A little bit of knowledge can be a bad thing. So can too much…
The acronym ESCHAPPM ( or something similar) will be familiar to most microbiologists. (a similar acronym SPICE, is sometimes used instead)
- Enterobacter spp.
- Serratia spp.
- Citrobacter freundii
- Hafnia spp.
- Aeromonas spp.
- Proteus spp.
- Providencia spp.
- Morganella morganii
Because we are clever microbiologists, we know this group of organisms may have inducible beta-lactamase activity, and we advise the clinicians of this, often provoking a reflex switch in anti-microbial therapy to carbapenems. Not only clinicians, but there are plenty of ID physicians who make this automatic transfer to carbapenems the moment the word ESCHAPPM is mentioned, my hospital included.
The thing is however, do all patients with infections by an ESCHAPPM organism require a carbapenem?
Almost certainly not…
If we use a carbapenem for every infection due to one of these organisms, then this amounts to a significant amount of carbapenems. This is therefore an important an important antimicrobial stewardship issue. We are supposed to be trying to decrease the use of broad spectrum antibiotics, not increase them.
But we have read the textbooks, and we are clever…
And yet, if we look at the literature, there is very little evidence to support the theoretical dangers of using a beta-lactam in such patients. In fact, there are several small studies out there that support the non-inferiority of beta-lactams in such patients, particularly in non-life threatening illnesses.
Not to mention there are other options out there, fluoroquinolones, sulphonamides, etc.
We are simply scared.
Here is what I generally do (rightly or wrongly):
- In a patient with bacteraemia due to an ESCHAPPM organism, as long as they are clinically improving I am happy to continue therapy based on the phenotypic susceptibility results.
- In patients with UTIs due to ESCHAPPM organisms, even if in hospital, I feel no need whatsoever to move to carbapenems.
- I reserve carbapenem use in “ESCHAPPM” patients to bacteraemic patients who are getting worse, and also for patients with chronic infections, e.g. prosthetic joint infection, on the rationale that the longer the treatment, the more chance you have of getting clinically relevant inducible beta-lactamase activity.
We need to take a more pragmatic approach to ESCHAPPM organisms and their treatment. We also need larger scale trials so we can be more confident in our decisions and adopt such approaches into guidelines.
and we need to be brave…