C-reactive protein (CRP) was isolated from equine serum by use of calcium-dependent affinity chromatography conjugated pneumococcal C-polysaccharide, anion exchange chromatography, and gel filtration. It was identified as genuine CRP by its immunochemical cross-reactivity with anti-human CRP, its homology with human CRP in amino acid composition, and its pentameric structure as revealed by electron microscopy. Purified equine CRP had a molecular weight of approximately 118,000 and was composed of 5 identical, nonglycosylated and noncovalently associated subunits with molecular weight of approximately 23,000 each. Equine CRP migrated in the region between beta- and gamma-globulin by results of immunoelectrophoresis, and its isoelectric point was about 7.0. In horses, increased CRP concentration was associated with clinical pneumonitis, enteritis, and arthritis, compared with values obtained in clinically normal horses by use of single radial immunodiffusion method. After IM administration of turpentine oil or castration, serum CRP concentration increased to 6 times higher than baseline values. Results indicate that CRP may be an acute-phase reactant protein in horses.

Flunixin meglumine has been reported to induce gastrointestinal lesions in dogs when administered at therapeutic dosages. We administered flunixin meglumine to dogs daily for 10 days to assess the effect of this drug on the gastrointestinal tract. We also evaluated the possibility of corticosteroid potentiation of gastrointestinal toxicosis by concurrent administration of prednisone to 1 group of dogs. Dogs were monitored for gastrointestinal toxicosis by means of serial endoscopic evaluation, measurement of fecal occult blood, PCV, and total solid concentration, and by physical examination. There were 3 treatment groups of 5 dogs each. Group-1 dogs were given 2.2 mg of flunixin meglumine/kg daily, in 2 divided doses IM; group-2 dogs were given 4.4 mg of flunixin meglumine/kg daily, in 2 divided doses IM; and group-3 dogs were given 2.2 mg of flunixin meglumine/kg daily, in 2 divided doses IM plus 1.1 mg of prednisone/kg/d orally, in 2 divided doses. A fourth group of 5 dogs served as a control group. Endoscopically visible gastric mucosal lesions developed in all treated dogs within 4 days of initiating treatment. Lesions first developed in the gastric pylorus and antrum and lesions at these sites were more severe than those observed elsewhere. Dogs treated with flunixin meglumine plus prednisone developed the earliest and most severe lesions; lesion scores in group-2 dogs were higher than those in group-1 dogs. All dogs treated had occult blood in their feces by day 5 and its presence appeared to correlate more closely with endoscopic findings than did physical examination findings or changes in values for PCV or total solids. Deep ulcers were observed in the pylorus of most treated dogs examined at necropsy on day 10. Shallow ulcers and erosions were in the small intestine of group-2 and -3 dogs. Capillary microthrombi, associated with lesions of coagulative necrosis of superficial epithelium, were found in the colonic and small intestinal mucosa of several dogs in groups 2 and 3, and were suggestive of vascular injury. From results of this study, it was concluded that flunixin meglumine, administered at therapeutic doses, induced early gastric mucosal injury in dogs and that concurrent administration of prednisone may have exacerbated the gastrointestinal injury induced by flunixin alone. Endoscopic evaluation and measurement of fecal occult blood appeared to be more sensitive than other methods evaluated for detection of gastrointestinal injury.

Microscopic anatomy of the horizontal part of the external ear canal was evaluated in 24 dogs. Sixteen dogs were from breeds known to have a predisposition to otitis externa. The remaining 8 dogs were from breeds that do not have a predisposition to otitis externa. Dogs were separated into groups according to predisposition to otitis externa: group 1--predisposed dogs without otic inflammation, group 2--predisposed dogs with otic inflammation, and group 3--nonpredisposed dogs without otic inflammation. Qualitative microscopic evaluation of distribution of hair follicles revealed hair within proximal, middle, and distal regions of the horizontal ear canal in all breeds. The degree of keratinization was directly proportional to the presence of otic inflammation and was excessive in group-2 dogs. Quality of sebaceous glands within the horizontal ear canal was similar among dogs with and without otitis externa, whereas the quantity of apocrine tubular glands was significantly increased (P < 0.05) in dogs with otitis. Quantity of apocrine tubular glands was also greater in group-1 dogs than in group-3 dogs. Thickness of the soft tissue in the external ear canal increased in direct proportion to the progression of disease and was greatest in the proximal region of the affected ear canal. Soft tissue located caudally between nonopposing ends of the annular cartilage, within the proximal region of the horizontal ear canal, contained few glands and hair follicles in dogs without otitis externa. In dogs with otitis externa, this region was infiltrated by distended apocrine tubular glands.

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.

A superovulatory and surgical protocol was developed for recovery of bovine zygotes. Holstein cows and heifers were given follicle-stimulating hormone and cloprostenol to induce superovulation. Surgical cannulation and lavage of the uterine tube was performed 40 to 48 hours after the start of standing estrus. In general, cows had more corpora hemorrhagica than did heifers, but a higher percentage (P < 0.05) of ova recovered from cows were infertile. Several heifers were subjected to the procedure twice, and embryo recovery rates were equivalent both times.

Cattle heterozygous for deficiency of uridine monophosphate synthase required more breeding services per calving when mated to other heterozygotes than did matings of normal cattle. Gestation length, number of breeding services per calving, and days from breeding to pregnancy examination were monitored on 759 complete gestations, 76 false-positive pregnancy diagnoses, 14 false-negative pregnancy diagnoses, and 413 negative pregnancy diagnoses in a dairy herd between 1983 and 1987. For complete gestations, 15 heterozygote X heterozygote matings required 3.13 +/- 0.37 breeding services per calving, which was significantly more than the 2.05 +/- 0.05 breeding services required for normal X normal matings; gestation length and days from breeding to pregnancy examination were similar between mating types. For false-positive pregnancy diagnoses, females diagnosed pregnant, but subsequently found not to be pregnant, 5 heterozygote X heterozygote matings averaged 51 +/- 23 days of gestation, which was less than the 93 +/- 6 days required for 71 normal matings; services and days from breeding to pregnancy examination were similar between mating types. All false-negative pregnancy diagnoses, females diagnosed not pregnant but later found to be pregnant, were made on cattle with normal matings. For negative pregnancy diagnoses, heterozygous matings averaged 0.3 more breeding services per examination than normal matings.

Fourteen ponies and 3 horses were inoculated with Ehrlichia risticii 2 to 20 months after a similar initial inoculation. Although all 17 had clinical signs of equine ehrlichial colitis after the first inoculation, 16 of 17 remained clinically normal following the second inoculation. The remaining pony had a transient fever and developed signs of depression. Before the initial inoculation, none of the animals had a detectable antibody titer to E risticii. All animals developed titers after the initial infection; however, a significant change of titer did not develop after reinoculation in most animals.