A key principle in the evolutionary ecology of disease is the degree to which hosts invest in defence against parasites and pathogens. Established concepts in this area include (1) that disease risk is a function of host density and (2) that risk of disease leads to selection on the host to minimize the potential costs of disease. A clear prediction that arises from these concepts is that hosts living at high densities should invest more in defence than those living at low densities: a hypothesis known as positive density-dependent prophylaxis (DDP).
For the past three years I have studied the African armyworm system (Spodoptera exempta), a devastating crop pest which expresses an extreme form of density-dependent phenotypic plasticity positive-DDP in response to host crowding. An equally destructive agricultural pest, the Australian Plague Locust (APL), Chortoicetes terminifera, has been suggested to exhibit negative-DDP, with certain key immune functions shown to be lower in gregarious than in the solitary insects. This project will attempt to determine why species with similar migratory activity appear to have evolved contrary behavioural and immunological strategies to combat disease transmission. The APL is an ideal model system to study the effects of crowding and migration, occurring in a socio-politically stable continent, allowing state-of-the-art field and laboratory experimentation.
I will use my knowledge of migratory host-pathogen dynamics and expertise in experimental biology to investigate three main objectives, a) to determine the spatial and temporal pattern of natural disease epizootics in APL populations, b) to compare immune function and disease resistance in gregarious and solitary locusts, and c) to quantify the impact of protein availability on immune function, host behaviour and disease resistance. This research will contribute to the knowledge-base in global food security and nutrition biology.
Funded under 7th FWP (Seventh Framework Programme)