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

A total of 2095 patients with fever were tested for malaria and classified according to ABO blood groups. Only 696 cases were malaria positive. While blood group A, B and O were equally susceptible to malaria infection, AB blood group had less number of persons with malaria parasites. A significantly lower frequency of Plasmodium falciparum was observed among individuals with blood groups A and O. In other two blood groups B and AB, no difference in P. vivax and P. falciparum proportions were observed. A two-year study showed that the frequency of repeated attacks between all blood groups was similar.
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PMID:ABO blood groups among malaria cases from district Mandla, Madhya Pradesh. 758 29

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

The possible relationship between erythrocyte antigens and the presence of malaria infection by P. vivax and P. falciparum was sought in four different ethnic groups of two departments of Colombia. Malaria infection by P. falciparum was found in 91.4% of malaria infected blacks. No significant differences were found between the presence of malaria infection and ABO antigens. In the other blood groups, it was observed that groups MNSs conferred black people a greater Rr for malaria by both species of Plasmodium and that Duffy-negative blacks and indians appeared to be resistant to P. vivax infection. A predominance of P. vivax infection was observed in Katio Indians while P. falciparum was predominant in Kuna Indians; the reason for this finding still needs to be explored.
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PMID:Blood groups and malaria. 799 71

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

It has been hypothesized that antibody induced by Plasmodium falciparum circumsporozoite protein vaccine would be effective against endemic human malaria. In a malaria endemic region of Kenya, 76 volunteers, in 38 pairs sleeping adjacently, were immunized with subunit circumsporozoite protein Asn-Ala-Asn-Pro tetrapeptide repeat-pseudomonas toxin A, or hepatitis B vaccine. After quinine and doxcycycline, volunteers were followed for illness daily, parasitemia weekly, antibody, T-lymphocyte responses, and treated if indicated. Anopheles mosquitoes resting in houses were collected, and tested for P. falciparum antigen, or dissected for sporozoites and tested for blood meal ABO type and P. falciparum antigen. Vaccine was safe, with side-effects similar in both groups, and immunogenic, engendering IgG antibody as high as 600 micrograms ml-1, but did not increase the proportion of volunteers with T-lymphocyte responses. Estimation of P. falciparum challenge averaged 0.194 potentially infective Anopheles bites/volunteer/ day. Mosquito blood meals showed no difference in biting intensity between vaccine and control groups. Both groups had similar malaria-free survival curves, cumulative positive blood slides, cumulative parasites mm-3, and numbers of parasites mm-3 on first positive blood slide, during three post-vaccination observation periods. Every volunteer had P. falciparum parastemia at least once. Vaccinees had 82% and controls 89% incidences of symptomatic parasitemia (P = 0.514, efficacy 9%, statistical power 95% probability of efficacy < 50%). Vaccine-induced anti-sporozoite antibody was not protective in this study. Within designed statistical precisions the present study is in agreement with efficacy studies in Colombia, Venezuela and Tanzania.
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PMID:Plasmodium falciparum circumsporozoite vaccine immunogenicity and efficacy trial with natural challenge quantitation in an area of endemic human malaria of Kenya. 881 30

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

Therapeutic erythrocytapheresis (TEA) has been used in different diseases such as polycythemia vera (PV), secondary erythrocytosis or hemochromatosis as a process of the less cumbersome but more expensive phlebotomy. TEA is preferred in emergency conditions such as thrombocytosis or in conditions such as porphyria cutanea tarda (PCT) or erythropoietic porphyria when plasma exchange (PEX) is often combined with TEA to reduce extracellular levels of uroporphyrin which contribute to plasma hyperviscosity. TEA is often combined with drug therapy that varies from etoposide in PV to EPO and desferoxamine which are used to mobilize and reduce iron stores in hemochromatosis. Benefits from this combination may be more long lasting than expected. Nonetheless for TEA, there is no standard protocol and, clinical experience with this therapy remains highly anecdotal. Therapeutic red cell-exchange (TREX) has been used with much interest over the years, starting with the management of hemolytic disease of the newborn and later used to correct severe anemia in thalassemia patients thereby preventing iron overload. It has also been used for the management of complications of sickle cell disease such as priapism, chest syndrome, stroke, retinal, bone, splenic and hepatic infarction or in preparation for surgery by reducing HbS to less than 30%. Automated apheresis has also favored the use of TREX in conditions such as paroxysmal nocturnal hemoglobinuria and aniline poisoning, arsenic poisoning, Na chlorate intoxications and CO intoxications, hemoglobinopathies, autoimmune hemolytic anemia, reactions due to ABO incompatibility, in preparation for ABO incompatible bone marrow transplantation or for preventing anti-D immunization after the transfusion of D(+) cells to D(-) recipients. Another field of application has been in the emergency management of intraerythrocytic parasite infections such as malaria and babesiosis. Application of TREX may be wide but its real use remains limited. In our personal experience, in 16 years, only 167 TREX procedures have been carried out in a total of 13,747 therapeutic procedures. This represents only 1.21% of the total.
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PMID:Clinical application of therapeutic erythrocytapheresis (TEA). 1083 21

HIV transmission is the greatest single risk of blood transfusion today. The World Health Organization estimated in late 1900 that 8-10 million persons worldwide were HIV seropositive. In Africa, 10% of adult and 25% of early childhood HIV infections are believed to be caused by contaminated transfusions. 90% of patients transfused with contaminated blood will become infected. The other serious infectious risks of transfusion are hepatitis B, malaria, and syphilis. Accidents and complications of transfusion can be avoided if transfusions are limited to absolute indications, clinical examinations of donors are thorough, the blood group is reliably determined, and testing of blood for HIV is reliably conducted. Transfusions not formally indicated are now formally contraindicated. The vital risk if the patient is not transfused must be assessed before the transfusion is done, as should the risk of transmitting infection through the transfusion. When emergencies occur in isolated areas, the donor is often a family member or person accompanying the patient. The blood of the donor as well as of the patient must be typed. The medical history and clinical examination of the donor to exclude contraindications must be thorough. The physical contraindications to blood donation are infectious disorders and especially AIDS, a history of untreated syphilis or jaundice, and recent malaria. Blood should never be donated by persons with fever, jaundice, cutaneous lesions suggesting syphilis or AIDS, clinical anemia, or cardiac insufficiency. Pregnant women and children under 15 should not donate blood. Aseptic conditions must be maintained during all handling of the blood. ABO and rhesus grouping and testing for HIV infection must be done in all cases. ELISA tests are most often used for blood screening, but the rapid tests developed a few years ago are equally reliable and more suited to isolated medical facilities or those that perform few transfusions. Because the tests give false positive results in a significant proportion of cases, they should be repeated before a positive result is reported. The results of an HIV test, whether positive or negative, should only be reported to the donor if information on the consequences of a positive test has been provided and consent to the test has been obtained, the screening test results have been confirmed by a diagnostic test, and the seropositive individual can receive medical follow-up and counselling. Prevention of syphilis transmission can be achieved by limitation of indications for transfusion, selection of low risk donors, clinical examination of donors, use of blood stored for 72 hours at 4 degrees celsius or lower, use of screening tests, and prophylactic administration of antibiotics. Clinical examination and a careful medical history are the main tools for preventing hepatitis B transmission. Systematic prophylaxis against malaria following national protocols is recommended.
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PMID:[Transfusion practice in isolated areas: prevention of HIV transmission]. 1228 4

Almost all individuals (182) belonging to an Amazonian riverine population (Portuchuelo, RO, Brazil) were investigated for ascertaining data on epidemiological aspects of malaria. Thirteen genetic blood polymorphisms were investigated (ABO, MNSs, Rh, Kell, and Duffy systems, haptoglobins, hemoglobins, and the enzymes glucose-6-phosphate dehydrogenase, glyoxalase, phosphoglucomutase, carbonic anhydrase, red cell acid phosphatase, and esterase D). The results indicated that the Duffy system is associated with susceptibility to malaria, as observed in other endemic areas. Moreover, suggestions also arose indicating that the EsD and Rh loci may be significantly associated with resistance to malaria. If statistical type II errors and sample stratification could be ruled out, hypotheses on the existence of a causal mechanism or an unknown closely linked locus involved in susceptibility to malaria infection may explain the present findings.
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PMID:The association of genetic markers and malaria infection in the Brazilian Western Amazonian region. 1293 53

The hypothesis that chloroquine-induced pruritus (CIP) may be determined by certain genetic factors was tested by investigating the epidemiology of CIP with respect to certain genetic red cell markers namely, haemoglobin genotype, glucose-6-phosphate dehydrogenase (G6PD) deficiency and the ABO blood groups. Three hundred consecutive patients treated for malaria with chloroquine at the University College Hospital, Ibadan, Nigeria were recruited into the study. They were observed over 3 days for presence of CIP. ABO blood groups, G6PD and Hb genotypes were determined appropriately for each patient. One hundred and twenty four (41.3%) of the patients responded positively to CIP. There was a reduced frequency of the sickle cell trait (HbAS) among itchers relative to non-itchers. This suggests that the trait may be protective against CIP. G6PD deficiency was also found to be relatively more common among itchers than non-itchers. This indicates that G6PD deficiency may increase susceptibility to CIP. There was however no difference in the distribution of itchers among the different ABO blood groups. It was concluded that CIP may be associated with certain genetic red cell markers particularly Hb and G6PD types which are known malaria markers but not ABO blood groups.
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PMID:Certain red cell genetic factors and prevalence of chloroquine-induced pruritus. 1502 76


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