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)

Immunization with avirulent Salmonella typhimurium strain SL3235, a smooth, aroA- derivative, was shown to induce high levels of resistance to challenge with virulent S. typhimurium in innately hypersusceptible C3H/HeJ mice and inherently resistant C3H/HeNCrlBR mice. Strain SL3235 is one of a class of avirulent aroA- derivatives made from various strains and species of Salmonella that are being considered as vaccine candidates for cattle and humans. This paper supports their efficacy and potential utility in this regard. In C3H/HeJ mice, immunity against over 1,000 50% lethal doses of virulent S. typhimurium was evident as early as 3 days after immunization and persisted for at least 7 months. Further, the vaccine was effective over a broad spectrum of doses, ranging from 10(4) to 10(6) organisms. Infection with SL3235 led to marked splenomegaly in both mouse strains. The relationship of splenomegaly to the growth kinetics and colonization by SL3235 in the spleens of infected C3H/HeJ and C3H/HeNCrlBR mice was followed. SL3235 initially multiplied slowly in the spleens of both mouse strains and then was rapidly cleared. Less multiplication was seen in the resistant C3H/HeNCrlBR mice than in C3H/HeJ mice. Maximum splenomegaly occurred after clearance of the organism had begun. Protection against virulent S. typhimurium persisted after virtually all of the SL3235 vaccine strain had been cleared from the spleen. Cross-protection against Listeria monocytogenes was evident, but had a later onset, waned by 21 days, and was not detectable by 1 month after vaccination. Demonstration of this cross-protection is consistent with the interpretation that SL3235 induces cellular immunity. One-week immune spleen cells adoptively transferred anti-S. typhimurium and anti-L. monocytogenes immunity. T cell-enriched fractions were ineffective in adoptive transfer, as were spleen cells taken 2 weeks or later after immunization. Protective capacity was in the adherent cell fraction and seemed to be associated with macrophages. Evidence for induction of a population of sensitized T cells was obtained by using a peritoneal exudate T-lymphocyte proliferation assay on peritoneal T lymphocytes collected 1 to 3 months after SL3235 infection.
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PMID:Immunity to Salmonella typhimurium infection in C3H/HeJ and C3H/HeNCrlBR mice: studies with an aromatic-dependent live S. typhimurium strain as a vaccine. 388 60

Infection of adult BALB/c mice with Friend disease virus results in a leukemia-like disease characterized by erythropoietic changes and splenomegaly. A marked depression of formation of cellular and serum antibody occurs in infected animals. Electron-microscopic examination of the ultrastructure of spleen sections from infected mice with depressed immunity revealed that virus particles can be detected only in immature blastlike lymphoid cells and not in plasmocytes characteristic of the immune response in spleens of noninfected mice immunized with sheep erythrocytes.
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PMID:Leukemia virus suppression of antibody-forming cells: ultrastructure of infected spleens. 563 63

Infection of A/J mice with Trypanosoma cruzi results in the polyclonal activation of B lymphocytes in vivo as assessed by the spontaneous plaque-forming cell (PFC) response to trinitrophenyl and to goat, equine, and sheep erythrocytes. The peak response to these antigens is found at 5 to 6 days of infection. Additionally, a polyclonal response to syngeneic erythrocytes can be detected in infected mice by using aged but not fresh indicator cells. Polyclonally stimulated PFC to human gamma-PFC found late in infection during a period of marked splenomegaly and parasitemia. This trypanosoma-induced polyclonal B cell activation may well be responsible for the abnormalities in immunoglobulin synthesis and secretion that have been reported to occur during human infection with T. cruzi.
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PMID:Polyclonal B lymphocyte activation during Trypanosoma cruzi infection. 615 88

A clinical and laboratory evaluation of 28 patients with hairy cells leukemia is performed. Twenty-two had splenomegaly and all but one had a pancytopenia with 5 to 70% of hairy cells in blood. A tartrate-resistant acid phosphatase activity was positive in the hairy cells of 11 patients of 14 studied. In all patients a myelofibrosis and a leukemic infiltration were found in a bone-marrow biopsy of iliac crest. Hemodilution by splenomegaly, mild hemolysis and dyshematopoiesis were observed in 10 patients by a 51Cr or 59Fe isotopic exploration. In seven cases an immunological study of the hairy cells was performed, a high percentage of the leukemic cells of these 7 patients had polyclonal surface Ig but without resynthesis of monoclonal S Ig which is a feature usually associated with B lymphocytes. In the blood of these patients normal T and B lymphocytes were decreased. A splenectomy was done in 12 patients (43%) always for severe pancytopenia Splenectomy was not randomised. Spleen weights ranged from 1 085 to 3 600 g. In splenectomised patients the level of hemoglobin, segmented cells and thrombocytes was significantly higher after surgery. The survival rate is better in the splenectomised group (median survival 57 months) than in the non-splenectomised group (median survival 19 months). Infectious diseases were frequent in all patients but less after splenectomy. Fourteen patients died, 8 owing to pancytopenia.
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PMID:[Hairy cell leukemia. I.--Clinical, biological and evolutive study on twenty-eight cases (author's transl)]. 627 Jul 94

Infection of mice with Brucella abortus strain 19 provides a most useful and interesting model in which to study chronic infection with intracellular bacteria. Most strains of mice develop a chronic infection. However, certain strains are better able to handle their infection. Long term bone marrow chimeras showed this to be due to bone marrow derived cells, rather than host physiology, although whether it is due T or B lymphocytes, macrophages or polymorphs is yet to be determined. In vitro treatment of lymphocytes from infected donors showed that the subpopulations transferring protection to naive mice was Thy 1+ 2+ Ia-. i.e. the same T cell which induces cell mediated immunity to Listeria. In vivo injection of an optimal regime of anti Ly1 monoclonal antibody exacerbated infection and removed the population of cells transferring immunity. Sub-optimal amounts of anti-Ly-1 abrogated IgG Brucella agglutinating antibody without affecting bacterial numbers, thus confirming the T dependence of IgG antibody and suggesting that it is not important in recovery from infection. Marked splenomegaly occurred about 3 weeks after infection of the mice. It was transferred by T lymphocytes and involved marked influx of macrophages, increased haemopoiesis, fibrin deposition and fluid in the spleen. Although the macrophages were immunosuppressive in vitro they did not appear to account for chronicity of infection. In seeking to account for this chronicity we have compared a number of aspects of the immune response in chronically infected mice and in mice which were able to control their infection. Although we have ruled out a number of possibilities, we have not yet established the basis of chronicity.
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PMID:Pathogenesis and cellular immunity in experimental murine brucellosis. 633 62

Patients with HCL are subject to a variety of medical problems. Many of these complications are caused by the cytopenias and splenomegaly produced by proliferating neoplastic cells. Infection is a common cause of morbidity in HCL, but it is not clear whether there is an inherent defect in the immune system. The incidence of infection is related to neutropenia and is increased by the administration of cytotoxic drugs and corticosteroids; such drugs should be used cautiously in these patients. Opportunistic or unusual pathogens occur frequently in HCL, but recovery from such infections is the rule if the diagnosis is made early. Marrow hypoplasia is not infrequently seen and may present diagnostic difficulties. Such patients may have a lower tumor burden and clinically milder anemia. Hemorrhagic complications are unusual in HCL, though many patients have platelet function abnormalities. Other medical problems occur with increased frequency in HCL, and failure to recognize them leads to increased morbidity in this disease. Autoimmune disease is seen in up to one fourth of patients. It takes the form of self-limited skin and joint disease, or a more progressive, systemic of patients. It takes the form of self-limited skin and joint disease, or a more progressive, systemic vasculitis. Both forms can usually be treated with splenectomy or corticosteroids, but alkylating agents can also be used successfully. Bone disease is usually localized and responds well to radiotherapy. Other problems such as amyloidosis, multiple myeloma, and paraproteinemia are uncommon in HCL.
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PMID:Clinical problems in hairy cell leukemia: diagnosis and management. 639 Jun 85

Malaria is an increasing hazard of tropical travel. Sixty-five cases were notified to the Health Department in 1980 and there is clear evidence of under notification. We reviewed the notes of 19 adults admitted to the infectious disease unit, Auckland Hospital, between 1 January 1979 and 31 March 1982. The typical patient admitted is a young caucasian New Zealander presenting three months after returning from Papua New Guinea where he took prophylaxis: he is febrile, infected with P. vivax, has splenomegaly but is not anaemic. Others presented atypically, especially with the potentially lethal P. falciparum. Four patients are described to highlight particular aspects of malaria management. Suggestions for prophylaxis and therapy are made in the light of changing global patterns of resistance of plasmodia, and particularly of P. falciparum to chloroquine.
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PMID:Imported malaria in adults in Auckland. 676 10

Infection of (C57BL/6 X DBA/2)F1 (BDF1) mice with 2,500 FFU of Friend virus complex (FV) resulted in erythroleukemia followed by recovery, at which time virus could not be detected in the spleens of mice, and with splenomegaly (progressor mice) or without splenomegaly (regressor mice). Progressor and regressor mice developed equally high amounts of FV-neutralizing activity in their sera. Progressor mice contained cells capable of producing virus, despite the lack of viral envelope antigen(s) in their spleens. The tropism of FV recoverable from the spleens of secondary recipients, injected with spleen cells from progressor mice, did not show any change, although the viral genome was present in Fv-I-restrictive host for at least 7 weeks. When the number of spleen colony-generating cells was enumerated, by the spleen colony assay, the frequency in normal syngeneic and in allogeneic hosts was approximately the same at the early stage of erythroleukemia but was about 1,000 times higher in the syngeneic recipients during leukemia progression. These spleen colony-generating cells were considered to be FV-transformed cells capable of self-renewal and capable of generating infectious centers (IC), respectively. Most of these transformed cells might be non-producer leukemia cells.
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PMID:Shut-down of virus synthesis during progression of erythroleukemia induced by Friend virus in mice. 695 90

Infection with Mycobacterium bovis (BCG) or injection of killed Corynebacterium parvum protected some strain B6D2 F1 (C57BL/6xDBA/2) mice but did not protect strain ICR or A mice from lethal challenge with Plasmodium berghei strain NYU-2. B6D2 mice were not protected against challenges delivered immediately after intravenous injection of these materials, but rather protection developed by day 7 and persisted through at least day 84. Infections in protected mice progressed to about 10% parasitemia in parallel with infections initiated with the same inoculum in untreated controls. However, infections in most of the protected mice were cleared subsequently, whereas infections in untreated controls were uniformly fatal. A small number of treated mice developed protracted high-level erythrocytic infections, which led to markedly delayed death. BCG-infected mice which survived P. berghei infections had a factor in their sera which protected passively immunized recipients from P. berghei. BCG-infected mice passively immunized with protective serum controlled P. berghei infections better than normal mice given the same amount of the same serum and challenged with the same P. berghei inoculum. The capacity of BCG-infected B6D2 mice to resist P. berghei infection was not directly related to the pattern of growth of BCG, to the degree of splenomegaly, or to the level of activation of macrophages (measured as microbicidal capacity) caused by BCG infection. Therefore, I concluded that (i) BCG infection or injection of killed C. parvum altered the immunological potential of B6D2 mice in such a way as to allow the production of measurable levels of a protective humoral factor in response to infection with P. berghei; (ii) BCG infection caused the generation of a capacity which, when expressed in the presence of immune serum, provided an anti-P. berghei capacity which was superior to that provided by BCG infection alone or immune serum in the absence of BCG infection; and (iii) not all strains of mice could be protected from P. berghei by BCG or C. parvum injection.
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PMID:Host defenses in murine malaria: nonspecific resistance to Plasmodium berghei generated in response to Mycobacterium bovis infection or Corynebacterium parvum stimulation. 702 24

Infection of mice with Friend erythroleukemia virus initially causes massive proliferation of erythroid precursors accompanied by splenomegaly and reticulocytosis. Strains of mice differ among themselves in susceptibility to Friend virus and one of the major genes affecting the early response to viral infection is Fv-2. Allophenic mice compounded from a resistant strain C57BL/6 (Fv-2rr) and a susceptible one DBA/2 (Fv-2ss) were infected with the polycythemic strain of Friend virus to determine whether susceptibility/resistance was limited to cells of the respective genotypes or if there was an influence across the genotypic barriers. The manifestations of viral pathogenesis monitored were splenomegaly, reticulocytosis and leukocytosis. In addition, the proportion of red cells of the two genotypes in each animal was monitored before and after viral infection by analyses for strain specific electrophoretic variants of hemoglobin and glucose phosphate isomerase. The group of allophenic mice with 25% or more susceptible-strain red blood cells all developed symptoms of virus-induced disease and also revealed dramatic increases in the number of red cells of the susceptible-strain genotype. Thus, no evidence for protection of susceptible-strain cells by ones of the resistant strain could be observed and the disease developed primarily in susceptible strain cells. On the other hand infected animals with 15% or less DBA/2 red cells were severely retarded in the development of Friend disease. Under these circumstances susceptible strain target cells might fail to undergo viral induced replication as a result of direct protection by resistant strain cells. Alternatively, other more complex mechanisms might be involved such as protective anti-viral immune reactions.
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PMID:Friend viral pathogenesis in C57BL/6 reversible DBA/2 allophenic mice. 717 42


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