Wednesday, April 15, 2009

Look! Over there! More MRSA!

Now that I have your attention, let’s talk about the greatest emerging antibiotic resistance challenge in healthcare settings:  multiply drug resistant gram negative rods (MDR-GNRs).  Reports keep coming in about the alarming rates of MDR-GNR carriage and infection in long term care facilities (LTCFs).  I just ran across one in a journal I don’t often read, the Journal of Gerontology.  This study, by Erika D’Agata’s group in Boston, found that MDR-GNRs (defined in this study as resistant to 3 or more antibiotic classes) were more prevalent in clinical cultures than were MRSA or VRE at one large LTCF in Boston.  Another recent report from Anthony Harris’ group in Maryland found that carriage of Acinetobacter baumannii was more common than MRSA among long-term acute-care residents.

Compared with the MDR-GNR universe, MRSA is very simple:  one gene (mecA), one altered target, one resistance phenotype.  For MDR-GNR?  Not so much.  Detection and prevention approaches remain a tremendous challenge, which is why Acinetobacter outbreaks are more likely to require closure of units to new admissions than are outbreaks due to any other organism.

In this context, I think what we really need are more laws that force hospitals to focus their antibiotic-resistance prevention resources on MRSA.  Don’t you agree?


  1. Here's our reply to Dr. Diekema's "They Write Comments":

    Many who oppose proactive control measures to control MRSA and VRE infections have vaguely implied that the ~180 controlled, epidemiologic studies showing control of MRSA or VRE with ADI were somehow inferior to the controlled epidemiologic studies available regarding isolation of all other nosocomial pathogens, and that we must therefore now have “controlled trials” of isolation for MRSA and VRE [but not other pathogens]. Most saying this have meant RCTs and explicitly said so (which is why we assumed Diekema meant RCTs). This call for RCTs began during this decade [after it became clear that the vast majority of available epidemiologic studies suggested that ADI was effective].
    Is the study by Harbarth “the best example of a well-designed, [unrandomized] controlled trial” of ADI efficacy as Dr. Diekema suggests? We don’t think so. Here are several reasons:
    1. Multiple recent studies of ADI to begin controlling MRSA HAIs already endemic to a hospital and its surrounding healthcare system, including the one by Huang praised by Diekema, required more than a year to begin showing any reduction, but Harbarth’s intervention phase lasted only 9 months.
    2. Interventions implemented as hospital policy (i.e., not a temporary experiment as in Harbarth’s study) may be more likely to obtain HCW buy-in and compliance.
    3. Harbarth’s definition of adequate isolation compliance was that barrier materials were available near the door of an isolation room. Most people who weren’t born yesterday know this to be inadequate documentation of compliance with donning and removing barrier materials at the right times.
    4. ADI doesn’t involve magic. The idea should be to find and isolate the full reservoir for spread, but Harbarth admitted that nothing was done to find and control the strains already being transmitted in the surgical wards when the study started—unlike the study by Huang. Despite the fact that 274 admission screen-negative patients were found by routine clinical culture to acquire MRSA in the study wards, no screening of inpatients was used to detect the reservoir for this spread. Given that routine clinical cultures usually detect only 15% to 30% of colonized hospital patients, the size of the undetected, unisolated reservoir likely extended well beyond these 274 [favoring a false negative result]. If spread continues when all patient reservoirs are found and isolated (which wasn’t attempted by Harbarth), then HCW screening should be considered as well because colonized HCWs occasionally have been responsible for epidemic spread [as emphasized by Harbarth himself in a recent review]. But this also wasn’t done. Given that ADI was used so poorly to find and isolate the reservoir for spread on the study wards, it’s hard to understand why anyone would call this study “well-designed.”
    5. Huang’s study confirmed the results of over 100 prior studies reporting MRSA control with ADI, adding credibility to Huang’s result. Based upon his data, Harbarth implied that ADI may not work in surgical patients, neglecting to mention that over 30 prior studies had reported controlling MRSA with ADI in surgical patients (including the study by Huang). This makes Harbarth’s result at odds with the bulk of the epidemiologic data regarding ADI efficacy in surgical patients.
    6. Lastly, it should be pointed out that of the 26 patients identified with MRSA prior to admission who received a full course of mupirocin treatment and chlorhexidine baths followed by vancomycin perioperative prophylaxis, none acquired an MRSA-HAI. The data for the rest were not as clearly presented, but it seems that the vast majority of the other patients identified as MRSA-colonized on admission didn’t receive the benefit of full decolonization therapy and 286 (> 70%) undergoing surgery reportedly didn’t receive vancomycin perioperative prophylaxis either. The point here is that screening doesn’t confer magical benefit—if suboptimal prophylactic therapy is prescribed to those found to be colonized, this won’t help prevent SSI.

    Barry M. Farr MD, MSc
    William R. Jarvis, MD

  2. We thank Farr and Jarvis for their continued interest in this blog!
    Regarding their critique of the Harbarth study, readers are referred to the letters to the editor (and the responses to those letters) that were published in JAMA 2008;300:503-506. Responding again to their arguments here serves no useful purpose, and might cause me to fall asleep and bang my head on the keyboard of my computer.

    I’ll make only a couple short points:

    1. We don’t know anyone who doesn’t want to be proactive about MRSA control. Farr and Jarvis have long divided the infection control community into two groups: those who believe active surveillance and isolation (or ADI) is absolutely necessary for MRSA/VRE control, and those who don’t care about the rampant spread of MRSA or VRE. This is wrong, and is counterproductive to a cause we all share, which is to reduce morbidity and mortality from all hospital acquired infections, MRSA and VRE included. Both Mike and I have been proactive about MRSA control at our respective hospitals, and those efforts have paid off.

    On a lighter note, if Farr and Jarvis could share with us a list of those who don’t want to be proactive about MRSA or VRE control, we’ll track them down and report them to the authorities.

    2. We look forward to Farr and Jarvis subjecting the multitude of observational studies they cite in support of ADI to the same intense scrutiny as they have the Harbarth study (and the yet-to-be-published NIH study!). Others have already done so, and we can provide them with those systematic reviews if they haven’t read them.

    If it is true that we can only prevent infections if we know in advance exactly who carries each drug resistant organism, then we’re all in very big trouble.