31 March 2008

Recommending a blog

The nonprofit New America Foundation has a new blog, the New Health Dialogue, that is largely written by my friend and colleague Joanne Kenen. Joanne was for many years the health policy reporter for the wire service Reuters; she and I were Kaiser Family Foundation media fellows a year ago. If you're at all interested in the deep questions of health care in America — what we spend, how we make decisions (or don't) on spending, and why it's all such a mess — Joanne's blog is an excellent place to start. I've added it to the blogroll on the right.

Healthcare-associated infections, the panel

The panel at the Association of Health Care Journalists' annual meeting exploring mandatory reporting of HAIs was very successful (she, the moderator, says modestly). Speakers were:
Notable points from the panelists:
  • Richards: The CDC acknowledges that its collaborators feel the agency took too long to take this issue seriously, but "we're there now."
  • Coyle: Hospitals think a uniform data standard should be set for reporting, so that rankings will be apples-to-apples comparable across the industry.
  • Moss: Victims and families are concerned that healthcare infections have become an industry, and that there is no financial incentive for hospitals to reduce infection rates.
  • McCaughey: HAIs are twice as prevalent as the CDC calculates: Not one out of 20 hospital admissions, but one out of 10. Arguments that infection control is too costly ignore the groundbreaking work done by Carlene Muto et al. at University of Pittsburgh Medical Center: Their enhanced surveillance and control of ICU patients achieved a 20-to-1 payback.
Pithy final comment from McCaughey: "We have the knowledge to reduce hospital-acquired infections. What we lack is the will."

28 March 2008

MRSA and animals and hospitals

I am at the annual meeting of the Association of Health Care Journalists, where last night we heard actor Dennis Quaid discuss the severe medical error that led to his infant twins being given 1000x the appropriate dose of heparin - twice. (Interesting tidbit: The twins were in the hospital because of a staph infection.) Quaid and his wife have set up a foundation that will work to reduce medical errors and is soliciting stories from victims and families.

Later today I'll be moderating a panel on mandatory reporting of hospital infections that we hope will provoke an, ahem, free and frank exchange of views. More on that to come.

Meanwhile, though, a wrinkle in the possibility that companion animals might spread MRSA: What if they are therapy animals?

An international collaborative group has contemplated that question and come out with a thoughtful set of guidelines that are published in this month's issue of the American Journal of Infection Control. The guidelines address both official therapy animals and also pets who live in long-term care facilities or are brought to visit patients.

Key considerations: Animals could not only spread disease to patients because they are colonized; they may also become colonized because they are handled by patients. Because transmission and colonization may be so dynamic, the most important preventive measure will be hand hygiene rather than attempting to evaluate the animal's bacterial carriage at any single point. And key points: To minimize opportunities for transmission, exclude animals that have come directly from a shelter or pound; animals that eat a raw-food diet; animals that haven't been or can't be housebroken or litter-trained.

The guidelines are here, and there's a good MSM summary by Helen Branswell of the Canadian Press here.

26 March 2008

Everything old (in plumbing) is new again?

Robyn asked below about some news about copper fixtures being antimicrobial. I thought I had seen it somewhere, and finally I tracked it down: a Bloomberg News story from yesterday.

Unfortunately the story seems to be based largely on a press release from the, wait for it, Copper Development Association. So it's just possible there may be a whiff of bias here.

The story says:
March 25 (Bloomberg) -- Copper doorknobs, bedrails and faucets can prevent the spread of deadly drug-resistant infections that have become a growing public-health threat in hospitals, according to a metal industry group.

The U.S. Environmental Protection Agency has found copper, brass and bronze can combat infections, including those caused by methicillin-resistant staphylococcus aureus, or MRSA, according to a statement today from the New York-based Copper Development Association.
Digging a little further, it seems the EPA on Tuesday ruled that metal-alloy manufacturers can make "health claims" about their products:
NEW YORK—The U.S. Environmental Protection Agency (EPA) has approved the registration of antimicrobial copper alloys, with public health claims. These public health claims acknowledge that copper, brass and bronze are capable of killing harmful, potentially deadly bacteria. Copper is the first solid surface material to receive this type of EPA registration, which is supported by extensive antimicrobial efficacy testing. ...

The following statements are included in the registration: "When cleaned regularly, antimicrobial copper alloys surfaces kill greater than 99.9% of (specific) bacteria within two hours, and continue to kill more than 99% of (these) bacteria even after repeated contamination," and "The use of a copper alloy surface is a supplement to and not a substitute for standard infection control practices; users must continue to follow all current infection control practices, including those practices related to cleaning and disinfection of environmental surfaces. The copper alloy surface material has been shown to reduce microbial contamination, but it does not necessarily prevent cross contamination."
There may be good science about some metals being sterilizing — there is at least one company producing silver-coated catheters to combat bloodstream infections — but I'm personally confused why this is an EPA ruling and not an FDA one, if the alloys are going to go into hospital fixtures. Perhaps bedrails and IV stands don't qualify as "devices"?

25 March 2008

Random MRSA research, ICEID

Came back from the conference and got slammed with work. (Also, snow, three days in succession. What is it about "Spring" that Minnesota does not understand?) So especial thanks to the 15 readers — you know who you are and Google Analytics does too — who have been diligently checking regardless.

I'm going to do a quick wrap on some of the remaining MRSA papers presented at the Emerging Infections conference. (For a wrap-up of flu and foodborne-disease research, see my final conference story at CIDRAP.)

A quick explainer for those who don't make a habit of going to science conferences, you lucky souls you: For many researchers, this is the first presentation of new or incremental findings. Thus, there's no publication to link to — that's why these ICEID posts aren't so content-rich. Many of these papers may end up in a medical journal in the next year, but for now, not even the abstracts are online.


  • To generate hypotheses about what leads to CA-MRSA infection, a team from the Minnesota Department of Health and the CDC analyzed the life circumstances of 150 people diagnosed with CA-MRSA or MSSA, and found the strongest correlation was between CA-MRSA and a prior history of boils or prior use of antibiotics. (Lead author: K. Como-Sabetti.)
  • In another Minnesota-based report, researchers from the VA Medical Center found that patients who developed MRSA in the hospital had a risk of dying within 6 months that was three times higher than for patients with non-resistant staph. (Lead author: C. Lexau.)
  • And, OK, Minnesota trifecta: A team from the MN DoH and the CDC checked the colonization levels of MRSA patients and their household members over a year and found that, even a year after the first diagnosis. one out of every five patients' households had at least one household member who was still colonized — and that use of Bactroban had made no difference. (Lead author: J. Buck.)
  • Confirming the hypothesis that MRSA can persist on surfaces and contribute to colonization, Texas researchers swabbed bathroom and common-room surfaces at a university and a jail and found the presence of MRSA was 5 times higher on the jail surfaces (6.1% of samples v. 1.2%). Jails are already known to be hotbeds of CA-MRSA — some of the earliest recognized outbreaks were recorded in jails — and this suggests that in a setting where there is a large amount of MRSA, environmental contamination may keep the bug circulating. (Lead author M. Felkner.)
  • An analysis by the Connecticut Department of Public Health of lab-confirmed diagnoses of invasive MRSA between 2001 and 2006 confirms how tricky sorting out HA- and CA-MRSA can be. The incidence of invasive MRSA stayed stable over those five years, but the proportion of community-associated MRSA rose while the proportion of "hospital-onset" (developed no sooner than 48 hours after admission to the hospital) decreased. That makes it sound as though CA-MRSA is increasing overall. But: When the Connecticut state laboratory finegrprinted the strains, they found that 2% of the hospital-onset and 4% of the "hospital-acquired/community-onset" cases were actually caused by community strains, and 76% of the community cases were actually caused by hospital strains. (Lead author: S. Petit.)
That's all on ICEID; tune in two years from now when the conference returns, or stay tuned for more on hospital-acquired infections, mandatory reporting, and disagreements over "search and destroy."

19 March 2008

MRSA and animals - not pets, meat

The International Conference on Emerging Infectious Diseases ended today with more news about a range of infections including MRSA. Most eyebrow-raising: Dr. J. Scott Weese of the Ontario Veterinary College in Guelph, an author of the original MRSA-in-cats paper I described a few posts ago.

Weese's news, tucked in at the end of a comprehensive presentation on MRSA and animals: Analysis of 212 raw pork products sold in four Canadian provinces reveals an average rate of MRSA contamination of more than 9%.

This shouldn't be surprising: Research by Weese and others has been revealing a complex and not well-understood interplay of infection between pigs and nearby humans.
  • A 2005 French paper reported a rate of resistant-staph nasal colonization in pig farmers that was twice as high as among human controls; 57% of the isolates from the farmers were identical to nasal isolates in pigs.
  • Last June, a Dutch study found 39% of pigs in nine major slaughterhouses in the Netherlands carried an identical novel MRSA strain.
  • In December, two studies filled out the picture. A Dutch study reported the prevalence of that novel MRSA strain (dubbed ST 398 and first found in a human in 2003) has risen to more than 21% of all MRSA isolates in the country. A Canadian study (with Weese as senior author), published online ahead-of-print, found MRSA colonization rates of 25% among Ontario pigs and 20% among pig farmers, with most of them sharing the ST 398 strain but some possessing the CA-MRSA strain USA100.
  • A Dutch study in January (first author Engeline van Duijkeren, who did the S. intermedius study from a few posts ago) found that pigs were colonized with MRSA on a variety of types of farms, such as ones that birth pigs and ones that raise them to slaughtering weight.
  • And just to erase any doubts, several Dutch studies have established that the ST 398 strain causes human disease: endocarditis, mastitis, severe hospital-acquired pneumonia and bloodstream infection.
Weese stressed today that his team's finding of MRSA in raw retail meat is very preliminary (though it is backed by a Dutch study from last November that found 34 MSSA strains and two MRSA strains — ST 398 and USA300 — in 79 pork samples). He added, though:

"People don’t tend to handle pork like it is biohazardous, unlike chicken. So there may be a theoretical concern that pork could be a vehicle of methicillin resistance colonization — but it is way too early to say anything about that."
But if you're not already handling raw meat in a careful manner (sterilizing cutting boards, avoiding cross-contamination), it might not be too early to start.

18 March 2008

More on pets and human infections

Another snippet from the International Conference on Emerging Infectious Diseases in Atlanta — again, not about staph, but about the unique role that pets may play in disease transmission:

In the exhibit hall that houses the "posters" (which are just what they sound like: broad swaths of shiny paper printed with graphical presentations of research), there is an intriguing report from West Virgina and the CDC about a novel infection in a cat. The infection is very serious: Corynebacterium diphtheriae, the bacillus that causes diphtheria (the "D" in the childhood DPT vaccine). Diphtheria seldom occurs in the United States — five or fewer cases per year — which is a good thing since it is a horrible disease that causes a membrane to grow across the throat and cut off breathing. It occurs so seldom because humans are the sole host for the disease, and when vaccination renders humans inaccessible territory, diphtheria fades away.

Well, make that: Humans were thought to be the sole host. The report at ICEID describes a pet cat (by the picture, a charming tortoiseshell) who came into a West Virginia veterinary hospital with a very severe ear infection. The infection turned out to be caused by C. diphtheriae that was present not only in that cat, but in a second household cat as well — but not in the cats' two human household members, nor in the eight vet personnel who had been exposed to the cats. Four isolates from the two cats had identical genetic fingerprints, but did not match any C. diphtheria isolates ever analyzed by the CDC.

And this means... what, exactly? It's not not clear how significant a development it is — "More research needed," the CDC says — but it's not good. A disease that was thought to exist only in humans, and thus could be chased out of humans if the percentage of vaccination is high enough, might instead be sustained in humans' environment by another species. And that species just happens to be a very common animal that shares our space very intimately. (Reports that my cats sleep on my pillow are merely vicious rumors. Anyway, it's only during the day.)

If vaccination coverage of the population were perfect, this would not matter: We would be protected anyway. But it's not.

17 March 2008

More on pets and staph

I am at the International Conference on Emerging Infectious Diseases, a biannual meeting sponsored by the CDC that is a disease geek's dream of heaven. The days are extremely packed — about 2,000 attendees and presentations every 15 minutes for most of three days — so blogging may be a little light. Lots of MRSA news here though, so there will be a lot to catch up on.

Here's one example: Engeline Van Duijkeren of Utrecht University reported this afternoon on an outbreak of Staphylococcus intermedius, a staph species that colonizes and causes disease in dogs and cats but is rarely found in humans. Between late 2006 and early 2007, the lab at Utrecht received samples for analysis from six animals, all of which had surgery at the same veterinary hospital: five dogs with orthopedic surgery, one cat with abdominal surgery. The samples yielded identical strains of S. intermedius that were all methicillin-resistant — and resistant to a host of other drugs as well, from 3d and 4th generation cephalosporins to clindamycin to tetracycline to Bactrim.

The lab group found the case cluster and the resistance pattern so striking that they looked around for a common source, including among the clinic's veterinary personnel. They swabbed the surgeon, six technicians, two healthy dogs who lived in the clinic, and the local environment. They found the identical strain in the noses of the surgeon, three of the technicians, and one of the house dogs. Conclusion, van Duijkeren said: The humans (who were colonized, not sick) picked up the strain and redistributed it to the animals under their care. It's the first recorded transmission of MRSI between humans and animals.

(Worth noting: A questioner from the University of Pennsylvania, which has done a lot of work on staph in animals, rose during the Q/A to suggest that the hospital was experiencing a clonal cluster of cases that arose independently, rather than a chain of transmission. Oooh, more fodder.)

As promised last month

Not MRSA but worth reading, I hope: My big project on post-Katrina New Orleans, a narrative profile of the leader of the city's "mental health SWAT team," has been published by MORE Magazine.

Read "After the Deluge" here, and then please take a moment to think what you might do to help the recovery of a fabled and shamefully abandoned city. New Orleans is not even close to being over Katrina. It needs all the help it can get.

13 March 2008

MRSA and cats - an earlier paper

In journalism, there sometimes arises a situation in which a reporter for a major outlet writes a story that is very similar to one that has already been published by a minor outlet, without crediting the minor outlet. We call it "bigfooting." It's not a compliment.

The flurry of attention to the new letter in the New England Journal of Medicine about a pet cat harboring MRSA and reinfecting the cat's owner has a whiff of bigfooting about it. The letter describes a German family with MRSA that particularly persisted in the wife/mother despite treatment until one of their three pet cats was swabbed and decolonized.

The three authors from the Bavarian Food and Health Safety Authority write, "There is evidence that companion animals, mainly dogs, harbor MRSA, and interspecies transmission has been shown in the members of a family and their dog. This case illustrates that MRSA transmission also occurs between humans and cats." There are five cites appended to the letter, on MRSA epidemiology and sequencing and MRSA in dogs. The inference that this is the first recorded case of cat-human MRSA exchange was picked up by several media outlets: — Associated Press, Reuters — and explicitly stated by HealthDay. com, whose story was carried by the Washington Post.

So, the bigfooting: This isn't the first report of cat-human transmission at all. A very nice paper published in December 2006 in Emerging Infectious Diseases (not NEJM, but not exactly obscure as it is published by the CDC) reports the first isolation of the CA-MRSA strain USA300 from a California cat along with an identical strain in the cat's human. And it shows up close to the top of a Medline search, so it wasn't exactly hard to find.

(There is also a 2005 Veterinary Microbiology paper that reports a PVL+ strain in a cat along with several from dogs, but the researchers didn't type the strains and were unable to say whether they were CA or HA; and two letters in the Veterinary Record in 2004 and 2006 citing multiple MRSAs in cats. Neither draw a direct link to human illness.)

OK, enough truth-squadding. Back to HAI and search-and-destroy soon.

10 March 2008

Cautionary tale: Unintended consequences, ripple effects

New story by me, up at the news website of the Center for Infectious Disease Research and Policy, where I am a contributing writer. It's on flu, not MRSA, but it contains lessons that apply to MRSA too.

Gist: This flu season turned out unexpectedly badly, with physicians across the country saying offices and ERs are overwhelmed with very sick patients. In ERs in particular, the dominos fall like this: More patients than usual come in for help; with some of them seriously sick, other patients get pushed further back in the triage queue; while the seriously sick wait in the ER for hospital admission, other patients back up in the waiting room; diversion (turning ambulances away) is called to relieve some of the pressure; and patients are taken instead to another ER, where the process begins again.

The irony here is that flu is an at least partially preventable disease: Under normal circumstances, get a flu shot, sharply reduce your chance of getting the flu. However, this year the flu vaccine and the circulating flu strains don't match well, and many people who stepped up and got the shot still developed flu. And why did the shot not match? It was partly a failure of luck — flu's perpetual genetic drift is unpredictable — but it was also a failure of infrastructure: Federal health planners knew a year ago that one strain was drifting, but that virus didn't grow well enough under lab conditions to get an isolate to vaccine manufacturers in time for it to be included in last fall's vaccine. (See Dr. Nancy Cox's comments in this CDC press briefing; the FDA discussions she refers to are archived here.)

And why did it have to be given to the manufacturers a year ago? Because it still takes 6 months to make commercial quantities of flu vaccine, using a technology that is essentially 50 years old. This despite either 10 years or 32 years of concern over the possibility of a flu pandemic (depending on whether you start counting from the appearance of avian flu H5N1 or the aftermath of the 1976 swine flu).

And why is any of this of concern for MRSA? Because many researchers and clinicians say that the only way to combat MRSA effectively is with a vaccine. Improving flu vaccination has been top of the public health wish-list, and a target of significant government funding, for years now, and yet it is still a disappointing mess. What chance for a lower-profile MRSA vaccine?

07 March 2008

Typing and fingerprinting: Who pays?

More on the issue of doing more microbiology to track the epidemiology of CA-MRSA (raised in an exchange below between me and Medifix, to whom many thanks for being my first commenter!). In my slog through the endless and growing MRSA literature, I came across a paper that poses the problem much better than I did.

In Use of Routine Wound Cultures to Evaluate Cutaneous Abscesses for Community-Associated MRSA (Annals of Emergency Medicine, July 2007; cite here, no abstract), Fredrick Abrahamian and Sunil Shroff of UCLA School of Medicine say that cultures and susceptibility testing are not always necessary. The tests might not be needed, for instance, if a skin/soft-tissue infection suspected of being MRSA is going to be incised and drained without antibiotics being prescribed; or if antibiotics are going to be prescribed, but physicians already know local susceptibility patterns and plan to order a drug that will provide coverage. In both cases, having additional information about the strain infecting the patient is not going to make any difference to the patient's treatment.

That information will make a difference to understanding the local, regional, national epidemic. But as Abrahamian and Shroff say: "One must determine if it is ethical to make an individual pay the cost of a test for a perceived public health benefit."

The obvious answer is to say the CDC should do it — they are after all the arbiters of population-level public health. Only, you know, their budgets have been being cut...

06 March 2008

And to Scott McPherson for the bloglove hat-trick!

Journalists aren't really accustomed to people liking us, so I'm a little dizzy. But huge thanks also to Scott McPherson, who was sweet enough to mention my first book, on the CDC's outbreak SWAT teams. Scott's day job is in the thick of politics — he's the chief information officer for the Florida House of Representatives — and he regularly nails the disconnect between public-health policy and the messy real world. Read him here.

And also to Crawford Kilian's readers!

Crof, dean of avian-flu bloggers and indefatigable proprietor of H5N1, very kindly called this "an excellent new site." To have the support of such experienced bloggers is a wonderful thing.

Big welcome to FLA_MEDIC's readers!

The energetic and always-thoughtful proprietor of Avian Flu Diary very kindly called out this blog today. (In the intro box over on the right, I invited reading by MRSA researchers, MRSA victims and major disease geeks — he says he's No. 3.) So welcome to anyone who found there way over here from there. And if you haven't been to his blog yet, go now: His essays and analyses on the possibility of pandemic flu are always worth reading.

"Leaky" hospitals: Is CA-MRSA really HA? Or v.v?

Within the community of scientists researching MRSA — which must be getting bigger all the time, since MedLine records about 25 new papers every week — there is some tension over whether hospital-acquired or community-associated MRSA causes the most disease and early death (morbidity and mortality, in epidemiologist-speak).

The latest paper to stoke this fire was a much-reported, CDC-authored Journal of the American Medical Association paper and an accompanying commentary that were published last Oct. 17. The paper found that invasive MRSA (the most serious cases, of bloodstream infections and endocarditis for instance) causes an estimated 94,360 infections and 18,650 deaths per year. The commentary famously and accurately said that MRSA accounts for more deaths in the United States each year than AIDS does. (Paper: Klevens RM, Morrison MA, Nadle J, et al. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA 2007;298:1763-71. Abstract here. Commentary: Bancroft EA. Antimicrobial resistance: it's not just for hospitals. JAMA 2007;298:1803-4. MedLine listing, but no abstract.)

An interesting feature of the Klevens paper, which was based on data from the CDC's Active Bacterial Core surveillance system, is that it re-sorts MRSA cases using a new set of definitions: community-associated, hospital-onset, and a new category they called "hospital-acquired, community-onset" — that is, colonized in the hospital but not symptomatic until after the person was discharged. Using these new definitions, the CDC group found that the vast majority of invasive MRSA cases were healthcare associated: 26.6% of the 8987 cases on which they based their study occurred while the patients were in hospital, and 58.4% after they left and were living at home again. Only 13.7 percent of the invasive MRSA cases turned out to be community-associated.

In other words, the most serious cases of MRSA look like they are CA cases, but actually are not.

That finding prompted the team to call for better infection control: "If, in fact, these infections represent acquisition during transitions of care from acute care, it follows that strategies to prevent and control MRSA among in-patients, if properly applied, may have an impact on these infections as well as on the traditional hospital-onset infections."

What's interesting about this is that it appears to return us to the "leaky hospitals" hypothesis of CA-MRSA. This view, which reigned from the emergence of MRSA in the 1960s to well into the 1990s, held that hospitals are the source of almost all MRSA cases if you just look hard enough. It was dislodged by microbiological analysis in several key papers in the late 90s, which showed that the strains causing CA-MRSA cases really were genetically different from the hospital strains.

The CDC paper seems to swing opinion back the other way, toward HA-MRSA as the source of the most serious cases of MRSA disease at least. But, here's an important point: The CDC paper bases its resorting on an assessment of risk factors, such as whether patients had prior exposure to the health care system. It does not sort the cases by microbiology: Of the 8987 cases used in the analysis, genetic-fingerprint (PFGE) results were available for only 864.

Now another group of researchers has arisen to say: That's not good enough. In a letter published in February, Michael David and colleagues of the University of Chicago Children's Hospital chide the CDC group for not considering that someone may have been in a healthcare environment, been discharged, and afterward picked up a community strain, In other words: Unless you do the microbiology, you won't know which cases are which. (David MZ, Siegel JD, Chambers HF, Daum RS. Determining whether methicillin-resistant Staphylococcus aureus is associated with health care. JAMA 2008;299:519. MedLine listing, but no abstract.)

Important note: The University of Chicago group, led by Dr. Robert Daum, were the first to challenge the "leaky hospitals" hypothesis and raise the alarm about CA-MRSA in a pathbreaking paper — really the first significant CA-MRSA paper — in 1998. (Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk. JAMA 1998;279:593-8. Abstract here.)

So: Are healthcare strains, with their unique resistance patterns, responsible for the worst community cases? Are community-staph cases really healthcare cases in disguise? And what if community staph was causing healthcare cases as well?

More on that to come.

04 March 2008

Rapid tests and detection of HAIs

From the New York Times' business section, a good discussion today of the new technologies that have made possible rapid detection and identification of patients colonized with MRSA.

The story focuses on Cepheid, a 12-year-old California biotech that may score its first-ever profits on the basis of its MRSA rapid test, which returns results in 60-90 minutes, compared to the several days required for a bacterial culture. (Other test manufacturers, with products already out or in the pipeline: Becton-Dickinson, Roche, GenProbe.) Among the early users: The company's own CEO, John L. Bishop, who picked up MRSA at his gym.

Rapid tests such as Cepheid's make "search and destroy" programs plausible: They return results so rapidly that hospitals can get started on treating or decolonizing patients before any staph that has been carried into the hospital can spread.

The piece does a nice job of exploring why hospitals would be opposed to "search and destroy." Among the reasons: Suspicion of being a new marketing opportunity for the test-producing companies; focusing on eradicating only one organism instead of instituting broad infection-control programs that will combat other HAIs as well.

03 March 2008

HAI reporting: Should it be legislated?

So assume for the purposes of argument that hospitals do not eliminate hospital-acquired infections, and that the states in which they operate require them to begin public reporting of their infection rates — as a means of (choose your motivator) shaming them into doing better, or warning the public if they do not.

This argument is not hypothetical: Nineteen states have enacted HAI-reporting legislation, and another half-dozen have HA-MRSA reporting requirements, with more states considering MRSA bills this spring.

On the one hand, we know that infection control is difficult: Bugs linger not just in obvious places — walls, floors — but on essential objects with complex, hard-to-clean surfaces such as computer keyboards and stethoscopes. But on the other hand, we know that good infection control saves not only lives, but money and time as well.

So, infection control — specifically, "search and destroy" — by legislation: Fair or not fair?

A set of articles published last year argues the two sides. From Dr. Barry Farr, professor emeritus at the University of Virginia Health System, long-time leader in infection control: Legislation is not the best solution, but it should be enacted because the healthcare industry has been dragging its feet for too long. From the boards of directors of the Association of Professionals in Infection Control and the Society for Healthcare Epidemiology of America: Legislating specific actions that hospitals must take creates an unfunded mandate and may have unintended consequences.

02 March 2008

More about hospital-acquired infections

As I said earlier, a panel of heavy hitters (and me, just the moderator) will meet later this month to debate the trend of states forcing hospitals to fess up to hospital-acquired infections. Nineteen states now require it and an additional handful have additional laws that specifically require MRSA reporting.

The unstated assumption behind those laws is that hospitals both should and can control hospital-acquired (AKA nosocomial) infections. But in the real world, the strategies for doing that are still being argued about. This is surprising, to say the least, since hospital-acquired MRSA has been brewing in the United States for 40 years. (First cite, for medical-history geeks: Barrett FF, McGehee RF Jr, Finland M.Methicillin-resistant Staphylococcus aureus at Boston City Hospital. Bacteriologic and epidemiologic observations. N Engl J Med. 1968 Aug 29;279(9):441-8.)

The tactic that has worked the best — in hospital units, whole hospitals, geographic areas and in Europe entire countries — goes by the jargon name "Active detection and isolation (ADI)" and the shorthand description "Search and destroy." Briefly, it calls for identifying new hospital patients whose recent history puts them at risk of being infected or colonized, testing them for the bug, and putting them under isolation until they are cleared of the bug.

It sounds straightforward, and currently there are about 150 studies to prove that it works. (Here is one of the most recent, about Evanston Northwestern Healthcare in Illinois.) But in the United States, hospitals take their infection-control cue from several official authorities, including the Healthcare Infection Control Practices Advisory Committee (HICPAC) chartered by the Centers for Disease Control; and a joint task force of the members of two professional organizations, the Society for Healthcare Epidemiology of America (SHEA) and the Association for Professionals in Infection Control (APIC). And those two groups do not agree: The task force says ADI should be used routinely — but HICPAC delinks detection from isolation and makes isolation just one of many options a hospital can try as a means of curbing a bug's spread.

The difference provokes furious debate among infection-control professionals, leaves hospitals confused, and has sparked a grassroots movement among families of victims of nosocomial infections. For a great overall exploration, check out Arthur Allen's recent article at the newly launched Washington Independent.