Eline L. Korenromp

We assessed the impact of HIV-1 on malaria in the sub-Saharan African population. Relative risks for malaria in HIV-infected persons, derived from literature review, were applied to the HIV-infected population in each country, by age group, stratum of CD4 cell count, and urban versus rural residence. Distributions of CD4 counts among HIV-infected persons were modeled assuming a linear decline in CD4 after seroconversion. Averaged across 41 countries, the impact of HIV-1 was limited (although quantitatively uncertain) because of the different geographic distributions and contrasting age patterns of the 2 diseases. However, in Botswana, Zimbabwe, Swaziland, South Africa, and Namibia, the incidence of clinical malaria increased by <28% (95% confidence interval [CI] 14%–47%) and death increased by <114% (95% CI 37%–188%). These effects were due to high HIV-1 prevalence in rural areas and the locally unstable nature of malaria transmission that results in a high proportion of adult cases.

Summary: Objective To review the impact of malaria control on haemoglobin (Hb) distributions and anaemia prevalences in children under 5 in malaria‐endemic Africa.Methods Literature review of community‐based studies of insecticide‐treated bednets, antimalarial chemoprophylaxis and insecticide residual spraying that reported the impact on childhood anaemia. Anaemia outcomes were standardized by conversion of packed cell volumes into Hb values assuming a fixed threefold difference, and by estimation of anaemia prevalences from mean Hb values by applying normal distributions. Determinants of impact were assessed in multivariate analysis.Results Across 29 studies, malaria control increased Hb among children by, on average, 0.76 g/dl [95% confidence interval (CI): 0.61–0.91], from a mean baseline level of 10.5 g/dl, after a mean of 1–2 years of intervention. This response corresponded to a relative risk for Hb < 11 g/dl of 0.73 (95% CI: 0.64–0.81) and for Hb < 8 g/dl of 0.40 (95% CI: 0.25–0.55). The anaemia response was positively correlated with the impact on parasitaemia (P = 0.005,P = 0.008 andP = 0.01 for the three outcome measures), but no relationship with the type or duration of malaria intervention was apparent. Impact on the prevalence of Hb < 11 g/dl was larger in sites with a higher baseline parasite prevalence. Although no age pattern in impact was apparent across the studies, some individual trials found larger impacts on anaemia in children aged 6–35 months than in older children.Conclusion In malaria‐endemic Africa, malaria control reduces childhood anaemia. Childhood anaemia may be a useful indicator of the burden of malaria and of the progress in malaria control.

Background We assessed whether Demographic and Health Surveys (DHS), a large and high-quality source of under-5 mortality estimates in developing countries, would be able to detect reductions in under-5 mortality as established in global child health goals. Methods and Results Mortality estimates from 41 DHS conducted in African countries between 1986 and 2002, for the interval of 0–4 years preceding each survey (with a mean time lag of 2.5 years), were reviewed. The median relative error on national mortality rates was 4.4%. In multivariate regression, the relative error decreased with increasing sample size, increasing fertility rates, and increasing mortality rates. The error increased with the magnitude of the survey design effect, which resulted from cluster sampling. With levels of precision observed in previous surveys, reductions in all-cause under-5 mortality rates between two subsequent surveys of 15% or more would be detectable. The detection of smaller mortality reductions would require increases in sample size, from a current median of 7060 to over 20 000 women. Across the actual surveys conducted between 1986 and 2002, varying mortality trends were apparent at a national scale, but only around half of these were statistically significant. Conclusions The interpretation of changes in under-5 mortality rates between subsequent surveys needs to take into account statistical significance. DHS birth history surveys with their present sampling design would be able to statistically confirm under-5 mortality reductions in African countries if true reductions were 15% or larger, and are highly relevant to tracking progress towards existing international child health targets.

To assess how the impact of sexually transmitted disease (STD) treatment on HIV incidence varies between stages of the HIV epidemic. We simulated the spread of curable STD, herpes simplex virus type 2 and HIV in the dynamic transmission model STDSIM. Parameters were quantified to represent a severe HIV epidemic as in Rakai, Uganda, using demographic, behavioural and epidemiological data from a recent STD treatment trial. The model fitted the HIV epidemic in Rakai if we assumed a considerable behavioural risk reduction, starting at the end of the Ugandan civil war in 1986. An improvement in STD treatment reduced HIV incidence in this population by 35% over 2 years if implemented in 1981, but only by 11 and 8% in 1988 or 1998. This trend resulted partly from the hypothesized behaviour change, which markedly reduced the prevalences of bacterial STD. In a simulated epidemic without behavioural change, the corresponding treatment impacts in 1988 and 1998 would be 19 and 15%. Enhanced herpetic ulceration in immunocompromised HIV patients contributed little to the reduced impact of treatment of bacterial STD over time. In HIV epidemics beyond the first decade, the impact of STD treatment programmes on HIV transmission may depend more on behavioural risk reduction than on the stage of the epidemic. Preceding behavioural change associated with restored civil stability may have contributed to the lack of impact of STD treatment on HIV in the Rakai trial. In advanced epidemics with less behaviour change, STD treatment may still be important for HIV prevention.

To assess the linkage of sexually transmitted disease (STD) symptoms and treatable STD to HIV incidence. Analysis of a randomized trial of STD control for HIV prevention, Rakai, Uganda. Consenting adults 15-59 years of age were seen at 10-monthly home visits, interviewed regarding STD symptoms, and asked to provide samples for HIV and STD diagnoses. HIV incidence was determined in 8089 HIV-negative subjects over 10457 person years. Adjusted rate ratios (RR) and 95% confidence intervals (CI) of HIV acquisition associated with genital ulcer disease (GUD) and discharge/dysuria were used to estimate the population attributable fraction (PAF) of HIV acquisition. HIV transmission risks associated with STD symptoms in HIV-positive partners of 167 HIV discordant couples and the numbers of sexual partners reported by HIV-positive subjects were used to estimate the PAF of HIV transmission attributable to STD. HIV prevalence was 16%. The risk of HIV acquisition was increased with GUD (RR 3.14; CI 1.98-4.98) and in males with discharge/dysuria (RR 2.44; CI 1.17-5.12), but not in females with discharge/dysuria. The PAF of HIV acquisition was 9.5% (CI 2.8-15.8%) with any of the three STD symptoms. The PAF for GUD was 8.8% (CI 3.7-13.8), but only 8.2% of reported GUD was caused by treatable syphilis or chancroid. The PAF for discharge/dysuria in males was 6.7% (CI 1.1-13.8), but only 25% of symptomatic males had concurrent gonorrhea or chlamydial infection. No significant differences were seen in PAF between study treatment arms. The PAF of HIV transmission associated with STD symptoms in HIV-positive persons was indirectly estimated to be 10.4%. In this mature, generalized HIV epidemic setting, most HIV seroconversion occurs without recognized STD symptoms or curable STD detected by screening. Therefore, syndromic management or other strategies of STD treatment are unlikely to substantially reduce HIV incidence in this population. However, STD is associated with significant HIV risk at the individual level, and STD management is needed to protect individuals.