You are here:
Effects of Forest Fragmentation on the Ecology of Trypanosoma cruzi, Etiologic Agent of Chagas DiseaseEPA Grant Number: F6F21338
Title: Effects of Forest Fragmentation on the Ecology of Trypanosoma cruzi, Etiologic Agent of Chagas Disease
Investigators: Gottdenker, Nicole Lynn
Institution: University of Georgia
EPA Project Officer: Jones, Brandon
Project Period: September 1, 2006 through August 31, 2009
Project Amount: $106,720
RFA: STAR Graduate Fellowships (2006) RFA Text | Recipients Lists
Research Category: Academic Fellowships , Ecological Indicators/Assessment/Restoration , Fellowship - Ecology
The objective of this study is to analyze the effects of forest fragmentation on the ecology and dynamics of the zoonotic protozoan parasite Trypanosoma cruzi, the agent of Chagas disease in humans. In particular, I will study relationships between forest fragmentation, Trypanosoma cruzi, wild mammal reservoir hosts, and the reduviid bug vector Rhodnius pallescens, in the Panama Canal Zone.
This study will measure relationships between forest fragmentation and the prevalence of T. cruzi within vector populations as an indicator for the risk of human infection. Forest patches of differing size, degree of isolation, connectivity, and matrix composition will be chosen as study sites. Rhodnius pallescens vectors will be caught at each study site using a variety of trapping techniques (i.e. yeast-baited traps, light traps, direct searching). Gut contents from R. pallescens will be analyzed via molecular genetic techniques to identify the species blood meal composition and measure T. cruzi prevalence. Within study sites, the abundance of common opossums and other small mammals will be estimated via mark-recapture methods. Blood samples will be taken from captured mammals for identification of trypanosomes, antibody testing of serum for T. cruzi antibodies and polymerase chain reaction for detection of T. cruzi. The quality of the forest patch for the insect vector will be determined by estimating densities of primary vector habitat, the palm tree Attalea butyracea.
I expect that more fragmented forest patches will have a higher prevalence of Trypanosoma cruzi infected vectors and hosts, a lower species diversity of host blood meals within vectors, a higher proportion of common opossum blood meals within vectors, and higher common opossum densities than in contiguous forests. Also, I expect forest patches with the highest Attalea sp. palm densities to harbor the greatest number of T. cruzi infected vectors.