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…
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”
Neisseria meningitidis is more classically known as the cause of meningococcal sepsis and meningococcal meningitis. However its role as a cause of urethritis/cervicitis has been the subject of ongoing speculation over the years, and several studies have backed such a link up. For example, check this study out, and this one.
A recent study has added more weight to this hypothesis, backing the assertion up with DNA studies of the N. meningitidis isolates showing adaptation to a genital environment. (loss of outer capsules, and acquisition of enzymes facilitating survival in a low oxygen environment)
So what does this all mean for clinical microbiology laboratories?
I guess it shows the inherent weakness of molecular diagnosis. There could be a widespread outbreak of urethritis due to Neisseria meningitidis in your local area, but the laboratory would be completely naïve to it, if it only performs molecular testing for C. trachomatis and N. gonorrhoeae. Particularly in the Sexual Health Clinic setting, adjunctive culture of STI samples is important, and not just to obtain the N. gonorrhoeae susceptibilities.
It is also possible that the selective molecular diagnosis and treatment of N. gonorrhoeae will therefore create a “niche” for organisms like Neisseria meningitidis to adapt physiologically and “gatecrash” the party.
And finally on this topic, there is also intriguing data coming out that suggests that some meningococcal vaccines may have a protective effect for N. gonorrhoeae infection. Suspected for some time, this suggestion has been backed up by some observational data in this study. More research is obviously needed. We are still a bit away I suspect from a gonococcal vaccine.
The physiological and evolutionary relationship between Neisseria meningitidis and Neisseria gonorrhoeae is a fascinating one. We shouldn’t think too much about one without considering the other…
Albert Ludwig Sigesmund Neisser was born in 1855 in Schweidnitz (now in Poland). He demonstrated the aetiological agent of gonorrhoea on microscopy in 1879, and the bacterium was named after him. Neisseria gonorrhoeae was not isolated in pure culture until 1885.
Neisser specialised in dermatology and sexually transmitted diseases and his other major discovery was as “co-founder” of the aetiological agent of leprosy, Mycobacterium leprae. (There was some dispute between Gerhard Hansen and Neisser over who had actually discovered the micro-organism first…
And what about Neisseria meningitidis? It was actually discovered by an Austrian bacteriologist called Anton Weichselbaum in 1887. It was initially called Diplococcus intracellularis meningitidis (!), but someone sensibly changed it to Neisseria meningitidis in due course.
Albert Neisser died of septicaemia in 1916, at the age of 61.
For a nice biography on the life and works of Albert Neisser, clickhere(about a 5 minute read)