Child deaths from flu + MRSA, an update

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

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

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

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

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

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?

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

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.

MRSA at the beach

Am I the only person whose grandmother said it was healthy to swim in the sea because the salt would disinfect any cuts or skin nastinesses? Well, apparently my grandmother — and who knows, maybe yours too — was wrong:

The annual meeting of the American Association for the Advancement of Science concluded today in Chicago. Among the presentations: Physicians at the University of Miami tested seawater at popular Florida beaches and found that swimmers have a 37% chance of coming into contact with drug-sensitive staph, and 3% chance of encountering MRSA. The organisms are deposited into the water by infected or colonized humans.

Dr. Lisa Pisano said in a precis distributed to press for the meeting (I don't think I am able to link to this, but am checking):

Our hypothesis is that the bathers using recreational waters not only contribute to the organisms in the water, and therefore serve as a source of staph, but they might also become colonized or infected by the organisms that they are exposed to while in the water or on the beaches. Investigators from our team had previously shown that staph was shed by adults into marine water filled pools after short exposures, supporting that people could serve as a source for the bacteria. In the studies I will present, we confirm that adults who are known to be colonized indeed shed their own bacteria into marine waters. We also show that children, in diapers, both known and some not known to be colonized with staph also shed bacterial into marine waters.
...
37% of the water samples contained staph and 3% of these were MRSA. Genetic analyses of the isolated organisms revealed that the majority of the staph, not MRSA, appeared to be non-aggressive strains lacking the key virulence factors known to be associated with more aggressive strains of bacteria. However the majority of the isolated MRSA were those likely to of the more aggressive variety.

To prevent colonization, or infection of any abrasions or open wounds, the researchers recommend showering before entering the water and before leaving the beach.

Until I figure out what of the materials can be linked to, or whether press releases were put online by funders of the research, here's a Reuters story carried by ScientificAmerican.com.

An inside look at combating HAIs

I've been moving my RSS feeds over to a new reader and so am behind in reading things. That's my lame excuse for not noticing an excellent story in the Washington Post Tuesday, a first-person account tracing the "conversion" of one skeptical physician to the cause of reducing hospital infections.

The story was highlighted at the New Health Dialogue, a must-read health-reform blog, by my friend and former fellow Kaiser fellow, Joanne Kenen.

HAI money in the stimulus bill

Constant readers, for those of you who are following the back-and-forth over the economic stimulus bill, I wanted to let you know that the Association of Professionals in Infection Control (APIC) is saying that the compromise may cut money for state programs to reduce hospital-associated infections.

Here is APIC's alert:

ACT NOW TO PRESERVE HAI AND PUBLIC HEALTH FUNDING IN STIMULUS BILL

Your urgent action is needed now to preserve public health funding related to HAIs in the stimulus bill pending in Congress.
The stimulus bill passed by the House of Representatives includes $3 billion in funding for overall public health, prevention and wellness programs. Part of this funding includes $150 million for carrying out activities to implement a national action plan to prevent healthcare-associated infections, $50 million of which would be provided to states to implement HAI reduction strategies.
Because of the fast-moving action on this legislation, and the fact that an agreement has been reached to remove prevention and wellness from the Senate stimulus bill, your Members of Congress need to hear from you today as the House and Senate prepare to confer over a final version of the bill. We need them to support the House-passed provisions for public health, prevention and wellness and the HAI language in the stimulus bill (the American Recovery and Reinvestment Act of 2009).

I apologize that, being deep in book production, I don't know the details of the HAI-reduction programs they are talking about, whether it means support for new mandatory reporting programs or some other thing. (I'll ask some of the HAI-focused organizations to weigh in back-channel if they can.)

But if you are concerned about the recent new initiatives in various states to report, track and control HAIs, this is probably worth looking at.

Hospital MRSA - taking local action

If you follow hospital-acquired infections, you know there's enormous debate nationally over the best strategies to use: "search and destroy" versus targeted surveillance; guidelines from SHEA, APIC, CDC, or elsewhere. The competing assertions and the lack of clarity can be dizzying.

Here's news though of one local area that has decided to cut through the fog. A private healthcare organization, state universities and a state hospital association have teamed together to create the South Carolina Healthcare Quality Trust, a partnership that says it will test evidence-based best practices and use IT tools to rapidly distribute them to the 60+ smaller hospitals in the state.

There's not a lot of detail up yet about what the trust plans, so let's applaud the effort while reserving judgment until we see what strategies they choose to test and why. Meanwhile, though, here is the announcement from Health Sciences South Carolina, which is a collaborative of several universities, and a FAQ; a story from the national publication Modern Healthcare; and one from the state newspaper, the Columbia State.

MRSA in kid athletes - simple but not easy

It's been almost a week since this came out — told you there had been a lot of research released — but I wanted to make sure everyone saw it: The Centers for Disease Control and Prevention released results of an investigation into an outbreak of MRSA on a high school football team in Brooklyn, NY. (My home town, in case anyone cares. But it must have gotten gentrified, since the only organized activities I remember were somewhat less, umm, licit.)

Out of 59 players who attended a pre-season training camp where they practiced all day and bunked in the gym at night, 6 had MRSA skin abscesses (4 confirmed by culture, 2 suspected). The four confirmed cases all began as a pustule or blister that the kids ignored until the infections blew up; three of them subsequently needed the abscesses surgically incised and drained and also took antibiotics.

So, this will sound like not a big deal, right? Fifty-nine kids, 6 infections, attack rate of 11.8%, no one harmed in the long term. Well, in one sense, yes. On the other hand, without sounding like a Cassandra, there have been plenty of sports infections that did not turn out to be so minor: Kellen Winslow, Kenny George, Brandon Noble, Ricky Lannetti. (And if you'll stay tuned til this book is published, there will be an entire chapter on MRSA and sports, both amateur and pro, and the story of a teen athlete who almost died of invasive MRSA following what looked like an innocuous minor infection.)

The difficult thing here is that the steps for preventing such infections — or, at least, vastly reducing their likelihood — are simple: Washing hands, showering after practice, not sharing towels or razors, keeping uniforms and gear clean, and keeping on top of what look like minor abrasions and bug bites. But, as this investigation demonstrates, it's not so easy to get kids to take those things seriously:

The school had supplied antibacterial soap in pump dispensers in the showers; however, several players brought their own soap. Players supplied their own towels. Players reported that they usually left their towels on their cots or on the floor when not in use. The school offered a daily laundry service for uniforms and towels during the camp; however, most players did not have their towels washed and wore their uniforms two or three times between launderings. Players often remained in sweat-soaked clothes between the morning and afternoon practices. (MMWR Jan.30, 2009. 58(03);52-55)

As with hospital infections, where the simple act of handwashing remains one of the most difficult tasks to accomplish, the steps that could prevent MRSA among kid athletes are not complex. What is challenging is getting the kids to understand — over-against the hypermasculinity of sports, where it's cool to be sweaty, dirty and banged-up — how important it is to perform those steps: routinely, thoughtfully, time after time after time.

A little sardonic (botanical) humor - "39 more 'oops' "...

Courtesy of ReACT, a Web-based international coalition on antibiotic resistance.

Back to bad news tomorrow.

"Alarming" increase in MRSA infections in children

I've been waiting to post on this paper from last week because there was something odd about the math in it. It's an important and troubling finding, though, so even though I haven't heard back from the authors, I'm going to describe it for you and explain where I think the error is. (NB, When corrected the error makes their findings more significant, not less.)

So: Authors from Emory University in Atlanta reviewed a national database of head and neck infections in children that were reported by 300 hospitals between 2001 and 2006. In those years, there were 21,009 S. aureus infections: ear infections, sinus infections and so on. But, in 2001, the proportion of S. aureus that was MRSA was 11.8%. In 2006, it was 28.1%. That's more than a doubling — it's a 138% increase. (Here's the error: The authors say it was a "16.3% increase". I believe they mean "16.3 percentage points," which would be correct but significantly undersells their finding.)

Because 60% of the infections were outpatient, the authors make the reasonable assumption that these are community-associated MRSA (CA-MRSA). CA-MRSA is generally resistant to fewer drug than the hospital (HA-MRSA) variety. Unfortunately, they also find that this community strain is gaining additional resistance factors: More than 48% of all MRSA stains in this study were resistant to clindamycin, which is not a traditional resistance for CA-MRSA but recently has been reported more and more. Also, head and neck infections are not traditional presentations for MRSA, suggesting the bug is expanding its range.

Their comment:

...[T]he results of this study depict an alarming increase in MRSA in the United States. There is an increasing trend of clindamycin resistance among MRSA isolates. Expeditious culture of suspected head and neck infections leading to more appropriate antimicrobial drug selection is highly recommended to avoid further resistant patterns.

The cite is: Iman Naseri; Robert C. Jerris; Steven E. Sobol. Nationwide Trends in Pediatric Staphylococcus aureus Head and Neck Infections. Arch Otolaryngol Head Neck Surg. 2009;135(1):14-16.

More MRSA, more meat - poultry, this time

Constant readers: Fresh from the journal Emerging Infectious Diseases — posted AOP (electronic publication/ahead of print) this afternoon — comes more news of MRSA ST 398, the "pig strain," in food animals. This time, it's chickens, in Belgium.

The authors (from Ghent University and the Veterinary and Agrochemical Research Center in Brussels) took swabs from living chickens — laying hens and broilers — from 24 farms, 50 layers and 75 broilers total; one broiler-raising farm was sampled twice. They found no MRSA in the layers, which is important for reasons I'll get to in a moment, and ST 398 in 8 broilers. From each chicken, they took two samples, nasal and cloacal, and in the 8 positive chickens, they got 15 MRSA isolations; one cloacal swab was negative. Of the positive chickens, several (I deduce three, but the math is a bit cloudy) were spread across the two visits to the farm that was sampled twice. Since chicken farms are depopulated between batches — yes, just what it sounds like, farms sell/kill all the birds and clean the place — that finding suggests that MRSA is persisting in the environment on that farm.

Important point: This strain was ST 398, which we here have been calling the pig strain from many previous findings, most of them in pigs. However, ST 398 is an identification using a particular technique called MLST (multi-locus sequence typing), which is used for this strain because the standard typing method, PFGE (pulsed-field gel electrophoresis), did not return a readable result when the strain was first identfied back in 2004. (Trivia: That's why the initial reports of this strain called it NT, for "nontypeable.") It's becoming increasingly clear, though, that ST 398 is actually a category, not a single strain. And within that category, today's research is a new find: a strain with the unusual spa type t1456, which has only been found 10 times in the past three years, in Germany and the Netherlands, not in Belgium. The author suggest that this particular strain may be adapting to poultry in the same manner that the ST 398 we have been talking about (different spa type — sorry, I will have to look it up) has adapted to pigs.

So, as before: Why do we care? We care for two reasons: First, because since this strain is in a food animal, the possibility exists that it could contaminate the chickens' meat during slaughter and pass to humans. As has happened with some ST 398, the humans could be only colonized, and not become ill. But, second, any increase in colonization is a bad thing: The more strains out there, the greater the chance that they will exchange virulence and resistance factors and become something unpredictable.

Now, about those layers, here's an interesting factor that the authors call out in their paper: Layers, unlike broilers, do not receive antibiotics. The layers did not carry MRSA. The broilers did. It's a pretty potent argument, in case anyone needed convincing, of the effect of the selective pressure that antibiotic use in food animals exerts on these strains.

The site is: Persoons D, Van Hoorebeke S, Hermans K, Butaye P, de Kruif A, Haesebrouck F, et al. Methicillin-resistant Staphylococcus aureus in poultry. Emerg Infect Dis. 2009 Mar; [Epub ahead of print] DOI: 10.3201/eid1503.080696