Maryn McKenna

Journalist and Author

Another new bad resistance factor. (Bonus: Another city stigmatized!)

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The subcontinent can cease fretting over the naming of that new bacterial resistance factor NDM, for New Delhi. There’s a newer resistance factor in town, and this one stigmatizes… Italy.

Welcome, Verona integron-encoded metallo-beta-lactamase, or VIM.

To be precise, VIM isn’t new — its very first identification was at the Verona University Hospital in 1999 — but it has just been found in the United States for the first time. The CDC said Wednesday evening that it has identified VIM in an American woman who took a Mediterranean cruise this summer, got diarrhea, was hospitalized (twice) in Greece, developed sepsis and C. diff, and eventually was transferred home and hospitalized here for a further 26 days. In the US, she was found to be infected with Klebsiella pneumoniae, a gram-negative bacterium that’s a common cause of serious-hospital acquired infections — urinary tract infections, abdominal infections and pneumonias. This strain, though, was resistant to all the drugs usually used to treat Klebsiella. (The woman did recover.)

To anyone who followed the NDM-1 news a few weeks ago, this should sound familiar. (If you didn’t, here’s my archive. No, go ahead; we’ll wait.) A resident of one country is unexpectedly hospitalized in another. That second country happens to have high rates of a novel, serious resistance factor — in Greece, 50 percent of Klebsiella isolates in ICUs are multi-drug resistant — that clusters in the organisms most likely to cause hospital infections. The person picks up a resistant infection without knowing it, travels home, and transports the novel resistance factor into his or her home country.

And because the gene that directs production of the problematic enzyme resides on a mobile genetic element — meaning it can move easily from one bacterium or species to another — the public health authorities in the unlucky person’s home country begin a very nervous waiting game.

That’s what happened with the identification of NDM-1, which was first noted in a man of South Asian origin, living in Sweden, who was unexpectedly hospitalized in India in 2007 and then hospitalized again in Sweden in 2008. (NDM was found in the US in June.) Like NDM, VIM has spread across the world; within a few years of its original identification it was in France, Spain and Taiwan. Nor are those two enzymes the only bad actors — they’re merely the most recent and notable in successive waves of multi-drug resistance in gram-negative organisms that are washing across the world. (Almost all of them, by the way, are named for their points of origin. GIM, Germany. SPM, Sao Paolo. DIM, Dutch. And so on.)

And those waves (to torture my metaphor until it whimpers) are really just the most visible points of an ocean of gram-negative resistance that has flooded the globe, and certainly the US. And, just to slosh home the point: These resistance mechanisms knock out the drugs of last resort for gram-negatives, the carbepenems, and there are no new drugs to replace them. The drug-development pipeline for gram-positives such as MRSA has a few drops still rolling down it; the pipeline for gram-negatives, as the Infectious Diseases Society of America has documented in several reports, has just about dripped dry.

The CDC on Thursday warned labs and hospitals to start taking action, in ways that will at least require additional staff time and attention, and probably will cost extra money too :

Cases of (carbepenem-resistant Enterobacteriaceae) are a significant, emerging public health problem regardless of the mechanism of carbapenem resistance, and procedures to rapidly recognize and report CRE cases to infection prevention personnel should be in place in all acute and long-term–care facilities. Facilities that have not identified cases of CRE should undertake periodic laboratory reviews to identify cases. Patients with CRE should be managed using contact precautions, and patients exposed to CRE patients (e.g., roommates) should be screened.

The problem with writing about increases in antimicrobial resistance is that, sooner or later, you inevitably end up sounding like Chicken Little. (Or Cassandra. I’m not sure which is worse. Chicken Little is probably cuter.) Every one of these sounds like the worst possible news. Problem is, every one of them is… until the next one comes along.

Image of Klebsiella pneumoniae courtesy of the Public Health Image Library, CDC.

Brain Amoebas. Organ Transplants. Brrr.

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Nightmare scenario: New disease arises. It’s rare enough that there aren’t many known patients, and so it isn’t well-studied — and because it isn’t well-studied, there aren’t agreed-upon treatments or accurate tests for it, and there isn’t a good understanding of situations where the infected might pose an unusual risk to others.

Situations, for instance, like organ transplants.

The CDC’s weekly bulletin today describes that nightmare scenario come true. Last year, four people received the kidneys, heart and liver of a 4-year-old boy who died in Mississippi of encephalitis that was assumed to be a rare reaction to flu infection. Weeks after the transplant, the two kidney recipients developed neurological symptoms — spasms, seizures, visual disturbances — and were hauled back to hospitals for evaluation. MRIs showed ring-shaped lesions in both their brains. That sent investigators back to re-examine the boy’s death — and revealed that while he did have encephalitis, it wasn’t because of flu.

It was because he was infected with a newly recognized pathogen, Balamuthia mandrillaris, a species of amoeba. It had passed to the four recipients via his organs, and grew in them with an assist from the immune-suppressing drugs they were taking to prevent rejection.

There have been only about 200 human cases of Balamuthia in the world since the infection was first recognized in 1990 (it got its name from its first-ever sighting the year before, in a sick mandrill at the San Diego Wild Animal Park). Treatment is prolonged and complex, an IV cocktail of multiple drugs that can drag on for months and optimally includes a drug, miltefosine, that isn’t even available in the United States except under an emergency plea to the Food and Drug Administration. When the amoeba develops in the brain, treatment is often unsuccessful anyway: Most cases of Balamuthia encephalitis are fatal.

And so it was in this cluster. One kidney recipient, a 31-year-old woman, developed her first neurological symptoms 20 days post-transplant and died on day 75. The other, a 27-year-old man, survived with “residual right arm paralysis, bilateral leg weakness, and intermittent vision loss,” the CDC says. The heart and liver recipients, both toddlers, mysteriously did better: They had not yet developed symptoms when the kidney recipients were diagnosed, and were hospitalized for evaluation and given a multi-drug cocktail in time.

Could this have been detected earlier? Probably not: It sounds simply random, rare and sad. The boy who was the donor was from Kentucky but was living with relatives in Mississippi when he first got sick in October 2009. He was diagnosed with the flu, got antivirals, got better, and then a week later developed headaches and seizures; was hospitalized for three days, diagnosed with acute disseminated encephalomyelitis, an immune reaction that can follow on flu, and was discharged. Four days later, his seizures recurred, and he died a week after that, on Nov. 18. In the course of his treatment, he’d been checked for viral, bacterial and fungal infections, and all had come up negative — so the family and hospital let his organs go for transplant. The recipients got them two days after that.

It wasn’t until the kidney recipients fell ill that the boy’s tissue, preserved after donation, was checked by CDC investigators, who found something that wasn’t viral, or bacterial, or fungal. They found the Balamuthia amoebas, distributed throughout his brain.

Balamuthia lives in soil around the world, but no one is confident yet of how people become infected; the predominance of encephalitis cases, and some facial infections in milder cases, suggest the route may be as simple as inhaling dust that contains amoebic cysts. It can only be diagnosed by brain biopsy, usually at autopsy, and so there’s some concern that it may be misdiagnosed and be more common than we know. A few cases in California have been analyzed, because California happens to have an encephalitis registry.

But it’s a funny thing about new, rare diseases: Once you know what to look for, you start seeing it where you wouldn’t have detected it before. And so it is with Balamuthia — while the CDC staff were writing up this cluster, another report came in, of another transplant cluster that happened just a few weeks ago in Arizona. In this case, the donor was a 27-year-old landscaper who died July 21 of what people thought was a stroke. Arizona residents, both men, got his liver, and one kidney and his pancreas; illustrating how far organ-donation networks can reach, his heart went to a man in California, and the other kidney to a man in Utah.

The liver recipient died Aug. 17. The kidney-pancreas recipient died Aug. 30. Their illnesses alerted the transplant network, and the other two donors were put on a multi-drug cocktail. So far, they have survived.

Because I spend so much time thinking about scary diseases, people often ask me if there’s anything that gets to me. I wash my hands a lot. I follow whatever precautions are being taken by scientists I hang around with. Most of the time, in most of my life, I don’t feel like I’m much at risk.

But amoebas, growing in your brain, because you happened to inhale the wrong speck of dust? That squicks me. A lot. Brrr.

Images of Balamuthia courtesy of the Parasite Image Library, CDC

New CDC flu numbers: This may not go well

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(Constant readers: Apologies for the slow blogging. Casa Superbug’s little medical crisis from a week ago has recurred, and things are a bit distracting. Back to normal soon, I hope.)

In public health, one of the numbers you hear most often — and especially so the past few years — is
36,000. That’s the number of deaths that the CDC estimates occur in an average year from influenza.

Or rather, estimated. Because today, in its weekly bulletin
MMWR and also in a teleconference for the press, the CDC announced that it is discarding that widely used number, in favor of newer numbers from newer studies that take into account the wide variation in illness and death from one flu season to the next.

The new estimate is:
23,607. Or, a range that goes
from 3,349 to 48,614. Or, in the language recommended by a CDC scientist and a communications specialist in the press call, ”
tens of thousands of people [who] may die each year in an average flu season.”

If that sounds difficult to communicate in a concise manner, well, the reporters on the CDC call today clearly thought so too. And while reporting study results forthrightly is transparent, and more precise numbers are almost always better, I can’t help but wonder whether this attempt at precision and transparency will not be received well. After all, we are only a few months (or a few weeks, depending whose end date you accept) away from the dribbling conclusion of a worldwide pandemic that was taken so not-seriously by the public that, in the US, 71 million doses of H1N1 vaccine went unused — and in Europe, some public representatives alleged that the entire emergency was a concoction by pharmaceutical companies.

Given that history, putting out a public message that
flu kills fewer people than we thought — but is, still, a serious disease that should be planned for and vaccinated against — sounds like a hard sell.

Here’s how today’s new numbers came about:

The mortality rate from flu has always been difficult to assess: People die of influenza directly, but they also die of underlying conditions — heart disease or chronic obstructive pulmonary disease, among others — that might not kill the person if influenza were not putting an extra strain on the system. In either case, but especially in the latter, the death may not be attributed to flu, particularly if the victim has not been tested for the presence of the flu virus.

So, to arrive at an estimate, the CDC has used a statistical model. As explained in the briefing today by Dr. David Shay of the CDC’s Influenza Division:

We have two categories that we look at… One is death certificates that have an underlying diagnosis of pneumonia or influenza. 99% of those deaths are actually coded as pneumonia. So, that’s to make an estimate of deaths in a particular season from pneumonia that are associated with flu. And typically, that’s about 8.5% of deaths over the time period that we looked at…  The broader category of respiratory and circulatory deaths we think encompasses the full picture of influenza-associated deaths, including things such as people who might die because of worsening chronic obstructive pulmonary disease or worsening congestive heart failure that results in death after an infection. And we estimate that about 2% of that broader category in any typical year is associated with influenza.

One other factor affects flu mortality: Which flu strain type is dominant in the season being measures. Flu is generally taken to cause the most severe disease, and the greatest number of deaths, in the elderly; but some strains cause more severe disease than others, and some (H1N1 “swine” flu, for instance) attack the young, who are healthier and less likely to die, more than they do the old. Again, Shay:

[I]t’s important to keep in context, which we don’t really describe in this article because of space, that there’s at least four factors that affect sort of flu mortality in any particular year, and those four would be the specific strain or influenza strains that are in circulation, sort of the length of the season or how long influenza is circulating in the united states, how many people get sick, because of course, the more people get sick, there is more likely to be more serious outcomes, and finally, who gets sick.

In the study released today, the CDC did two things: It
broadened the range of flu seasons from which it took data to feed into the statistical model, and it
took a second look at the years on which the previous model, the one that produced the 36,000-death estimate, was based.

When the range of years was broadened to 31 flu seasons (1976-77 to 2006-07), here’s what shook out:

  • For deaths from influenza and pneumonia:
    from 961 in 1986-87 to 14,715 in 2003-04, an average of 6,309
  • For deaths from respiratory and circulatory complications:
    from 3,349 in 1986-87 to 48,614 in 2003-04, an average of 23,607.

(When asked which number should be used for shorthand, Shay said: “The broader category of respiratory and circulatory deaths we think encompasses the full picture of influenza-associated deaths.”)

When the 36,000-death estimate was re-examined, Shay said:

The 36,000 number that’s often used pertains to a very specific time period from 1990 to 1999. And in that decade, where we had prominent circulation of H3N2 viruses, they were prominent in eight of the nine seasons that are contained within the data that were used to make that estimate, and those are, as you know, typically more severe seasons. We had a high mortality for that nine-year period.

According to the MMWR analysis, mortality rates in the H3N2 years were 2.7 times higher than in years when other types were dominant.

So that’s the rationale behind today’s dialed-down numbers. Here’s the potential problem with it: It just took me about 1,000 words to (somewhat talkily) explain. It requires patience and detail to impart, which in the current media environment are in very short supply. As one of the participants on the call said today:

I’m really scratching my head here wondering what I’m going to use, because we really don’t have a lot of time … to present a lot of numbers, and I think in a sense to say that the range is 3,000 or 3,300 to 49,000 raises a lot of questions, and I think we don’t have time to answer those questions in every report. And I also wonder if it’s not a bit misleading to use 3,300 as the bottom number since it’s been 20 years since it was that low, and even in the last 20 years, the mortality has never been much below 12,000.

You see the problem.

To repeat: This is an effort at transparency and accountability; those are worth applauding. But it’s also a nuanced and difficult health-communication message, launched into a zeitgeist already tuned toward conspiracy theories and a media marketplace with little time or expertise to counter them.

Pessimistically, I wonder how long it will be before this message gets transformed into something like, “See? I told you so. Flu isn’t that big a deal after all.” I hope the CDC is prepared when it does.

(Here’s today’s MMWR article, the transcript of the press briefing, and a Q&A on the new calculation. The cite is: Morbidity and Mortality Weekly Report, “Estimates of Deaths Associated with Seasonal Influenza — United States, 1976–2007.” August 27, 2010. 59(33);1057-1062)

Update: Access to dental care

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A couple of days ago, I talked about the link between a potentially massive hepatitis B outbreak in West Virginia and the lack of access to primary dental care. I was mushy qualitatively descriptive, ahem, about the number of people who lack access to dental insurance.

Comes now the CDC to save the day. In a statistical brief posted today, the National Center for Health Statistics gives a concise but thorough overview of the state of dental insurance in the US. Short version: Ain’t pretty.

Crude preliminary population math:

  • There are currently 309 million Americans.
  • Based on census tables from last summer, 39 million are 65 or older (i.e., eligible for Medicare).
  • Based on other census tables from last summer, 52 million are 17 or younger (of which some percentage, based on family income, would be eligible for Medicaid).
  • That leaves, with wiggle room, about 218 million working adults.

According to the NCHS:

  • 172 million non-elderly Americans have private health insurance. (NB, leaving 46 million non-elderly with no health insurance, which matches the usually accepted figures.)
  • Of them, 45 million have no dental coverage — which, added to the 46 million with no insurance at all, means that more than 90 million Americans have no dental coverage at all. (I believe the technical term for a number that large is a crapton. Maybe a metric crapton.)

In addition:

  • If you have employer-provided health insurance, your chances of having dental coverage are pretty good: 80%.
  • If you have privately purchased insurance of any kind, not so much: 30%.

So, reinforcing Monday’s point: There are multiple millions of Americans who get no assistance paying for dental care, which is a largely cash-only business. (And judging from my own experience — thanks to my childhood in the UK, I have teeth like chalk and consume more than my share of dental care — dental insurance negotiates discounts. So self-pay dental care is relatively more costly.) And therefore, it is not surprising that thousands of people attended that free dental clinic in northeastern West Virginia, and were potentially exposed to hepatitis B as a result.

Dept. of Unintended Consequences: Hepatitis B in West Virginia

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Via ProMED Mail comes a news report that about 2,000 people in 5 states are being sought by health departments so they can be checked for hepatitis B infection. The potential source: the Mission of Mercy Dental Clinic, a free dental-care fair held just about a year ago in Berkeley County in the far north-east corner of West Virginia. The potentially infected include 1,137 people who were treated at the two-day clinic and 826 of the volunteers who worked there, from West Virginia, Washington, D.C., Virginia, Maryland, Pennsylvania and North Carolina. Three patients and two volunteers have already been diagnosed. The virus in four of the five matched on molecular fingerprinting, suggesting a common source; the fifth patient refused further testing.

Hepatitis B is blood-borne, so on the surface, this is a story of the tragic consequences of some failure somewhere in the clinic’s infection-control procedures. (One reason why it caught my eye, since I’m interested in healthcare-associated infections.) Except that it’s not — or not only. It’s important to unpick why such an extraordinarily large number of people may have been exposed at one time. Looked at through that lens, it becomes a story about what can happen when we don’t fund basic health care in a timely way.

Some background: West Virginia is one of the poorest states in the country and has some of the highest rates of the usually recognized diseases of poverty: tobacco use, chronic kidney disease, asthma, cardiovascular disease. (Look for West Virginia on these CDC maps of incidence of heart disease and stroke.) But it also has extraordinarily high rates of another health problem that ought to be linked in the public mind to low socioeconomic status, but usually isn’t: untreated dental disease. Eric Eyre of the Charleston Gazette (disclosure: a friend and fellow Kaiser Foundation Fellow) took a year-long close look at dental disease in the state in 2006-07 (slideshow, stories). If you’re squeamish, I advise skipping the one about the woman yanking her own teeth with pliers after a few shots of moonshine.

Dental disease — that’s not just cavities, but tooth loss, bone loss, abscess, Ludwig’s angina, septicemia in the most serious cases — isn’t only a problem for West Virginia, though it happens to be worst there. It’s a problem all over the US because, without ever intending to, we’ve allowed dental care to become a primarily cash-based form of medicine.

If you have a job, you may have dental insurance, though it’s a less-common employment benefit than health insurance, and covers comparatively less of the cost of any procedure. If you don’t have a job, dental care is entirely out of pocket. If you’re poor enough to be on Medicaid, whether or not you have dental coverage depends on which state you live in, because Medicaid dental coverage for adults falls under the portion of Medicaid funded by the states, not the federal government. In the past 12 months, California, Hawaii, Massachusetts, Michigan, Minnesota, North Carolina, and Washington state all cut or tried to cut their contributions to dental Medicaid from their state budgets. If you’re the child of a poor family, you are hypothetically entitled to Medicaid-funded dental care, though that depends on being able to find a local dentist willing to accept Medicaid reimbursement; last year, the Government Accountability Office said that children have trouble finding Medicaid-accepting dentists in 43 out of 50 states.

Net result: Untreated dental disease is now the most common disease of childhood, five times more common than asthma according to a 2000 Surgeon General’s report, and emergency room visits for dental crises are rising steadily. ERs are not the right place to treat dental problems — they don’t fill cavities or do extractions, though they can drain abscesses and give antibiotics and pain meds — but as with so much else in US medicine, ERs offer a mandated clinic of last resort when there’s nowhere else to go. (For more about the interplay between dental care and ER overcrowding, here’s a story I wrote for the June Annals of Emergency Medicine.)

All of that explains why thousands of people from a wide swath of the East Coast were so desperate for free dental care that they were willing to stand in line overnight in a high school parking lot. (The first free dental clinic in West Virginia had to close its doors early after it got 1,100 patients in the first 2 hours.) And also why hundreds of dental-care professionals and students and community volunteers were so eager to help. And why they’re all now waiting by the mailbox, wondering whether they’re in line for a letter that will tell them where to get tested for infection with a life-long chronic disease.

Hospital infections – good, bad, or too little data?

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Some of you may have spotted an announcement last week from the Centers for Disease Control and Prevention about a release of data from the National Healthcare Safety Network (NHSN), a repository of hospital infection data. You can guess the big news in the report from its title,  “First State-Specific Healthcare-Associated Infections Summary Data Report”: For the first time, database users are able to calculate healthcare-associated infections (let’s call them HAIs for short) by state, as well as nationally.

Good news, you would think. And it is. According to the CDC’s announcement (press release, press conference transcript), the national rate of one particular type of HAIs, central line associated bloodstream infections or CLABSIs (like it looks — pronounced “klab-sees”) is down 18% from the previous 3 years. Taken together, all HAIs kill at least 100,000 Americans each year (an old number that is probably an underestimate) and cost at least $30 billion per year. CLABSIs are an important component of the spectrum of HAIs and may account for a third of all HAI deaths — so any reduction is a positive development.

And yet: The bigger news about this report, unfortunately, is that it lays bare how little we really know about HAIs, and how little progress has been made in preventing or even documenting them.

Consider:

  • The report includes data from only 17 states
  • The data does not match state to state, so state rates cannot be compared
  • Participation in the NHSN by hospitals is voluntary (except in states that recently have passed mandatory reporting laws) and data is self-reported
  • Hospitals that report to the NHSN are not identified (in fact, unless state laws say otherwise, they are guaranteed anonymity)
  • The NHSN does not collect data on the most problematic HAI organisms, MRSA and C. difficile.

If you think for a moment about how incomplete this data is, and how much the data collection allows hospitals to avoid saying, then Dr. Peter Pronovost‘s remarks to the Association of Health Care Journalists in April begin to make sense. Pronovost is a MacArthur Fellow for his championship of evidence-based infection prevention, and said (sorry, no verbatim record that I know of, but I live-tweeted his speech) that if hospital infection reporting were truly transparent and truly accountable — right now, it’s neither — the problem of HAIs would end tomorrow, because consumers would be so shocked that they would rise up and demand change.

The CDC says there will be additional data and a new comparison with this first snapshot within about 6 months. Again, that’s all good news. But it’s worth taking a deep look at this report to really understand how little we know — which will also help to explain why this problem so persistently fails to get better.

(NB: The CDC announcement and the relevant background were covered thoughtfully by my friends Dan DeNoon of WebMD and Barbara Feder Ostrov of Reportingonhealth.org, whose post, FWIW, quotes me.)

Quick alert: Congressional hearing Wednesday

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Constant readers, I’m on the road again: Georgia Center for the Book tonight in Decatur, 7:15 p.m. But if you can’t make that, take a look at this: The Energy and Commerce Subcommittee of the US House of Representatives has announced a hearing for Wednesday on “Antibiotic resistance and the threat to public health.”

This is not a hearing on PAMTA, but apparently a broader hearing on the whole issue, featuring two VIPs: Dr. Anthony Fauci of NIH and Dr. Tom Frieden of the CDC. To my eye, this indicates that official, policy interest in this issue is (finally, at last) ramping up.

The hearing page is here and the preliminary memo on it is here.

Get Smart About Antibiotics Week, Oct. 5-11 (now!)

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Every year, the CDC sponsors a week-long observance called Get Smart About Antibiotics Week, intended to bring attention to this issue of antibiotic misuse that all of us here are so concerned about, and to link the efforts of federal and state agencies, nonprofit groups, and anyone else with an interest.

Today marks the start of the 2009 week, and of course it comes as a crucial time: With the H1N1 flu pandemic causing so many people to seek care for upper respiratory illnesses, the possibility of antibiotics being misprescribed for a viral illness is greater than usual.

The homepage for the CDC campaign is here. There is an abundant list of materials, images, campaign strategies and suggestions for framing the conversation, along with graphics (I’ve lifted the one at left from a poster aimed at parents of young children), PSA sound files, and cute little web widgets such as the image at right above (sorry for the poor layout skills, it’s a busy morning).

Since this comes from the CDC and is therefore taxpayer-funded, all of it is open-access. So go, already.

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.

Special bonus for disease-detection wonks

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Constant readers: Some of you know that my first book, published five years ago, was a narrative and history of the CDC’s Epidemic Intelligence Service, the young, committed corps of MDs and PhDs who give up two years of their lives to serve on front-line outbreak SWAT teams.

The EIS are very important right now, because there are almost 100 CDC people in the field, in Mexico and in US cities and other countries where H1N1 swine flu is emerging.

My next book — the one for which this blog is the whiteboard — is being published by the same imprint, Free Press, part of Simon & Schuster. So because the EIS is so crucial to the outbreak investigation, FP has relaxed their rights and very graciously allowed me to fling up some parts of Beating Back the Devil on the web, for free, to my regular readers.

My web skills are not magnificent, and my site has outgrown the program I used to build it. However: If you go to this page, you’ll see a section that announces Excerpts! And in it you’ll find a prologue and two chapters in various formats. (We did this fast; it is messy. Sorry.)

I particularly recommend Chapter 13 [pdf], which is a narrative of the SARS outbreak in Asia, starting with an EIS officer named Dr. Joel Montgomery staring down a tray of blood samples in a laboratory in Vietnam. (I wrote about the importance of serology — blood-analysis — surveys to swine flu at CIDRAP tonight.) The description of that outbreak response should give you a good flavor of what the CDC investigators are doing and thinking about now. And, bonus, it talks about some little-known cases of avian flu H5N1; we did not know at the time how important those cases would turn out to be.

If you have time, there are also links to sections that FP has posted on their own site: Chapter 1, which will tell you who the EIS are and why the corps exists (Korean War veterans will know already); and the book’s Prologue, which takes you inside the first bioterror-response training that EIS members ever endured.

I hope you enjoy.