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Spatial and Genetic Epidemiology of Hookworm in a Rural Community in Uganda
Authors:Rachel L. Pullan  Narcis B. Kabatereine  Rupert J. Quinnell  Simon Brooker
Affiliation:1. Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom.; 2. Vector Control Division, Ministry of Health, Kampala, Uganda.; 3. Institute of Integrative and Comparative Biology, University of Leeds, Leeds, United Kingdom.; 4. Malaria Public Health and Epidemiology Group, Kenya Medical Research Institute-Wellcome Trust Research Programme, Nairobi, Kenya.;George Washington University, United States of America
Abstract:There are remarkably few contemporary, population-based studies of intestinal nematode infection for sub-Saharan Africa. This paper presents a comprehensive epidemiological analysis of hookworm infection intensity in a rural Ugandan community. Demographic, kinship, socioeconomic and environmental data were collected for 1,803 individuals aged six months to 85 years in 341 households in a cross-sectional community survey. Hookworm infection was assessed by faecal egg count. Spatial variation in the intensity of infection was assessed using a Bayesian negative binomial spatial regression model and the proportion of variation explained by host additive genetics (heritability) and common domestic environment was estimated using genetic variance component analysis. Overall, the prevalence of hookworm was 39.3%, with the majority of infections (87.7%) of light intensity (≤1000 eggs per gram faeces). Intensity was higher among older individuals and was associated with treatment history with anthelmintics, walking barefoot outside the home, living in a household with a mud floor and education level of the household head. Infection intensity also exhibited significant household and spatial clustering: the range of spatial correlation was estimated to be 82 m and was reduced by a half over a distance of 19 m. Heritability of hookworm egg count was 11.2%, whilst the percentage of variance explained by unidentified domestic effects was 17.8%. In conclusion, we suggest that host genetic relatedness is not a major determinant of infection intensity in this community, with exposure-related factors playing a greater role.
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