Joseph Lister (1827-1912) was a surgeon who pioneered anti-septic surgery while working at Glasgow Royal Infirmary (where I did my microbiology training…)
In 1867, Lister utilised carbolic acid (phenol) to sterilise both surgical instruments and disinfect wounds, leading to reductions in post-operative infections. All this was done long before the “germ theory” of infection was completely understood. Impressive indeed.
So who discovered Listeria monocytogenes?
The credit for this goes to a man called Everitt Murray (1890-1964) Murray was born in South Africa, but discovered Listeria in 1926 whilst working as a bacteriologist in laboratories in Cambridge, England. Along with his colleagues, he noticed that the bacterium was infecting and killing experimental rabbits in the laboratory. Initially it was named Bacterium monocytogenes, then Listerium monocytogenes, and finally Listeria monocytogenes in 1940, in order to honour Joseph Lister’s work on surgical antisepsis. The monocytogenes refers to the peripheral monocytosis often seen in animals infected with this bacterium.
It was not until much later that Listeria monocytogenes was recognised as a foodborne pathogen, possibly as late as 1981.
Listeria monocytogenes is interesting in its ability to both harmlessly colonise and to cause devastating infection. See “The Danger Period”.
I guess Joseph Lister is probably one of the few surgeons to have had a bacterium named after him…
p.s. I have added a few MCQs on Hepatitis B serology to the website.
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