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Information on hookworm infection and re-infection in a cohort of primary school children and interview data on their socioeconomic background and behavior were combined with environmental data using a geographic information system (GIS). Multivariate models served to explore the covariation of environmental and infection patterns adjusted for possible confounders. Our aim was to identify environmental factors that might serve to predict infection and thus guide control efforts when epidemiologic information is insufficient. Furthermore, we wanted to establish whether soil type has a genuine influence on hookworm infection. Prevalence maps and spatial statistics showed considerable spatial clustering of infection in the small (
28 x 16 km) study area. The multivariate logistic regression models showed strong positive associations of infection at baseline (baseline prevalence = 83.2%) with settlement density (odds ratio [OR] = 1.24, 95% confidence interval [CI] = 1.10–1.38) and vegetation density (OR = 1.66, 95% CI = 1.25–2.22) and a strong negative association with the clay content of the soil (OR = 0.67, 95% CI = 0.62–0.73). Similar but weaker correlations were found after re-infection. Socioeconomic status and behavior did not seem to confound these associations. Spatial analysis of the model residuals suggested that because the models accounted for most of the spatial pattern, the model standard errors were not affected by spatial clustering. Our study shows that the pattern of hookworm infection is strongly influenced by several environmental factors. The GIS-aided prediction of areas in need of treatment is therefore a promising tool to guide control efforts when epidemiologic information is insufficient.
Received May 27, 2004. Accepted for publication November 4, 2004.
Acknowledgments: We thank the pupils, staff, and parents of the participating schools for their cooperation and their patience, and the KwaZulu-Natal Department of Health for providing treatment, laboratory space, and general assistance.
Financial support: This study was supported by the Danish Bilharziasis Laboratory. Elmar Saathoff was supported by a PhD scholarship from Evangelisches Studienwerk Villigst/Germany.
Authors’ addresses: Elmar Saathoff, Harvard School of Public Health, 665 Huntington Avenue, Boston MA 02115, E-mail: elmarsaathoff{at}compuserve.de. Annette Olsen, Danish Bilharziasis Laboratory, Jaegersborg Allé 1 D, DK-2920, Charlottenlund, Denmark, E-mail: ao{at}bilharziasis.dk. Brian Sharp and Immo Kleinschmidt, Malaria Lead Programme of the Medical Research Council, PO Box 17120, Congella 4013, Durban, South Africa, E-mails: sharpb{at}mrc.ac.za and immo.kleinschmidt{at}mrc.ac.za. Jane D. Kvalsvig, Child, Youth and Family Development, Human Sciences Research Council, Private Bag X07, Dalbridge 4014, South Africa, E-mail: JKvalsvig{at}hsrc.ac.za. Chris C. Appleton, School of Life and Environmental Sciences, University of KwaZulu-Natal, Durban 4041, South Africa, E-mail: appleton{at}biology.und.ac.za.
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