Quantitative evaluation of neutrophil chemotaxis was performed on cells obtained by hypotonic-lysis techniques from heparinized blood samples from clinically normal dogs. The techniques resulted in neutrophil recovery rates between 60 and 80%. Chemotaxis comparisons were based on cellular migration in microchambers equipped with polycarbonate membranes with 5-micrometer pores. Chemo-attractant comparisons were based on neutrophil migration to medium, normal canine plasma, zymosan-activated plasma, and xanthine oxidase. Cellular migration to zymosan-activated plasma in buffer (1:100 dilution) was significantly (P less than 0.001) enhanced over random baseline medium migration. Neutrophil migrations to normal canine plasma and xanthine oxidase were quantitatively less than to zymosan-activated plasma, but were equivalent to each other and significantly greater than for random migration. Migration to xanthine oxidase was maximal at concentrations near 1 U/ml within 30 minutes.

The restriction endonuclease digestion DNA patterns from Brucella abortus strains 19 and 2308 were examined with 11 restriction enzymes (AvaI, BamHI, BglII, BstEII, DdeI, EcoRI, HindIII, KpnI, PstI, XbaI, and SalI)). The DNA electrophoretic banding patterns between the strains were highly similar, using this restriction enzyme analysis. Differences were not discernable between B abortus strains 19 and 2308 in any of the restriction banding patterns examined. Methylation at CCGG or GATC sites was not detectable on the basis of digestion with isoschizomers (HpaII and MspI, and DpnI, Sau3AI and MboI). Homology between B abortus strains 19 and 2308 was assessed, using solution-hybridization techniques followed by S1 nuclease assays. Results of these reassociation experiments indicated 98.6 to 99.3% homology between B abortus strains 19 and 2308 with 13.5 to 18.6% homology between B abortus (strains 19 and 2308) and the E coli HB101 control. We concluded that any DNA differences between the 2 B abortus strains are small and will require analysis at the DNA sequence level.

Lesions in 32 calves that died or were euthanatized during the course of severe natural infection with bovine respiratory syncytial virus (BRSV) are described. All calves had been dyspneic for 1 to 2 days. At necropsy, lesions that could be related to dyspnea included congested and cyanotic mucosae and widespread petechiae. The lungs had various lesions in the cranioventral (CV) and caudodorsal (CD) portions. The CV portion of the lungs was consolidated, firm, and edematous. Histologically, the main characteristic was degenerative, necrotic bronchiolitis, with few syncytial cells. Signs of repair, such as epithelial hyperplasia, fibrosis, and bronchiolitis obliterans, often were observed. The CD portion of the lungs was markedly distended, owing to severe edema and emphysema. Bronchiolar lesions were lacking in the CD portion. In 14 calves, hyaline membranes were seen in the CV and CD portions. Results of immunofluorescence for BRSV were positive in 24 calves, but only in the CV portion of the lungs. The calves had variable concentrations of BRSV-specific IgG1 and IgM in serum, lung lavage fluid, or both. The BRSV-specific IgA, on the contrary, was seldom detected. Thus, 2 discrepancies existed. Although the clinical picture appeared to be acute, bronchiolar lesions and serotest results suggested infection of longer duration. Also, although virus and viral cytopathologic features were detected only in the CV portion of the lungs, the CD portion had extensive lesions that consisted of emphysema and edema.

We evaluated the efficacy of buparvaquone in eliminating Babesia equi of European origin in carrier horses and in experimentally infected splenectomized ponies. When administered at the rate of 2.5 mg/kg of body weight, IM, 4 times at 96-hour intervals, buparvaquone was effective in eliminating B equi carrier infection in 1 horse. Such results could not be repeated at the same dosage or at 3.5 or 5 mg/kg, IM. Buparvaquone given at the rate of 4 to 6 mg/kg IV and/or IM was therapeutically effective in 4 of 5 acute B equi infections in splenectomized ponies. The treated ponies became carriers.

Data were collected for 3,636 full-term pigs born in a commercial swine herd to determine the effects of birth weight and clinical disease on survival during the first 3 weeks of life. Logistic regression models were constructed for 7-day survival for all live-born pigs, and for 21-day survival for pigs surviving the first week of life. Estimates of birth weight and disease effects were adjusted simultaneously for other risk factors including litter size, parity, and within-litter variation in birth weight. The 7-day survival model indicated that survival odds improved significantly with increasing birth weight. Maximal survival, relative to pigs weighing less than 601 g at birth, was evident in pigs weighing greater than 2 kg atbirth (odds ratio [OR] = 349). Diarrhea (OR = 2.7) and splayed limbs (splay leg; OR = 37.3) significantly (P less than 0.05) reduced 7-day survival. Models of 21-day survival indicated a smaller, but still significant, effect of birth weight on survival. Adjusted survival odds for pigs in the heaviest weight group (greater than 2 kg) were 20.1 times higher than pigs weighing less than 801 g. Diarrhea (OR = 2.7) and lameness (OR = 2.6, 2 limbs) significantly (P less than 0.05) decreased 21-day survival.

Hereford heifer calves were experimentally infested with Psoroptes ovis. Histologic examination of skin specimens was conducted at weekly intervals before and after treatment with ivermectin on postinfestation week 7. Electron microscopy revealed numerous degranulating mast cells in the skin of infested but not in control calves. Many active, as well as degenerate, neutrophils were in the scab on infested calves. Microscopic epidermal ulcers developed on infested calves when live mites were present but not after treatment. Numbers of dermal neutrophils and plasma cells decreased and numbers of circulating neutrophils increased 1 week after treatment. Numbers of dermal eosinophils and mast cells in calves with eosinophilia increased for several weeks after treatment. Statistical analysis indicated significant correlations (P less than 0.05) among numbers of dermal inflammatory cells, hemogram values, and changes in dermal thickness. Seemingly, mite-induced epidermal damage was the key pathogenic event in psoroptic scabies in calves. Mast cell degranulation contributed to the pathogenesis of the dermatitis, and neutropenia was caused by sustained, poorly compensated efflux of neutrophils into the scab through mite-induced breaks in the epidermis.

Capsular polysaccharide (CP) of Pasteurella haemolytica (type A1) was first deposited by fiberoptic bronchoscopy in the lungs of sheep to examine lesions and changes in bronchoalveolar lavage cell populations and, later, was mixed with pulmonary surfactant to investigate alterations in physical properties or surface tension. At 22 hours after deposition, minimal lesions were seen in the lungs only at and contiguous to the site of CP deposition in 2 of 4 sheep. Microscopically, alveoli and interlobular septa were filled with edema fluid. Terminal airways and alveoli contained a moderate amount of neutrophils that varied between sheep. Significant differences in number or type of bronchoalveolar lavage cells were not observed in the weekly lavages between each group or among sheep within each group, either before or after deposition of CP or physiologic saline solution. After 6 hours of incubation at 37 C, CP-surfactant mixtures were examined with a surface tensiometer and centrifuged in sucrose gradients. The CP bound to surfactant, resulting in formation of a precipitate with a surface tension of 31.6 +/- 0.1 dynes/cm and a density of 1.07 to 1.08 g/ml. Lipopolysaccharide of P haemolytica, used as a control, also bound to surfactant, resulting in a complex with a surface tension of 57.7 +/- 0.4 dynes/cm and a density of 1.06 to 1.10 g/ml. Surfactant alone had a surface tension of 32.6 +/- 0.2 dynes/cm and density of 1.05 to 1.06 g/ml. The CP appears by itself not to be a direct major factor in the lung damage that develops in cases of pneumonic pasteurellosis. However, the precipitation of surfactant by CP may be a lectin reaction that would allow the attachment of the organism to the lining of the alveolus and become established during an infection.

The abdominal portion of the aorta was catherized in 27 cows. Local analgesia was achieved by infiltration of anesthetic agents. A 10-cm skin incision was made caudal and parallel to the 13th rib at the lateral border of the epaxial muscles. The dorsal costoabdominal artery was exposed at its first lateral cutaneous branch by careful dissection through fascial layers. A sterile polyvinyl catheter (1.52 mm OD) was inserted into the artery and was advanced 35 to 40 cm to the abdominal portion of the aorta. Catheter patency was maintained for up to 5 weeks. Concentrations of plasma progesterone and estradiol-17 beta in samples obtained from the abdominal portion of the aorta were similar to simultaneously obtained concentration in samples from the jugular vein before and after parturition.

Microvascular circulation of the ascending colon in healthy horses was studied using microangiography, light microscopy, and scanning electron microscopy. The pelvic flexure with 30 cm of ventral and dorsal colon attached was removed from 14 adult horses immediately after horses were euthanatized. The lumen was flushed with warm water, and this section of the ascending colon was placed in a 37-C bath of isotonic NaCl. In sections from 8 horses, colic vessels were perfused with a radio-opaque medium for microangiography. After angiographic evaluation, tissue sections were prepared for light microscopic observation, using standard histologic methods. In sections from 6 horses, injection replicas were made by perfusing the vessels with 2 types of plastics. The results of microangiography, light microscopy, and scanning electron microscopy of vascular replicas were correlated, providing acomprehensive documentation of the microvasculature of the ascending colon at the pelvic flexure. Arteries branched from mesenteric colic vessels approximately every 2 cm toward the colonic tissue. Immediately after branching, arterial vessels formed an anastomotic plexus, the colonic rete. However, each branch from the colic vessel eventually continued into the colonic tissue. A second set of vessels originated from the colonic rete and supplied the mesenteric lymph nodes. Arterial vessels penetrated the tunica muscularis into the sub-mucosa 3 to 4 cm toward the antimesenteric border forming a submucosal vascular network. From the submucosal arterioles, branching took place at right angles to supply the mucosal capillaries. Capillaries surrounded the colonic glands and anastomosed at the luminal surface, forming a superficial luminal honeycomb-appearing vascular plexus. Venules, sparsely distributed, drained the superficial plexus. Arterial venous anastomoses were not observed within the mucosa.

The normal radiographic anatomy of the equine larynx was determined by use of xeroradiography and dissection. The body and laminae of the thyroid cartilage, the muscular process of the arytenoid cartilages, and the dorsal lamina and arch of the cricoid cartilage had radiographic evidence of mineralization (calcification) and/or ossification in clinically normal horses. There was a significant (P less than 0.01) increase in the degree of mineralization of the thyroid and arytenoid cartilages with advancing age. Horses with diagnosis of arytenoid chondrosis (arytenoid chondral dysplasia, arytenoid chondropathy) by use of endoscopy had radiographic changes that included: enlargement with increased density of the arytenoid cartilage region, abnormal patterns of mineralization (dystrophic mineralization or osseous metaplasia), abnormal contour of the corniculate process(es) and laryngeal masses, sometimes obliterating part or all of the lateral laryngeal ventricles.