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

115 blood donors were screened for the presence of malaria and other blood parasites at the Blood Bank, University College Hospital, Ibadan, between January and July, 1984. 11.3% of these had blood parasites; 7.8% had Plasmodium falciparum with parasitaemias from 0.03-0.2%, and 3.5% had Loa loa microfilaraemia. No other blood parasites were observed. Serological examination by the indirect fluorescent antibody test revealed that 86% of the donors had malaria antibody with reciprocal titres ranging from 16 to 512. There was no significant association between ABO blood group and malaria parasitaemia or antibody titre.
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PMID:Malaria and loaisis among blood donors at Ibadan, Nigeria. 331 17

A total of 736 patients with fever was tested for malaria and classified according to ABO blood group. Of these, 476 cases had patent parasitaemia at the time of investigation. The distribution of blood groups in this group was significantly different from that in 1300 controls from the same area. While group A was found to be more common in malaria cases than in normals, the reverse situation was found for group O. Possible explanations for this are discussed.
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PMID:Relationship between ABO blood groups and malaria. 697 Nov 87

Rosette formation in 154 fresh Plasmodium falciparum isolates from Kenyan children with mild (n = 54), moderate (n = 64), or severe (n = 36) malaria was studied to determine whether the ability to form rosettes in vitro is correlated with malaria severity. There was a wide distribution of rosette frequencies within each clinical category; however, a clear trend towards higher rosette frequency with increasing severity of disease was seen, with the median rosette frequency of the mild-malaria group (1%; range, 0 to 82%) being significantly lower than those of the moderate-malaria group (5%; range, 0 to 45%; Mann-Whitney U test, P < 0.02) and the severe-malaria group (7%; range, 0 to 97%; Mann-Whitney U test, P < 0.003). Within the severe-malaria category there was no difference in rosetting among isolates from cerebral malaria patients or those with other forms of severe malaria. We also examined the ABO blood groups of the patients from whom isolates were obtained and found that isolates from group O patients (median rosette frequency, 2%; range 0 to 45%) rosetted less well than those from group A (median, 7%; range 0 to 82%; Mann-Whitney U test, P < 0.01) or group AB (median, 11%; range 0 to 94%; Mann-Whitney U test, P < 0.03). We therefore confirm that rosetting is associated with severe malaria and provide further evidence that rosetting is influenced by ABO blood group type. Whether rosetting itself plays a direct role in the pathogenesis of severe malaria or is a marker for some other causal factor remains unknown.
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PMID:Plasmodium falciparum rosetting is associated with malaria severity in Kenya. 776 16

Spontaneous rosette formation of uninfected erythrocytes around an erythrocyte infected with Plasmodium falciparum is a recently described in vitro phenomenon which is also present in infections with some other malarial species where sequestration of parasite infected erythrocytes is a characteristic. In the present studies, rosetting was established as a P. falciparum virulence factor, the expression of which is modified by a variety of host factors, such as host immunity, ABO blood group and haemoglobin phenotype. The molecules involved in rosetting seem to be distinct from those involved in endothelial cytoadherence, although they are often co-expressed on the same parasitised red cell. Rosette formation was shown not only to be a phenomenon of laboratory-propagated strains, but also to exist in wild clinical isolates from all major malarious areas of the world. In two studies performed in The Gambia, comprising 211 children with uncomplicated or cerebral malaria, a strong association was found between in vitro rosette formation and cerebral malaria, indicating that rosetting plays a role in the pathogenesis of severe P. falciparum disease. Anti-rosetting activity, presumably mediated by antibodies, was found in sera from patients in malaria-endemic areas, and it was demonstrated that such activity was more abundant in individuals with uncomplicated malaria than in those with cerebral disease, suggesting that humoral immunity protects against rosette formation in vivo. It was also demonstrated, by the use of several independent assays, that erythrocytes from individuals with sickle-cell trait, alpha- and beta-thalassaemia trait or with HbE, formed smaller and weaker rosettes than did normal (HbAA) red cells. The results also suggest that microcytosis per se is correlated to impaired rosette formation. Differences in rosetting ability were also seen between red cells of different ABO blood groups, with a diminished rosetting potential in blood group O red cells. Impaired rosette formation may thus contribute to the innate resistance to severe P. falciparum malaria that is known to exist in certain red cell disorders and in individuals of blood group O. Rosette formation was found to be governed by strong adhesive forces, with lectin-like bindings between parasite-derived proteins exposed on the P. falciparum-infected red cell surface, rosettins, and various carbohydrate moieties present on the uninfected erythrocyte. The strongest carbohydrate receptors seem to be contained within the blood group A or B antigens, and the rosettes were abolished by oligosaccharides mimicking these antigens. The binding between infected and uninfected erythrocytes was dependent on divalent cations and was sometimes sensitive to pH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Erythrocyte rosetting in Plasmodium falciparum malaria--with special reference to the pathogenesis of cerebral malaria. 849 54

The malaria parasite Plasmodium falciparum utilizes molecules present on the surface of uninfected red blood cells (RBC) for rosette formation, and a dependency on ABO antigens has been previously shown. In this study, the antirosetting effect of immune sera was related to the blood group of the infected human host. Sera from malaria-immune blood group A (or B) individuals were less prone to disrupt rosettes from clinical isolates of blood group A (or B) patients than to disrupt rosettes from isolates of blood group O patients. All fresh clinical isolates and laboratory strains exhibited distinct ABO blood group preferences, indicating that utilization of blood group antigens is a general feature of P. falciparum rosetting. Soluble A antigen strongly inhibited rosette formation when the parasite was cultivated in A RBC, while inhibition by glycosaminoglycans decreased. Furthermore, a soluble A antigen conjugate bound to the cell surface of parasitized RBC. Selective enzymatic digestion of blood group A antigen from the uninfected RBC surfaces totally abolished the preference of the parasite to form rosettes with these RBC, but rosettes could still form. Altogether, present data suggest an important role for A and B antigens as coreceptors in P. falciparum rosetting.
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PMID:Blood group A antigen is a coreceptor in Plasmodium falciparum rosetting. 1076 96

Several human genetic factors, including red blood cell polymorphisms (ABO blood group, sickle-cell trait, G6PD deficiency) as well as point mutations in the mannose binding protein (MBP) and in the promoter regions of both the TNF-alpha and NOS2 genes, influence the severity of disease due to infection with Plasmodium falciparum. We assessed their impact on mild P. falciparum malaria, as part of a longitudinal investigation of clinical, parasitological and immunological parameters in a cohort of 300 Gabonese schoolchildren. We found the following frequencies: blood group O (0.54), sickle-cell trait (0.23), G6PD deficiency (0.09), MBP gene mutations (0.34), TNF-alpha promoter mutations (at positions -238: 0.17 and -308: 0.22) and NOS2 promoter mutation (0.18). Blood group O or hemoglobin AA were associated with protection against higher parasitemia. Girls with normal G6PD enzyme activity were protected against clinical malaria attacks. In addition, we demonstrated for the first time that the mutation at position -238 of the gene coding for the promoter region of TNF-alpha was positively correlated with the level of the antibody response specific for epitopes of the antigens MSA-2 and RAP-1 of P. falciparum.
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PMID:Human genetic factors related to susceptibility to mild malaria in Gabon. 1119 74

Although the ABO blood group of the human host has been reported to influence malarial infection, there have been few clinical observations on this effect. A hospital-based, comparative study was therefore performed to investigate the relationship between blood-group type and severe disease i nPlasmodium falciparum malaria. Overall, 243 cases of malaria (163 uncomplicated and 80 severe) and 65 patients with severe, non-malarial infections were studied. In terms of ABO-blood-group composition, the patients with severe malaria were significantly different from the patients with the uncomplicated disease (P<0.001) and also from a population control described previously (P<0.0001). The patients with uncomplicated malaria or severe but non-malarial disease were, however, similar to the population control. The cases of severe malaria were significantly less likely to be of blood group O (P=0.0003), and significantly more likely to be of group AB (P<0.0001), than the patients with nonsevere malaria. It appears that individuals who are of blood-group O are relatively resistant to the severe disease caused by P. falciparum infection.
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PMID:ABO-blood-group types and protection against severe, Plasmodium falciparum malaria. 1581 30

Haptoglobin (Hp) levels were investigated in relation to host genotype in a malaria-endemic area in Gabon. A cross-sectional study of 1-12-year-old children was conducted in the rainy season, a period of high malaria transmission, to examine this relationship. Variables that influenced Hp levels were Hp genotype, location, and age interacting with parasite density. At low parasite densities, there was a negative correlation between Hp levels and age. At higher densities, there was a positive correlation with age. This suggests that in the presence of greater parasite-induced hemolysis, older children are capable of increased production of Hp. Sickle cell trait and ABO blood group was not associated with Hp levels in this population.
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PMID:Association of haptoglobin levels with age, parasite density, and haptoglobin genotype in a malaria-endemic area of Gabon. 1640 42

There is increasing evidence that Plasmodium falciparum malaria is influenced by ABO blood group but the extent of association between both is yet to be well defined. Studies that investigated association between P. falciparum malaria and ABO blood group were identified using MEDLINE search and were systematically reviewed. There were apparent discrepancies and contradictions in the studies as some reported significant association between both while others observed no significant association. This outcome may reflect the complex interaction between P. falciparum malaria and the host immune responses. However, findings from all studies reviewed suggested that individuals of blood group O are relatively resistant to severe disease caused by P. falciparum infection. It was established that parasitized erythrocytes form rosettes more readily with red blood cells (RBCs) of A, B, or AB groups than with blood group O and this parasite-triggered RBC rosette formation is associated with the severity of clinical disease and with the development of cerebral malaria. Differences in rosetting ability were based on the P. falciparum strain-specific preference of rosetting with non-O blood groups and not only a phenomenon of laboratory-propagated strains, but also exist in wild clinical isolates from all major malarious areas of the world.
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PMID:Plasmodium falciparum malaria and ABO blood group: is there any relationship? 1704 97

Malaria has been a major selective force on the human population, and several erythrocyte polymorphisms have evolved that confer resistance to severe malaria. Plasmodium falciparum rosetting, a parasite virulence phenotype associated with severe malaria, is reduced in blood group O erythrocytes compared with groups A, B, and AB, but the contribution of the ABO blood group system to protection against severe malaria has received little attention. We hypothesized that blood group O may confer resistance to severe falciparum malaria through the mechanism of reduced rosetting. In a matched case-control study of 567 Malian children, we found that group O was present in only 21% of severe malaria cases compared with 44-45% of uncomplicated malaria controls and healthy controls. Group O was associated with a 66% reduction in the odds of developing severe malaria compared with the non-O blood groups (odds ratio 0.34, 95% confidence interval 0.19-0.61, P < 0.0005, severe cases versus uncomplicated malaria controls). In the same sample set, P. falciparum rosetting was reduced in parasite isolates from group O children compared with isolates from the non-O blood groups (P = 0.003, Kruskal-Wallis test). Statistical analysis indicated a significant interaction between host ABO blood group and parasite rosette frequency that supports the hypothesis that the protective effect of group O operates through the mechanism of reduced P. falciparum rosetting. This work provides insights into malaria pathogenesis and suggests that the selective pressure imposed by malaria may contribute to the variable global distribution of ABO blood groups in the human population.
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PMID:Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting. 1795 77


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