Severe anemia in young children after high and low malaria transmission seasons in the Kassena-Nankana district of northern Ghana.

Koram, Kwadwo A.; Owusu‐Agyei, Seth; Utz, G; Binka, Fred; Baird, J. Kevin; Hoffman, S. L.; Nkrumah, Francis

doi:10.4269/ajtmh.2000.62.670

Cited by 69 publications

(58 citation statements)

References 7 publications

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“…The relatively brief respite in transmission between February and May appeared sufficient to allow recovery of most severe anemia to above the 6.0 g/dl level. The work reported here and by Koram and others 10 demonstrates the need for longitudinal studies of seasonal risk of severe anemia in northern Ghana.…”

Section: Discussionmentioning

confidence: 54%

“…The infants and young children in these studies showed dramatic distinctions with respect to the prevalence of severe anemia as seen at enrollment at the end of the dry and wet seasons. 10 In effect, an epidemic of severe malarial anemia occurred in these children as the wet season progressed: apparently starting at 1% in May and increasing to 24% in October. Given the fact that we have now documented that intense transmission continues at least to February, the prevalence of severe anemia may even worsen relative to the 25% rate measured in October.…”

Section: Discussionmentioning

confidence: 99%

“…10 Incidence density was measured as the post-radical cure attack rate for P. falciparum parasitemia. This work provides relatively precise measures of incidence that may be linked to established patterns of disease risk in the region, i.e., high risk of severe anemia among infants and young children.…”

Section: Introductionmentioning

confidence: 99%

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

Baird

Owusu‐Agyei²,

Utz³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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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.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

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

Baird

Owusu‐Agyei²,

Utz³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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“…The mechanism we propose here may be a major contributor to the anemia seen in children in Africa at the end of the intense transmission season. 23 If this is the case, it will be extremely important to monitor hemoglobin status during trials of malaria vaccines that are designed not to prevent blood stage infection, but rather to limit it. 24 this study.…”

Section: Discussionmentioning

confidence: 99%

Anemia in parasite- and recombinant protein-immunized aotus monkeys infected with Plasmodium falciparum.

Jones

Stroncek²,

Gozalo³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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Abstract. Plasmodium falciparum-induced anemia was characterized in Aotus monkeys repeatedly immunized by infection with P. falciparum (FVO strain) parasites, then cross-challenged with CAMP strain, or in monkeys receiving blood stage challenges as part of malaria vaccine trials. In 4 studies, 25 (30.5%) of 82 monkeys had at least a 50% reduction in hematocrit; mean day of maximum parasitemia was 12.5, whereas the mean day of minimum hematocrit was 18.8 (P < 0.0009). Decreased hematocrit levels were not associated with reticulocytosis until parasite densities decreased significantly from peak levels. Direct antibody tests to detect IgG and C3d on the surface of erythrocytes were negative. Nonantibody/noncomplement-mediated lysis of uninfected erythrocytes seems to be the principal cause of the anemia, and it also seems that bone marrow suppression and lysis of infected erythrocytes contributed to the anemia. Partial immunity-whether induced by repeated immunization with whole parasites or with vaccine-seems important to the development of anemia.

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“…1 In areas with intense Plasmodium falciparum transmission, severe malarial anemia is the primary symptom of serious malarial disease among children less than two years of age and accounts for more than half of all malarial deaths in African children. 2,3 In malariaendemic areas, anemia is usually multifactorial in origin, but P. falciparum infection is the major factor in the etiology of severe anemia. 3 In areas of stable malaria transmission, anemia appears in the first few months of life, and has the highest prevalence towards the end of the first year.…”

Section: Introductionmentioning

confidence: 99%

A Comparison of Iron and Folate with Folate Alone in Hematologic Recovery of Children Treated for Acute Malaria

Gara

Madaki²,

Thacher³

2010

The American Society of Tropical Medicine and Hygiene

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Abstract. Concern has been raised that iron supplementation for treatment of acute malaria may worsen the severity of malaria. We compared the effect of iron and folate with folate alone on hematologic recovery in children treated for acute malaria. We randomized 82 children 6-60 months of age from Nigeria with smear-positive malaria and anemia (hematocrit < 33%) to receive iron (2 mg/kg/day) plus folate (5 mg/day) or folate alone in addition to antimalarial drugs. The mean ± SD hematocrit at baseline was 28.5% ± 2.9%. At four weeks, the mean hematocrit increased by 2.5% ± 1.6% in the iron plus folate group and by 1.4% ± 1.0% in the folate alone group ( P = 0.001). Baseline hematocrit, iron supplementation, weight for height, and weekly meat intake were significant predictors of final hematocrit. The effect of iron was not significantly modified by baseline hematocrit, weekly meat intake, nutritional status, mother's education, sex, or age of the child. Iron supplementation improved hematologic recovery in children with malarial anemia.

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Severe anemia in young children after high and low malaria transmission seasons in the Kassena-Nankana district of northern Ghana.

Cited by 69 publications

References 7 publications

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

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

Anemia in parasite- and recombinant protein-immunized aotus monkeys infected with Plasmodium falciparum.

A Comparison of Iron and Folate with Folate Alone in Hematologic Recovery of Children Treated for Acute Malaria

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