The putative binding of porcine parvovirus (PPV) to semen components in vitro was examined along with the shedding pattern of PPV in oronasally infected boars. Porcine parvovirus DNA was determined to be bound to spermatozoa that had been incubated in vitro with PPV and washed to remove loosely adherent virus. To determine whether PPV was shed in the semen, four 8-month-old boars, seronegative for PPV, were inoculated oronasally with a virulent strain of PPV. Prior to virus inoculation, a catheter was surgically implanted in the vas deferens for the purpose of collecting cauda epididymal semen free of extrinsic contamination. Epididymal semen specimens were collected prior to inoculation and daily thereafter for 21 days. A fifth boar was inoculated oronasally with PPV, but semen was collected by electroejaculation twice weekly for an equal period of time. Reproductive glands and semen specimens from all boars were examined by nucleic acid hybridization for the presence of viral DNA. All boars seroconverted to PPV, as evidenced by serum antibody titers ranging from 512 to 8,192 hemagglutinating inhibition units/50 microliter. Porcine parvovirus DNA was detected in epididymal semen of 3 of 4 catheterized boars on postinoculation days 5 through 9, but not in semen obtained by electroejaculation. Viral DNA was consistently detected in tissue samples collected on postinoculation days 8 and 21 from the scrotal lymph nodes (4 of 5 boars) and epididymides (3 of 5 boars).

At an abattoir, lesion specimens from 140 condemned sheep livers were collected for bacteriologic culture and for pathologic examination. Grossly, 23 lesions were abscesses; from 9 of which, Fusobacterium necrophorum biovar A (3 in pure culture and 6 in mixed culture) was isolated and from 14 of which, biovar B (6 in pure culture and 8 in mixed culture) was isolated. Escherichia coli was the predominant facultative anaerobic bacterium and Clostridium perfringens was the predominant obligate anaerobic bacterium isolated from the 14 lesions with mixed bacterial infection. Histologically, these lesions had a core of coagulation necrosis, encircled by a zone of necrotic phagocytic cells and bacteria with cellular characteristics of F necrophorum biovars A or B, and a connective tissue capsule. Of the 117 lesions without F necrophorum, 49 were culture-positive (for other organisms) and 69 were culture-negative. These 117 lesions were fibrous and were smaller than the 23 abscesses. A variety of gram-positive and gram-negative facultative anaerobic and obligate anaerobic bacteria was isolated from the culture-positive lesions, but always in low numbers. Eleven culture-negative and 18 culture-positive lesions were examined and had histologic characteristics of parasite-induced granulomas, with numerous eosinophils and epithelioid giant cells. Results of the study indicated that the histologic appearance of ovine hepatic lesions with F necrophorum was similar to bovine liver abscesses caused by F necrophorum, but unlike bovine liver abscesses, F necrophorum biovar B was isolated more frequently than was biovar A and often in pure culture. Most of the lesions in the condemned livers were parasite-induced granulomas.

Five dogs with mucopolysaccharidosis I, 3 of which had been treated with bone marrow transplantation (BMT), were evaluated for 20 months with electrocardiography, thoracic radiography, and M-mode and 2-dimensional echocardiography. Treated and untreated (control) dogs had widened P waves on ECG. Thoracic radiographs remained normal for all dogs throughout the study. Thickening of the mitral valve was observed on echocardiograms of dogs in both groups, but the untreated dogs appeared to have thicker valves. Concentrations of glycosaminoglycans in the mitral valves and myocardium were higher in control dogs than in treated dogs. Markedly large aortic root diameters were observed on echocardiograms in both untreated dogs, but aortic root diameters remained normal in treated dogs. Echocardiography, but notelectrocardiography, was useful in monitoring heart enlargement in each dog. Dogs treated with BMT generally had less-severe cardiac changes and slower disease progression than control dogs.

To determine the effects of long-term thyroxine treatment, histomorphometric analysis was performed on the pituitary and thyroid glands of healthy dogs, dogs treated for 9 weeks with a replacement dose of L-thyroxine, and dogs at 6 weeks after cessation of thyroxine treatment. In treated dogs, the volume density of thyrotropes decreased during thyroxine treatment and increased 6 weeks after cessation of treatment, compared with thyrotropes of healthy nontreated dogs. The activity of the thyroid gland was decreased in dogs during thyroxine treatment, as evidenced by decreases in epithelial volume density, epithelial height, and follicular area, and increase in colloid volume density, compared with thyroid gland activity in nontreated dogs. After cessation of thyroxine treatment, the thyroid gland had decreased colloid area, follicular area, and epithelial volume density, and increased interstitial volume density, compared with the thyroid gland of healthy nontreated dogs. Thyroxine treatment resulted in suppression of pituitary thyrotropes and thyroid follicular activity.

The response of blood neutrophils to the chemotactic peptide formyl-methyl-leucyl-phenylalanine varies among species. Our results indicate that this peptide does not activate the respiratory burst of porcine neutrophils. Specifically, concentrations less than or equal to 10-6M did not cause production of either superoxide or hydrogen peroxide. Studies designed to delineate the biochemical deficit responsible for these results indicated that these cells do not express specific chemotactic peptide receptors on the external surface of the plasma membrane. Although these data do not rule out the possibility that internal stores of chemotactic peptide receptor exist, attempts to induce expression of the receptor by priming the cells with either lipopolysaccharide or calcium ionophore were unsuccessful.

This work was an attempt to develop an in vitro adherence model for Mycoplasma hyopneumoniae, using monolayers of human and porcine lung fibroblasts and porcine kidney cells. Mycoplasma hyopneumoniae grown in Friis mycoplasma broth was radiolabeled with 35[S]-methionine, washed, concentrated, and inoculated on the monolayers. After 15 minutes of centrifugation to facilitate adherence, monolayers were washed 3 times, dissolved with 0.1N NaOH, and suspended in scintillation liquid, and the radioactivity was determined in a liquid scintillation counter. Adherence, measured as a percentage of counts added, varied according to the mycoplasma strain and the cell line used. Comparison of strains J, 144L, and 232 of M hyopneumoniae revealed 7.5 +/- 5.9, 31.9 +/- 13, and 9.6 +/- 5% adherence to porcine kidney cells, respectively. Slightly different, but proportionally the same relationships were obtained with swine or human fibroblasts. Adherence was decreased slightly by repeated washings of the mycoplasma-treated cell monolayers; however, a plateau was reached, indicating irreversibility of the adherence process. Pretreatment of cell monolayers with nonlabeled organisms substantially blocked adherence by labeled organisms. Dilution of labeled organisms resulted in an increased proportion adhering. Therefore, it appears that the adherence was a receptor-dependent event. Treatment of the mycoplasmas with trypsin prior to the inoculation of monolayers resulted in a marked reduction in adherence. Treatment of the mycoplasmas with hyperimmune swine serum against M hyopneumoniae or normal swine serum resulted in 80 to 90% reduction of adherence; however, no inhibition occurred when mycoplasmas were treated with purified IgG from the hyperimmune serum.

The influence of variable zinc content (29.1, 250, 1,000 and 2,000 mg/kg of dry weight) in a basic diet containing 7.7 mg of copper/kg on the ability of weanling foals to maintain normal copper balance was investigated. Serum copper and zinc concentrations were monitored, and terminal hepatic copper and zinc contents were measured in 4 weanling foals fed the basic diet containing 29.1 mg of zinc/kg and in 2 foals each fed the higher-zinc diets. Foals fed the lower-zinc diets (29.1 and 250 mg/kg) maintained normal serum copper and zinc concentrations for 14 to 15 weeks, whereas those fed the 2 higher-zinc diets became hypocupremic within 5 to 6 weeks and were lame within 6 weeks, owing to cartilaginous disease characteristic of osteochondritis dissecans. Serum zinc concentration in the foals fed the 2 higher-zinc diets increased to > 2 microgram/ml within 2 weeks. Foals fed the high-zinc diets became lame after serum copper concentration had remained at 0.3 microgram/ml for > 1 week. Serum copper concentration in these arthritic foals was less than or equal to 0.2 microgram/ml at the end of the study. In lame foals, fractures of the cartilage of the articular and growth physes occurred through the zone of hypertrophic cells, and varied from bilateral to unilateral and from small to large. Free masses and flaps of cartilage attached to one side were numerous.

Eight adult female cattle (6 Holstein, 1 Jersey, 1 Brown Swiss) were used to determine the antagonistic effects of tolazoline, an alpha 2-adrenoceptor antagonist, on xylazine-induced (via caudal epidural administration) depression of CNS, respiratory, and cardiovascular activity and rumen motility. A 2% solution of xylazine HCl was injected into the epidural space at the first coccygeal interspace, using a dosage of 0.05 mg/kg of body weight, diluted to a 5-ml volume with sterile water, and administered at a rate of approximately 1 ml/30 s. Eight minutes after xylazine injection, either tolazoline (0.3 mg/kg) or saline solution (4 ml) was administered IV. All 8 cattle were treated, using both regimens in a random sequence; at least 1 week elapsed between treatments. Epidurally administered xylazine induced caudal analgesia (S3 to coccyx), as evaluated by no response to superficial and deep muscular pinprick, and induced sedation, cardiopulmonary depression, and inhibition of rumen motility, but all cattle remained standing. Tolazoline effectively reversed xylazine-induced rumen hypomotility, and partially antagonized xylazine-induced cardiopulmonary depression without affecting sedation and desirable local (S3 to coccyx) analgesic effects.

A radiopaque marker was injected, using needles of various lengths, into the cervical musculature, the lumbar epaxial musculature, and the cranial and caudal muscular masses of the thighs of anesthetized dogs. After this procedure, the dogs were euthanatized and deep-frozen. The bodies were then sectioned, and the slices were radiographed to determine the fate of the injected material. Material that was injected into the neck or caudal region of the thigh was determined to be located in the muscle bellies or dispensed throughout the intermuscular fascial sheaths. In contrast, material injected into the lumbar area and cranial region of the thigh was located entirely in the muscle bellies. It was concluded that the best sites for injection in dogs are the lumbar epaxial musculature or the quadriceps femoris muscle when IM administration is imperative.

Samples of pleural fluid from 20 horses with effusive pleural diseases of various causes were evaluated; samples from 19 horses were used for the study. There were differences for pH (P = 0.001) and partial pressure of oxygen (P(O2)) between arterial blood and nonseptic pleural fluid (P = 0.0491), but there were no differences for pH, P(O2), partial pressure of carbon dioxide (P(CO2)) and concentrations of bicarbonate (HCO3-), lactate, and glucose between venous blood and nonseptic pleural fluid. Paired comparisons of venous blood and nonseptic pleural fluid from the same horse indicated no differences. There were differences (P = 0.0001, each) for pH, P(O2), P(CO2), and concentrations of HCO3- between arterial blood and septic pleural fluid. Differences also existed for pH (P = 0.0001), P(CO2) (P = 0.0003), and concentrations of HCO3- (P = 0.0001), lactate (P = 0.0051), and glucose (P = 0.0001) between venous blood and septic pleural fluid. Difference was not found for values of P(O2) between venous blood and septic pleural fluid, although 4 samples of septic pleural fluid contained virtually no oxygen. Paired comparisons of venous blood and septic pleural fluid from the same horse revealed differences (P < 0.05) for all values, except those for P(O2). These alterations suggested functional and physical compartmentalization that separated septic and healthy tissue. Compartmentalization and microenvironmental factors at the site of infection should be considered when developing therapeutic strategies for horses with septic pleural disease.