All models included a random effect at the individual level to ac

All models included a random effect at the individual level to account for the within-individual correlation of titre measurements at different time points. Geographical clustering of parasite prevalence, antibody prevalence or age-adjusted antibody density was assessed as described previously [18, 19] using satscan software on binary (Bernouilli model) or continuous (normal model) variables (http://www.satscan.org/, Accessed 2 February 2012). A total of 509 individuals

were enrolled in the longitudinal study; 249 children ≤5 years of age, 126 children between 6 and 10 years of age and 134 adults who were ≥20 years (Table 1). The overall P. falciparum parasite prevalence www.selleckchem.com/products/Gefitinib.html by microscopy at enrolment was 38·1% (194/509). Microscopic P. falciparum parasite prevalence was significantly higher in children SB203580 6–10 years of age compared with younger children (P = 0·002) and lowest in adults (P < 0·001); parasite density in parasitaemic individuals decreased with age (test for trend between age groups, P = 0·012). Baseline P. falciparum parasite prevalence by PCR was 57·1% (284/493) and showed the same age-pattern as microscopically detectable parasite carriage, that is, higher in children 6–10 years compared with younger children (P < 0·001) and lowest in adults (P = 0·002). As expected, given that all participants were given curative antimalarial therapy at enrolment, P. falciparum

parasite prevalence decreased during the study in all age groups (Figure 1). During the last cross-sectional survey, none of the adults had microscopically detectable infections, but 14·2% (16/113) had submicroscopic P. falciparum infections. We found no evidence for geographical clustering of parasite carriage at any time point (data not shown). We evaluated the prevalence and titre of antibodies against P. falciparum AMA-1,MSP-119, MSP-2,

and CSP and against An. gambiae salivary protein gSG6. The baseline prevalence of antibodies to MSP-119, MSP2 and CSP all increased with increasing age group (P < 0·001). Prevalence of anti-AMA-1 antibodies showed an initial increase and then decrease with age; antibody prevalence was higher in 6- to 10-year-old children compared with younger children (P < 0·001) and compared with adults (P = 0·005). Phosphatidylinositol diacylglycerol-lyase Antibody titre increased with increasing age group for MSP-119, MSP-2 and CSP (P ≤ 0·009; Figure 2, Table 1). AMA-1 antibody titre was again higher in 6- to 10-year-old children compared with younger children (P < 0·001) and adults (P < 0·001). Baseline anti-gSG6 antibody prevalence showed a borderline significant increase with age (P = 0·053); antibody titre increased significantly with age (P = 0·004). We found no evidence for geographical clustering of the prevalence or age-adjusted titre of antibodies against any of the antigens at any time point (data not shown).

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