Maryn McKenna

Journalist and Author

News break: “Pig MRSA” ST398 involved in the death of a child?

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The latest postings to the website of the CDC journal Emerging Infectious Diseases include a sad and very troubling letter from physicians in Lyon and Paris, reporting the death from necrotizing pneumonia of a previously healthy 14-year-old girl. That would be sad under any conditions, but here’s what makes the death so troubling: It appears to have been caused by MRSA — but not by the community strain, USA300, that has been implicated in a number of deaths from necrotizing pneumonia. (Several such stories are told in SUPERBUG the book.)

Instead, her death appears to have been caused by infection with MRSA ST398 — the livestock-associated strain that was first noted in pigs raised with antibiotics, and the pig-farm workers caring for them, in the Netherlands 6 years ago, and that has since spread across the European Union, Canada and into the United States. (My 3-year archive of ST398 posts is here.)

This may be the first death associated with ST398, though I can’t say that for sure as I am away from my big computer and working without my database. I’ll update later today and confirm or knock that down.

The physicians say that the girl came in with flu-like symptoms and abdominal pain, was put on IV antibiotics (cefotaxime and amikacin), underwent an exploratory laparotomy that showed nothing, and shortly afterward developed acute respiratory distress and was put on a vent. A chest X-ray was shadowy on both sides. She went rapidly downhill and died 6 days later.

On analysis, the staph strain infecting her was ST398; there was no indication where she had picked it up. The strain had an unusual characteristic: It possessed the ability to make the cell-destroying toxin Panton-Valentine leukocidin, PVL for short, a genetic trick that until now has been a property only of community MRSA strains such as USA300. Though its role is disputed, PVL has been linked to community MRSA’s ability to start infections on intact skin, and to the cellular damage that destroys children’s lungs in cases of pneumonia caused by USA300. Until now, ST398 has been PVL-negative.

The physicians’ letter is short and there’s much more to find out about this case. But if the report and analysis are correct, this is bad news. One of the repeated themes in the 50-year evolution of MRSA has been its ability — all staph’s ability — to promiscuously swap and share the bits of DNA that confer resistance and enhance virulence. Another, since the emergence of ST398, has been the potential peril of a staph strain adapting and mutating in the millions of farm animals around the world that are routinely given antibiotics — and that for the most part are not checked to see whether they harbor resistant organisms. If this report (and my interpretation) are correct, then those two trends are converging in a way that cannot bode well.

Once again, flu and bacterial co-infection

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With the H1N1 pandemic trending down, it may seem that the question of how much bacterial co-infection affects the outcome of flu is less important than it was. But though the pandemic is subsiding — for ever, for this season, or just until a third wave, who can say — researchers are just now getting enough good data to be able to make solid observations about what happened during the past 10 months.

Case in point: Writing in the journal Public Library of Science (PLoS) ONE, a team of researchers from Australia has pinpointed the incidence of MRSA co-infection during flu in two hospitals in Perth last summer, which was the Australian winter and the height of their flu season. Of 252 patients admitted for H1N1 infection, 3 were identified during treatment as having MRSA pneumonia. They survived, but two other patients who died were found to have MRSA pneumonia during post-mortem exams.

There were 3 female and 2 males, aged between 34 and 79 years… Two patients lived at the same long-term care facility, whilst the other patients lived independently in the community. Four of the 5 patients had conditions that may have increased their risk of pneumonia, including quadriplegia (two patients) asthma (one patient), cirrhosis (one patient) and diabetes mellitus (one patient). Two of the 5 cases (patients 3 and 4) had known MRSA infection/colonization prior to the onset of their illness (with the same cMRSA clone that subsequently caused their co-infection).

 There are some interesting points embedded here. First, incidence: In the Australian patients, MRSA pneumonia was much more common. The Perth researchers found 5 MRSA cases out of 252 flu patients. When the CDC analyzed the occurrence of MRSA pneumonia in flu last summer, it found only 1 case out of 272. Second, treatment: None of the 5 patients got antibiotics that would have affected MRSA — even though two of them were already known to be MRSA carriers. The possibility of MRSA pneumonia subsequent to flu seems not to have occurred to the health professionals taking care of them.

And third, the pathogen: The 5 Australian cases were caused by 3 community MRSA strains that are common in Australia — but only one of the 3 made PVL, the toxin that has so frequently been associated with MRSA pneumonia. That is interesting, and troubling at the same time. At this point, the association of PVL and necrotizing pneumonia has become practically taken for granted; and yet here are two strains that did not make PVL and yet caused severe and fatal pneumonia. It may be an indication that the inflammation that flu causes in the lung can open the door to more severe damage even when PVL is not present; it’s certainly an indication that the absence of PVL does not signal a mild or not-dangerous strain.

The cite is: Murray RJ, Robinson JO, White JN, et al. 2010 Community-Acquired Pneumonia Due to Pandemic A(H1N1)2009 Influenzavirus and Methicillin Resistant Staphylococcus aureus Co-Infection. PLoS ONE 5(1): e8705. doi:10.1371/journal.pone.0008705.
Simultaneously, a new paper in the American Journal of Pathology seeks to clarify how often and in what circumstances bacterial superinfection becomes a risk during flu. Using a range of mice — both healthy ones, and “knockout” mice bred to be without particular immune-system components — researchers from San Diego confirmed that infections with flu and with Haemophilus influenzae can be lethal when the flu infection precedes the bacterial one. That was true even for infections that, if experienced separately, would not have been lethal; it was the synergy of the two infections, flu first followed by the bacterial infection, that caused the high mortality rate. The results may not be directly applicable to human medicine (Do you all know the old flu-research saying, “Mice lie and ferrets mislead?”), but they are an important indicator both of the seriousness of bacterial infection after flu, and also of the potential vulnerability of even healthy beings to that one-two punch.
The cite is: Lee LN, Dias P, Han D, et al.: A mouse model of lethal synergism between influenza virus and Haemophilus influenzae. Am J Pathol 176: 800-811.

While taking a flu break, a MRSA round-up

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Constant readers, the H1N1 (Virus Formerly Known as Swine) Flu story remains a bit intense. I’ve missed a few MRSA stories over the past few days, so here is a round-up.

First, though, if you’re curious about what the swine flu reaction says about our ability to handle a pandemic, you might take a look at this story I wrote Friday at CIDRAP. Quick version: Over-reaction on the part of the “worried well” — and people seeking testing and not knowing where to get it — put ERs into meltdown nationwide. If we were facing a virus that was not only fast-spreading but virulent, we could be in serious trouble.

On to MRSA:

  • Therapy animals as a vector: In a letter to the Journal of Hospital Infection, Drs. J. Scott Weese and Sandra L. Lefebvre of the Ontario Veterinary College at the University of Guelph report on two therapy dogs that became transiently colonized with C. difficile (on its paw pads) and MRSA (on its coat; found on the hands of its handler) after visiting health care facilities, demonstrating how easily bacteria can move in and out of hospitals. Constant readers will recognize Weese’s name: He is one of the most important investigators of MRSA in food animals and pets, and among other things has written infection-control guidelines for therapy animals.
  • In the Canadan Medical Association Journal, Drs. Anne G. Matlow and Shaun K. Morris of the University of Toronto and the Hospital for Sick Children caution that while hospitals may be getting better at infection control, there is not yet as much attention to it as there should be in ambulatory-care settings: urgent care centers, surgery centers and doctors’ offices. They offer a checklist of the minimal things that a physician practice should do.
  • And in the UK, Baroness Masham of Ilton, a member of the House of Lords, offers her online notes on serious infections with community MRSA, which the Brits are calling PVL-MRSA in recognition of the toxin that the strain produces. The notes are in advance of a series of questions that she intends to pose to government ministers during a Question Time on Wednesday.

More soon.

“Sick as a pig” – from ST398

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

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

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

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

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

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

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

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.