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

Seventy five patients with large spleens were investigated in order to establish the causes of splenomegaly in Northern Nigeria, to define further the diagnostic criteria of tropical splenomegaly syndrome (TSS), and to study its pathogenesis. Investigations included examination of liver biopsy, bone marrow cytology, lymphocyte response to phytohaemagglutinin (PHA), serum immunoglobulins and complement, and the presence of immunoglobulin and complement fixed in Kupffer cells. Thirty patients had TSS, five chronic lymphatic leukaemia (CLL), four a syndrome of gross lymphoid hyperplasia (GLH) distinct from TSS, CLL and the lymphomas, and twenty three miscellaneous conventional diseases. In thirteen cases no definite diagnosis could be established. TSS was found to be predominantly a disease of female Fulani cattle herders. Its essential characteristics were splenomegaly in the presence of acquired immunity to malaria, a grossly raised serum IgM, a lowered serum complement, and the presence of IgM fixed in Kupffer cells. There was lymphoid hyperplasia in bone marrow, hepatic sinusoids and often blood which may be indistinguishable from that in CLL. Lymphocytes undergo normal blastogenesis to PHA. There was clinical and haematological response to proguanil therapy. Reticuloendothelial phagocytosis of IgM, probably as a complex, seems to be the essential feature of the condition. As it was impossible to identify early cases of TSS it is unclear whether IgM overproduction or phagocytosis of IgM complexes is the first stage of the disease. The precise nature of the association with malaria remains obscure. The diagnosis of CLL demanded the demonstration of an abnormally low immunoglobulin level and impaired lymphocyte responsiveness to PHA by blast transformation or 3H-thymidine incorporation, in addition to the usual haematological findings. The syndrome GLH occurred in multiparous Hausa women. It was characterised by intense lymphocytosis with active, PHA-responsive cells, and normal immunoglobulin levels. Patients responded to proguanil therapy. It is suggested that these patients have a depressed immune response to malaria, perhaps through repeated pregnancies, and to a leukaemogenic agent, both of which stimulate lymphocytosis. Antimalarial treatment at this stage may prevent the development of frank leukaemia or lymphoma. The usefulness of the various investigative procedures and the problem of managing the large number of undiagnosed cases are discussed.
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PMID:Splenomegaly in Northern Nigeria. 1 54

Lymphocyte subpopulations in thirty-nine patients with the tropical splenomegaly syndrome (TSS) were studied using the E-rosette, EAC rosette and direct immunofluorescent staining techniques. In the peripheral blood a decrease in the percentage of T-lymphocytes was found which was accompanied by an increase in the percentage and number of B-lymphocytes. These abnormalities reverted towards normal on treatment. Splenic aspirates contained an increased proportion of T-lymphocytes. The relative T-cell lymphoenia in TSS is probably due to specific trapping or non-specific sequestration of lymphocytes in the liver and splen. B-cell lymphocytosis is probably due to persistent antigenic or mitogenic stimulation by malaria.
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PMID:T- and B-lymphocyte subpopulations in the tropical splenomegaly syndrome (TSS). 30 10

Ten captive-reared African black-footed penguins (Spheniscus demersus) from a large outdoor colony were monitored for avian malaria, using several diagnostic tests. One treatment regimen was evaluated. Thin smear blood evaluation enabled detection of seven parasitemias involving Plasmodium relictum and Plasmodium elongatum in the penguins. Leukocytosis (relative lymphocytosis) was characteristic of infected birds. Parasitemia was detected as early as 21 days prior to onset of clinical signs (depression, anorexia, regurgitation, pale mucous membranes, and respiratory distress). The single bird that died had clinical signs only a few hours prior to its death. Treatment consisted of 0.03 mg of primaquine phosphate base/kg body weight, administered orally once daily for 3 days. Oral chloroquine phosphate therapy, given simultaneously, was administered in an initial loading dose of 10 mg of chloroquine phosphate base/kg body weight, followed by doses of 5 mg/kg at 6, 18 and 24 hours after the initial chloroquine dose. This treatment regimen prevented mortality and cleared parasites from the blood. Recurrences of malaria occurred in two birds that had received this treatment.
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PMID:Avian malaria in African black-footed penguins. 52 78

We report the clinical picture, treatment and evolution of a child with hyperreactive malarious splenomegaly treated outside the endemic area of malaria. The patient presented gross splenomegaly, proceeded from an area where malaria is endemic, showed increased immunoglobulins levels, high antimalarial antibody titres and hepatic sinusoidal lymphocytosis. The child did not return to an area where malaria is endemic and showed a favorable response to only one course of quinine. The response of this patient to limited antimalarial therapy suggests the importance of reinfection with malaria in the development and maintenance of this syndrome.
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PMID:Reduction of spleen size in a child with hyperreactive malarious splenomegaly (HMS) treated outside the Brazilian endemic area of malaria with only one course of quinine. 134 May 41

Levels of platelets and other hematological values were monitored in 21 Saimiri and 12 Aotus monkeys over a period of three weeks post-infection with monkey-adapted Indochina CDC-1 strain of Plasmodium falciparum. In both Saimiri sciureus boliviensis and Aotus nancymai karyotype-1 monkeys the severest thrombocytopenia was observed at 14 days post-infection coinciding with peak parasitemia, neutropenia, lymphocytosis, and anemia associated with severe hemoglobinemia and elevated fibrinogen degeneration products(FDP's). MCH and MCV profiles in Aotus monkeys decreased with ascending parasitemia. In contrast, these parameters in Saimiri were characterized by a significant compensatory increase correlating with parasitemia. In general, thrombocytopenia was one of the earliest clinical manifestations of the infection with the platelets returning to normal levels shortly after peak parasitemia at 14 days. Platelet kinetics had a strong correlation with hematologic and parasitologic values in the Aotus model. No consistent associations were observed between platelet kinetics and other parameters in the Saimiri model. These data indicate that the Aotus model for malaria is more predictable than the Saimiri. Further, platelet turnover rates and recovery provide a useful prognostic parameter during malaria infection. The results are discussed in relation to the value of the two species of monkeys as models for the pathogenesis of human malaria.
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PMID:Platelet kinetics and other hematological profiles in experimental Plasmodium falciparum infection: a comparative study between Saimiri and Aotus monkeys. 142 30

This paper presents changes in the bone marrow of patients with malaria; it is based primarily on observations of bone marrows of 89 Gambian children with P. falciparum malaria and includes a review of the literature. Erythroid hyperplasia with dyserythropoiesis was found to be more common in patients with severe anemia and low grade parasitemia than in those with acute malaria. The dyserythropoietic changes are illustrated both with light photomicropraphs and with electron micrographs. The significance of the dyserythropoiesis and possible causes are discussed. Other changes in these patients with acute malaria include lymphocytosis in the bone marrow and reactive lymphocytes, monocytosis and mild neutrophilia in the peripheral blood. Giant metamyelocytes were also commonly seen in bone marrow of patients but were thought to be part of dysmyelopoiesis and not due to B12 or folate deficiency. Phagocytosis of erythrocytes, parasitized cells and nucleated cells was more commonly seen in macrophages in acute malaria, while phagocytosis of small particles such as merozoites was observed in neutrophils. Megakaryocytes were found to be increased in number in patients with acute malaria; a proportion of these cells had rounded nuclei, probably indicating accelerated platelet turnover.
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PMID:Hematopoiesis in human malaria. 225 20

A series of peripheral blood films taken from Gambian children with either acute or low-grade Plasmodium falciparum infections were examined for abnormal features of the red and white cells. Hypochromia and polychromasia with cytoplasmic stippling were predominant features in both groups. Lymphocytosis, granulocytosis and plasmacytosis were common white cell abnormalities. An additional feature in films from patients with acute malaria was the presence of numerous atypical lymphocytes. A comparison of the features in the two groups indicated that some abnormalities are associated with an acute attack of malaria and that others have a nutritional or genetic aetiology.
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PMID:Abnormal features of peripheral blood films from Gambian children with malaria. 247 97

Inoculation of adult C57/BC mice with 10(6) red cells infected with Plasmodium chabaudi induces an acute primary parasitaemia peaking around the 8th or 9th day and lasting 10-14 days. Concomitantly, the spleen enlarges to reach 6-7 times its normal weight by the 11th day. The major component of this increase is between day 9 and 11, due primarily to an increase in erythropoietic cells in the red pulp. Although initially the white pulp increases in size, by day 11 it shows partial lymphocyte depletion which coincides with the occurrence of massive absolute lymphocytosis in the peripheral blood. 3H-Thymidine labelling in vivo suggests that this lymphocytosis is not due to lymphocytopoiesis. Collectively, these findings suggest a redistribution of lymphocytes. Lymphocyte migration was investigated around peak parasitaemia, using enriched populations of T and B cells labelled with 51Cr. The traffic patterns of these cells were followed over 36 h. These studies show decreased uptake (or decreased retention) of T and B cells by spleens of infected mice. Concomitantly, there is increased retention of T and B cells in the liver and lungs of infected mice, suggesting a complex redistribution of these cells. Lymphocyte migration to lymph nodes was unimpaired in these animals. Similar changes in T and B cell migration do not occur in Babesia microti infections in C57/BL mice. We relate our findings to histological and histochemical changes in the liver and spleen of malarious mice and discuss the significance of these findings to immunosuppression in malaria and to the development of parasiticidal immunity.
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PMID:Lymphocyte migration in murine malaria during the primary patent parasitaemia of Plasmodium chabaudi infections. 349 67

In Burkitt's lymphoma, dental structures may provide the route for Epstein-Barr virus (EBV) in saliva to penetrate the jaws, thereby promoting tumor formation. In children, EBV could enter tooth sockets exposed following deciduous tooth loss and thereby contact jaw marrow lymphocytes stimulating neoplastic transformation. Marrow contact by EBV probably also occurs through carious teeth. Jaw tumors are rare in adults because their jaw marrow is no longer hematopoietic and so lacks the lymphoid substrate for the virus. In adults, jaw marrow lymphocytosis, as accompanies infectious mononucleosis and perhaps malaria, or which could develop around the roots of carious teeth having chronic periapical infection, could provide the substrate for EBV. EBV could then contact the jaw marrow lymphocytes when teeth are extracted and so favor jaw tumor development. Therefore, prevention of dental caries might reduce jaw tumor prevalence in Burkitt's lymphoma except among children ages 6-13 whose jaw marrow would unavoidably become infected by salivary EBV when the latter is present at the time of deciduous tooth loss.
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PMID:Circumstances favoring jaw tumors in Burkitt's lymphoma. 632 20

The clinicohaematological findings of acute state (Group A, 30 patients) and chronic state (Group B, 34 patients) of falciparum malaria in paediatric patients are compared. The children with chronic falciparum malaria were apyrexic and presented with features of moderate to severe anaemia with hepato-splenomegaly. Greater severity of anaemia and haemolysis, higher incidence and severity of neutropenia, atypical lymphocytosis, monocytosis and thrombocytopenia were observed in patients with chronic falciparum malaria as compared to patients with acute falciparum malaria despite lesser degree of parasitaemia in the former as compared to the latter. While mechanical destruction of parasitised RBC's, ineffective and dysplastic erythropoiesis either due to unmasking of border line dierty folic acid deficiency or otherwise, transient hypoplasia of bone marrow, impaired utilization of iron and immune destruction of RBCs with hypersplenism may be the mechanisms for anaemia, transient hypoplasia of bone marrow and hypersplenism may be the factors responsible for thrombocytopenia and neutropenia.
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PMID:Clinico-haematological profile in acute and chronic Plasmodium falciparum malaria in children. 796 80


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