Prevalence and risk factors of malaria among children in southern highland Rwanda.

BACKGROUND: Increased control has produced remarkable reductions of malaria in some parts of sub-Saharan Africa, including Rwanda. In the southern highlands, near the district capital of Butare (altitude, 1,768 m), a combined community-and facility-based survey on Plasmodium infection was conducted early in 2010. METHODS: A total of 749 children below five years of age were examined including 545 randomly selected from 24 villages, 103 attending the health centre in charge, and 101 at the referral district hospital. Clinical, parasitological, haematological, and socio-economic data were collected. RESULTS: Plasmodium falciparum infection (mean multiplicity, 2.08) was identified by microscopy and PCR in 11.7% and 16.7%, respectively; 5.5% of the children had malaria. PCR-based P. falciparum prevalence ranged between 0 and 38.5% in the villages, and was 21.4% in the health centre, and 14.9% in the hospital. Independent predictors of infection included increasing age, low mid-upper arm circumference, absence of several household assets, reported recent intake of artemether-lumefantrine, and chloroquine in plasma, measured by ELISA. Self-reported bed net use (58%) reduced infection only in univariate analysis. In the communities, most infections were seemingly asymptomatic but anaemia was observed in 82% and 28% of children with and without parasitaemia, respectively, the effect increasing with parasite density, and significant also for submicroscopic infections. CONCLUSIONS: Plasmodium falciparum infection in the highlands surrounding Butare, Rwanda, is seen in one out of six children under five years of age. The abundance of seemingly asymptomatic infections in the community forms a reservoir for transmission in this epidemic-prone area. Risk factors suggestive of low socio-economic status and insufficient effectiveness of self-reported bed net use refer to areas of improvable intervention.

Molecular markers of Plasmodium falciparum drug resistance in southern highland Rwanda.

In Rwanda, frequent mutations in the pfdhfr and pfdhps genes of Plasmodium falciparum have suggested intense sulfadoxine-pyrimethamine resistance. However, data on pfmdr1 are not available but might be important in the context of the first-line treatment with artemether-lumefantrine. During a survey among 749 children under five years of age in southern highland Rwanda, 104 P. falciparum isolates were obtained. Parasite polymorphisms associated with drug sensitivity were typed including the genes pfdhfr, pfdhps, pfmdr1, and pfcrt. Plasma concentrations of chloroquine and pyrimethamine were measured by ELISA. Treatment with artemether-lumefantrine within the preceding two weeks was stated by 12.5% of the respondents; chloroquine in plasma was detected in 17.6%, pyrimethamine in none. Isolates with pfdhfr triple and pfdhps double/triple mutations occurred in 75% and 93%, respectively; 69% of the isolates comprised pfdhfr/pfdhps quintuple or sextuple mutations associated with high-grade sulfadoxine-pyrimethamine resistance. Pfdhfr L164 was absent. The pfmdr1 pattern revealed more than 50% of the F184 polymorphism and almost 40% of the N86-F184-D1246 allele combination known to be selected in infections reappearing following artemether-lumefantrine treatment. Molecular markers demonstrate intense antifolate drug resistance of P. falciparum in southern Rwanda. The present, first-time data on pfmdr1 alleles from Rwanda reveal a pattern which might reflect a predominance of wild types for some alleles or, alternatively, substantial artemether-lumefantrine pressure on the local parasite population.

High prevalence of Giardia duodenalis Assemblage B infection and association with underweight in Rwandan children.

BACKGROUND: Giardia duodenalis is highly endemic in East Africa but its effects on child health, particularly of submicroscopic infections, i.e., those below the threshold of microscopy, and of genetic subgroups (assemblages), are not well understood. We aimed at addressing these questions and at examining epidemiological characteristics of G. duodenalis in southern highland Rwanda. METHODOLOGY/PRINCIPAL FINDINGS: In 583 children <5 years of age from communities and health facilities, intestinal parasites were assessed by triplicate light microscopy and by PCR assays, and G. duodenalis assemblages were genotyped. Cluster effects of villages were taken into account in statistical analysis. The prevalence of G. duodenalis as detected by microscopy was 19.8% but 60.1% including PCR results. Prevalence differed with residence, increased with age, and was reduced by breastfeeding. In 492 community children without, with submicroscopic and with microscopic infection, underweight (weight-for-age z-score <-2 standard deviations) was observed in 19.7%, 22.1%, and 33.1%, respectively, and clinically assessed severe malnutrition in 4.5%, 9.5%, and 16.7%. Multivariate analysis identified microscopically detectable G. duodenalis infection as an independent predictor of underweight and clinically assessed severe malnutrition. Submicroscopic infection showed respective trends. Overall, G. duodenalis was not associated with gastrointestinal symptoms but assemblages A parasites (proportion, 13%) were increased among children with vomiting and abdominal pain. CONCLUSIONS/SIGNIFICANCE: The prevalence of G. duodenalis in high-endemicity areas may be greatly underestimated by light microscopy, particularly when only single stool samples are analysed. Children with submicroscopic infections show limited overt manifestation, but constitute unrecognized reservoirs of transmission. The predominance of assemblage B in Rwanda may be involved in the seemingly unimposing manifestation of G. duodenalis infection. However, the association with impaired child growth points to its actual relevance. Longitudinal studies considering abundant submicroscopic infections are needed to clarify the actual contribution of G. duodenalis to morbidity in areas of high endemicity.