Maryn McKenna

Journalist and Author

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)

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.

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 extra 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.

For flu wonks: Hear from a CDC expert on novel H1N1 “swine” flu

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Folks, I am a member of the Association of Health Care Journalists, a US-based organization of 1,100 journalists from North America and elsewhere committing to practicing science/health/medical journalism to a high standard. (No matter how much the collapse of the MSM undermines us. But that’s a different blog post…)

One of the things the AHCJ tries to do is to get its membership in direct touch with newsmakers as much as possible. We have a conference, we have podcasts, we have newsmaker briefings. And on Tuesday, we had a live webcast/call-in with Dr. Carolyn Bridges, associate director for epidemiologic science in the influenza division of the CDC, taking questions for 45 minutes on aspects of the new flu.

Participation in the call was limited to AHCJ members, but the archived version is open to all on BlogTalkRadio. Link is here.

(And yes, the moderator/interviewer is, umm, me.)

Child deaths from flu + MRSA, an update

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As predicted earlier this week: The Centers for Disease Control and Prevention (CDC) has announced more deaths of children from flu, and from flu followed by MRSA pneumonia.

My colleagues at the Center for Infectious Disease Research and Policy are tracking the case count, and here’s what they said this evening:

The CDC received eight reports of influenza-related deaths in children during the week ending Feb 21, bringing the seasonal total to 17. Four of the deaths occurred in Texas, 2 in Colorado, and 1 each in Arizona and Massachusetts.
Bacterial coinfections have been confirmed in 10 (59%) of the 17 children. Staphylococcus aureus was identified in 8 of the 10 children—3 of the isolates were sensitive to methicillin, 4 were not, and results were not reported for 1. Eight of the 10 children who had coinfections were age 12 or older. (Byline: Lisa Schnirring)

Just to recap, that’s four deaths so far this flu season from flu+MRSA, twice the number we knew of last week.

And just to remind: The CDC and its Advisory Committee on Immunization Practices now recommends flu shots for all children and adolescents, up through the age of 18. A flu shot is one defense against MRSA pneumonia. It is worth considering.

Child deaths from flu + MRSA, again

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Folks, I am close to manuscript deadline and so keep disappearing down the rabbit hole; forgive me if I don’t post as regularly as usual, I’ll be back as soon as I can.

I wanted to point out the announcement by the Centers for Disease Control late Friday that we are starting to see children dying from MRSA this flu season. (The architecture of the linked page is unfortunately way clumsy; at the link, scroll down to the subhead “Influenza-Associated Pediatric Mortality.”)

Since September 28, 2008, CDC has received nine reports of influenza-associated pediatric deaths that occurred during the current season.
Bacterial coinfections were confirmed in six (66.7%) of the nine children; Staphylococcus aureus was identified in four (66.7%) of the six children. Two of the S. aureus isolates were sensitive to methicillin and two were methicillin resistant. All six children with bacterial coinfections were five years of age or older.

We’ve talked before (here, here and here, among other posts) among the emerging understanding of the particular danger that MRSA poses during flu season, when (it is hypothesized) inflammation from flu infection makes the lungs more vulnerable to secondary bacterial infection.

(For those paying attention to the hospital v. community MRSA debate, this is a community-associated infection, not a hospital one.)

This current CDC bulletin underlines, just in case we have forgotten, that drug-sensitive S. aureus (MSSA) can be a serious foe as well. Let’s remember, resistance makes MRSA less treatable than MSSA, but it does not change its virulence; MSSA by itself can be a very serious foe. Yes, there are other changes in some strains, especially the community ones, that do appear to increase virulence, but the original MSSA strain is nothing to trifle with.

Also, here’s an important addition to this unfolding story: My colleagues at the Center for Infectious Disease Research and Policy are keeping track of kid deaths around the country. According to them, these CDC numbers are already out of date; they have uncovered more that the CDC has not yet posted, but may take note of in future weekly updates.

MRSA reductions in ICUs – good news, but qualified

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Constant readers, you will no doubt have seen the overnight news about a paper by CDC authors in the Journal of the American Medical Association, reporting a significant decline in catheter-associated bloodstream infections (known by the uncatchy acronym CLABSIs, and yes, people pronounce it “klab-seez”) in intensive care units.

Our results show that the 6 most common adult ICU types reporting central line–associated BSIs to the CDC, which together account for 96% of all reported MRSA central line–associated BSIs among studied ICU types, have experienced declines of 50% or more in the incidence of MRSA central line–associated BSI since 2001. This means that the risk of primary MRSA bloodstream infections among patients with central lines in these ICUs has substantially decreased in recent years.

First, let’s stipulate that any reduction in healthcare-associated infections is good, good news.

Having said that, let’s drill down into the paper a bit. Because in some of the coverage last night and this morning, this paper is being represented as “Hooray, the MRSA problem is over,” and that’s an over-reaction. Here are some reasons why.

The data come from several overlapping CDC databases: the National Nosocomial Infections Surveillance system (NNIS) and the National Healthcare Safety Network (NHSN). The NNIS existed from 1970 to 2004; there was a data gap in 2005, and the NHSN sprang up in 2006. There were 300 hospitals in 37 states reporting to the NNIS when it shut down, and in 2007 there were 518 reporting to the NHSN, many of which joined that year as a result of new mandatory HAI reporting in New York, Colorado and South Carolina. Participation in either database was/is voluntary.

The CDC analysis abstracts data from the reports to those systems for the years 1997-2007. But, as you can guess from those numbers above, the data does not cover all 7,500 US hospitals; and because it is more weighted to certain states, it does not represent a nationally representative sample. In addition, hospitals came into the system(s) during the study, and also dropped out; an accompanying editorial estimates that only 6% of the 599 hospitals in the study reported data for all 11 years.

Second, it’s important to note that all CLABSIs went down: MRSA infections, drug-sensitive staph (MSSA) and other organisms. So something is going on — but it is not MRSA-specific. Optimistic interpretation: Enhanced infection control in hospitals is suppressing all HAIs. Pessimistic interpretation: Enhanced scrutiny, in the states that account for the most additional hospitals, is negatively affecting HAI reporting. Can we distinguish which? Probably not. On the one hand, CLABSIs started trending down in 2001, before the earliest mandatory reporting legislation became effective. On the other hand, the study doesn’t/can’t associate declines in CLABSIs with any specific interventions — so it is not possible to know from this study whether one particular strategy was responsible for this decline.

Third, to put the study focus in context, MRSA accounts for only about 7% of CLABSIs; according to the paper, it is not those infections’ most common causative organism. And CLABSIs do not account for the largest proportion of MRSA HAIs; according to a 2007 paper, they fall third on the list behind nosocomial pneumonia and septicemia.

Fourth, since it is abstracted from a hospitals data base, this study doesn’t address community MRSA infections — and there are some scientists in the family of MRSA researchers who would insist that it is the increasing prevalence of community infection that is the true driver of the MRSA epidemic.

So: Decreased MRSA HAIs, good news. Reasons, unfortunately unclear. Significance, possibly less than the headlines this morning maintain. But whatever it is that those hospitals were doing, let us hope they keep doing it.

The cite is: Burton, DC, Edwards, JR, Horan, TC et al. Methicillin-resistant Staphylococcus aureus Central Line-Associated Bloodstream Infections in US Intensive Care Units, 1997-2007. JAMA. 2009. 301(7): 727-36.
The accompanying editorial is: Climo, MW. Decreasing MRSA Infections: An End Met by Unclear Means. JAMA. 2009. 301(7)772-3.

MRSA in kid athletes – simple but not easy

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It’s been almost a week since this came out — told you there had been a lot of research released — but I wanted to make sure everyone saw it: The Centers for Disease Control and Prevention released results of an investigation into an outbreak of MRSA on a high school football team in Brooklyn, NY. (My home town, in case anyone cares. But it must have gotten gentrified, since the only organized activities I remember were somewhat less, umm, licit.)

Out of 59 players who attended a pre-season training camp where they practiced all day and bunked in the gym at night, 6 had MRSA skin abscesses (4 confirmed by culture, 2 suspected). The four confirmed cases all began as a pustule or blister that the kids ignored until the infections blew up; three of them subsequently needed the abscesses surgically incised and drained and also took antibiotics.

So, this will sound like not a big deal, right? Fifty-nine kids, 6 infections, attack rate of 11.8%, no one harmed in the long term. Well, in one sense, yes. On the other hand, without sounding like a Cassandra, there have been plenty of sports infections that did not turn out to be so minor: Kellen Winslow, Kenny George, Brandon Noble, Ricky Lannetti. (And if you’ll stay tuned til this book is published, there will be an entire chapter on MRSA and sports, both amateur and pro, and the story of a teen athlete who almost died of invasive MRSA following what looked like an innocuous minor infection.)

The difficult thing here is that the steps for preventing such infections — or, at least, vastly reducing their likelihood — are simple: Washing hands, showering after practice, not sharing towels or razors, keeping uniforms and gear clean, and keeping on top of what look like minor abrasions and bug bites. But, as this investigation demonstrates, it’s not so easy to get kids to take those things seriously:

The school had supplied antibacterial soap in pump dispensers in the showers; however, several players brought their own soap. Players supplied their own towels. Players reported that they usually left their towels on their cots or on the floor when not in use. The school offered a daily laundry service for uniforms and towels during the camp; however, most players did not have their towels washed and wore their uniforms two or three times between launderings. Players often remained in sweat-soaked clothes between the morning and afternoon practices. (MMWR Jan.30, 2009. 58(03);52-55)

As with hospital infections, where the simple act of handwashing remains one of the most difficult tasks to accomplish, the steps that could prevent MRSA among kid athletes are not complex. What is challenging is getting the kids to understand — over-against the hypermasculinity of sports, where it’s cool to be sweaty, dirty and banged-up — how important it is to perform those steps: routinely, thoughtfully, time after time after time.

A timely reminder on using antibiotics well (and badly)

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The Infectious Diseases Society of America, the professional organization for ID physicians, is criticizing large grocery store and pharmacy chains for giving antibiotics away for free. (Yes, you read that right: Not generic, not cheap, free. Here is a Wall Street Journal Health blog post explaining the practice, which has become quite common over the past two years.)

IDSA is concerned of course that these antibiotics will be used inappropriately because, being free, they will have a perceived lesser value. The Centers for Disease Control and Prevention has been campaigning for years against inappropriate antibiotic use, via its Get Smart: Keep Antibiotics Working campaign.

(Why is it important to use antibiotics only for the things they work against? All together now: Because if used inappropriately — in too-low doses, too-short courses, or against an illness where they are not useful — they will encourage the development of resistant bacteria, and also may kill your own commensal bacteria, clearing a niche that resistant ones can then occupy. Very good, class, early dismissal today.)

There’s an additional, interesting twist to these campaigns, though, which IDSA very rightly raises: They are taking place now, in flu season. One of the most common inappropriate uses of antibiotics is against viral diseases such as flu; the CDC says:

Tens of millions of antibiotics prescribed in doctors’ offices each year are for viral infections, which cannot effectively be treated with antibiotics. Doctors cite diagnostic uncertainty, time pressure on physicians, and patient demand as the primary reasons why antibiotics are over-prescribed.

IDSA is quite rightly concerned that the launch of these free-pill programs in flu season will reinforce the association between flu and antibiotics, which is precisely the association that causes antibiotics to be most overused. An excellent point.