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)
We are fortunate with Chlamydia trachomatis, in that the organism so far, retains almost universal susceptibity to a range of oral antimicrobials, including tetracyclines, erythromycin, azithromycin and even amoxycillin.
This is just as well really as Chlamydia trachomatis is almost exclusively diagnosed by molecular means and antimicrobial susceptibility testing is both difficult and non-standardised.
What we don’t really know about Chlamydia trachomatis is whether continued heavy usage of tetracyclines and azithromycin are leading to “MIC creep” to these antimicrobials. It may be that we only start worrying about this when we start to see treatment failures in significant numbers.
The worry would be that as now Neisseria gonorrhoeae moves towards molecular diagnosis, we will apply the same “out of sight, out of mind” philosophy to this micro-organism. However we definitely cannot afford to go down this route for Neisseria gonorrhoeae as there are already significant resistance problems with this particular bacterium.
We need to remember for both C. trachomatis and N.gonorrhoeae, that just because we aren’t doing susceptibility testing, it doesn’t mean these micro-organisms have suddenly stopped selecting out resistant mutants under antimicrobial pressure….
p.s. While on the subject of GU microbiology, here is a really nice article on the conditions of cytolytic vagnosis and lactobacillosis, well worth a read.