Around 50 million children a year are unlucky enough to become infected with one of two closely-related coccobacilli: Bordetella pertussis and B. parapertussis.
Both cause similar acute symptoms: severe coughing that can progress to coma, convulsions and death.
Intriguingly, both these Bordetella subspecies appear to have evolved independently — and very recently — from a third (B. bronchiseptica) that infects a range of mammals, including humans.
Why has this progenitor twice given rise to a virulent, highly transmissible, human-specific pathogen? Ottar Bjornstad and Eric Harvill propose a possible answer.
Based on epidemiogical theory, they point out that a virulent pathogen can spread in a host population as long as it has a high enough transmission rate. High transmission rates lead to rapid spread, and to extinction in small host populations (as all susceptible individuals become infected, then die or become immune). But even a virulent pathogen can persist when the host population size is large and clustered enough to maintain a supply of susceptible individuals — as in some urban human communities during recent historical times.
They also suggest that the human immune response favors expression of different virulence factors by the two subspecies. B. pertussis produces a toxin that appears to slow antibody production. B. parapertussis retains the genes for this toxin but does not express them. Instead, it (like B. bronchiseptica) makes an O-antigen — a polysaccharide that is thought to shield the bacterium from immune recognition.
Bjornstad and Harvill show how experimental, epidemiological and phylogenetic data support the hypothesis that B. parapertussis was better able to invade and persist in human populations by avoiding cross immunity to B. pertussis. They also propose that toxin production by B. pertussis was advantageous in historical human populations that had been exposed to O-antigens during infection with B. bronchiseptica.
Thus, evolution of the two virulent pathogens that we see today appears to have been favored by immune-mediated competition between subspecies, high transmission rates and large host population size.
Written By: Ottar N. Bjнџrnstad& Eric T. Harvill
Paper Url: http://www.trends.com/tim/default.htm
Journal: 13: 355-359
Journal Reference: 13: 355-359