UC Santa Barbara

Emerging infections in both humans and wildlife can often be traced back to human mediated changes in host densities, host communities, and the environment. In Chapter 1, I reviewed how humans affect wildlife nematodes. Nematode responses to human actions vary, thus knowing host and parasite natural history, and the mechanisms underlying disease dynamics are critical for predicting parasite responses and managing disease.

Among wildlife nematodes, raccoon roundworm (Baylisascaris procyonis) is infamous for its ability to cause fatal disease in both humans and wildlife. This parasite infects millions of raccoons in North America. Although adult worms cause little pathology in raccoons, larval worms undergo extensive tissue migrations in other hosts, often causing neurological damage. Disease risk is driven by environmental egg contamination, which increases with raccoon density, worm intensity, and worm prevalence. In Chapter 2, I examined 189 raccoons from southern California to investigate how host age and season affect parasite abundance, demography, and fecundity. Roundworm infected 90% of Santa Barbara County raccoons, juveniles hosted more worms than adults, and more heavily infected raccoons released more eggs.

In Chapter 3, I investigated whether animals can avoid raccoon roundworm contaminated sites, and if such avoidance balances disease costs and foraging preferences. Using wildlife cameras, I monitored animal behavior at raccoon latrines — sites that concentrate both seeds and pathogenic parasite eggs, and found that latrine contact rates reflected background activity, diet preferences and disease risk. Disease-tolerant raccoons and rats displayed significant site attraction, while susceptible birds and small mammals avoided these high-risk sites.

The introduced black rat, Rattus rattus, occurs throughout the native range of the raccoon roundworm, Baylisascaris procyonis, and frequently forages in latrines. In Chapter 4, I examined the role of these rats and other California rodents in B. procyonis transmission. I surveyed wild rodents for B. procyonis and found that B. procyonis infected R. rattus at intensities more than 100 times greater than loads in co-occurring native Reithrodotomys megalotis and Peromyscus maniculatus. I also conducted scavenger trials using motion activated cameras and found that rodent carcasses were scavenged by opossums, skunks and raccoons, suggesting that these infected rodents, particularly R. rattus, contribute to B. procyonis transmission in this coastal California ecosystem.

Raccoon roundworm infects both rodents and raccoons in southern California, but we know little about infection risk for other species. In Chapter 5, I used information on animal time allocation and behavior to build a model for predicting community-wide exposure risk for raccoon roundworm. This model suggests that larval worms are likely widespread in the animal community and provides a novel non-invasive method for identifying “at-risk” species.

Raccoon roundworm infection can cause devastating pathology in humans, but there is growing evidence that subclinical cases also occur. As there is limited information on the frequency of these subclinical human infections, in Chapter 6 I surveyed 150 adults from California for B. procyonis antibodies. Eleven participants were seropositive suggesting that subclinical infection does occur and that previously undetectable infections warrant further study.