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)

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

Marble spleen disease (MSD) is a contagious disease of captive-reared ring-necked pheasants (Phasianus colchicus) characterized by variable mortality and high morbidity. The etiologic agent is a type II avian adenovirus closely related to hemorrhagic enteritis virus of turkeys and splenomegaly virus of chickens. Gross lesions of MSD consist of enlargement and mottling of the spleen and pulmonary edema. Microscopic alterations are most pronounced in the spleen and are characterized by reticuloendothelial (RE) cell hyperplasia and lymphoid necrosis. Intranuclear viral inclusions occur within hyperplastic RE cells. Serologic detection of MSD is routinely accomplished using an agar gel precipitin test. Oral vaccination with hemorrhagic enteritis virus or avirulent strains of MSD virus is effective in preventing MSD. There is no specific treatment available for MSD but supportive care, strict sanitation and good management practices are helpful in reducing mortalities and limiting the spread of an epizootic.
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PMID:A review of marble spleen disease of ring-necked pheasants. 255 99

Avian malaria (Plasmodium relictum) caused significant mortality in wild-caught Magellanic penguins (Spheniscus magellanicus) in 1986 at the Blank Park Zoo in Des Moines, Iowa (USA). In early winter, wild birds were captured off the southern coast of Chile and flown to Detroit, Michigan for a 38 day quarantine. After quarantine, 18 birds were dispersed to Lansing, Michigan, six to a facility in Maine, and 46 to Des Moines, Iowa. Upon arrival in Des Moines, several penguins became weak and inactive, had to be force-fed, and died after 2 days. Gross lesions at postmortem included splenomegaly, hepatomegaly, and pulmonary edema. Histopathological examination revealed numerous intraendothelial schizonts in spleen, lung, liver, heart and kidney. Schizonts were generally 16 to 28 micron by 11 to 16 micron and contained merozoites of two distinct sized (macromerozoites, nuclei 1.0 micron; micromerozoites, nuclei 0.5 micron). Based on the morphology of the abundant exoerythrocytic forms, a tentative diagnosis of avian malaria (Plasmodium sp.) was made. Subsequent transmission electron microscopic examination of schizonts in formalized tissue revealed merozoites with tear-shaped rhoptries. Antimalarial therapy was initiated early but deaths continued for 5 mo. Mortality, which eventually totaled 83%, occurred in three distinct waves, each separated by a hiatus of approximately 1 mo. Despite examinations of repeated blood smears, intraerythrocytic Plasmodium relictum was not detected until late in the outbreak. Diagnosis was based on morphologic characteristics including schizonts with eight to 12 merozoites/segmenter and round gametocytes that displaced and turned the infected erythrocyte nucleus. In addition to malaria, penguins showed evidence of aspergillosis, bacterial enteritis (Escherichia coli; Proteus sp.; and Edwardsiella sp.), and helminthiasis (Contracaecum sp. and Tetrabothrius sp.). Based on gross and histological lesions, disease prevalence in this group of penguins was malaria 58%, aspergillosis 61%, enteritis 60%, helminthiasis 26%. Epidemiologic investigation including group transport history, disease prevalence in co-quarantined birds not sent to Des Moines and climatological data implicated Des Moines as the likely site for initial exposure, although information is not conclusive. Stress and concurrent disease certainly contributed to the severe mortality in this group of penguins infected with P. relictum.
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PMID:Plasmodium relictum as a cause of avian malaria in wild-caught magellanic penguins (Spheniscus magellanicus). 319 55

Studies were performed to characterize the toxic effects of human rIL-2 in mice and to examine the mechanism of toxicity. Intraperitoneal administration of rIL-2 at doses greater than or equal to 2 X 10(6) U/kg twice each day for greater than or equal to 4 days led to toxicity in several strains of mice. The toxic effects of rIL-2 included the vascular leak syndrome (manifested by pulmonary edema, pleural effusions, and ascites), elevated hepatic transaminases, hyperbilirubinemia, hypoalbuminemia, pre-renal azotemia, anemia, thrombocytopenia, mild eosinophilia, and death. Marked lymphoid cell infiltration of pulmonary and hepatic vasculature was present in mice suffering from rIL-2 toxicity, and the pleural and ascitic fluids also contained high numbers of mononuclear cells. Mononuclear cells isolated from the pleural fluids and livers of these mice were 74 to 98% Thy-1+, 55 to 83% asialo-GM1+, 29 to 45% Lyt-2+, and less than 10% L3T4+. These cells possessed potent lymphokine-activated killer (LAK)-like activity in that their ability to lyse cells of the NK-resistant P815 mastocytoma line was 10- to 100-fold higher on a per cell basis than splenocytes from the same animals. A correlation was found between the dose level, duration, and frequency of dosing with rIL-2 required to induce pleural effusions and hepatotoxicity and the dosage regimens required to produce the LAK-like cells in the pleural cavities and livers, respectively, of rIL-2-treated mice. Moreover, treatment of mice with anti-asialo-GM1 (anti-ASGM-1) antiserum in vivo at the same time they were receiving toxic doses of rIL-2 abolished or greatly reduced the severity of the vascular leak syndrome and hepatotoxicity and significantly prolonged the survival of the mice. Administration of anti-ASGM-1 to mice receiving toxic doses of rIL-2 resulted in a marked reduction in the LAK-like cytolytic activity of their pleural and liver lymphoid cells and a corresponding reduction in the percentage of ASGM-1+ cells in pulmonary and hepatic lymphoid infiltrates. Nevertheless, the overall extent of pulmonary and hepatic lymphoid infiltration, as well as other consequences of rIL-2 administration, including splenomegaly, hypoalbuminemia, eosinophilia, and thrombocytopenia, were not diminished as a result of anti-ASGM-1 treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of asialo-GM1-positive lymphoid cells in mediating the toxic effects of recombinant IL-2 in mice. 325 67

A 54 year old man, hospitalised for thoraco-abdominal pain resulting from a septicemia which gives positive hemocultures for streptococcus D Bovis, is diagnosed to have a splenic abscess which will require splenectomy. At the same time, an endocarditis develops and gets worse, with auriculo-ventricular blockade and, especially, major aortic insufficiency, which is the cause of death by a brutal and massive pulmonary oedema. In the progression of an endocarditis, the occurrence of a splenic abscess, primary localisation of the initial septicemia or the secondary of an arterial septic embolism, is a rare contingency compared to the frequency of splenomegaly or splenic infarction: less than 2 percent of the cases in the literature. This very atypical and exceptional case serves as a reminder, on the one hand, of the diagnostic inadequacy of echocardiography which cannot visualise vegetation in the course of progressive endocarditis, and, on the other, of the prognostic importance of auriculoventricular blockade in septal and aortic endocardial lesions.
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PMID:[Splenic abscess disclosing endocarditis]. 393 91

Interleukin 12 (IL-12) activates natural killer (NK) and T cells with the secondary synthesis and release of interferon-gamma (IFN-gamma) and other cytokines. IL-12-induced organ alterations are reported for mice and the pathogenetic role of IFN-gamma is investigated by the use of mice deficient in the IFN-gamma receptor (IFN-gamma R-/-). IL-12 caused a rapid infiltration of liver and splenic red pulp with activated macrophages; this and increased NK cells resulted in a fivefold increase of splenic weight in wild-type mice. Splenomegaly was associated with myelosuppression and decreasing peripheral leukocyte counts. IL-12-induced changes in wild-type mice were associated with markedly increased IFN-gamma serum levels and up-regulation of major histocompatibility complex (MHC) class I and II expression in various epithelia. IL-12 induced a qualitatively similar macrophage infiltration in IFN-gamma R-/- mice, less marked splenomegaly (to 2 x normal), and no MHC upregulation. Strikingly increased vascular endothelial intercellular adhesion molecule-1 expression was apparent in both IFN-gamma R-/- and IFN-gamma R+/+ mice. Restricted to mutant mice was a severe, invariably lethal, interstitial, and perivascular pulmonary macrophage infiltration with diffuse pulmonary edema. Extensive quantitative reverse transcriptase polymerase chain reaction analysis revealed an increase of only IL-6 and IL-10 pulmonary gene transcripts in IFN-gamma R-/- mice compared with wild-type mice. IL-12-induced myelosuppression is due to IFN-gamma-release from NK cells and T cells, and is associated with macrophage activation and distinct MHC class I and II antigen upregulation. The pulmonary pathology in IFN-gamma R-/- mice, however, reveals a toxic potential for IL-12 and suggests that endogenous IFN-gamma plays a protective role in preventing fatal pulmonary disease in these mice.
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PMID:Role of interferon-gamma in interleukin 12-induced pathology in mice. 749 76

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Twenty-six patients, whose B-cell lymphoma had relapsed after conventional therapies, were treated in a phase I dose escalation study with an immunotoxin consisting of a mouse CD22 monoclonal antibody (RFB4:IgG1K) coupled to chemically deglycosylated ricin A chain (dgA). Two to 12 doses of the immunotoxin were infused intravenously at 48-hour intervals. The peak serum concentration and half-life (T1/2) did not correlate directly with the dose and averaged 3.8 micrograms/mL and 7.8 hours, respectively. The main dose-limiting toxicity was caused by the vascular leak syndrome (VLS) consisting of weight gain, edema, serum albumin decrease, and critically by pulmonary edema. Myalgia occurred frequently and was only dose limiting in one patient who developed rhabdomyolysis. The presence of lymphoma cells in the blood (> or = 10(10)/L) and clinically detectable splenomegaly were associated with reduced toxicity and a shorter T1/2. Nine of 24 evaluable patients (37.5%) made antibody to either mouse Ig or dgA. There were five partial responses (PR) and one complete response (CR) lasting 30 to 78 days. High peak concentrations of immunotoxin in the serum, a long T1/2, and large areas under the curve (AUC) correlated with both clinical response and toxicity. None of three patients with CD5+ lymphomas (including two CLL patients) had more than mild toxicity or responded to the immunotoxin.
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PMID:A phase I study of an anti-CD22-deglycosylated ricin A chain immunotoxin in the treatment of B-cell lymphomas resistant to conventional therapy. 821 17

Plasmodium falciparum malaria is endemic in the northern KwaZulu areas of South Africa. The clinical morbidity produced by this parasite has not been studied since the institution of the present malaria control programme. Fifty-nine patients were prospectively studied at a peripheral clinic during the peak malaria season; symptoms and signs of the infection, parasite loads, haemoglobin values and leucocyte counts were recorded in all patients. Haemoglobin and leucocyte counts were also measured in 37 control subjects without malaria. The commonest symptoms were persistent headache (100%), rigors (98%) and myalgia (93%). None of the patients presented with coma, pulmonary oedema, hypoglycaemia or algid malaria. Splenomegaly was found in 49%, hepatomegaly in 20% and mental confusion in 5% of patients. Mean parasite load was 1.71% and 57% of patients had parasite loads of < 1%. Anaemia of < 10 g/dl was significantly more frequent (P < 0.0001) in the patient group than in the control group. Leucopenia (white cell count < 4.0 x 10(9)/l) was present in 12 of 50 patients in whom it was measured compared with 2 controls (P = 0.0175). The results show a wide range of morbidity, without severe complications as presenting manifestations. Symptomatic infection in the presence of low parasite loads suggests that there may be little or no immunity in this population.
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PMID:Morbidity from falciparum malaria in Natal/KwaZulu. 845 85

Interleukin 12 (IL-12) activates natural killer and T cells with the secondary synthesis and release of interferon-gamma (IFN-gamma) and therefore enhances a Th1- or cell-mediated immune response. The immunostimulatory property of IL-12 may be used clinically in cancer and viral diseases. Safety studies in rodents and primates demonstrated a rather small therapeutic window with hepato- and splenomegaly, myelodepression, and lung edema. Investigations in mutant mice deficient for the IFN-gamma receptor (IFN-gamma R-/-) revealed that both the biologic and toxic effects are indirect and largely due to IL-12-induced IFN-gamma. The significance of these findings for the safety in man needs to be explored.
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PMID:Interleukin-12: role of interferon-gamma in IL-12 adverse effects. 907 24


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