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The virulence of bacteria, their capacity to cause disease, is generally dependent on the expression of a variety of properties which create a complex series of interactions between the invading pathogen and a susceptible host. Different factors may be required at different stages of infection : initially, the bacteria will usually need to adhere to tissues in sufficient numbers to establish infection; then they will need to obtain nutrients and to multiply while at the same time evading the host defence mechanisms. In some instances, they may need to invade host cells for survival or further dissemination within the host (Finlay & Falkow, 1989). The recognition that bacterial pathogenicity is multifactorial has been followed by the more recent finding that many pathogens regulate the expression of sets of virulence factors in a coordinated manner as a response to changes in their environment (J. F. Miller et al., 1989a). These changes would be seen when the pathogen first enters the host from an outside environment, when it transfers to different sites within the host or as a response to changing conditions within the host as a result of inflammation or an increased immune response. Coordination is achieved by a regulatory locus whose expression is itself responsive to environmental signals and which then in turn alters the expression of virulence-associated genes. This review will focus on the expression of the virulence factors of Bordetella pertussis, a Gram-negative bacterium that causes the human respiratory disease whooping cough. The techniques of molecular genetics found early application with B. pertussis during attempts to define important virulence factors and to ascertain

Antigenic switching and pathogenicity: environmental effects on virulence gene expression in Bordetella pertussis