Malaria in the first 6 months of life in urban African infants with anemia.

A total of 446 infants in the first 6 months of life who presented at an urban children's hospital with complaints of any illness whatsoever were recruited into a study with the aim of determining the contribution of malaria to infant morbidity in a malaria-endemic urban area in Nigeria. Sixty-eight of the infants were in their first month of life and 79, 77, 61, 97, and 64 were in their second, third, fourth, fifth and sixth month of life, respectively. Overall, 107 (24.0%) infants were clinically diagnosed as having malaria. This included 3 who were in the first month of life, 12 in the second, 15 in the third, 17 in the fourth, 33 in the fifth, and 27 in the sixth months of life (4.4, 15.2, 19.5, 27.9, 34.0, and 42.1%, respectively). Laboratory investigations confirmed 35 (32.7%) of those clinically diagnosed and 86 (25.4%) of those not clinically diagnosed (n = 339) as having malaria parasitemia, giving an overall malaria parasite rate of 27.1% among the infants. Acute respiratory infection was the major diagnosis (41.3%) among those that were not initially diagnosed as malaria but turned out to have malaria parasitemia followed by gastroenteritis (11.8%) and failure to growth (1.5%). Overall geometric mean parasite density was 202.5 parasites/microL of blood (range, 12-65,317 parasites/microL of blood). The mean hematocrit of infants with parasites (33.0%) was significantly lower (P < 0.005) than that of infants without parasites (35.1%). The mean hematocrit of infants with malaria parasites in each age group was lower than that of infants without malaria parasites in the corresponding age group. Among the infants with malaria parasites, those aged 2 to 2.9 months recorded the lowest mean hematocrit (30.1%), and those aged < 1 month recorded the highest mean hematocrit (42.7%). Axillary temperature increased and hematocrit decreased with increase in parasite density. The percentage of infants with anemia likewise increased as the parasite density increased. Plasmodium falciparum was present in all infected infants, but mixed infection with P. malariae was present in only 2.5% of infections. Analysis of our data suggests an urgent need for health education of caretakers and for training of clinicians for increased awareness of malaria as an important cause of illness and anemia in infants aged < 6 months so as to reduce children's wasting due to an easily preventable and treatable disease.

Antimalarial drug response of Plasmodium falciparum from Zaria, Nigeria.

The sensitivity of Zaria strains of Plasmodium falciparum to chloroquine, mefloquine, quinine and sulphadoxine/pyrimethamine was investigated 5 years after the appearance of in vivo/in vitro chloroquine resistance in urban Zaria. Infections in 36/43 children (83.7%) treated with chloroquine were sensitive while those in 7 (16.3%) were resistant. 8/13 isolates cultured (61.5%) were sensitive in vitro to chloroquine and 5 (38.5%) were resistant. Of the cultured isolates, 13/13 (100%), 12/13 (92.3%) and 5/7 (71.4%) showed mefloquine, quinine and sulphadoxine/pyrimethamine sensitivity, respectively. The results confirmed chloroquine and sulphadoxine/pyrimethamine resistance in urban Zaria and revealed emerging quinine resistance. Resistance to chloroquine and sulphadoxine/pyrimethamine is at RI level and chloroquine should continue to be the first-line drug for the treatment and prevention of P. falciparum infection in the Zaria area of northern Nigeria. We suggest that, while quinine serves as second-line drug, mefloquine should be reserved for infections resistant to chloroquine, quinine and sulphadoxine/pyrimethamine.

Extra-hepatic biliary atresia preoperative and surgical assessment in 25; cases seen in Zaira

Admission in a seven year period of 25 infants with biliary atresia. We note that prelaparatomy percutaneous liver established the diagnosis of extrahepatic biliary atresia; which were confirmed at laparatomy. Fifty percent of the patients had liver cirrhosis before surgery. Therefore; bile drainage was not established in any of the 25 patients following hepatic surgery. Six (24 percent) died of hepatic failure during the period of follow-up. Factors responsible for the poor success rate of surgery included late presentation and grossly non correctible lesions