“…A genetic analysis of hookworm infection in Zimbabwe (Williams-Blangero et al, 1997) estimated a heritability of 0.37 in the population indicating genetic factors to be responsible for 37% of the variation (after correcting for confounding environmental factors) seen in faecal EPG. A strong genetic effect (37–44%) was also detected in intestinal schistosomiasis caused by S. mansoni in a population in Brazil (Bethony et al, 2001; Bethony et al, 2002) and shared household environment was also shown to be important and accounted for 12–21% of the phenotypic variation seen in infection intensity. In contrast, a family based study in Kenya that investigated the aggregation of S. haematobium infection, obtained a low heritability score for the trait (King et al, 2004).…”
Despite the success of extensive control measures that have been implemented in China for over 50 years, the number of individuals infected with Schistosoma japonicum remains high in the remaining endemic areas. A variance components analysis was undertaken to estimate the heritable and environmental components that contribute to S. japonicum infection in the Poyang Lake region of Jiangxi Province, PR China. The total target population was 3148 from four separate administrative villages. Two thousand seven hundred and five of these comprised 400 families ranging in size from 3 to 188. After adjustments were made for gender, water contact and past history of having had schistosomiasis, the heritable component was estimated to account for as much as 58% of the phenotype variation under the polygenic model. Household was not shown to be an important environmental factor. Incorporating village effects indicated that the results were valid for the total population. We conclude that genetic heritability in this region is high and plays an important role in determining risk of infection with S. japonicum.
“…A genetic analysis of hookworm infection in Zimbabwe (Williams-Blangero et al, 1997) estimated a heritability of 0.37 in the population indicating genetic factors to be responsible for 37% of the variation (after correcting for confounding environmental factors) seen in faecal EPG. A strong genetic effect (37–44%) was also detected in intestinal schistosomiasis caused by S. mansoni in a population in Brazil (Bethony et al, 2001; Bethony et al, 2002) and shared household environment was also shown to be important and accounted for 12–21% of the phenotypic variation seen in infection intensity. In contrast, a family based study in Kenya that investigated the aggregation of S. haematobium infection, obtained a low heritability score for the trait (King et al, 2004).…”
Despite the success of extensive control measures that have been implemented in China for over 50 years, the number of individuals infected with Schistosoma japonicum remains high in the remaining endemic areas. A variance components analysis was undertaken to estimate the heritable and environmental components that contribute to S. japonicum infection in the Poyang Lake region of Jiangxi Province, PR China. The total target population was 3148 from four separate administrative villages. Two thousand seven hundred and five of these comprised 400 families ranging in size from 3 to 188. After adjustments were made for gender, water contact and past history of having had schistosomiasis, the heritable component was estimated to account for as much as 58% of the phenotype variation under the polygenic model. Household was not shown to be an important environmental factor. Incorporating village effects indicated that the results were valid for the total population. We conclude that genetic heritability in this region is high and plays an important role in determining risk of infection with S. japonicum.
“…Population size and the extent of the study area prevented us from introducing adjustment for exposure based on water contact, as has been done in some previous studies. 7,13,14 Water contact in the present study area takes place in multiple dispersed surface ponds, and both snail infection levels and water use vary extensively from season to season. 3,33,34 Previous multivariate analysis of environmental predictors of infection risk in the Msambweni study area have shown the degree and duration of water contact to be much less effective predictors of infection/reinfection than age, gender, and location of residence.…”
Section: Discussionmentioning
confidence: 96%
“…Heritable risk for S. mansoni infection intensity has also been suggested by recent population-based family studies in Brazil, which have indicated that 20−44% of the variance in their infection levels appears related to heritable effects. 13,14 In addition, population-based studies of intestinal helminthic infections (Ascaris lumbricoides [roundworm], Trichuris trichiura [whipworm], and hookworm) suggest a moderate but significant heritable component to risk for these other worm infections. 13,15−17 With this in mind, we undertook the present study to estimate the influence of hereditary factors in determining risk for infection and urinary tract disease caused by the parasite S. haematobium in a high transmission area of coastal Kenya.…”
To estimate their heritable component of risk for Schistosoma haematobium infection intensity and disease, we performed a community-based family study among an endemic population in coastal Kenya. Demography and family linkages were defined by house-to-house interviews, and infection prevalence and disease severity were assessed by standard parasitologic testing and by ultrasound. The total population was 4,408 among 912 households, with 241 identified pedigree-household groups. Although age- and sex-adjusted risk for greater infection intensity was clustered within households (odds ratio = 2.7), analysis of extended pedigree-household groups indicated a relatively low heritability score for this trait (h2 = 0.199), particularly after adjustment for common household exposure effects (adjusted h2 = 0.086). Statistical evidence was slightly stronger (h2 = 0.353) for familial clustering of bladder morbidity, with an adjusted h2 = 0.142 after accounting for household exposure factors. We conclude that among long-established populations of coastal Kenya, heritable variation in host susceptibility is low, and likely plays a minimal role in determining individual risk for infection or disease.
“…Unaccounted household-level variability may alternatively be explained by intrinsic host-related factors such as genetics [51],[52], nutrition [53], immune response [54],[55] or concomitant infection with other parasites [56]. Despite an increasing number of studies suggesting a genetic component to variation in intensity of helminth infection, the relative importance of host genetics and exposure remain unclear and vary considerably between the settings studied (reviewed in [57] and [58]).…”
BackgroundIndividuals living in areas endemic for helminths are commonly infected with multiple species. Despite increasing emphasis given to the potential health impacts of polyparasitism, few studies have investigated the relative importance of household and environmental factors on the risk of helminth co-infection. Here, we present an investigation of exposure-related risk factors as sources of heterogeneity in the distribution of co-infection with Necator americanus and Schistosoma mansoni in a region of southeastern Brazil.MethodologyCross-sectional parasitological and socio-economic data from a community-based household survey were combined with remotely sensed environmental data using a geographical information system. Geo-statistical methods were used to explore patterns of mono- and co-infection with N. americanus and S. mansoni in the region. Bayesian hierarchical models were then developed to identify risk factors for mono- and co-infection in relation to community-based survey data to assess their roles in explaining observed heterogeneity in mono and co-infection with these two helminth species.Principal FindingsThe majority of individuals had N. americanus (71.1%) and/or S. mansoni (50.3%) infection; 41.0% of individuals were co-infected with both helminths. Prevalence of co-infection with these two species varied substantially across the study area, and there was strong evidence of household clustering. Hierarchical multinomial models demonstrated that relative socio-economic status, household crowding, living in the eastern watershed and high Normalized Difference Vegetation Index (NDVI) were significantly associated with N. americanus and S. mansoni co-infection. These risk factors could, however, only account for an estimated 32% of variability between households.ConclusionsOur results demonstrate that variability in risk of N. americanus and S. mansoni co-infection between households cannot be entirely explained by exposure-related risk factors, emphasizing the possible role of other household factors in the heterogeneous distribution of helminth co-infection. Untangling the relative contribution of intrinsic host factors from household and environmental determinants therefore remains critical to our understanding of helminth epidemiology.
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