Monthly Archives: December 2018

“Making a difference to gonorrhoea treatment”

Confessions of a Microbiologist, , ,


For several years now, the core empirical treatment for gonorrhoea has been intramuscular ceftriaxone. This wasn’t always the case, but the resistance rates for both penicillin and ciprofloxacin have crept up to levels that meant using them as empirical antibiotics was no longer a satisfactory option.

N. gonorrhoeae is particularly vulnerable to antibiotic resistance, essentially because it has no hiding place.

There are not many viable options left after ceftriaxone, so we end up using ceftriaxone on everybody with gonorrhoea or suspected gonorrhoea. And as a result we are starting to see ceftriaxone resistance…

Selection pressure…

The solution of course is to avoid using ceftriaxone on every patient for empirical treatment of gonorrhoea. 

And this is now becoming achievable with the release of a commercial rapid diagnostic PCR assay, ResistancePlus® GC ,that not only detects the presence of N. gonorrhoeae (using both OPA and PorA targets), but also looks for the mutation conferring ciprofloxacin resistance (GyrA S91 F).

In the patients who have ciprofloxacin susceptible gonorrhoea, this will allow oral ciprofloxacin to be prescribed in a timely fashion, thus allowing the selection pressure of ceftriaxone on N. gonorrhoeae to be reduced.

This is a great example of how good diagnostic stewardship can lead to good antimicrobial stewardship. Hopefully such advances in molecular diagnostics will prevent the rather ugly scenario of “untreatable gonorrhoea”

Michael

“Cohort Bias”

Data Interpretation, The Science of Microbiology, , ,

At my laboratory we only test nasal Staphylococcus aureus susceptibility to mupirocin in the following two circumstances:

  • Prior to joint replacement surgery as part of a Staphylococcal decolonisation bundle
  • In patients where the clinical details state recurrent skin infections

In the patients about to get their joints replaced, our nasal Staph aureus resistance rate to mupirocin is 3%. Not surprising really. This is a generally older cohort, less likely to suffer from impetigo and skin boils etc., and thus less likely to have been exposed recently to mupirocin.

In the patients who have recurrent skin infections, our nasal Staph aureus resistance rate to mupirocin is 15%. This is not surprising either. This cohort is generally young, and due to their clinical history are much more likely to have been exposed to a lot of mupirocin. As a cohort, they potentially have a lot of physical contact with each other (in kindergartens, in the school playground, on the sports field, in cinemas, backs of cars etc..,) facilitating cross-transmission.

This is a good demonstration of how much antibiotic resistance can vary, depending on what population you are looking at. 3% is markedly different from 15% and management of these different rates might be very different from an antibiotic stewardship point of view.

It also reflects the difficulties in measuring antibiotic resistance and then how to report such results in a meaningful manner.

We like to simplify things, and have just one result regardless of what biases might be at play. Measuring resistance rates is complicated enough due to the sheer number of microbe-antimicrobial combinations that can be permutated. To add another level of complexity by calculating different values for any one microbe-antimicrobial combination is too much for most of us to handle! 

But sometimes the difference in values between different population cohorts (as demonstrated above) is just too much to be ignored…

Michael