We investigated fibrin(ogen)-related antigens in liver tissues of rabbits infected with rabbit haemorrhagic disease (RHD) virus. Fibrin(ogen)-related antigens were detected in the sinusoids of liver at six hours post infection (pi). At 18 hours pi, the antigens were clearly detected in the hepatocytes infiltrated with heterophils rather than in the sinusoid. In the rabbits that spontaneously died (30 hours pi), fibrin(ogen)-related antigens were detected in both degenerating and some intact hepatocytes. They were also expressed in the necrotic foci of hepatocytes infiltrated by heterophils. By immunoprecipitation fibrin(ogen)-related antigens were extracted from the infected liver homogenates and analysed by sodium dodecyl sulphate polyacrylamide gel electrophoresis and Western blot analysis. There was an increase in fibrinogen and A alpha polypeptide chains in the liver homogenates from rabbits sacrificed at 18 and 24 hours pi, including those that died. Disseminated intravascular coagulation developed after progress of degeneration and necrosis of hepatocytes in RHD. It is assumed that the resultant consumption of fibrinogen triggers replenishment of fibrinogen by hepatocytes.

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Distribution of rabbit haemorrhagic disease virus RNA in experimentally infected rabbits.

Adult rabbits were inoculated with liver homogenate from a rabbit that died in a Japanese outbreak of rabbit haemorrhagic disease (RHD). All experimentally infected rabbits died with typical clinical, gross and histological findings of RHD. Distribution of RHD virus in tissues of the infected rabbits was studied by non-isotopic in-situ hybridization. Both viral plus- and minus-strand RNAs were detected within the cytoplasm of hepatocytes, Kupffer cells and splenic and alveolar macrophages, mainly in morphologically intact cells. Strand-specific reverse transcriptase-polymerase chain reaction also demonstrated viral minus-strand RNA as well as plus-strand RNA in the liver, lung and spleen of infected rabbits. These results suggest that viral replication occurs not only in hepatocytes but also in macrophages. The infected macrophages may contribute to viral dissemination in RHD.

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Evidence for a new lethal gene causing cardiomyopathy in Japanese black calves.

Sudden death with severe dyspnea in new-born or infant calves confined to a family of Japanese black cattle was studied. Neither environmental nor bacteriological factors seemed to be involved in the etiology of the disease. Histopathological examination revealed focal degeneration and necrosis of the muscle fibers in the myocardium, to which a diagnosis of idiopathic cardiomyopathy was proposed. The pedigree and mating type analyses suggested that a new autosomal recessive lethal gene was responsible for the syndrome. Rates of incidence of the affected calves in five sire families were tested for an expectation of 12.5 percent incidence by the chi-square method.

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The hypotrophic axonopathy mutant in Japanese quail.

A new behavioral mutant showing either head or body quivering, or both, was found in Japanese quail. This trait was characterized by neurofilament deficiency in the axons of the cervical spinal cord and the optic and sciatic nerves and was named "hypotrophic axonopathy." This character was shown to be controlled by an autosomal recessive gene, for which the gene symbol hax was proposed.

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Neurotoxic effects of 2,5-hexanedione on normal and neurofilament-deficient quail.

The neurotoxic effects of 2,5-hexanedione (2,5-HD) were investigated using neurofilament (NF)-deficient (Quv) Japanese quail in comparison with normal Japanese quail. Both Quv and normal Japanese quail were inoculated intraperitoneally with 350 mg/kg/day 2,5-HD for 6 consecutive wk. The results of 2,5-HD exposure differed substantially between the 2 strains of Japanese quail. The 2,5-HD-exposed normal quail showed leg paralysis about 4 wk after initiation of dosing. Some treated normal quail fell into dysstasia and died of nutritional disturbances. Histologically, 2,5-HD-treated normal quail had NF-rich axonal swellings and degeneration in the distal parts of the peripheral nerves, spinal cord, and cerebellar peduncles. In contrast, 2,5-HD-injected Quv quail showed tonic convulsion, ataxia gait, severe quivering, and excitation about 2-3 days after administration. Some treated Quv birds died immediately after systemic tonic convulsion, probably because of asphyxia. Although all treated Quv quail showed neurologic signs, there were no recognizable 2,5-HD-induced lesions in the nervous system. After about 4-6 wk of dosing, 2,5-HD induced distal axonopathy in normal quail and acute neurotoxicity in Quv quail.

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Esophageal/gastric adenocarcinoma in a dog.

A nine-year-old, intact female, mixed-breed dog was presented with a history of chronic regurgitation and weight loss. Endoscopy and contrast radiography confirmed the presence of a distal esophageal mass. The dog was euthanized, and histopathological diagnosis of the mass was an esophageal/gastric adenocarcinoma.

Adenocarcinoma↗

PubMedDate not supplied

Pathological study of lead poisoning in whooper swans (Cygnus cygnus) in Japan.

During spring 1989, thirty-three whooper swans (Cygnus cygnus) died at Lake Miyajima in Hokkaido, Japan; 15 were examined. The birds were diagnosed as having subacute lead poisoning due to ingestion of spent lead shot. The main gross findings were bile-stained liver, edematous or gelatinous bone marrow, bile-stained lining with hyperkeratosis and lead pellets in the gizzard, and proventricular impaction. Histopathologically, there was lead-hemolytic jaundice of the liver, hemosiderosis in the liver and spleen, and hypoplasia of the bone marrow with increased numbers of polychromatic erythroblasts. Acid-fast intranuclear inclusion bodies were seen in kidneys of seven swans. Under electron microscopy, inclusion bodies had frayed contours and consisted of high-electron-dense fine granules. The lead concentration of the liver ranged from 5.5 to 44.3 mg/kg wet weight. It was suggested that these changes resulted from excess breakdown of erythrocytes, inhibition of heme synthesis, and impaired erythropoiesis caused by lead shot.

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