Cardiopulmonary function values were determined before and after surgical removal of adult heartworms in 25 dogs with spontaneous and 4 dogs with drug-induced caval syndrome (CS). Fifteen dogs with spontaneous CS (recovery group) and 4 dogs with drug-induced CS (drug-induced CS group) recovered after removal, and 10 dogs with spontaneous cs were euthanatized or died (nonsurviving group). Before heartworm removal, injected radiographic contrast medium was regurgitated from the right ventricle to the right atrium. Mean pulmonary arterial pressure and total pulmonary resistance were not statistically different between the recovery and nonsurviving groups of dogs, but the end-diastolic right ventricular pressure (mean +/- SD, 6.9 +/- 9.1 mm of Hg) and the a (8.7 +/- 9.2 mm of Hg)- and v (6.3 +/- 8.5 mm of Hg)-waves of the right atrial pressure curve in the recovery group were less, respectively, than the end-diastolic right ventricular pressure (17.3 +/- 6.0 mm of Hg) and the a (15.8 +/- 6.1 mm of Hg)- and v (21.4 +/- 6.9 mm of Hg)-waves in dogs of the nonsurviving group. After heartworm removal, contrast medium regurgitation disappeared, and cardiac output of the right ventricle increased in dogs of the recovery (from 2.08 +/- 0.72 to 2.38 +/- 0.68 L/min; P < 0.05) and drug-induced CS (from 1.42 +/- 0.19 to 1.88 +/- 0.26 L/min, P < 0.05) groups. However, regurgitation remained, and cardiac output did not increase in some dogs of the nonsurviving group. Mean pulmonary arterial pressure decreased significantly (from 37.7 +/- 18.3 mm of Hg to 32.0 +/- 16.1 mm of Hg; P < 0.01) at 1 week after heartworm removal in dogs of the recovery group, but not in those of the nonsurviving group. Total pulmonary resistance (from 12,612 +/- 7,670 dynes.sec.cm-5.kg of body weight to 9,776 +/- 6,089 dynes.sec.cm-5.kg; P < 0.01) and right atrial pressure (a-wave: from 8.7 +/- 9.2 mm of Hg to 4.1 +/- 5.6 mm of Hg; v-wave: from 6.3 +/- 8.5 mm of Hg to 2.1 +/- 4.6 mm of Hg) decreased after heartworm removal in dogs of the recovery group. Total pulmonary resistance (from 20,309 +/- 9,682 dynes.sec.cm-5.kg to 15,970 +/- 6,798 dynes.sec.cm.5.kg; P < 0.05) and right atrial pressure (a-wave: from 15.8 +/- 6.1 mm of Hg to 10.1 +/- 6.3 mm of Hg; v-wave: from 21.4 +/- 6.9 mm of Hg to 11.1 +/- 3.7 mm of Hg) also decreased in dogs of the nonsurviving group. However, pressures in the right side of the heart and total pulmonary resistance after heartworm removal were greater in dogs of the nonsurviving group than in dogs of the recovery group. At necropsy pulmonary arterial emboli containing dead heartworms were found in almost all dogs with spontaneous CS, but not in dogs with drug-induced CS. The severity of pulmonary arterial embolism correlated significantly with mean pulmonary arterial pressure before (r = 0.710; P < 0.01) and 1 week after (r = 0.728; P < 0.01) heartworm removal.

Thirty-six of 50 young equids examined at necropsy for gross pathologic and histopathologic evidence of osteochondrosis were determined to have lesions characteristic of this disorder in the distal joints of the tarsus. Abnormalities ranged from retained endochondral cores underlying undisturbed articular cartilage surfaces to clefts, subchondral osseous cyst-like lesions, and cartilage ulceration. Our findings supported the conclusion that osteochondrosis may cause spavin in the juvenile equid.

Milk samples were collected at onset of 508 episodes of clinical mastitis on a 1,700-cow dairy farm in Michigan. Daily milk production and disease events were recorded for all cows in the herd. Despite statistical association with severity of mastitis, this association was too weak for N-acetyl-beta-D-glucosaminidase (NAGase) activity to be of great value as a prognostic test for clinical mastitis. High milk NAGase activity was significantly (P < 0.0001) associated with: increased duration of treatment; increased duration of clinical signs of mastitis; decreased daily milk production; and increased risk of the cow being culled because of mastitis. The NAGase value was combined with days in milk production, baseline milk production before mastitis onset, parity, and season of onset to predict the outcome of clinical cases as measured by the first 3 aforementioned variables. Statistical models explained little of the variability among cows in duration of treatment (R2 = 0.11), duration of clinical signs of infection (R2 = 0.11), and milk production change (R2 = 0.09).

Evaluation of pudendal reflexes and effects of pudendal branch conditioning on those reflexes was carried out in 2 studies. In the first study of pudendal reflexes, 20 adult male and female mixed-breed cats underwent surgical isolation of the anal branch, urethral branch, and distal trunk (consisting primarily of the dorsal nerve of the penis/clitoris) of the pudendal nerve. Reflexes were tested in all possible ipsilateral and contralateral test-response combinations. Latency values and effects of increasing stimulus rate on response amplitude were recorded. Reflexes were detected in all combinations, with response latencies between 6.3 and 13.0 ms. Response amplitudes were diminished at stimulus rates of 3 to 5 Hz, and responses were apparently abolished at 4 to 16 Hz, suggesting that pudendal reflexes are polysynaptic. In the second study of conditioning effects, 9 adult male and female mixed-breed cats underwent preparation similar to that for study 1. A train of conditioning stimuli was applied to branches of the pudendal nerve prior to attempting to induce reflex responses, as performed in study 1. Conditioning completely abolished reflex responses for a period of 70 to 130 ms. Reflex responses were diminished in amplitude, compared with those observed during preconditioning trials, for 180 to 300 ms after conditioning.

A series of experiments was performed in vitro and in vivo to determine the influence of FK-565, a heptanoyl tripeptide, on lymphocyte and macrophage function in swine. Compared with values for control cultures, mitogen-stimulated lymphocyte blastogenesis and interleukin-2 production were unaffected in cells preincubated with 0.1, 1.0, and 10.0 microgram of FK-565/ml. Natural killer cell activity was increased by preincubation with 1.0 microgram of FK-565/ml; however, this increase was not statistically significant. In vitro treatment of porcine alveolar macrophages with FK-565 did not enhance cytolytic activity or bactericidal activity. In in vivo experiments, FK-565 given orally to pigs at concentrations of 6 or 60 microgram-kg-l.-d-1 for 5 days did not affect lymphocyte blastogenesis, interleukin-2 production, or alveolar macrophage bactericidal activity. A trend toward increased natural killer cell activity was evident in pigs treated with FK-565. In contrast, pigs treated with 6 microgram-kg-1.-d-1 had significantly (P less than 0.01) decreased alveolar macrophage cytolytic activity. These data indicate that at the dosages tested, FK-565 is not a suitable immunomodulator for enhancement of nonspecific immunity in swine.

The relationship of muscle and bone structure to limb weakness was examined in 60 Duroc pigs from 3 lines divergently selected for thoracic limb weakness. The lines were designated high, control, or low, with the low line having inferior thoracic limb structure. At approximately 100 kg, 10 pigs of each line and gender were scored for thoracic limb structure and movement. Right and left thoracic limbs were collected at slaughter. A computerized morphometric image analysis system was used to determine cross-sectional areas of muscles, bones, and soft tissues at levels through the brachium, antebrachium, metacarpus, and digits. The statistical model that was used to analyze the data included the effects of line, sire, gender, and side (left vs right), with weight as a covariate. Total bone area was similar for all 3 lines of pigs at all cross-sectional levels, but significant differences in muscle and other soft tissue areas were observed, including significantly greater extensor area for the antebrachium (P less than 0.001) in low-line pigs than in control- and high-line pigs, smaller total area (P less than 0.05) of the metacarpus in low-line pigs than in control and high-line pigs, and less total area of the medial digit (P less than 0.01) in low-line pigs than in control- or high-line pigs. Total area of bone and soft tissue for each cross-sectional region was significantly greater (P less than 0.05) in boars than in gilts. Side differences also were observed in total cross-sectional areas of bone and soft tissue of the antebrachium, metacarpus, and digits. Pigs selected for inferior thoracic limb structure had less total soft tissue cross-sectional areas in distal limb regions than did control- or high-line pigs. Limb weakness may be related to altered distribution of soft tissue supporting structures of the thoracic limb.

Blood, feces, nasal secretions, and tears werecollected weekly from 5 randomly selected 1- to 8-week-old calves in a large commercial dairy herd. Clinical signs and bovine coronavirus (BCV) shedding from the respiratory and enteric tracts of calves were monitored through the 8-week period by direct immunofluorescence of nasal epithelial cells, protein A-gold immunoelectron microscopy on feces, and ELISA on nasal secretions and feces. All samples were analyzed for antibody isotypes to BCV structural proteins by immunoblotting. All calves had BCV respiratory tract infections and 4 of 5 calves shed virus in feces. Several calves had multiple or prolonged periods of BCV respiratory tract or enteric tract shedding or both. All calves (except 1) had passive IgG1 antibodies to some BCV proteins (mainly the E2 and E3 proteins) in their serum when they were 1 week old. The presence of these passive serum antibodies (mainly to the E2 and E3 BCV proteins) was associated with decreased or delayed systemic and mucosal antibody responses in calves, in particular IgA responses in nasal secretions and tears to the E2 and E3 BCV proteins, but not to the N protein. Moderate amounts of maternal BCV E2- and E3-specific antibodies in serum did not prevent BCV enteric tract or respiratory tract infections in calves, but may have delayed the development of active antibody responses to these BCV proteins. However, calves with BCV respiratory tract or enteric tract infections had no detectable passive antibodies to any BCV proteins in nasal secretions or feces.

The beige (bgJ/bgJ) mouse is a well-described murine model of Chediak-Higashi syndrome. Platelet function was examined in normal and beige mice to better characterize the defective aggregation response in platelets from mice with Chediak-Higashi syndrome. Platelet aggregation after collagen, thrombin, and phorbol-12-myristate 13-acetate stimulation was significantly (P < 0.025) decreased in platelets from beige mice, relative to platelets from normal mice. Compared with beige and normal mice, those heterozygous for the bg trait had intermediate responses to collagen and thrombin, but not phorbol-12-myristate 13-acetate. The defect(s) in aggregation of platelets from beige mice was associated with a dense granule storage pool deficiency and decreased stores of serotonin and adenine nucleotides in platelets. Mice heterozygous for the bg trait had normal platelet serotonin and adenine nucleotide concentrations. Platelets from beige mice were approximately 10 times more sensitive to prostacyclin inhibition of collagen-induced aggregation than were platelets from control mice. However, a significant difference in platelet cyclic AMP concentration was not apparent between beige and normal mice after prostacyclin stimulation. Platelet endoperoxide synthesis measured by quantification of thromboxane B2, was normal in beige mice. Protein phosphorylation patterns in mouse platelets were similar to those seen in human platelets. Thrombin and collagen-induced [32P] phosphorylation of 40- and 20-kD proteins in platelets from normal and beige mice was similar. Results indicate that the biochemical defect(s) in platelet function in beige mice is partially attributable to storage pool deficiency and does not result in an absolute defect in phosphorylation of 40- and 20-kD proteins.

Twenty-six clinically normal colostrum-fed dairy calves were allotted to 5 groups. Calves of groups 1 and 2 served as nonvaccinated controls and were challenge-exposed with variable numbers of organisms. Group-3 calves were vaccinated SC with a modified Salmonella typhimurium bacterin. The bacterin was composed of killed acid-hydrolyzed S typhimurium G30/C21 (Re-mutant) whole cells coated with alkali-hydrolyzed S typhimurium LT-2 lipopolysaccharide, as antigen, and monophosphoryl lipid A, as adjuvant. Calves of groups 4 and 5 were vaccinated with a 2% mineral oil-in-water emulsion containing lipopolysaccharide as antigen and monophosphoryl lipid A and trehalose 6-6'-dimycolate as adjuvants. Calves of groups 3-5 were vaccinated at 2 weeks of age and again at 4 or 6 weeks of age. Adverse reactions were not observed after vaccination. Calves were challenge-exposed orally at 6 or 8 weeks of age with 1.5 X 10(11) (groups 1 and 4), or 3.0 X 10(11) (groups 2, 3, and 5) colony-forming units of S typhimurium UCD 108-11. Mortality after challenge exposure was 2 of 5 group-1 calves; 4 of 5 group-2 calves; 5 of 6 group-3 calves; 1 of 5 group-4 calves; and 4 of 5 group-5 calves. Statistical difference between calves of similarly challenge-exposed groups was not evident, indicating failure of either vaccine to protect calves of this age from oral challenge exposure with virulent S typhimurium.

Blood culture and serologic testing were used to study the prevalence of Trypanosoma cruzi infection in a group of 85 dogs from southern Louisiana rural environment. These dogs were known to have been in contact with wild mammalian hosts of the hemoflagellate. Results were compared with blood culture and serologic test results in 103 dogs from a rural environment and with limited known wild mammalian T cruzi host contact. Serologic test results for the 188 dogs from the rural environment were compared with results for 176 dogs from an urban animal shelter and for 100 household pet dogs from an urban southern Louisiana environment. Blood culture was not performed on urban dogs. Culture results were negative in all dogs from rural environments. Serologic evidence of infection was obtained for 4 of the 85 (4.7%) dogs of rural environment with known host contact. Of 176 dogs from the animal shelter, 4 (2.3%) had high antibody titer to T cruzi, and 11 others had low titer (< 2 adjusted ELISA units [aEU]). Two and 4 dogs of the housed urban and rural groups, respectively, had antibody titer to T cruzi that was < 2 aEU. Results indicate that prevalence for exposure to T cruzi antigen is higher in dogs with high potential contact with the vector and wild mammalian hosts of T cruzi, whether they are from rural or urban environment. Furthermore, results indicate that similar studies on high-risk human populations may be indicated.