Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inocula of S. mansoni and T. gondii well tolerated by albino mice when given singly, were given concomitantly to groups of animals. Few notable effects were observed when toxoplasmosis preceded schistosomiasis, but the S. mansoni leads to T. gondii model, with an interval of 59 days between infections, led to massive mortality, great weight loss and a striking splenomegaly. These findings are very similar to data from previous work on the S. mansoni leads to Trypanosoma cruzi model. The authors believe that other examples of such a type of potentialization should be searched for in human schistosomiasis also.
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PMID:Mortality and other parameters of concomitant infections in albino mice: the Schistosoma-Toxoplasma model. 61 25

A 37 year old male developed fever for 20 days, along with headache, anorexia, malaise, sweating, pharyngitis, lymphadenopathy and splenomegaly. At this stage, Ag p24 was positive and anti HIV was negative. The patient recovered fully but 6 months later positive HIV titers were demonstrated by immunofluorescence and Western-blot. A retrospective diagnosis of acute retroviral syndrome was made. The difficult differential diagnosis with infectious mononucleosis, cytomegalovirus, measles, rubella, toxoplasmosis and influenza is discussed. Thus, anti HIV antigenemia should be investigated in any patient with a mononucleosis like syndrome belonging in a high risk group for AIDS, even if Paul-Bunnell-Davidson or IgG anti VCA-EB reactions are positive.
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PMID:[Acute retroviral syndrome]. 182 45

A 38-year-old man with AIDS presented with fever of unknown origin, splenomegaly, anemia, and thrombocytopenia. Admission laboratory data revealed a positive toxoplasmosis titer in the blood. The initial chest x-ray showed small bilateral pleural effusions, a normal cardiac silhouette, no infiltrates, and no interstitial edema. Ga-67 imaging revealed markedly abnormal uptake in the myocardium. A diagnosis of toxoplasmosis myocarditis was made based on laboratory and imaging data. The patient was treated for toxoplasmosis. No myocardial uptake of tracer was demonstrated on a follow-up Ga-67 scan, performed after completion of treatment for toxoplasmosis.
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PMID:Ga-67 citrate myocardial uptake in a patient with AIDS, toxoplasmosis, and myocarditis. 205 84

This report describes toxoplasmosis lesions in Australian marsupials. Clinical signs, necropsy findings and histopathological changes are summarized for 43 macropods, two common wombats, two koalas, six possums, 15 dasyurids, two numbats, eight bandicoots and one bilby. Animals either died suddenly without clinical signs or exhibited signs associated with respiratory, neurological or enteric disease. At necropsy, many marsupials had no visible lesions. Where present, common necropsy findings included pulmonary congestion, oedema and consolidation, adrenal enlargement and reddening, haemorrhage and ulceration of stomach and small intestine, and lymphadenomegaly and splenomegaly. Microscopically, affected lungs showed interstitial pneumonia and macrophage accumulation. Myocardial, skeletal and smooth muscle necrosis and neutrophilic inflammation were common. Organs had focal necrosis and/or fibrosis and lymphoid infiltrates. Toxoplasma gondii tissue cysts were common in muscle and nervous tissue. Free tachyzoites were commonly present in areas of necrosis. Selected sections from four macropods, two koalas, two dasyurids, one wombat and one possum stained specifically with avidin-biotin complex and anti-Toxoplasma gondii serum.
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PMID:Lesions of toxoplasmosis in Australian marsupials. 224 91

A 45-year-old Caucasian female with seropositive rheumatoid arthritis was found coincidentally to have a circulating lymphocytosis (6.4 x 10(9)/l) and neutropenia (0.1 x 10(9)/l). Initial presentation was with mouth ulceration and recurrent infections. A spleen scan showed no evidence of splenomegaly and serum titres against EBV, CMV and toxoplasmosis were negative. No anti-neutrophil antibodies were found. Marrow aspiration demonstrated a lymphocytosis of 60% with reduced numbers of granular precursors. Lymphocytes in both blood and bone marrow were CD3, CD8, CD16 and HLA-DR positive. Lymphocyte conditioned medium (LCM) generated from the patient's blood lymphocytes (without phytohaemagglutinin) was found to inhibit allogeneic colony-forming unit, granulocyte-macrophage (CFU-GM) stem cells in semi-solid culture compared with control LCM. This inhibitory activity was abrogated by the cytolytic removal of CD8 cells prior to LCM production and was significantly reduced by co-culture with indomethacin. Culture of the patient's marrow at autostimulatory light density marrow cell concentrations showed poor spontaneous CFU-GM colony formation until marrow CD8 lymphocytes were removed cytolytically. Prednisolone was used therapeutically (40 mg/d) and resulted in the patient's neutrophil count rising from 0.06 x 10(9)/l to 1.1 x 10(9)/l and a fall in the total lymphocyte count to 1.9 x 10(9)/l. Reevaluation of the patient's LCM post steroid therapy showed loss of the previous inhibitory effect. The patient's neutrophil count is maintained on oral azathioprine and indomethacin.
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PMID:Inhibition of CFU-GM by prostaglandins in a case of chronic T-cell lymphocytosis and neutropenia. 281 37

An animal model for the study of transient lymphadenopathy-splenomegaly during toxoplasmosis is presented. Injection of CBA/J mice with the low virulent, cyst-forming strain of Toxoplasma gondii (Pe strain) induces a three to four fold increase in weight and cellularity of spleen and lymph nodes with peak changes at 30-50 days after infection. The spleen displays marked haemopoiesis, a 30 fold increase in mononuclear phagocytes, and a two fold increase in Lyt2+ lymphocytes. Lymph nodes show a five fold increase in mononuclear phagocytes and a four and a half fold increase in Lyt2+ T cells. The increase in mononuclear phagocytes significantly alters T cell/macrophage ratios and this is associated with decreases in in vitro cell proliferation to mitogen and toxoplasma antigen. The relationship between alterations in cell balance of mononuclear phagocytes and T cell subsets and the expression of transient immune dysfunction can now be examined by modulating changes in these cell types.
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PMID:Spleen and lymph node cell populations, in vitro cell proliferation and interferon-gamma production during the primary immune response to Toxoplasma gondii. 310 Oct 32

Murine toxoplasmosis caused by a low virulence, cyst-forming strain of Toxcoplasma gondii (Pe strain) is characterized by splenomegaly, lymphadenopathy, decreased delayed-type hypersensitivity (DTH), and the presence of toxoplasma cysts in brain tissue. Cyclophosphamide (CY) in a single dose of 100 mg/kg injected 3 days before infection, or splenectomy 3 weeks before infection, augmented DTH and decreased the number of toxoplasma brain cysts. CY-induced augmentation of resistance during the first 3 weeks of murine toxoplasmosis was associated with: (1) an increase in mononuclear phagocytes and a decrease in T lymphocytes (including Lyt2+ cells) in spleens and lymph nodes; (2) suppressed toxoplasma antigen induced proliferation of cultured spleen cells: (3) augmentation of antigen induced proliferation of cultured lymph node cells; and (4) low levels of interferon-gamma production in both spleen and lymph node cultures. The best correlate of the enhanced in-vivo effects of CY was proliferation of nylon wool-purified lymph node cells to toxoplasma antigen. The presence of Lyt2+ cells in lymph nodes of toxoplasma infected mice inhibited maximal proliferation.
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PMID:Murine spleen and lymph node cellular composition and function during cyclophosphamide and splenectomy induced resistance to Toxoplasma gondii. 310 64

The tropical splenomegaly syndrome, described by Charmot as a chronic splenomegaly without any acute malaria attack, appears to be the prototype of hyperimmune malaria. A very small number of red cells or even no red cells are infected. IgG and/or IgM rates are greatly increased, as are anti-Plasmodium antibodies. The ratio T. helper/T. suppressor is normal or slightly increased. Serological tests show often cross reactions, mainly with African trypanosomiasis and toxoplasmosis, also with leishmaniasis. Undefined genetic factors in the host could explain the syndrome.
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PMID:[Cellular and humoral immunity in hyperimmune malaria]. 393 94

A 29-year-old male with sarcoidosis autoimmune haemolytic anaemia and paroxysmal nocturnal haemoglobinuria is described. Throughout his illness the chest films showed fibrosis in the right hilar region and he had had several pneumonias in the right lung. He had had massive splenomegaly and a splenectomy was performed. He was treated with prednisone and cyclophosphamide. Because his blood group was initially confused, several incompatible blood transfusions were given. Two types of antibody were detected: an autoantibody with "s" specificity and an alloantibody with Rh "D" specificity. Other interesting features in this case revealed at autopsy were a viral pneumonia and Toxoplasma gondii infection of the brain. As far as we know, this is the first reported patient with this unusual association.
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PMID:Sarcoidosis associated with autoimmune haemolytic anaemia and paroxysmal nocturnal haemoglobinuria red cell abnormality. 678 61

The original TORCH complex described clinically similar congenital infections caused by Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus, types 1 and 2. Cutaneous manifestations, including petechiae, purpura, jaundice, and dermal erythropoiesis, are commonly seen in toxoplasmosis, rubella, and cytomegalovirus infections. In herpes simplex virus infections, 80% of symptomatic infants show single or grouped cutaneous vesicles, oral ulcers, or conjunctivitis. Extracutaneous signs and symptoms are variable and can be severe. Significant clinical signs in congenital toxoplasmosis include diffuse intracerebral calcification, chorioretinitis, and microcephaly; congenital rubella can result in deafness, congenital heart disease, retinopathy, and brain calcification. Cytomegalic inclusion disease can include hepatomegaly, splenomegaly, paraventricular calcification, and intrauterine growth retardation. Localized or disseminated congenital herpes virus infection often involves the central nervous system and the eye. Diagnosis is confirmed by culture and identification of species-specific immunoglobulin M within the first 2 weeks of life. Histological examination contributes to the diagnosis in herpes simplex virus infection. Treatment for toxoplasmosis includes pyrimethamine with sulfadiazine or trisulfapyrimidine; congenital herpes simplex virus infection is treated with acyclovir. No specific therapy for congenital rubella or cytomegalovirus infections has been established, and so treatment is primarily supportive.
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PMID:TORCH syndrome. 764 Feb


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