Changes in host suitability by microsporidia

Investigations on the host-parasitoid- pathogen system Lymantria dispar - Glyptapanteles liparidis - Vairimorpha sp. in a previous research project revealed that the microsporidian infection of the host larva had a negative impact on the development of the endoparasitic wasp without causing infection of the parasitoids themselves. It is the aim of the proposed research to study the causes of this reduced performance of the parasitoid. Therefore, gypsy moth larvae will be inoculated with the microsporidium before or after parasitization. Hemolymph and total insect body samples will be taken at certain intervals and analyzed for changes in the host nutrient content of carbohydrates, amino acids, and lipids, which might consequently lead to malnutrition of G. liparidis larvae. Moreover, the study could yield new insight on the effects of a microsporidian infection on the host`s physiology, a topic that is only poorly understood, as well as on the impact of parasitism by G. liparidis on the host`s amino acids and lipids content which also has not been investigated yet.

The gypsy moth, Lymantria dispar, is one of most devastating forest pests feeding on the foliage of oaks or other deciduous trees. To promote its control by natural enemies like parasitoids and pathogens, more knowledge about their synergistic or inhibitory interactions is of particular importance. In this project, we studied the influence of a specific pathogenic infection of the gypsy moth larva by an unicellular organism (microsporidia) on the development and mortality of an endoparasitic wasp. The parasitoid species belongs to one of the most important natural enemies of gypsy moth in our oak forests. The results of this study show that the parasitoid larvae in microsporidian-infected hosts are not directly infected by the pathogen. However, their growth is significantly reduced due to changes in the host`s nutrient budget. We observed a drastic decline of the blood sugar level and the reduced content of fatty acids in the haemolymph of infected host larva after the 5th day of infection. At this time the excessive multiplication of the pathogen in the fat body starts, the organ which is responsible for carbohydrate and fat metabolism.