The rocket-science of a CPE screen & isolate policy

Last weeks’ blog from Jon Otter on the practice of CPE screening and isolation raised some interesting comments (on twitter) emphasizing the difficulties in policy making for infection control. The two comments that struck me were: (1) … screening for CPE sounds logical “but does it work in long-term care facilities with high-levels of endemicity?” And “I use it in my hospital, but face difficulties in convincing others because of lacking scientific evidence for CPE.”

The answer to the first question (does it work in settings with high endemicity?) is most probably NO. The evolution of the hospital epidemiology of any MDR pathogen starts with “in the beginning it is not there”. The first encounters are sporadic monoclonal outbreaks. In the absence of an effective response, this stage will proceed to “more frequent and larger monoclonal outbreaks”, and if the hospital is still asleep it will end in polyclonal endemicity. The likelihood of succes of infection control measures to reverse a situation to a previous state  declines rapidly. Controlling a monoclonal outbreak, in the absence of introduction of similar strains in the hospital, is (relatively) easy. Definitely  easier than eradicating all carriage from the hospital if there is repeated introduction leading to multiple simultaneously occurring monoclonal outbreaks. And I am not aware of a succesful change from polyclonal endemicity back to a setting with sporadic and small (rapidly controlled) monoclonal outbreaks (happy to be enlightened on this).

The message here – for CPE – is: act immediately, with the first outbreak you see, and keep on doing this. Waiting for better times is elusive (in the end someone will say “penny wise, pound foolish”). If you are “blessed” with polyclonal endemicity, all you can do is to taper the endemicity level, prevent invasive infections, wait for new antibiotics (or combinations) and publish your difficult-to-treat infections.

The answer to the second question (where is the evidence for CPE?) is more difficult. Those that request scientific evidence probably think that we are scientists, as in scientists that can provide undisputable proof of something. Here we must lay off our pride and convince those people that we are not true scientists, but intelligent physicians (or alike), with capacity for biological and epidemiological reasoning, susceptible to conventional  wisdom and able to learn from past experience.  As long as CPE is not in the community (as is ESBL) and depends on healthcare settings for transmission, as does MRSA (real MRSA, not LA-MRSA) and VRE, old-fashioned infection control measures can prevent further spread from identified carriers, if applied. Doesn’t seem ethical to me to make that a research question that needs a control group for an answer.

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