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J Stace

Publications and source records attributed to J Stace.

15 recordsLinked to original sources
PubMed1992

Chemoprophylaxis against malaria in Papua New Guinea: a trial of amodiaquine and a combination of dapsone and pyrimethamine.

A placebo-controlled chemoprophylaxis trial was carried out in 1980 in 318 semi-immune school children in the Madang area of Papua New Guinea, where there was a high prevalence of strains of Plasmodium falciparum resistant to 4-aminoquinolines. Since prophylaxis with amodiaquine at 5 mg/kg weekly had failed, amodiaquine at a dose of 10mg/kg weekly and Maloprim (half a tablet or one tablet depending on body weight, which gave ranges of dapsone of 1.7-3.3mg/kg and pyrimethamine 0.2-0.4 mg/kg) weekly were tried. Neither regimen was completely successful in preventing parasitaemia, though after 13 weeks of prophylaxis the slide positivity rate was 16% for the amodiaquine group and 2% for the Maloprim group, which was in each case significantly lower than the normal baseline rate in the controls of 42%. Amodiaquine was completely successful in suppressing Plasmodium vivax infections. Breakthrough parasitaemia occurred, with either P. falciparum or P. vivax, in 5% of subjects on Maloprim at some time during the 13-week period of prophylaxis. Significantly more children in both the amodiaquine and Maloprim groups than in the placebo group showed a reduction in spleen size. All groups showed an unexplained fall in haemoglobin level over the study period but the fall was significantly less in both the prophylaxis groups. There was no adverse effect on white cell counts by either drug regimen. Chemoprophylaxis as a component of an integrated malaria control program should not be overlooked, provided that compliance can be maintained. However, in this particular case the principal purpose of the study had been to evaluate the proposed chemoprophylactic regimens in school children before embarking on an intervention study in young children. As a result of this study it was decided not to go ahead with the chemoprophylactic intervention in young children but to adopt an approach based on early presumptive treatment.

Antimalarials↗
PubMed1986

Characterisation of the host response to Plasmodium falciparum infection in acute non-complicated malaria.

In this study we have examined serum from patients with Plasmodium falciparum malaria, collected at the time of acute attack and 14 days later. We have also examined sequential samples of sera taken from children living in Madang Province, Papua New Guinea, an area endemic for malaria. The total amount of antibody directed against P. falciparum in acute phase sera was less than that found in matched controls. An in vitro assay measuring inhibition of penetration of uninfected erythrocytes by merozoites of P. falciparum revealed less inhibitory activity in acute phase sera than in matched controls. The longitudinal study of sera from village children demonstrated that non-specific inhibition of intracellular parasite growth was fairly stable, while merozoite inhibiting activity was unstable and varied with time. A cloned P. falciparum species has been used to directly demonstrate the specific growth enhancement by serum in vitro.

Acute Disease↗
PubMed1986

Characterisation of the host response to Plasmodium falciparum infection. I. Cerebral malaria.

Cerebral malaria is a major form of complicated malaria consequent upon cerebral damage associated with endothelial cell necrosis. We have used assays of Plasmodium falciparum growth inhibition in vitro to study serum inhibitory factors in patients with cerebral malaria. Serum from children with cerebral malaria inhibited parasite growth in a non-synchronised 72-hour assay to a greater extent than did sera from immune adults or asymptomatic children (p less than 0.001). The high level of non-specific inhibition of parasite growth was particularly evident when sera were tested against three P. falciparum isolates, and contrasted with the inhibitory effect of sera from non-malaria febrile controls. In this study, serum from patients with cerebral malaria was more inhibitory than serum from the other groups (p less than 0.001) and its between-isolate variation, when tested against a panel of P. falciparum isolates in growth assays, was significantly less than that of the other groups tested (p less than 0.005). These results are consistent with the hypothesis of toxin-induced endothelial cell damage, with the sequence of pathogenic events involving host-derived serum factors capable of damaging P. falciparum.

Adolescent↗
PubMed1985

Pharmacokinetics of quinine in children.

Serum quinine concentrations were measured in seven children after intravenous infusion of quinine dihydrochloride, in eight children after intramuscular injection of quinine dihydrochloride, and in six children after nasogastric administration of a solution of quinine dihydrochloride. The mean (+/- SD) half-life of quinine was 11.1 +/- 4.8 hours, and the volume of distribution was 1.39 +/- 0.37 L/kg. To attain a serum level of 10 microgram/ml quinine, we suggest that children with severe malaria be given a loading dose of 20 mg/kg quinine dihydrochloride parenterally, followed by 7.5 mg/kg every 8 hours. Once recovery begins, quinine sulphate 10 mg/kg may be given orally every 8 hours. Serum concentrations should be monitored, if possible, because they vary greatly from person to person. Quinine is rapidly and completely absorbed after either intramuscular or nasogastric administration.

Child↗
PubMed1983

Serum levels of quinine following intramuscular administration to children.

The serum quinine level was assayed in 31 children four hours after receiving an intramuscular injection of quinine dihydrochloride; in 14 children the level was also assayed 2 hours after the injection. The quinine was quickly absorbed from muscle, with serum quinine levels being significantly higher at 2 hours than at 4 hours. The injections were not particularly painful, and muscle necrosis was not observed. Quinine is rapidly absorbed following intramuscular injection, and is a safe and reliable method of administering the drug to children with severe malaria. In most situations in Papua New Guinea (PNG), intramuscular administration of quinine is preferable to intravenous infusion.

Body Weight↗
PubMed1982

Sulfadoxine-pyrimethamine for the treatment of acute malaria in children in Papua New Guinea. I. Plasmodium falciparum.

Chloroquine-resistant Plasmodium falciparum malaria is increasing in prevelance in Papua New Guinea and alternative therapies for acute malaria are being sought. A trial of sulfadoxine-pyrimethamine for the treatment of acute falciparum malaria in children has been carried out in Madang, Papau New Guinea. Eighty-five children were treated with sulfadoxine-pyrimethamine, either alone or in combination with a single 10 mg/kg dose of chloroquine. Of 78 children completing 28-days follow-up, treatment failures occurred in 15 (19.2%) and of these, 8 (10.3%), are believed to be sulfadoxine-pyrimethamine resistant; the others remain equivocal. There was no advantage in this study in combining a single dose of chloroquine with sulfadoxine-pyrimethamine; indeed, this combination was associated with an increased incidence of vomiting. It is argued that sulfadoxine-pyrimethamine should not become the standard presumptive treatment for acute malaria in Papua New Guinea.

Child↗
PubMed1982

Sulfadoxine-pyrimethamine for the treatment of acute malaria in children of Papua New Guinea. II. Plasmodium vivax.

In Papua New Guinea, Plasmodium falciparum and P. vivax are common causes of acute malaria in children and P. malariae an uncommon cause. The increasing prevelance of chloroquine-resistant strains of P. falciparum in Papua New Guinea has prompted the search for alternatives to chloroquine as standard presumptive treatment. Sulfadoxine-pyrimethamine, either alone or in combination with a single dose of chloroquine, was compared with chloroquine alone for treatment of acute vivax malaria in children in Madang. Fever resolution was slowest in the group treated with sulfadoxine-pyrimethamine alone, and time to clearance of parasitemia was significantly longer in this group (P less than 0.001). Where possible, species identification should be undertaken in acute malaria and cases of P. vivax treated with chloroquine.

Child↗
PubMed1982

Cerebral malaria in children: a retrospective study of admissions to Madang Hospital, 1980.

A review was undertaken of sixty-eight children admitted with cerebral malaria to Madang Hospital, Madang, Papua New Guinea (PNG) in 1980. Children with cerebral malaria were significantly older than those with uncomplicated malaria, and older than children admitted with other conditions causing fits or coma. The nutritional status of children with cerebral malaria did not differ from that of children admitted with other diagnoses. The cerebrospinal fluid was normal in 80% of children with cerebral malaria, and in 20% mildly elevated protein or leukocytes were noted. Of the 68 children with cerebral malaria, four died (5.9%). This is a low mortality rate in comparison wih other centres in PNG and with reports from other countries.

Brain Diseases↗
PubMed1981

Acute malaria in children in Madang: endemicity, clinical presentation and treatment.

Much of the present knowledge of the status of malaria in Papua New Guinea stems from a few studies carried out in the past. In the present situation there are many areas of uncertainty not least the effects of poor acceptance of residual spraying programmes and the emergence of chloroquine-resistant falciparum malaria. New anti-malarials are being developed, new methods of vector control may become useful and immunization may soon become possible. In order to assess the impact of these measures it is essential that they are studied in an area with a well defined population and where the current epidemiological situation is known.

Amodiaquine↗
PubMed1980

Plasmodium falciparum strains from Papua New Guinea: culture characteristics and drug sensitivity.

Seven strains of Plasmodium falciparum from Papua New Guinea have been established in continuous in vitro culture. Samples with a high initial parasitaemia were more likely to form continuous lines, possibly due to the time required for transport of infected blood samples from Papua New Guinea to laboratories in Australia. Most but not all established lines were resistant to chloroquine and all were resistant to pyrimethamine, possibly reflecting the parasite strain characteristics in that region.

Adolescent↗