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)

Infection of BALB/c mice with chemically induced metacyclic forms of Trypanosoma cruzi clone Dm28c led to characteristic changes of experimental Chagas' disease, with protracted but marked parasitemia, intense splenomegaly, and splenic T cell hyporeactivity to TcR;CD3-dependent stimulation. Infection of BALB/c mice with either chemically induced or triatomine-derived Dm28c metacyclic forms led to comparable parasitemias, a synchronous increase in the number of splenic large lymphocytes, and a similar reduction in T cell responsivity to immobile anti-CD3 antibody. A marked and selective reduction in the level of CD8 expression per cell was also seen in mice infected with either form of metacyclic parasites. Large inflammatory mononuclear cell infiltrates were present in the hearts of mice infected with either chemically induced or insect vector-derived metacyclic forms, at both acute and chronic stage, with predominance of CD8 over CD4 T cells in the lesions, in both cases. These results indicate that infection with chemically induced metacyclic forms of T. cruzi can be a useful model of Chagas' disease, resembling infection caused by the insect vector.
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PMID:Trypanosoma cruzi: both chemically induced and triatomine-derived metacyclic trypomastigotes cause the same immunological disturbances in the infected mammalian host. 789 31

Visceral leishmaniasis is an infectious disease with a classical clinical presentation of fever, anaemia and splenomegaly forming the three cardinal signs. A rare presentation of the disease is described where cervical lymph node enlargement was the only sign and there were no symptoms. It is emphasised that with extensive travel to and from areas of endemic leishmaniasis now established, it is important that clinicians and pathologists become acquainted with the characteristics of the disease.
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PMID:Visceral leishmaniasis: an unusual cervical presentation. 799 44

Infection of mice with LP-BM5 elicits an immunodeficiency state referred to as murine acquired immune deficiency syndrome (MAIDS). Shortly after infection, retrovirus particles become associated with follicular dendritic cells (FDC) and this study was undertaken to determine whether retroviruses alter FDC functions. The FDC functions examined included the ability to: (1) retain antigen (Ag) trapped prior to infection; (2) trap new Ag after infection; (3) maintain specific IgG responses; and (4) provide co-stimulatory signals to B cells. Mice were infected with LP-BM5 and the ability of their FDC to trap and retain 125I-Ag (HSA) was assessed. Serum anti-HSA levels were monitored and FDC co-stimulatory activity was indicated by increased B-cell proliferation. HSA trapped on FDC prior to infection began to disappear by 3 weeks and was practically gone by 6 weeks. Serum anti-HSA titres were maintained normally for about 3 weeks after infection and then declined precipitously. The ability of FDC to trap new Ag began to disappear around the second and third week of infection and was markedly depressed by the fourth week. However, FDC recovered from infected mice retained their ability to co-stimulate anti-mu- and interleukin-4 (IL-4)-activated B cells throughout a 5-week period. In short, the ability of FDC to trap and retain specific Ag and maintain specific antibody levels was markedly depressed after retrovirus infection. However, FDC from infected mice continued to provide co-stimulatory signals and these signals may contribute to the lymphadenopathy and splenomegaly characteristic of MAIDS.
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PMID:Follicular dendritic cell function and murine AIDS. 813 18

We describe a case of spontaneous bacterial peritonitis in a 53 year old man affected by cryptogenic micro-macronodular cirrhosis, portal hypertention, splenomegaly and hypersplenism, who was admitted with hepatic failure and septic shock and successfully treated with antibiotics (combination of clindamycin and netilmycin), surgical abdominal drainage and splenectomy. This case gave reason for a literature review and an update on the therapeutic options in these high risk patients, especially concerning the role of surgery. Spontaneous Bacterial Peritonitis (SBP) is defined as a bacterial infection of ascitic fluid in the absence of any septic focus. It is a typical life-threatening complication of hepatic cirrhosis with ascites. Mortality is very high and ranges from 75% to 97% of patients, due to septic shock and hepatic failure (hepatorenal syndrome, hepatic encephalopathy, gastrointestinal bleeding). Infection with a single organism is found in most cases. Gram negative bacilli are present in about 70% of cases and E. coli (less frequently Klebsiella, Serratia, Pseudomonas) is principally found. Gram positive cocchi comprise an additional 30% of cases. Anaerobic and microaerophilic organisms seem to be rare causes of SBP (2.7-6%); this finding is probably due to the intrinsic bacteriostatic activity of ascites, which contains high oxygen tension (70 mmHg) and is an inhospitable environment for bacteroides and Clostridia. The prevalent isolation of enteric organism suggest that the gut is the most frequent source of infection, even if the pathogenetic mechanism is not yet well known. The right treatment depends on differentiating primary (SBP) from secondary peritonitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is the surgical treatment of spontaneous bacterial peritonitis still up-to-date?]. 824 98

Infection with Rauscher leukaemia virus (RLV) causes erythroleukaemia, anaemia, viraemia, and splenomegaly, features which develop very quickly in mice of strains susceptible to RLV but more slowly or not at all in strains resistant to RLV. We compared the effects of bone marrow transplantation (BMT) of donor cells obtained from a mouse strain resistant to the virus with the effects of BMT of donor cells obtained from strains susceptible to the virus, in recipient virus-susceptible mice which had previously been inoculated with RLV. Our results indicated that bone marrow transplantation from a marrow-resistant donor, but not from a susceptible donor, delayed the expression of leukaemia and delayed death, although such treatment did not appear to inhibit viral infection in susceptible recipients.
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PMID:Bone marrow transplantation therapy using resistant donors for retrovirus-induced leukaemia in mice. 828 97

Infection of severe combined immunodeficient mice, which lack T and B lymphocytes, with polyomavirus (PyV) induced an acute hematological disorder leading to the death of the mice by 2 weeks postinfection. The disease was characterized by a dramatic decrease in megakaryocytes, multiple hemorrhages, anemia, thrombocytopenia, splenomegaly, a massive myeloproliferation and splenic erythroproliferation with a defect in maturation of the myeloid elements similar to that in acute leukemia. This pathology in severe combined immunodeficient mice is very different from that of the well-characterized tumor profiles induced by PyV in normal newborn or nude mice. Viral T and capsid (VP1) antigens and viral genome were detected in some cells in the spleen, but not in the majority of the proliferating myeloid cells. This suggests that the myeloproliferation is induced by some indirect mechanism, such as secretion of growth factors or cytokines by virus-infected cells, rather than by direct transformation by PyV. Neither the spread of PyV, its replication in different organs, nor the pathogenesis or the time of death were altered by depleting natural killer cells in vivo by anti-natural killer cell antibodies. Analysis of the spleen leukocyte population indicated that the cells expressed high levels of class I major histocompatibility complex antigens and were resistant to lysis by activated natural killer cells.
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PMID:Acute, lethal, natural killer cell-resistant myeloproliferative disease induced by polyomavirus in severe combined immunodeficient mice. 831 Nov 19

A follow-up study of 179 cases of human immunodeficiency virus (HIV) seropositive neonates born from HIV seropositive mothers is reported. At the time of the present study, HIV infection resulting from maternofetal transmission was found in 50 cases, while 108 infants were not infected; HIV infection remained uncertain in 16 cases; 5 infants were lost for follow-up. Out of the 50 infected cases, 20 were less than two-year old, 17 were 2-5 year old and 13 were older than 5 years. Very few remained asymptomatic after the age of 6 months, the most common symptoms being adenopathies and/or hepatomegaly and/or splenomegaly. Twenty-six had an acquired immunodeficiency syndrome (AIDS). Six died, from pneumocystosis (3), cytomegalovirus infection (1) and septicemia (2). Virus culture and polymerase chain reaction were the most efficient laboratory methods for early diagnosis of HIV infection, both being positive in more than 95% of the infected cases after the age of 3 months. A close clinical and biological supervision is recommended in these infants and children because of the permanent threat of infectious diseases in relation to their immunodeficiency. Treatment associates: 1) antiviral therapy with AZT as soon as the HIV infection is diagnosed; 2) primary prophylaxis against pneumocystosis with trimethoprim-sulfamethoxazol; 3) IV immunoglobulins in the case of repeated bacterial infection; 4) regular evaluation of the nutritional status and psychological assistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Management of HIV-seropositive newborn infants. Personal experience apropos of 179 cases]. 839 76

Murine gammaherpesvirus is a natural pathogen of wild mice. The virus infects alveolar cells and spleen cells during the primary infection and establishes a latent/persistent infection in B lymphocytes. Little is known about the immunological response to gammaherpesviruses during a primary infection. To address this issue, we investigated the pathogenesis of murine herpesvirus 68 (MHV-68) infection in mice deficient in CD4 or CD8 T-cell populations. Infection of the lung and spleen were greatly exacerbated in CD8-deficient mice, reflected by elevated virus titers in the lung and an increase in the number of infected splenocytes located around germinal centers. This finding contrasts with clearance of virus from the lung and spleen by day 12 postinfection in CD4-depleted animals. These data clearly indicate a major role for CD8 T cells in recovery from an acute MHV-68 infection. Whereas CD4 T cells fail to influence the course of infection in the lung, they do contribute to lymphoproliferation seen in the spleen (splenomegaly) during the primary infection. The significance of these results are discussed in relation to the immune response to other herpesviruses, in particular Epstein-Barr virus, with which MHV-68 shares similar molecular and biological properties.
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PMID:Pathogenesis of murine gammaherpesvirus infection in mice deficient in CD4 and CD8 T cells. 839 47

Recent evidence suggests that interactions between spleen focus-forming virus (SFFV) env products and the erythropoietin receptor (EpoR) are responsible for viral pathogenicity. Infection of factor-dependent cell lines expressing epoR (the cloned gene for EpoR) with SFFVP is mitogenic, generating cell lines that are no longer dependent on added growth factor, and an immunoprecipitable complex between EpoR and immature env protein in the endoplasmic reticulum has been identified. The dependence of these in vitro activities on env protein processing and their relationship to pathogenicity of SFFV were explored by using glycosylation site mutants of SFFV env. Mutants carrying Asn-->Asp mutations at each of the two consensus signals for N-linked glycosylation in the N-terminal domain of SFFVAP-L env (gs1 and gs2), the gs1-2- double mutant, and the gs0 quadruple mutant (mutated at all four signals utilized for N-linked glycosylation in SFFVAP-L env) were made. The primary translation products (gp52) of single-site mutant envs were processed into more highly glycosylated forms, and the corresponding viruses induced splenomegaly in susceptible mice, whereas the gs1-2- and gs0 proteins were not processed, and these viruses were not pathogenic. Unprocessed env proteins of both pathogenic and nonpathogenic mutants coprecipitated with EpoR. In the BaF3 cell assay for epoR-dependent mitogenicity, the pathogenic single mutants induced factor-independent growth efficiently whereas the nonpathogenic gs1-2- and gs0 mutants did not. These data demonstrate that the ability of gp52 to form complexes with EpoR in the endoplasmic reticulum is not sufficient for either mitogenicity in cell culture or induction of splenomegaly in mice while supporting the hypothesis that pathogenicity and mitogenicity of SFFV both result from an interaction between EpoR and SFFV env protein.
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PMID:Erythropoietin receptor (EpoR)-dependent mitogenicity of spleen focus-forming virus correlates with viral pathogenicity and processing of env protein but not with formation of gp52-EpoR complexes in the endoplasmic reticulum. 843 18

Atraumatic splenic ruptures in the course of infectious diseases are rare but have been reported. Various germs of viruses can be at the origin of such rupture. The more often quoted viral disease is infectious mononucleosis. The more frequently involved bacteria are Streptococcus non pneumoniae, Pseudomonas, staphylococci and Clostridium. Rupture mechanism is not clearly elucidated; it can be connected with sepsis diffusion at spleen level via haematogenic way and consequently splenomegaly. Splenic rupture following septicaemia does not always entail major splenomegaly nor abscess formation but the attack of the splenic tissue itself is sometimes sufficient to bring about the rupture. The present case of atraumatic splenic rupture on spleen sepsis, no abscess, starting from a pulmonar infection with Streptococcus pneumoniae is, to our knowledge, the first case reported in literature.
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PMID:Atraumatic splenic rupture in the course of a pneumonia with Streptococcus pneumoniae. Case report and literature review. 847 Apr 45


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