The sense of smell in dogs infected with canine distemper virus (CDV) was examined by use of EEG olfactometry, behavioral olfactometry, and electro-olfactography. Infection with CDV was confirmed by a direct immunofluorescence technique in 8 active cases and was suggested by clinical history compatible with canine distemper 10 to 26 weeks earlier in 6 cases. Pathologic alterations of the olfactory mucosa in 3 clinically affected dogs was examined by light microscopy. Infection with CDV was found to be associated with anosmia and lack of recorded responses on electro-olfactogram in 8 of 8 dogs with clinical signs of acute distemper from naturally acquired infections. Anosmia was found in 5 of 6 dogs that had recovered from acute distemper 10 to 26 weeks earlier. The sixth dog had hyposmia, with abnormalities on the electro-olfactogram. Histologic examination was not performed on the 6 dogs that had recovered. Histologic lesions observed at necropsy in 3 dogs that had had clinical signs of acute distemper were those of subacute purulent rhinitis and atrophy of the olfactory epithelium. Altered olfactory function could be explained by mucopurulent exudate blocking odors from olfactory receptors in the acutely affected dogs, but alteration of olfactory function in the dogs that had recovered without clinical evidence of rhinitis could not be explained.

The minimum anesthetic dose (MAD) and the cardiopulmonary dose-response for halothane were determined in male chickens. The MAD for halothane was 0.85 +/- 0.09% (mean +/- SD), with a range of 0.75% to 0.98%. There was a significant (P less than 0.002) positive correlation between increasing concentrations of halothane and PaCO2, and significant negative correlations of halothane concentration with respiratory rate (P less than 0.04), arterial blood pH (P less than 0.008), and mean arterial blood pressure P less than 0.008). A significant correlation was not found between halothane concentration and heart rate or arterial blood bicarbonate concentration. It was concluded that the MAD for halothane in chickens is similar to values for minimum alveolar concentrations of halothane in mammalian species, and that there is substanial dose-dependent depression of cardiopulmonary function in chickens.

Bovine fibroblast interferon (BoF-IFN), produced in bovine embryonic kidney cell cultures by priming and infection with bluetongue virus, was partially purified by controlled pore glass chromatography. The partially purified B0F-IFN then was subjected to beaded agarose affinity chromatography. The IFN eluted by affinity chromatography in 2 distinct fractions-1 after the addition of 1M NaCl and the other one after the addition of 1.5M NaCl containing 50% ethylene glycol. Analysis of fractions by sodium dodecyl sulfate/polyacrylamide-gel electrophoresis revealed a broad molecular weight range (14,900 to 27,900) for the IFN eluted by 1M NaCl, and 2 discrete molecular weight ranges (16,000 to 19,500 and 28,300 to 34,000) for IFN eluted by 1.5M NaCl containing 50% ethylene glycol. The specific activity of the IFN eluted with 1.5M NaCl containing ethylene glycol was 2.85 X 10(6) U/mg of protein, compared with 5.7 X 10(5) U/mg of protein in the controlled pore glass-purified IFN.

Relative pathogenicity of 151 Escherichia coli isolates from 36 calves with bacteremia after necropsy was studied by measurement of the LD50 after mice were inoculated IP with E coli isolates. Study of virulence factors and markers revealed that the pathogenicity of E coli was associated with the production of hydroxamate siderophores and with resistance to serum bactericidal effects. Production of colicins, including colicin V, and of surface antigen 31A was correlated with virulence. The close association between phenotypic expression of virulence factors and markers was consistent with a hypothesis of a localization of genes coding for virulence factors and markers on the same plasmid.

Fifty-five horses were inoculated IV and/or SC with materials containing Ehrlichia risticii, ie, infected whole blood, buffy coat cells, or cell culture, to study clinical and hematologic features of equine monocytic ehrlichiosis (Potomac horse fever). Major clinical and hematologic features of induced E risticii infection were biphasic increase in rectal temperature with peak increases of 38.9 C and 39.3 C on postinoculation days (PID) 5 and 12, respectively; depression; anorexia; decreased WBC count (maximal decrease of 47% on PID 12); and diarrhea from PID 14 to PID 18. Increased WBC count was an inconsistent feature, with a maximal increase of 51.5% on PID 20. During times of decreased and increased WBC counts, lymphocyte/neutrophil ratios remained fairly constant. However, not all horses had all clinical and hematologic features, and these features were present in different degrees among horses. Increased rectal temperature, depression, anorexia, and decreased WBC count were more consistent features, whereas diarrhea developed in 73% of the horses. Of 55 horses, 39 (71%) had all clinical and hematologic features of the disease (classic disease), whereas 16 (29%) horses did not have greater than or equal to 1 of these features (nonclassic disease). The E risticii titer in the blood (ehrlichemia) was maximum during the peak increase in rectal temperature. In 55 horses, mortality was 9%. Significant differences (P > 0.5) in clinical and hematologic features were not detected between horses that survived and those that died of E risticii infection.

A kinematic analysis of the instant centers of rotation analysis was performed on 21 metacarpophalangeal joints from 11 horses. Manual and computerized methods were used to locate the instant center of rotation on photocopies of transparent composite tracings of a series of radiographs of each joint. The instant centers of rotation of the proximal phalanx about the distal portion of the third metacarpal bone were located consistently on or near the eminence for attachment of the collateral ligaments. The instant centers of rotation of the sesamoids about the distal portion of the third metacarpal bone were consistently located near the dorsal articular margin of the distal portion of the third metacarpal bone. Rotation of the joint as it extended caused minor variation in radiographic projection. This variation in radiographic projection limited the precision of the analysis of the instant center of rotation and prevented the identification of a single instant center of rotation or an instant center of rotation pathway for the articulation of the proximal phalanx or the proximal sesamoids with the distal portion of the third metacarpal bone. The articular surface velocity vectors determined from the instant centers of rotation indicated that the joint surfaces slide on each other. The motion of the joint caused compression at the dorsal articular margins at maximal extension and thereby limited further extension. At this degree of extension, the proximal sesamoidsarticulated only with the proximal sesamoid-metacarpal articular surface of the distal portion of the third metacarpal bone.

During initial studies, we found that many fluorescein isothiocyanate-labeled anti-immunoglobulin conjugates were unstable and tended to aggregate and precipitate when used for indirect immunofluorescence microscopy. In some instances, the precipitate was extensive enough to interfere with interpretation of the test results. Attempts to resolve this problem resulted in a procedure by which such conjugates were digested with papain to Fab and Fc fragments before use. Aggregation and precipitation were prevented, while desired antibody activity was retained. Digestion with papain also reduced the diffuse background fluorescence (commonly referred to as nonspecific fluorescence or staining) that is often associated with conjugates before they are sorbed with tissue powders or chromatographed to remove highly labeled immunoglobulin molecules.

Bovine alveolar macrophages, obtained by bronchoalveolar lavage, were labeled with tritiated arachidonic acid. The cells were stimulated with calcium ionophore A23187, and the radiolabeled arachidonic acid metabolites that were released were identified by reverse-phase high-performance liquid chromatography. Leukotriene B4 and 5-hydroxyeicosatetraenoic acid were consistently observed. The lipoxygenase inhibitor, nordihydroguaiaretic acid, blocked production of these metabolites. The cyclooxygenase products, prostaglandin F2 alpha and thromboxane B2, were observed infrequently in comparison with leukotriene B4 and 5-hydroxyeicosatetraenoic acid.

Adherence of Streptococcus dysgalactiae isolates from cattle and S equi isolates from horses to their respective host epithelial cells was compared with the adherence of S pyogenes to human epithelial cells. The adherence was quantitatively determined by use of fluorescein-labeled streptococci. All 3 streptococcal species adhered selectively to their respective host cells. The mechanism of adherence was evaluated by binding studies with adhesive plasma protein, fibronectin. Although all 3 streptococcal species bound fibronectin, S dysgalactiae and S equi interacted preferentially with a 210-kilodalton (kD) C-terminal fragment of fibronectin, whereas S pyogenes bound only a 29-kD N-terminal fragment. A synthetic peptide Gly-Arg-Gly-Asp-Ser, representing the host cell attachment site of fibronectin, partially inhibited the binding of fibronectin and of its 210 kD fragment to S dysgalactiae, but not to S equi. The binding of fibronectin and its 29-kD fragment to S pyogenes was not inhibited by Gly-Arg-Gly-Asp-Ser. These differences in binding activities corresponded to the ability of fibronectin to mediate the adherence of the streptococci to the epithelial cells: fibronectin strongly inhibited the adherence of S pyogenes and S equi to the epithelial cells, but only weakly inhibited that of S dysgalactiae.

For 10 years, 42 female Herefords (as they progressed from weanling calves to aged cows) were fed diets individually, with phosphorus (P) content being the only variable. During growth and the first 3 gestations, clinically evident differences were not associated with 2 dietary treatments (approx 12 and 38 g of P/day). During the next 2 gestations (2 years), half the cows from each original treatment group were fed less than 6 g of P (n = 21 cows, 11 from the group fed 12 g of P/day and 10 from the group fed 38 g of P/day) daily. The other half were fed diets supplying approximately 8 g of P (n = 11 cows fed 12 g of P/day) and 35 g of P (n = 10 cows fed 38 g of P/day) daily. During the last 3 years of the experiment, all remaining cows were fed diets containing 12 g (n = 19 cows originally fed 12 g) or 19 g (n = 17 cows originally fed 38 g) of P/day. Cows fed diets containing less than 6 g of P/day developed an insidious and subtle complex syndrome characterized by weight loss, rough hair coat, abnormal stance, and lameness. Spontaneous fractures occurred in the vertebrae, pelvis, and ribs. In severely affected cows, fractures did not heal properly. Some bones were demineralized markedly, and the cortical surfaces were porous, chalky white, soft, and fragile. Osteoid tissue was not properly mineralized. Radiography revealed diminished bone density osteoporosis), cortical thinning, and resorption of trabeculae. Time-related availability of dietary P initiated excessive turnover of bone, with resultant structural changes and impaired function. Bone structure and general health of the P-deficient cows improved rapidly when they were fed a diet containing greater than 12 g of P/day.