Musculature from 198 Canadian cattle with suspected lesions of eosinophilic myositis were examined histologically and by pepsin digestion. Sera from 51 of the 198 animals were also examined by enzyme-linked immunosorbent assay (ELISA) for anti-Trichinella antibodies. Viable larvae of Trichinella were not recovered from any of the cattle but one animal from Ontario tested positive for anti-Trichinella antibodies. Histologically, focal and/or diffuse eosinophilic myositis lesions were observed in 149 (75.2%) of the animals studied. Other conditions identified were sarcocystiosis, abscesses, cysticercosis, steatosis, fibrosis, granuloma, lymphosarcoma and necrosis. Sarcocystiosis was identified in 105 of the 198 animals in both normal and affected musculature. The study indicates that trichinosis is not a primary cause of eosinophilic myositis in cattle.

Sixty-nine specific pathogen-free male Wistar rats approximately eight weeks of age were used to evaluate the efficacy of an attentuated strain of sialodacryoadenitis (SDA) virus in providing protection against infection on subsequent challenge with virulent SDA virus. Fifty-four animals were inoculated intranasally with approximately 10-1.5 median cell culture infectious doses of the 25th passage of SDA virus in L-2 cells. Randomly-selected vaccinated animals were killed in order to evaluate the safety and efficacy of attenuated virus by histopathological examination of the salivary glands, lacrimal glands, and lower respiratory tract, and titration of sera for antibody to SDA virus. At three months and six months post-vaccination (pv), animals were selected at random and challenged with virulent SDA virus. Seronegative, age-matched animals were also challenged, and served as controls. In animals examined at six to ten days pv, lesions were absent in submandibular and parotid salivary glands and lacrimal glands, but transient lesions were present in major airways of the lower respiratory tract. In a comparison of the incidence and extent of lesions, and antibody titers in challenged vaccinates and seronegative controls, lesions were minimal or absent in vaccinates compared to challenged naive rats, particularly in animals inoculated at three months pv. In addition, antibody titers in challenged vaccinates were much higher than were postinoculation titers in inoculated controls. In a comparison of lesions in salivary and lacrimal glands in vaccinated and control animals challenged at six months pv, there was a significant reduction in the number of animals without lesions in the vaccinated group (p = < 0.0001). Based on the incidence of lesions in target tissues and the marked antibody response in vaccinates on challenge with virulent SDA virus, it was concluded that prior inoculation with the attenuated strain of SDA virus provided a significant level of protection for up to six months postvaccination.

Tissues from cattle that died of experimentally induced mucosal disease (n = 3), naturally acquired mucosal disease (n = 6), or naturally acquired chronic bovine viral diarrhea (n = 4) were examined. Consistent findings were lymphocytic depletion of lymphoid tissues, degeneration of myenteric ganglion cells, and mild adrenalitis. Intracytoplasmic viral antigen was detected in myenteric ganglia and in endocrine glandular cells. Noncytopathic virus was isolated from all cattle, and cytopathic virus was isolated from 12 of 13 cattle.

We compared the frequency and severity of osteochondrosis lesions in young Thoroughbred horses with cervical stenotic myelopathy (CSM) vs that in clinically normal Thoroughbreds of the same age. All lesions of the cervical vertebrae and appendicular skeleton were classifiedhistologically as osteochondrosis or nonosteochondrosis and were measured for severity. Minimal sagittal diameter was significantly smaller in horses with CSM from C2 through C6; no difference was detected at C7. Severity of cervical vertebral osteochondrosis was greater in the horses with CSM, however frequency was not different. Frequency and severity of nonosteochondrosis lesions were not different in cervical vertebrae or appendicular skeleton. Frequency and severity of appendicular skeleton osteochondrosis lesions were both greater in horses with CSM. Osteochondrosis and nonosteochondrosis lesions were more severe on facets at sites of compression than on facets at noncompressed sites in horses with CSM. However, compression was also observed at sites with no articular facet lesions. The association of widespread osteochondrosis and spinal canal narrowing with CSM suggests CSM may represent a systemic failure in the development or maturation of cartilage and bone.

A comparison of immune variables following lung sensitization with live Pasteurella haemolytica serotype 1 (Ph1)-impregnated agar beads was done in 2 separate trials. The Ph1 immune variables studied were blood bactericidal activity, serum bacteriolysis, total classical complement, and indirect hemagglutination antibody. Each trial had 16 male weanling goats: 6 controls and 10 principals. In trial 1, each goat was surgically catheterized through the trachea, then the material was deposited in a bronchus. The controls received only agar beads and the principals received agar beads impregnated with live Ph1. These goats were studied for 32 days, euthanatized, and necropsied. In trial 2, the controls were each transthoracically injected with agar beads into the left lung and the principals were similarly injected with agar beads impregnated with live Ph1. These goats were studied for 35 days, then challenge exposed transthoracically by injection of Ph1 in saline solution (1.2 X 10(7) CFU/ml) into the right lung. Four days later, they were euthanatized and necropsied. The volume of lung consolidated tissue was an excellent measure of Ph1 immunity. Principal goats generated solid protective immunity to subsequent challenge exposure because minimal or no lung consolidation was observed, whereas large volumes of lung consolidation were seen in the controls. The principal goats in trial 1 gave a weak serum indirect hemagglutination Ph1 antibody response, which was attributed to the bronchial method of depositing the Ph1. The corresponding response of the control group remained negative. The Ph1 agar beads (1 X 10(6) CFU in 0.5 ml) protected the bacteria from immediate phagocytosis and lysis as indicated by the induced pneumonic deaths of 2 principals 5 days later. Also, live Ph1 were isolated on day 32 during necropsy of respiratory tracts of 3 principals. At necropsy, no Ph1 isolates were found in the controls. Bacteriolytic activity was not induced against Ph1 in either control or principal groups in this trial. the study, but antibody titers of the principals increased to a geometric mean of 1:250 seven days after lung injection (1 X 10(5) CFU in 0.5 ml). Serum bacteriolytic titers on day 0 indicated that both principals and controls could be subgrouped to high or low subgroups on the basis of their bacteriolytic activity. The bacteriolytic activities of the controls remained unchanged during the experiment, and neither control subgroup was protected from Ph1 challenge exposure. Bacteriolytic activities of the high and low principal subgroups responded differently to Ph1 agar bead lung injection, but both principal subgroups were protected from lung challenge exposure. The low principal subgroup generated high titers of indirect hemagglutination Ph1 antibody, whereas, the high principal subgroup generated lower antibody titers. Total complement, serum bacteriolytic, and blood bactericidal profiles were similar in the principal group with high bacteriolytic activity. The immune factors that protected 2 principal subgroups did not appear to be associated with Ph1 serum bacteriolysis.

The effect of humidity on the histologic lesions induced by high-frequency jet ventilation was investigated in 12 healthy cats. After 16 hours of ventilation, the appearance of the tracheal epithelium ranged from normal to necrotic. The damage was considerably more severe in the trachea of cats of the group ventilated without added humidity. Increasing the relative humidity to 63% at 24 C had a protective effect, but further increasing the relative humidity to 92% at 35 degrees C did not appear to provide significantly more protection. The bronchi and distal airways had minimal, if any, damage in all groups.

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56. Leptomeres were observed in cardiac myocytes of ducklings that had been fed furazolidone, but not in those fed only the control ration. Our clinical, gross pathologic, and ultrastructural findings indicate that regression of the cardiac lesions of furazolidone toxicosis may be essentially complete by 28 days after cessation of furazolidone intake. Our ultrastructural findings indicate that furazolidone consumption may result in cardiac dilatation by altering myofibrillar/cytoskeletal attachments of myocytes.

Enterotoxemia was induced in 4 lambs and 4 goat kids by continuous intraduodenal infusion of a whole culture of Clostridium perfringens type D. Clinical signs, hematologic values, biochemical alterations, and postmortem lesions in the lambs and goat kids were compared. The 4 lambs and 4 goat kids died within 25 hours of beginning the infusions. Lesions were not observed in the gastrointestinal tract of the 4 lambs; however, severe hemorrhagic enterocolitis was found in the 4 goat kids. This difference between the lambs and goat kids in the lesions caused by experimentally induced enterotoxemia may explain the discrepancies reported between sheep and goats in clinical signs, response to treatment, and efficacy of vaccination observed in naturally induced enterotoxemia in the 2 species.