Samuel J. Black
Professor of Veterinary and Animal Sciences, University of Massachusetts
Ph.D.: University of Edinburgh, Postdoctoral Training: Cologne University, Germany Stanford University, USA International Laboratory for Research in Animal Diseases, Kenya
We are studying host control of African trypanosomes, tsetse fly-transmitted flagellate protozoa that live and replicate in the fluid compartment of host blood. The organisms cause fatal disease in people and domestic animals. Human trypanosomiasis is restricted to a few regions of Africa but likened to a sleeping dragon that can awake and spread like wildfire. Cattle trypanosomiasis is endemic in and excludes cattle from about 10 million square kilometers of Africa lying between 15° North and 20° South and comprising much of the humid and semi-humid zones. This region is haven to Cape buffalo which are resistant to trypanosomiasis. Our investigations show that control of trypanosome infection in Cape buffalo correlates with broad-acting anti-trypanosome serum activity involving oxygen radicals generated during catabolism of purines by serum xanthine oxidase. Two features of the buffalo response are noteworthy. First, the presence of a high concentration of serum xanthine oxidase ensures the extracellular capability of producing significant quantities of reactive oxygen radicals. Secondly, an infection-associated decline in blood catalase activity occurs co-incident with clearance of the first parasitemic wave and augments the efficacy of the oxidative response by limiting the rate of catabolism of hydrogen peroxide which is the trypanocidal radical. We want to characterize features of xanthine oxidase that affect its presence and concentration in serum, the sources and regulation of purine substrates in serum, and how infection causes the decline in serum and erythrocyte-associated catalase. These questions are of fundamental interest because whilst oxygen radicals can slay dragons they can also turn on their maker.