Showing papers on "Plasmodium vivax published in 1979"

Treatment of vivax malaria with sulfadoxine-pyrimethamine and with pyrimethamine alone.

Abstract: The effect of pyrimethamine and the combination of pyrimethamine-sulfadoxine (Fansidar) upon the termination of the acute attack of vivax malaria was studied in Thailand. Pyrimethamine was found to be ineffective, providing clearance of parasitaemia in only two of six patients by the end of seven days following treatment. The combination, administered in a two-tablet single dose (sulfadoxine 1 gm, pyrimethamine 50 mg) eliminated parasitaemia in only six of ten patients within seven days. Three tablets (sulfadoxine 1 . 5 gm, pyrimethamine 75 mg) given to 11 patients, provided clearance of parasitaemia in all within seven days; however, mean parasite and fever clearance times in this group were prolonged at 90 and 50 hours respectively. Chloroquine remains the drug of choice for the termination of the acute attack of vivax malaria. Subsequent primaquine is necessary for the prevention of relapse.

Hepatic dysfunction in childhood malaria.

Abstract: Hepatic function of 80 children aged under 3 years with Plasmodium vivax malaria were studied during the acute attack and 6 weeks after antimalarial treatment. Raised levels of serum aspartate transaminase (serum AST; SGOT), serum alanine transaminase (serum ALT; SGPT), and alkaline phosphatase were observed in 68%, 39% and 46% of cases respectively. AST levels were higher than ALT ones and the mean level of both enzymes was much higher in patients with hepatomegaly. The hepatic dysfunction which these observations reflect is transient, as these enzymes were found to be at their normal levels 6 weeks after treatment. A transient derangement of liver function is thus a common feature of childhood malaria, and hepatic dysfunction takes place to a significant degree even in P. vivax malaria.

Effect of sequential infection with Plasmodium vivax and P. falciparum in the Aotus trivirgatus monkey.

Abstract: Aotus trivirgatus monkeys with prior experience with Plasmodium vivax were inoculated with P. falciparum via the bites of infected mosquitoes. The animals with prior malaria had higher parasitemias and significantly higher levels of mosquito infectivity than monkeys with no prior P. vivax experience. Monkeys with a history of P. falciparum that were inoculated with P. vivax had essentially the same parasitemias as those with no prior malaria. However, levels of mosquito infectivity were markedly increased in those monkeys with a history of P. falciparum. The results imply that the introduction of another malaria species into a malarious area may result in higher levels of mosquito infection and more rapid establishment and distribution of that species.

Malaria in Birmingham and a London teaching hospital.

Abstract: During the past five years the incidence of imported malaria increased among patients seen in East Birmingham Hospital and in St Thomas's Hospital, London. Plasmodium vivax was the predominant species in Birmingham, and was almost always acquired by Asian immigrants visiting the Indian subcontinent. In St Thomas's P falciparum was most commonly imported, usually by African immigrants visiting Nigeria and Ghana. Two patients (one Irish, one Japanese) died of falciparum malaria after visiting tropical Africa. In both hospitals the immigrant patients had seldom taken prophylactic drugs, and the few who had, ceased to do so on arrival in the UK and sometimes before leaving the malarious country. Apparently immigrants who visit their homeland do not consult their general practitioners before travelling, are given inappropriate advice, or do not take appropriate advice when given. Since the incidence of imported falciparum malaria in the UK is rising, the following points should be considered: the infection may be lethal, particularly in patients lacking immunity; it can mimic other diseases, which may lead to delayed diagnosis; severe disease may be associated with few parasites on a blood film, and even if the result is negative further tests should be performed; clinicians and hospital pharmacists should be aware of the need to keep permanent stocks of parenteral chloroquine and quinine preparations.

Studies on the 2,4-diamino-6-substituted quinazolines. II. Activities of selected derivatives against infections with various drug-susceptible and drug-resistant strains of Plasmodium falciparum and Plasmodium vivax in owl monkeys.

Abstract: Four 6-thio-, one 6-sulfinyl-, and two 6-sulfonyl-substituted 2,4-diaminoquinazolines were evaluated for capacities to cure established infections with the chloroquine-resistant Vietnam Oak Knoll and pyrimethamine-resistant Malayan Camp-CH/Q strains of Plasmodium falciparum in owl monkeys. As compared with the doses of standard drugs required for cure of infections with drug-susceptible strains or doses of the newly developed aminoalcohols required for cure of either drug-susceptible or drug-resistant strains, each of these quinazolines effected cure of infections with the Oak Knoll strain at a remarkably small daily dose. However, doses required for cure of infections with the Camp-CH/O strain were from 4-48 times those required for cure of infections with the Oak Knoll strain, suggesting that the activities of these quizanolines, like those of 6-amino-substituted derivatives, were compromised by pyrimethamine resistance. This suggestion received support from expanded studies involving WR-158,122 and WR-159,412, the most active of the agents examined, and the multidrug-resistant Vietnam Smith strain of P. falciparum and Vietnam Palo Alto strain of P. vivax, as well as the Oak Knoll and Camp-CH/Q strains. These studies also showed that significant fractions of infections with the Oak Knoll, Camp-CH/Q, and Palo Alto strains treated previously with subcurative doses of the above derivatives failed to respond to doses that regularly cured previously untreated infections. These treatment failures proved to be due to emergence of parasites resistant to the quinazolines.

Studies on the 2,4-diamino-6-substituted quinazolines. III. The capacity of sulfadiazine to enhance the activities of WR-158,122 and WR-159,412 against infections with various drug-susceptible and drug-resistant strains of Plasmodium falciparum and Plasmodium vivax in owl monkeys.

Abstract: Previous studies showed: 1) that the activities of the 2,4-diamino-6-substituted quinazolines. WR-158,122 and WR-159,412, against Plasmodium falciparum and Plasmodium vivax infections in owl monkeys, were seriously impaired when infecting strains were pyrimethamine-resistant; and 2) that primary treatment failure with either agent led frequently to emergence of parasites resistant to these derivatives. Taking advantage of the potencies of WR-158,122 and WR-159,412 as dihydrofolic acid reductase inhibitors, the current studies were aimed at determining whether the above liabilities could be reduced to manageable levels or eliminated by concomitant administration of a rho-aminobenzoic acid inhibitor such as sulfadiazine. Application of these combinations prevented emergence of parasites resistant to WR-158,122 or WR-159,412, but did not abolish the differences in effectiveness of either compound against infections with pyrimethamine-susceptible and pyrimethamine-resistant strains; however, activities against infections with either susceptible or resistant strains were enhanced markedly. With WR-158,122, this enhancement ranged from greater than 7-fold to 75-fold; with WR-159,412, it ranged from greater than 5-fold to 13-fold. Maximal increases in activity were attained with a remarkedly small dose of sulfadiazine, 5.0 mg per kg of body weight daily. With this augmentation of activity, acceptably small doses of WR-158,122 regularly cured infections with even the most highly pyrimethamine-resistant strain.

The role of platelets in infections. I. Observations in human and murine malaria.

Abstract: The interaction between platelets and microorganisms may be underestimated. Our in vivo studies support a direct role of thrombocytes in malarial infections. We have found intrathrombocytic parasites of Plasmodium vivax (in 10% of men naturally infected) and P berghei (in 53% of mice experimentally infected); these were both merozoites and trophozoites. Neither the mechanism of parasitization (whether by active penetration or by phagocytosis) nor the outcome of this phenomenon is known. However, structures suggestive of partially digested parasitic material were seen in platelets of almost 50% of the men and 75% of the mice. These findings suggest that other microoganisms (fungi, bacteria, and viruses) may also enter thrombocytes in vivo. If so, platelets could play important roles, either favorable or deleterious, in infections.

Chloroquine-resistant Plasmodium vivax malaria in infancy and childhood.

Abstract: Cases of malaria are increasing day by day in the vicinity of Delhi. A large number of cases attends this department for screening of malarial parasites. Several thousand cases were screened since October 1976 and only 10 cases were detected who were resistant to chloroquine treatment. The peripheral blood smears on repeated examination even after chloroquine therapy given on more than 2 to 3 occasions showed heavy parasitisation ofP. vivax. Subsequent treatment with primaquine for 5 days was inadequate as persistence ofP. vivax was present. Primaquine therapy extended to 14 days showed complete disappearance ofP. vivax from the peripheral blood on subsequent repeated examinations.

[Imported malaria in a tropical unit in Paris. About 100 cases (author's transl)].

Abstract: From a hundred cases of imported malaria observed in Paris, the authors emphasize the following points: annual increase of cases, lack or inadequacy of prophylaxis, frequent reinfestations among black africans living in France, and comming back in endemic area for a brief journey, high risks for pregnant women.

Plasmodium gallinaceum-parasitized chicken erythrocytes in a practical hemagglutination test for IgM antibodies in human malaria.

Abstract: A new hemagglutination test for human malaria, done with Plasmodium gallinaceum-parasitized, aldehyde-fixed, chicken erythrocytes as a stable lyophilized reagent, is described. The test was positive in every human case of falciparum or vivax malaria in which there was parasitemia. It detected only IgM anti-plasmodial antibodies and usually became negative within a few weeks after treatment. As a practical and sensitive test for active malaria, the P. gallinaceum hemagglutination test should be complementary tool for seroepidemiological studies.

Immunobiology of malaria.

Abstract: Malaria, the number one disease in the world, is caused by intracellular protozoans belonging to the Subphylum, Sporozoa; Suborder, Haemosphoridia; and Family, Plasmodiidae. The four classical organisms producing disease in man are Plasmodium vivax, P. falciparum, P. malariae, and P. ovale. Although malaria has been known to man for centuries, attempts are still being made to control and eliminate its devastating effects in tropical and subtropical areas of the world. Current active interest in malarial immunology and immunopathology derives from two main facts: (1) that human malaria is still one of the chief health problems in a broad tropical and subtropical zone in which lie most of the developing countries; and (2) most of the seminal leads in basic immunology are being applied to malarial immunology, either directly in human patients, or using laboratory animals as test objects. This paper addresses the nature of malarial immunity and target organs in malarial pathology.