Meeting Abstract
Parasite-mediated anorexia is a ubiquitous, but poorly understood component of host-parasite interactions. These temporary but substantial reductions in food intake (range: 4-100%) limit exposure to parasites and alter within-host physiological processes that regulate parasite development, production, and survival, such as energy allocation, immune function, host-microbiota interactions, and gastrointestinal conditions. By altering the duration, severity, and spread of infection, anorexia could substantially alter ecological, evolutionary, and epidemiological dynamics. However, these higher-order implications are typically overlooked and remain poorly understood — even though medical (e.g., non-steroidal anti-inflammatory drugs, vaccines, targeted signaling pathways, calorie restriction) and husbandry practices (e.g., antibiotic and diets used for rapid growth, nutrient supplementation) often directly or indirectly alter host appetite and nutrient intake. We develop theory that helps elucidate why reduced food intake (anorexia) can enhance or diminish disease severity and illustrates that the population-level outcomes often contrast with the individual-level outcomes: treatments that increase the intake of high-quality nutrients (suppressing anorexia), can drive rapid individual-level recovery, but inadvertently increase infection prevalence and select for more virulent parasites. Such a theory-guided approach offers a tool to improve targeting host nutrition to manage disease in both human and livestock populations by revealing a means to predict how nutrient-driven feedbacks will affect both the host and parasite.
