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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malaria pigment is most abundant and distinct in gametocytes. Trophozoites have variable amounts of pigment, depending on the species of Plasmodium and the stage of infection. In Plasmodium falciparum infection, blood smear preparations fall into two categories that are distinguishable at all levels of parasitemia; one type of preparation contains only pigment-deficient trophozoites, and the other type contains only pigment-rich trophozoites. Pigment accumulates in the residual body of the mature schizont and is lost upon rupture of the schizont. In contrast, pigment remains associated with the macrogametocyte and developing oocyst. Certain antimalarial drugs, such as chloroquine, have distinct effects on pigment clumping. These observations raise questions regarding the current idea of pigment as an inert excretory product of hemoglobin metabolism. It is suggested that pigment particles represent stacked utilizable intermediates of hemoglobin digestion that accumulate in the gametocyte to serve as a food reserve during the growth cycle in the mosquito.
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PMID:Formation and role of malaria pigment. 305 84

This paper describes changes in the circulating platelets of 25 patients with acute malaria within 2 to 6 days of onset of illness. Thrombocytopenia was observed in 10 out of 15 patients with Plasmodium falciparum infection, and in 4 out of 9 patients with P. vivax infection. One patient with a mixed infection of both species had a disseminated intravascular coagulation. Platelet antibody was detected in the sera of 8 out of 11 cases by the complement lysis inhibition technique and indirect immunofluorescence. The mean platelet antibody concentrations in the sera of 11 patients and 53 control subjects were 122.70 +/- 80.25 ng/10(7) platelets and 36.69 +/- 18.72 ng/10(7) platelets, respectively. An inverse relationship between the platelet count and platelet antibody levels in serum supported the view that thrombocytopenia in malaria may be partly immune-mediated. Platelet aggregation responses to agonists such as ADP, adrenaline, collagen and ristocetin revealed hyperactivity. Ultrastructural study of unstimulated platelets from patients revealed several changes such as centralization of dense granules, glycogen depletion, and formation of pseudopods and microaggregates, indicating in vivo activation of the platelets, which may also lead to thrombocytopenia.
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PMID:Functional and ultrastructural changes of platelets in malarial infection. 306 47

The renal pathology of 9 squirrel monkeys (Saimiri sciureus) with acute Plasmodium falciparum infection was studied by light and electron microscopy. Endocapillary proliferative glomerulonephritis was the major pathological change observed. The peroxidase anti-peroxidase method demonstrated the presence of IgG, IgM, and P. falciparum antigens in the mesangium and basement membrane. These findings were consistent with those seen in humans with acute P. falciparum infection and indicates that squirrel monkeys are likely to be a good model for the study of renal pathology in malaria research.
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PMID:Glomerulopathy in squirrel monkeys with acute Plasmodium falciparum infection. 327 66

One hundred and ninety-two male malaria patients admitted to two different hospitals within 1 year, were studied. There were 74 malaria cases with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and 118 G-6-PD normal malaria cases, randomly selected as a control group. History of dark urine, and the presence of jaundice, haematocrit, total bilirubin and parasite count on day of admission were not significantly different comparing both groups. The number of observed complications did not differ either. Distinctions were detected in abnormal symptoms and in some laboratory parameters in patients with Plasmodium falciparum infection. G-6-PD deficient patients had significantly less gastrointestinal disturbances (P = 0.006), higher serum glutamic oxalacetic transaminase (P = 0.009) and significantly lower blood urea nitrogen (P = 0.007) when compared with the control group. These findings indicate that G-6-PD deficiency when the variants are aggregated, in male adult patients has no significant influence on the clinical presentation of malaria.
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PMID:Glucose-6-phosphate dehydrogenase deficiency in Thailand: the influence on the clinical presentation of malaria in male adult patients. 329 88

This report describes a Danish patient with severe Plasmodium falciparum infection and Pseudomonas aeruginosa septicaemia. The patient had been sailing along the coast of West Africa for ten years without taking any antimalaria prophylaxis and without any apparent previous history of malaria. He presented with severe form of malaria, progressing rapidly into coma and died within a short time. P. aeruginosa was isolated from his blood taken on the day of admission. His neutrophils were all occupied by P. falciparum. The unusual combination of severe falciparum malaria infection and P. aeruginosa septicaemia with extensive involvement of neutrophils lends further support for the role of phagocytic defence in malaria.
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PMID:Pseudomonas aeruginosa septicaemia in a patient with severe Plasmodium falciparum. 332 35

Amodiaquine was compared to chloroquine in two groups of Filipino patients with uncomplicated falciparum malaria. Every patient received 25 mg/kg of base orally given over three days. In a hospital study, all eight patients receiving chloroquine cleared their parasitemia by day 6, but six of eight patients receiving amodiaquine failed to clear parasitemia and in four patients there was no response at all (RIII resistance); this difference was significant (P less than 0.01). In a village based study, there was initial clearing of parasitemia in each patient. However, recrudescent infection occurred in all five patients receiving amodiaquine (RI resistance). Five of six falciparum infections were sensitive to chloroquine, while parasitemia reappeared in one patient. In this village, resistance to amodiaquine was significantly more common than resistance to chloroquine (P less than 0.05). To our knowledge, this is the first report of amodiaquine being substantially worse than chloroquine in the treatment of Plasmodium falciparum infection.
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PMID:Amodiaquine less effective than chloroquine in the treatment of falciparum malaria in the Philippines. 354 92

A clinical case of Black Water Fever following Plasmodium falciparum infection is reported. The patient had no previous history of malaria and had not taken anti-malarials as prophylasis. He was free from G-6-PD deficiency and abnormal haemoglobins. He had acute intravascular haemolysis, haemoglobinurea and renal failure after the third dose of quinine infusion. His life was saved by peritoneal dialysis and Artemether injection. In in vitro test, his blood haemolysed suddenly in 36 hours when incubated with quinine (10 mg per lit) at 37 degrees C in test tube while control blood took over a week for natural slow haemolysis. Thus quinine plays an important part in the cause of Black Water Fever.
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PMID:A case of black water fever treated with peritoneal dialysis and artemether (quinghaosu derivative). 366 74

The immune status of patients in Harare modifies their response to acute P.falciparum infection. Malnourished children were the group at greatest risk and fits were a feature of malaria in this age group. Fever and headache were the commonest symptoms overall, but 12,5% of patients were never pyrexial. Splenomegaly was common in young children but uncommon in adults. A leukocytosis, thrombocytopenia and normochromic normocytic anemia were common features of acute P. falciparum malaria as were hyponatremia and hypokalemia. The leukocytosis and hypokalemia are not well documented features of acute malaria and genetic differences may account for varying responses. The diagnosis was proven in only 26% of cases thought clinically to have malaria. In several cases malaria was not considered in the differential diagnosis. More than 1/2 the patients with positive blood slides received antibiotics as well as chloroquine. Bacteria were isolated from blood cultures in 8 patients. Septicemia may be an uncommonly recognized complication of acute P. falciparum malaria.
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PMID:The clinical features and laboratory findings in acute Plasmodium falciparum malaria in Harare, Zimbabwe. 391 Feb 59

Folacin deficiency in malaria endemic areas is not reported other than in severely malnourished children. This is surprising in view of the high incidence in these areas of malaria in pregnancy, with its complications of prematurity and low birth weight, all of which can predispose to folacin deficiency. This paper reports results of folacin and cobalamin activities of blood samples collected from women at parturition and their newborns in a holoendemic area in West Kenya. Evidence is given that Plasmodium falciparum infection has little influence on cord plasma or red cell folacin activities. Mean values for folacin and cobalamin are not low when compared with reported values from neonates from temperate climates.
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PMID:A comparison of maternal and foetal folacin and cobalamin activities at parturition in relation to Plasmodium falciparum infection. 409 47

The morphology of the erythrocyte in Plasmodium falciparum infection is still obscure. In a study of 27 cases, uninfected erythrocytes were found to be thinner, but greater in diameter and surface area, than such cells in 10 normal individuals. The changes were not correlated with the severity of the disease or the degree of reticulocytosis. Megaloblastic anaemia was not present in the malaria cases.
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PMID:Red blood cell morphology in falciparum malaria. 457 16


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