Look at any local antimicrobial susceptibility profile worldwide and you are likely to find that E.coli susceptibility to trimethoprim is sitting at somewhere around 75-80%.
So why therefore does trimethoprim remain such a popular choice on empirical antibiotic protocols?
There may be a few reasons for this:
- The urine specimens that come into the lab are essentially a biased cohort. i.e. they do not represent everyone who will be diagnosed (and treated) with a UTI as many patients will get the diagnosis on the basis of symptoms or dipstick urinalysis alone.
- Institutes that set antimicrobial susceptibility breakpoints may well err on the side of caution when setting the breakpoints. i.e. they will not want to call an antibiotic susceptible to a bacterium when it is actually resistant.
- Trimethoprim usually acheives higher concentrations in the urine than elsewhere in the body.
So the reason that trimethoprim remains on the empirical antibiotic protocols for UTI in so many institutions is because it generally works, and it works in almost certainly a higher percentage than we suggest it does (in the lab).
I am sure there are many stakeholders who have been disconcerted by the in-vitro trimethoprim susceptibility rates to E.coli in their local institution, and may have changed prescribing habits because of it.
In my area, E.coli susceptibility rates to trimethoprim have remained stubbornly stable at around 78-80% for the past 20 years. Trimethoprim has been an empirical choice for uncomplicated UTI in local guidelines for the whole of that time period.
Sometimes you just need to look at the data, then work out how it translates into reality.
I published a similar post several months ago but it was lost from the website due to technical problems. Apologies if this post looks familiar!