One of the strains has been around for at least 87 years and causes severe cystic acne in Europe. There is enough variation that there's likely at least a little genetic susceptibility or vulnerability to some strains in the population. They confirmed that some strains release irritating fatty acids and are likely initiators of the acne cycle.
However, the previously predicted metabolism of hyaluronic acid by certain strains was not associated with acne; exactly the opposite, in fact. So normal P.acnes on healthy individuals might make use of that. In contrast, unhealthy P.acnes strains may have an increased dependent symbiotic relationship with the fungus Malassezia, which is normally on the skin, metabolizing its chitin... as well as glycoprotein (previously discovered “neuraminidase activity”) from the cell walls of the human pore. The possibly fungal eating part of their genotyping is surprising on the bad strains, because prior, albeit mostly old, research hasn't shown much help when antifungals are combined with antibiotics & antibacterial agents.
The study here did learn there's a very strong core gene base for P.acnes with a much lower "distance" or genetic differentiation between various P.acnes strains than, say, bad strains of Strep or Staph or other bugs that attack mucous membranes. That might have something to do with the difficulty in fooling the more powerful immune systems of those membranes.
There seems to be a lot of complex factors at work in the skin that’s allowing the acne cycle to start up and then continue, much like an airline crash where it’s often not just one issue at cause since there’s redundancy.
Edited by Reti, 10 April 2011 - 02:46 PM.