Epidemiologic data were evaluated from all dogs admitted to the University of Minnesota, Veterinary Teaching Hospital (UMVTH) between June 1981 and November 1989. Of 69,890 admissions, 2,077 were Miniature Schnauzers. Uroliths were retrieved from 63 of the 2,077 Miniature Schnauzers admitted. In 20 of the 63 urolith episodes, calcium oxalate was the predominant mineral identified. By comparison, calcium oxalate uroliths were identified in only 56 of the remaining 67,813 non-Miniature Schnauzer canine admissions. The odds that uroliths from Miniature Schnauzers were composed of calcium oxalate was 11.8 times greater than for other canine breeds evaluated at the UMVTH (95% confidence interval = 6.8 to 20.1). Data also were evaluated from files of uroliths retrieved from dogs and submitted to the Minnesota Urolith Center for quantitative mineral analysis between June 1981 and November 1989. Of 3,930 uroliths analyzed, 615 (15.6%) uroliths were obtained from Miniature Schnauzers. Of the 615 uroliths, 175 (28.4%) were calcium oxalate. By comparison, only 550 (16.6%) of the remaining 3,315 from dogs of breeds other than Miniature Schnauzers were calcium oxalate. The odds that uroliths submitted for analysis were composed of calcium oxalate was 2 times greater for Miniature Schnauzers than for dogs of other breeds (95% confidence interval = 1.6 to 2.4). Calcium oxalate uroliths were retrieved more frequently in males than females. The risk for males developing calcium oxalate uroliths was > 3 times the risk for females in both groups of data evaluated. The mean age of all Miniature Schnauzers admitted to the UMVTH with calcium oxalate uroliths was 9 years. Calcium oxalate uroliths were not detected in Miniature Schnauzers younger than 1.7 years.

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 classified histologically 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.

During the hunting season of 1992, 322 black bears from Pennsylvania were examined for Toxoplasma gondii- and Trichinella spp-induced infections. Toxoplasma gondii antibodies were found in 79.8% of 322 bears--titer < 1:25 in 65 (20.2%), 1:25 in 18 (5.6%), 1:50 in 11 (34.5%) and 1:500 in 128 (38.7%) bears--by use of the modified agglutination test. Muscle tissues from 89 of these bears were bioassayed for T gondii parasites. Muscles from 64 bears, including heart from 1 bear, and heart alone from another bear, were digested in pepsin, and the digested samples were bioassayed in mice. Toxoplasma gondii was isolated from 5 bears; from the heart of 1, heart and skeletal muscles of 1, and skeletal muscles of 3. The T gondii antibody titers for the 5 bears with detectable T gondii were: greater than or equal to 1:25 in all 5 bears by use of the modified agglutination test; < 1:10 (3 bears, considered Toxoplasma-negative), 1:20 and 1:320 by use of the Sabin-Feldman dye test; < 1:64 (3 bears, considered Toxoplasma-negative), 1:128, 1:512 by use of the indirect hemagglutination test, and < 1:16 (2 bears, considered Toxoplasma-negative), 1:32, 1:64, and 1:512 by use of the latex agglutination test. Toxoplasma gondii was not isolated from feces of 5 cats fed muscles from the remaining 25 bears with T gondii antibody titer < 1:25. Tissue cysts of the 4 T gondii isolates from bears were rendered noninfective by freezing at -13 C. Antibodies against Trichinella spp were found in 6 (1.8%) of 319 bear sera; Trichinella spp larvae were detected in muscle digests of 2 of 63 bears, and in histologic sections of muscles from 3 of 162 bears. Genetic typing indicated that the 2 Trichinella isolates from bears were a sylvatic genotype and were not the species found in domestic pigs.

Four shed-lambing operations in western Colorado were monitored during the 1984 spring lambing season to determine the causes and rates of perinatal lamb mortality. The number of lambing ewes per flock ranged from 513 to 1,712, and lambing percentages ranged from 131 to 180%. Overall perinatal lamb mortality ranged from 8.2 to 12.2%. Most lamb deaths occurred during parturition or within 24 hours after parturition. More than 85% of all lamb deaths were in lambs born to ewes having 2 or more lambs. The leading causes of lamb death were starvation, dystocia, stillbirth (unknown cause), and infectious diseases. A wheel model was used to categorize factors causing lamb deaths into 4 groups: physical, social, host, and biological, and to present data on perinatal lamb mortality in a simple visual model. In all flocks, social and biological factors resulted in most of the lamb deaths. On the basis of our findings, we suggest that interventions designed to improve ewe-lamb bonding and to reduce infectious agents and the incidence of prolonged parturition may reduce lamb mortality.

In a survey of 666 sheep at a slaughterhouse, gallstones (concretions with a diameter greater than or equal to 1 mm) were found in the gallbladder of 50 sheep (7.5%), sludge (concretions with a diameter < 1 mm) was found in 9 sheep (1.4%), and sludge plus gallstones were found in 7 sheep (1.1%). Gallstones and sludge were associated, and were more frequent in lambs and females, compared with adults and males. Qualitative analysis of the stones revealed all to be pigment (bilirubin) stones. There was a statistically significant increase of biliary bilirubin (total and indirect quota) only in sheep with gallstones plus sludge, compared with control sheep without sludge or gallstones. Concentrations of bilirubin, cholesterol, phospholipids, total and single bile aids, and total and ionized calcium were similar in the bile of sheep with gallstones, sludge, or both and control sheep. Bacteriologic analysis of the bile in 10 sheep with gallstones and 10 controls revealed bacteria in 50% of the first group and in 75% of the second group (Escherichia coli in all sheep and Salmonella spp also in 1 sheep with gallstones). These findings confirm our earlier findings of a high prevalence of black pigment gallstones in sheep. On that basis, we suggest that gallstones are associated with high total bilirubin concentration in the bile, and deconjugating bacteria are common in the biliary tract of these animals.