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A Japanese Black calf became dehydrated on the first day of life and died on the third day. Gross examination revealed a large amount of yellowish-brown serous fluid in the abdominal cavity and whitish-yellow fibrin in the serosa of the abdominal organs. Patchy red spots were observed throughout the peritoneum, and the outer membrane of the umbilical arteries was dark red. Bacteriologically, Mannheimia haemolytica serotype 2 was isolated from the umbilical arteries and vein, liver, and kidney. Histopathology revealed inflammation with M. haemolytica serotype 2 in the outer membrane of the umbilical arteries and in the serosa of the bladder and intestinal tract. This is the first case of bovine peritonitis with histopathologic and immunohistochemical identification of M. haemolytica.

Lolitrem B, a causative toxin for ryegrass staggers, is produced by Neotyphodium lolii infecting perennial ryegrass (Lolium perenne). Japanese black cattle have been suspected to be more sensitive to lolitrem B than to other strains, and there has been a concern about the public health hazard of eating beef contaminated with lolitrem B. We carried out a feeding experiment to examine the sensitivity of Japanese black cattle to lolitrem B and the residual level of lolitrem B in several animal tissues. Japanese black steers were fed a 0, 500, 750, 1000, 1500 or 2000 µg kg(-1) diet of lolitrem B provided by endophyte-infected perennial ryegrass straw for 12 weeks. All six animals in the 2000 µg kg(-1) diet group exhibited ryegrass staggers symptoms. Furthermore, two out of three animals in the 1500 µg kg(-1) diet group, three out of six animals in the 1000 µg kg(-1) diet group and one out of three animals in the 750 µg kg(-1) diet group presented clinical signs of ryegrass staggers. These results suggest that a daily intake of 18 µg kg(-1) body weight of lolitrem B can produce ryegrass staggers in Japanese black steers. Perirenal fat tissues of the steers from those groups having one or more animals exhibiting ryegrass staggers symptoms contained approximately 150 ng g(-1) of lolitrem B, while only small amounts of lolitrem B were detected in muscle, liver and kidney. Because the residual amount of lolitrem B in tissues of Japanese black cattle is small, the exposure to lolitrem B in consumers of the beef is likely to be low.

Seven of 92 lactating Holstein cows on a dairy farm developed urticaria with alopecia and decreased milk production, and three of the seven died over the course of 7 to 18 days. Pathologic examination of the three cows, including the two dead and one euthanized cow, revealed that the skin, liver, spleen, kidneys, heart, salivary glands, pancreas, adrenal glands, mammary glands, lymph nodes, and trigeminal ganglia had lymphocytic to lymphogranulomatous inflammation. Inflammation predominated by lymphocytic infiltration was prominent in the heart, pancreas, mammary glands, adrenal gland, and trigeminal ganglia. Severe granulomatous inflammation with multinucleated giant cells was present in the spleen and kidneys. These lesions and their distributions were most similar to those seen in suspected cases of citrus pulp toxicosis and hairy vetch toxicosis. The outbreak of this disease resolved with the elimination of Citrus pulp from the feed. Immunohistochemical detection of lymphocytes and macrophage markers confirmed dramatic hyperplasia of CD3-positive T lymphocytes in these lesions. This strongly suggested that a type 4 hypersensitivity reaction played a role in the development of the lesions.

Intranuclear eosinophilic inclusion bodies were seen in the lactiferous duct and sinus epithelium of mammary tissues collected from a cow with clinical mastitis. Transmission electron microscopy revealed herpesvirus particles in these cells. Immunolabeling against anti bovine herpesvirus type 4 (BHV-4) rabbit serum was detected in nuclei that had intranuclear inclusion bodies. In addition, BHV-4 was isolated from the mammary tissue. The viral DNA was detected by nested PCR from the same tissue. This is the first report to describe mammary lesions in association with BHV-4.

A holstein calf with congenital chondrodysplastic dwarfism was histopathologically examined. The head of the calf was relatively flat giving a dog-like appearance with its short nose and sloping forehead. Limb bones were dumbbell-like with short diaphysis and hypertrophied metaphyses. Bone marrow was pale, whitish and fatty. In the metaphyseal plates most of chondrocytes were pyknotic with swollen and ghost-like cytoplasm, and were irregularly arranged. Column of calcified cartilage were poorly formed losing comb-like structure. Bone marrow was ischemic with poor hematopoiesis and was moderately replaced by adipose tissue. In articular cartilage, most of chondrocytes were degenerated with ghost-like cytoplasm. Many cartilage canals and occasional bone marrow-like structure were formed. The characteristics lesions of the calf were chondrodysplasia and dyshematopoiesis.

Ten calves ("group 4") were inoculated endobronchially with Pasteurella haemolytica 4 days after inoculation with bovine herpesvirus 1 (BHV-1). Four calves (group 3) were similarly inoculated with P. haemolytica alone, and three (group 2) with BHV-1 alone. All group 4 animals showed severe respiratory signs and had bilateral lobar pneumonia; one died 6 days after inoculation with P. haemolytica. Two types of pneumonic lesion were observed. One was characterized by interlobular and interstitial lymphatic thrombosis, fibrinous pleuritis and coagulative necrosis, and the other by necrotizing bronchiolitis with intranuclear inclusion bodies. The former type of lesion was associated with the presence of P. haemolytica antigen and the latter with the presence of BHV-1 antigen. The weight of infection of BHV-1 and P. haemolytica in bronchoalveolar (BAL) fluid was clearly reflected in the immunohistochemical demonstration of the corresponding antigens in BAL fluid cells. Group 4 calves differed from the calves of groups 1-3 in showing 10-1530 times more endotoxin in BAL fluid. These findings suggested that BHV-1 infection partly destroyed the clearance mechanisms of the respiratory tract epithelium and exacerbated the subsequent P. haemolytica infection., (Copyright 2000 Harcourt Publishers Ltd.)

Each of six calves inoculated endobronchially with bovine herpesvirus 1 (BHV-1) by means of a bronchoscope developed viral pneumonia. Gross and histopathological lesions were mainly localized to the right diaphragmatic lobe (middle to caudal region) of the lung and were closely associated with the site of the deposition of the inoculum. The lesions were characterized by intranuclear inclusion bodies associated with focal necrosis of the epithelium in the lower respiratory tract. BHV-1 antigen and BHV particles were detected in the degenerating bronchial, bronchiolar and alveolar epithelial cells. After infection, the total cell count in the broncho-alveolar lavage (BAL) fluid increased. In addition, BHV-1 antigen and virus were detected in the desquamated cells and macrophages of BAL fluid from the right diaphragmatic lobe, but not from the left diaphragmatic lobe. It is concluded that examination of BAL fluid is valuable for immunohistopathological and virological confirmation of BHV-1 infection.

Nine calves infected percutaneously with graded doses of Strongyloides papillosus (SPL) were examined for hematological, biochemical and histological changes during the infection. Six of the calves infected with the highest larval doses died suddenly and the three calves given lower doses survived. No changes were observed in blood cell counts except for a transient eosinophilia. Parameters of the blood coagulation system and blood gas remained normal. A decrease in blood glucose was observed in four of the calves that died after the prepatent period of the parasite. However, endotoxic shock could be ruled out as a cause of death because of normal platelet counts, no intravascular coagulation and low levels of serum endotoxin. A transient increase of creatine kinase was observed in three of the calves that died; however, myocardial infarction or myocarditis were not observed. No lesions were observed except for minor inflammatory changes in the lungs and slight cellular infiltrations in the heart. In the absence of any consistent hematological, biochemical or histological changes in the calves that died, the present study failed to demonstrate mechanisms underlying sudden death due to SPL infection.