Some effects of the nematode Mermis nigrescens upon carbohydrate metabolism in the fat body of its host, the desert locust Schistocerca gregaria.

Abstract

Adult desert locusts were experimentally infected with 50 Mermis nigrescens ova and changes in the fat body carbohydrate levels and glycogen phosphorylase activities recorded. At both 2 and 3 weeks after infection, the parasitism caused a significant reduction in the level of glycogen and non-glycogen carbohydrates in the host fat body, together with a progressive depletion of active and inactive glycogen phosphorylases. By feeding extensively upon the blood carbohydrates of the host, the developing nematode deprives the fat body of carbohydrates and thereby effects a reduction in glycogenesis by the host fat body. Increased catabolism (and (or) decreased anabolism) of the fat body phosphorylases, together with a possible suppression of the host "hyperglycaemic factor" by the nematode, prevent further glycogenolysis by the fat bodies of mermithid-infected locusts and allow a low, constant level of fat body glycogen to be maintained in these insects.