Design and implementation of a health systems strengthening approach to improve health and nutrition of pregnant women and newborns in Ethiopia, Kenya, Niger, and Senegal.

Maternal and neonatal mortality are unacceptably high in developing countries. Essential nutrition interventions contribute to reducing this mortality burden, although nutrition is poorly integrated into health systems. Universal health coverage is an essential prerequisite to decreasing mortality indices. However, provision and utilization of nutrition and health services for pregnant women and their newborns are poor and the potential for improvement is limited where health systems are weak. The Community-Based Maternal and Neonatal Health and Nutrition project was established as a set of demonstration projects in 4 countries in Africa with varied health system contexts where there were barriers to safe maternal health care at individual, community and facility levels. We selected project designs based on the need, context, and policies under consideration. A theory driven approach to programme implementation and evaluation was used involving developing of contextual project logic models that linked inputs to address gaps in quality and uptake of antenatal care; essential nutrition actions in antenatal care, delivery, and postnatal care; delivery with skilled and trained birth attendant; and postnatal care to outcomes related to improvements in maternal health service utilization and reduction in maternal and neonatal morbidity and mortality. Routine monitoring and impact evaluations were included in the design. The objective of this paper is to describe the rationale and methods used in setting up a multi-country study that aimed at designing the key maternal and neonatal health interventions and identifying indicators related to inputs, outcomes, and impact that were measured to track change associated with our interventions.

Integrating nutrition into health systems at community level: Impact evaluation of the community-based maternal and neonatal health and nutrition projects in Ethiopia, Kenya, and Senegal.

Maternal undernutrition and mortality remain high in several African countries. Key nutrition and health interventions improve maternal and birth outcomes. Evidence is scarce on how to strengthen health systems to ensure pregnant women and newborns are reached with these interventions. We conducted three quasi-experimental nonrandomized Community Based Maternal and Neonatal Health and Nutrition projects in regions of Ethiopia, Senegal, and Kenya to demonstrate how proven nutrition interventions could be integrated into health programs to improve knowledge and practices during pregnancy, birth, and postpartum. We evaluated impact on knowledge and practices related to maternal and neonatal care using logistic regression and repeated-measures models with districts as a fixed variable and adjusted for covariates. Combined country analyses show significant positive effects of the intervention on women receiving first antenatal care visit (ANC) during first trimester (OR = 1.44; p < .001), those consuming any iron and folic acid supplement during their latest pregnancy (OR = 1.60; p = .005), those whose <6 months infants were exclusively breastfed (OR = 2.01; p=.003), those whose delivery was facility based (OR = 1.48; p=.031), and those whose postnatal care was facility based (OR = 2.15; p<.001). There was no significant differences between intervention and control groups regarding one or more and four or more ANC visits, women consuming iron and folic acid for ≥90 days, and early initiation of breastfeeding. We conclude that integrating proven nutrition interventions into health programs at community level improved components of access to and use of ANC, delivery services, and postnatal care by women in three African countries.

Effects of HIV-1 serostatus, HIV-1 RNA concentration, and CD4 cell count on the incidence of malaria infection in a cohort of adults in rural Malawi.

BACKGROUND: To assess the effects of human immunodeficiency virus (HIV) infection on susceptibility to malaria, we compared the incidence rates of malaria by HIV type 1 (HIV-1) serostatus, baseline blood HIV-1 RNA concentration, and baseline CD4 cell count, over the course of a malaria season. METHODS: We followed a cohort of 349 adults in Malawi. For the 224 HIV-1-seropositive adults (64% of the cohort), we measured HIV-1 RNA concentration (n=187) and CD4 cell count (n=184) at baseline. Parasitemia was defined as presence of asexual parasites on a thick film of blood and was treated with sulfadoxine/pyrimethamine (SP), in accordance with national policy. Hazard ratios (HRs) of parasitemia were estimated using Cox regression. Demographics were adjusted for. RESULTS: HIV-1 seropositivity was associated with parasitemia (adjusted HR, 1.8 [95% confidence interval {CI}, 1.2-2.7] for a first parasitemia episode; adjusted HR, 2.5 [95% CI, 1.5-4.2] for a second parasitemia episode [> 14 days after the first episode]; adjusted HR, 1.9 [95% CI, 1.4-2.6] for parasitemia overall). Treatment failure (parasitemia < or = 14 days after SP treatment) did not differ by HIV-1 serostatus (risk ratio, 1.3 [95% CI, 0.5-3.2]). HIV-1 RNA concentrations and CD4 cell counts were moderately but inconsistently associated with parasitemia. A high parasite density with fever was associated with HIV-1 seropositivity and low CD4 cell count. CONCLUSION: HIV-infected adults in malaria-endemic areas are at increased risk for malaria. Where possible, additional malaria prevention efforts should be targeted at this population.

Cross-reactivity of anti-HIV-1 T cell immune responses among the major HIV-1 clades in HIV-1-positive individuals from 4 continents.

BACKGROUND: The genetic diversity of human immunodeficiency virus type 1 (HIV-1) raises the question of whether vaccines that include a component to elicit antiviral T cell immunity based on a single viral genetic clade could provide cellular immune protection against divergent HIV-1 clades. Therefore, we quantified the cross-clade reactivity, among unvaccinated individuals, of anti-HIV-1 T cell responses to the infecting HIV-1 clade relative to other major circulating clades. METHODS: Cellular immune responses to HIV-1 clades A, B, and C were compared by standardized interferon- gamma enzyme-linked immunospot assays among 250 unvaccinated individuals, infected with diverse HIV-1 clades, from Brazil, Malawi, South Africa, Thailand, and the United States. Cross-clade reactivity was evaluated by use of the ratio of responses to heterologous versus homologous (infecting) clades of HIV-1. RESULTS: Cellular immune responses were predominantly focused on viral Gag and Nef proteins. Cross-clade reactivity of cellular immune responses to HIV-1 clade A, B, and C proteins was substantial for Nef proteins (ratio, 0.97 [95% confidence interval, 0.89-1.05]) and lower for Gag proteins (ratio, 0.67 [95% confidence interval, 0.62-0.73]). The difference in cross-clade reactivity to Nef and Gag proteins was significant (P<.0001). CONCLUSIONS: Cross-clade reactivity of cellular immune responses can be substantial but varies by viral protein.

Effect of Plasmodium falciparum malaria on concentration of HIV-1-RNA in the blood of adults in rural Malawi: a prospective cohort study.

BACKGROUND: Raised HIV viral load in blood has been associated with accelerated disease progression and increased transmission of infection. To assess the effect of Plasmodium falciparum malaria on concentrations of HIV in blood, we did a prospective cohort study in Malawi. METHODS: We recruited 367 HIV-1-infected adults. Among 334 people aparasitaemic at baseline, 148 had at least one malaria episode during follow-up and received antimalarial treatment. Of these, 77 had HIV-1-RNA measurements at baseline, during malaria, and post-malaria. We used linear regression with generalised estimating equations to assess effect of four definitions of malaria (any parasitaemia, parasite density > or =2000/microL, febrile parasitaemia, and febrile parasitaemia with parasite density > or =2000/microl) on changes in log HIV-1 RNA, overall and by baseline CD4 count. FINDINGS: With malaria defined as any parasitaemia, HIV-1-RNA concentration almost doubled between baseline (median 96215 copies per mL) and malaria (168901 copies per mL), a 0.25 (95% CI 0.11-0.39) log increase in mean RNA concentration. HIV-1-RNA concentration fell to median 82058 copies per mL by about 8-9 weeks post-malaria. Increases in HIV-1-RNA were greatest for people with fever, parasite density 2000/microL or greater, and CD4 count more than 300 cells per muL, in whom concentrations rose from median 38483 copies per mL at baseline to 196098 copies per mL during malaria, a mean log increase of 0.82 (95% CI 0.55-1.10, p<0.0001), and fell to median 75331 copies per mL post-malaria. People who remained aparasitaemic showed no changes in HIV-1-RNA concentration. INTERPRETATION: HIV-infected individuals with malaria have a significantly increased viral load, which might enhance HIV transmission and accelerate disease progression.