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.

Ten colostrum-deprived calves were assigned to 1 of 2 treatment groups (5 calves/group), and fed colostrum that had either low (naturally infected cows) or high (immunized cows) antibody titers to bovine coronavirus (BCV). All calves were inoculated orally and intranasally with virulent BCV when they were 24 to 48 hours old and challenge exposed 21 days later. Blood, feces, nasal secretions, tears, saliva, and bronchoalveolar lavage (BAL) fluids were collected weekly from each calf for 5 weeks after inoculation. The titers to whole BCV or the relative amounts of isotype-specific antibodies to BCV structural proteins were evaluated in these samples by ELISA or immunoblotting, respectively. Both pools of colostrum contained primarily IgG1, IgG2, and IgA antibodies to the E2 and E3 BCV proteins. Calves fed the high-titer colostrum had correspondingly higher amounts of passive IgG1 and IgA antibodies to whole BCV and to the E2 and E3 BCV proteins in serum, feces, and BAL fluid at postinoculation week 1 than those calves fed low-titer colostrum. Active IgG1, IgA and IgM antibody responses in serum and active IgA and IgM antibody responses in most mucosal secretions to whole BCV and to the E2 and E3 proteins were lower or delayed in calves fed high-titer colostrum, compared with responses in calves fed low-titer colostrum. In contrast, increased responses to the BCV N protein were observed in all samples (except in serum and BAL fluid) in the calves fed high-titer colostrum, compared with calves fed low-titer colostrum. Upon challenge exposure, responses to E2 and E3 BCV proteins in serum and BAL fluid were lower in the group fed high-titer colostrum, compared with those in the group fed low-titer colostrum. Our findings indicate that the level of passive immunity in calves at the time of BCV inoculation can influence the development of active antibody responses in serum, feces, and mucosal secretions to whole BCV and to some BCV proteins individually.

Periosteal autograft were used for repair of large osteochondral defects in 10 horses aged 2 to 3 years old. In each horse, osteochondral defects measuring 1.0 X 1.0 cm2 were induced bilaterally on the distal articular surface of each radial carpal bone. Control and experimental defects were drilled. Periosteum was harvested from the proximal portion of the tibia and was glued into the principal defects, using a fibrin adhesive. Control defects were glued, but were not grafted. Sixteen weeks after the grafting procedure, the quality of the repair tissue of control and grafted defects was assessed biochemically. Total collagen content and the proportion of type-II collagen were determined. Galactosamine and glucosamine contents also were determined. From these measurements, contents of chondroitin and keratan sulfate and total glycosaminoglycan, and galactosamine-to-glucosamine ratio were calculated. All biochemical variables were compared with those of normal equine articular cartilage taken from the same site in another group of clinically normal horses. Total collagen content was determined on the basis of 4-hydroxyproline content, using a colorimetric method. The proportions of collagen types I and II in the repair tissue were assessed by electrophoresis of their cyanogen bromide-cleaved peptides on sodium dodecyl sulfate slab gels. Peptide ratios were computed and compared with those of standard mixtures of type-I and type-II collagens. Galactosamine and glucosamine contents were determined by use of ion chromatography. In general, the biochemical composition of repair tissue of grafted and nongrafted defects was similar, but clearly differed from that of normal articular cartilage. Total glycosaminoglycan content, galactosamine and glucosamine contents, and galactosamine-to-glucosamine ratio of grafted and nongrafted defects were all significantly (P < 0.05) less than corresponding values in normal equine articular cartilage. By contrast, total collagen content of neocartilaginous tissues of grafted and nongrafted defects was greater than that of normal articular cartilage, although the difference was not significant. The proportion of type-I and type-II collagens in repair tissue in grafted and nongrafted defects was 70 and 30%, respectively. The fibrous nature of the repair tissue reported in a companion morphologic and histochemical study was substantiated by the biochemical results. We concluded that use of periosteal autograft did not improve the healing of osteochondral defects.

Nine 115- to 180-kg, hay-adapted, Holstein steers were fed an experimental diet with added sodium sulfate that induces polioencephalomalacia (PEM). Five calves developed the disease. Thiamine concentrations in blood, CSF, brain, and liver were not indicative of thiamine deficiency. The odor of hydrogen sulfide in eructated rumen gas was associated with the onset of PEM. Sulfide concentrations in rumen fluid were measured 1 or 2 times a week by 2 techniques. Sulfide concentrations progressively increased in all 9 calves after the feeding of the PEM-inducing diet commenced. The highest concentrations coincided with the onset of clinical signs of PEM and were significantly higher in the calves that developed PEM than in those that did not. This suggests that PEM can result from sulfide toxicosis following excess production of sulfide in the rumen.

Canine and human platelets (washed 4 times in a solution containing EDTA, prostaglandin E1, and theophylline to prevent release of alpha-granule constituents) were lysed by being frozen and thawed in the presence of detergent. Radioelectroimmunoassay for von Willebrand factor (vWf) in 5 human platelet lysates produced precipitin rockets, shaped like those produced from vWf in plasma from healthy human beings, and indicated that the mean von Willebrand factor antigen (vWf:Ag) content in platelets from healthy human beings was 526 +/- 87 human U/10(12) platelets. Radioelectroimmunoassay for vWf in platelet lysates from 17 healthy dogs with normal plasma vWf:Ag concentration produced precipitin rockets that looked different from those produced from canine plasma and indicated vWf:Ag content of 59 +/- 35 canine U/10(12) platelets. Inclusion of protease inhibitors in the lysing solution did not normalize the appearance of the precipitin rockets or substantially alter the measured platelet content of vWf:Ag. The array of vWf multimers revealed by sodium dodecyl sulfate-agarose gel electrophoresis of canine platelet lysates had a distinct appearance that differed from that of vwf in canine or human plasma and platelets; the intensity of the canine platelet vWf multimer bands was skewed, with relatively greater density in the lower molecular weight region and faint or undetectable multimer bands in the higher molecular weight region. Electrophoretograms with visible multimers in the high molecular weight region had vwf components that had higher molecular weight than did any vWf components in canine plasma. Radioelectroimmunoassay for fibronectin in these same canine platelet lysates indicated that the fibronectin content in platelets was 2.89 +/- 1.10 mg/10(12) platelets. An Airedale Terrier with type-I von Willebrand disease (vWd), but lacking clinical signs of vWd, had normal platelet content of vwf:Ag (28 +/- 12 canine U/10(12) platelets), whereas a German Shorthaired Pointer with moderately severe type-II vWd and a mildly affected Doberman Pinscher with type-I vWd had only a trace or undetectable amounts of vWf:Ag in their platelets. The concentration of vWf:Ag in platelet lysates from the Doberman Pinscher with vWd remained undetectable when the platelets were isolated from the Doberman Pinscher's blood mixed with citrated plasma from dogs with normal plasma vWf:Ag concentration. In all 3 dogs with vWd, platelet fibronectin content was within the normal range.

Three commonly used keratin monoclonal antibodies (MAB)--AE1:AE3, CAM 5.2, and MAK-6--were compared with routinely used cytokeratin antibody. The expression of these antibodies was analyzed in several tissues obtained from clinically normal dogs and in a variety of neoplasms from dogs. Using appropriate enzymatic digestion, paraffin-embedded tissues processed in routine manner retained their typical keratin expression. Differentiated and poorly differentiated epithelial neoplasms, lymphomas, and melanomas were studied by use of the avidinbiotin-peroxidase technique. All 4 of the aforementioned antibodies had similar staining profiles. Of 3 anaplastic carcinomas, 2 had positive reaction to all 4 antibodies. All lymphomas, plasma cell tumors, and amelanotic melanomas had negative reaction to MAK-6, CAM 5.2, AE1:AE3, and cytokeratin MAB. Three basal cell epitheliomas had positive reaction to all 4 antibodies, whereas 1 basal cell tumor with a solid pattern had negative staining reaction. Two carcinoids had negative reaction to all markers and 1 of 2 malignant chemodectomas and 1 transitional cell carcinoma had staining reaction to only AE1:AE3 MAB. Comparing the 4 antibodies, use of AE1:AE3 MAB produced the strongest staining intensity followed by cytokeratin, MAK-6, and CAM 5.2 MAB. All 4 antibodies had low background staining. In conclusion, AE1:AE3 and MAK-6 MAB are as useful as cytokeratin MAB for identification of poorly differentiated epithelial neoplasms in dogs and cats.

To provide information about oncogenes for molecular biological studies of tumors in domestic animals, theproto-oncogenes homologous to the c-myc, c-erbB-2, c-ros-1, c-yes-1, v-myc, v-Ki-ras, and v-Ha-ras oncogenes of genomic DNA in cattle, horses, pigs, dogs, cats, and chickens were investigated by Southern blot hybridization. High molecular weight genomic DNA in each of the animals contained proto-oncogenes that had a certain homology with the oncogenes used, but the extent of nucleotide homology of the proto-oncogenes differed in number and molecular weight: ie, 1 or 2 bands at 1.6 to 22.0 kilobase (kb) in the c-myc probe, 1 or 2 bands at 1.1 to 16.0 kb in the c-ros-1 probe, 1 to 3 bands at 0.7 to 23.0 kb in the c-erbB-2 probe, 1 to 4 bands at 0.6 to 18.0 kb in the c-yes-1 probe, 1 to 3 bands at 1.6 to 30.0 kb in the v-myc probe, 1 to 7 bands at 1.0 to 36.0 kb in the v-Ki-ras probe, and 1 to 4 bands at 1.0 to 27.0 kb in the v-Ha-ras probe. Furthermore, signal strength of each band, as determined by autoradiography, was not always the same for each probe in the various animals. Our findings indicate that these proto-oncogenes are well conserved with species specificities in each animal.

In the silver fox, as in its wild ancestor, the red fox (Vulpes vulpes L.), the annual growing phase (anagen) of guard hair follicles occupies at least four months. Severe damage to the hair coat near the end of this growing period was reported in 1985 on many ranches in New Brunswick and Nova Scotia. A histological analysis of serial sections of skin biopsies showed a marked increase in nuclear aberrations in the hair matrix of anagen guard hair follicles. These nuclear aberrations indicated that cells were undergoing apoptosis, a controlled form of cell death. Tissues from affected and unaffected foxes for histological and toxicological analysis, as well as other data, were obtained during visits to 26 ranches in 1986 and 34 ranches in 1987. Histological sections of the 1987 skin samples showed the mean percentage of nuclear aberrations in 43 unaffected foxes to be 0.08 +/- 0.01 (SEM), while that for 49 affected foxes was 0.51 +/- 0.23. The four foxes with the most severe coat damage also had the highest incidences of guard hair matrix cells with nuclear aberrations, ranging from 20 to 100 times greater than the mean for unaffected foxes. The mitotic index of the hair matrix, which normally remains fairly constant during the hair growth phase, was similar for unaffected and affected foxes (1.83 + 0.06 and 1.97 +/- 0.07 respectively). Although our analyses of field data have not established a specific environmental factor associated with increased nuclear aberrations, the possible involvement of toxic agents in follicle damage may warrant further investigation.

The effect of intestinal microflora on digestible energy (DE) value and fiber digestion was studied in single-comb White Leghorn chickens fed a low-fiber diet (experiment 1) or a high-fiber diet with low or adequate metabolizable energy (ME) value (experiment 2). Fecal energy excretion was calculated from the difference between total energy excretion in urinary and fecal droppings and urinary energy excretion, which was estimated from the energy values for individual urinary nitrogenous compounds extracted with Li2CO3. When the birds were fed the low-fiber diet, no differences in growth, DE, or ME were observed between germ-free and conventional environments. Of birds fed the high-fiber diet, growth of those in the conventional environment was similar to that of the birds in the germ-free environment at the adequate ME value, whereas birds in the conventional environment grew faster than the birds in the germ-free environment at the low ME value. Changes in observed dietary ME values of the high-fiber diets, being higher in birds in the conventional environment than in birds in the germ-free environment (experiment 2), were almost entirely accounted for by those in dietary DE values, most of which was contributed by crude fiber digestion. It was concluded, therefore, that by means of fiber digestion, the intestinal microflora may benefit the host bird by supplying extra energy, which would result in growth promotion, particularly when the bird is deficient in energy.

Detection of capsular polysaccharide (CP) in milk of cows with natural intramammary infection caused by Staphylococcus aureus was attempted. Five quarters of 5 cows harboring S aureus strains that produce type-8 CP were selected. Using an ELISA with a monoclonal antibody, type-8 CP was not detected in extracts prepared from fresh milk collected aseptically. By contrast, CP was easily detectable after incubation of infected milk at 38 C for 20 hours. Quantitation of CP in extracts from incubated milk samples by use of ELISA indicated a great variation of CP expression by strains. Although an incubation step was necessary to detect CP, results of the study indicate that CP may be expressed in vivo during intramammary infection caused by S aureus.