Maryn McKenna

Journalist and Author

MRSA research at Society for Healthcare Epidemiology of America meeting

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As promised, a round-up of some of the research presented at the annual meeting of the Society for Healthcare Epidemiology of America (SHEA), held last weekend in San Diego. (Disclosure: I was on the faculty for the meeting; in exchange for co-hosting a session, SHEA will be reimbursing me for airfare and hotel. I wasn’t otherwise paid, though.) There were 143 presentations on MRSA; here are a few.

I’m going to put in links to the online abstracts — I have SHEA’s permission to do this — but I can’t guarantee how long they will stay up. For those outside the science world, what happens at these meetings is that research is presented, in slide/PowerPoint sessions or in a poster, as a preliminary step to getting it published in a journal. Once a journal expresses interest, a cone of silence descends, the researchers are asked not to discuss the research until the paper is printed, and the abstract will probably be taken offline.

So, efforts to control hospital MRSA are showing some success:

  • Invasive hospital-onset MRSA infections declined 16% from 2005 to 2007, and hospital-associated community-onset infections went down almost 9% — probably, though not provably, because of in-hospital prevention campaigns. (A. Kallen et al.)
  • MRSA control in a small ICU (22 beds) leads to MRSA reductions throughout a 270-bed Montana community hospital. (P.J. Chang et al.)

But those efforts face some complexities:

  • Swabbing the nose and culturing the swab, the classic test to check for MRSA colonization, misses 30% of positive patients because they are colonized in the groin or armpit. (C. Crnich et al.)
  • If a hospital does not use AST (active surveillance and testing, or “search and destroy”) it may seriously underestimate its MRSA incidence, though it may be able to detect general trends. (P.J. Chang et al.)
  • But medical centers of similar size and situation that did v. did not use AST achieved similar reductions in hospital infections. (K. Kirkland et al.)

Community strains are moving into hospitals:

  • Most of the cases of MRSA colonization identified in a Delaware healthcare system were found so soon after admission that they must have begun out in the community and were not due to hospital transmission. (K. Riches et al.)
  • The proportion of MRSA bloodstream infections caused by community strains (proven microbioogically) doubled at Chicago’s main public hospital between 2000 and 2007. (K. Popovich et al.)
  • One out of every 7 ICU cases of MRSA in Atlanta’s major public hospital involved a community strain. (H. Blumberg et al.)
  • The number of MRSA infections brought to a Chicago-area ER increased 566% between 2002 and 2007, and was seasonally clustered (D. Buchapalli et al.)

And at the same time, hospital strains are moving out into the community:

  • Hospital-associated community-onset cases accounted for 58% of all invasive MRSA in the US between 2005 and 2007, with patients undergoing dialysis or those who have been in long-term care the most vulnerable. (J. Duffy et al.)

Bill in Congress: “Preservation of Antibiotics for Medical Treatment” Act

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Important news for anyone concerned about the spread of “pig MRSA” ST398: Rep. Louise Slaughter (D-NY) and Sen. Edward Kennedy (D-MA) have introduced a bill that would restrict important classes of antibiotics for use against disease only, taking them out of the realm of subtherapeutic use or growth promotion in agriculture. The bill would allow the use of the antibiotic classes for disease in animals as well as in humans; the intent is to preserve the drugs’ effectiveness for as long as possible.

The text of the bill, the Preservation of Antibiotics for Medical Treatment Act of 2009, is here.

A Reuters story in which Slaughter predicts the bill will have a difficult time is here; she has introduced it several times in the past decade, but it has never made it through.

Support from the Pew Commission on Industrial Farm Animal Production is here. An earlier version was supported by the American Academy of Family Physicians here.

The National Pork Producers’ Council’s response is here.

(Hat tip to Barry Estabrook at Politics of the Plate and to Melinda Hemmelgarn, the FoodSleuth.)

Kindle owners: My first book now available, with a MRSA chapter

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It was news to me, until a friend of mine went and bought it: My first book, Beating Back the Devil: On the Front Lines with the Disease Detectives of the Epidemic Intelligence Service, has been put into a Kindle edition.

BBtD was the first and so far only book to go inside the CDC’s “outbreak police.” It tells a year in the life of the first class of young physicians and PhDs to join the Epidemic Intelligence Service after the anthrax attacks — the first year, in other words, in which the EIS officers knew in advance that the possibility of confronting bioterrorism was no longer hypothetical. It tracks members of the class around the planet, from West Nile virus to foodborne illness to malaria prevention in Malawi to SARS. In alternating chapters, it also tells the hidden history of the EIS, which was founded in 1951 as a post-Korean War force for bioterror detection. Its members were in on every major disease event of the second half of the 20th century: the launch and near-failure of the polio vaccine, the end of smallpox, the beginning of AIDS, and the emergency investigation of the anthrax attacks (during which I was embedded with a CDC team).

Most important for our purposes here, BBtD takes you inside an investigation of a MRSA outbreak — in Los Angeles in 2003, when gay men who frequented sex clubs began developing cripplingly serious skin infections, and a young CDC investigator had to determine whether to call on the city to shut the clubs down…

Ten tips for avoiding hospital infections

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ScientificAmerican.com (disclosure: I have written a story for them, and it is edited by a friend) has a great interview with a hospital epidemiologist about things to do to avoid hospital infections.

It’s a smart list, with some non-obvious things on it. For instance:

5. Make sure you’re kept warm
The air temperature in operating rooms typically hovers between 65 and 69 degrees Fahrenheit (18 and 20 degrees Celsius). That’s great for the doctors and nurses bundled head to toe in scrubs, but not necessarily for the person on the table. [Stephen Streed, an epidemiologist who oversees infection control at the Lee Memorial Health System in Fort Myers, Fla.] says that the body responds to chilly air by constricting vessels supplying blood to the skin and the tissues just below it; diverting blood away from the body’s surface and toward its core is the body’s strategy for conserving heat. With less blood supplying oxygen to the incision site, the immune cells there become oxygen-deprived and therefore less effective at battling invading germs. Ask the surgical team how they intend to keep you warm — if they will crank up the room temperature by a few degrees, cover you in blankets, or warm you with IV fluids, for instance.

6. Ask about presurgery antibiotics
For many operations, including those involving the heart and bone, doctors routinely give patients preventive antibiotics to nip infections in the bud. One dose is typically given via IV an hour before the surgeons make the first cut, and sometimes two more doses are given over the next 24 hours, Streed says. If you think there is any possibility that you have an infection before going into surgery, tell your doctor so that he or she can treat you first. (Having an existing infection in, say, the bladder or skin ups the risk of developing a second, surgery-related infection, Streed warns.)

The whole list is worth reading.

More on “pig MRSA” and the havoc it can do

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Folks, before I get to the SHEA abstracts, one more post on ST398 in humans, and a sad and difficult story. It is the first (to my knowledge) report of ST398 spreading into a nursing home, in the January 2009 issue of Eurosurveillance Weekly.

It was very thoroughly investigated, because it took place in the Netherlands, where by national policy there is active surveillance and testing — AKA “search and destroy” — for MRSA in health care facilities.

To me it is both an object lesson in the unpredictable spread of this newly recognized organism, and also an exploration of the deep human cost of combatting it.

The nursing home, in a town called Doorn, is described as a residence for “visually and intellectually disabled” people, and it sounds like a good place, made of 35 household-like units that hold 8 residents each, with a pretty high ration of staff to residents. One resident in one unit was an adult man (age not given) who was completely blind and significantly mentally disabled. Since 2004, he had been living with hidradenitis suppurativa, a condition of painful, recurring, weeping infections of the skin that can be caused by staph. Periodically, he was treated with a variety of antibiotics — tetracycline,erythromycin, flucloxacillin, trimethoprim/sulfamethoxazole, clindamycin, minocycline, rifampicin — but none of them seem to have made much difference to the infections. (Hidradenitis is an awful condition; there are times when the only treatment is skin grafts.)

In October 2007, the regular swabs taken of his infections suddenly showed not drug-sensitive staph, but MRSA. Confirmatory swabs showed that he was colonized with MRSA in the nose, throat and groin. After analyzing whom he might have been in contact with, the home identified 43 resident and staff at risk, swabbed them all, and found 2 other residents and 3 staff members colonized. That led to another round of swabbing, of 160 people, but no other cases of colonization were found.

So, just to recap, that is the index case, with MRSA infections and colonization in various places on his body, plus five others who were only colonized.

Sequencing/typing of the isolates found that all 6 were carrying ST398, falling into one of two spa types, t2383 and the more rare t011. None of the residents or staff had had any contact with livestock. They did have play/therapy animals at the residence — rabbits, chickens and goats — but they were checked and were all negative. The source was never found.

The five who were only colonized were given 5 days of decolonization therapy: mupirocin gel (Bactroban) in the nose and showers with chlorhexidine soap (Hibiclens). Afterward, they had to be proved negative on three successive nasal cultures; the paper does not say how far apart the cultures were. Until the third negative culture, staff had to stay home, and residents were banned from group activities. Underlining that: Physically or mentally disabled adults living in an enclosed, supportive society had to be isolated from it because they acquired this bug. Just think how difficult that must have been. The paper notes: “The outbreak caused commotion among the staff members, and they had a lot of practical questions as they were unfamiliar with MRSA and an MRSA-outbreak in particular. Furthermore, it turned out that the use of gloves, surgical masks and aprons during washing and clothing was perceived as threatening by the clients.“

The index case’s situation is even sadder. He was given a private bath and shower, and essentially restricted to there and to his private room. He had been in group day-care, but was switched to being minded by himself. His “social contacts with other residents who lived in other units was restricted to a minimum” — presumably he was not able to be fully secluded from the other members of his household. However, anyone who came into direct contact with him — for instance, to bathe and dress him — had to be on contact precautions: gloves, aprons and surgical masks. This went on for six months while his very refractory MRSA was treated with oral antibiotics and surgical incision and drainage of his abscesses; after six months, his symptoms had not resolved, but swabs of his wounds were MRSA-negative, and some of the isolation precautions were lifted.

Underlining: Someone blind and mentally disabled, presumably fairly secure in the enclosed, supportive society of the residential home, has to be restricted from his routine, from people who are probably his friends, and from all skin-to-skin contact, for half of a year.

Now, mind you: If you or I had a relative in that home, we might want them to do exactly what they did do. It is difficult to say how well the staff might have succeeded in getting mentally disabled residents to cooperate with, for instance, hand-washing.

But this is not the first case I have heard of where the cost of protecting a group from MRSA has fallen very, very hard on one individual. I am not going to argue with the Dutch policies, but in this case, I find their unintended consequences terribly sad.

“Sick as a pig” – from ST398

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Constant readers, I am at the annual meeting of the Society for Healthcare Epidemiology of America, where there is a lot of news about MRSA in hospitals. I hope to post on that over the next few days.

In the meantime, though, I want to pass on several pieces of news about ST398, the “pig strain” that we have talked so much about.

First, the Soil Association, the British organic/sustainable farming group that has done much work elucidating the spread of ST398 and making the link between that bug and antibiotic use on farms, has released an online documentary about ST398 called Sick as a Pig. You can watch it here, and here is the Soil Association’s press release:

…40% of Dutch pigs and up to 50% of Dutch pig farmers are now carrying the new strain, which is also spreading to the wider population. Although this type of MRSA was first detected in humans in the Netherlands as recently as 2003, it now causes almost one in three cases of MRSA treated in Dutch hospitals.
It is not yet known whether any British pigs are affected by the new strain of MRSA (called ST398) since the results of testing, which was required by the EU and carried out in 2008, have not been made public.
Several countries have already published the results of their own tests revealing significant levels of MRSA in national pig herds. The European Food Safety Authority has said that, ‘It seems likely that MRSA ST398 is widespread in the food animal population, most likely in all Member States with intensive animal production’.

Second, here is a paper from last fall that somehow slipped by me: in the CDC journal Emerging Infectious Diseases, a report of two cases of ST398 infection in men in Sweden. Neither had any contact with farming or animals.

The first patient, a previously healthy 36-year-old male physiotherapist, sought medical care in March 2006 for a small abscess in his axilla. Culture of the abscess grew MRSA. Presence of mecA gene was confirmed by PCR. During the next 2 months, furunculous [sic] developed twice, caused by the same strain. His youngest child, adopted from China, had been found to be MRSA positive (throat, perineum, and a small wound) a month earlier during routine screening for adopted children. During subsequent screening of the family, the older sister, adopted from South Korea, was also found positive (throat). Both parents were negative for MRSA at that time, which suggests that the father was newly infected when his abscess developed and that he had not acquired the strain abroad. Also, spa typing indicated that the children carried different strains from that of the father and from each other (t286, t1434). Subsequent screening of family members for MRSA on several occasions found only the father to be repeatedly positive.
The second patient, a 43-year-old male clerk, also previously healthy, sought medical attention during the summer of 2007 for a MRSA-infected elbow wound. Follow-up examination determined that he carried MRSA also in the perineum and in a chronic external otitis eczema. He was later hospitalized for a larger abscess that required surgical drainage. His family members reported no symptoms and were thus not screened for MRSA.

Of note, the men’s strain (ST398, t034) carried the two genes that express the toxin PVL, which is unusual in ST398, though characteristic of CA-MRSA USA300, the dominant community strain in the US. The role that PVL plays is very controversial: Some research groups believe it is responsible for the rapid tissue destruction that can accompany USA300 infection (in penumonia and some soft-tissue infections, for instance), while others vociferously disagree.

More MRSA in meat, in Austria

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There’s a new publication out that I haven’t been able to lay my hands on yet, except for the abstract. But here’s what I know: A group from the Austrian Agency for Health and Food Safety and two Austrian national reference laboratories have published a paper saying that ST 398, the “pig strain” of MRSA that we have been talking about here for a year now, has surfaced in Austria in environmental samples, in humans and also in food — presumably meat, but the abstract doesn’t say that.

The abstract in Wiener Klinischer Wochenshrift (Viennese weekly clinical review, if my college German is still with me) says:

…the emergence of ST398 is not just a Dutch problem, as reports on livestock colonization and human infections are appearing worldwide. In Austria, the ST398 lineage has been detected in dust samples from pig breeding facilities and in food samples. Since the first Austrian detection of this emerging lineage in 2006, 21 human isolates, partially associated with infections, have been observed. MRSA has to be regarded as a new emerging zoonotic agent and livestock may constitute a growing reservoir of the ST398 lineage.

The University of Minnesota (where, as you all know, I work part time for the excellent infectious-disease news site CIDRAP; please go) does not have electronic access to this journal, and ILL is slow. If anyone else has a copy and would like to share, I would be grateful.

The cite is: Springer, B. et al. Methicillin-resistant Staphylococcus aureus: A new zoonotic agent? Wien Klin Wochenschr. 2009 Feb;121(3-4):86-90. Abstract here.

New York Times takes up “pig MRSA” ST398

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Constant readers, I know that many of you are very interested in ST 398, the “pig strain” of MSRA that has caused both mild and life-threatening human infections in Europe and has been found in retail meat in Canada and on farms and in farmers here in the Midwest. So I just want to bring to your attention that New York Times columnist Nicholas Kristof takes up the topic today, in the first of two promised columns: Our Pigs, Our Food, Our Health.

In today’s piece, he describes an apparent epidemic of skin and soft-tissue infections in a pig-farming area of Indiana that caught the attention of a local family physician, who subsequently died.

What we’d need to know, of course — and may never know, given that the investigation may have ended with the doctor’s death — is what strain of MRSA those local folks had. They may have ST 398, picked up if they worked on farms, or if it migrated out of the farms via groundwater or dust or flies. Or they may have USA300, the human community-associated strain, which in some areas is astonishingly common — a fact that most people don’t appreciate if they have heard only about the invasive child-death cases or the outbreaks in sports teams.

The full archive of posts on MRSA in animals is here and stories only about ST398 are here.

MRSA and animals — an elephant, this time.

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So, constant readers, I have wrestled another chapter to the ground — and thus have a few minutes’ breathing space to talk about a story that some of you have asked about privately. I’ve been wondering whether to post on this, because the entire episode is in the book, and I don’t want to scoop myself. But it’s so interesting, and so sad, that it seems worthwhile.

This episode happened a year ago, and was reported at a couple of medical meetings last fall, but it is in the news now because it was written up last week in the CDC’s Morbidity and Mortality Weekly Report or MMWR. (Which is the best-read magazine that you have never heard of. Hundreds of thousands of people all over the world read it every week for the latest in disease news. It’s free. Go, already.)

So, the brief synopsis: In late January 2008, the San Diego Zoo’s Wild Animal Park noticed that a baby African elephant, born in late November 2007, had broken out in pustules on her ear, neck, elbow and leg. Three of her caretakers had skin infections also. The zoo launched an investigation, assisted by a CDC Epidemic Intelligence Service officer who is assigned to California; they were concerned that the caretakers had unknowingly picked up a disease from the baby, who had been born early, was not thriving and was being intensively hand-reared by the zoo staff.

But in fact, it was more complicated than that. The pustules were MRSA, of course — but they were not ST 398, the animal strain that we have talked about so much here. Instead, they were USA300, the community-associated human strain that has zoomed to dominance all over the country. But there was no MRSA in the elephant herd, which the baby had not had contact with since late December. The reconstructed chain of transmission looked more like this: from an unknowingly colonized human to the baby elephant, who was medically fragile and had been isolated from her herd, and then from the elephant to the rest of the human “herd” who were caring for her. The strain involved was USA300, In the end, five human infections and three colonizations were laboratory-confirmed, and 15 other infections were suspected but not confirmed.

The humans recovered; most of their infections were so minor as to need no treatment, though three of them took oral antibiotics. The poor little elephant was not so lucky. She had multiple other illnesses, and she was euthanized on Feb. 4, 2008. The MRSA did not cause her death — by the time she died, the infection had resolved — but as one of the zoo staff told me, “It certainly didn’t help.”

So what does this tell us? Well, for zoo personnel, it tells them what to do for next time: More complete infection control especially around vulnerable animals. For microbiologists, it’s an expansion of MRSA’s range: No one had ever seen it in an elephant before.

For animal owners, it’s a warning and reminder. We’ve known for a while that community strains can transiently colonize pets, staying in the animal’s nose or elsewhere on the body just long enough to reinfect a human — in fact, an emerging piece of advice for physicians dealing with recurrent MRSA in families is, “Check the dogs and cats, too.”

And for the rest of us, it suggests, one more time, how extremely adaptive and inventive MRSA is, and that we should never underestimate its ability to surprise.

Resistant bacteria on health care workers’ phones

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Here’s some of the news that I mentioned Friday – no, I’m not hoarding, I’m just desperately behind on some writing (and falling further down the curve all the time, but thanks for the concern).

A team from Ondokuz Mayis University in Turkey, publishing in the open-access journal Annals of Clinical Microbiology and Antimicrobials, looked beyond the concern over health care workers’ hands being clean, and decided to interrogate what those workers hold in their possibly-not-clean hands. They swabbed and tested the hands of 200 health care workers (“15 senior, 79 assistant doctors, 38 nurses and 68 healthcare staff “), and 200 phones. Their results:

  • 94.5% of phones colonized with bacteria
  • 49% of the phones grew one bacteria
  • 34% grew two species, 11.5% three or more

The language in the paper is a bit difficult, but if I’m reading it right, the colonization rates look like this:

  • 50 of the phone and 53 health care workes carried S. aureus (approximately 25%)
  • 52% of the S. aureus strains on phones were MRSA
  • 37.7% of the S. aureus strains on hands were MRSA.

Other organisms on the phones and the hands were other staph species, coliform, enterococci, moulds and yeasts.

The health care workers were certainly not infection-control outlaws: They washed their hands regularly. But only 10% of them had ever thought to clean their phones — which are held by the mouth and nose, a prime site for staph colonization, and go with them everywhere in the hospital, including to the OR and the ICU. (The paper doesn’t make clear whether the phones in question are hospital-supplied, with potentially many users, or personal, with one user, but going from hospital to home and back again.)

So: We’ve talked in the past about the many challenges of infection control in hospitals — all the many, tiny details in multi-person, highly technological health care that can trip up even well-intended infection control. (Remember the sinks?) Here’s just one more example of the unfathomable complexity of the journey of attempting to get to zero in healthcare-associated infections — a place, of course, where we all want to be.

The cite is: Ulger, F., Esen, S., Dilek, A. et al. Are we aware how contaminated our mobile phones are with nosocomial pathogens? Annals of Clinical Microbiology and Antimicrobials 2009, 8:7doi:10.1186/1476-0711-8-7

Industrial farming, bacterial spread 2 – or: Flies. Ick.

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There’s a brand-new paper in the journal Science of the Total Environment that has some unnerving things to say about the link between very large scale farming, use of antibiotics in food animals, development of resistant organisms, and transmittal out into the larger environment.

Via flies.

Not to be unscientific, but: Ick.

A team from the Bloomberg School of Public Health at Johns Hopkins (who have done a number of studies on the spread of antibiotic-resistant organisms from farms to the outside world) decided to test the links in a chain of hypothesis that goes like this:

  • Antibiotics are used in large amounts in poultry production.
  • Antibiotic-resistant organisms are produced within the birds.
  • Antibiotic-resistant organisms leave the batteries via poultry litter (“excreta, feathers, spilled feed, bedding material, soil and dead birds“).
  • Poultry litter is stored in open sheds until it can be used as a soil amendment.
  • Flies have unrestricted access to poultry litter.

The tests were: sampling poultry litter from three farms in the Delmarva Peninsula (for non-US readers, that’s a portmanteau word for contiguous areas of the states Delaware, Maryland and Virginia, home to about 600 million chickens each year); trapping flies at 8 locations within 100 meters of farm boundaries; and assaying both litter and flies for the presence of resistant organisms and resistance genes.

And the findings were: Oh, lots and lots. Litter piles at all three farms contained resistant organisms — E. faecium, E. faecalis and our particular interest, Staphylococcus (multiple species, including three strains of S. aureus) — throughout the 120-day study period. All 8 fly traps did as well. All of the litter contained enterococci and staph strains that were resistant to 3 or more antibiotic classes. Seven of the 8 fly traps yielded multi-drug resistant enterococci, and 3 yielded multi-drug resistant staph. The resistance factors identified were for drugs that the FDA classifies as “critically or highly important” to human medicine: “penicillin, tetracyclines, macrolides, lincosamides, aminoglycosides and streptogramins.” Oh, and the fly species captured in the traps had an average range of 2 miles.

Of note, among the isolates discovered was one staphylococcus with high-level resistance to vancomycin.

The authors say:

This study strongly suggests that flies in intensive poultry production areas, such as the Delmarva Peninsula, can disperse antibiotic resistant bacteria in their digestive tracts and on their exterior surfaces. Dispersion of resistant bacteria from poultry farms by flies could contribute to human exposures, although at present it is difficult to quantify the contribution of flies. Flies may also transfer bacteria from fields amended with poultry waste.

The cite is: Graham JP et al., Antibiotic resistant enterococci and staphylococci isolated from flies collected near confined poultry feeding operations, Sci Total Environ (2009), doi:10.1016/j.scitotenv.2008.11.056. The ahead-of-print abstract is here.

Child deaths from flu + MRSA, an update

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As predicted earlier this week: The Centers for Disease Control and Prevention (CDC) has announced more deaths of children from flu, and from flu followed by MRSA pneumonia.

My colleagues at the Center for Infectious Disease Research and Policy are tracking the case count, and here’s what they said this evening:

The CDC received eight reports of influenza-related deaths in children during the week ending Feb 21, bringing the seasonal total to 17. Four of the deaths occurred in Texas, 2 in Colorado, and 1 each in Arizona and Massachusetts.
Bacterial coinfections have been confirmed in 10 (59%) of the 17 children. Staphylococcus aureus was identified in 8 of the 10 children—3 of the isolates were sensitive to methicillin, 4 were not, and results were not reported for 1. Eight of the 10 children who had coinfections were age 12 or older. (Byline: Lisa Schnirring)

Just to recap, that’s four deaths so far this flu season from flu+MRSA, twice the number we knew of last week.

And just to remind: The CDC and its Advisory Committee on Immunization Practices now recommends flu shots for all children and adolescents, up through the age of 18. A flu shot is one defense against MRSA pneumonia. It is worth considering.

Industrial farming, bacterial spread – another connection

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We’ve talked a lot here about the spread of MRSA ST 398, the “pig strain,” subsequently found in other animals and in retail meats in various countries; and also about the likelihood that antibiotic use in large-scale farming fosters the growth of resistant organisms; and also about the way that resistant bacteria from large-scale industrial farms end up in the larger environment via groundwater and airborne dust. (Use these links to call up all the ST 398 stories and related agriculture and food stories.)

Here’s an emerging story that should illuminate some of the dangers we are discussing. Note, it’s not about MRSA, and it’s not about resistant organisms, but it is an object lesson on how industrial-size farms can spread bacteria through the environment.

Last year, there was an outbreak of an unusual type of E. coli — a strain called O111 — in Oklahoma. There were 341 known cases, 72 hospitalizations, one death. The outbreak centered on a Locust Grove, OK restaurant called the Country Cottage, which used a private well. Here’s the Oklahoma State Department of Health wrap-up of that outbreak; no source for the E. coli was ever identified.

Now comes the Oklahoma Attorney General to say that the source has been identified: Poultry DNA has been found in wells in the area, and the AG contends it is because of the use of poultry litter — manure, feathers, the stuff that falls to the bottom of a chicken house — as fertilizer on local fields.

Now, some cautions: There is no indication in the media reports (I’m looking for a report or release from the AG’s office but haven’t found one) that the particular E. coli strain has been found; that outbreak has burned itself out. And also, the Oklahoma AG has apparently been fighting with the poultry industry and the state of Arkansas for several years over poultry-litter pollution in the Illinois River watershed. The poultry industry, naturally, disagrees that this practice is a health threat.

But if the Oklahoma AG is correct, and there is evidence that poultry manure is putting pathogens into the water supply far from poultry farms, then that would be one more link in the chain of evidence that connects industrial-scale farming, agricultural antibiotic use, development of resistant organisms, presence of those organisms in the environment, and human health effects.

Do not, do not, do NOT do this

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Hi from down the rabbit hole, readers (is there an echo?) — I am deep into a chapter and not surfacing much. Therefore, I’m once again behind in my reading, and so just stumbled across this from last week: a New York Times article called out by Liz Borkowski on the excellent public health blog Pump Handle.

The NYT story — which ran in the New York regional section and thus may not even have made it (on paper) out here to the Great Flyover — is primarily about young adults going naked on health insurance, what happens when that goes wrong, and how they practice a kind of do-it-yourself medicine to cope. But what made Liz’s hair stand on end (and mine, now that I’ve read it), is the way that the characters describe taking each other’s unused antibiotics:

Nicole Polec, a 28-year-old freelance photographer living in Williamsburg, Brooklyn, said she has attention deficit hyperactivity disorder and has a client who procures Ritalin on her behalf from a sympathetic doctor who has seen Ms. Polec’s diagnosis. Ms. Polec’s roommate, Fara D’Aguiar, 26, treated her last flu with castoff amoxicillin — “probably expired,” she said — given to her by a friend. (Byline: Cara Buckley)

You all got what was going on there, right? Flu — or even a cold — is a viral illness. Antibiotics don’t work against viruses. But antibiotics taken inappropriately do contribute to the evolution of drug-resistant bugs everywhere, and do make you more vulnerable to such bugs if they wipe out your own protective bacterial flora.

(NB: Let’s be clear, by criticizing this, I do not at all mean to be unsympathetic to the plight of the uninsured. My brother, a film composer, has been uninsured his entire career; as a freelancer, I have insurance only by the generosity of my in-all-ways-excellent spouse. And, just to editorialize, I consider it an international embarrassment that, what, one-sixth? of our population lacks the ability to pay for their health care. But there are things that are smart to do, in coping with the unworkability of the American health care system, and there are things that are not smart. Under-dosing and self-mis-dosing are, categorically, not smart.)

If you have time, please go read Liz’s analysis, it’s very good. If you don’t, please just listen to this take-away message: DON’T DO THIS. (Sorry to shout.)

Bad news from Australia: MRSA in water supplies

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The Brisbane Courier-Mail reports that scientists in Australia have found MRSA and VRE from hospital sewage in rivers and lakes throughout the state of Queensland, and have been trying for two years to get their provincial government to pay attention.

Secret tests on waste water discharged from 28 Queensland hospitals and clinics revealed the widespread presence of MRSA (Methicillin resistant Staphylococcus aureus) and VRE (Vancomycin resistant Enterococci).
However there was no evidence the potentially lethal organisms had made their way into drinking water.
A Central Queensland University scientist who helped carry out the research told me 97 per cent of hospital sewage discharge lines tested positive for antibiotic resistant bacteria.
He said 70 per cent of hospital discharges tested positive for both MRSA and VRE.
“We got a lot more of those bacteria than we thought possible,” he said. … “Even though they have passed through a treatment process, the bacteria are most likely getting back into natural waterways, dams and ponds used for swimming, boating, fishing and in food production.” (Byline: Des Houghton)

The report was presented to the Queensland parliament by a member in 2007, ignored, and presented again last week. (Note for US readers who click through to the story, from my UK childhood: “Tabled,” in parliamentary parlance, means “brought forward” or “introduced” — not “postponed” as we would interpret it.)

The wastewater was treated in a sewage plant and then tested — but the usual tests look for enteric pathogens such as E. coli, not for MRSA, so the water passed testing without MRSA’s presence being detected.

There have been similar studies in Portugal, South Africa and Nigeria. In the US, MRSA and other resistant bacteria have been found in groundwater and airborne dust, but that has been due to leakage from industrial farming. I’m not aware of anyone doing this sort of study, with organisms escaping from hospitals, in this country. If anyone does know of one, and has a cite, please comment!

Child deaths from flu + MRSA, again

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Folks, I am close to manuscript deadline and so keep disappearing down the rabbit hole; forgive me if I don’t post as regularly as usual, I’ll be back as soon as I can.

I wanted to point out the announcement by the Centers for Disease Control late Friday that we are starting to see children dying from MRSA this flu season. (The architecture of the linked page is unfortunately way clumsy; at the link, scroll down to the subhead “Influenza-Associated Pediatric Mortality.”)

Since September 28, 2008, CDC has received nine reports of influenza-associated pediatric deaths that occurred during the current season.
Bacterial coinfections were confirmed in six (66.7%) of the nine children; Staphylococcus aureus was identified in four (66.7%) of the six children. Two of the S. aureus isolates were sensitive to methicillin and two were methicillin resistant. All six children with bacterial coinfections were five years of age or older.

We’ve talked before (here, here and here, among other posts) among the emerging understanding of the particular danger that MRSA poses during flu season, when (it is hypothesized) inflammation from flu infection makes the lungs more vulnerable to secondary bacterial infection.

(For those paying attention to the hospital v. community MRSA debate, this is a community-associated infection, not a hospital one.)

This current CDC bulletin underlines, just in case we have forgotten, that drug-sensitive S. aureus (MSSA) can be a serious foe as well. Let’s remember, resistance makes MRSA less treatable than MSSA, but it does not change its virulence; MSSA by itself can be a very serious foe. Yes, there are other changes in some strains, especially the community ones, that do appear to increase virulence, but the original MSSA strain is nothing to trifle with.

Also, here’s an important addition to this unfolding story: My colleagues at the Center for Infectious Disease Research and Policy are keeping track of kid deaths around the country. According to them, these CDC numbers are already out of date; they have uncovered more that the CDC has not yet posted, but may take note of in future weekly updates.

MRSA reductions in ICUs – good news, but qualified

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Constant readers, you will no doubt have seen the overnight news about a paper by CDC authors in the Journal of the American Medical Association, reporting a significant decline in catheter-associated bloodstream infections (known by the uncatchy acronym CLABSIs, and yes, people pronounce it “klab-seez”) in intensive care units.

Our results show that the 6 most common adult ICU types reporting central line–associated BSIs to the CDC, which together account for 96% of all reported MRSA central line–associated BSIs among studied ICU types, have experienced declines of 50% or more in the incidence of MRSA central line–associated BSI since 2001. This means that the risk of primary MRSA bloodstream infections among patients with central lines in these ICUs has substantially decreased in recent years.

First, let’s stipulate that any reduction in healthcare-associated infections is good, good news.

Having said that, let’s drill down into the paper a bit. Because in some of the coverage last night and this morning, this paper is being represented as “Hooray, the MRSA problem is over,” and that’s an over-reaction. Here are some reasons why.

The data come from several overlapping CDC databases: the National Nosocomial Infections Surveillance system (NNIS) and the National Healthcare Safety Network (NHSN). The NNIS existed from 1970 to 2004; there was a data gap in 2005, and the NHSN sprang up in 2006. There were 300 hospitals in 37 states reporting to the NNIS when it shut down, and in 2007 there were 518 reporting to the NHSN, many of which joined that year as a result of new mandatory HAI reporting in New York, Colorado and South Carolina. Participation in either database was/is voluntary.

The CDC analysis abstracts data from the reports to those systems for the years 1997-2007. But, as you can guess from those numbers above, the data does not cover all 7,500 US hospitals; and because it is more weighted to certain states, it does not represent a nationally representative sample. In addition, hospitals came into the system(s) during the study, and also dropped out; an accompanying editorial estimates that only 6% of the 599 hospitals in the study reported data for all 11 years.

Second, it’s important to note that all CLABSIs went down: MRSA infections, drug-sensitive staph (MSSA) and other organisms. So something is going on — but it is not MRSA-specific. Optimistic interpretation: Enhanced infection control in hospitals is suppressing all HAIs. Pessimistic interpretation: Enhanced scrutiny, in the states that account for the most additional hospitals, is negatively affecting HAI reporting. Can we distinguish which? Probably not. On the one hand, CLABSIs started trending down in 2001, before the earliest mandatory reporting legislation became effective. On the other hand, the study doesn’t/can’t associate declines in CLABSIs with any specific interventions — so it is not possible to know from this study whether one particular strategy was responsible for this decline.

Third, to put the study focus in context, MRSA accounts for only about 7% of CLABSIs; according to the paper, it is not those infections’ most common causative organism. And CLABSIs do not account for the largest proportion of MRSA HAIs; according to a 2007 paper, they fall third on the list behind nosocomial pneumonia and septicemia.

Fourth, since it is abstracted from a hospitals data base, this study doesn’t address community MRSA infections — and there are some scientists in the family of MRSA researchers who would insist that it is the increasing prevalence of community infection that is the true driver of the MRSA epidemic.

So: Decreased MRSA HAIs, good news. Reasons, unfortunately unclear. Significance, possibly less than the headlines this morning maintain. But whatever it is that those hospitals were doing, let us hope they keep doing it.

The cite is: Burton, DC, Edwards, JR, Horan, TC et al. Methicillin-resistant Staphylococcus aureus Central Line-Associated Bloodstream Infections in US Intensive Care Units, 1997-2007. JAMA. 2009. 301(7): 727-36.
The accompanying editorial is: Climo, MW. Decreasing MRSA Infections: An End Met by Unclear Means. JAMA. 2009. 301(7)772-3.

Did MRSA kill an Ontario nurse?

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Here is a story that was flagged by several commenters (welcome, Canadian readers), and is being reported by a number of Canadian news outlets: A nurse who worked in the critical care unit at Victoria Hospital in London, Ont. has died, possibly of MRSA, and the Ontario Ministry of Labor is investigating whether her death is an occupational exposure — that is, whether she caught the bug in the process of working in the hospital.

There’s not a lot of detail in the stories published so far. The St. Thomas (Ont.) Times-Journal, the London (Ont.) Free Press and the Canadian Press suggest that the nurse was a patient in her own hospital and acquired the infection while a patient. The Toronto Globe and Mail, on the other hand, casts the story as the nurse working, becoming sick, and then becoming a patient.

Occupational infections with MRSA have certainly been recorded. A Texas firefighter and EMT died of invasive MRSA in 2006, and his widow alleged it was because of his exposure to MRSA patients; an Illinois EMT almost lost a leg to the infection in 2007.

Let’s stipulate that this Ontario nurse’s death is terribly sad. The question will be whether it is also scientifically confounding. A hospital is going to have a substantial background rate of MRSA, in infected patients, colonized patients and colonized personnel. If her death turns out to be caused by MRSA, it will be important to ascertain both the timeline — did she become sick while working, or while undergoing care for some other health problem — and also the microbiology: Did she have whatever strain is predominant in her hospital? Or was it on the other hand a strain that is circulating in the community (provided that community strains have not moved into hospitals in Ontario as they have in the US)?

That sort of microbiological differentiation provided an important clue in the death of Maribel Espada, a British nurse who died of invasive MRSA in 2006, six days after giving birth at the hospital where she worked. Unusually for the UK, Espada was infected with a PVL+ strain of MRSA, something that is very common in US community strains, but unusual in the UK until recently. That allowed her infection to stand out from the background, and suggested that she had been infected by a patient in her hospital:

The Health Protection Agency said it was investigating the possibility Mrs Espada caught PVL MRSA from a patient who died at the hospital in March.
A spokesman for University Hospitals of North Staffordshire NHS Trust said all staff who had come in contact with the two people originally diagnosed with PVL MRSA had been screened by the hospital’s infection control team.
A further nine cases were subsequently identified, of which one was a former patient.
The eight other cases were either members of staff or people staff had come into contact with. (BBC News)

MRSA and sports — and a sportswriter

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Chris Harry, NFL beat reporter and blogger at the Orlando Sentinel, recently covered the Superbowl in Tampa — and, possibly coincidentally, developed a MRSA infection of his own that required three surgeries and IV antibiotics, including a PIC line.

He writes about the experience here.

We’ve talked in the past about the unique affinity that MRSA seems to have for both student and pro athletes, including the disputed role of artificial turf (check the comments under the “pro athletes” post for more on that). As a reminder, the CDC has posted specific recommendations for schools, athletic trainers and parents in an attempt to reduce MRSA among student athletes.