A case-control study was done to identify factors associated with the development of equine degenerative myeloencephalopathy (EDM). Questionnaires were mailed to the owners of 146 horses admitted to the New York State College of Veterinary Medicine between November 1978 and June 1987 and diagnosed as having EDM by histologic examination. Questionnaires also were sent to owners of 402 clinically normal horses admitted to the college during the same period. Data were compared between the EDM-affected and control groups (56 and 179 questionnaires returned, respectively). Risk factors identified included the use of insecticide applied to foals, exposure of foals to wood preservatives, and foals frequently spending time on dirt lots while outside. Foals spending time outside on green pastures was a protective factor. Foals from dams that had had an EDM-affected foal were at higher risk of developing EDM than were foals from other dams.

A prospective cohort study was undertaken in a farrow-to-farrow swine herd to describe patterns of pneumonia, and to identify host risk factors associated with the extent of pneumonic lesions in 2 weight groups of slaughter swine. The risk of coughing and pneumonic lesions increased with increasing age of pigs within the herd (P < 0.0001). The age-specific prevalence of pneumonic lesions was low (2.7%) in pigs < 16 weeks old at slaughter, but increased rapidly when pigs were between 16 and 22 weeks old (8.6 to 67.9%). After 22 weeks, the prevalence remained relatively constant at about 80%. Associations between possible risk factors and pneumonia were investigated by use of multiple-regression models. Age at weaning (< 24 days) and birth weight (< 1 kg) exerted small, but significant (P < 0.002), effects on the extent of pneumonic lesions in pigs slaughtered at 30 to 50 kg live weight. For pigs slaughtered at 90 to 110 kg, pneumonic lesions were more extensive (P = 0.007) in pigs sired by Yorkshire boars than pigs sired by non-Yorkshire sires (Duroc, Hampshire, Chester White, or American Spotted). Other host factor variables including weaning weight and clinical diseases (atrophic rhinitis, diarrhea, and arthritis) were not associated with pneumonia extent in either weight group. Higher pneumonia percentages were also associated with reduced growth rates in the grower/finisher phase. Pigs sired by Yorkshire boars grew significantly (P < 0.0001) more slowly from entry into shed 2 (mean, 38 kg) until about the time of exit (mean, 92 kg) than pigs sired by other breeds (747 g/d and 795 g/d, respectively).

Polioencephalomalacia (PEM) was induced in calves by feeding a semipurified, low-roughage diet of variable copper and molybdenum composition. Two formulations resulting in Cu-insufficient and Cu-sufficient forms of the diet were fed (n = 10 and 4 calves, respectively); both diets induced PEM. Clinical signs of disease developed as early as 15 days after transition to the experimental diets and included impaired vision, decreased response to external stimuli, and abnormal gait. Grossly evident cerebrocortical lesions consisted of laminar areas of cavitation and/or autofluorescence seen under UV illumination. Hepatic Cu concentration was decreased in calves fed the Cu-insufficient diet, but not below normal range. During the course of feeding either diet, rumen pH decreased, rumen volatile fatty acid concentrations increased, rumen and blood lactic acid concentrations increased, and rumen and plasma thiamine concentrations increased. The thiamine pyrophosphate effect on erythrocyte transketolase activitywas unaltered in calves of either diet group. This nutritionally induced form of PEM does not appear to be related to Cu deficiency or reduction in plasmaor rumen thiamine concentration.

Hypochloremic metabolic alkalosis accompanied by hypokalemia and hyponatremia was induced experimentally in 7 adult sheep by diversion (loss) of gastric contents through an Ivan and Johnston cannula placed in the cranial part of the duodenum just distal to the pylorus. Cannula placement was easily accomplished, and cannulae were tolerated well by the sheep. Volume of effluent produced during the 60- to 120-hour period of diversion ranged from 7.7 to 14.9 L and tended to be greatest during the first 24 hours. All sheep became dehydrated, with mean PCV and plasma total protein concentration increases of 94.2 and 61.7%, respectively. Plasma chloride concentration decreased in linear fashion from a prediversion mean of 113 mEq/L (range, 111 to 117 mEq/L) to an end-point mean of 54 mEq/L (range, 45 to 65 mEq/L). Plasma sodium and potassium concentrations also decreased, though potassium concentration increased terminally. There were rapid increases in arterial blood pH and bicarbonate and base excess concentrations during the first 48 hours after diversion. However, during the final stages of diversion, sheep developed superimposed metabolic acidosis with increased plasma lactate concentration and high anion gap.

The influence of recombinant bovine interferon gamma (rBOIFN-gamma) treatment on resistance of clinically normal and dexamethasone-treated calves to Haemophilus somnus infection was evaluated. Four groups of 6 calves each were treated with saline solution (controls), dexamethasone (0.04 mg/kg of body weight/for 3 days), rBOIFN-gamma (2 micrograms/kg for 2 days), or dexamethasone and rBOIFN-gamma (aforementioned dosages). All treatments were started 24 hours before intrabronchial challenge exposure with 5 x 10(9) colony-forming units of H somnus. Rectal temperature and WBC count were monitored daily. Two of the dexamethasone-treated calves died of pneumonia 4 days after challenge exposure and were necropsied. All other calves were euthanatized and necropsied 7 days after challenge exposure. All calves had pneumonia of variable intensity. Dexamethasone-treated calves had increased volume of pneumonic lung (P < 0.05) and increased severity of pneumonia, compared with control calves. Recombinant bovine interferon gamma treatment resulted in reduction in pneumonic lung volume and severity of pneumonia in dexamethasone-treated calves (P < 0.05), although it did not influence severity of pneumonia in nondexamethasone-treated calves.

The chemotactic activity of turkey peritoneal macrophages in response to an atherosclerotic plaque extract from a hypertensive strain of turkeys was determined. Atherosclerotic plaque extract stimulated macrophage chemotaxis, whereas normal aortic extract did not stimulate macrophage chemotaxis. However, differences were not revealed by sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of extracts of atherosclerotic plaque and normal aorta. Chemotactic activity was diminished with pronase treatment, suggesting the chemoattractant is a protein. Seemingly, atherosclerotic plaque of turkeys contains a macrophage chemotaxin.

The clinicopathologic manifestations of bovid herpesvirus-4 (BHV-4; FCAHV strain)-induced infection of the lower portion of the urinary tract were characterized in 12 adult neutered male and 6 female specific-pathogen-free cats, and were compared with those in 12 neutered male control cats. Six neutered male and 6 female cats were given immunosuppressive doses of methylprednisolone acetate prior to inoculation of their urinary bladders with BHV-4. Six neutered male control cats were given immunosuppressive doses of methylprednisolone acetate prior to inoculation of their urinary bladders with uninfected tissue culture control inoculum. Six additional neutered male control cats were exposed only to uninfected tissue culture control inoculum. All cats were observed for 90 days following inoculation. Dysuria and gross hematuria were observed in only 1 BHV-4-exposed cat. Radiographic abnormalities of the lower portion of the urinary tract were not observed. Microscopic hematuria, crystalluria, and lipiduria were identified with similar frequency in BHV-4-exposed and control cats. Results of urine culturing for bacteria, mycoplasma, ureaplasma, and viruses were negative. Viruses were not isolated from blood leukocytes collected from exposed or control cats. Three to 6 weeks after inoculation, high concentrations of BHV-serum 4 antibodies were detected in all exposed cats by an indirect fluorescent antibody test. Light microscopic examination of the urinary tract revealed multifocal lymphoid cystitis in 2 BHV-4-exposed cats. Except for suppurative bronchitis in 1 BHV-4-exposed cat given glucocorticoids, morphologic differences in urinary and extraurinary tissues were not observed. In urinary bladder tissue collected 90 days after inoculation, BHV-4 was reisolated from urinary bladder explants of all but 1 exposed cat. Virus was also isolated from a kidney explant of 1 exposed male cat, and spleen cell cocultures of 1 exposed female cat given glucocorticoids. Bovid herpesvirus-4 (FCAHV strain) caused persistent urinary tract infections in male and female specific-pathogen-free cats. Detection of occult BHV-4 infection required isolation of virus from tissues by explantation, or demonstration of specific BHV-4 antibodies by immunofluorescent fluorescent techniques. Administration of glucocorticoids prior to inoculation did not enhance morbidity associated with BHV-4 urinary tract infection. Further investigations are needed to determine the pathogenic role of BHV-4 in 4 noninduced feline lower urinary tract disease.

Twelve horses, with acute laminitis (primarily in the forefeet) at 12 hours after intragastric dosing with an aqueous extract of black walnut (Juglans nigra) heartwood, were studied. The distribution of perfusion of blood to the foot and to outlined regions within the foot was quantified, using gamma scintigraphy of regionally 99mTC. labeled macroaggregated albumin, before and 12 hours after extract administration. Horses 1 to 3 were not studied further. Perfusion was quantified again for horses 4 to 12 at 84 hours after extract administration. At the onset of acute laminitis, horses 7 to 12 were administered a single dose of prazosin (0.025 mg/kg of body weight, IV) immediately after scintigraphy of the right forelimb and before scintigraphy of the left forelimb. When compared with baseline images, perfusion to the forefoot of horses after the development of acute laminitis was quantitatively decreased vs perfusion to the entire distal portion of the forelimb. Also with the onset of laminitis, perfusion also decreased to the dorsal laminar and coronary corium regions vs the distal portion of the forelimb. The acute laminitis-associated deficit in perfusion to the dorsal lamina was greater in magnitude than the deficit in perfusion to either the coronary corium or the entire forefoot. Equivalent deficits in the distribution of perfusion were not detected in forelimbs from horses with acute laminitis and which had been treated with prazosin. When compared with baseline images, perfusion to the dorsal lamina was increased in relation to perfusion to the distal portion of the limb at postdosing hour 84. Prazosin treatment did not influence that increase in perfusion to the dorsal lamina.

Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P < 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia. The results indicated that young calves are susceptible to 3-methylindole-induced pulmonary injury and that nonciliated bronchiolar epithelial cells, type-I alveolar epithelial cells, and pulmonary endothelial cells are most susceptible to injury. The results failed to indicate that 3-methylindole pulmonary toxicosis significantly enhances respiratory disease induced by bovine respiratory syncytial virus.

Leukocytosis (34,600 WBC/microliter of blood) was detected in an apparently healthy 7-day-old Holstein heifer. Analysis of blood samples obtained over the next 41 days revealed chronic progressive neutrophilia, which peaked at greater than 85% neutrophils and exceeded 100,000 WBC/microliter. In vitro assessment of isolated blood neutrophils obtained from the heifer at 38 and 45 days of age revealed selected functional abnormalities. Endocytosis of immunoglobulin-opsonized Staphylococcus aureus and killing of this test organism by the calf's neutrophils were significantly diminished, as were phagocytosis-associated superoxide generation, chemiluminescence activity, and myeloperoxidase-catalyzed iodination. Diminished H2O2 elaboration by the calf's neutrophils was evident during ingestion of opsonized zymosan or on exposure to phorbol myristate acetate. Extracellular release (secretion) of elastase during ingestion of zymosan was also diminished, although total cell content of elastase was normal, compared with that of neutrophils from age-matched calves, and granular or other morphologic abnormalities of the calf's neutrophils were not evident by ultrastructural examination. Abnormalities of random migration were inconsistently detected, and normal or high degree of antibody-dependent cytotoxicity or natural killing by the calf's neutrophils was observed. Similar in vitro assessment of neutrophils obtained from the calf's dam revealed no functional abnormalities. The calf died at 48 days of age, with persistent fever and chronic diarrhea despite administration of antibiotics. Histologic examination at necropsy revealed large numbers of intravascular neutrophils in most tissues, including massive neutrophil sequestration in spleen. However, a striking lack of extravascular neutrophils was evident in inflamed submucosa mucosa adjacent to intestinal ulcers heavily contaminated with enteric microorganisms. Bone marrow examination revealed diffuse myeloid hyperplasia, but no other abnormalities. The clinical and pathologic features in this calf were similar to those in previously reported human patients or Irish Setters with genetic deficiency of the CD11/CD18 leukocyte glycoprotein complex, thus prompting further postmortem evaluations. Results of immunoblot analyses of the neutrophil lysates of the heifer calf (isolated and stored prior to death) documented severe deficiency of Mac-1 (CD11b/CD18). Results of immunofluorescent analyses indicated substantially diminished (intermediate) amounts of the Mac-1 beta subunit (CD18) on blood neutrophils of the calf's dam and sire and on neutrophils of 8 of 15 paternal half-siblings; findings were consistent with an autosomal recessive trait in the proband's kindred. Findings also indicate that genetic abnormalities of CD11/CD18 proteins may underlie the molecular pathogenesis of disease in this calf as well as other previously described examples of the granulocytopathy syndrome in Holstein cattle.