In healthy adult goats, closure of the esophageal groove was induced by thirst, IV administered vasopressin, and intracarotid administration of hypertonic NaCl solutions. The efficiency of stimulation was tested directly by visual inspection of the course taken by orally administered solutions through a ruminal or abomasal fistula, palpation of the lips of the esophageal groove through a ruminal fistula, and indirectly by following the glucose dynamics in the blood after oral administration of glucose solution. Esophageal groove closure was observed during drinking after a 48-hour period of water deprivation. Intracarotid administration of 1.5 ml of a saturated solution or 10.5 ml of a 1.5% solution of NaCl also stimulated groove closure; however, groove closure stimulated by administration of vasopressin is the most satisfactory procedure for passing compounds of therapeutic importance directly from the cardiac orifice to the abomasum.

Concentrations of serum IgA, IgG, and IgM were determined for 829 adult Beagles from a commercial kennel in which several IgA-deficient dogs had been identified previously (index kennel). These values were compared with measurements of 100 adult dogs from another Beagle kennel (control kennel). After adjustment for differences in the ages and gender of the dogs, dogs from the index kennel had significantly (P less than 0.0001) lower IgA concentrations (mean, 46 mg/dl). Regardless of kennel, males had significantly (P less than 0.01) higher IgA concentrations than did females. Dogs in the control kennel had significantly (P less than 0.04) higher IgG concentrations (mean, 2,649 mg/dl) than did dogs in the index kennel (mean 2,478 mg/dl), and female dogs in the control kennel had significantly (P less than 0.05) higher IgM concentrations (mean, 189 mg/dl) than dogs of either sex in the index kennel (mean, 162 mg/dl) or male dogs in the control kennel (mean, 163 mg/dl). For both sexes, concentrations of IgA, IgG, and IgM increased with age.

Kinetics of large-scale production of naturally derived bovine leukocyte interferon (IFN) was investigated using Sendai virus, Newcastle disease virus, and infectious bovine rhinotracheitis virus inducers. Cultures were tested for IFN production every 6 hours for 66 hours. The effect of varying the priming dose of Sendai virus from 0 to 50% of total virus dose and the effect of varying the priming time from 0 to 4 hours before induction also were investigated. Other factors explored were effects of varying the fetal bovine serum concentration (from 0 to 8%) and individual cow donors on bovine IFN titers. Highest bovine leukocyte IFN titers (15,314 U/ml) were obtained using Sendai virus (priming dose, 60 hemagglutinating units/ml;inducing dose, 240 hemagglutinating units/ml) and incubating for 12 hours. Up to 24 L (over 360 million U) of naturally derived leukocyte IFN were produced at one time.

The efficacy of a single dose of ivermectin (0.2 mg/kg), in injectable or paste formulations, against microfilariae of Onchocerca cervicalis and associated skin lesions was evaluated in 20 naturally infected horses during midsummer months in Louisiana. All horses had clinical signs of dermatitis of the ventral midline and/or limbs, shoulders, thorax, and withers. Efficacy was monitored at 21, 42, and 63 days after treatment. Procedures done at these intervals included microfilarial counts of 6-mm skin biopsy specimens of affected ventral midline, grading of gross lesions, and photography and histologic assessment of ventral midline biopsy specimens. Microfilarial numbers were reduced to 0 by 21 days after treatment in all but one horse. Active lesions improved or were resolved completely by 63 days after treatment. Total inflammation, as judged by histologic methods, was reduced in all horses by 63 days after treatment, but there was a residual population of inflammatory cells in all horses. Adverse reactions after treatment were not observed in any of the horses.

Pituitary function and short-term clinical effects after transsphenoidal hypophysectomy were investigated in clinically normal dogs. In study, I, 8 dogs were given polyionic fluids IV during the first 12 hours after surgery. In study II, 4 dogs were given polyionic fluids IV and glucocorticoid supplementation for 7 days. Pituitary function was assessed by evaluating basal ACTH concentrations and results of a growth hormone stimulation test before and 1 and 12 weeks after hypophysectomy, an ACTH stimulation test, a thyrotropin-releasing hormone-stimulation test, and a modified water deprivation/vasopressin response test before and 1, 4, 8, and 12 weeks after hypophysectomy. Gross and histologic evaluations of the surgery site, thyroid and adrenal glands, and skin were done at 12 weeks after surgery. Four dogs from study I died within 27 hours after hypophysectomy. Postmortem examinations of these dogs revealed liver and lung congestion compatible with circulatory collapse. None of the dogs in study II died. For the surviving dogs in both studies, diabetes insipidus developed immediately after hypophysectomy and resolved within 2 weeks. Hypernatremia also developed immediately after hypophysectomy and resolved by 1 week. Production of ACTH was evident at 1 and 12 weeks after hypophysectomy in all dogs, and results of ACTH stimulation tests after surgery were not notably different from results obtained before surgery. Results of thyrotropin-releasing hormone stimulation and growth hormone-stimulation tests supported the diagnosis of hypothyroidism and hyposomatotropism attributable to hypophysectomy. Histologic examination revealed thyroid atrophy, epidermal and dermal atrophy, and normal adrenal glands in all dogs and remnants of the hypophysis in 2 dogs from study I. Continued ACTH production suggested that complete hypophysectomy was not accomplished in any dog.

The umbilical arteries urachus, and umbilical vein were scanned ultrasonographically in 13 clinically normal foals that ranged in age from 6 hours to 4 weeks. Sonograms were obtained using a 7.5-MHz sector scanner transducer placed across the midline of the ventral portion of the foal's abdominal wall. The umbilical vein was scanned from the umbilical stalk to its entrance into the hepatic parenchyma. The mean (+/- SD) diameter of the umbilical vein was 0.61 +/- 0.20 cm immediately cranial to the umbilical stalk, 0.52 +/- 0.19 cm midway between the umbilicus and liver, and 0.6 +/- 0.19 cm at the liver. The urachus and umbilical arteries were scanned from the umbilical stalk to the apex of the urinary bladder and had a mean total diameter of 1.75 +/- 0.37 cm at the bladder apex. The umbilical arteries also were scanned along either side of the bladder and had a mean diameter of 0.85 +/- 0.21 cm. These measurements and the ultrasonographic appearance of the internal umbilical structures from clinically normal foals can be used as references to diagnose abnormalities of the umbilical structures in neonatal foals.

Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extra-cellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells.

Inoculation of lambs with an ovine isolate of respiratory syncytial virus (RSV) by a combined intranasal and intratracheal route resulted in mild respiratory tract illness, with respiratory tract lesions. Lung lesions were characterized by bronchitis and bronchiolitis, hyperplasia of bronchial and bronchiolar epithelium, peribronchiolar and perivascular accumulations of lymphocytes, alveolar and perivascular accumulations of lymphocytes, alveolar septal thickening, and collapse. Respiratory synctial virus was recovered from the respiratory tract of inoculated lambs, and RSV antigen was demonstrated by immunoperoxidase staining of bronchiolar and alveolar epithelial peroxidase staining of bronchiolar and alveolar epithelia cells in pneumonic lesions of lambs euthanatized on post-inoculation days 5 and 6. Other primary respiratory tract pathogens were not isolated. Clinical signs of respiratory tract illness or respiratory tract lesions did not develop in the in-contact control lamb. Inoculation of the ovine RSV isolate into calves and deer fawns resulted in infection in both species, and at necropsy, pneumonic lesions were present. A mild to moderate respiratory tract illness developed in the calves, but clinical disease was not seen in the fawns. Lung lesions in fawns were similar to those seen in lambs; lesions in calves were characterized by collapse, scattered areas of parenchymal necrosis, and bronchiolitis. Respiratory synctial virus was reisolated from the lower respiratory tract of inoculated calves and fawns, and immunoperoxidase positive epithelial cells were seen in pneumonic lesions Other primary respiratory pathogens were not detected. Respiratory syncytial virus infection was not demonstrable in control animals that were in contact with inoculated animals. We concluded that an ovine RSV isolate, when inoculated in a severe challenge regime, caused mild primary pneumonia in lambs and lesions similar to those described in epizootics of naturally occurring ovine respiratory tract disease. Also, the ovine RSV caused lower respiratory tract lesions in infected calves and deer.

In vitro testing of bacterial susceptibility to a combination of ticarcillin and clavulanic acid was done, using 406 aerobic gram-positive and gram-negative isolates (considered to be pathogens) cultured from equine and small animal specimens. A microdilution broth technique of susceptibility testing was performed, using trays with wells containing a range of doubling concentrations of dehydrated ticarcillin (range, 0.50 to 128 microgram/ml) with fixed concentration of clavulanic acid (4 microgram/ml). The following isolates of equine origin were (90%) susceptible to concentrations of ticarcillin and clavulanic acid combinations of less than or equal to 16 and 4 microgram/ml, respectively: Staphylococcus aureus, S intermedius, Klebsiella pneumoniae, Enterobacter aerogenes, Ent agglomerans, Ent cloacae, Escherichia coli, Actinobacillus sp, Corynebacterium pseudotuberculosis, Rhodococcus equi, Proteus vulgaris, and Bordetella bronchiseptica. Isolates of small animal origin (90%) susceptible to less than or equal to 16 and 4 microgram of ticarcillin-clavulanic/ml included S aureus, S intermedius, Ent aerogenes, Ent agglomerans, Pasteurella multocida, B bronchiseptica, Pr mirabilis, and Serratia sp.

Ninety-nine nonclassical serogroups isolated from newborn pigs with neonatal diarrhea were tested for fimbrial antigens F4(K88), F5(K99), F6(987P), F41, and F165, and for heat-labile enterotoxin, heat-stable enterotoxin a (STa), heat-stable enterotoxin b, verocytotoxin, and cytolethal-distending toxin. Thirty-two strains, belonging mostly to serogroups O64:K"V142,", O9:K103, and O20:K101, were F5-positive and usually produced STa, although 5 strains produced only heat-stable enterotoxin b. Fifteen strains, belonging mostly to serogroups O64:K"V142" and O20:K101, were F41 positive and usually produced STa. Twenty-three strains belonging mostly to serogroups O64:K"V142," O9:K103, and O20:K101, were F6-positive and usually produced STa. Several strains produced more than one fimbrial antigen, either F5 and F41, F5 and F6, F6 and F41, F6 and F165, or F5, F6, F41, and F165. None of the strains produced heat-labile enterotoxin, verocytotoxin, or cytolethal-distending toxin. The indirect immunofluorescence test was much more sensitive than was the slide agglutination test for the detection of each of the fimbrial antigens F5, F6, F41, and F165 on strains grown in vitro. The production of F6 by certain strains for which only a low proportion of cells were F6-positive in vitro as demonstrated by immunofluorescence, was confirmed by experimental infection of newborn pigs.