story, virginiamycin is an allowed, widely used veterinary antibiotic in the US. However, it is not used in the European Union: It was banned there in 1998 because the EU’s ag authorities believed that it promoted resistance to the drug Synercid (quinupristin+dalfopristin), which is a drug of last resort against vancomycin-resistant bacteria such as VRE. (Here’s a Lancet paper that talks about that resistance mechanism.) Synercid was approved by the FDA in 1999 — two years after Synercid resistance had already been found in the US. (For a long but cogent explanation of the complex story of virginiamycin, see the book The Killers Within.)

So, just to recap: We have an industry whose long-term earnings are shaky, whose economic survival is partially secured by the sale of its waste product, and which via that waste product is putting antibiotic residues and antibiotic-resistant bacteria into the environment, and is conveying them into food animals, and is making particular use of an antibiotic that other countries have banned because they believe that, via its use in animals, it exerts an adverse impact on human health.

Something to remember the next time ethanol subsidies come up.

How sewage plants birth resistant bacteria

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At the always-excellent public health blog Effect Measure, there’s a fascinating dissection of a new paper still in press at the journal Science of the Total Environment. The paper unpacks what happens to Acinetobacter in effluent as they move through sewage treatment. Answer: Many are eliminated, but the ones that survive become significantly more resistant.

I am deep in the final book chapter, so blogging will be light for a week. In the meantime, I recommend this paper and the accompanying post for explicating a little-explored aspect of antibiotic resistance in the environment (which we also talked about in this earlier post.)

The cite is: Zhang, Y. et al. Wastewater treatment contributes to selective increase of antibiotic resistance among Acinetobacter spp. Sci Tot Env doi:10.1016/j.scitotenv.2009.02.013.

Back soon.

More MRSA in pigs, in Portugal

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A brand-new report, in a letter to the International Journal of Antimicrobial Agents, indicates that ST398 “pig MRSA” has been found in Portugal for the first time.

Constanca Pomba and colleagues from the Technical University of Lisbon swabbed and cultured the noses of pigs and veterinarians on two pig farms in different regions of Portugal, and also checked the air at both farms.

What they found:

  • On Farm A: All pigs and the veterinarian positive for ST398, the pig-origin strain that has been found so far in Iowa, Ontario, the Netherlands, France, Denmark, Germany and Austria and has, depending on the country, caused human disease and/been found on retail meat. The veterinarian was transiently colonized, which is to say that he was not carrying the bug long-term.
  • On Farm B: All pigs — but neither of two veterinarians — positive for a different MRSA strain, CC (or ST) 30. This is very interesting, because CC30 is usually a drug-sensitive strain (MSSA, methicillin-sensitive S. aureus), and has been found in pigs primarily in Denmark and France. In Portugal, it is a human MSSA hospital-infection strain.

Strains from both farms were resistant to tetracycline; this is turning out to be a great marker for these strains having emerged due to antibiotic pressure in animals, because tetracycline is very commonly used in pigs. but not much used for MRSA in humans. The strains have the genes tetK and tetM, so they are resistant not just to tetracycline itself, but to the whole class of tetracyclines including doxycycline and minocycline. The Farm B strains also carried the gene ermC, which encodes resistance to erythromycin.

So what does this tell us?

  • First, that (once again), every time people look for ST398, they find it; it is now a very widely distributed colonizing bug in pigs, and is repeatedly spreading to humans. What we don’t know, because all these studies are so new, is whether ST398 is actively expanding its range, or has been present in all these countries for a while. We have been anticipating its presence or spread (take your pick at this point) through the European Union because of open cross-border movement of food animals, meat, and agriculture and health care workers.
  • And second, it should tell us that it is really past time to start looking for this more systematically. Every finding of ST398 that we have (long archive of posts here) is due to an academic research team who decided to look for the bug. None of the findings, to date, have come from any national surveillance system. (NB: Except for the first human colonizations in the Netherlands, which were found as a result of the national “search and destroy” rules in hospitals.)

Of note, the European Union is running a study now that is supposed to report ST398 prevalence at any moment (as they have been saying since 2007). It is not expected to be comprehensive, since it was piggy-backed onto another study, but it is something. The US government has not been so enterprising.

The cite is: Pomba, C. et al. First description of meticillin-resistant Staphylococcus aureus (MRSA) CC30 and CC398 from swine in Portugal. Intl J Antimicrob Agents (2009), doi: 10.1016/j.ijantimicag.2009.02.019

Appearing today on The Ethicurean

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Constant readers, I want to let you know that the terrific food policy blog The Ethicurean (motto: “Chew the right thing“) very kindly had me over to do a Q&A on MRSA in meat. Please take a look and let them have some clicks: They are smart people thoughtfully elucidating a difficult subject, and worth following.

(And I would say that even if they hadn’t called me the “Superbug supersource,” honest.)

MRSA in a hospital nursery

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Via the Boston Globe and the blog of the hospital’s CEO comes work of an ongoing outbreak of community-associated MRSA in the newborn nursery at Beth Israel Deaconess Medical Center in Boston:

…between last November and March, BIDMC experienced several occurrences or “clusters” of methicillin-resistant Staphylococcus aureus, or MRSA, infections that have affected some of our patients (19 newborns and 18 mothers) days to weeks after discharge from our obstetrics and newborn services. These infections have been, for the most part, superficial skin infections and breast infections. It is important to note that no babies in our Neonatal Intensive Care Unit have been affected. (Paul Levy, president and CEO, BIDMC)

The paper and the blog post report that the Massachusetts Department of Public Health (DPH), the Boston Public Health Commission (BPHC), and the federal Centers for Medicare and Medicaid Services (CMS) are all investigating, and the Centers for Disease Control and Prevention (CDC) has sent epidemiologists to sort out transmission. Levy, the CEO, admits on his blog that in sorting out this outbreak, the hospital has found its staff’s infection-control procedures to be not-adequate.

By sheer chance, this occurs as I am writing a chapter on just this phenomenon of the blurring of the MRSA epidemics of hospital-acquired and community-associated staph. As constant readers know, the original MRSA strains arose in hospitals in the 1960s (1961 in the UK, 1968 in the US), and the separate community strain was first noticed in the 1990s. (Though there are intriguing hints about earlier cases that a few smart physicians noticed and no one else took seriously.)

But for about 5 years now, the community strain has been moving into hospitals and causing outbreaks there, particularly in mothers and newborns: first in New York City, and then in Houston, and now quite widely. The Globe article references some others.

Why this is important: Because CA-MRSA and HA-MRSA are different, and not just because they originally occurred in different settings or had different resistance profiles. CA-MRSA (which is a term that is obviously becoming much less useful than it once was) also appears, in newer research, to colonize the body in different ways — not just the nostrils, but also the armpit, groin, and genitals, possibly including vaginal colonization. So there may be an additional risk of transmission from mother to child during birth that has not been anticipated — or from mother to child to health care worker to another child to that child’s mother.

Now, mind you: Good infection control ought to anticipate all those posibilities, because good infection control does the right thing every time. But as we’re finding out, very few institutions manage to train their staff in such a way that they do the right thing every time or close to it (Novant Health Care, creators of the Soapacabana video, seem to have managed it, and won a major award for it). Most health care workers, even very well-intentioned ones, find themselves in time crunches or responding to unexpected emergencies, and make risk-based judgments about what they must do, and what they can afford to let slide.

If CA-MRSA is becoming a hospital organism, and its unique risks of colonization are not recognized by the hospital staff, then their judgments of relative risk will be off — and what would have been a relatively safe risk to take in one instance becomes a significantly unsafe risk in another.

That’s all speculation, of course: I’m not reporting on Beth Israel and have no inside knowledge of their outbreak. But it does describe a phenomenon that has been occurring in other medical centers, and it underlines one of the risks attendant on these epidemics blurring. When CA-MRSA moves into a hospital, the MRSA ecology changes, and the risks of transmission change. It is essential that staff training keep up with that, or additional mistakes will be made.