Tag Archives: colonisation

“Looking after Pseudomonas aeruginosa in chronic ulcers, from a laboratory point of view”

There are a reasonable amount of papers in the medical literature about Pseudomonas aeruginosa in chronic ulcers but not a lot of concrete evidence nor definitive guidelines.


Here are my personal thoughts on the topic:

  • All chronic ulcers will become colonised with bacteria, of which some might be Pseudomonas aeruginosa. Moist lesions full of nutrients are perfect for bacterial breeding. A bacterial swab taken from any chronic ulcer will almost always grow bacteria, which may or may not include Pseudomonas aeruginosa.
  • Whether a chronic ulcer is infected is a clinical judgement. The laboratory result may occasionally affect treatment in a clinically infected ulcer, but should almost never be used to decide whether an ulcer is infected or not.
  • Pseudomonas aeruginosa colonises approximately 10-15% of chronic ulcers. This is my anecdotal experience , but will obviously depend to some extent on the cohort that you are studying.
  • Pseudomonas aeruginosa probably only causes infection in a small minority of ulcers in which it is found. Most chronic ulcers are not infected, including most which grow Pseudomonas aeruginosa. Chronic ulcers may be slow to heal for a variety of other reasons, which is why they are “chronic”!
  • An ulcer colonised with Pseudomonas aeruginosa may have a charcteristic odour and colour. Yes, the distinctive colour and odour of Pseudomonas aeruginosa can be visible on the ulcer. This however does not mean it is necessarily infected, despite what others might say…
  • A heavy load of Pseudomonas aeruginosa is probably associated with slower wound healing. There is some evidence to support this assertion in the literature. However reduction of this load does not necessarily need to be with systemic antibiotic therapy. Various types of dressings, including acetic acid, silver, and medical honey have all shown at least anecdotal evidence of doing this job.
  • I would not feel compelled to report a light growth of Pseudomonas aeruginosa when mixed with other enteric flora. Pseudomonas aeruginosa is enteric flora so no need to report separately unless a heavy growth out of proportion to rest of the flora.
  • I try and avoid doing antimicrobial susceptibility testing on Pseudomonas aeruginosa in chronic ulcers unless specifically requested or some exceptional circumstances, such as pre-grafting, transplant patient etc.. If antimicrobials are routinely reported on Pseudomonas aeruginosa isolates from chronic ulcers, then you can be sure that antimicrobials will be used to treat these ulcers far more often than is clinically necessary. 

Good “management” of Pseudomonas aeruginosa by the laboratory leads to Pseudomonas aeruginosa isolates in the population which are generally susceptible and thus more amenable to treatment when they really do require attention….



“The Danger Period..”

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.

Listeria monocytogenes
Listeria monocytogenes

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