MRSA research round-up: hospitals, vitamins, pets

Because I've been so behind, there's so much to cover! So let's dive in:

In today's Archives of Surgery, researchers from Seattle's Harborview Medical Center report that one simple addition to the routine of caring for trauma patients made a significant difference to the patients' likelihood of acquiring a hospital-associated infection: bathing them once a day with the antiseptic chlorhexidine (in an impregnated wipe). Patients who were bathed with the antiseptic wipe, compared with patients wiped down with an inert solution, had one-fourth the likelihood of developing a catheter-related bloodstream infection and one-third the likelihood of ventilator-associated MRSA pneumonia. Cite: Evans HL et al. Effect of Chlorhexidine Whole-Body Bathing on Hospital-Acquired Infections Among Trauma Patients. Arch Surg. 2010;145(3):240-246.

How important are hospital-acquired infections? Here's a piece of research from a few weeks ago that I sadly failed to blog at the time: Just two categories of HAIs, sepsis and pneumonia, account for 48,000 deaths and $8.1 billion in health care costs in a single year. Writing in the Archives of Internal Medicine, researchers from the nonprofit project Extending the Cure analyzed 69 million hospital-discharge records issued in 40 states between 1998 and 2006. Hospital charges and number of days that patients had to stay in the hospital were 40% higher because of those infections, many of which are caused by MRSA — and all of which are completely preventable. Cite: Eber, MR et al. Clinical and Economic Outcomes Attributable to Health care-Associated Sepsis and Pneumonia. Arch Intern Med. 2010; 170(4): 347-53.

 What else could reduce the rate of MRSA infections? How about Vitamin D? South Carolina scientists analyze data from the NHANES (National Health and Nutrition Examination Survey 2001-2004), a massive database overseen by the CDC, and find an association between low blood levels of Vit. D and the likelihood of MRSA colonization. More than 28% of the population is Vitamin D deficient. MRSA colonization is increasing in the US. Can giving Vit. D decrease MRSA carriage? More research needed. Cite: Matheson EM et al. Vitamin D and methicillin-resistant Staphylococcus aureus nasal carriage. Scand J Infect Dis. 2010 Mar 8. [Epub ahead of print]

And finally: Who else carries MRSA? Some unlucky pet owners have found that animals can harbor human strains, long enough at least to pass the strain back to a human whose colonization has been cleared. So it makes sense to ask whether humans who spend time with pets are carrying the bug. Last month's Veterinary Surgery reports that the answer is Yes. Veterinarians are carrying MRSA in very significant numbers: 17% of vets and 18% of vet technicians at an international veterinary symposium held in San Diego in 2008. Cite: Burstiner, LC et al. Methicillin-Resistant Staphylococcus aureus Colonization in Personnel Attending a Veterinary Surgery Conference. Vet Surg. 2010 Feb;39(2):150-7.

MRSA and pets

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

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

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

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

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

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

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

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

More MRSA in pigs, in Portugal

A brand-new report, in a letter to the International Journal of Antimicrobial Agents, indicates that ST398 "pig MRSA" has been found in Portugal for the first time.

Constanca Pomba and colleagues from the Technical University of Lisbon swabbed and cultured the noses of pigs and veterinarians on two pig farms in different regions of Portugal, and also checked the air at both farms.

What they found:

• On Farm A: All pigs and the veterinarian positive for ST398, the pig-origin strain that has been found so far in Iowa, Ontario, the Netherlands, France, Denmark, Germany and Austria and has, depending on the country, caused human disease and/been found on retail meat. The veterinarian was transiently colonized, which is to say that he was not carrying the bug long-term.
• On Farm B: All pigs — but neither of two veterinarians — positive for a different MRSA strain, CC (or ST) 30. This is very interesting, because CC30 is usually a drug-sensitive strain (MSSA, methicillin-sensitive S. aureus), and has been found in pigs primarily in Denmark and France. In Portugal, it is a human MSSA hospital-infection strain.

Strains from both farms were resistant to tetracycline; this is turning out to be a great marker for these strains having emerged due to antibiotic pressure in animals, because tetracycline is very commonly used in pigs. but not much used for MRSA in humans. The strains have the genes tetK and tetM, so they are resistant not just to tetracycline itself, but to the whole class of tetracyclines including doxycycline and minocycline. The Farm B strains also carried the gene ermC, which encodes resistance to erythromycin.

So what does this tell us?

• First, that (once again), every time people look for ST398, they find it; it is now a very widely distributed colonizing bug in pigs, and is repeatedly spreading to humans. What we don't know, because all these studies are so new, is whether ST398 is actively expanding its range, or has been present in all these countries for a while. We have been anticipating its presence or spread (take your pick at this point) through the European Union because of open cross-border movement of food animals, meat, and agriculture and health care workers.
• And second, it should tell us that it is really past time to start looking for this more systematically. Every finding of ST398 that we have (long archive of posts here) is due to an academic research team who decided to look for the bug. None of the findings, to date, have come from any national surveillance system. (NB: Except for the first human colonizations in the Netherlands, which were found as a result of the national "search and destroy" rules in hospitals.)

Of note, the European Union is running a study now that is supposed to report ST398 prevalence at any moment (as they have been saying since 2007). It is not expected to be comprehensive, since it was piggy-backed onto another study, but it is something. The US government has not been so enterprising.

The cite is: Pomba, C. et al. First description of meticillin-resistant Staphylococcus aureus (MRSA) CC30 and CC398 from swine in Portugal. Intl J Antimicrob Agents (2009), doi: 10.1016/j.ijantimicag.2009.02.019

MRSA in a hospital nursery

Via the Boston Globe and the blog of the hospital's CEO comes work of an ongoing outbreak of community-associated MRSA in the newborn nursery at Beth Israel Deaconess Medical Center in Boston:

...between last November and March, BIDMC experienced several occurrences or “clusters” of methicillin-resistant Staphylococcus aureus, or MRSA, infections that have affected some of our patients (19 newborns and 18 mothers) days to weeks after discharge from our obstetrics and newborn services. These infections have been, for the most part, superficial skin infections and breast infections. It is important to note that no babies in our Neonatal Intensive Care Unit have been affected. (Paul Levy, president and CEO, BIDMC)

The paper and the blog post report that the Massachusetts Department of Public Health (DPH), the Boston Public Health Commission (BPHC), and the federal Centers for Medicare and Medicaid Services (CMS) are all investigating, and the Centers for Disease Control and Prevention (CDC) has sent epidemiologists to sort out transmission. Levy, the CEO, admits on his blog that in sorting out this outbreak, the hospital has found its staff's infection-control procedures to be not-adequate.

By sheer chance, this occurs as I am writing a chapter on just this phenomenon of the blurring of the MRSA epidemics of hospital-acquired and community-associated staph. As constant readers know, the original MRSA strains arose in hospitals in the 1960s (1961 in the UK, 1968 in the US), and the separate community strain was first noticed in the 1990s. (Though there are intriguing hints about earlier cases that a few smart physicians noticed and no one else took seriously.)

But for about 5 years now, the community strain has been moving into hospitals and causing outbreaks there, particularly in mothers and newborns: first in New York City, and then in Houston, and now quite widely. The Globe article references some others.

Why this is important: Because CA-MRSA and HA-MRSA are different, and not just because they originally occurred in different settings or had different resistance profiles. CA-MRSA (which is a term that is obviously becoming much less useful than it once was) also appears, in newer research, to colonize the body in different ways — not just the nostrils, but also the armpit, groin, and genitals, possibly including vaginal colonization. So there may be an additional risk of transmission from mother to child during birth that has not been anticipated — or from mother to child to health care worker to another child to that child's mother.

Now, mind you: Good infection control ought to anticipate all those posibilities, because good infection control does the right thing every time. But as we're finding out, very few institutions manage to train their staff in such a way that they do the right thing every time or close to it (Novant Health Care, creators of the Soapacabana video, seem to have managed it, and won a major award for it). Most health care workers, even very well-intentioned ones, find themselves in time crunches or responding to unexpected emergencies, and make risk-based judgments about what they must do, and what they can afford to let slide.

If CA-MRSA is becoming a hospital organism, and its unique risks of colonization are not recognized by the hospital staff, then their judgments of relative risk will be off — and what would have been a relatively safe risk to take in one instance becomes a significantly unsafe risk in another.

That's all speculation, of course: I'm not reporting on Beth Israel and have no inside knowledge of their outbreak. But it does describe a phenomenon that has been occurring in other medical centers, and it underlines one of the risks attendant on these epidemics blurring. When CA-MRSA moves into a hospital, the MRSA ecology changes, and the risks of transmission change. It is essential that staff training keep up with that, or additional mistakes will be made.

More news on ST398, "pig MRSA," in Europe

Two new papers have been posted ahead-of-print to the website of Emerging Infectious Diseases, the free journal published monthly by the CDC. (It's a great journal. Just go.)

One, from the Austrian National Reference Center for Nosocomial Infections, reports that out of 1,098 isolates from infected or colonized hospital patients collected between 2006 and 2008, 21 were ST398, the "pig strain" that we have talked so much about here. Of the 21, 15 were colonized and 5 had actual infections (one person lost to followup, apparently); of the 5 infections, 4 were minor, and one was a very serious infection in a knee replacement in a 64-year-old farmer.

In a separate piece of math that is not fully explained, the researchers note that the prevalence of ST398 in Austria has risen to 2.5% of MRSA isolations, from 1.3% at the end of 2006 — close to double, and especially rapid given that Austria's very first ST398 sample was found during 2006.

The second paper is much more complex; it deals with the prevalence of multiple MRSA strains in the cross-border region where Germany, Belgium and the Netherlands bump up. (Apparently EU bureaucracy calls an area like this a "Euregio." Ah, jargon. This is the EMR, the Euregio Meuse-Rhin.) The concern here is that MRSA prevalence is very different in different EU countries; in the Netherlands, which has an active surveillance "search and destroy" policy in its hospitals, MRSA represents only 0.6% of all staph — but the rates are 13.8% in Germany and 23.6% in Belgium, which either do not do active surveillance or began to much more recently. So as people move freely across borders, from a high-prevalence area to a low-prevalence one, they could bring a resistant bug with them that then could find a foothold because there is an open ecological niche.

This study analyzed 257 MRSA isolates from hospitals in the border region that were collected between July 2005 and April 2006: 44 from Belgium, 92 from Germany, and 121 from the Netherlands. Of the Dutch isolates, according to typing, 12 (10%) were ST398. These were all from patients who were identified as colonized when they checked into hospitals practicing "search and destroy"; none represented actual infections.

So, what does this tell us? A couple of things, I think. First, it documents the continued presence of ST398 in Europe; in other words, it wasn't a blip and doesn't appear to be going away. Second, it underlines both that you find it when you look for it, and also that it remains a small portion of the overall MRSA picture. But, we immediately have to add, it's a small portion that wasn't present at all just a few years ago.

And it should underline that what we need, and are not getting in this country or in Europe, is much more comprehensive surveillance and research to understand ST398's place in MRSA's natural history, so that we can understand where it is only an emerging disease, or truly an emerging threat.

The cites are:
Krziwanek K, Metz-Gercek S, Mittermayer H. Methicillin-resistant Staphylococcus aureus ST398 from human patients, Upper Austria. Emerg Infect Dis. 2009 May; [Epub ahead of print]
Deurenberg RH, Nulens E, Valvatne H, et al. Cross-border dissemination of methicillin-resistant Staphylococcus aureus, Euregio Meuse-Rhin region. Emerg Infect Dis. 2009 May; [Epub ahead of print]

MRSA news from Europe - Society for General Microbiology

The annual meeting of the UK's Society for General Microbiology is taking place this week, so here's a quick roundup of MRSA-related news. As with these posts from a year ago, abstracts are not online; in a few cases there are press releases from the science-news service EurekAlert.

• MRSA-colonized patients who have been identified in a hospital by active surveillance culturing may not need to be isolated to prevent their bacteria being transmitted to other patients by healthcare workers — provided hospital staff and visitors adhere to very vigorous handwashing. (P. Wilson, University College Hospital, London; press release)
• An engineered coating made of titanium dioxide with added nitrogen could be employed as an antibacterial surface in hospitals; exposure to ordinary white light activates the compound to kill E. coli and may be useful against MRSA also. (Z. Aiken, UCL Eastman Dental Institute; press release)
• The natural antiseptics tea tree oil and silver nitrate enhance bacterial killing when combined, which may also allow them to be used in lower doses – important for avoiding toxicity. It may also be possible to deliver them encapsulated in engineered sphere made of lipids called liposomes. (W.L. Low, University of Wolverhampton; press release)
• Overuse of antibiotics in farming is not only breeding resistant bugs in animals, it is also changing soil ecology and depleting nitrogen-fixing bacteria that improve soil fertility. The antibiotics are affecting soil when manure from drug-using farms is spread as fertilizer. (H. Schmitt, University of Utrecht; press release)

MRSA research at Society for Healthcare Epidemiology of America meeting

As promised, a round-up of some of the research presented at the annual meeting of the Society for Healthcare Epidemiology of America (SHEA), held last weekend in San Diego. (Disclosure: I was on the faculty for the meeting; in exchange for co-hosting a session, SHEA will be reimbursing me for airfare and hotel. I wasn't otherwise paid, though.) There were 143 presentations on MRSA; here are a few.

I'm going to put in links to the online abstracts — I have SHEA's permission to do this — but I can't guarantee how long they will stay up. For those outside the science world, what happens at these meetings is that research is presented, in slide/PowerPoint sessions or in a poster, as a preliminary step to getting it published in a journal. Once a journal expresses interest, a cone of silence descends, the researchers are asked not to discuss the research until the paper is printed, and the abstract will probably be taken offline.

So, efforts to control hospital MRSA are showing some success:

• Invasive hospital-onset MRSA infections declined 16% from 2005 to 2007, and hospital-associated community-onset infections went down almost 9% — probably, though not provably, because of in-hospital prevention campaigns. (A. Kallen et al.)
• MRSA control in a small ICU (22 beds) leads to MRSA reductions throughout a 270-bed Montana community hospital. (P.J. Chang et al.)

But those efforts face some complexities:

• Swabbing the nose and culturing the swab, the classic test to check for MRSA colonization, misses 30% of positive patients because they are colonized in the groin or armpit. (C. Crnich et al.)
• If a hospital does not use AST (active surveillance and testing, or "search and destroy") it may seriously underestimate its MRSA incidence, though it may be able to detect general trends. (P.J. Chang et al.)
• But medical centers of similar size and situation that did v. did not use AST achieved similar reductions in hospital infections. (K. Kirkland et al.)
  

Community strains are moving into hospitals:

• Most of the cases of MRSA colonization identified in a Delaware healthcare system were found so soon after admission that they must have begun out in the community and were not due to hospital transmission. (K. Riches et al.)
• The proportion of MRSA bloodstream infections caused by community strains (proven microbioogically) doubled at Chicago's main public hospital between 2000 and 2007. (K. Popovich et al.)
• One out of every 7 ICU cases of MRSA in Atlanta's major public hospital involved a community strain. (H. Blumberg et al.)
• The number of MRSA infections brought to a Chicago-area ER increased 566% between 2002 and 2007, and was seasonally clustered (D. Buchapalli et al.)

And at the same time, hospital strains are moving out into the community:

• Hospital-associated community-onset cases accounted for 58% of all invasive MRSA in the US between 2005 and 2007, with patients undergoing dialysis or those who have been in long-term care the most vulnerable. (J. Duffy et al.)

This is what hand hygiene looks like

Contant reader Robyn pointed out an amazing image in the New England Journal of Medicine issue I discussed below. I missed it (thanks, Robyn!), so I went back and retrieved it. Here's what you're looking at:

The Cleveland Veterans Affairs Medical Center discovered via a routine nasal swab that a quadriplegic patient was colonized with MRSA; the patient had not had any signs that would have indicated an infection. To satisfy their curiosity over how much MRSA a healthcare worker might pick up from a patient whom they did not know was colonized, they had a health care worker do an abdominal exam of the patient — let's underline that: abdominal; nowhere near his nose. Then they pressed the worker's hand onto a growth medium that had been tuned with antibiotics so that it would allow MRSA to grow but suppress other bacteria.

That's what you're looking at above. All of that red is MRSA. The image on the right is what grew after the same worker did hand-sanitizing with alcohol foam and then pressed the same hand onto an identical culture plate. What's growing? Nothing at all.

Here's the back story, quoted from NEJM (re-paragraphed):

A 24-year-old man who had quadriplegia due to a traumatic spinal cord injury was found on routine surveillance cultures to have methicillin-resistant Staphylococcus aureus (MRSA) colonization of his anterior nares. He had no history of MRSA infection or colonization.
To assess the potential implications of the patient's MRSA carriage for infection control, an imprint of a health care worker's ungloved hand was obtained for culture after the worker had performed an abdominal examination of the patient. The MRSA colonies grown from this handprint on the plate (CHROMagar Staph aureus), which contained 6 µg of cefoxitin per milliliter to inhibit methicillin-susceptible S. aureus, are pink and show the outline of the worker's fingers and thumb (Panel A).
With the use of a polymerase-chain-reaction assay, the mecA gene, which confers methicillin resistance, was amplified from nares and imprint isolates. After the worker's hand had been cleaned with alcohol foam, another hand imprint was obtained, and the resulting culture was negative for MRSA (Panel B).
These images illustrate the critical importance of hand hygiene in caring for patients, including those not known to carry antibiotic-resistant pathogens.

The cite is: Donskey, Curtis J., Eckstein, Brittany C. IMAGES IN CLINICAL MEDICINE: The Hands Give It Away. N Engl J Med 2009 360: e3

UPDATE: The tireless and too-seldom-thanked crew at ZoneGrippeAviare, who provide pandemic news for the Francophone community, have translated this post into French. Mes mercis respectueuses!

Brilliant entrepreneur asks: "So why CAN'T you fix this?"

Constant readers, you'll note that posting has slowed down a bit: I am deep into a chapter that is giving me some difficulty. (And I seem to be playing holiday host to an unexpected bout of bronchitis. I'm sure I didn't need both lungs...)

But here's something that crossed my monitor this morning, and it's worth looking at. Sir Richard Branson, founder of Virgin Air and many other extremely successful entrepreneurial efforts. has accepted a post as vice-president of the Patients Association, a nationwide nonprofit that advocates for hospital patients in the UK. Speaking up in his new position, Branson gave an interview to the BBC in which he talked about hospitals' failure to curb MRSA:

It feels like they have tinkered with the problem rather than really got to the heart of the problem. The hospitals are there to cure people. They are not there to kill people.

It's a marvelous interview — read the whole thing, it's not long — because it's such a breath of fresh air. Branson is an outsider to health care, but he knows how to make businesses work. And as the head of an airline, he's extremely familiar with what we in the US call "never events":

Sir Richard says the health service could learn a lot from the airline and rail industries on how to avoid mistakes."In the airline industry if we had that kind of track record we would have been grounded years ago," he said."In the airline industry if there is an adverse event that information is sent out to every airline in the world. And every airline makes absolutely certain that that adverse event doesn't happen twice."

So his advice is brutally practical: Health care workers carry MRSA? Screen and swab them. Workers are positive for MRSA? Treat them, and take them out of direct patient contact for two weeks. That costs money? Spend the money: It's less costly in the end than killing your patients.

MRSA in newborns on Prince Edward Island: HA? CA? Matters?

There's been a running story for several weeks now about the Queen Elizabeth Hospital on Prince Edward Island (home to mussels and Anne of Green Gables). The hospital struggled earlier this year with an outbreak of MRSA and a second outbreak of VRE among adult patients. It got those under control, but since earlier this month has been dealing with a new outbreak of MRSA in its newborn nursery, according to the PEI Guardian:

Nine newborns and one mother have now tested positive for MRSA. Five of those nine cases can be connected to the same source. (Byline: Wayne Thibodeau)

The stories are detailed, for a small paper — they go into depth about the cleaning measures the hospital is taking — and yet they don't answer the questions that we here want to know. Does "tested positive" mean colonized or infected? Does "connected to the same source" mean they all have the same strain, or does it mean there is an epidemiologic link?

In the latest news (Tuesday's paper and online edition), the hospital reports that it is doing nasal swabs on more than 300 staff, with the intention to do a 7-day decolonization regimen on anyone who turns up positive. They won't however, disclose the source when they find it — though, again, it's not clear whether that means not identifying the staffer (appropriate) or not admitting that it is a nosocomial outbreak (inappropriate and at this stage lacking in credibility):

Rick Adams, CEO of the Queen Elizabeth Hospital, said about 290 staffers have already been screened.
“In terms of the test results, we’re not going to be making anything public,’’ Adams told The Guardian.
“We want to make sure the environment here is supportive of staff and create a climate where they can feel comfortable and open to come forward and be screened knowing that any results will be kept strictly confidential.’’
Adams said he realizes a solid argument can be made that the public should be informed if the source is found and that source is a staff member.
But he said the public should also realize the hospital is doing everything it can to prevent a further spread of the superbug.
“The staff are under enormous pressure. They feel like they are under a microscope.’’ (Byline: Wayne Thibodeau)

Some readers may know that it is outbreaks among newborns that have demonstrated that the designations "community-associated" and "hospital-acquired" are passing out of usefulness. There have been several MRSA outbreaks in newborns and their mothers in the US (in New York City, Houston, Chicago, Los Angeles and Houston again because Baylor College of Medicine has been particularly alert to this) that were clearly nosocomial, and yet when the microbiology was done, were found to be caused by community strains.

Why does this matter? Well, for the PEI hospital, it may not: They have an outbreak, it appears to be nosocomial in nature, and whether it is HA left over from their earlier outbreak, or CA that came in via a health care worker or a pregnant woman, mostly affects what drugs they give the children and mothers if those patients do in fact have infections. And for those of us who are primarily concerned with nosocomial infections, the distinction may also feel not-relevant: Failures of infection control are failures of infection control and should not happen period full stop.

But for those of us who are are also interested in the natural history of this perplexing bug, the answer to what is going on at the Queen Elizabeth will be an important piece of information, because it could underline that the distinction between HA and CA is becoming increasingly artificial. The epidemics are converging.

New newspaper series on HA-MRSA

The Seattle Times this morning launched an three-day investigative project on incidence of HA-MRSA in Washington State that is worth reading.

As readers here already know, MRSA is not a reportable disease, and there are no diagnosis codes that directly correspond to MSRA that make infection or death easily trackable through hospital records or death certificates. The Times' team came up with some innovative data-drilling techniques and apparently did a massive amount of number-crunching to come up with the incidence estimates that underpin their reporting. They use those to challenge hospitals' reluctance to undertake surveillance and treatment that would wipe out MRSA on colonized patients and thus reduce the likelihood of MRSA infecting those patients or spreading to others via healthcare workers who neglect infection control. (NB, Michael Berens, the series' co-author, did a huge project on nosocomial infections when he was at the Chicago Tribune a number of years ago.)

I am puzzled by one thing I am seeing on the story's web page — one of the items in the break-out box that sums the story up very quickly to attract eyeballs to it. It says: "About 85 percent of people infected with MRSA get the germ at a hospital or other health-care facility. " That figure doesn't make sense to me; it sounds as though it is a mis-translation of the CDC finding a year ago (in the Klevens JAMA paper) that approximately 85% of invasive cases of MRSA have hospital-associated risk factors. Constant readers will remember that estimate has been challenged by researchers on community MRSA, who believe that CA-MRSA accounts for a much larger proportion of the current epidemic than has been acknowledged, and think that the wide spread of the community strain is the actual driver of the overall epidemic. I can't see where in the text the Times team has done the math to support that assertion, so if anyone else spots it, or knows the reference it comes from, please let me know.

MRSA in meat in Louisiana: pig meat, human strain

On Nov. 3, I posted on an enterprising group of TV stations in the Pacific Northwest who had retail meat in four states tested for MRSA. I said at the time that it was the first finding of MRSA in meat in the US that I knew of.

Turns out that I was wrong by three days. On Oct. 31, the journal Applied and Environmental Microbiology published an electronic version of a study that they will be printing in the paper journal on some future date. Journals do this when a finding is so important or timely that it should see the light immediately, rather than wait through the additional weeks or months of print production.

And this finding is certainly timely. Shuaihua Pu, Feifei Han, and Beilei Ge of the Louisiana State University Agricultural Center have made what appears to be the first scientifically valid identification of MRSA in retail meat in the United States. But — and this is an important point — it is not the swine strain, ST 398, that has been found in meat in Canada and Europe, and in hospital patients in Scotland and the Netherlands, and in pigs in Iowa; and in humans in New York, though that strain was drug-sensitive.

Instead, what the researchers found (in 5 pork and 1 beef samples, out of 120 bought in 30 grocery stores in Baton Rouge, La. over 6 weeks in February-March 2008) was USA300, the dominant community MRSA strain, and USA100, the main hospital-infection strain. In other words, they found meat that had been contaminated during production by an infected or colonized human, not by a pig. As they say:

...the presence of MRSA in meats may pose a potential threat of infection to individuals who handle the food. ... (G)reat attention needs to be taken to prevent the introduction of MRSA from human carriers onto the meats they handle and thereby spreading the pathogen.

As we've discussed before, the primary danger from MRSA in meat is not that people will take the bug in by mouth (though that is a danger, since S. aureus because of its toxin production can cause severe foodborne illness — and these researchers found, overall, an S. aureus contamination rate of 46% of their pork samples and 20% of their beef samples). Rather, the danger is that people handling the raw meat will be careless in preparing it, and will colonize themselves by touching the meat and then touching their own noses or mucous membranes, leading to a possible future infection. As reader Rhoda pointed out in a comment last week, people could also infect themselves directly, by getting MRSA-laden juice or blood into an abrasion or cut.

So: Be careful in the kitchen, keep meat separate from other foods, wash cutting boards and knives, and (say it with me, now) wash your hands, wash your hands, wash your hands.

The cite for the new paper: Pu, S. et al. Isolation and Characterization of Methicillin-Resistant Staphylococcus aureus from Louisiana Retail Meats. Appl. Environ. Microbiol. doi:10.1128/AEM.01110-08. Epub ahead of print 31 Oct 08.

Housekeeping note: This is the 16th post I've written on MRSA in food animals and/or meat. Providing all the links to the previous posts is starting to obstruct the new news. So if you are looking for all those past posts, go to the labels at the end of this post, below the time-stamp, and click on "food." You should get something that looks like this.

Outbreak of Zyvox-resistant staph (breaking news from ICAAC 2)

Physicians from Madrid reported today on what's believed to be the first outbreak of MRSA caused by a strain that was resistant to linezolid, usually known as Zyvox, a relatively new and costly drug that is used for complicated MRSA infections and when older drugs fail.

Linezolid resistance in single cases has been recorded before — the first isolate I can see in a quick scan of the literature dates to 2002 — but this appears to be the first outbreak.

Dr. Miguel Sanchez of the Hospital Clinico San Carlos said the outbreak was discovered April 13, 2008 in an ICU patient and subsequently spread to 11 other patients in the ICU and two elsewhere in the hospital. The patients, 8 men and 4 women, had been in the unit for at least three weeks for a variety of reasons; they were intubated, had central venous catheters, and had been receiving broad-spectrum antibiotics. None of them were colonized with MRSA on admission. The outbreak went on for 12 weeks, until June 27.

It was eventually shut down by a combination of strategies: taking the patients off linezolid in favor of other anti-staph drugs (vancomycin and tigecycline); drastically restricting linezolid use, a policy that is already followed by many US hospitals; checking the patients very frequently for colonization; and cohorting them, which means grouping them together physically, away from uninfected patients, and putting them under isolation.

In a quick briefing with reporters, Sanchez seemed to suggest that the hospital does not believe its infection control failed. The hospital swabbed 91 environmental surfaces (such as bed rails and room furniture) and the hands of 47 health-care personnel and found only one sample that grew the linezolid-resistant strain on a culture. A case-control study to find the cause is being conducted, he said.

Half of the patients died, he said, but not as a result of the linezolid-resistant strain.

Sanchez' data slides were not available to reporters this evening. (More precisely, they were delivered to the press room, but in a format that wasn't readable). I'll update with more details if/when we get access to them. Meanwhile, the cite is: M. De la Torre, M. Sanchez, G. Morales et al. "Outbreak of Linezolid-Resistant Staphylococcus aureus in Intensive Care." Abstract C2-1835a.

Much new news on hospital-acquired infections

There's a ton of new, and conflicting, findings on prevention and detection of hospital-acquired MRSA and other infections.

First: Today, in the journal Infection Control and Hospital Epidemiology, three researchers from Virginia Commonwealth University add to the ferocious debate on "search and destroy," the colloquial name for active surveillance and testing: that is, checking admitted patients for MRSA, isolating them until you have a result, and and if they are positive, treating them while continuing to isolate them until they are clear. "Search and destroy" has kept in-hospital MRSA rates very low in Europe, and has proven successful in some hospitals in the United States; in addition, four states (Pennsylvania, Illinois, California and New Jersey) have mandated it for some admitted patients at least. Nevertheless, it remains a controversial tactic, with a variety of arguments levelled against it, many of them based on cost-benefit.

Comes now Richard P. Wenzel, M.D., Gonzalo Bearman, M.D., and Michael B. Edmond, M.D., of the VCU School of Medicine, to say that the moment for MRSA search and destroy has already passed, because hospitals are now dealing with so many highly resistant bugs (Acinetobacter, vancomycin-resistant enterococci (VRE), and so on). They contend that hospitals would do better to pour resources into aggressive infection-control programs that broadly target a spectrum of HAIs.

The abstract is here and the cite is: Richard P. Wenzel, MD, MSc; Gonzalo Bearman, MD, MPH; Michael B. Edmond, MD, MPH, MPA. Screening for MRSA: A Flawed Hospital Infection Control Intervention. Infection Control and Hospital Epidemiology 2008 29:11, 1012-1018.

Meanwhile, the US Government Accountability Office recently released a substantive examination of HAI surveillance and response programs, in states and in hospitals, that looks at:

• the design and implementation of state HAI public reporting systems,
• the initiatives hospitals have undertaken to reduce MRSA infections, and
• the experience of certain early-adopting hospitals in overcoming challenges to implement such initiatives. (from the cover letter)
  

The report is too thick to summarize here, but here are some key points:

• No two places are doing this the same way — which means that data still does not match state to state
• Experts are still divided about how much MRSA control is necessary
• Hospitals that have undertaken MRSA-reduction programs have taken different paths
• But MRSA control does work: It does reduce in-hospital infections, but at a cost.

This report is an important bookend to an earlier GAO report from last April that explored the poor state of MRSA surveillance nationwide. Read it if you wonder why we don't really know how much MRSA - in hospitals or in the community - we have.

I am stillworking my way through the new Compendium of Strategies to Prevent Healthcare-Associated Infections in Acute Care Hospitals, released a week ago by a slew of health agencies (Joint Commission, CDC, et al.) and health organizations (American Hospital Association, ACIP, SHEA, IDSA et al.), to see how much the MRSA strategies have actually changed. If anyone has any comments, please weigh in!

Five-fold increase in flu+MRSA deaths in kids

I have a story up this evening at CIDRAP News about a new paper in the journal Pediatrics that analyzes the incidence of child deaths from pneumonia caused by the combination of MRSA and flu, a sad and scary development that we've talked about here, here and here.

(NB: CIDRAP News is the original-reporting and news-aggregation arm of the Center for Infectious Disease Research and Policy at the University of Minnesota, an infectious disease research center headed by noted epidemiologist Michael Osterholm, PhD. I have a part-time appointment there. CIDRAP News is the best-read infectious-disease website you have never heard of, with about 10 million visitors a year, and is a notable resource for news on seasonal and pandemic flu, select agents and bioterrorism, and foodborne disease.)

It is bad netiquette and not fair use to reproduce another publication's entire story here, even if I wrote it. Here though are the highlights:

• 166 children died of influenza in the past three seasons (2004-05, 2005-06, 2006-07) according to 39 states and 2 local health departments (86 this year in preliminary reporting)
• The proportion of deaths from bacterial co-infection rose each year, from 6% to 15% to 34%, a five-fold increase
• Almost all of the bacterial co-infections were staph; 64% of them MRSA
• The rapid rise in MRSA colonization (from 0.8% of the population in 2001 to 1.5% in 2004 — that's more than 4 million people) may be playing a role
• And, some of these deaths could have been avoided if children had had flu shots — but overall, only 21% of under-2s and 16% of 2- to 5-year-olds get the two shots they need to be fully protected against flu.
  

Please click through to CIDRAP for more.

The cite is: Finelli L, Fiore A, Dhara R, et al. Influenza-associated pediatric mortality in the United States: increase of Staphylococcus aureus coinfection. Pediatrics 2008;122:805-11.

News round-up

I'm deep into writing again and therefore slipping on posting; apologies to regular readers! But here are some items of importance from the past week:

• Wednesday (Aug. 20) marked the first anniversary of Illinois' signing and immediately enacting the MRSA Screening & Reporting Act, the first state law to mandate that hospitals screen all ICU and other high-risk patients for MRSA colonization and to isolate and treat them until they are clear. This law would never have been passed without the extraordinary advocacy of MRSA survivor Jeanine Thomas, founder of the MRSA Survivors Network (site here and in the blogroll).
• Also as of Wednesday, California came within one step of passing its own MRSA laws, SB 1058 and SB 158. They await the signature of Gov. Arnold Schwarzenegger — but with California's budget in a $15.2 billion deficit freefall, new legislation there may be held hostage until a budget deal is agreed. Important addition: SB 1058 is also called "Nile's Law," after Nile Calvin Moss, who died of MRSA in April 2006. His parents Carole and Ty have pushed relentlessly for a MRSA law in his memory.
• Plus, a great find thanks to Carole Moss: The Washington State Department of Health has put together an excellent pamphlet, Living with MRSA, that explains MRSA infection, colonization, decolonization and infection-control care at home in excellent everyday language.
• And finally, another blog worth knowing about: GERMblog, written by Dr. Harley Rotbart, professor and vice-chair of pediatrics at University of Colorado School of Medicine and author of Germ Proof Your Kids: The Complete Guide to Protecting (Without Overprotecting) Your Family from Infections. I interviewed Dr. Rotbart recently for a magazine story and his advice was clear, science-based and sensible. His blog is now in the blogroll.

MRSA colonization - the long-term risk

One of the ongoing puzzles of MRSA's behavior is the significance of colonization, that situation of MRSA living on the skin — or in the nostrils or other locations close to the body's external surface — without causing illness. It's not known how frequently MRSA colonization occurs, for one thing: The long-standing estimate of 1% of the population has been challenged by a number of recent studies.

Another persistent question has been whether the risk of illness and death changes as colonization continues. It has been established that up to one-third of newly colonized carriers will become seriously ill within a year of their acquiring the bug (Huang, SS. et al., Society for Healthcare Epidemiology of America Annual Meeting 2006, abstract 157 - not online that I can find)— but what happens beyond that? Does the risk of illness persist or decrease?

In Clinical Infectious Diseases, the same team that defined the risks of recent colonization report that there are significant risks to long-term carriage as well: 27% of invasive illness in the second year and 16% thereafter, based on a review of 281 patients who were followed for at least one and up to four years at Brigham & Women's Hospital, a Harvard Medical School teaching hospital. These patients become very ill, and in addition use a significant amount of health-care resources:

At our hospital, there are 2–3 times as many hospital admissions involving patients previously known to harbor MRSA than there are hospital admissions of individuals who are newly detected as MRSA carriers each year.

What is the precipitating event that tips MRSA carriage over into MRSA illness? It may be health care. In other words, the long-term carriers do not become ill with MRSA disease and then come to the hospital. Instead, they come to the hospital for some other reason, and the surgery, IV placement, dialysis etc. they receive allows their MRSA strain to slip past the protective barrier of their skin and begin an invasive infection.

We submit that these high risks of MRSA infection among culture-positive prevalent carriers are not only preferentially detected because of hospitalization but may, in fact, be incurred because of the device-related, wound-related, and immunologic declines associated with a current illness.

This raises the question of whether any admitted patient found to be colonized should undergo the routine known as decolonization before any other procedures are performed — and whether institutions and insurance companies will be open to the additional hospital days and drug costs that will represent.

The cite is: Datta, R. and Huang, SS. Risk of Infection and Death due to Methicillin-Resistant Staphylococcus aureus in Long-Term Carriers. Clinical Infectious Diseases. 2008 47:176-81.

Isolation: Doesn't work if healthcare workers contaminate themselves afterward

In the new Emerging Infectious Diseases, there is a small but very smart study that ought to get wider play. It was done by a PhD candidate at University of North Carolina, Chapel Hill named Lisa Casanova, with the help of faculty and the local health department.

Background: In certain highly infectious environments — including in-hospital isolation — healthcare workers wear what is usually known as "personal protective equipment" or PPE. PPE generally includes gloves, gown and an eye shield, goggles or face-splash guard (also called "barrier precautions") as well as a mask or a respirator ("respiratory protection"). PPE protects the healthcare worker while he or she is in the patient's presence, but it poses a problem when the worker leaves that environment, because the PPE is likely to be carrying the disease organism on its surface. If the worker doesn't doff the PPE very carefully, he or she might contaminate himself/herself and become infected or colonized, or spread the organism further in the healthcare environment.

This accidental contamination was a significant problem in the 2003 SARS epidemic — so after SARS was over, the Centers for Disease Control and Prevention came up with a recommended procedure for taking off PPE (on this page, half-way down). Casanova decided to test how well the protocol actually works.

Answer: Not so much. She had 10 volunteers (men and women, left- and right-handed) dress in PPE, contaminated the equipment in certain spots ("front shoulder of gown, back shoulder of gown, right side of N95 respirator, upper right front of goggles, and palm of dominant hand") with a benign virus, had the volunteers take off their PPE, and then tested them for the virus's presence. Results:

Transfer of virus to both hands, the initially uncontaminated glove on the nondominant hand, and the scrub shirt and pants worn underneath the PPE was observed in most volunteers.

Casanova recommends changes: additional PPE; different PPE and doffing protocols, such as are used in surgical suites; or PPE impregnated with antimicrobials. (#1 and #3 of course would be more costly; #2 would require procedural change but not necessarily additional garments).

She also raises a vital ongoing issue for MRSA infection control: that healthcare workers may not be punctilious about hand hygiene because they believe that gloves are adequate protection. Only, as this study demonstrates, they are not:

This study also indicates the need for continued emphasis on hand hygiene. A barrier to improving hand hygiene compliance rates is the belief that gloves make hand hygiene unnecessary (14). This is contradicted by our study and others showing that organisms can spread from gloves to hands after glove removal (15). Even if double gloving is incorporated into protocols for PPE use, it is not a substitute for proper hand hygiene.

The cite is: Casanova L, Alfano-Sobsey E, Rutala WA, Weber DJ, Sobsey M. Virus transfer from personal protective equipment to healthcare employees’ skin and clothing. Emerg Infect Dis. 2008 Aug; [Epub ahead of print]

The "vicious cycle" of HA-MRSA

In the new issue of Lancet Infectious Diseases there's a marvelous analytical review of the complex relationship between hospital overcrowding and understaffing and the rise of hospital-acquired MRSA.

You can feel intuitively that these phenomena must be linked:

• If a hospital has more patients, its staff will be more stressed;
• If they are more stressed, they may neglect handwashing and other infection-control measures;
• If budget shortfalls cause staff cuts, the remaining staff will be more stressed still;
• If infection control is neglected, more patients will acquire MRSA;
• Since MRSA patients are sicker and stay longer, more beds will be full;
• Since there are more patients, staff will be more stressed;
• Since MRSA patients are more costly, budgets will be more stressed.

And so on. Because it is a review article it is also an excellent guide to the medical literature on this aspect of the MRSA problem, with 140 cites.

The citation is: Clements, A. et al. Overcrowding and understaffing in modern health-care systems: key determinants in meticillin-resistant Staphylococcus aureus transmission. The Lancet Infectious Diseases 2008; 8:427-434.

Natural remedies - upsides and downsides

For obvious reasons there is a lot of interest in finding new sources for antimicrobial compounds that work against MRSA, and in finding non-drug remedies as well. There's been a small upsurge in reports of such research recently, which may be coincidence or may simply be due to the timing of certain scientific meetings.

Notably there was the report of "four or five super-active peptides" found in the blood of alligators and reported at the American Chemical Society's annual meeting a few weeks ago (first author Lancia Darville. Louisiana State University; Science News' take on the story is here), and another report at the same meeting of antimicrobial compounds in clay (authors Lynda Williams and Shelley Haydel of Arizona State University; press release here).

And just a few days ago, the journal Clinical Infectious Diseases posted ahead-of-print a study from the Netherlands on a "medical-grade honey" named Revamil that reduced skin colonization by resistant bacteria 100-fold.

That study's authors raise a red flag: that while honey has an antibacterial reputation that reaches back into prehistory, most investigations of honey as an antimicrobial have tripped up on the lack of product standardization, with batches from different areas, or even the same area at different times, showing significant variations in antibacterial activity. (Standardization of active ingredient is a long-standing problem for herbal remedies as well; regulatory authorities in Europe, where herbal preparations are more mainstream, are far ahead of the US on tackling this.)

It's important to remember that, naturally-sourced or not, antimicrobials are antimicrobials and must be handled with care, or they may invoke the sort of unintended consequences that brought us resistant organisms in the first place. For an excellent example of this, see a little-noticed paper from Irish researchers published last year in the the Journal of Antimicrobial Chemistry. That group found problems with the well-researched natural antimicrobial tea tree oil (Melaleuca alternifolia), which is commonly used in "natural" toiletries and cleaning products (and which I have in my own medicine cabinet). When tea tree oil was applied to bacterial colonies at a lower-than-lethal dose, the surviving bacteria developed resistance not only against the oil's active ingredient, but also against a range of antibiotics including vancomycin.