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The patient was a 60-year-old man with the chief complaints of bloody stools, and their abnormal motion. The diagnosis was sigmoid colon cancer. Esophageal cancer and cholelithiasis were also found by several preoperative examinations. Subtotal esophagectomy, cholecystectomy and sigmoidectomy were performed. Resected Specimen: There was an early cancer measuring 2.5 X 2.0 cm at the abdominal esophagus. It was a poorly differentiated squamous cell carcinoma. There were two polyps at the gallbladder, in which carcinoma in situ was found. A well-differentiated papillotubular adenocarcinoma of type Borr 2 was found at the sigmoid colon.

In pigs inoculated with Aujeszky's disease virus (ADV), recrudescence of herpesvirus infection was induced by daily administration of 1,000 mg of prednisolone for 5 days at 2 (group A) or 5 (group B) months after the primary infection. At necropsy in group A pigs, ADV was recovered from nasal secretions 3 to 9 days after prednisolone treatment initiation and from the brain cortex 10 days after treatment initiation; ADV was not recovered from group B pigs. In pigs of both groups killed 10 days after treatment initiation, 2 types of characteristic lesions were found. One type was a nonsuppurative encephalitis that consisted of neuronal necrosis, neuronophagia, and formation of eosinophilic intranuclear inclusion bodies. The 2nd type had basophilic intranuclear inclusion bodies in the enlarged endothelial cells of the kidneys, liver, lungs, adrenal glands, and lymph node sinusoids. Cells containing intranuclear inclusion bodies had immature and mature herpesvirus particles. Therefore, the brain lesions containing the eosinophilic inclusion bodies were considered to be due to ADV. Basophilic inclusion bodies in the endothelial cells were due to porcine cytomegalovirus. These observations indicated that prednisolone treatment resulted in recrudescence of ADV and porcine cytomegalovirus infections.

Akabane disease, an infectious disorder causing congenital abnormalities in calves, was studied in naturally affected calves between 1972 and 1974 in Japan. The animals included one three-month fetus from which a strain of Akabane virus (OBE-1) was isolated, and a total of 177 stillborn or premature fetuses and deformed or infirm newborn calves that died within a few days of birth. The three-month fetus had nonpurulent encephalomyelitis in the undifferentiated central nervous system, characterized by necrosis of the nerve tissue and endothelial proliferation in the encephalitic process; and polymyositis in the myotubule phase with parenchymal degeneration and cellular infiltrates in the skeletal muscle. The full-term fetuses and newborn calves had nonpurulent encephalomyelitis in the early stage of the epizootic. In the middle to late stages, a dysplastic muscular change which we call runt-muscle disease was seen simultaneously with a decrease in number of ventral horn neurons in the spinal cord and arthrogryposis in the legs. Cystic cavities and thick vascular walls sometimes were seen in the central nervous system in these stages. Hydranencephaly was prominent in the late stage.