SYMP 1-1 - Ecological and social mechanisms driving multi-host vector borne pathogen transmission in rural landscapes

Monday, August 12, 2019: 1:30 PM
Ballroom E, Kentucky International Convention Center
Nicole Gottdenker1, Luis Fernando Chaves2, Azael Saldana3, Jose Calzada3, Diana Carolina Erazo4, Julie Velasquez-Runk5, Christina Pilar Varian6, Chystrie Rigg7, Milixa Perea8, Kadir Gonzalez7, Vanessa Pineda7, Anamaria Santamaria7, Richard J. Hall9, John M. Drake10, Caitlin Mertzlufft11 and Susan Tanner12, (1)University of Georgia, (2)Costa Rican Institute for Research and Education on Nutrition and Health, Tres Rios, Costa Rica, (3)Parasitology, Gorgas Memorial Institute for Health Studies, Panama City, Panama, (4)Universidad de los Andes, Bogota, Colombia, (5)Anthropology, University of Georgia, Athens, GA, (6)College of Veterinary Medicine: Pathology, University of Georgia, Athens, GA, (7)Parasitología, Instituto Conmemorativo Gorgas de Estudios de la Salud, Panama, (8)Parasitology, Instituto Conmemorativo Gorgas de Estudios de la Salud, (9)Odum School of Ecology, University of Georgia, Athens, GA, (10)Center for the Ecology of Infectious Diseases, University of Georgia, Athens, GA, (11)Geography, University of Georgia, Athens, GA, (12)Anthropology, Associate Professor, Athens, GA
Background/Question/Methods:

Land use change in rural landscapes, driven by local, regional, and international socioeconomic and political processes, is associated with emergence of vector-borne pathogens in animals and humans. Mechanisms by which anthropogenic drivers can lead to increased vector-borne disease transmission include changes in vector and host niches and behavior, food web changes, loss of host and vector diversity, host community shifts favoring human-associated wildlife (e.g. opossums, rats) and ‘r-selected’ hosts that, in theory, invest less in acquired immunity (pace of life hypothesis), resulting in higher community competence. Predicting how vector-borne pathogens respond to land use is complicated by the fact that many of these vector-borne pathogens co-occur, and they may have differing dynamic responses to anthropogenic change. We describe theoretical and empirical studies of ecological and social relationships between deforestation and transmission of two co-occurring vector-borne zoonotic diseases, Chagas disease (CD), and American Cutaneous Leishmaniasis (ACL), in rural Panama.

Results/Conclusions

Both pathogens exhibit differing ecological and social responses to deforestation. In response to deforestation, CD vector infection is ‘hump-shaped’, with lower vector infection in contiguous forests, peak prevalence in fragmented forest sites, and declines in deforested sites. CD infection prevalence in dog sentinels in communities surrounded by differing degrees of deforestation also mirror this pattern. Although theoretical models support the ‘pace of life’ hypothesis as a key driver of CD vector infection in deforested landscapes, they under-estimate field measures of vector infection. For ACL, vector diversity declines in response to deforestation, ands shifts to a predominance of generalist and anthropophilic vectors. Although dog ACL exposure does not differ in communities surrounded by forest cover and in fragmented forests, self-reported ACL infections tend to peak in more recently established communities near protected forest edges surrounded by more forest cover.

In terms of social responses, there tends to be greater local knowledge about ACL transmission compared to CD, which may be due to obvious skin lesions caused by ACL and the cryptic nature of CD. There are no clear associations between socioeconomic status and CD and ACL transmission in areas undergoing deforestation in Panama, therefore individual human behavior, household and yard management, may also influence CD and ACL human transmission risk. We conclude the presentation by discussing theoretical and empirical consideration of CD and ACL transmission in dynamic rural landscapes, incorporating predictions of how different land use states post-deforestation (e.g. palm oil plantations, regenerating forests, timber plantations) can influence vector-borne disease risk.