Despite high pertussis vaccine coverage, pertussis incidence has increased substantially in recent years in many countries including Australia. Epidemic cycles occur every 3 to 5 years and Australia has been experienced a prolonged epidemic between 2008 and 2012. A significant factor that may be contributing to the increase of pertussis is adaptation to the acellular vaccine (ACV) by Bordetella pertussis, the causative agent of pertussis. Many studies have shown that B. pertussis populations have changed after the introduction of vaccination. This talk will present an overview of evolution of B. pertussis and the effect of selection pressure from ACV induced immunity on the changes in Australian B. pertussis population.
B. pertussis is a highly homogenous pathogen with very low levels of variation between strains. Most changes observed are singe base changes referred to as single nucleotide polymorphisms (SNPs). Our genotyping studies have shown that the predominant strains currently circulating in Australia and other developed countries belong to Cluster I, defined by the presence of certain SNPs. SNP Cluster I is associated with a change in the pertussis toxin (Ptx) promoter (from ptxP1 to ptxP3) that has been linked to increased production of Ptx and several other virulence factors. SNP cluster I contains the alleles ptxA1 and prn2, which code for two of the three antigens used in the ACVs commonly used in Australia. Significantly, the Ptx and pertactin (Prn) protein variants found in Cluster I strains are different from those of the strain used to manufacture the ACV used in Australia and many other countries. We have also found that strains that did not produce Prn emerged and expanded during the 2008-2012 epidemic, providing further evidence of vaccine-driven evolution. Using a mixed infection mouse model, we found that Prn negative strains are fitter over Prn positive strains under ACV induced immunity. These findings have significant implications for control of pertussis and vaccination strategies.