Affiliation:
1. Department of Biology, Colorado State University, Fort Collins, Colorado 80523;
Abstract
Rather than being fixed, pathogen transmission varies and is thus an object of natural selection. I examine how opportunities for selection on pathogen transmission depend on (a) pathogen fitness, (b) genetic variability, and (c) forces acting at within- and between-host levels. The transmission rate, β, influences processes such as epidemic spread, postepidemic fade-outs, and low-level persistence. Complexity of infection processes within hosts leads to different transmission rates among hosts and between types of pathogens (viruses, bacteria, eukaryotic Protozoa). Generality emerges, however, by “unpacking” β into within- and between-host opportunities for selection. This is illustrated by evolutionary biology of the bacterium Yersinia pestis, which causes plague in mammals, remains highly virulent and is transmitted by multiple routes, including fleas and direct contacts with infected hosts. The strength of within-host selection is manifested through infectivity, replication, pathogenicity, and dissemination from hosts. At the between-host level, responses to selection are less predictable because of environmental variation, whereas vector-borne transmission (usually by arthropods) provides additional opportunities for selection and trade-offs between vectors and hosts. In subdivided host populations, selection favors transmission before local pathogen extinction occurs, but key components (e.g. infectious periods of hosts) are determined by within-host dynamics. Pathogen transmission is often viewed in the context of transmission-virulence trade-offs, but within-host dynamics may cause host damage unrelated to transmission, and thus transmission-virulence trade-offs are not universal.
Subject
Ecology,Ecology, Evolution, Behavior and Systematics
Cited by
35 articles.
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