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91.
Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis 总被引:5,自引:0,他引:5
Disseminated intravascular coagulation was induced in kittens by intraperitoneal inoculation of feline infectious peritonitis virus (FIPV). Kittens seronegative to FIPV survived significantly (P less than 0.05) longer than those seropositive to FIPV. Pyrexia, anemia, icterus, hyperbilirubinemia, and elevated concentrations of liver-specific enzymes were detected in the inoculated cats. Lesions induced included disseminated fibrinonecrotic and pyogranulomatous inflammation, hepatic necrosis, and widespread phlebitis and thrombosis. Localization of FIP viral antigen and immunoglobulin G was demonstrated in foci of heptic necrosis by immunofluorescence miroscopy. Lymphopenia, thrombocytopenia, hyperfibrinogenemia, and increased quantities of fibrin-fibrinogen degradation products were present in cats after the onset of clinical illness. Depression of factor VII, VIII, IX, X, XI, and XII plasma activities and prolongation of prothrombin and partial thromboplastin times also developed in infected cats. The accelerated onset of clinical disease and mortality in seropositive kittens vs seronegative kittens and the association of virus and antibody in multiple foci of hepatic necrosis suggest an immune-mediated component is involved in the pathogenesis of this disease. 相似文献
92.
Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extracellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells. 相似文献
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Etiology of ammoniated hay toxicosis 总被引:4,自引:0,他引:4
Some animals consuming hay treated with anhydrous ammonia have developed neurological signs including hyperexcitability, circling and convulsions. A series of experiments was conducted to identify tentatively the toxin and determine its mode of action. Three out of four sheep fed ammoniated orchardgrass hay (approximately 4% ammonia on a dry basis) developed convulsions. Two of the three sheep died within 18 h of the onset of signs. The concentrations of blood lactate and pyruvate were elevated in the symptomatic sheep (P less than .05). A proposed toxin, 4-methyl imidazole, did not induce the syndrome when 750 mg/d (approximately 10 times the dietary amount) were administered orally. Four out of five calves that received milk from cows fed ammoniated oat hay (approximately 5% ammonia on dry basis) displayed hyperexcitability and circling. Concentrations of blood lactate and pyruvate were also elevated in the calves. The crude alkaloid fraction of the toxic milk produced neurological signs similar to those of the calves when injected into mice. A fluorescent compound was found in the alkaloid fraction of toxic milk and ammoniated hay, but not in control milk or untreated hay. The fluorescent compound was quite labile; hence, characterization has been unsuccessful thus far. 相似文献
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Weiss DJ 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2005,19(2):147-154
Dysmyelopoiesis is defined as a hematologic disorder characterized by the presence of cytopenias in the blood and dysplastic cells in one or more hematologic cell lines in the blood or bone marrow. The causes of dysmyelopoiesis include acquired mutations in hematopoietic stem cells (i.e., myelodysplastic syndromes [MDSs]), congenital defects in hematopoiesis, and dysmyelopoietic conditions associated with various disease processes, drug treatments, or toxin exposure. Two major subtypes of MDSs (i.e., MDS with refractory cytopenias and MDS with excess myeloblasts) have been described that differ in clinical presentation, response to treatment, and survival time. The most frequently occurring causes of secondary dysmyelopoiesis include immune-mediated hematologic diseases, lymphoid malignancies, and exposure to chemotherapeutic drugs. Differentiation of the various causes of dysmyelopoiesis is essential for establishing an appropriate therapeutic plan and for determining prognosis. 相似文献