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…
What do Listeria monocytogenes and Neisseria meningitidis have in common?
Quite a lot of things probably, but one characteristic that sets them apart from most other organisms is that they are both very virulent bacteria and also colonise a significant proportion of the population.
Neisseria meningitidis, when it causes disease has a mortality of approx. 10%, yet manages to colonise asymptomatically the nasopharynx of 10-15% of the population.
Along the same lines, Listeria monocytogenes has a mortality rate of approximately 20% when it causes invasive disease, yet manages to colonise the intestines of approximately 15% of the population.
So what is going on here?
Some factors point towards invasive disease caused by these micro-organisms being much more prevalent when the bacterium has been recently acquired by the host. For example during outbreak investigations we know that Listeria isolates from patients often have the same strain type as Listeria isolates from food eaten by the patient in the period before the onset of symptoms. We also know that contacts of patients with confirmed meningococcal disease have up to a 800 times greater risk than the general population of developing meningococcal disease in the ensuing couple of weeks.
Both these facts suggest that in many cases, if not all, it is the recent acquisition of Listeria monocytogenes or Neisseria meningitidis where the real risk lies. After acquisition there is a “danger period” where the host/patient either learns to live with the bacterium (colonisation) or the bacterium goes on to cause disease.
It is unclear whether listeriosis or meningococcal disease can result from reactivation of colonising strains. Such a study would be very difficult to carry out.
It is my gut feeling that most cases of disease caused by these particular bacteria are caused by “recent acquisition and control failure.”
The relationship between colonisation and disease in these very virulent bacteria is a fascinating topic, and an area we still don’t really know a lot about….
p.s. I have added a short powerpoint to the website on Listeria