Maryn McKenna

Journalist and Author

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.

MRSA at the beach

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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.

MRSA in kid athletes – simple but not easy

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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.

“Alarming” increase in MRSA infections in children

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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

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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

Prevention v. treatment (1st Global Health Blog Carnival!)

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Constant readers, about a dozen of us who are interested in global health are co-blogging today in a Global Health Blog Carnival. If you are on Twitter, search the hashtag #ghnews. If you’re not, we will try to get them all linked somewhere. This was organized (to the degree that blogger organize, which as you can guess is like herding small felines) by reporter and blogger Christine Gorman, formerly of TIME Magazine.

Our theme for today is prevention v. treatment. Fortuitously, the New England Journal of Medicine today is publishing an editorial (for which they have posted the free full text) that reminds us of the full burden and cost of MRSA. Drs. Cesar A. Arias and Barbara E. Murray say:

Faced with this gloomy picture, 21st-century clinicians must turn to compounds developed decades ago and previously abandoned because of toxicity — or test everything they can think of and use whatever looks active. …
It is more difficult than ever to eradicate infections caused by antibiotic-resistant “superbugs,” and the problem is exacerbated by a dry pipeline for new antimicrobials with bactericidal activity against gram-negative bacteria and enterococci. A concerted effort on the part of academic researchers and their institutions, industry, and government is crucial if humans are to maintain the upper hand in this battle against bacteria — a fight with global consequences. (NEJM 360(5):439-443)

As we’ve discussed time and time again, MRSA is increasingly common worldwide and increasingly costly to treat. Moreover, what has been presented by some as the first line of prevention for hospital-acquired MRSA — active surveillance and testing programs, also called “search and destroy” — is deeply controversial.

So what’s the next step? Well, in the past, when medicine has wanted to nullify an infectious disease threat, it did not rely only on surveillance or asepsis; it developed a vaccine. And there have been a few efforts to develop a MRSA vaccine, which are recapped in a new article in Infectious Disease Clinics of North America (yes, that’s a journal):

The most extensively tested vaccine against S aureus, which is a capsular polysaccharide-based vaccine known as StaphVAX, showed promise in an initial phase 3 trial, but was found to be ineffective in a confirmatory trial, leading to its development being halted. Likewise, a human IgG preparation known as INH-A21 (Veronate) with elevated levels of antibodies to the staphylococcal surface adhesins ClfA and SdrG made it into phase 3 testing, where it failed to show a clinical benefit. … Given the multiple and sometimes redundant virulence factors of S aureus that enable it to be such a crafty pathogen, if a vaccine is to prove effective, it will have to be multicomponent, incorporating several surface proteins, toxoids, and surface polysaccharides. (23 (1): 153-171)

Several longtime MRSA researchers, including Dr. Robert S. Daum of the University of Chicago, who wrote the first paper calling attention to community-associated MRSA in 1998, have called for a vaccine to be made a research priority.

Any thoughts, constant readers? In the public mind, right now, vaccines are at a low point: People are turning away from them, manufacturing problems have led to shortages, and pharma no longer finds vaccine manufacturing a lucrative business sector. If a MRSA vaccine were developed, would you take it yourself before surgery, or give one to your children?

More MRSA in meat, and not just pork

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In my excitement over the paper by Tara Smith and team on Friday, I failed to sufficiently emphasize an important new finding. (I included it in my story for ScientificAmerican.com, but it was toward the end.) I feel it deserves a post of its own, so here it is:

The Food and Consumer Product Safety Authority of the Netherlands has found MRSA in 12% of 2,217 samples of meat on sale in the country, including not just pork, but beef, lamb, chicken, turkey and game birds, and 85% of the bacterial isolates were the”pig strain” ST 398.

We have talked before (all posts here) about the potential risk of MRSA in meat, especially ST 398 because it seems to have found a preferred host in pigs. In this study, however, the meat most likely to carry ST 398 was not pork, but turkey, followed by chicken and then by veal, and then by pork.

So what does all this mean? It’s still probably too early to tell: Recall that the first isolations of this bug were in 2004, there have still been only a few papers on it, and this finding by Smith and team is the first identification of the strain in the United States. (Though not in North America, as it was identified in Canada in 2007.) It seems likely that ST 398 may have found a niche in other food animals, and that it contaminates the meat when the animals are slaughtered.

The consensus among the Dutch, though, is that this is an effect of the use of antibiotics in food animals. The romantic image of the Netherlands is as a cute little collection of postage-stamp family farms, but the reality, especially in the southeast of the country, is that they have substantial industrial-sized farms housing thousands of animals on relatively small properties. The only way to grow animals efficiently under such conditions is to keep very close tabs on potential illness, and liberally deploy antibiotics when necessary. (NB, I am not talking here about sub-therapeutic, growth-promoting use, but rather prophylactic antibiotics, given to an entire herd when a certain percentage of the herd shows sign of illness.) Evidence for this, according to the current study’s authors: Meat sold as “biologic” — that’s “organic,” in the US — had a much lower rate of contamination with ST 398.

There are still very few reports of human illness from ST 398, though of those reports, some are quite serious, including wound infections and endocarditis. The concern here, as the researchers interested in it have been saying from the start, is that someone will inadvertently colonize themselves with the organism by touching their eyes or nose while handling meat contaminated with ST 398. Colonization does not necessarily lead to disease, but it does lead to a far greater pool of organism potentially spreading unmonitored through human and animal populations, swapping resistance and virulence factors as it goes.

So, you know what I’m going to say: Wash your hands, wash your hands, wash your hands.

This is what hand hygiene looks like

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Contant reader Robyn pointed out an amazing image in the New England Journal of Medicine issue I discussed below. I missed it (thanks, Robyn!), so I went back and retrieved it. Here’s what you’re looking at:

The Cleveland Veterans Affairs Medical Center discovered via a routine nasal swab that a quadriplegic patient was colonized with MRSA; the patient had not had any signs that would have indicated an infection. To satisfy their curiosity over how much MRSA a healthcare worker might pick up from a patient whom they did not know was colonized, they had a health care worker do an abdominal exam of the patient — let’s underline that: abdominal; nowhere near his nose. Then they pressed the worker’s hand onto a growth medium that had been tuned with antibiotics so that it would allow MRSA to grow but suppress other bacteria.

That’s what you’re looking at above. All of that red is MRSA. The image on the right is what grew after the same worker did hand-sanitizing with alcohol foam and then pressed the same hand onto an identical culture plate. What’s growing? Nothing at all.

Here’s the back story, quoted from NEJM (re-paragraphed):

A 24-year-old man who had quadriplegia due to a traumatic spinal cord injury was found on routine surveillance cultures to have methicillin-resistant Staphylococcus aureus (MRSA) colonization of his anterior nares. He had no history of MRSA infection or colonization.
To assess the potential implications of the patient’s MRSA carriage for infection control, an imprint of a health care worker’s ungloved hand was obtained for culture after the worker had performed an abdominal examination of the patient. The MRSA colonies grown from this handprint on the plate (CHROMagar Staph aureus), which contained 6 µg of cefoxitin per milliliter to inhibit methicillin-susceptible S. aureus, are pink and show the outline of the worker’s fingers and thumb (Panel A).
With the use of a polymerase-chain-reaction assay, the mecA gene, which confers methicillin resistance, was amplified from nares and imprint isolates. After the worker’s hand had been cleaned with alcohol foam, another hand imprint was obtained, and the resulting culture was negative for MRSA (Panel B).
These images illustrate the critical importance of hand hygiene in caring for patients, including those not known to carry antibiotic-resistant pathogens.

The cite is: Donskey, Curtis J., Eckstein, Brittany C. IMAGES IN CLINICAL MEDICINE: The Hands Give It Away. N Engl J Med 2009 360: e3

UPDATE: The tireless and too-seldom-thanked crew at ZoneGrippeAviare, who provide pandemic news for the Francophone community, have translated this post into French. Mes mercis respectueuses!

Seriously, a global problem

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Serendipitously, as I was preparing the previous post (an intro to GlobalPost.com, which will be featuring posts from SUPERBUG), an auto-push email from the National Library of Medicine‘s PubMed service landed in my inbox.

For those of you whose bedtime reading is not obscure medical journals (I know: This is what you have me for), PubMed is a search interface that allows you to pull articles for medical journals wordwide. It also offers a push option: Set a search term, fill in your email, and links to the latest articles on your term of choice are delivered. I have my search set to “MRSA” and have the results pushed once a week; there are never fewer than 25 new papers, which is a great gauge of how active an area of research — and how important a topic — MRSA is.

The latest push — 26 articles — vividly reminded me that, as NIAID Diretor Dr. Anthony Fauci said a few months ago, we are in the midst of “a global pandemic.”

Here is a sampling of those latest papers, from, again, a single week:

No question, constant readers: What we are talking about here is an international problem, a truly global bug.

“Pig MRSA” in New York City – via the Dominican Republic?

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Folks: Back in October, I broke the news for you of an intriguing poster presentation at the ICAAC meeting. It revealed the discovery of ST 398, the anomalous staph strain found in pigs, pig farmers and health care workers in Europe, in residents of a Dominican-immigrant neighborhood in northern Manhattan, and also in the Dominican Republic.

Because there is so much traffic back and forth between those neighborhoods, the authors theorized that people are providing an “air bridge” for the bacterium — though they were unable to say whether the bug is moving from the Dominican Republic to the United States, or vice versa.

I was unable to link to that presentation at the time, because it was a meeting poster – yes, literally a poster, the authors stand by it to discuss it with anyone who wanders by. However, now it has been published as a paper, in the CDC journal Emerging Infectious Diseases; and because it is a CDC journal, the full text is available free online here.

Just to underline, despite my headline above, the strain found in NYC was not MRSA: It actually is MSSA, drug-sensitive staph. The ST 398 found in Europe, Canada and the American Midwest is MRSA. The authors hypothesize that the NYC strain is at risk of becoming MRSA also.

To see the multiple posts in this blog about MRSA ST 398 and other strains in the food chain, food animals, and pets, go to the labels under the time stamp on this post, and click “animals” or “food.”

The cite for the paper is: Bhat M, Dumortier C, Taylor B, Miller M, Vasquez G, Yunen J, et al. Staphylococcus aureus ST398, New York City and Dominican Republic. Emerg Infect Dis. 2009 Feb; [Epub ahead of print]

Brilliant entrepreneur asks: “So why CAN’T you fix this?”

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Constant readers, you’ll note that posting has slowed down a bit: I am deep into a chapter that is giving me some difficulty. (And I seem to be playing holiday host to an unexpected bout of bronchitis. I’m sure I didn’t need both lungs…)

But here’s something that crossed my monitor this morning, and it’s worth looking at. Sir Richard Branson, founder of Virgin Air and many other extremely successful entrepreneurial efforts. has accepted a post as vice-president of the Patients Association, a nationwide nonprofit that advocates for hospital patients in the UK. Speaking up in his new position, Branson gave an interview to the BBC in which he talked about hospitals’ failure to curb MRSA:

It feels like they have tinkered with the problem rather than really got to the heart of the problem. The hospitals are there to cure people. They are not there to kill people.

It’s a marvelous interview — read the whole thing, it’s not long — because it’s such a breath of fresh air. Branson is an outsider to health care, but he knows how to make businesses work. And as the head of an airline, he’s extremely familiar with what we in the US call “never events”:

Sir Richard says the health service could learn a lot from the airline and rail industries on how to avoid mistakes.”In the airline industry if we had that kind of track record we would have been grounded years ago,” he said.”In the airline industry if there is an adverse event that information is sent out to every airline in the world. And every airline makes absolutely certain that that adverse event doesn’t happen twice.”

So his advice is brutally practical: Health care workers carry MRSA? Screen and swab them. Workers are positive for MRSA? Treat them, and take them out of direct patient contact for two weeks. That costs money? Spend the money: It’s less costly in the end than killing your patients.

Terribly sad story from Florida

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Cody Shrout, a 12-year-old 6th-grader who lived in Daytona Beach, Fla., was found dead in bed a week ago today by his 8-year-old sister.

His death was initially put down to chickenpox, which was circulating in his school, but the Volusia County medical examiner determined Tuesday that his death was due to MRSA.

Two weeks ago, he scraped his knee skateboarding, subsequently spiked a 103+ degree fever, was treated at a local ER and sent home. The story describing his treatment quotes his grandfather in a way that suggests the scrape was treated as a sports injury, with ice and ibuprofen.

Cody lived with his mother, sister, 3-year-old brother and grandfather. His mother, who is single, could not afford a funeral. With extraordinary generosity, Heather and Jason Jenkins, who own a plumbing business in Apopka, Fla., have paid for the funeral. He will be buried Tuesday.

An odd tidbit in this very sad story: Ten months ago, according to the Daytona Beach News-Journal, he was treated at that same medical center for a staph infection. The story doesn’t say whether he was an admitted patient or seen in the ER, and also doesn’t say whether it was MRSA or drug-susceptible staph. Interesting, though.

File under Unintended Consequences, 2

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Via the BBC comes a report, from a conference hosted by the journal Lancet Infectious Diseases, that some healthcare-infection experts in the UK are publicly questioning efforts to reduce hospital-acquired MRSA.

The argument is that, by focusing so tightly on MRSA, hospitals neglect other drug-resistant HAIs to such an extent that the overall rate of illness in the hospital remains approximately the same. They argue instead for a broader focus on all resistant and nosocomial organisms:

“It’s not clear that overall things have got better,” … said [Dr Mark Millar, a medical microbiologist at St. Bartholomew’s Hospital and the London NHS Trust].
“Rates of E. coli are going up and it almost compensates for MRSA.
“All you’ve done is replaced one problem with another one,” he said. … “”There’s no evidence that overall we have fewer hospital infections or fewer people are dying.” (Byline: Emma Wilkinson)

This is a highly contentious debate in the US as well, with no resolution in sight. I’ve covered some aspects of it here, and there is a long point-counterpoint from Infection Control and Hospital Epidemiology here and here.

More on MRSA pneumonia, flu and ER delays

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Folks, yesterday I posted the very sad story of 39-year-old Robert Sweitzer of Tucson, who died of MRSA pneumonia after being triaged to an 8-hour wait, in an overcrowded emergency room, during the height of flu season.

As a follow-up, I want to emphasize that while necrotizing pneumonia may seem an unusual circumstance, there is one thing in his story that is very, very common: The ER wait.

Emergency departments all over the country are suffering extraordinary stresses thanks to a confluence of factors: The unfunded mandate of mandatory ER care or at least treatment and stabilization, through the federal legislation known as EMTALA. The closure of large numbers of in-hospital beds, which make it more difficult to get patients admitted. The lack of adequate primary care, which drives people to seek ER care because they cannot get into a regular doctor’s office. The extraordinary percentage of Americans who have no health insurance — a percentage that is likely to increase as the economic meltdown continues.

How crowded are emergency departments? On average in the United States, an ambulance is diverted — denied admittance because an ER is too full to take new patients — once every minute.

To quote a bumper sticker that got a lot of use over the past few years: If you aren’t outraged, you’re not paying attention.

(Disclosure: I was a Henry J. Kaiser Family Foundation fellow in 2006-07, and spent an average of eight nights a month, for a year, as an ER observer. So ER overcrowding is something I both have witnessed up close, and feel passionately about.)

I mention all this in order to let you know that the American College of Emergency Physicians released today a state-by-state “report card” on the condition of ER care in the United States. Our average national grade? C-. (If you don’t have time for the full report, the New York Times sums it up here. If you want to do more research, three Institute of Medicine reports on the issues, from 2006, are here.)

So, again: While Robert Sweitzer’s death may seem end-of-the-curve extraordinary, the conditions that contributed to his death — a crushing overload in a community-hospital ER — are very, very common. And that should frighten all of us.

MRSA in newborns on Prince Edward Island: HA? CA? Matters?

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There’s been a running story for several weeks now about the Queen Elizabeth Hospital on Prince Edward Island (home to mussels and Anne of Green Gables). The hospital struggled earlier this year with an outbreak of MRSA and a second outbreak of VRE among adult patients. It got those under control, but since earlier this month has been dealing with a new outbreak of MRSA in its newborn nursery, according to the PEI Guardian:

Nine newborns and one mother have now tested positive for MRSA. Five of those nine cases can be connected to the same source. (Byline: Wayne Thibodeau)

The stories are detailed, for a small paper — they go into depth about the cleaning measures the hospital is taking — and yet they don’t answer the questions that we here want to know. Does “tested positive” mean colonized or infected? Does “connected to the same source” mean they all have the same strain, or does it mean there is an epidemiologic link?

In the latest news (Tuesday’s paper and online edition), the hospital reports that it is doing nasal swabs on more than 300 staff, with the intention to do a 7-day decolonization regimen on anyone who turns up positive. They won’t however, disclose the source when they find it — though, again, it’s not clear whether that means not identifying the staffer (appropriate) or not admitting that it is a nosocomial outbreak (inappropriate and at this stage lacking in credibility):

Rick Adams, CEO of the Queen Elizabeth Hospital, said about 290 staffers have already been screened.
“In terms of the test results, we’re not going to be making anything public,’’ Adams told The Guardian.
“We want to make sure the environment here is supportive of staff and create a climate where they can feel comfortable and open to come forward and be screened knowing that any results will be kept strictly confidential.’’
Adams said he realizes a solid argument can be made that the public should be informed if the source is found and that source is a staff member.
But he said the public should also realize the hospital is doing everything it can to prevent a further spread of the superbug.
“The staff are under enormous pressure. They feel like they are under a microscope.’’ (Byline: Wayne Thibodeau)

Some readers may know that it is outbreaks among newborns that have demonstrated that the designations “community-associated” and “hospital-acquired” are passing out of usefulness. There have been several MRSA outbreaks in newborns and their mothers in the US (in New York City, Houston, Chicago, Los Angeles and Houston again because Baylor College of Medicine has been particularly alert to this) that were clearly nosocomial, and yet when the microbiology was done, were found to be caused by community strains.

Why does this matter? Well, for the PEI hospital, it may not: They have an outbreak, it appears to be nosocomial in nature, and whether it is HA left over from their earlier outbreak, or CA that came in via a health care worker or a pregnant woman, mostly affects what drugs they give the children and mothers if those patients do in fact have infections. And for those of us who are primarily concerned with nosocomial infections, the distinction may also feel not-relevant: Failures of infection control are failures of infection control and should not happen period full stop.

But for those of us who are are also interested in the natural history of this perplexing bug, the answer to what is going on at the Queen Elizabeth will be an important piece of information, because it could underline that the distinction between HA and CA is becoming increasingly artificial. The epidemics are converging.

British infection control: Epic fail

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Via the Guardian comes news that British hospitals are failing miserably at hygiene and infection-control targets set by the Healthcare Commission, a government-funded but independent watchdog agency somewhat analogous to the United States’ Joint Commission (formerly called JCAHO).

While community-associated MRSA is still a somewhat new story in the the UK, hospital or nosocomial MRSA is a major epidemic, with resistant Clostridium difficile (“C.diff”) coming close behind. So there has been significant attention paid in the UK to improving infection control programs in hospitals, through the vehicle of benchmarks set for the National Health Service trusts (essentially, regional organizational groupings of hospitals).

And the results, according to unannounced spot-checks made by the UK commission, are appalling. Only 5 of 51 trusts ( 51 = 30% of all acute-care hospitals in the UK) that were checked hit the mark. For those slow at math, that means 3% of UK hospitals are doing what they should to protect patients from infections they cause. (UPDATE: To be fair, if we assume the “5 out of 51” holds true across the NHS, then 10% are doing what they should. That’s still appalling.)

“At nearly all trusts we have found gaps that need closing,” said Anna Walker, the commission’s chief executive. “It is important to be clear that at these trusts we are not talking about the most serious kind of breaches. But these are important warning signs to trust boards that there may be a weakness in their systems.” (Byline: Sarah Boseley)

How weak? This weak, according to the commission’s own report:

  • 27 of the 51 trusts inspected were failing to keep all areas of their premises clean and well maintained. These lapses covered issues ranging from basic cleanliness, to clutter which makes cleaning difficult, to poorly maintained hospital interiors.
  • One in five trusts in this sample did not comply with all requirements for the decontamination of instruments and other equipment used in the care of patients. Trusts that breached this duty tended to have no clear strategy for decontamination or to lack an effective process to assure compliance.
  • In one in eight trusts, the provision of isolation facilities was not adequate. The containment of infections is extremely important to managing outbreaks. Hospitals without adequate facilities must ensure they have contingency plans so that the risk of infections spreading between patients is minimised.
  • For over one in five trusts there were issues related to staff training, information and supervision. While training on preventing and controlling infection was often in place, boards could not always ensure that training days were well attended or that staff used their knowledge in practice.

UK hospitals have until next April to learn to hit these benchmarks or be held accountable under a new Care Quality Commission.

For infection-control geeks, the full text of the “hygiene code” which the hospitals must abide by is here. Details of inspections at individual trusts are here.