Some symbiotic associations are nasty, and some are nice – why is there so much variation in interspecific interactions?
One idea is that competition between parasite genotypes can select for higher virulence (Frank 1996). When different parasite strains or species infect the same host, they may compete for host resources. The more competitive genotype will win out, producing more transmissible stages. This genotype’s competitive ability may also correspond to elevated virulence – it is more competitive because it can exploit its host more rapidly and aggressively. If hosts are commonly infected with multiple parasite genotypes, we’d then predict the evolution of higher virulence in the parasite population.
I assisted Manuela López-Villavicencio, Tatiana Giraud and many others in an experimental test of this hypothesis. We found that the virulence of the fungus Microbotryum violaceum, the agent of anther-smut, is elevated when multiple strains infect its host Silene latifolia. This elevated virulence seems to result from an increase in the growth and reproduction of fungal strains in the presence of competitors, in particular unrelated ones. This aggressive growth results in more sterilization of the host and more transmissible stages (spores) produced by the parasite ( López-Villavicencio et al. 2010 Evolution).
I explored a similar question in the protozoal parasites Toxoplasma gondii and Sarcocystis neurona. These are terrestrial parasites – T. gondii‘s definitive hosts are felines (like house cats) and S. neurona‘s definitive hosts are opossums. However, both can infect a wide range of intermediate hosts. With land-to-sea runoff, this range increasingly includes marine mammals like harbor porpoises and seals. We surveyed a sample of marine mammals that stranded on beaches in the Pacific Northwest and found high rates of protozoal parasitism. Nearly half of infected individuals were infected with both T. gondii and S. neurona, and these cases were associated with more severe disease (Gibson et al. 2011PLoS NTD). This study calls for additional work to determine if dual infections select for more virulent strains.
- Frank, S. A. 1996. Models of parasite virulence. Quart Rev Biol 71:37-78.