Chloroquine-resistant Plasmodium falciparum with reduced sensitivity in vitro to mefloquine and quinine in Zaria, northern Nigeria.

Thirty-six P. falciparum isolates collected from children with malaria were tested for their susceptibility to chloroquine, mefloquine and quinine in vitro using the WHO microtest system. 37% of the isolates grew in the presence of 1.6 mumol chloroquine 1(-1) blood, indicating resistance. The sensitivity to both mefloquine and quinine was markedly reduced. The inhibitory endpoints for quinine correlated with those for chloroquine and mefloquine, but no such correlation was found between chloroquine and mefloquine.

Resistance of Plasmodium falciparum to sulfadoxine-pyrimethamine combination in semi-immune children in Zaria, northern Nigeria.

The World Health Organization (WHO) extended field test was employed to assess the in vivo sensitivity of Plasmodium falciparum to sulfadoxine-pyrimethamine combination in 44 children in Zaria urban area. 36 children (82%) were fully sensitive to the drug and 8 (18%) were resistant at the RI level. 8 parasite isolates were obtained from the children and successfully cultured in vitro using the WHO microtest (mark II) system. The 8 isolates underwent schizogony at concentrations of 10,000 pmol sulfadoxine/125 pmol pyrimethamine per well, indicating in vitro resistance.

Chloroquine resistance of Plasmodium falciparum in semi-immune children in Zaria, northern Nigeria.

Fifty-nine children with Plasmodium falciparum malaria were subjected to the World Health Organization (WHO) extended field test to assess the in vivo sensitivity of the parasite to chloroquine in Zaria urban area, Nigeria. The parasites in 53 children (90%) were positive but those in 6 (10%) were resistant at the RI-RII level. 36 isolates from the patients were successfully cultured in vitro for the WHO standard microtest. 13 (37%) of the isolates underwent schizogony at chloroquine concentrations of 1.6 microM/litre and above. Probit analysis showed that the chloroquine concentrations producing 50% (EC50), 90% (EC90) and 99% (EC99) schizont inhibition were 0.4, 1.6 and 4.9 microM/litre, respectively. The results indicate a rapid decline in the sensitivity of P. falciparum to chloroquine in the study area during the past 3 years.

In-vivo sensitivity of Plasmodium falciparum to chloroquine in Zaria, Nigeria.

In 33 children with confirmed Plasmodium falciparum malaria, the WHO Extended Field Test was employed to test the sensitivity of the parasite to chloroquine in Zaria urban area. No evidence of resistance to the drug was found. In 82% of the patients parasitaemia had disappeared within 3 days, while the remaining 18% were parasite negative on day 4 or 5. The mean parasite clearance time was calculated as 3.45 +/- 1.23 days. The results suggest that chloroquine sensitivity of P. falciparum may be decreased in this part of Nigeria.

Familial hyperphosphatasaemia in a Nigerian child.

A 5-year-old Nigerian girl of normal intelligence had grotesque crippling skeletal deformities, multiple pathological fractures and dwarfism dating back to the end of the first year of life. She also suffered from recurrent lower respiratory tract infection since infancy. The clinical, biochemical and radiological profile were compatible with the diagnosis of familial hyperphosphatasaemia.

Treatment of iron deficiency in Nigerians with daily intramuscular Ferastral.

Treatment of severe iron deficiency with iron-poly(sorbitol-gluconic acid) complex (Ferastral) intramuscular 10 ml (iron 500 mg) on alternate days has been shown highly effective and well tolerated. In order to see whether the time of treatment could be shortened, 20 Nigerians with severe iron deficiency (mostly from hookworm infection) were treated with daily intramuscular Ferastral 10 ml until their calculated total requirement of iron was met. The total iron deficit was 877-2763 mg (mean 1875 mg). Supportive treatment included antimalarials, folic acid and anthelmintics. No patient complained of undue pain at injection sites or of any other undesirable side-effects. There was no evidence of hepatic or renal toxicity in any patient, including eight who were followed at intervals up to eight weeks from the start of treatment. The initial haemoglobin (Hb) level was 2.2-7.8 g/dl (mean 4.6 g/dl). Daily regeneration of Hb in the first 14 days was 0.12-0.49 g/dl (mean 0.30 g/dl), and haematological indices were generally normal by eight weeks. Recovery was slow or incomplete in six patients, all of whom had complications other than iron deficiency. Serum iron was measured in five patients, rose to around 8000 micrograms/dl on about day 4, and fell to physiological levels by day 14. The serum unsaturated iron binding capacity fell to nil in five out of six patients on around day 3, and reappeared between days 7 and 10. Five patients who had persistent blood loss from continued hookworm infestation received a further single dose of Ferastral (iron 1000 mg) 10 ml into each buttock after four weeks, and one patient after two weeks. This large dose was also acceptable to patients if given slowly; it was followed by an accelerated Hb regeneration, but no toxicity. Daily intramuscular Ferastral 10 ml until the calculated iron requirements are met (usually in less than five days) is recommended for the treatment of severe iron deficiency. Patients with continued blood loss or Hb less than 10 g/dl after four weeks without other cause of anaemia, may receive a boost of one intramuscular injection of Ferastral 20 ml (10 ml into each buttock).