Cell proliferation kinetic values were established for the epidermis, hair follicle epithelium, and sebaceous glands of 8 Cocker Spaniels with primary idiopathic seborrhea. Values were established by intradermal pulse labeling injections of tritiated thymidine followed by cutaneous biopsy and autoradiography.The epidermal basal cell-labeling index was 4.96 +/- 0.97%, and the epidermal nucleated cell-labeling index was 3.33 +/- 0.71%. Calculated epidermal cell renewal time for the viable layers of the epidermis was 7.85 +/- 1.80 days. The hair follicle infundibulum basal cell-labeling index was 5.48 +/- 2.01%, and the sebaceous gland basal cell-labeling index was 5.94 +/- 4.15%. When compared with previously reported cell kinetic values for Cocker Spaniels and Beagles with healthy skin, these data indicate accelerated cellular proliferation in all 3 cutaneous structures in seborrheic Cocker Spaniels.

A porcine rotavirus isolate was titrated in neonatal colostrum-fed and colostrum-deprived pigs. The stock rotavirus suspension had a titer of 10 /ml and was in its fifteenth cell culture passage in MA-104 cells. Fourteen colostrum-fed pigs were orally inoculated with dilutions of the stock virus suspension ranging from undiluted to 10-5. These pigs did not develop notable clinical signs during the 7-day experimental trial and no pathologic changes were found in intestine, liver, lung, kidney, spleen, or brain. However, rotavirus was detected in feces of the colostrum-fed pigs, using virus isolation and electron microscopic techniques. Rotavirus was also isolated from lung, brain, or spleen of 4 of 12 of these pigs. Sixteen colostrum-deprived pigs were orally inoculated with dilutions of the stock virus suspension ranging from 10-1 to 10-8. Diarrhea developed in 10 of 12 pigs that were given up to the 10-6 dilution. Seven of these 12 pigs died because of the severity of diarrhea. Pigs that died of rotavirus-induced diarrhea had severe villus loss in the jejunum and ileum. Villi of the small intestine of colostrum-deprived pigs that survived the severe diarrhea were within normal limits at the end of the 7-day trial. The colostrum-deprived pigs that were inoculated with a dilution less than 10-6 and survived past 96 hours underwent seroconversion. Rotavirus was detected by virus isolation and electron microscopy in the feces of all colostrum-deprived pigs that survived beyond 18.5 hours after inoculation. Virus was isolated from lungs, brain, or spleen of 12 of 16 colostrum-deprived pigs.

Bovine pulmonary artery cells in cell culture were exposed to lipopolysaccharide (LPS) purified from Pasteurella haemolytica serotype A1. This resulted in severe membrane damage, which caused a time- and dose-dependent release of lactate dehydrogenase that was first detected 4 hours after exposure and reached a maximal mean release of 67% after 24 hours of exposure to 1 microgram of LPS/ml. Mean release of 51chromium followed by a similar pattern and reached a maximum of 61% following 24 hours of exposure to 10 micrograms of LPS/ml. Morphologically, endothelial cells responded to LPS by marked cell membrane retraction, the formation of numerous cytoplasmic blebs, and ruffling of the cell membrane. Subsequently, the cells became round and detached. Cell detachment reached a mean of 95% following 8 hours of exposure to 1 microgram of LPS/ml. These studies demonstrated that P haemolytica LPS is capable of causing direct damage to bovine pulmonary arterial endothelial cells, which may be important in the pathogenesis of bovine pneumonic pasteurellosis.

A study was designed to determine the effect of Pasteurella haemolytica infection on the rate and extent of penetration of sulfadiazine and trimethoprim into tissue chambers implanted SC in cattle. Thermoplastic tissue chambers were implanted SC in 6 calves. At 35 days after implantation, sulfadiazine (25 mg/kg of body weight) and trimethoprim (5 mg/kg) were administered IV to 5 of the calves. Chamber fluid and blood samples were collected from each animal at various time intervals for 24 hours after administration. Ten days later, all chambers were inoculated with P haemolytica serotype 1. At 36 hours after inoculation, a second pharmacokinetic study was conducted, using sulfadiazine and trimethoprim. Drug doses and sampling schedules were identical to those used prior to inoculation. A histologic study of infected chamber tissue was conducted, using the calf not included in the pharmacokinetic studies. Disposition curves of antimicrobials in serum and chamber fluid were well described by 2-compartment and 1-compartment pharmacokinetic models, respectively. Inoculation of P haemolytica into tissue chambers was accompanied by marked changes in the composition of chamber fluid. Increased total protein and albumin concentrations, decreased pH, and disruption of chamber tissue vasculature were associated with a significant increase in the penetration of sulfadiazine and trimethoprim into infected tissue chambers, compared with that in noninfected chambers. This increased penetration was accompanied by increases in the apparent volume of distribution for sulfadiazine and trimethoprim.

The relationship between the palpebral conjunctival oxygen index, mixed venous oxygen tension, and cardiac index were compared, using a canine hemorrhagic shock model. The cardiac output was reduced by reducing the blood volume in 5% increments until the initial cardiac output was reduced by one half. In each of 7 dogs, the palpebral conjunctival oxygen index and mixed venous oxygen tension were found to have good correlation with cardiac index; however, the correlation coefficients were markedly reduced when the data from all of the dogs were combined. It was concluded that the palpebral conjunctival oxygen index provides an excellent means of assessing changes in cardiac index over time in the same dog; however, it cannot be used to estimate cardiac index in an individual dog with a degree of accuracy that would be clinically significant.

Turkey enteric coronavirus (TCV) from intestinal contents of diarrheal poults was isolated and serially propagated in HRT-18 cells, an established cell line derived from a human rectal adenocarcinoma. In these cells, TCV induced cytopathic changes, including polykaryocytosis, which depended on trypsin in the medium and incubation at 41 C. Viral antigens could be demonstrated in the cytoplasm by immunofluorescence, and extracellular virus was detected by an ELISA and negative electron microscopy. The cell-free virus had characteristics of TCV: shape, surface projections, buoyant density of 1.18 to 1.20 g/ml in sucrose, and hemagglutination of rat RBC. The one-step growth curve was complete by postinoculation hours 14 to 16, and maximal titers reached 9 to 9.5 log10 TCID50/ml during 5 passages, after which the titer remained stable. Electron microscopic examination of infected cell monolayers revealed budding of typical coronavirus particles through intracytoplasmic membranes and accumulation of complete virus in cytoplasmic vesicles. Late in the infection, aggregated progeny vial particles were detected near the outer surface of infected cells. One-day-old turkey poults inoculated orally with tissue culture-adapted TCV isolates developed mild to severe diarrhea.

Strips of trachealis muscle were dissected from the mid-cervical portion of the trachea from horses that were free of respiratory tract disease. The epithelium and mucosa were removed from one group of tissues and were left intact in a second group of tissues. Each tissue was suspended in a bath filled with Krebs-bicarbonate solution that was aerated with 5% CO2 in oxygen and maintained at 37 C. Isometric tension was continuously recorded. The contractile response to square-wave electrical stimulations increased as frequency (3, 5, 10, 15, 20, 25, and 30 Hz), voltage (10, 15, 18, and 25 V), and pulse duration (0.2, 0.5, 1.0, 1.5, and 2.0 ms) increased in tissues with the epithelium and mucosa intact. A stimulus of 18 V, 20 Hz, and 0.5 ms induced maximal contraction. Atropine (10(-6) M) abolished the response to 18 V and 0.5 ms at all frequencies. The increase in active isometric tension was concentration dependent when acetylcholine (10(-9) to 10(-4) M) was added to the baths in 0.5-logarithmic increments. Tissues that were contracted in response to acetylcholine (10(-5) M) had a concentration-dependent decrease in active isometric tension when isoproterenol was added to the baths in 0.5-logarithmic increments (10(-9) to 10(-4) M). The contraction and relaxation curves were qualitatively similar, but quantitatively different in tissues with and without the epithelium and mucosa. Removing the epithelium and mucosa increased the contractile response to acetylcholine at bath concentrations of 3.1 X 10(-7) M and 10(-6) M. The presence of epithelium and mucosa enhanced the magnitude of isoproterenol-induced relaxations. We concluded that electrical stimulation released acetylcholine from isolated equine trachealis muscle, that isoproterenol induced relaxation of the trachealis muscle, and that the magnitude of the responses to exogenous agonists depended on the presence of epithelium and mucosa.

A clinical trial examining the efficacy of 2 drugs for treatment of a natural epizootic of infectious bovine keratoconjunctivitis was performed. The study was conducted in 103 grazing Hereford calves during the summer of 1985. The calves were prospectively and randomly assigned to 1 of 3 groups at the beginning of the study on June 17, and were examined 3 times weekly thereafter until the final observation on August 6. Calves in group 1 (n = 34) were not treated and were used as controls. Calves of group 2 (n = 34) with corneal ulcers were treated with a long-acting oxytetracycline formulation (OTC group). The parenteral treatment was repeated in 72 hours. Affected calves of group 3 (n = 35) were treated topically with furazolidone spray when they developed new corneal ulcers, or when existing lesions worsened during subsequent examination periods (NFZ group). Healing times of the corneal ulcers were reported in 3 ways: the combined times for ulcers present in both eyes of a calf simultaneously (method A), independent times of each ulcer on a calf (method B), and time of the first ulcer for each calf (method C). Censored healing times were examined as left censored (ulcer present at the beginning of the study), right censored (ulcer not healed at the end of the study), or uncensored (true) healing times. The effect that the treatments had on healing times were investigated by use of notched box and whisker plots, life tables, and Cox regression models. The analysis indicated that treatment of calves with either antimicrobial reduced the healing time of corneal ulcers, compared with untreated controls. Calves treated with OTC had shorter periods with ulcers present on both eyes than did NFZ-treated calves. The healing time of the first ulcer on a calf was faster when treated with either antimicrobial than when not treated, but no significant difference between periods for OTC and NFZ treatments was found. Censored healing times were consistently longer than uncensored healing times. Box and whisker plots indicated that both treatments shortened healing times more than those for controls, and OTC shortened healing times more than did NFZ for responses A and B (but not C). Life tables showed that OTC healing times were shorter than those for controls, and NFZ shorter than controls for response B and C (but not A). Cox regression model (for response A) showed a borderline significant difference between times for OTC group and controls, and no significant difference between times for NFZ group and controls.

Cytoplasmic proteins from unsporulated and sporulated Eimeria maxima oocysts were analyzed by gel-filtration column chromatography. Unsporulated oocysts were characterized as having 3 major cytoplasmic proteins and sporulated oocysts as having 5 major cytoplasmic proteins. Molecular weights ranged from 5 X 10(3) to 1.4 X 10(6). Larger molecular weight proteins were detected in sporulated and unsporulated oocysts, but were associated more with sporocysts of sporulated oocysts.

In vitro activities of 9-([2-hydroxyethoxy] methyl) guanine (acyclovir), (E)-5-(2-bromovinyl)-2'deoxyuridine, 9-beta-D-arabinofuranosyladenine (vidarabine), 5-iodo-2'-deoxyuridine (idoxuridine), and 5-trifluoromethyl-2'-deoxyuridine (trifluridine) were studied against 6 strains of feline herpesvirus-1. A significant difference was not detected among viral strains in their susceptibility to these compounds (P = 0.442). The relative potency of these compounds was trifluridine greater than greater than idoxuridine greater than virdarabine greater than bromovinyldeoxyuridine greater than greater than acyclovir. Concentrations of trifluridine and idoxuridine (0.67 and 6.8 micromole, respectively) required to reduce plaque numbers by 50%, compared with that of controls, were significantly lower (P less than 0.001) than were those of other compounds.