Abstract

Host immune responses against parasitic infection undoubtedly exert significant selective pressures on the evolution of parasite traits, such as virulence. The majority of theoretical and empirical work in this area has focused on the evolutionary consequences of immune responses that are purely protective, acting solely to decrease parasite density and thus to reduce disease severity and risk of host death. Using rodent models of malaria and whooping cough, I will present results of experiments exploring how parasite exploitation strategies might evolve in two different, but commonly encountered ‘immune scenarios’; those of (i) immunopathology (defined here as immune responses that increase the risk of host death) and (ii) imperfect vaccines (defined here as vaccines which confer partial/incomplete immunity against infection), respectively. (i) Using a rodent malaria model (Plasmodium chabaudi), we show that infection-induced immunopathology and parasite genetic variability may together have the potential to shape malaria virulence evolution. In accord with recent theory, the data show that some forms of immunopathology may select for malaria parasites that make hosts less sick. (ii) Using a rodent model of human whooping cough infection (Bordetella pertussis and B. parapertussis), we demonstrate how the commonly used acellular whooping cough vaccine (aP) interferes with the optimal clearance of a sub-species of the human infecting bordetellae (Bordetella parapertussis) and enhances the performance of this pathogen. These data raise the possibility that widespread aP vaccination can create hosts more susceptible to B. parapertussis infection and may ultimately lead to an increase in B. parapertussis prevalence. The fitness consequences to parasites of variations in immune environment must be better understood in order to predict trajectories of parasite evolution in heterogeneous host populations and in response to medical interventions.