Maryn McKenna

Journalist and Author

Community MRSA rates rising, and epidemics converging

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A study published Tuesday in Emerging Infectious Diseases makes me happy, despite its grim import, because it confirms something that I will say in SUPERBUG: Community MRSA strains are moving into hospitals, blurring the lines between the two epidemics.

The study is by researchers at the excellent Extending the Cure project of Resources for the Future, a group that focuses on applying rational economic analysis (think Freakonomics) to the problem of reducing inappropriate antibiotic use. (Here’s a post from last year about their work.)

Briefly, the researchers used a nationally representative, commercial (that is, not federal) database of isolates submitted to clinical microbiology labs, separated out MRSA isolates, divided them into whether they originated from hospitals or outpatient settings (doctors’ offices, ambulatory surgery centers, ERs), and analysed them by resistance profile, which has been a good (thogh not perfect) indicator of whether strains are hospital or community types (HA-MRSA or CA-MRSA). They cut the data several different ways and found:

  • Between 1999 and 2006, the percentage of staph isolates from outpatient settings that were MRSA almost doubled, increasing 10% every year and ending up at 52.9%. Among inpatients, the increase was 25%, from 46.7% to 58.5%.
  • Among outpatients, the proportion of MRSA isolates that were CA-MRSA increased 7-fold, going from 3.6% of all MRSA to 28.2%. Among inpatients, CA-MRSA also increased 7-fold, going from 3.3% of MRSA isolates to 19.8%.
  • Over those 7 years, HA-MRSA did not significantly decrease, indicating that CA-MRSA infections are not replacing HA-MRSA, but adding to the overall epidemic.

So what does this mean? There are a number of significant aspects — let’s say, bad news, good news, bad news.

Bad: CA-MRSA strains are entering hospitals in an undetected manner. That could simply be because patients entering the hospital are colonized by the bug and carry it with them. But it could also be because healthcare staff who move back and forth between outpatient and in-patient settings — say, an ambulatory surgical center and a med-surg ward — could be carrying the bug with them as well.

Good: If they are detected (analyzed genotypically or for drug sensitivity), CA-MRSA strains are less expensive to treat because they are resistant to fewer drugs, and some of the drugs to which they are susceptible are older generics, meaning that they are cheaper.

Very Bad: The entrance of CA-MRSA strains into hospitals risks the trading of resistance factors and genetic determinants of transmissibility and colonization aptitude in a setting where bacteria are under great selective pressure. Several research teams have already seen this: In several parts of the country, CA-MRSA strains have become resistant to multiple drug families.

Is there a response? The work of Extending the Cure focuses on developing incentives that will drive changes in behavior around antibiotic use. These results, lead author Eili Klein told me, call for developing incentives for creating rapid diagnostic tests that will identify not just that a bug is MRSA, but what strain it is, so that it can be treated appropriately and not overtreated.

The results also underline the need for something that is particularly important to me: enhanced, appropriately funded surveillance that will define the true size of the MRSA epidemic and delineate the behavior of the various strains within it. Right now, surveillance is patchy and incomplete, done partially by various CDC initiatives and partially by the major MRSA research teams at academic medical centers. As we’ve discussed, there is no national requirement for surveillance of patients, and very few state requirements; there is no incentive for insurance companies to pay for surveillance, since it benefits public health, not the patient whose treatment the insurance is paying for; and there is a strong disincentive for hospitals to disclose surveillance results, because they will be tarred as dirty or problematic. Yet to know what to do about the MRSA epidemic, we first have to know the size and character of what we are dealing with, and we do not now.

The cite is: Klein E, Smith DL, Laxminarayan R. Community-associated methicillin-resistant Staphylococcus aureus in outpatients, United States, 1999–2006. Emerg Infect Dis. DOI: 10.3201/eid1512.081341

MRSA and H1N1 “swine” flu – still not a lot of evidence

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Hello again, constant readers. It’s busy out there.

The CDC said Wednesday that new infections with the novel H1N1 virus (Formerly Known As Swine Flu) may be trending down. Nevertheless, there is still a lot of rumor and speculation out there regarding what role MRSA pneumonia may have played in serious cases.

The CDC commented on this in its May 19th press briefing:

Q: Is anybody looking for, and is anybody finding any evidence of, coinfection with MRSA?
A: We′re very interested in that question. As you know, the seasonal influenza in children we′ve been tracking pediatric deaths, and we have seen MRSA among seasonal flu cases in children at a higher rate than we had expected. MRSA is a big problem in the United States right now in terms of the community associated resistant staff or its infections. So far as we′ve been looking at the patients with the H1N1 virus, we don′t have evidence of coinfection. Not everybody has been tested for bacterial infections. But among the ones that have been tested, we aren′t seeing an important role for bacterial coinfection, including MRSA. I think this is an important issue for us to continue to follow, whether bacterial co-infections or bacterial pneumonias following the illness are featured. It′s a feature we′re interested in but haven′t seen this turn up yet.

We’ve talked a number of times before here about MRSA necrotizing pneumonia, and about the apparent importance of secondary bacterial infections to the death rates in prior flu pandemics.

But for anyone who needs a refresher, I recommend an excellent new paper by researchers at Emory University, published last week in the journal Lancet Infectious Diseases. It recounts the clinical course of two people who were treated at Atlanta’s Grady Memorial Hospital for MRSA pneumonia. Both were adults, and both survived, but their courses were complicated; the clinicians note that they did not improve until they were given additional antibiotics aimed at shutting down MRSA’s toxinproduction, a step that is not universally considered by doctors treating a MRSA patient.

The cite is: Hidron, AI et al. Emergence of community-acquired methicillin-resistant Staphylococcus aureus strain USA300 as a cause of necrotising community-acquired pneumonia. Lancet Infect Dis. 2009 Jun;9(6):384-92. The abstract is here.

MRSA strains crossing borders: US CA-MRSA to Italy

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Swine flu continues to dominate the headlines, but other pathogens don’t read the papers. Case in point: New news about a US community strain being found and treated in a woman in Italy — better treated, as it turns out, than she was in California, where she was infected.

In a new letter in Emerging Infectious Diseases (a free journal published online and in print by the CDC — it’s your tax dollars at work, just read it, already), Carla Vignaroli, Pietro E. Varaldo, and Alessandro Camporese of the Polytechnic University of Marche in Ancona amd the Santa Maria degli Angeli Regional Hospital, Pordenone report the case of

a 36-year-old Italian woman (who) was seen at Pordenone Hospital (northeastern Italy) for spider-bite–like skin lesions on the face, characterized by rapid evolution to furuncles and small abscesses. The infection had started ≈1 month earlier in California, where she had spent several months on business (wine import-export), and where she had been treated empirically with amoxicillin/clavulanate for 10 days (1 g, 3×/day), with no clinical improvement.

(At this point, I know every clinician reader and everyone who has had a MRSA skin infection is shaking his or her head. Surely by now the knowledge that “spider bite” is practically diagnostic for CA-MRSA has penetrated? But apparently not, since she was given amoxicillin/clavanulate, AKA Augmentin, which is partially penicillin-based.)

When the woman’s lesions were cultured, they turned out to be caused by USA400, the original community strain, which back in the 1990s was known as MW2. That’s interesting, especially in California, since USA300 has become such a dominant strain. Nevertheless, the key point is that USA400, as with USA300, has barely been recorded in Italy:

All 3 previously reported cases of CA-MRSA infection in Italy were caused by type IV SCCmec, PVL-positive strains, none of which, however, belonged to the ST80 clonal lineage that predominates in Europe (7). The first case (in 2005) was a necrotizing pneumonia caused by an ST30 isolate; the 2 other cases (2006) were severe invasive sepsis and a neck abscess, both caused by ST8 (USA300) isolates.

The concern, of course, is that once imported, they will not remain rare:

The case we note here documents the importation of a US pathogen into a country in Europe, from an area where the pathogen is widespread and has been highly virulent since the late 1990s, to an area where its penetration in the past has been poor.

The cite is: Vignaroli C, Varaldo PE, Camporese A. Methicillin-resistant Staphylococcus aureus USA400 clone, Italy [letter]. Emerg Infect Dis. 2009 Jun; [Epub ahead of print]. DOI: 10.3201/eid1506.081632

MRSA in a hospital nursery

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

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

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

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

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

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

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

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

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

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.

MRSA in meat in Louisiana: pig meat, human strain

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On Nov. 3, I posted on an enterprising group of TV stations in the Pacific Northwest who had retail meat in four states tested for MRSA. I said at the time that it was the first finding of MRSA in meat in the US that I knew of.

Turns out that I was wrong by three days. On Oct. 31, the journal Applied and Environmental Microbiology published an electronic version of a study that they will be printing in the paper journal on some future date. Journals do this when a finding is so important or timely that it should see the light immediately, rather than wait through the additional weeks or months of print production.

And this finding is certainly timely. Shuaihua Pu, Feifei Han, and Beilei Ge of the Louisiana State University Agricultural Center have made what appears to be the first scientifically valid identification of MRSA in retail meat in the United States. But — and this is an important point — it is not the swine strain, ST 398, that has been found in meat in Canada and Europe, and in hospital patients in Scotland and the Netherlands, and in pigs in Iowa; and in humans in New York, though that strain was drug-sensitive.

Instead, what the researchers found (in 5 pork and 1 beef samples, out of 120 bought in 30 grocery stores in Baton Rouge, La. over 6 weeks in February-March 2008) was USA300, the dominant community MRSA strain, and USA100, the main hospital-infection strain. In other words, they found meat that had been contaminated during production by an infected or colonized human, not by a pig. As they say:

…the presence of MRSA in meats may pose a potential threat of infection to individuals who handle the food. … (G)reat attention needs to be taken to prevent the introduction of MRSA from human carriers onto the meats they handle and thereby spreading the pathogen.

As we’ve discussed before, the primary danger from MRSA in meat is not that people will take the bug in by mouth (though that is a danger, since S. aureus because of its toxin production can cause severe foodborne illness — and these researchers found, overall, an S. aureus contamination rate of 46% of their pork samples and 20% of their beef samples). Rather, the danger is that people handling the raw meat will be careless in preparing it, and will colonize themselves by touching the meat and then touching their own noses or mucous membranes, leading to a possible future infection. As reader Rhoda pointed out in a comment last week, people could also infect themselves directly, by getting MRSA-laden juice or blood into an abrasion or cut.

So: Be careful in the kitchen, keep meat separate from other foods, wash cutting boards and knives, and (say it with me, now) wash your hands, wash your hands, wash your hands.

The cite for the new paper: Pu, S. et al. Isolation and Characterization of Methicillin-Resistant Staphylococcus aureus from Louisiana Retail Meats. Appl. Environ. Microbiol. doi:10.1128/AEM.01110-08. Epub ahead of print 31 Oct 08.

Housekeeping note: This is the 16th post I’ve written on MRSA in food animals and/or meat. Providing all the links to the previous posts is starting to obstruct the new news. So if you are looking for all those past posts, go to the labels at the end of this post, below the time-stamp, and click on “food.” You should get something that looks like this.

Final report from ICAAC-IDSA 08 (news from ICAAC, 3)

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The ICAAC-IDSA (48th Interscience Conference on Antimicrobial Agents and Chemotherapy and 46th annual meeting of the Infectious Diseases Society of America) meeting ended a week ago, and I’m still thrashing my way through the thousands of abstracts.

Here’s my final, highly unscientific selection of papers that caught my eye:

* Evidence that the community-strain clone USA300 is a formidable pathogen: It first appeared in the San Francisco jail in 2001. By last year, it had become the sole MRSA strain found in the jail — it crowded out all others. (P. Tattevin, abstract C2-225)
* Another paper from the same UCSF research group finds that the emergence of USA300 has caused a dramatic increase in bloodstream infections, most of which are diagnosed in the ER, not after patients are admitted to the hospital. (B. Diep, abstract C2-226)
* And the CDC finds that USA300 is picking up additional resistance factors, to clindamycin, tetracycline and mupirocin, the active ingredient in the decolonization ointment Bactroban. (L. McDougal, abstract C1-166)
* An example of the complexity of “search and destroy,” the active surveillance and testing program that seeks to identify colonized patients before they transmit the bug to others in a health care institution: Patients spread the bug within hours, often before test results judging them positive have been returned from the lab. (S. Chang, abstract K-3379b)
* In addition to the report from Spain I posted on during the meeting, there is a report of emerging linezolid resistance in France. (F. Doucet-Populaire, abstract C1-188)
* And in addition to the abundant new news about MRSA in pork, and “pork-MRSA” or ST 398, in humans, over the past few days, there were reports of MRSA in milk in Brazil (W. Gebreyes, abstract C2-1829) and Turkey (S. Turkyilmaz, abstract C2-1832), and beef and chicken in Korea (YJ Kim, abstract C2-1831), as well as ST 398 itself acquiring resistance to additional drugs. (Kehrenberg, abstract C1-171)
* Echoing many earlier findings that MRSA seems most common among the poor, the poorly housed and the incarcerated, BR Makos of the University of Texas found that children are more likely to be diagnosed with the bug if they are indigent, or from the South (which I imagine is a proxy for lower socio-economic status, since the South is a more rural, more poor region). (abstract G2-1314)
* And finally, to the long list of objects (ER curtains, stethoscopes) that harbor MRSA, here are more: The ultrasound probes in emergency rooms (B. Wessman, abstract K-3377). Also: Dentures. (Ick.) (D. Ready, abstract K-3354)

UK grapples with community MRSA

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Regular readers in the US will have noticed that the MRSA situation here is quite different from Europe. In the UK, for instance, hospital MRSA has been an enormous scandal, but community MRSA — both skin and soft-tissue infections, and fatal invasive infections such as necrotizing pneumonia — has been much less of a concern.

That appears to be changing. Today, the BBC’s Radio 4 broadcast a documentary, “The Bug That Can Kill Within Hours,” that focuses on fears of a dramatic rise in the UK of cases of serious community MRSA. According to the UK’s Health Protection Agency, lab-confirmed cases of community MRSA strains hit 1,361 in 2007, three times what they were the year before. (Soundfile here, starts automatically.)

The documentary refers to CA-MRSA as “PVL-MRSA,” a recognition of the fact that most of the community strains produce the toxin Panton-Valentine leukocidin, or PVL. (PVL is known to destroy white blood cells, but whether it is responsible for the virulence of CA-MRSA is a hotly disputed question in MRSA research.) Aside from the difference in terminology, any of the statements from the accompanying BBC website story could have been said here any time in the past 10 years:

Professor Brian Duerdan, the Inspector of Infection Control at the Department of Health, admits however that many aspects of this virulent bug are a mystery.
“We do know that it spreads in the community amongst close contacts, families, people who share the same sporting events. But we still need to know a lot more about its exact prevalence in the community,” he said.

People who have been tracking the relentless expansion of CA-MRSA, espeially its dominant clone USA 300, are likely to find some of the statements in the documentary both troubling and poignant. The UK is beginning to deal with some of the wuestiosn that the US has struggled with: how much surveillance to do, how to spend scarce research dollars, and what the consequences may be if CA-MRSA is not focused on now.

Hugh Pennington, Emeritus Professor at the University of Aberdeen, and President of MRSA Action, told the BBC that the HPA lacks the resources to keep proper surveillance on outbreaks of infection from this strain of bugs.
“The scandal here is that we know what to do, the technology’s there to spot these things as they are appearing and we know how to react to them.
“It would be quite wrong if we allow these things to develop and of course history tells us that it we do neglect these bugs, we neglect them at our peril.”

Indeed.