COS 74-9
Consequences of co-infection for hosts and parasites: Importance of host nutrition and parasite species identity

Wednesday, August 7, 2013: 4:20 PM
L100E, Minneapolis Convention Center
Sarah A. Budischak, Odum School of Ecology, University of Georgia, Athens, GA
Kaori Sakamoto, Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA
Joseph F. Urban, Diet, Genomics and Immunology Lab, USDA, Beltsville, MD
Vanessa O. Ezenwa, Odum School of Ecology, University of Georgia, Athens, GA

Most animals are concurrently infected with multiple parasites. Compelling, but limited, evidence suggests that interactions among co-infecting parasites can influence disease dynamics and host fitness. Human and laboratory animal studies provide strong evidence of resource-based and immune-based mechanisms driving interactions between pairs of parasite species. Although both mechanisms likely operate within individual hosts, most studies typically focus on each mechanism independently. Additionally, decreased condition and/or nutrition can influence an individual’s ability to mount adequate immune responses. However, it is unclear how reductions in host immunocompetence will affect both resource- and immune-mediated interactions among co-infecting parasites. To test concurrent interactions among parasites, immune function, and host nutrition, we conducted a factorial experiment using laboratory mice (Balb/c). Specifically, mice were given high or low quality diets, dosed with two species of helminths (alone and in combination), and challenged with bovine tuberculosis.


We found that diet quality and co-infection status strongly influenced host immune function and condition, the proportion of supershedders, and parasite survival and reproduction. Importantly, the magnitude and direction of responses in both hosts and parasites depended on parasite species identity, diet quality, and the combination of co-infecting parasites. For example, a low-quality diet increased egg production of one helminth by 1.4-fold, but decreased egg production of the other by 2.7-fold. Also, both helminth and bovine tuberculosis co-infections increased the proportion of supershedders of one helminth, but not the other. Importantly, effects of bovine tuberculosis on helminth egg production were detectible only in mice fed the low-quality diet. Parasite reproduction influences the number of infective stages released into the environment and, consequently, transmission within host populations. Mouse weight, a correlate of condition and fecundity, increased at a lower rate during peak helminth egg production, but single infections were no more pathogenic than dual infections. However, hosts co-infected with all three parasites (two helminths + bovine tuberculosis) gained the least weight. Our findings highlight the importance of investigating parasite communities, not simply single parasites, to understand the responses of both host and parasite populations to additional pathogens and changing resource availability.