Seasonal malaria attack rates in infants and young children in northern Ghana.

Abstract

Abstract. The incidence density of infection and disease caused by Plasmodium falciparum in children aged six to 24 months living in the holoendemic Sahel of northern Ghana was measured during the wet and dry seasons of 1996 and 1997. At the beginning of each season, a cohort composed of 259 and 277 randomly selected children received supervised curative therapy with quinine and Fansidar and primaquine for those with normal glucose-6-phosphate dehydrogenase activity. The 20 weeks of post-therapy follow-up consisted of three home visits weekly and examination of Giemsastained blood films once every two weeks. Blood films were also taken from children brought to clinic with illness. The incidence density of parasitemia after radical cure was 4.7 infections/person-year during the dry season and 7.1 during the wet season (relative risk ‫ס‬ 1.51, 95% confidence interval [CI] ‫ס‬ 1.25-1.81; P ‫ס‬ 0.00001). Although the mean parasitemia count at time of reinfection in the dry season (3,310/l) roughly equaled that in the wet season (3,056/l; P ‫ס‬ 0.737), the risk ratio for parasitemia > 20,000/l during the wet season was 1.71 (95% CI ‫ס‬ 1.2-2.4; P ‫ס‬ 0.0025). The risk ratio for parasitemia > 20,000/l with fever during the wet season was 2.45 (95% CI ‫ס‬ 1.5-4.1; P ‫ס‬ 0.0002). The risk ratio for anemia (hemoglobin < 8 g/dl) at first post-radical cure parasitemia showed no difference between seasons (1.0; 95 % CI ‫ס‬ 0.73-1.4; P ‫ס‬ 0.9915). We did not see seasonal differences in anemia known to exist in this region, probably because the longitudinal cohort design using first parasitemia as an end point prevented the subjects from developing the repeated or chronic infections required for anemia induction. These findings bear upon the design of malaria drug and vaccine trials in holoendemic areas.

A quantitative analysis of transmission efficiency versus intensity for malaria

“…Other studies have come to similar conclusions about the lack of infection blocking immunity early in childhood 17,43 , although it might still develop in adults 17 . Bloodstage immunity is unlikely to be a factor in the young children considered in these studies, but it could be a factor in older children or adults: one study found that malaria attacks were less common in older children 37 , but another found very similar attack rates in children and adults 32,33 . An acute immune system response, such as to mosquito biting, could explain the variability in transmission efficiency.…”

“…A preliminary literature search identified five kinds of studies that estimated transmission efficiency either directly by exposing people to the bites of infectious mosquitoes, or indirectly as the ratio of the FOI and the EIR, the number of infections per infectious bite: (1) human subjects were challenged by exposing them to the bites of infectious mosquitoes [28][29][30][31] ; (2) synthetic cohorts of uninfected people were created by curing infections with antimalarial drugs, and the cohorts were followed over time to estimate the attack rate: the proportion of the cohort that was infected 16,32,33 ; (3) cross-sectional parasite surveys were used to estimate the FOI by fitting models to the rise in malaria prevalence with age, after accounting for infections that were cleared [12][13][14] ; (4) cross-sectional serological surveys were used to estimate the SCR by fitting models to the rise in seroprevalence with age, after accounting for waning immunity (or sero-reconversion) 34,35 ; and (5) longitudinal studies were used to estimate the FOI by following individuals over time as they naturally acquired infections, and several study designs and methods were used to infer the attack rates from a sequence of parasite positive or negative observations 15,36,37 . These studies were reanalysed and the results assembled to evaluate the functional relationship between the FOI (denoted h in equations, which Ross called the 'happenings' rate 1 ) and the EIR (denoted E in equations).…”

Successful Induction of CD8 T Cell-Dependent Protection Against Malaria by Sequential Immunization with DNA and Recombinant Poxvirus of Neonatal Mice Born to Immune Mothers

“…A major protective factor is thought to be maternally acquired Abs that provide enough protection to limit morbidity and mortality. However, in areas with extremely intense transmission of P. falciparum, such as northern Ghana (20) and western Kenya (21), a significant proportion of serious disease and P. falciparumassociated mortality occurs between 4 and 8 mo of age. This means that to be optimally effective in preventing serious morbidity and mortality, a P. falciparum vaccine will have to be first administered to neonates or young infants, and the immunization series will have to be completed by 4 -6 mo of age.…”

An investigation of the protective effect of alpha+‐thalassaemia against severe Plasmodium falciparum amongst children in Kumasi, Ghana

“…A few studies in Ghana have reported various rates of prevalence of G6PD deficiency (Allison et al, 1961, Lewis et al, 1965, Acquaye et al, 1973, Burchard et al, 2001, Baird et al, 2002. Current studies have suggested prevalence rates of 8.33% in the northern part of Ghana (Baird et al, 2002), 19.0% in the middle belt of Ghana (Amoako et al, 2010, personal communication) and 30.4% and 2.6%…”