Maryn McKenna

Journalist and Author

A parent's plea and confusion

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I want to highlight a comment that was left on Labor Day by a woman named Valorie in Arkansas (thank you for reading, Valorie). She said:

I am just now learning about all of this and am very concerned about my 12 year old daughter. We were only 10 days into the school year, and she came down with the flu about a week ago. The rate at which it spread within her school as well as to me (her mother) and 2younger siblings was astonishing! We were all running high fevers within 24 hours of the onset of her first noticeable symptoms. Her junior high (which has approximately 500 students) had between 130 and 140 students absent last week due to flu like symptoms. However, the school is saying this is not H1N1 because it is too early in the season to be the actual flu. (This is absurd in my opinion.) Now, on our oldest daughter’s 5th day into the illness she has developed an MRSA infection from a small boil on her tummy. Within a day, it has swollen from a golf ball size to larger than a baseball in size. She now has 2 places of infection and is running a fever of about 101.7 on her 6th, almost 7th day of illness. Her doctor has placed her on a high powered antibiotic, but she is feeling so ill that I am scared to death for her, especially reading about the complications from having both the flu and MRSA. Do you think the oral antibiotics should take care of it, or do you think we need to have her admitted for IV antibiotics. I’ve just been surprised at how long this illness has lasted and how ill she still seems to be. No one seems to want to talk about the flu, much less any other possible complications in order to keep everyone else from panicking. I just want to get my daughter well and keep her safe. Any advice? Thanks so much for your time.

I wanted to highlight Valorie’s comment for a couple of reasons.

First, because it captures the way in which H1N1 has been ripping through schools in most places where school has returned to session. Schools in the Southeast tend to go back before the Northeast or the West; in Atlanta, where I used to live and where schools reopen long before Labor Day, H1N1 has gone through schools like a hot knife. Second, it shows how little the education about flu being pushed out by the CDC (and by others including my colleagues at CIDRAP) has penetrated: There has been H1N1 flu all over the place this summer, and it’s precisely because it is “too early in the season” that we know it is H1N1 and not the seasonal flu.

But what is most concerning and touching is Valorie’s confusion over which drugs her daughter should be taking, and whether her daughter’s physician is giving enough attention to her illness. Despite years of clinical experience, figuring out which drugs to give for MRSA is not easy. That’s first because many of them are old and now generic-only drugs for which clinical trials (in the context of this disease) were never done; and second because community MRSA’s resistance profile keeps changing as it picks up additional resistance factors.

The CDC dealt with this problem of what drugs to give in a meeting held in 2004 and a report issued in 2006. The report, going drug by drug, is here (caution, it’s 24 pages) and a flow chart summarizing the findings is here. Either is useful to have and to take to doctors if you feel uncomfortable about what is being prescribed or about a patient’s lack of progress.

Valorie, I hope your daughter does better. Keep us posted.

Child deaths from flu + MRSA: CDC confirmation

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Hello again, constant readers. It’s been an exciting few weeks at Casa Superbug. I’ll spare you the details — most of them are both grueling and trivial — but out of the murk, here is a piece of excellent news: SUPERBUG has been edited, revised and sent back to the publisher, who has sent it into production. Yes, it’s actually beginning to become a book. There are many more steps to go, but it it is finally, really on its way.

Meanwhile, there is a ton of MRSA news to catch up on, which I will roll out over the next week or so. First: For those of you who don’t read the CDC’s weekly bulletin (called the MMWR, for Morbidity and Mortality Weekly Report. It’s the best-read magazine you’ve never heard of. It’s free. Go already), there was an important and disturbing report last Friday, reporting the case details of children who have died from H1N1 flu.

As of August 8, the CDC said, 477 people had died in the US from H1N1, and 36 of them were children and teenagers. Out of those 36:

  • 7 were younger than 5
  • 24 had at least one high-risk medical condition, many of them neurological (developmental delay, cerebral palsy) or pulmonary; 12, or one-third, did not
  • 23 had some pathologic analysis done during their illness or after their deaths
  • 10 had bacterial co-infections
  • of those 10, 5 had staph infections
  • 3 of the staph infections were MRSA.

Let’s bring the first and last terms of that equation together: 36 children; 3 known MRSA infections. Though it could be an underestimate (because 13 children had no pathology done), that is a non-trivial 8%.

The report splits the data on the child deaths a number of different ways, and reveals details that are important to note. Six of the bacterial infections (four staph) were in children older than 5 who did not have any underlying conditions; they were healthy, normal kids before developing flu. Of the 7 kids younger than 5, 2 had a bacterial infection; again, neither child had a high-risk condition.

How worrisome are these numbers? It’s hard to say with precision, but they are certainly not good news. The CDC has only been counting child deaths from flu for a few years, and the totals they have come up with are very variable: 153 in 2003-04, 47 in 2004-05, 46 in 2005-06 and 73 in 2006-07. But, important point: Those deaths were during the regular flu season, which goes from roughly October to March. These new deaths occurred between late April and early August, when there is not supposed to be any flu. What this will mean for this fall and winter, when H1N1 will still be around, and may co-circulate with seasonal flu, no one yet can say.

For our purposes, the most important point is that lethal MRSA co-infections are now confirmed to be happening in the setting of H1N1 flu. And, as the CDC paper notes, these infections happened in children who would not have been expected to have a tough course, because they had no underlying high-risk conditions:

This report also highlights the prominence of laboratory-confirmed bacterial coinfections, which were identified in 10 (43%) of the 23 children who had culture or pathology results reported. All six children who were aged ≥5 years, did not have a high-risk medical condition, and had culture or pathology results reported had an invasive bacterial coinfection, suggesting that bacterial infection, in combination with 2009 pandemic influenza A (H1N1) virus infection, can result in severe disease in children who might be otherwise healthy. Clinicians should be aware of the potential for severe bacterial coinfections among children diagnosed with influenza and treat accordingly.

Obviously those of us who are concerned about MRSA and the potential for MRSA pneumonia alongside flu have been worried about this (long archive of posts here). If there is any good news in the sad saga of these deaths, it is that the CDC has confirmed that MRSA pneumonia in H1N1 flu is a real and dangerous possibility.

So if you are concerned about this, first, bookmark the MMWR report, because it will be something to show to a physician if necessary. And second, keep in mind the potential for pneumonia if you have a young child who contracts H1N1. I am not suggesting being alarmist; if H1N1 circulates widely, doctors and ERs will be overwhelmed, and we should try not to add to their case load unless really necessary.

But on the other hand, if a child has chest pain or breathing difficulty, don’t hold back. There are online tools such as this one by Children’s Healthcare of Atlanta that can help a worried parent assess whether and when a child with flu should be taken to the ER. If you click through its steps, you’ll see that breathing difficulties and the possibility of pneumonia are things that it takes seriously, and so should we.

Another death from H1N1 flu + MRSA

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Thanks to a commenter who alerted me to this sad story: A teenager in Austin died of a combination of H1N1 flu and MRSA pneumonia. Constant readers will know that we have been watching for this for a while; MRSA pneumonia is a known and dangerous complication of any flu infection.

For stories for CIDRAP and the Annals of Emergency Medicine, I’ve been talking to ER physicians about their expectations for the fall, when the regular flu season begins and H1N1 is expected to intensify. (A friend’s school already has cases circulating.) It’s fair to say that emergency departments are unsettled about the possibility of severe complications from this flu.

One more set of recommendations

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… and then next week I’ll be back to analyzing the medical literature: A stack of interesting new journal articles is threatening to topple and bury my computer.

For the moment, though:

First, the Hearst newspapers chain has conducted a nationwide investigation into medical errors that should be required reading for anyone who wonders why hospitals can’t do a better job controlling hospital-acquired infections. It is a 7-part series focusing on the 5 states (New York, Texas, California, Connecticut, Washington) where there are Hearst papers, and hosted on the site of the San Francisco Chronicle. The introductory article says:

Ten years ago, a highly publicized federal report called the death toll shocking and challenged the medical community to cut it in half — within five years.
Instead, federal analysts believe the rate of medical error is actually increasing.
A national investigation by Hearst Newspapers found that the medical community, the federal government and most states have overwhelmingly failed to take the effective steps outlined in the report a decade ago.
… in five states served by Hearst newspapers — New York, California, Texas, Washington and Connecticut — only 20 percent of some 1,434 hospitals surveyed are participating in two national safety campaigns begun in recent years.
Also, a detailed safety analysis prepared for Hearst Newspapers examined discharge records from 1,832 medical facilities in four of those states. It found major deficiencies in patient data states collect from hospitals, yet still found that a minimum of 16 percent of hospitals had at least one death from common procedures gone awry — and some had more than a dozen. (Byline: Cathleen F. Crowley and Eric Nalder)

From that opening statement, the investigation goes on to explore many patient stories that individually are tragedies and collectively — as we here know all to well — are a scandal.

There is just one notable MRSA story in the mix, the death of a retired hospital president who contracted the bug in his own hospital. But they are all worth reading.

Second, an executive and apparently new writer named David Goldhill has written for The Atlantic a passionate and well-thought out piece on his father’s death from a hospital-acquired infection and on what needs to change for such deaths to never happen again. “My survivor’s grief has taken the form of an obsession with our health-care system,” he writes:

My dad became a statistic—merely one of the roughly 100,000 Americans whose deaths are caused or influenced by infections picked up in hospitals. One hundred thousand deaths: more than double the number of people killed in car crashes, five times the number killed in homicides, 20 times the total number of our armed forces killed in Iraq and Afghanistan. Another victim in a building American tragedy.

You may not agree with his conclusions, but it is worth reading through to the end to experience how one intelligent citizen from outside health care understands and attempts to re-think our broken system.

Catching up on some reading: health care reform, food bugs, vaccine, MRSA+flu

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Folks, while I was caught in travel hell, some excellent stories and blogposts were released. Here’s a quick round-up of recommendations for a rainy weekend:

  • At Roll Call (covers Congress like a blanket), Ramanan Laxminarayan, PhD MPH, of the rational-use-of-antibiotics project Extending the Cure and infection-control physician Ed Septimus, MD make a strong argument for including control of hospital infections in health care reform. Hard to argue against when you realize that HAIs cost the United States more than $33 billion each year.
  • At Meat Wagon, a blog of the online magazine Grist, the always-excellent Tom Philpott digs into the ongoing outbreak of antibiotic-resistant Salmonella in hamburger meat. Key quote: “Outbreaks of [antibiotic-resistant foodborne illnesses] are really ecological markers — feedback that our way of producing meat is deeply unsustainable and really quite dangerous.”
  • The Associated Press reports that the long-in-development staph vaccine made by Nabi Pharmaceuticals may have received a second life: It’s been purchased by international pharma giant GlaxoSmithKline in a $46-million deal.
  • And finally and sadly, the Sacramento Bee reports that a California nurse who died of H1N1/swine flu also had MRSA pneumonia. Karen Ann Hays, 51, died despite being extremely healthy: she was a triathlete, skydiver and marathon runner. No one yet has been able to say whether she caught the flu — or MRSA — at work (though her partner believes that to be true), but her death has fueled disquiet among members of the California Nurses Association, who are protesting a lack of protective equipment for nurses.

For those of us concerned about MRSA pneumonia — and we have been talking here since the start of the H1N1 pandemic about the danger of MRSA co-infection — that last item about Hays’ very sad death should underline a vital point. Public health authorities have been stressing that H1N1 is most deadly when the infected person has a pre-existing condition: pregnancy, heart disease, obesity, diabetes, cystic fibrosis. It is possible that MRSA infection is also a pre-existing condition that will put anyone infected with flu at risk of deadly complications.

If you have had MRSA, even a minor skin infection — and especially if you have experienced recurrent infections — you should probably discuss with your personal physician whether you should take the H1N1 vaccine when or if it becomes available. It could be the step that prevents a minor case of flu from tipping over into something much more serious.

Decolonization: disappointing news

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I know that many of you who are MRSA patients, especially with recurrent infections, are especially interested in the issue of decolonization, the grueling regimen of antibiotic nasal gel (containing mupirocin; usually sold as Bactroban) combined with body washes with chlorhexidine (Hibiclens) that is believed to eradicate MRSA carriage in the nose and on the skin. Decolonization is an essential part of the “search and destroy” measures practiced by zero-tolerance hospitals who want to detect any MRSA transport in their institution, and it is a last-ditch hope in recurrent community-strain infections. (I told the story of several women’s struggles with recurrent infections in SELF and Health magazines.)

It’s disheartening, then, to realize that decolonization is not a universally agreed-upon measure, and there is relatively little research that can say in which setting (household, hospital, ICU) it works best, and why. There have been a few studies, and a few review papers summing up studies, on the role that decolonization can play in reducing the risk of infection in already hospitalized, colonized patients — ones about to undergo surgery, for instance. A meta-analysis by the Cochrane group, of 8 trials, found that decolonization in the hospital did reduce the likelihood of infections in surgical patients.

The role that decolonization can play in short-circuiting community infections is much less clear, though there are many, many people who have suffered recurrent infections and testify that it worked for them. (Please speak up in the comments if you are!) One problem is that outside hospitals, there is no one recommended regimen: One physician might tell her patient to use mupirocin and chlorhexdine only, whereas another might tell his patient to also take bleach baths, or bleach all the laundry or household surfaces. The CDC has so far declined to put its muscle behind decolonization in community-strain infections, recommending only that frustrated patients with recurrences seek the advice of an infectious-disease specialist. (See this flowchart of treatment options (.pdf) that the CDC published in 2007.)

Comes now the infectious-diseases division of Evanston Northwestern Healthcare, whom some of you will recognize as being among the most successful and evangelical practitioners of “search and destroy” in the United States. (ENW has recently been renamed NorthShore University HealthSystem and is affiliated with Northwestern University. Disclosure, in case you care: I went to grad school at Northwestern, though not in medicine.) In a paper published in Infection Control and Hospital Epidemiology, the group evaluates the use and success rate of decolonization in ENW/NorthShore’s 3 hospitals and finds, well, not such good news: a temporary reduction in patients’ being colonized with MRSA, but no success in preventing infection.

This is an important and troubling finding, because decolonization comes with costs. There is the obvious cost to hospitals (and the follow-on cost to insurance companies and consumers) of paying for mupirocin and chlorhexidine themselves. But there is also a hidden cost that we here should be particularly sensitive to: Because mupirocin is being used so lavishly, mupirocin resistance is rising.

In the same issue of ICHE (which, yes, is pronounced Itchy), a related editorial by Dutch researchers reviews the difficulty of conducting decolonization trials, but summarizes the ENW/NorthShore study as not an endorsement of decolonization regimens:

It is clear that staphylococcal carriage is an important risk factor for infection and that eradication of carriage has proven successful for patients who are undergoing elective surgery. For other groups of patients, it is still unclear what the benefits are. It is obvious that indiscriminate use of mupirocin is associated with development of resistance. Therefore, additional studies are warranted to define the optimal MRSA decolonization strategy, including what should be given, to whom, and at what moment and who should guide and supervise the regimen.

The cites are:
Robicsek A, Beaumont JL, Thomson RB Jr et al. Topical therapy for methicillin-resistant Staphylococcus aureus colonization:impact on infection risk. Infect Control Hosp Epidemiol. 2009 Jul;30(7):623-32.
Kluytmans J, Harbarth S. Methicillin-resistant Staphylococcus aureus decolonization: “Yes, we can,” butwill it help? Infect Control Hosp Epidemiol. 2009 Jul;30(7):633-5.

New England Journal editorial: MRSA, H1N1 parallels

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There’s a very interesting piece in a recent New England Journal of Medicine (unfortunately, only the abstract is online) that draws parallels between MRSA and public expectations for pandemic flu. Written by Dr. Kent Sepkowitz, chief of infection control at Memorial Sloan-Kettering Cancer Center in New York and one of the authors of the “Medical Examiner” column at Slate, it’s an exploration of microbial sleight of hand: We were looking in one direction for a problem to develop, and — like Wile E. Coyote staring after the Road Runner but missing the Acme anvil — the problem came around and socked us in the back of the head.

In the case of flu, Sepkowitz writes, we concentrated on the threat of H5N1 avian influenza — the focus, until H1N1/swine flu arrived, of billions of dollars and years of effort in pandemic preparation — but were surprised by the sudden catastrophic emergence of seasonal flu strains resistant to oseltamivir (Tamiflu), one of the few antiviral drugs that can reduce illness and death from flu if taken early enough. In the case of MRSA, medicine focused on containing the spread of hospital MRSA and its rare transformation into VRSA, vancomycin-resistant staph — and mostly discounted, until far too late, the enormous threat of community MRSA strains:

The intensity of our concern and the frequency of the doomsday dispatches were appropriate. We were simply chasing the wrong microbe. It is community-acquired MRSA, not VRSA… that now occupies the center of the public health stage. And just about everything predicted for VRSA has come true for community-acquired MRSA. It’s everywhere; it’s deadly; it has changed the day-to-day management of skin infections and pneumonia in clinics, emergency rooms and intensive care units. It’s a true public health disaster. It’s just a different disaster from the one we were exercised about.

As we wrangle the new threat of H1N1, Sepkowitz warns that it is vital to remember how many millennia of practice microbes have in foiling our expectations:

We should marvel at the raw, restless power of microbes. They have the numbers — trillions and quadrillions and more that replicate wildly, inaccurately and disinterestedly. Nothing microbes do, whether under the duress imposed by antimicrobials or from some less evident pressure, should surprise us. It’s their world; we only live in it.

(Image courtesy Sansceo Design)

Bad news from California

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Constant readers, some of you may be aware that one major nexus of MRSA infection gets very little attention, though I’ve tried to raise it here periodically. That’s MRSA in jails and prisons: Thanks to poor hygiene and extraordinary overcrowding, jails and prisons are hotbeds of the bug, and it is very common for people to develop an infection after they are incarcerated, and then to be unable to shake it because they cannot keep up with hygiene, cannot get access to a doctor, etc.

Some commenters, here and elsewhere online, have suggested that this is no more than prisoners deserve. This seems to me both extraordinarily uncompassionate and epidemiologically foolish. In case no one has noticed, prison overcrowding is so serious that many prisoners don’t stay in prison for their sentenced time. And when they come out, and come back to their communities, they bring MRSA with them. That’s not even to mention the risk to the very large numbers of people who are not themselves incarcerated, but go in and out of jails and prisons every day: correctional officers, cooks, medical staff, and on and on.

All of which makes the news from California on Friday more than usually depressing.

Prison medical care in California has been so bad (see Gov. Arnold Schwarzenegger’s 2006 emergency declaration) that it is no longer under control of the state, but rather administered by a court-appointed receiver, who said in 2007:

Across the board we see delays in diagnosis and access to care and needed tests; misfiled, incomplete or illegible medical records; lack of space, sanitation and staffing; botched hand-offs of medical information during inmate transfers; failures by clinicians to recognize and evaluate “red flag” symptoms, follow published guidelines, perform basic physical examinations or respond to patient complaints; abdication of responsibility for patient care and lack of critical thinking or requests for help in difficult cases.

The prevalence of MRSA in California prisons is an important part of that picture : Correctional officers have sued over MRSA they acquired at work. (And yes, you can read all about it in SUPERBUG.)

Now, you may also know that California is in the midst of a gruesome budget crunch — and on Friday, the push for better prison medical care and the deficit in the state budget collided, and the deficit won. According to the Associated Press and the San Francisco Chronicle, the Schwarzenegger administration backed off an agreed-upon plan that would have ended the receivership and returned control of the medical system to the state at a cost of $1.9 billion, one-fourth of what was originally thought to be needed.

Schwarzenegger said in a statement Thursday that California cannot afford the additional cost.
“We cannot agree to spend $2 billion on state-of-the-art medical facilities for prisoners while we are cutting billions of dollars from schools and health care programs for children and seniors,” he said.
Schwarzenegger and lawmakers are considering eliminating or significantly reducing education, state parks and core social programs to address the $24.3 billion budget shortfall. (AP, byline Don Thompson)

The Chronicle story makes clear that the prison spending would not have made the deficit any worse, because the money was coming from new bonds, not from the state’s general fund. Its online commenters don’t seem to have paid attention to that, as they hit the same familiar themes:

  • “Why should the public have to babysit them for the medical problems they brought on themselves… Let them rot.”
  • “In my opinion bad medical services in prison should be only one of the deterrents that keeps one from wanting to go to jail. “
  • “Prison should be a place that is so intolerable, that no sane person would ever want to go there.“

It’s easy to moralize. It’s much harder, as we know here, to control the continuing spread of a microbe that has already gotten a solid foothold in the community. California’s decision to not improve medical care in its prisons — and therefore not address the threat of MRSA to its prisoners and staff — is practically a guarantee that the state’s already substantial community MRSA problem is going to get much worse.

Restricting antibiotics in animals: Start by restricting access

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Constant readers, those of you who follow the pressing issue of MRSA in animals will know the work of J. Scott Weese, DVS, associate professor of pathobiology at the University of Guelph in Ontario and supervising author of many crucial papers on MRSA in food and companion animals, including the first finding of MRSA in pigs and pig farmers in North America.

You may not know that Weese and his postdoc Maureen Anderson publish an excellent blog on veterinary and zoonotic diseases called Worms and Germs. This weekend they have an important post that deserves wider attention: Antibiotics: A Dose of Common Sense. In it, they propose that one way to reduce the overuse of drugs in food animals is to make animal antibiotics prescription-only. It’s worth taking the time to read it.

Those of you in the cities may not know this, but out here in the Great Flyover, antibiotics for veterinary use are surprisingly easy to buy (as I discovered when I stumbled into a farm-related store in search of a Carhartt jacket against the Minnesota winter). They’re not even over-the-counter — they’re on the shelf, or stacked on the floor with the implements and feed, or blended into the feed itself. And as Weese points out in this post, they are also available without prescription over the Internet (as human antibiotics are too).

It’s a potentially controversial proposal: I don’t think I have any farming readers, but I would imagine their response would start with an objection to the extra cost of hiring a veterinarian to assess whatever situation might require the drugs. And since most farmers (NB: not the overarching ag-biz companies, but the farmers themselves) exist on razor-thin economic margins, they would have a point. But as we know from the excellent work of Extending the Cure and the Center for a Livable Future, unnecessary antibiotic use comes with a cost as well — one that is borne by all of us when antimicrobial resistance prevents antibiotics from working.

MRSA legislation in Congress

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Readers, on Monday, Rep. Jackie Speier (D-CA, 12th District) introduced a bill: HR 2937, the MRSA Infection Prevention and Patient Protection Act.

It requires:

  • hospitals to screen all patients entering high-risk units for MRSA infection
  • adoption of best practices including contact precautions among health care professionals to prevent MRSA’s spread within hospitals.
  • patients testing positive for MRSA be informed of the result and given instructions on how to prevent the spread of their infection when discharged.
  • hospitals to report the number of cases of hospital-acquired MRSA that occur within their facilities.

In other words, it seeks to enact nationally what advocates such as Jeanine Thomas, Carole Moss, Michael Bennett and others have done in individual states. (Find their organizations in the right-hand column.)

Speier’s announcement is here and the text of the bill is here.

MRSA and pets

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It’s been a while since we’ve focused on the presence of MRSA strains in pets, and the complications that can cause for the pets’ human owners/custodians/companions (or, in the view of my own two cats, abject servants. No, I will not post their pictures. I have some shreds of pride).

The problem with MRSA and pets is not the same as the problem of MRSA ST398 in food animals. Rather, pets tend to carry human strains, passed to them by their owners. The carriage is usually asymptomatic, but not always; there are cases in the medical literature of cats and dogs suffering serious skin and soft-tissue infections from community-strain MRSA, usually USA300. But the emerging consensus seems to be that pets carry the bug transiently — not long, but long enough to reinfect the person who passed the bacterium to the pet in the first place. (This can be, but is not always, the source of recurrent infections in humans: The human takes antibiotics and recovers, but the animal holds onto the bug long enough to pass it back to the now-clear human.)

For anyone who needs to go deeper on this, the current issue of Lancet Infectious Diseases has a good overview of the problem that community MRSA strains pose to pets and their humans. There’s a thorough review of the major papers:

  • Cefai, 1994: hospital outbreaks traced to two nurses and through them to their dog
  • Simoons-Smit, 2000: household epidemic of three humans, one cat, one dog
  • Manian, 2003; dog is source for owner’s recurrences
  • Vitale, 2006: owner is (apparently) source of cat’s MRSA.

(This is a good place to say that this entire history, including personal stories of human and animal infection, is covered in a chapter of SUPERBUG. Publication date coming soon!)

The Lancet paper incorporates reminders of some powerful and troubling trends. As with MRSA ST398, one thing can distinguish MRSA that has been in an animal is a resistance pattern that is slightly different from what we expect but that has arisen because the animals receive different drugs. In the case of pigs and ST398, the intriguing marker is tetracycline resistance; humans don’t usually get tetracycline for MRSA, but pigs do. In the case of companion animals, it tends to be fluoroquinolone resistance; pets are more likely to get that class of drugs for a skin/soft-tissue infection. But, the authors caution, that may mean that pets serve as a breeding ground for multi-drug resistant MRSA, with their fluoroquinolone treatment adding another resistance factor into the bug’s already potent arsenal.

The authors also remind us that MRSA can come from animals much more directly than through silent carriage: that is, in a bite. Both dog and cat bites have been found infected with MRSA, due to bacterial contamination of the wound either from the pet or from colonization on the human’s skin.

The cite is: Oehler RL et al. Bite-related and septic syndromes caused by cats and dogs. The Lancet Infectious Diseases, 9(7):439 – 447, July 2009. doi:10.1016/S1473-3099(09)70110-0.

H1N1 and MRSA – first disclosed case

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Readers, once again there’s a lot of MRSA-related news piling up, and I’ll try to roll some of it out over the next few days. But first, today we have to deal with an event that many of us have been anticipating, though not with any pleasure: the first known report of a MRSA death secondary to H1N1 “swine” flu infection.

We’ve talked about this possibility for weeks, because bacterial pneumonia, especially due to MRSA, is a known and frequently deadly follow-on to flu infection. (Archive of posts here.) With swine flu so common, CDC has said several times that they have been looking for post-flu bacterial pneumonia, but had not seen it. And commenters to this blog have relayed rumors — or, to be more precise, stories with no names attached — of flu patients so ill with MRSA that they have to be put on an ECMO, what we used to call a “heart-lung machine,” and sometimes do not come off.

Today, however, the Buffalo News carries the story of a New York State teen’s death from MRSA pneumonia as a sequela of flu:

Matthew Davis was a healthy Buffalo teenager who participated in sports before complaining of headaches June 13.
Within a few days, the 15-year-old student at Harvey Austin School 97 on Sycamore Street arrived seriously ill at Women & Children’s Hospital and then died Saturday, making him the first known fatality in Erie County caused by swine flu, officially known as novel H1N1 influenza.
… By the time Matthew entered the hospital, he was seriously ill with the flu, as well as co-infected with a type of bacteria known as methicillin-resistant staphylococcus aureus, or MRSA, according to health officials. (Byline Henry L. Davis)

Under normal circumstances — as in, during the past flu season — the public health advice has been to protect against MRSA pneumonia by getting a flu shot, which by preventing flu prevents the microtrauma to the lungs that allows MRSA and other bacteria to gain a foothold. In this case, though, with no H1N1 vaccine available, ir’s not clear what protective actions could have been taken.

Still, it’s terribly sad.

H1N1 flu and swine surveillance – more relevance for MRSA

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Constant readers, you probably know that yesterday the World Health Organization declared the first flu pandemic in 41 years. I want to point out for you a side issue in the H1N1 story that has great relevance for MRSA, especially ST398.

As described in this article I wrote last night for CIDRAP, three medical journal articles have now pointed out that the virus, or its major components, could have been recognized in swine months to years ago. We missed it, though, because there is so little regular surveillance in pigs for diseases of potential importance to humans. As the authors of the most recent article, in Nature, said yesterday: “Despite widespread influenza surveillance in humans, the lack of systematic swine surveillance allowed for the undetected persistence and evolution of this potentially pandemic strain for many years.”

This is important for our purposes because we know that we are in the same situation with MRSA ST398: The strain was first spotted in France, and has been a particular research project in the Netherlands, but has been found pretty much wherever researchers have looked for it, throughout the European Union, in Canada, and most recently in the United States. All told, though, the scientists concerned with it are still a small community; there is no broad surveillance looking for this bug.

And that’s a problem, for MRSA, for influenza, and for any number of other potentially zonotic diseases: We cannot anticipate the movement of pathogens from animals to humans if we don’t know what’s in the animals to start with. That’s the argument behind the “One Health” movement, which has been arguing for several years now for including veterinary concerns in human health planning. (The human health side would probably say that the animal health side just wants more money. This is also true, which does not make it unimportant.)

To understand the need to look at animal health in order to forecast threats to human health, you can’t do better than the map I’ve inserted above (because Blogger, annoyingly, won’t let me put it below). It has appeared in various forms in various publications for about 10 years but originates I think from the IOM’s Emerging and Reemerging Diseases report in the early 90s. (This iteration comes from the One Health Initiative website.) It depicts the movement of new diseases from animals to humans over about 30 years. It’s up-to-date through SARS and through the 2003-05 movement of H5N1 avian flu around the world. I’m sure H1N1 will be added soon. How many of those outbreaks could we have shortcircuited if we had been warned of their threat in good time?

Farm animals and antibiotics – a new campaign

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I was gobsmacked to discover today, a few days late, that the Pew Campaign on Human Health and Industrial Farming (authors of the report discussed here) have launched a marvelously in-your-face series of ads in Washington DC, aimed at bringing the issue of antibiotic use in farm animals to people who might not think about it.

The ads have been placed in the Capitol South and Union Station Metro stops, which are the stops that bracket Capitol Hill, and in Metro cars on the red and blue/orange line trains, which are the main commuter trains down to the Hill. In other words, they’ve been made to be the morning reading of the people most engaged in the health reform debate right now — and if you think those folks are not thinking about healthcare spending and the growth of antibiotic resistance, well, umm, oh never mind.

The campaign says:

The American Medical Association, the American Academy of Pediatrics and other leading medical groups agree that the growth of bacterial infections resistant to antibiotic treatment is a looming public health challenge. The groups also agree the misuse of antibiotics on industrial animal farms plays a significant role in this crisis. While antibiotics are prescribed to people for short-term disease treatment, these same critically important drugs—like tetracycline, erythromycin and ciproflaxin—are fed in low doses to large herds or flocks daily, often for the lifespan of the animal. This creates ideal conditions for the breeding of new and dangerous antibiotic-resistant bacteria.

For statistics and arguments, along with more images — cows! chickens! pills! — go to the site of the commission’s campaign, Save Antibiotics.

MRSA in pig-farm workers – very high rates

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Let’s go back for a moment to what I think of as the “third epidemic” of MRSA: ST398 and the other strains that reside in animals and cross to humans. (In my personal taxonomy, the first and second epidemics are hospital-acquired and community-associated.)

Via Emerging Infectious Diseases, the open-access journal published by the CDC (Do I have to keep telling you to read it? It’s free. It’s good. Your tax dollars pay for it.), comes a report of surveillance for MRSA colonization of pig-farm workers, conducted in Belgium by researchers from Erasmus Hospital of the Free University of Brussels, and the Veterinary and Agrochemical Research Centre of Brussels. The group persuaded 127 farm workers on 49 farms to be tested for colonization, or asymptomatic carriage, of MRSA; at the same time, they tested 30 randomly selected pigs on each farm.

They found very high rates of colonization, higher than have been found in patients in hospitals or residents of nursing homes: 38% of the farm workers carried MRSA ST398, the pig strain (plus, an additional 17% carried various strains of MSSA, drug-susceptible staph). There was a clear association between colonized farmers and colonized pigs: Out of 1500 pigs sampled, 44% carried ST398 — and half of the workers on farms with colonized pigs were colonized also, compared to only 3% of workers on farms where pigs did not carry the bug.

In a bit of good news, the researchers found only one farm worker who had suffered any MRSA disease from ST398, a man with a lesion on his hand. There was no invasive disease, though ST398 has been associated in the past with pneumonia and endocarditis.

Workers were more likely to acquire the bug if they had regular contact with pigs, dogs or horses, which makes intuitive sense. But in an odd finding, their odds of acquiring ST398 did not go down if they wore protective clothing — which is to say, aprons, gloves and masks did not protect them from picking up the bug, leading the researchers to wonder whether airborne spread or contaminated surfaces are playing a role in transmission.

So what does this mean? The lack of invasive disease in this population must be good news; and it’s consistent with a number of papers that have reported low rates of disease from ST398 even when colonization is present. But to me, the high rate of colonization must be bad news. The more of this bug there is (and every researcher who looks for it seems to find it), the more chance there is of the bug adapting in an unpredictable — potentialy more resistant, potentially more virulent — way. If that did happen, it could well go undetected for a while — because as swine flu has been teaching us, disease surveillance in animals is patchy at best, and new pathogens can and do arise and ciruclate for years before being detected.

For more on the paucity of surveillance in animals, see my CIDRAP colleague Lisa Schnirring’s story here. For a complete archive of posts on “pig MRSA” ST398, go here.

The cite is: Denis O, Suetens C, Hallin M, Catry B, Ramboer I, Dispas M, et al. Methicillin-resistant Staphylococcus aureus ST398 in swine farm personnel, Belgium. Emerg Infect Dis. 2009 Jul; [Epub ahead of print] DOI: 10.3201/eid1507.080652.

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 in space

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No, really — but not quite the way you think. The weekly geekfest that is Aviation Week and Space Technology reports that the payload of the space shuttle Atlantis includes a MRSA experiment. The goal is to investigate whether bacteria held in the microgravity of space become more virulent — this was done earlier with salmonella — and then to determine whether any new virulence markers suggest targets for a potential staph vaccine.

A vaccine of course, is the Holy Grail of MRSA research — and it has remained frustratingly out of reach. For a great review of past research and future challenges, see this review article from March.

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 colonizedwith 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.

Quick update: Yes on bacterial pneumonia and new flu

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Constant readers, I thought you;d like to know that there are a few more indications that secondary bacterial pneumonia (as discussed in this post the other day) does seem to be playing a role in the severe cases of the new flu.

That’s according to this account of the WHO’s technical briefing from Wednesday, along with this item (there are three entries, go to the bottom one) from the excellent disease-alert list ProMED.

More soon.

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