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Haematological measurements were made in 198 Nigerian children aged three months to two years who received weekly malaria chemoprophylaxis with chloroquine from shortly after birth until the age of one or two years and in 185 age-matched control children. Children protected against malaria had a higher mean haemoglobin level and a higher packed cell volume than control children, and they showed fewer abnormalities of their red cells. Total and differential white blood cell counts, mean plasma folate and mean serum ferritin concentrations were similar in both groups of children. However, the geometric mean red cell folate level of children exposed to malaria was significantly higher than the mean level of control children; and it may be that malaria raises the red cell folate through intracellular synthesis by malaria parasites. Children with malaria parasitaemia had a significantly lower haemoglobin and packed cell volume and a significantly higher geometric mean red cell folate and ferritin level than children without parasitaemia. Serum ferritin is probably an unreliable index of iron status in children with malaria.

Haematological indices, malarial parasitaemia, serum and red cell folate (SFA, RCF), serum vitamin B12 and haemoglobin (Hb) electrophoretic patterns were studied in 228 non-elite young Hausa primigravidae at less than 24 weeks of gestation. The study was conducted in the guinea savanna of Nigeria, where malaria is hyperendemic. Ninety-nine (43%) were anaemic (Hb less than 11.0 g dl-1). The commonest cause of anaemia was malaria, in 28% of all and 40% of anaemic subjects. Plasmodium falciparum was predominant; P. malariae was seen in 1.3% and P. ovale was not recorded. Parasitaemia was more frequent and more dense in the wet than the dry season. Iron deficiency was diagnosed in 18% of all and 25% of anaemic women; 14% of all patients were folate-deficient; high MCV and MCH correlated with anaemia, and low SFA was associated weakly with anaemia and malaria. Serum vitamin B12 was normal or high in all 145 in whom it was measured; 3% had congenital elliptocytosis, but this did not contribute to the anaemia. Sickle-cell trait was present in 26% and Hb-AC in less than 1%. Hb-AS was associated with significantly lower frequency and density of P. falciparum; this has not been demonstrated in pregnancy in Africa previously. However, the parasitological advantage was not reflected in any haematological advantage. The roles of malaria, folate-deficiency and iron-deficiency in the causation of anaemia in Hausa primigravidae will be defined further by a double-blind trial of antimalarial prophylactics, iron supplements and folic acid supplements.

The prevalence of different haemoglobins and their interaction with malaria have been studied in Garki, Kano State, Nigeria. Sickle cell trait was present in 24% of newborn and 29% of those aged over five years. Hb.AC was present in 0.7%. Frequency of both haemoglobin variants was greater in Hausa than Fulani. Sickle cell anaemia was almost invariably fatal in early childhood. The distribution curve of percentage of Hb.S in sickle cell trait subjects was normal, and did not demonstrate any high frequency of a gene for alpha-thalassaemia. The presence of beta-thalassaemia minor could not be tested, but Hb.S/beta-thalassaemia was not detected. Hb.S gene frequency appears to have been maintained by a fitness in heterozygotes of 21% over normal homozygotes; increased fertility and high mutation rate did not make any apparent contribution. Hb.AS subjects had on average lower frequency and considerably lower densities of Plasmodium falciparum trophozoites than Hb.AA from the age of 30 to 59 weeks; density was less in sickle cell trait up to age three years in the dry season only. It is suggested that the survival advantage and hence the prevalence of sickle cell trait may be greatest in some hyperendemic areas and less where malaria transmission is extremely high or when it is high and unvaried.

Plasmodium falciparum and P. malariae were found less frequently in blood obtained from Nigerian children under the age of two years who had the haemoglobin genotype AS than in blood films obtained from those who had the genotype AA. However, differences between the two groups were statistically significant only for P. falciparum asexual forms. The prevalence of malaria antibodies, as measured by an ELISA, did not differ significantly between the two groups.

The efficacy of chloroquine and pyrimethamine as malaria chemoprophylactics was investigated in young Nigerian children. Chloroquine resistance had not been documented in the study area; pyrimethamine resistance was probably present but uncommon. Children who received weekly chemoprophylaxis with pyrimethamine had a lower prevalence of malaria parasitaemia and malaria antibodies than children who received weekly chemoprophylaxis with chloroquine. Pyrimethamine given monthly gave a comparable degree of protection to chloroquine given weekly. Chloroquine frequently induced vomiting in young children and this may have impaired its efficacy as a prophylactic. We conclude that, in an area where neither chloroquine nor pyrimethamine resistance is prevalent, pyrimethamine is a better chemoprophylactic for young children than chloroquine.