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OBJECTIVES: Both chronic and acute malnutrition in children under 5 remain a persistent problem in low and low-middle income countries. Haiti faces the highest burden of childhood malnutrition in the Western Hemisphere. We attempted to describe the prevalence of malnutrition in children in a farming community in Haiti and record characteristics of the those experiencing the disease. METHODS: A household survey was conducted within the town of Fontaine in the Nord department of Haiti on all children under the age of 5. A total of 535 children were assessed. Anthropometric data was taken on the children and household information was assessed via a population-based survey. RESULTS: Of the children assessed, 28% (149/535) were either chronically or acutely malnourished. Of the children who were malnourished: 36.4% (43/118) had 3 or more bouts of diarrhea in the past 3 months and only 5.3% (7/132) had stopped breastfeeding before 1 year of age. On average, the mothers of these children had completed 6.2 years of formal schooling. A slight majority of mothers, 54.7% (81/148), either “never” or “rarely” were concerned their child was malnourished. Of the households with malnourished children 88.4% (130/147) had reported running out of food in the last month. When asked what caused children in Fontaine to be malnourished, mothers of malnourished children cited a lack of food, 56.2% (82/146), and a lack of access to employment, 25.3% (37/146), most frequently. CONCLUSIONS: Malnutrition commonly affects children in Fontaine. Efficacious prevention interventions could possibly include decreasing food insecurity, or increasing girls’ education level. FUNDING SOURCES: None.

We have utilized Caenorhabditis elegans to study human methylmalonic acidemia. Using bioinformatics, a full complement of mammalian homologues for the conversion of propionyl-CoA to succinyl-CoA in the genome of C. elegans, including propionyl-CoA carboxylase subunits A and B (pcca-1, pccb-1), methylmalonic acidemia cobalamin A complementation group (mmaa-1), co(I)balamin adenosyltransferase (mmab-1), MMACHC (cblc-1), methylmalonyl-CoA epimerase (mce-1) and methylmalonyl-CoA mutase (mmcm-1) were identified. To verify predictions that the entire intracellular adenosylcobalamin metabolic pathway existed and was functional, the kinetic properties of the C. elegans mmcm-1 were examined. RNA interference against mmcm-1, mmab-1, mmaa-1 in the presence of propionic acid revealed a chemical phenotype of increased methylmalonic acid; deletion mutants of mmcm-1, mmab-1 and mce-1 displayed reduced 1-[(14)C]-propionate incorporation into macromolecules. The mutants produced increased amounts of methylmalonic acid in the culture medium, proving that a functional block in the pathway caused metabolite accumulation. Lentiviral delivery of the C. elegans mmcm-1 into fibroblasts derived from a patient with mut(o) class methylmalonic acidemia could partially restore propionate flux. The C. elegans mce-1 deletion mutant demonstrates for the first time that a lesion at the epimerase step of methylmalonyl-CoA metabolism can functionally impair flux through the methylmalonyl-CoA mutase pathway and suggests that malfunction of MCEE may cause methylmalonic acidemia in humans. The C. elegans system we describe represents the first lower metazoan model organism of mammalian propionate spectrum disorders and demonstrates that mass spectrometry can be employed to study a small molecule chemical phenotype in C. elegans RNAi and deletion mutants.