Epidemiological consequences of reproductive senescence in a long-lived vector

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Tsetse flies transmit single-celled parasites - trypanosomes - to livestock with a single infectious bite. Once infected, the animal develops animal African trypanosomiasis (AAT), a fatal disease which kills 1-2 million cattle and costs sub-Saharan Africa 3-5 billion USD in lost agricultural potential each year. Strategies to control this disease are informed by mathematical models describing rates of parasite transmission between tsetse and hosts and changes in the numbers of tsetse. A crucial aspect of an insect's ability to transmit a disease-causing parasite is its longevity and susceptibility to infection. For a wide variety of animals, longevity and susceptibility to infection are affected by the investment made by an individual's mother. This maternal effect is likely to be very important for tsetse because of their unusual reproductive biology. Unlike most other insects, female tsetse get pregnant, lactate and give birth to live young, which weigh more than the mother. Tsetse can survive over six months in the field with females producing a single larva every ~10 days. The close link between an individual fly and its mother suggests that there will be a marked maternal effect on tsetse longevity and immunity and hence parasite transmission. Models for trypanosomiasis are based on the Ross-Macdonald model for human malaria, however, and do not consider the role of maternal investment in tsetse population dynamics or epidemiology as malaria mosquitoes - like most other vectors - reproduce through egg laying.This project will investigate how maternal investment changes with age and nutrition in tsetse, the consequences for offspring survival and ability to spread trypanosomes, and the contribution of these processes to tsetse population and disease transmission dynamics. We will conduct parallel observations of tsetse in the laboratory - using a large colony of flies at the Liverpool School of Tropical Medicine - and in the field, using flies of estimated age caught using an innovative sampling method in their natural habitat in Zimbabwe. We will experimentally manipulate nutrition in females and measure the costs of reproduction by preventing females from mating until they are older, to assess whether late-life declines in reproductive output (such as those reported in humans) reflect depleted resources or build-up of damage as a by-product of reproduction. We will develop new evolutionary models to understand whether such patterns represent adaptive strategies to maximize the total number of offspring produced in a lifetime, constraints due to physiology, or a combination of these processes.We will follow offspring born to mothers of varying age and nutritional state to test whether offspring born to older or nutritionally stressed mothers are more likely to die young or become infected by trypanosomes. We will also test whether maternal effects are stronger in sons than daughters. Finally, we will use insights from these experimental observations and evolutionary models to improve epidemiological models predicting the spread of tsetse-borne diseases. These diseases can persist at low prevalence and vector density, only to flare up when control efforts are relaxed or new habitats become suitable. Our new models will be used to predict the role of mothers in helping tsetse populations to persist or shift range as a result of human-related and environmental change. The accuracy of these models will be validated against existing data on the distribution and abundance of tsetse, their hosts and disease prevalence.