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The possibility that positive or negative associations occur between the filarial nematode Onchocerca volvulus and the gastrointestinal nematodes Ascaris lumbricoides and Trichuris trichiura was investigated in 205 children attending three schools in central Cameroon. Despite the closeness of their locations, marked differences between the schools were detected with respect to the number of species carried, the prevalence of O. volvulus and T. trichiura and the interaction between the prevalence of these two species. The number of species carried and these same prevalences varied significantly across the narrow age range of the study group. In addition, we observed an interaction between the prevalences of O. volvulus and A. lumbricoides that was dependent upon school but independent of host age and sex. Quantitative analyses revealed that the abundances of O. volvulus, A. lumbricoides and T. trichiura were affected by both school and age whereas host sex was significant only for O. volvulus. Finally, we observed significant positive interactions between the intensities of A. lumbricoides and T. trichiura and between O. volvulus and T. trichiura, that were school, age and sex independent. Our data suggest that associations do occur between filarial and gastrointestinal nematodes and that certain individuals are prone to multiple and high-level infections.

In persons naturally exposed to high transmission, how significant, in terms of immune protection, is the occurrence or non-occurrence of a malaria attack during a given observation period? This question was studied in a West African village where Plasmodium falciparum malaria is holoendemic with intense and perennial transmission. A cohort of 94 children aged 4 months-14 years from Dielmo village, Senegal, was studied over 4 months, June-September 1990. 41 children had no malaria attack and 53 children suffered between one and 6 attacks. The average number of attacks was 1·80, 2·25, 1·87, 0·29 and 0·07, respectively, in children aged 4–11 months, 1–2, 3–6, 7–10 and 11–14 years. The transmission level was 75 infective bites per person. Analysis of the distribution of the number of attacks in individual children suggested that all children within the same age group had either the same, or a very similar, level of protection. This suggests that the acquisition of clinical protection in areas where malaria is highly endemic involves a progressive and homogeneous decrease of the probability of having a malaria attack (attacks occur less frequently as age increases, in all children), rather than the acquisition of complete protection by an increasing number of children. The differences between the number of clinical attacks observed in young children and their presumed exposure suggest that protective mechanisms become effective from the first reinfection onwards, and are independent of the cumulative exposure to a great variety of antigens.

In highly malaria-endemic areas, thick smears are usually positive regardless of the clinical context. Therefore the simple positivity or negativity of the thick smear is not an adequate criterion for distinguishing malaria from other causes of fever. In order to define simple parasitological and clinical criteria for diagnosing clinical malaria with a small risk of error, a study was undertaken in a rural area in the Congo where malaria transmission is intense and perennial. Results of the systematic determination of the parasite density of 1562 samples from persons of all ages considered representative of the population of the studied area are compared to those from 327 febrile patients, 204 patients detected during medical consultations held in the villages and 123 febrile schoolchildren detected during surveys for fever. The analysis of the clinical data and the parasitological results clearly demonstrates the importance of the parasite density determination for the diagnosis of clinical malaria. Clinical Plasmodium falciparum malaria is unlikely to occur in children under 15 years if the parasite/leucocyte ratio is less than 1·5. On the contrary this diagnosis is very probable if the parasite/leucocyte ratio is higher than 2. Clinical criteria were too non-specific to serve as useful diagnostic criteria.

In order to determine the incidence and prevalence of clinical malaria in children exposed since birth to intense and perennial transmission, two successive longitudinal surveys, a weekly survey over four months and a daily survey over 10 days, were carried out in 1983-1984 among 182 children aged 5-13 years in Linzolo, Republic of the Congo, a village where malaria is holoendemic. By age group, prevalence of clinical malaria was found to be between 3.2% and 2.4% at ages 5-6 years, between 2.5% and 1.8% at ages 7-8 years, between 1.6% and 1.1% at ages 9-10 years, and between 0.5% and 0.3% at ages 11-13 years. For these four age groups, respectively, the annual incidence of clinical malaria was estimated during the first survey as 3.0, 2.1, 1.8, and 1.2 attacks, and during the second survey as 5.2, 2.7, 2.0, and 0.8 attacks. No difference was observed in the incidence of malarial attacks between children who use bed-nets and those who do not use them. Also investigated were the customs of the inhabitants of the village in the presence of febrile syndromes in the children, and the importance of antimalarial drug consumption in these cases. It was observed that almost all of these syndromes were rapidly treated with antimalarials, and that in half of the cases these drugs were administered by the parents themselves.

The lack of serum haptoglobin in Africans has been investigated in the Congo, Central Africa, where HpO prevalence is about 30%. This study shows that it is possible to suppress ahaptoglobinaemia within a few weeks by antimalarial chemoprophylaxis, that it does not occur in protected individuals, that ahaptoglobinaemia reappears at its original incidence levels after interruption of chemoprophylaxis, and that some individuals are more susceptible in relation to Hp2 gene. Malaria is the only significant cause of ahaptoglobinaemia in subjects both with and without detectable parasitaemia. The possible mechanisms involved are discussed.