An intramammary device (IMD) was adapted for use in ewes; this device was made of abraded poly. ethylene material (1.7 mm in diameter, 47 mm long) and formed a 15-mm-diameter loop in the gland cistern. The IMD was inserted in 1 gland in each of 43 ewes. A significant (P < 0.0001) increase in milk somatic cell count (SCC) was observed in glands provided with an IMD. This increase was attributable to an increase in neutrophil numbers and was observed during the first 12 weeks after insertion. The IMD had a protective effect against experimentally induced staphylococcal mastitis (Staphylococcus aureus and S epidermidis), although different milk SCC were required for protection from each bacterial species in most ewes (10(6) and 2 X 10(5) cells/ml, respectively). Histologic studies revealed that the IMD induced local squamous metaplasia in the glandular part of the lactiferous sinus. Erythrocytes were found in milk from glands provided with an IMD throughout the studied period (35 days of the 45-day lactation) and, in some cases, blood clots were observed during the first 2 weeks of lactation. Glands with IMD also had lower milk production and quality at 30 and 32 days of lactation. Eight ewes with IMD were studied throughout a subsequent lactation. Milk from the IMD-containing glands had an increase in SCC, as in the previous lactation period; did not contain blood clots or erythrocytes; and had normal composition (similar to that in glands without the IMD).

Current medical management of dogs with Portosystemic shunt (PSS) includes dietary protein restriction. After establishment of baseline values, 32 dogs underwent portosystemic anastomosis to induce PSS. They were assigned to 1 of 4 dietary treatments, and given 11 or 24% crude protein (CP); 20% of the protein was derived from branched chain or aromatic amino acids. The apparent digestibility of CP and of total digestible energy were not affected by PSS. The apparent digestibility of fat decreased from 92% to 85% in dogs with PSS (P < 0.01). Across all diets, the apparent dietary protein requirement (ADPR) was 2.07 g of CP/kg of body weight/d in clinically normal dogs and 2.11 g of CP/kg/d after PSS. Dietary amino acid composition had no effect on ADPR. The ADPR for dogs fed the 11% protein diets was 1.69 g of CP/kg/d in clinically normal dogs and 1.62 g of CP/kg/d after PSS, whereas the ADPR in dogs fed the 24% protein diets was 3.94 g of CP/kg/d before PSS and 3.31 g of CP/kg/d after PSS. Serum total protein, urea nitrogen, and albumin concentrations were lower in dogs with PSS fed the 11% protein diets, compared with those fed the 24% protein diets. We conclude that there is no difference in ADPR in dogs with PSS; however, the low protein intake of 1.62 g of CP/kg/d appeared inadequate to maintain normal protein stores. Dietary protein that provides at least 2.1 g of CP/kg/d is recommended for dogs with PSS.

In this study, we compared hepatic ultrastructure in healthy cats, in cats with severe hepatic lipidosis, and in cats with experimentally induced, chronic, extrahepatic bile duct occlusion. Ultrastructural features unique to the lipidosis syndrome included an apparent reduction in number of peroxisomes and alteration in their morphologic features. The quantity of endoplasmic reticulum, Golgi complexes, and lysosomes was subjectively reduced, and paucity of cytosolic glycogen was observed. Bile canaliculi appeared collapsed because of cytosolic distention with lipid. Mitochondria were reduced in number and were markedly pleomorphic. Cristae assumed a variety of shapes, lengths, and orientations. Ultrastructural features of bile duct occlusion were similar to those described in other species and differed from those in cats with hepatic lipidosis.

The genetic basis of drug-resistant strains of Actinobacillus pleuropneumoniae in Japan was studied. The A pleuropneumoniae strains AV277 and AV281 that belong to serotype 2 were resistant to streptomycin (SM) and sulfonamide (SA). Both strains had an 8.1-kilobase (kb) SM-SA plasmid that was previously classified in the H1 group. The AV177 (serotype 1) strain was resistant to SM, SA, ampicillin, and kanamycin (Km), but did not have any plasmids. The AV319 and AV324 (serotype 1) strains were resistant to Sm, SA, tetracycline (TC), and chloramphenicol (CP). The AV318 (serotype 12) strain was resistant to SM, SA, TC, minocycline, and CP. These 3 strains (AV319, AV324, and AV318) had a 4.3-kb SM-SA plasmid and a 5.2-kb CP plasmid. The 4.3-kb plasmid was classified in the H2 group. The AV263 (serotype 1) strain was resistant to SM, SA, KM, TC, and CP. It had a 5.2-kb CP plasmid and a 6.6-kb SM-SA-KM plasmid. Both plasmids did not replicate stably in Escherichia coli strains. The former 5.2-kb plasmid was mobilized in E coli strains by plasmid RP4, which belonged to incompatibility P with broad host range, but the latter 6.6-kb plasmid was not so mobilized. Three 5.2-kb CP plasmids isolated from strains AV319, AV324, and AV318, had the same restriction endonuclease pattern after digestion with Ava I and EcoRI. They coexisted with H1 group plasmids in the incompatibility test, and coexisted also with H2 group plasmids of the original A pleuropneumoniae strains. Results indicated that the 5.2-kb CP plasmids could be classified in a new incompatibility group, H3. In this study, 4 types of plasmids were isolated, but no plasmids encoded TC and minocycline resistance.

The effect of triamcinolone acetonide (0.09 mg/ kg of body weight, IM) on serum osteocalcin concentration was studied. Two groups of horses were investigated and included clinically normal horses (group 1, n = 5) and horses with chronic obstructive pulmonary disease (group 2, n = 5). Before treatment, results of a t-test did not reveal any significant difference in serum osteocalcin concentration between the 2 groups. After treatment, a significant (P < 0.05) decrease in serum osteocalcin concentration was observed for both groups. Osteocalcin concentration in individual horses reached a minimum by 24 to 48 hours after treatment. In both groups of horses, serum osteocalcin response to glucocorticoid administration was similar. In 7 of 10 horses, return to pretreatment values was observed after 28 days. Pretreatment values for the other 3 horses were reached between 62 and 150 days.

Eighteen female lambs with prior exposure to Haemonchus contortus infections were ovariectomized and assigned to 1 of 3 replacement regimens: 0, 25, or 250 mg of progesterone/d delivered IM. After 3 weeks of hormonal treatment, all lambs were inoculated with 100,000 infective larvae of H. contortus. After 8 weeks of hormonal treatment, a blastogenic assay was performed on blood lymphocyte populations, and the abomasum from each lamb was obtained for larval and adult worm recoveries of H. contortus. Lambs of the 25 mg of progesterone group had significantly (P < 0.05) reduced blastogenic response to concanavalin A and greater adult and larval populations, compared with controls. Lambs of the 250 mg of progesterone group had worm burdens and lymphocyte blastogenesis values intermediate between those of the other treatment groups.

A semiquantitative heartworm test of antigen concentration was evaluated as a predictor of thromboembolism after adulticide treatment. Seventeen dogs with naturally acquired infections of Dirofilaria immitis (heartworms) were studied before and after thiacetarsamide treatment, using physical examinations, arterial blood gas analyses, thoracic radiography, and pulmonary hemodynamic and arteriographic tests. Eight dogs were considered to have a low burden of heartworms and 9 had a high burden. Dogs with a high worm burden had more severe pulmonary thromboembolism with pulmonary hypertension, dilated pulmonary arteries, flow obstruction of the caudal pulmonary arteries, and parenchymal lesions in the caudal lung lobes. Dogs with a low worm burden had minimal changes. Within each group of dogs, the severity of thromboembolism was less in some dogs in which all heartworms were not killed. Six of the 9 dogs with a high burden of heartworms had surviving heartworms, and 1 of these dogs had 38 live heartworms. Only 4 of the 8 low worm burden had complete heartworm mortality, but only 1 dog had more than 3 surviving heartworms. We concluded that dogs with a high worm burden were more likely to have pulmonary thromboembolism after thiacetarsamide treatment and that dogs with a low worm burden were more likely to have minimal changes. A semiquantitative heartworm test of antigen concentration is recommended as part of the pretreatment evaluation of dogs infected with heartworms.

Serum interleukin-6 (IL-6) concentration was measured in 11 colostrum-fed (CF) and 8 colostrum. deprived (CD) 2- to 3-day-old foals after foals were infused with lipopolysaccharide LPS; Escherichia coli O55:B5 endotoxin, 0.5 micrograms/kg of body weight in sterile saline [0.9% NaCl] solution. Four CF and 2 CD foals were given saline solution alone. Serum IL-6 concentration was estimated by use of an in vitro proliferative bioassay, using the IL-6 dependent B.13.29 clone 9 cells. Interleukin-6 concentration increased in all LPS-infused foals, and geometric mean serum IL-6 concentration was significantly higher in CF than CD foals 30 and 90 minutes after infusion. Both LPS-infused. groups had multiple spikes of mean IL-6 concentration that peaked at 120 minutes in CF foals and 150 minutes in CD foals. Results indicated that IL-6 is produced in neonatal foals in response to LPS infusion. Furthermore, colostrum deprivation resulted in longer times to peak mean serum IL-6 concentration and tended to reduce serum IL-6 concentration in neonatal foals.

Desoxycorticosterone pivalate was administered IM to juvenile Beagles at 0, 2.2, 6.6, or 11 mg/kg of body weight daily over a consecutive 3-day period every 28 days (equivalent to a cumulative monthly dosage of 0, 6.6, 19.8, or 33 mg/kg) for 6 months. Polyuria, polydipsia, and decreases in serum potassium and BUN concentrations were detected while the dogs were being treated. Transient increases in serum sodium concentrations also were detected. The treated males had significant decreases in body weight gain, resulting in an 18% decrease in body weight in the 11-mg/kg dosage group, compared with the controls. The weights of the adrenal glands, epididymides, and testes also were lower in the treated males. Organ weights for the 2.2, 6.6, and 11-mg/kg dosage groups were: 86, 79, and 69%, respectively, of the controls (adrenal glands); 80, 70, and 68%, respectively, of the controls (epididymides); and, 79, 75, and 67%, respectively, of the controls (testes). When normalized to body weight, these decreases in organ weight were still dosage-dependent, but the differences were less remarkable. In contrast, the relative weight (to body weight) of the kidneys (males and females) and of the thyroid and parathyroid glands (males) were higher dosage-dependently. All of the treatment-related effects, other than organ and body weight changes, appeared to be reversible following the cessation of treatment. On the basis of these results, it was concluded that treatment with desoxycorticosterone pivalate could be tolerated, even when given at dosages 15-fold the therapeutic dosage of 2.2 mg/kg every 25 days.

Pharmacokinetic variables of ibuprofen were studied in 6 adult lactating dairy goats after single administration of the drug (14 and 25 mg/kg of body weight, IV, and 50 and 100 mg/kg, PO). Each of the goats was given all doses, with a minimum of 1 week between doses. Ibuprofen concentration in serum was analyzed by use of high-performance liquid chromatography. The lower limit of detection for the ibuprofen assay was 50 ng/ml. Ibuprofen pharmacokinetic variables after IV administration best fit an open two-compartment model. Geometric mean (range) volume of distribution at steady state was 0.16 (0.11 to 0.19) and 0.17 (0.15 to 0.19) lag, and terminal half-life was 1.08 (0.79 to 1.70) and 1.27 (1.03 to 1.88) hours, for ibuprofen dosages of 14 and 25 mg/kg, respectively. After 50 and 100 mg/kg administered orally, bioavailability was 90.8 and 106%, respectively. Area under the curve increased linearly with dose administered. Adverse effects were not observed in goats given ibuprofen.