Last Thursday, I had to write an essay under exam conditions for the module BS3012: Infection and Immunity. We had a list of essay titles that we could choose from and I chose: Compare and contrast the structure, regulation and contributions to pathogenesis of the pertussis and adenylate cyclase toxins in Bordetella pertussis. Bordetella pertussis being the primary pathogen responsible for whooping cough.
The topic itself is quite interesting as I am basically detailing the different effects B. pertussis‘ primary virulence factors have on the immune system’s ability to eradicate the pathogen, where there are only slight differences in these toxins’ structure and genetic regulation. In the case of B. pertussis, a slight difference in location of the genes responsible for expression of these toxins means that their actions on the temporal events involved with *neutrophil clearance are quite different, but profound enough to allow further infection in the host’s airways.
*cellular component responsible for uptake of pathogenic material after primary infection alerts the immune system to the invader’s presence.
This research is important considering the recent rise in whooping cough infections in developed countries such as the UK and USA. In the UK, we are all given vaccines to this infection in a series of stages, from an early age, predominantly in combination with tetanus, diptheria, polio and influenza (type B). Compulsory jabs for whooping cough were established from the late 70s and the incidence has declined over the decades. However, the resurgence in whooping cough has caused for more research into novel vaccines against the bacteria. Now, to limit the possibility of very young babies getting whooping cough, mothers are vaccinated after 28 weeks, while the baby is still in utero.
Part of the resurgence is due to not everybody having the vaccine. For whatever reason, if the whole population isn’t vaccinated, this allows for the bacteria to survive in a population by infecting hosts not vaccinated. Persistent survival gives the pathogen the ability to adapt to vaccines within several generations (in bacteria’s lifetime we’re talking hours to days for the next generation to form). Mutations in the genes responsible for antibody susceptibility can occur and persist in the population if it means that B. pertussis can continue to infect new hosts and survive. Some of these antibodies targeted the virulence factors I had to research, and if these mutations are conferring the toxins’ cumulative ability to avoid these antibodies, then more research into the structure, regulation and contribution to pathogenesis of these toxins does need discerning.
And either the vaccines can be manipulated to complement these toxins’ changes or new targets need to be elucidated!