We explore the evolution and ecology of socially mediated immunity in termites. My group focuses on understanding the role of sociality in host-parasite interactions. We apply life-history theory to understand how behavioural and physiological host responses vary across species, and how ecology and caste shape individual and social immunity.
Nature is complicated. Hosts and parasites do not interact in closed one-to-one systems. We are looking at the issue of complex multi-host-pathogen dynamics by using the intracellular gut parasites of bees: Nosema (Phylum Microspora, once thought to be unusual protists, they are now known to be highly derived fungi). Microsporidia have evolved a unique and very impressive host-invasion strategy. Spores eject a filament that uncoils like a spring, probably via an osmotic trigger.
The force of the filament's growth pierces the host cell membrane and once fully ejected, the spore contents are transmitted through the filament into the cell. How do similar pathogens compete when in the same host? Does order of infection, or dosage matter?
Does being a parasite impact the rate of evolution? Is rapid evolution adaptive, or is it simply correlated with (and not causally responsible for) shifts in conditions? We used the parasitic order Strepsiptera (the 'twisted-wing parasites') as a model to investigate this issue. Strepsiptera also contain a very interesting lineage of parasites (Myrmecolacidae: pictured below), wherein males and females of the same species infect different host species. Males typically parasitize ants, while females parasitize crickets or preying mantises. We investigated whether this very unusual host-parasite relationship influenced the history of diversification.
I am also interested in understanding how changes in selective pressures (e.g. host switching, other traits influencing virulence or transmission) affects molecular evolution in pathogenic organisms. Many of the world's most serious disease threats to humans (e.g. Ebola, Influenza), agricultural animals (e.g. Tuberculosis), crops (e.g. Rice blast) and wild organisms (e.g. Chytridiomycota in Amphibians)) are due to zoonosis or other sudden changes in the environment, reflecting rapid but sustained shifts in selective pressures. How do organisms adapt to selection, and how is this reflected in the genome? We are seeking to address this question by using rapidly evolving RNA viruses in bee pollinators.
As part of a larger project during my postdoc, we investigated the impacts of emerging infectious diseases (EIDs) on bee pollinators, focussing on RNA viruses and the exotic gut parasite: Nosema ceranae. Specifically, with the aim of exploring the wider risk of EIDs to managed and wild (e.g. bumble bees) pollinators.