In order to investigate the renal pathology of spontaneously occurring renal lesions, basic macroscopic inspection was conducted to 3,850 pigs randomly collected from local slaughter houses, and a total of 355 pigs (9.2 %) were detected with various gross pathological conditions. Renal morphologic patterns for gross lesions were classified histopathologically as 123 (34.5 %) congestion, 81 (22.8 %) acute interstitial nephritis, 52 (14.7 %) chronic interstitial nephritis, 49 (13.8 %) hemorrhage, 39 (11.0 %) renal cyst, 29 (8.2 %) chronic glomerulonephritis, 18 (5.1 %) acute glomeruonephritis, 14 (3.9 %) infarction, 11 (3.1 %) thrombosis, 5 (1.4 %) atrophy, 5 (1.4 %) pyelonephritis and 1 (0.3 %) lymphosarcoma.

A clinical trial examining the efficacy of 2 drugs for treatment of a natural epizootic of infectious bovine keratoconjunctivitis was performed. The study was conducted in 103 grazing Hereford calves during the summer of 1985. The calves were prospectively and randomly assigned to 1 of 3 groups at the beginning of the study on June 17, and were examined 3 times weekly thereafter until the final observation on August 6. Calves in group 1 (n = 34) were not treated and were used as controls. Calves of group 2 (n = 34) with corneal ulcers were treated with a long-acting oxytetracycline formulation (OTC group). The parenteral treatment was repeated in 72 hours. Affected calves of group 3 (n = 35) were treated topically with furazolidone spray when they developed new corneal ulcers, or when existing lesions worsened during subsequent examination periods (NFZ group). Healing times of the corneal ulcers were reported in 3 ways: the combined times for ulcers present in both eyes of a calf simultaneously (method A), independent times of each ulcer on a calf (method B), and time of the first ulcer for each calf (method C). Censored healing times were examined as left censored (ulcer present at the beginning of the study), right censored (ulcer not healed at the end of the study), or uncensored (true) healing times. The effect that the treatments had on healing times were investigated by use of notched box and whisker plots, life tables, and Cox regression models. The analysis indicated that treatment of calves with either antimicrobial reduced the healing time of corneal ulcers, compared with untreated controls. Calves treated with OTC had shorter periods with ulcers present on both eyes than did NFZ-treated calves. The healing time of the first ulcer on a calf was faster when treated with either antimicrobial than when not treated, but no significant difference between periods for OTC and NFZ treatments was found. Censored healing times were consistently longer than uncensored healing times. Box and whisker plots indicated that both treatments shortened healing times more than those for controls, and OTC shortened healing times more than did NFZ for responses A and B (but not C). Life tables showed that OTC healing times were shorter than those for controls, and NFZ shorter than controls for response B and C (but not A). Cox regression model (for response A) showed a borderline significant difference between times for OTC group and controls, and no significant difference between times for NFZ group and controls.

To evaluate the effect of exogenous testosterone on the development of T-2 toxin-induced necrosis of adrenal glands, mice were allotted to 3 treatment groups. Each treatment group contained castrated male, and castrated and sexually intact female mice. Each mouse in group 1 was given 0.16 mg testosterone propionate at 48-hour intervals for a total of 12 infections, group-2 mice were given similar injections of only the vehicle, and group-3 mice were given no treatment. Twenty-four hours after the last injection, the mice in all 3 groups were exposed for 10 minutes to an aerosol of T-2 toxin. All mice alive at 24 hours after exposure were euthanatized and the adrenal glands and thymuses were examined histologically. Necrosis of the adrenal cortex was not found in any of the mice given preexposure treatment with exogenous testosterone, whereas all mice given vehicle only or no treatment had T-2 toxin-induced necrosis of the inner portion of the adrenal cortex. Lymphocytolysis in the cortex of the thymus confirmed that each mouse of all 3 treatment groups had experienced systemic mycotoxicosis. The uniform severity of the lesion in all mice suggests that the thymus was not protected by exogenous testosterone administration or by the castration status of the mice. We propose that T-2 toxin-induced adrenal necrosis in mice is prevented by the presence of testosterone.

Ninety-one equine aortic and cranial mesenteric arterial segments were evaluated ultrasonographically in a water bath. On the basis of pathologic evidence of verminous arteritis, arterial segments were classified into 4 categories, and the ultrasonographic characteristics of each group were evaluated. Normal arteries (class 1) were ultrasonographically characterized by a smooth luminal surface layer and uniform wall thickness and echogenicity. Arteries with only histopathologic evidence of verminous arteritis (class 2) were ultrasonographically characterized by a smooth luminal surface layer, uniform thickness, uniform echogenicity, and the presence of a hyperechoic luminal layer. Arteries with both gross and histopathologic evidence of verminous arterities (class 3) were characterized ultrasonographically by an irregular luminal surface layer, varying wall thickness, varying wall echogenicity, and the presence of a hyperechoic luminal layer. The ultrasonographic characteristics of arteries with luminal thrombosis (class 4) were an irregular luminal surface, varying wall thickness, and nonuniform echogenicity.

The normal radiographic anatomy of the equine larynx was determined by use of xeroradiography and dissection. The body and laminae of the thyroid cartilage, the muscular process of the arytenoid cartilages, and the dorsal lamina and arch of the cricoid cartilage had radiographic evidence of mineralization (calcification) and/or ossification in clinically normal horses. There was a significant (P less than 0.01) increase in the degree of mineralization of the thyroid and arytenoid cartilages with advancing age. Horses with diagnosis of arytenoid chondrosis (arytenoid chondral dysplasia, arytenoid chondropathy) by use of endoscopy had radiographic changes that included: enlargement with increased density of the arytenoid cartilage region, abnormal patterns of mineralization (dystrophic mineralization or osseous metaplasia), abnormal contour of the corniculate process(es) and laryngeal masses, sometimes obliterating part or all of the lateral laryngeal ventricles.

Thirteen 3-week-old pigs that had been allowed to nurse for the first 16 to 18 hours after birth were orally inoculated with 1 X 10(6.5) TCID(50) of porcine rotavirus. All developed diarrhea, anorexia, and vomiting by postinoculation (PI) hour 30. These signs had abated by PI day 6. Villus blunting in the small intestine was most severe in the jejunum and ileum of pigs euthanatized between PI days 3 and 5. Villi had returned to nearly normal length by PI day 6, although fused villi were seen in a few locations in the distal portion of the jejunum and in the ileum. Virus was detected in the feces of inoculated pigs by isolation in cell cultures and by electron microscopy during the 7-day course of the experiment. There was 1 extraintestinal virus isolation from the lung of 1 pig at PI day 2. Infection and disease developed in the presence of serum-neutralizing antibody obtained by nursing seropositive sows. There was no significant change in neutralizing antibody titers in the 3-week-old pigs over the course of the experiment. In this experimental work, a model to study rotavirus infection in 3-week-old pigs has been developed.

Transverse sections of snouts from 171 cross-bred (principally Yorkshire X American Landrace) pigs were evaluated for evidence of turbinate atrophy by use of conventional (atrophic rhinitis [AR] score) and morphometric methods. Of the 171 pigs, 35 were clinically normal (AR score, 0), 65 had mild AR (AR score, 1), 41 had moderate AR (AR score, 2), and 30 had severe AR (AR score, 3). Turbinate cross-sectional area (TA) and the ratio of TA to nostril cross-sectional area, called turbinate area ratio (TAR), had the lowest correlations (r = 0.24 to 0.55) with conventional AR score. Among clinically normal pigs, TA was greater in older pigs as expected, but the TAR values also were significantly (P less than 0.0001) different betwee n 15-week-old pigs (55 kg) and 22-week-old pigs (100 kg). Turbinate perimeter and turbinate perimeter ratio (TPR) were not influenced by pig age or source. The TPR values were closely correlated with subjective visual AR scores (r = 0.73), with AR scores derived by measuring the space between the ventral portion of the scroll and the floor of the nasal cavity (r = 0.72), and the actual size of this space in millimeters (r = 0.71). Mean TPR values for pigs assigned visual AR scores of 0, 1, 2, or 3 were 1.54, 1.25, 0.97, and 0.73, respectively. The 95% confidence intervals around these mean TRP values were discreet and did not overlap. Turbinate perimeter ratio, therefore, may be a more reliable morphometric measure of atrophic rhinitis and also provides parametric data suitable for quantitative analysis.

To determine the sites of replication and the evolution of pseudorabies virus infection in boar genital organs, 5 Belgian Landrace boars were inoculated with pseudorabies virus unilaterally in the cavum vaginale of the testis. Virus replication took place only in cells of the tunica vaginalis of both cava vaginalia. Infection of the serosa led to exudative periorchitis and increased scrotal fluid, resulting in a severely swollen scrotal region. These experimental findings were similar to findings in boars with naturally aquired pseudorabies virus infection. Scrotal fluid contained large amounts of virus, making it a useful specimen for diagnosis of the disease in affected boars.

Leukotoxin activity from culture supernatants of Pasteurella haemolytica serotype 1 in logarithmic growth phase caused rapid (less than 5 min) release of intracellular K+, uptake of extracellular Ca2+, and swelling of cultured bovine lymphoma cells (BL3 cells). Release of 51CrO(4)(2-) and lactate dehydrogenase (LDH) from BL3 cells began after 15 minutes of incubation with leukotoxin at 37 C and was completed between 60 and 120 minutes of incubation. In addition, leukotoxin exposure of BL3 cells resulted in cell aggregation and adherence to glass surfaces. Scanning electron microscopy indicated that after 10 minutes of leukotoxin exposure, BL3 cells increased in size, and large membrane defects developed between 20 and 60 minutes of exposure. The rate of release of LDH from leukotoxin-exposed BL3 cells was proportional to the amount of leukotoxin added. At high cell concentrations, the activity of LDH released at completion was directly proportional to the amount of leukotoxin added. Leukotoxin-induced release of LDH required a divalent cation, whereas K+ release and cell swelling did not. The addition of Ca2+, Mn2+, and Ba2+ resulted in increased leukotoxin-induced release of LDH. Divalent cation concentrations of 0.5 to 2.5 mM resulted in 50% of maximal stimulation. Ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid blocked increased release of LDH caused by Ca2+ addition, but had no effect on K+ release or cell swelling. Leukotoxin action on BL 3 cells (K+ release, cell swelling, Ca2+ uptake, and release of LDH) was prevented by incubation at 4 C.

Cell proliferation kinetic values were established for the epidermis, hair follicle epithelium, and sebaceous glands of 8 Cocker Spaniels with primary idiopathic seborrhea. Values were established by intradermal pulse labeling injections of tritiated thymidine followed by cutaneous biopsy and autoradiography.The epidermal basal cell-labeling index was 4.96 +/- 0.97%, and the epidermal nucleated cell-labeling index was 3.33 +/- 0.71%. Calculated epidermal cell renewal time for the viable layers of the epidermis was 7.85 +/- 1.80 days. The hair follicle infundibulum basal cell-labeling index was 5.48 +/- 2.01%, and the sebaceous gland basal cell-labeling index was 5.94 +/- 4.15%. When compared with previously reported cell kinetic values for Cocker Spaniels and Beagles with healthy skin, these data indicate accelerated cellular proliferation in all 3 cutaneous structures in seborrheic Cocker Spaniels.