Maryn McKenna

Journalist and Author

Brand-new research: Vast increase MRSA, CA-MRSA diagnoses among kids

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I’m on the road today and have what feels like seconds between commitments, but there’s a brand new piece of research this morning that I think you folks should know about. It’s an early-online release from Pediatrics by researchers from 3 states. It uses a database called the Pediatric Health Information Systems analyze diagnosis codes and antibiotic treatment of kids treated for staph at 25 US children’s hospitals  from 1999 to 2008, and it finds:

The incidence of methicillin-resistant S aureus (MRSA) infections during this period increased 10-fold, from 2 to 21 cases per 1000 admissions, whereas the methicillin-susceptible S aureus infection rate remained stable. Among patients with S aureus infections, antibiotics that treat MRSA increased from 52% to 79% of cases, whereas those that treat only methicillin-susceptible S aureus declined from 66% to <30% of cases. Clindamycin showed the greatest increase, from 21% in 1999 to 63% in 2008.

To translate, for those not used to reading scientific literature:

  • a 10-fold increase in MRSA diagnoses over 10 years
  • a 3-fold increase in what was not the most commonly prescribed drug, one useful for the different resistance profile of community infections
  • clindamycin (used in mild and also invasive infections) eclipsing vancomycin (last-resort drug for invasive cases) as the most-used drug — which could be a sign of changes in prescribing patterns, changes in seriousness of the cases seen, or a warning that with so much use, clindamycin resistance could emerge more quickly, as happened when vancomycin came off the shelf in the 1990s and began to be used more.

It will take me a while to download and read the paper (hard to do in the car), but that’s the topline news. Update to come.

Community MRSA rates rising, and epidemics converging

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A study published Tuesday in Emerging Infectious Diseases makes me happy, despite its grim import, because it confirms something that I will say in SUPERBUG: Community MRSA strains are moving into hospitals, blurring the lines between the two epidemics.

The study is by researchers at the excellent Extending the Cure project of Resources for the Future, a group that focuses on applying rational economic analysis (think Freakonomics) to the problem of reducing inappropriate antibiotic use. (Here’s a post from last year about their work.)

Briefly, the researchers used a nationally representative, commercial (that is, not federal) database of isolates submitted to clinical microbiology labs, separated out MRSA isolates, divided them into whether they originated from hospitals or outpatient settings (doctors’ offices, ambulatory surgery centers, ERs), and analysed them by resistance profile, which has been a good (thogh not perfect) indicator of whether strains are hospital or community types (HA-MRSA or CA-MRSA). They cut the data several different ways and found:

  • Between 1999 and 2006, the percentage of staph isolates from outpatient settings that were MRSA almost doubled, increasing 10% every year and ending up at 52.9%. Among inpatients, the increase was 25%, from 46.7% to 58.5%.
  • Among outpatients, the proportion of MRSA isolates that were CA-MRSA increased 7-fold, going from 3.6% of all MRSA to 28.2%. Among inpatients, CA-MRSA also increased 7-fold, going from 3.3% of MRSA isolates to 19.8%.
  • Over those 7 years, HA-MRSA did not significantly decrease, indicating that CA-MRSA infections are not replacing HA-MRSA, but adding to the overall epidemic.

So what does this mean? There are a number of significant aspects — let’s say, bad news, good news, bad news.

Bad: CA-MRSA strains are entering hospitals in an undetected manner. That could simply be because patients entering the hospital are colonized by the bug and carry it with them. But it could also be because healthcare staff who move back and forth between outpatient and in-patient settings — say, an ambulatory surgical center and a med-surg ward — could be carrying the bug with them as well.

Good: If they are detected (analyzed genotypically or for drug sensitivity), CA-MRSA strains are less expensive to treat because they are resistant to fewer drugs, and some of the drugs to which they are susceptible are older generics, meaning that they are cheaper.

Very Bad: The entrance of CA-MRSA strains into hospitals risks the trading of resistance factors and genetic determinants of transmissibility and colonization aptitude in a setting where bacteria are under great selective pressure. Several research teams have already seen this: In several parts of the country, CA-MRSA strains have become resistant to multiple drug families.

Is there a response? The work of Extending the Cure focuses on developing incentives that will drive changes in behavior around antibiotic use. These results, lead author Eili Klein told me, call for developing incentives for creating rapid diagnostic tests that will identify not just that a bug is MRSA, but what strain it is, so that it can be treated appropriately and not overtreated.

The results also underline the need for something that is particularly important to me: enhanced, appropriately funded surveillance that will define the true size of the MRSA epidemic and delineate the behavior of the various strains within it. Right now, surveillance is patchy and incomplete, done partially by various CDC initiatives and partially by the major MRSA research teams at academic medical centers. As we’ve discussed, there is no national requirement for surveillance of patients, and very few state requirements; there is no incentive for insurance companies to pay for surveillance, since it benefits public health, not the patient whose treatment the insurance is paying for; and there is a strong disincentive for hospitals to disclose surveillance results, because they will be tarred as dirty or problematic. Yet to know what to do about the MRSA epidemic, we first have to know the size and character of what we are dealing with, and we do not now.

The cite is: Klein E, Smith DL, Laxminarayan R. Community-associated methicillin-resistant Staphylococcus aureus in outpatients, United States, 1999–2006. Emerg Infect Dis. DOI: 10.3201/eid1512.081341

A parent's plea and confusion

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

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

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

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

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

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

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

MRSA and pets

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

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

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

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

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

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

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

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

While taking a flu break, a MRSA round-up

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Constant readers, the H1N1 (Virus Formerly Known as Swine) Flu story remains a bit intense. I’ve missed a few MRSA stories over the past few days, so here is a round-up.

First, though, if you’re curious about what the swine flu reaction says about our ability to handle a pandemic, you might take a look at this story I wrote Friday at CIDRAP. Quick version: Over-reaction on the part of the “worried well” — and people seeking testing and not knowing where to get it — put ERs into meltdown nationwide. If we were facing a virus that was not only fast-spreading but virulent, we could be in serious trouble.

On to MRSA:

  • Therapy animals as a vector: In a letter to the Journal of Hospital Infection, Drs. J. Scott Weese and Sandra L. Lefebvre of the Ontario Veterinary College at the University of Guelph report on two therapy dogs that became transiently colonizedwith C. difficile (on its paw pads) and MRSA (on its coat; found on the hands of its handler) after visiting health care facilities, demonstrating how easily bacteria can move in and out of hospitals. Constant readers will recognize Weese’s name: He is one of the most important investigators of MRSA in food animals and pets, and among other things has written infection-control guidelines for therapy animals.
  • In the Canadan Medical Association Journal, Drs. Anne G. Matlow and Shaun K. Morris of the University of Toronto and the Hospital for Sick Children caution that while hospitals may be getting better at infection control, there is not yet as much attention to it as there should be in ambulatory-care settings: urgent care centers, surgery centers and doctors’ offices. They offer a checklist of the minimal things that a physician practice should do.
  • And in the UK, Baroness Masham of Ilton, a member of the House of Lords, offers her online notes on serious infections with community MRSA, which the Brits are calling PVL-MRSA in recognition of the toxin that the strain produces. The notes are in advance of a series of questions that she intends to pose to government ministers during a Question Time on Wednesday.

More soon.

MRSA strains crossing borders: US CA-MRSA to Italy

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Swine flu continues to dominate the headlines, but other pathogens don’t read the papers. Case in point: New news about a US community strain being found and treated in a woman in Italy — better treated, as it turns out, than she was in California, where she was infected.

In a new letter in Emerging Infectious Diseases (a free journal published online and in print by the CDC — it’s your tax dollars at work, just read it, already), Carla Vignaroli, Pietro E. Varaldo, and Alessandro Camporese of the Polytechnic University of Marche in Ancona amd the Santa Maria degli Angeli Regional Hospital, Pordenone report the case of

a 36-year-old Italian woman (who) was seen at Pordenone Hospital (northeastern Italy) for spider-bite–like skin lesions on the face, characterized by rapid evolution to furuncles and small abscesses. The infection had started ≈1 month earlier in California, where she had spent several months on business (wine import-export), and where she had been treated empirically with amoxicillin/clavulanate for 10 days (1 g, 3×/day), with no clinical improvement.

(At this point, I know every clinician reader and everyone who has had a MRSA skin infection is shaking his or her head. Surely by now the knowledge that “spider bite” is practically diagnostic for CA-MRSA has penetrated? But apparently not, since she was given amoxicillin/clavanulate, AKA Augmentin, which is partially penicillin-based.)

When the woman’s lesions were cultured, they turned out to be caused by USA400, the original community strain, which back in the 1990s was known as MW2. That’s interesting, especially in California, since USA300 has become such a dominant strain. Nevertheless, the key point is that USA400, as with USA300, has barely been recorded in Italy:

All 3 previously reported cases of CA-MRSA infection in Italy were caused by type IV SCCmec, PVL-positive strains, none of which, however, belonged to the ST80 clonal lineage that predominates in Europe (7). The first case (in 2005) was a necrotizing pneumonia caused by an ST30 isolate; the 2 other cases (2006) were severe invasive sepsis and a neck abscess, both caused by ST8 (USA300) isolates.

The concern, of course, is that once imported, they will not remain rare:

The case we note here documents the importation of a US pathogen into a country in Europe, from an area where the pathogen is widespread and has been highly virulent since the late 1990s, to an area where its penetration in the past has been poor.

The cite is: Vignaroli C, Varaldo PE, Camporese A. Methicillin-resistant Staphylococcus aureus USA400 clone, Italy [letter]. Emerg Infect Dis. 2009 Jun; [Epub ahead of print]. DOI: 10.3201/eid1506.081632