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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

Serum-IgM is always abnormally high in tropical splenomegaly syndrome. It is postulated that patients with this disease have an abnormal immunoglobulin response to malaria because they lack effective T suppressor cells. This defect may be genetically determined, thus explaining the tribal and familial aggregation of the disease. Hypermacroglobulinaemia is associated with the formation of large amounts of high-molecular-weight immune complexes. These complexes are important in the pathogenesis of the clinical features of the syndrome.
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PMID:A suppressor T-cell defect in tropical splenomegaly syndrome. 6 46

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

For the last few years it has been known that high molecular weight circulating immune complexes containing IgM, other immunoglobulins and complement are usually present in TSS. Similar material to be found in the Kupffer cells of affected patients, and on the surfaces of their red cells. The recent demonstration that the immune complexes contain malarial antibody activity strengthens the belief that they also contain malarial antigen and are due to the basic immunological abnormality. As indicated in this review, further studies are required fully to confirm their role in the production of the splenomegaly, the auto-immune phenomena and the haemolysis of TSS. The balance of evidence favours a genetic rather than a purely environmental basis for development of the syndrome. Treatment is simple, inexpensive and relatively free of risk. It is feasible even in rural communities pending the advent of successful malaria eradication, the ultimate means of prevention and cure.
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PMID:The pathogenesis of tropical splenomegaly syndrome--the role of immune complexes. 33 8

Serum immunoglobulin concentrations, malarial antibodies and schistosomal antibodies were measured in 33 patients with a provisional diagnosis of schistosomal splenomegaly, 16 with TSS of presumed malarial aetiology and in 52 controls. IgG and IgM were higher in both splenomegaly groups than in the controls and IgG was significantly higher in patients with schistosomal splenomegaly than in TSS. Although a very high IgM was found more often in the TSS group, there was no significant difference between the mean IgM levels in the two splenomegaly groups. The mean antischistosomal antibody titres were significantly higher in the schistosomal group than in those with TSS but there was no difference in the antimalarial antibody titres. These results emphasise the problems of diagnosis of gross splenomegaly in areas where schistosomiasis and malaria coexist.
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PMID:Serum immunoglobulin concentrations, malarial and schistosomal antibodies in patients with massive splenomegaly in Malawi. 39 37

The Leishmanin skin test was performed on 1353 people in a kala-azar endemic region of south-west Ethiopia. Physical examinations were also carried out on 2723. Two of these individuals, both males, had active visceral leishmaniasis with Leishmania organisms demonstrated by spleen puncture. Two other males, including one member of the research team, had parasitologically proven cutaneous leishmaniasis. Because there was negligible migration and little movement of individuals outside of their tribal territories, the geographical distribution of skin test positivity and clinical findings could be determined and correlated with environmental parameters. The level of positive skin tests for the groups tested ranged from over 64% for the three tribes collectively inhabiting the lower regions of the Omo Valley (altitude approx. 500 m) to 6.4% for the Suri tribe, which lives at 1400 m. Skin test positivity was highest in areas of deeply fissuring montmorillonite soils and where Phlebotomus langeroni orientalis have been collected. Termite mounds of the pipe-organ type seemed to occur independently of the proportion of positive skin tests, possibly because alternative resting and breeding sites for sandflies were available in the cotton clay soil or because of the cultural patterns of the people. Almost always, males had a markedly higher prevalence of positive skin tests than did females. The degree of positivity was strongly correlated with increasing age, most positive conversions occurring in the ten to 20 year olds, the age at which males join cattle camps as part of their herding activities. Splenomegaly reached a prevalence of nearly 50% among the Hamar speaking people to the east of the Omo River, where the pattern of disease suggests malaria as the principal cause. Hepatomegaly, however, was highest in the lower Omo Basin among the Nyangatom, Dassanetch and Kerre, where hydatid disease was a major cause of liver enlargement, but seemed unrelated to the proportion of positive Leishmanin skin tests.
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PMID:Kala-azar in Ethiopia: survey of south-west Ethiopia. The Leishmanin skin test and epidemiological studies. 53 46

In a village population in N. Nigeria the Fulani form a heterogeneous group in comparison with the Hausa and Maguzawa people. It was demonstrated that, apart from having a different body build, Fulani men have on the average lower haemoglobin concentrations, more splenomegaly and higher IgM and IgG concentrations. Splenomegaly and higher IgM levels were correlated in the Fulani only, and this probably is a manifestation of their altered immune response to malaria, which is manifested by the prolonged parasitaemia in Fulani men suggesting that their control over malaria parasites is less effective. Very high IgM levels (more than 9.6 g/l) were present in 6/70 (9%) of Fulani and in none of the others. According to the criteria used the Tropical Splenomegaly Syndrome could be diagnosed in 4/70 (6%) of Fulani and in 2/89 (2%) of Hausa and Maguzawa. A nutritional factor, presumably iron intake, and Schistoma haematobium infections appeared to be determinants of haemoglobin concentration in the Hausa and Maguzawa. In Fulani a different pattern emerged characterised by the nutritional factor and a haemolytic factor related to the sickle cell trait. The frequency of the sickle cell trait, however, was similar in all tribes. The significance of the findings is discussed and it is suggested that the heterogeneity of Fulani is possibly due to their less complete adaptation to stable malaria.
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PMID:Differences in blood status of three ethnic groups inhabiting the same locality in Northern Nigeria. Anaemia, splenomegaly and associated causes. 54 94

Rat-adapted Plasmodium chabaudi caused a syndrome characterized by hemolytic anemia, splenomegaly, and glomerulonephritis. All rats recovered and appeared normal after 4 weeks despite persistence of proteinuria. Serologic studies on the malarious rats revealed that the infection was associated with a soluble antigen which was present concurrently with antibody in plasma, in material eluted from blood cells, in extracts of kidney tissues, and in the urine. This antigen appeared to be identical with one extracted from P. chabaudi parasites and did not cross-react with antigens of Plasmodium gallinaceum. Tests for the cold-active hemagglutin (CAH) and the globulin associated serum antigen (SA) previously associated with acute malaria, revealed that CAH, but not SA, was present. From these observations it is suggested that soluble complexes of the parasite antigen and its antibody may have been causal in this syndrome.
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PMID:Experimental infection with Plasmodium chabaudi in rats: antigen and antibody associated with anemia and glomerulonephritis of acute infection. 59 39

Levels of species and class-specific malarial antibody were studied in 249 New Guineans with tropical splenomegaly syndrome (TSS) and in 87 control subjects living in the same area. Titres of IgG and IgM antibody to Plasmodium falciparum, P. vivax and P. malariae were estimated by indirect immunofluorescence. Both Ig and IgM antibody levels were higher in subjects with TSS than in controls; IgM titres were highest in those with the greatest splenic enlargement. Responses to all three species were comparable. It is concluded that there is no evidence from this study to incriminate any one species of malaria parasite in the production of tropical splenomegaly syndrome.
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PMID:Malarial antibodies in tropical splenomegaly syndrome in Papua New Guinea. 59 79

Immunologically competent mice and mice with defined immunological deficiencies were infected with Plasmodium yoelii. Splenomegaly, enhanced phagocytosis, and anemia were most marked in infected mice having intact thymic tissue. Whereas the spleens of infected nude mice increased minimally in size, the relative blood hemoglobin levels and the rates of carbon clearance in these mice were similar to those of noninfected, immunologically intact mice. Thymus-reconstituted nude mice and B-cell-deficient mice responded to infection in a manner similar to that of infected immunocompetent mice. These data demonstrate that the hallmarks of malaria, i.e., splenomegaly, enhanced phagocytosis, and anemia, are thymus-dependent responses to infection.
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PMID:Splenomegaly, enhanced phagocytosis, and anemia are thymus-dependent responses to malaria. 66 20


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