Borrelia in rodents
Borrelia afzelii is a tick-transmitted bacterium which infects rodents and other small mammals. It can occasionally infect humans where it causes Lyme disease, the most important vector borne disease in the northern hemisphere. We use B. afzelii and its rodent hosts to address a number of questions regarding the evolutionary ecology of host-parasite interactions:
What determines transmission success? The fitness of a pathogen is ultimately determined by its ability to transmit itself to new hosts, so natural selection should maximize the ability of a pathogen to transmit. Yet, there is often considerable variation in the rate at which infected hosts transmit the pathogen. In the case of B. afzelii, the rate of transmission from an infected host individual to ticks varies from 0 to 100%. What are the host and pathogen factors behind this variation?
What are the causes and consequences of multiple infections? Infections with pathogenic microorganisms often consist of a number of different strains of a particular pathogen. In the case of B. afzelii, infections can consist of up to six different bacterial genotypes. Such 'multiple infections' can be expected to lead to within-host interactions between coinfecting strains. For example, coinfecting strains may compete over limited resources. Alternatively, coinfections may facilitate parasite growth by interfering with the host's immune response. The relative importance of different types of interactions, and their evolutionary consequences are as yet poorly understood.
How does natural selection act on host immune genes? Parasitism is considered one of the most important selective agents. In theory, parasite-mediated selection can either enhance or reduce the variation at host genes involved in defence, for example immune genes. However, the relative importance of these different kinds of selection is largely unclear. We use the Borrelia–rodent system to investigate how parasite-mediated selection acts on a variety of immune genes, including MHC and toll-like receptors.