A new rat cytomegalovirus (RCMV) isolated from the placenta/uterus of a house rat (Rattus rattus diardii) was found to productively infect rat embryo fibroblast (REF) cells. The virus produced typical herpesvirus-like cytopathic effects characterized by a lytic infection. The well-known herpesvirus morphology was confirmed by electron microscopy. Its slow growth in cell culture indicated that the virus is belonging to subfamily Betaherpesvirinae. Electron microscopy techniques and immunohistochemistry confirmed the presence of herpesviral inclusion bodies and virus related particles in the cytoplasm and nucleus of infected cells. Hyperimmune serum against the Maastricht strain of RCMV revealed the virus identity in neutralization test, immunoperoxidase and immunofluorescence techniques. Despite typical characteristics of CMV, the viral genome is significantly different from that of Maastricht, English, UPM/Sg and UPM/Kn strains. The dissimilarities, which have not been reported before, had been confirmed by mean of restriction endonuclease analysis. The new RCMV strain, a virus that infects placenta and uterus of rats, has been named as ALL-03.

Postmortem radiographic examinations of animals are commonly performed in judicial investigations to rule out gunshot and fractures. However, there was no available data on radiographic postmortem changes of animals. Forty-one sets of abdominal radiographs of feline cadavers made within 12 h of death were evaluated for postmortem changes. Intravascular gas was detected in 11 of 41 (27%) cadavers. The most common site of intravascular gas was the liver. Intravascular gas was also present in the aorta, femoral artery, celiac and cranial mesenteric arteries, and caudal superficial epigastric artery. Intrasplenic gas was detected in two cadavers. Only two cadavers had distended small intestine. One cadaver had pneumatosis coli. The changes detected were most likely due to putrefaction.

One of 13 healthy dogs used in a pharmacokinetic study of imidocarb dipropionate died due to difficulty in breathing, tachycardia, weakness and profuse diarrhoea. Autopsy findings showed marked pulmonary congestion and oedema. Kidneys were grossly enlarged and markedly congested with extensive haemorrhage in the cortex and medulla. Marked tubulonephrosis was also exhibited microscopically. Liver and spleen were moderately enlarged and congested. The adverse effects of imidocarb may be due to excessive acetylcholine action.

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Sixteen 8- to 9-week-old Pasteurella multocida-free New Zealand White rabbits were divided into two equal groups. The first group was inoculated intranasally with P multocida serotype D:1 strain and the second group that was inoculated with phosphate-buffered saline (PBS) only was used as a control group. Pasteurella multocida was isolated from the nasal cavity of all infected rabbits in group 1 and from tracheal swabs of seven rabbits in this group. Four rabbits in group 1 died with clinical signs of septicaemia, two rabbits had mucopurulent nasal discharge and pneumonic lesions and the other two did not show any clinical signs or gross lesions. The ultrastructural changes detected were deciliation or clumping of cilia of ciliated epithelium, cellular swelling, vacuolation and sloughing. The subepithelial capillaries showed congestion, intravascular fibrin deposition, platelets aggregation and endothelial injury. Pasteurella multocida was observed attached to the injured endothelial cells. Heterophils, mast cells, vacuolated monocytes and macrophages infiltrated the lamina propria and between the degenerated epithelial cells.