Showing papers on "Plasmodium vivax published in 1971"

The simian malarias: zoonoses, anthroponoses, or both?

Abstract: It now appears that Plasmodium cynomolgi, Plasmodium knowlesi, Plasmodium inui, and Plasmodium schwetzi are true zoonoses, although the latter, as Plasmodium ovale, may be an anthroponosis as well. Plasmodium malariae and Plasmodium rodhaini are generally accepted as being synonymous; if this is true, and it probably is, then this African quartan parasite is either one, i.e., a zoonosis or an anthroponosis, depending on which group of primates gave it origin. Certain African-Asian forms, Plasmodium gonderi for example, appear to be neither. The Central and South American primate malarias pose a different problem, for it is held that these malarias appeared only after 1492 when man, carrying P. malariae and Plasmodium vivax invaded this area from Europe. Consequently, each infection appeared in the monkeys as an anthroponosis. If this is true, synonymy is inevitable. If, on the other hand, Plasmodium brasilianum is a valid species, it acts as a zoonosis. There is reasonable doubt that Plasmodium simium acts in the same capacity.

Malaria and the tropical splenomegaly syndrome in New Guinea

Abstract: The pattern of malarial parasitaemia and the incidence and degree of splenomegaly have been studied in the population of the Upper Watut Valley in New Guinea. Malaria is the only apparent cause of splenomegaly found in this area, and all cases of gross splenomegaly in adults conform to the descriptions of the tropical splenomegaly syndrome. Malaria is meso-endemic and moderately stable. The incidence of parasitaemia is similar in villages at 3300 feet and 5200 feet above sea level, although the incidence of splenomegaly in adults is lower at the higher altitude. Peak parasitaemia is recorded at 3 years of age and then declines slowly, and parasite rates are significantly lower in adult subjects with splenomegaly than in those without palpable spleens. No difference in distribution of species of plasmodia was found between individuals with different grades of splenomegaly or in different age groups or at different altitudes. P. vivax was the predominant species in all groups.

Malaria Transmission by Leukocyte Component Therapy

Abstract: A 38-year-old man with chronic myelogenous leukemia received 203 units of blood and blood products. On Aug 8, 1969, a lung biopsy was performed because of recurrent fever and chills, and malaria-like forms were found which led to identification of Plasmodium vivax on peripheral blood smears. Only one highly suspect infective donor was found—a Vietnam veteran who had donated blood on June 27, from which the leukocytes were administered to the patient on the same day.

Serological malaria survey in the Ethiopian highlands.

Abstract: The indirect fluorescent-antibody (IFA) test was used to examine serum samples from 1,141 residents of 11 villages in north-central Ethiopia for the presence of antibodies to malaria parasites. The antigens used were Plasmodium falciparum, Plasmodium malariae, Plasmodium ovale, and Plasmodium vivax. Positive serologic responses were obtained with one or more of these antigens for 36.7% of persons living at elevations of 6,000 feet or less; whereas only 4.3% of serum specimens from persons living at elevations of 6,300 feet or higher had positive responses. Positive responses were found more often in serum from males than from females; this may be owing to the work habits of males, which exposes them to greater chance of infection. In general, serologic results correlated with parasitologic findings and suggested that P. falciparum was the most prevalent species, followed by P. ovale and P. vivax.

Symptomless Plasmodium vivax parasitemias and malaria eradication in Santa Catarina State, Brazil

Abstract: Thirty-nine symptomless carriers of P. vivax parasites in the blood gave blood films at monthly intervals for four to six months during the non- transmission season. It was found that parasitaemias can continue for many months. Thirteen of those studied relapsed with symptoms and were treated with chloroquine at a dosage of 600 mg for adults with proportionate doses for children. Of these nine relapsed silently while under observation: a symptomless relapse rate of approximately 70 per cent. One case had symptoms attributable to malaria close to the time of the original survey (the day before). Of the remaining 38 asymptomatic parasite carriers four showed microgametocytes in a density that suggested a potentially high infectivity and six showed microgametocytes in a density suggesting a potentially low to moderate infectivity for mosquito vectors. There was thus a proportion of one smptomatic case of malaria to 10 potentially infective symptomless parasite carriers. Because they feel no need to seek treatment, such persons may form an important reservoir of infection when vectors cannot be fully controlled by spraying. Some possible methods of dealing with such situations are discussed.

An Australian experience with malaria.

Abstract: The clinical and laboratory findings In 48 cases of malaria treated in a single hospital are described. The commonest infecting parasite was Plasmodium vivax, and the largest group of patients came from South Vietnam. A therapeutic regime is suggested, and the importance of completing this as a supervised in‐patient in order to prevent the recurrence of malaria is Illustrated.

Plasmodium vivax from Vietnam. Response to chloroquine-primaquine.

Abstract: From 1965 to 1968 in Vietnam, there was a dramatic increase in the proportion of malaria infections caused by Plasmodium vivax. We studied 30 patients with acute vivax malaria in Vietnam and 12 at Walter Reed General Hospital to assess the responsiveness of their infections to suppressive amounts of chloroquine with primaquine (C-P). Each patient was treated with a single C-P tablet containing chloroquine (base) 300 mg and primaquine (base) 45 mg. Clinical and parasitological responses were prompt in all patients. No urine-chloroquine tests performed upon the patients on admission to the hospital in Vietnam showed detectable chloroquine excretion owing to previous drug administration. Failure to take the prescribed C-P chemoprophylaxis probably accounts for the high proportion of vivax malaria in Vietnam.

Case of Plasmodium vivax malaria contracted in Southern Europe.

Abstract: A 24-year-old sociologist and his male companion left England on 9 August 1970 on a hitch-hiking holiday, travelling through France and Switzerland and down the Adriatic coast of Italy to Sicily. They then embarked for Sardinia and from there to Corsica, where they spent 12 days on a seaside camping site. On all three islands they slept in the open, some nights without a tent, and sustained multiple insect bites; these were most numerous at St. Florent in Corsica. They left Corsica on 8 September and, travelling by boat and train to London, arrived home on the 9th. Two days later the patient developed malaise, aching pains in the leg muscles, and fatigue. Febrile episodes occurred, lasting up to 18 hours, with intervening afebrile periods of about 24 hours. He was treated initially with antibiotics by his general practitioner without improvement. On day 7 of the illness he had a rigor and his temperature was recorded as 103'F (39-4'C). On day 9 he was admitted to hospital. There was no history of previous illness, and apart from a short holiday in Greece three years previously he had never travelled abroad. He did not admit to any injections apart from the usual immunization procedures. On examination he looked well but his temperature was 101'F (38 3'C). The throat was clear and there were no rashes or skin punctures and no lymphadenopathy apart from a few shotty inguinal nodes. The spleen was soft and enlarged to 8 cm below the costal margin, and the liver was felt 3 cm below the right costal margin. He was not jaundiced. On the evening of the day of admission his temperature rose to 105'F (40 50°C). Investigations.-Haemoglobin 12 3 g/100 ml; white cell count 6,100/mm3 (53% neutrophils, 2% eosinophils, 36% lymphocytes, 9% monocytes); platelet count 36,000/mm3. Blood film examination showed moderate anisocytosis of the red cells, and malaria parasites identified as Plasmodium vivax were seen. There were approximately 20 plasmodia per 10,000 red cells, mainly gametocytes, and also very occasional ring forms. The species was later confirmed by Mr. P. G. Shute, of the Malaria Reference Laboratory. Urine testing showed no haematuria or haemoglobinuria, and a stain of urine deposit for iron granules was negative. Serum bilirubin 10 mg/100 ml, Van den Bergh negative, remaining liver function tests normal. Blood urea 59 mg/100 ml, plasma electrolytes normal.