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A large-scale longitudinal cohort project was initiated in western Kenya in June 1992. Between June 1992 and July 1994, 1,848 children less than 15 years of age were monitored prospectively for a mean of 236 days. During this period, 12,035 blood smears were examined for malaria and only 34% were found to be negative. Parasite prevalence (all species) decreased with age (from a high of 83% among children 1-4 years old to 60% among children 10-14 years old). Even more dramatic decreases were noted in the prevalence of high density falciparum infection (from 37% among children 12-23 months old to Ͻ 1% among 10-14-year-old children) and in clinical malaria (20% to 0.3% in the same age groups). Children Ͻ 1 year of age accounted for 55% of all cases of anemia detected. Anemia was consistently associated with high density infection in children Ͻ 10 years of age (20% to 210% increased risk relative to aparasitemic children). These results demonstrate the relationship between high-density malaria infection and two clinical manifestations of malarial illness.

Abstract. A large-scale longitudinal cohort project was initiated in western Kenya in June 1992. The primary purpose of the project was to study Plasmodium falciparum malaria in a highly endemic area using a comprehensive and multidisciplinary approach, which included epidemiology, entomology, and immunology. Between June 1992 and July 1994, pregnant women living in 15 rural villages were identified during a monthly census and 1,164 were enrolled. The women were followed-up throughout their pregnancy and they, along with their newborn infants and direct siblings of the infants' less than 15 years of age, were monitored over time. As of May 1995, 1,017 infants had been born to these women. This paper presents the design and general methodology used in this study and describes the initial experience with intense monitoring of a large population over a prolonged period.Plasmodium falciparum infection can present with a wide spectrum of signs, symptoms, and history, from a fatal disease to an apparently asymptomatic infection, from a rapidly progressing, fulminant illness to a chronic insult. Many of the reasons for this wide variation in the presentation of this disease have been known for years, such as the protection afforded by some hemoglobinopathies.1,2 Recent scientific advancements and closer coordination of work done in various disciplines have begun to explain other observations for which there previously has been no satisfying explanation. For instance, application of newer genetic techniques to large populations has linked a particular human leukocyte antigen (HLA) type to increased risk of cerebral malaria, 3 partly explaining the observation that there are some people who develop cerebral malaria while most of their neighbors, with presumably the same exposures and histories, do not. 4 Combining the work of entomologists with that of clinical epidemiologists has demonstrated an effect of exposure pressure on disease development. 5 Because of the growing realization of complex interrelationships among the parasite, vector, environment, and host, advancing our understanding of falciparum malaria will require investigation of most if not all of these factors simultaneously. Conducting studies with similar designs in a variety of epidemiologic settings may also be necessary to understand the determinants of the full range of malarial illness. While a tremendous amount has been and can still be learned from cross-sectional studies, many of the questions that remain can only be addressed by monitoring larger numbers of people over longer periods of time, such as has been done in Senegal, 6 Ghana, 7 and Nigeria. 8A study initiated in June 1992 in western Kenya was designed to address the epidemiology, entomology, immunology (both humoral and cellular responses to defined antigens), host factors, molecular biology and antigenic variation, and population genetics of P. falciparum in a large cohort of women, newborn infants, and older children monitored over an extended period. Taken as a whole, this project wil...

Plasmodium falciparum infection is an important cause of the high childhood mortality rates in sub-Saharan Africa. Increasingly, the contribution of P. falciparum-associated severe anemia to pediatric mortality is being recognized while the impact of chloroquine resistance on mortality has not been evaluated. To address the issues of pediatric mortality, causes of death among hospitalized children less than five years of age in western Kenya were identified using standardized clinical examinations and laboratory evaluations. Follow-up examinations were conducted to determine the child's clinical status posthospitalization. Of the 1,223 children admitted to Siaya District Hospital from March to September 1991, 293 (24%) were severely anemic (hemoglobin level < 5.0 g/dL). There were 265 (22%) deaths; 121 (10%) occurred in-hospital and 144 (13%) occurred out-of-hospital within eight weeks after admission; 32% of all deaths were associated with malaria. Treatment for malaria with chloroquine was associated with a 33% case fatality rate compared with 11% for children treated with more effective regimens (pyrimethamine/sulfa, quinine, or trimethoprim/sulfamethoxazole for five days). The risk of dying was associated with younger age (P < 0.0001) and severe anemia (relative risk [RR] = 1.52, 95% confidence interval [CI] = 1.22, 1.90), and was decreased by treatment with an effective antimalarial drug (RR = 0.33, 95% CI = 0.19, 0.65). Effective drug therapy for P. falciparum with regimens that are parasitocidal in areas with a high prevalence of severe anemia and chloroquine resistance can significantly improve the survival of children in Africa.

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In the United States (US), travelers who have had malaria or who have taken antimalarial chemoprophylaxis are deferred as blood donors for 3 years to prevent transfusion-transmitted malaria. To assess the impact of shortening this 3-year exclusion period, national malaria surveillance data from 1972 to 1988 were reviewed. The average annual rate of transfusion-transmitted malaria is 0.25 cases per million units of blood collected. Of 45 reported cases, 38 percent were caused by Plasmodium malariae, 29 percent by P. falciparum, 24 percent by P. vivax, and 9 percent by P. ovale. Thirty-two donors were implicated in 34 cases of transfusion-transmitted malaria. Of 30 implicated donors whose native country was identified, 23 (77%) were foreign nationals and 7 (23%) were from the US. In a review of all imported malaria cases by species and by interval between date of entry and onset of illness, 98 percent of P. falciparum, 86 percent of P. malariae, 76 percent of P. vivax, and 74 percent of P. ovale infections became symptomatic within 6 months of the patient's arrival in the US, regardless of the use of prophylaxis. Shortening to 6 months the donor exclusion period for US travelers to malarious areas would result in a minimum of 70,000 additional blood donors' being made available, with a maximum annual increase of 0.03 additional cases of transfusion-transmitted malaria. The potential benefit of bringing healthy travelers back into the donor pool after a shorter period of exclusion merits consideration by the blood banking industry.

Severe anaemia among women in sub-Saharan Africa is frequently treated with blood transfusions. The risk of transmission of human immunodeficiency virus (HIV) through blood products has led to a re-evaluation of the indications for transfusions. Prospective surveillance of women admitted to a district hospital in western Kenya was conducted from 1 December 1990 to 31 July 1991, for haemoglobin (Hb) transfusion status, and outcome. Of the 2986 enrolled women (mean Hb 10.4 g/dL, SD +/- 2.6, median age 24.4 years), 6% were severely anaemic (Hb < 6.0 g/dL). Severe anaemia was associated with a higher mortality rate (10.7% vs. 1.4%, odds ratio (OR) = 8.2, 95% confidence interval (CI) 2.6, 34.2) compared with women with Hb > or = 6.0 g/dL. Decreased mortality rates in hospital were observed with increasing Hb values (OR = 0.43, 95% CI 0.19, 0.98), but blood transfusions did not improve survival in hospital (OR = 1.56, 95% CI 0.22, 11.03). The attributable mortality due to HIV infection and severe anaemia was 75% and 31%, respectively. Maternal/child health care services must include prevention strategies for HIV transmission and the prevention, recognition, and treatment of severe anaemia.