Eight rabbits exhibited head tilt and subsequently died. At necropsy, three rabbits had crusty deposits in ears and four had reddish lungs. The main histopathological features were severe diffuse suppurative meningoencephalitis (75.0% of rabbits), fibrinopurulent pneumonia (37.5%), and otitis externa (37.5%). Pasteurella multocida (P. multocida) was isolated from brains, ears, and lungs. The capsular serogroups of the isolates were untypable. Based on histopathological features and bacterial analysis results, the rabbits were diagnosed as P. multocida infection. P. multocida infections might result in considerable economic loss in commercial rabbit production facilities in Korea.

This paper describes a naturally occurring case of meningoencephalitis associated with Listeria monocytogenes in a 4 month-old Korean native goat. The goat was raised in a herd consisting of seventy goats, and fed on straw and leftover vegetables including onions, cauliflower, and bean sprouts. The clinical symptoms of the goat were depression, inappetence, anorexia, circling, and recumbency before death. No conspicuous gross lesions were found except consolidation of the lung.

To elucidate the involvement of interleukin-1beta converting enzyme (ICE) in the courseof experimental autoimmune encephalomyelitis (EAE), we induced EAE by immunizing rats with an emulsion of rat spinal cord homogenate with complete Freund's adjuvant supplemented with Mycobacterium tuberculosis(H37Ra, 5mg/ml) and then examined the expression of ICE in the spinal cord of rats with EAE. In normal rate spinal cords, ICE is constitutively, but weakly, expressed in ependmal cells, neurons, and some neuroglial cells. In EAE, many inflammatory cells are positive for ICE, and the majority of ICE+ cells were identified as ED1+ macrophages. During this stage of EAE, the number of ICE+ cells in brain cells, including neurons and astrocytes, increased and these cells also had incresed ICE immunoreactivity. These findings suggest that the upregulation of ICE in both brain cells and invading hematogenous cells is stimulated by a secretory product from inflammatory cells, and that this enzyme is involved in the pathogenesis of EAE via the production of IL-1 beta.