Effects of immunosuppression were compared in newly hatched chickens given cyclophosphamide (CY) after inoculation with avian nephritis virus (ANV). All CY-treated infected chickens died within 13 days after inoculation of the virus and had heavy urate deposits throughout the body. However, non-CY-treated infected, CY-treated noninfected, and non-CY-treated noninfected control chickens survived through the observation period. In a chronologic study, the value of serum uric acid in CY-treated infected chickens was more than 3 times higher than that in non-CY-treated infected chickens, and more than 9 times higher than in noninfected chickens. Serum uric acid values were coincident with the positive degree of ANV antigen in the tubular epithelial cells in the kidneys and with the severity of renal degeneration. Serologic and immunohistologic examinations did not reveal detectable antibody and IgG- and IgM-containing cells in the spleen and kidneys of CY-treated infected chickens. However, non-CY-treated infected chickens had an increased number of IgM- and IgG-containing cells and antibody against ANV on postinoculation day 6. These findings demonstrated that CY treatment enhanced the susceptibility of chickens to ANV infection.

A specific thromboxane synthetase inhibitor, 3-methyl-2 (3-pyridyl)-1-indoleoctanoic acid (CGS 12970) was administered orally to 6 healthy adult Beagles at a dosage of 30 mg/kg of body weight. Blood generation of thromboxane B2 and urinary excretion of thromboxane B2 were measured before and after administration of CGS 12970. Although 97 +/- 0.4% inhibition of thromboxane B2 generation was observed within 2 hours after a single dose of CGS 12970 was administered orally, an effect on urinary excretion of thromboxane B2 was not observed. Additionally, oral administration of 30 mg/kg every 12 hours resulted in 80 +/- 14% inhibition of thromboxane B2 generation but had no effect on urinary thromboxane B2 excretion.

Numbers of mast cells in the cornea, sclera, choroid, ciliary body, iris, and retina of sections of globes from 35 clinically normal dogs and 34 dogs with secondary glaucoma was determined. Fixed globes were trimmed along a vertical midsagittal plane and embedded in paraffin. Tissue sections, approximately 6 micrometer thick, were stained with toluidine blue for identification of mast cells. In normal globes, most of the mast cells were observed in the anterior portion of the uvea, and fewer mast cells were seen in the choroid and sclera. Mast cells were not observed in the retina and were seldom observed in the cornea of dogs with or without glaucoma. In sections of glaucomatous globes, mast cells were distributed evenly in the uvea and sclera, and fewer mast cells were present than in normal globes, regardless of the cause of glaucoma.

The connective tissue structures commonly referred to as the periorbita, orbital septum, muscular fasciae, and vagina bulbi or collectively, as the orbital fasciae were dissected then illustrated and described. Two sheets (layers) of the periorbita (endorbita) were found in our dogs. The periorbita should be renamed endorbita because of its anatomic relations. The periorbita did not always fuse with the periosteum of frontal and sphenoid bones. Rather, the periorbita and the periosteum were often distinct and separate; only medioventrally did several fibrous bands unite the superficial sheet of the endorbita with the periosteum. Two layers of the endorbita fused with the periosteum of the margin of the bony orbit and with the orbital ligament. The muscular fasciae were divided into 3 layers. The superficial layer extended caudally from the orbital septum, was thick, and was pierced by arteries, veins, and nerves. The middle layer was attached to the sclerocorneal junction and, at the temporal canthus of the eye, was divided into superficial and deep sheets. The deep portion was attached to the lateral angle of the third eyelid, similar to a strong ligament. The deep layer of the muscular fasciae extended caudally from the sclerocorneal junction in intimate contact with recti and oblique muscles of the eyeball. The deep portion of the deep muscular fascia covered the deep surface of all recti muscles and separated them from the retractor bulbi muscle. Intermuscular septa were observed between middle and deep muscular fascia layers. The body of the third eyelid was located between superficial and middle muscular fascia layers and was fixed ventrally to the lateral angle of the eye by the deep sheet of the middle muscular fascia.

Sera and tracheal washings (TW) were used to identify antigens of Bordetella avium recognized during experimentally induced bordetellosis in young turkeys. Pooled sera and TW were examined for antibody by a microtitration agglutination test and by western immunoblotting. In addition, comparable samples collected from 1-day-old turkeys and uninoculated control turkeys also were examined. At least 8 outer membrane proteins of B avium were recognized in immunoblots of sera and TW from infected turkeys. Reactivity of TW in immunoblots was qualitatively similar but less intense, compared with reactivity of corresponding sera collected on postinoculation (PI) weeks 2, 3, and 4. Molecular weights of the major outer membrane proteins of B avium recognized by sera and TW at PI week 4 were 100,000, 97,000, 36,000, 31,000, 21,000, 18,000, 14,000, and < 14,000. A protein with a molecular weight of 55,000 reacted nonspecifically in all samples tested. Antibody, detectable by microtitration agglutination, was in sera of 1-day-old turkeys and in sera and TW of B avium-infected turkeys during PI weeks 2 to 4.

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.

Fifty-six samples of feces and intestinal contents from nonvaccinated diarrheal pigs with rotavirus infections were tested, using a subgroup (SGP)-specific ELISA, to determine rotavirus SGP classification. Forty-one percent (23/56) were SGP 1, 25% (14/56) were SGP 2, and 34% (19/56) were not classifiable. For classifiable samples, the geographic distribution for SGP 1 and SGP 2, respectively was: 60%/40% from Ohio (n = 15), 63%/37% from other midwestern states (Iowa, Minnesota, Nebraska, South Dakota: n = 16), and 67%/33% from Canada (n = 6). Thirty-seven SGP-classifiable samples were categorized according to age of pigs. Of pigs less than or equal to 1 week old, 22% of samples were SGP 1 (n = 8), and 14% (n = 5) were SGP 2. Of samples from 1- to 2-week-old pigs, 8% were SGP 1 (n = 3), and 5% were SGP 2 (n = 2). Of samples from 2- to 3-week-old pigs, 5% were SGP 1 (n = 2), and 8% were SGP 2 (n = 3). Of samples from 3- to 4-week-old pigs, 5% were SGP 1 (n = 2), and 3% were SGP 2 (n = 1). Of samples from pigs > 4 weeks old, 22% were SGP 1 (n = 8) and 8% were SGP 2 (n = 3). Double-stranded RNA extracted from positive controls and from 10 selected field samples (5 from SGP 1 and 5 from SGP 2) was electrophoresed in polyacrylamide gels to detect correlation between subgroup classification by ELISA and long or short double-stranded RNA electrophoretic-migration patterns. All SGP-1 and -2 rotavirus samples tested had typical long double-stranded RNA electrophoretic-migration patterns.

Morphologic changes in the small intestine were investigated during development of naturally acquired wheat-sensitive enteropathy in Irish Setters. To distinguish underlying morphologic abnormalities from non-specific effects of intestinal damage, progeny of affected dogs reared on a normal wheat-containing diet were compared with their own littermates reared on a cereal-free diet and with age-matched clinically normal Irish Setters fed the same wheat-containing diet. Peroral jejunal biopsy specimens were taken sequentially between 4 months and 1 year of age. At 4 months of age, there were no differences in villus height, comparing the 3 groups, but increased numbers of intraepithelial lymphocytes and goblet cells were already present in biopsy specimens from the affected Irish Setters fed wheat. Dietary wheat resulted in a progressive reduction in virus height in the jejunum of affected Irish Setters from 6 months onward. Underlying morphologic abnormalities were not found, and the characteristic morphologic changes of this enteropathy were secondary to the presence of dietary wheat. However, development of partial villus atrophy was preceded by increased numbers of intraepithelial lymphocytes and goblet cells.

In 6 female goats, the mean threshold for glucosuria was 159.5 +/- 4.3 mg/dl. During increasing filtered loads of glucose, renal reabsorption of glucose reached maximal capacity, which was not exceeded when plasma glucose concentration was increased further. Measured in 10 female goats, the transport maximum for glucose was 119.1 +/- 9.1 mg of glucose reabsorbed/min. During infusion of glucose, there was a significant (P < 0.05) time-dependent reduction in inulin clearance indicating that IV glucose administration may be inappropriate in goats with compromised renal function.

The kinetics of specific IgM and IgG antibody response was characterized in four 9-month-old Beagles after inoculation of 2 x 10(2) plaque-forming units (PFU) of Sheila Smith strain of Rickettsia rickettsii. Immunoglobulin M antibodies were first detected by indirect immunoflorescence on postinoculation (PI) day 9, peaked by PI day 20, and were no longer detectable by PI day 80. Immunoglobulin G antibodies became detectable between PI days 22 and 28, peaked by PI day 42, and decreased gradually through PI day 130. Subsequent challenges with R rickettsii on PI days 216 (2 x 10(2) PFU/dog) and 1,029 (5 x 10(4) tissue culture infective dose [TCID50]/dog) resulted in slightly different serologic responses. The initial challenge exposure failed to increase the concentration of IgG antibodies and induced only low concentrations of IgM antibodies. After the second challenge inoculation, IgM antibodies were not detectable and the concentration IgG antibodies increased slightly. Clinical abnormalities and seroconversion were documented in control dogs following each challenge exposure. Examination of acute and convalescent serum samples from 55 dogs in which Rocky Mountain spotted fever was suspected clinically suggested that sole evaluation of IgM antibodies in acute-phase serum would result in inaccurate diagnoses because of false-positive and -negative results. Use of a composite conjugate that detects IgM and IgG antibodies to R rickettsii appears to be satisfactory for diagnostic purposes; however, concurrent quantitation of IgM antibodies may facilitate serodiagnosis in a select group of dogs in which a four-fold increase in convalescent antibody titer is not detected by use of the composite conjugate. With the exception of a dog with a serum antibody titer of 1:8,192, we were unable to detect IgM or IgG antibodies in CSF samples from 9 dogs with experimentally and 3 dogs with naturally acquired infections.