Health education and awareness involves providing knowledge about causes of illness and choices to promote a change in individual behaviour and, thus, improves survival of individuals. Studies have, however, shown that improved knowledge and awareness is not always translated into appropriate actions. This study aimed at exploring the factors determining mothers’ choices of appropriate child health and nutrition practices in the Gambia. Eight focus-group discussions (FGDs) were held with 63 women whose children had been seen at the Keneba MRC Clinic within the 12 months preceding the study. The FGDs were analyzed using a thematic framework. Gender inequality, presence or absence of support networks, alternative explanatory models of malnutrition, and poverty were identified as the main factors that would determine the ability of a mother to practise what she knows about child health and nutrition. The findings highlight the need to consider the broader social, cultural and economic factors, including the value of involving men in childcare, when designing nutritional interventions.

BackgroundThe nature of the association between ghrelin, an orexigenic hormone produced mainly in the stomach, and Helicobacter pylori (H pylori), a bacterium that colonises the stomach, is still controversial. We examined available evidence to determine whether an association exists between the two; and if one exists, in what direction.MethodsWe reviewed original English language studies on humans reporting circulating ghrelin levels in H pylori infected and un-infected participants; and circulating ghrelin levels before and after H pylori eradication. Meta-analyses were conducted for eligible studies by combining study specific estimates using the inverse variance method with weighted average for continuous outcomes in a random effects model.ResultsSeventeen out of 27 papers that reported ghrelin levels in H pylori positive and negative subjects found lower circulating ghrelin levels in H pylori positive subjects; while 10 found no difference. A meta-analysis of 19 studies with a total of 1801 participants showed a significantly higher circulating ghrelin concentration in H pylori negative participants than in H pylori positive participants (Effect estimate (95%CI) = -0.48 (-0.60, -0.36)). However, eradicating H pylori did not have any significant effect on circulating ghrelin levels (Effect estimate (95% CI) = 0.08 (-0.33, 0.16); Test for overall effect: Z = 0.67 (P = 0.5)).ConclusionsWe conclude that circulating ghrelin levels are lower in H pylori infected people compared to those not infected; but the relationship between circulating ghrelin and eradication of H pylori is more complex.

There is consensus that the pathophysiology of malaria-associated anaemia is multifactorial, but the precise mechanisms behind many of the haematological changes during malaria remain unclear. In this review, we attempt to build a composite picture of the pathophysiology of malarial anaemia using evidence from experimental, human and animal studies. We propose that cytokine- and hepcidin-mediated iron delocalisation, a principal mechanism in the anaemia of inflammation, plays an important role in the aetiology of malarial anaemia, and can explain some of the clinical and laboratory findings. These mechanisms interact with other aetiological determinants, such as dietary iron and micronutrient supply, helminth load, other infections and genetic variation, in determining the severity and associated features of anaemia. We suggest that iron delocalisation as a mechanism for malarial anaemia could be exploited for the development of alternative therapeutic strategies for post-malaria anaemia.

BackgroundMalaria is one of the strongest recent selective pressures on the human genome, as evidenced by the high levels of varying haemoglobinopathies in human populations–despite the increased risk of mortality in the homozygous states. Previously, functional polymorphisms of Hp, coded by the co-dominant alleles Hp1 and Hp2, have been variously associated with several infectious diseases, including malaria susceptibility.Methodology/Principal FindingsRisk of a clinical malarial episode over the course of a malarial transmission season was assessed using active surveillance in a cohort of Gambian children aged 10–72 months. We report for the first time that the major haplotype for the A-61C mutant allele in the promoter of haptoglobin (Hp)–an acute phase protein that clears haemoglobin released from haemolysis of red cells–is associated with protection from malarial infection in older children, (children aged ≥36 months, >500 parasites/ul and temperature >37.5°C; OR = 0.42; [95% CI 0.24–0.73] p = 0.002) (lr test for interaction, <36 vs ≥36 months, p = 0.014). Protection was also observed using two other definitions, including temperature >37.5°C, dipstick positive, plus clinical judgement of malaria blinded to dipstick result (all ages, OR = 0.48, [95% CI 0.30–0.78] p = 0.003; ≥36 months, OR = 0.31, [95% CI 0.15–0.62] p = 0.001). A similar level of protection was observed for the known protective genetic variant, sickle cell trait (HbAS).Conclusions/SignificanceWe propose that previous conflicting results between Hp phenotypes/genotypes and malaria susceptibility may be explained by differing prevalence of the A-61C SNP in the populations studied, which we found to be highly associated with the Hp2 allele. We report the -61C allele to be associated with decreased Hp protein levels (independent of Hp phenotype), confirming in vitro studies. Decreased Hp expression may lead to increased oxidant stress and increased red cell turnover, and facilitate the development of acquired immunity, similar to a mechanism suggested for sickle cell trait.

ObjectiveTo determine if low-dose weekly chloroquine (CQ) therapy improves recovery from malaria-associated anaemia.DesignProof of concept randomised clinical trial.SettingWest Kiang District, Lower River Region, The Gambia.ParticipantsChildren resident in participating communities, aged 12–72 months, with uncomplicated malaria identified using active case detection over two consecutive malaria transmission seasons.InterventionsIn 2007, eligible children were randomised to chloroquine-sulfadoxine/pyrimethamine (CQ-SP) or co-artemether (ACT) antimalarial therapy, and after parasite clearance on day 3 were subsequently re-randomised (double-blind) to weekly low-dose CQ (5 mg/kg) or placebo. In 2008, all eligible children were treated with ACT and subsequently randomised to CQ or placebo.Outcome measuresThe primary outcome was a change in haemoglobin from baseline (day 3 of antimalarial treatment) to day 90 in the CQ and placebo treatment arms. Secondary outcomes were changes in urinary neopterin as a marker of macrophage activation, markers of erythropoietic response and prevalence of submicroscopic parasitaemia. Change in haemoglobin in the placebo arm by initial antimalarial treatment was also assessed.ResultsIn 2007, 101 children with uncomplicated malaria were randomised to antimalarial treatment with CQ-SP or ACT and 65 were subsequently randomised to weekly CQ or placebo. In 2008, all children received ACT antimalarial treatment and 31 were subsequently randomised to receive weekly CQ or placebo. Follow-up to day 90 was 96%. There was no effect of weekly CQ vs placebo on change in haemoglobin at day 90 (CQ+10.04 g/L (95% CI 6.66 to 13.42) vs placebo +7.61 g/L (95% CI 2.88 to 12.35)). There was no effect on the secondary outcomes assessed, or effect of initial antimalarial therapy on haemoglobin recovery. Higher day 90 haemoglobin correlated independently with older age, not being stunted, higher haemoglobin at day 0 and adequate iron status at day 3.ConclusionsWeekly low-dose CQ after effective antimalarial treatment is not effective in improving recovery from postmalarial anaemia.Trial registrationThe clinical trial registration number is NCT00473837 (ClinicalTrials.gov).

Several reports suggest that antimicrobial resistance is an increasing global problem; but like most pandemics, the greatest toll is in the less developed countries. The dismally low rate of discovery of antimicrobials compared to the rate of development of antimicrobial resistance places humanity on a very dangerous precipice. Since antimicrobial resistance is part of an organism's natural survival instinct, total eradication might be unachievable; however, it can be reduced to a level that it no longer poses a threat to humanity. While inappropriate antimicrobial consumption contributes to the development of antimicrobial resistance, other complex political, social, economic and biomedical factors are equally important. Tackling the menace therefore should go beyond the conventional sensitization of members of the public and occasional press releases to include a multi-sectoral intervention involving the formation of various alliances and partnerships. Involving civil society organisations like the media could greatly enhance the success of the interventions

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Summaryobjective To retest our previous finding that the haptoglobin (Hp) 22 genotype is associated with seasonal anaemia, and to investigate the role of malaria in this effect.methods Haemoglobin (Hb) and peripheral parasitaemia were assessed at pre-and post-malarial season cross-sectional surveys in rural Gambian children aged 10-72 months. Between the surveys, active longitudinal surveillance was conducted to detect febrile episodes.results Unlike previously, no overall reduction in Hb was observed (Hb = 106.1 vs. 107.2 g ⁄ l, P = 0.13, n = 545). However, multi-variable linear regression revealed differences in Hb over the season by Hp and Hb-sickle (HbS) genotype ()2.20 g ⁄ l per copy of the Hp2 allele, P = 0.043; HbAS vs. HbAA + 3.13 g ⁄ l, P = 0.11, n = 536). There was no effect of malarial episodes during follow-up; this suggests that when effective treatment is given, Hb levels recover. The A61-C Hp promoter SNP, associated with the Hp2 allele, had no effect.conclusion The effect of the Hp2 allele appears to be independent of effects on malaria incidence but may affect Hb levels through increased oxidant stress and red cell turnover. This may be supported by our previous observations that the effect of Hp22 was independent of markers of iron status and zinc protoporphyrin measured at the cross-sectional surveys and therefore also of iron availability for erythropoiesis.