The role of bile salt in biliary lipid excretion was studied in 3 healthy ponies with chronic external biliary fistulas. After endogenous bile salt pool depletion, micelle-forming taurocholate or taurochenodeoxycholate was infused to replace excreted bile salt. Enterohepatic circulations were held open (total biliary diversion) throughout each study. Results indicated that biliary lipid excretion in ponies (113 +/- 21 nmol/in/kg of body weight) is approximately 10 times less than that reported in rodents. Although the lipid composition (4.4% cholesterol, 5.6% phospholipid, and 90% bile salt) was within the predicted range for a single phase of micellar (or vesicular) liquid in solution, it was supersaturated with cholesterol because of low absolute concentrations of bile salt and phospholipid. Ponies, like guinea pigs, were determined to have a high bile salt-independent secretion of biliary lipid with little (or no) coupling to endogenous bile salt output. However, bile salt excretion induced by higher taurocholate infusion rates (ie, those greater than the physiologic range of 61 to 125 nmol/min/kg) was positively correlated with an increase in biliary phospholipid excretion, but not cholesterol excretion, thus indicating that a threshold intracellular bile salt concentration may be associated with enchanced biliary phospholipid excretion in ponies. The apparent cholerectic effects of endogenous bile salts, taurocholate, and taurochenodenoxycholate (that is, the increment in bile flow per increment in bile salt recovered) were greater in ponies than reported for any other mammal.

Serum protein electrophoresis was performed on 71 clinically healthy juvenile and adult llamas (6 juvenile males, 7 juvenile females 25 adult males, 13 adult females, and 20 pregnant females) to determine normal serum protein concentrations. Values were reported for each of the 5 groups because the groups were not homogeneous in all 8 peaks. Although the values reported here may serve as reference values for adults, they represent only a guideline for the juveniles because of the limited number of animals in each of these groups.

A field study was performed to determine the effectiveness of benzathine cloxacillin for the treatment of infectious bovine keratoconjunctivits in cattle from 2 farms located in northern California. The study was performed between June and September of 1987. Affected calves ranging from 2 to 9 months of age were selected from the main herd when signs of corneal ulceration were observed. The study was conducted in 2 phases. For phase I, the affected calves of herd 1 (n = 21; Holsteins) and herd 2 (n = 43 Angus crossbred), were randomly assigned to 1 of 3 groups, and were either treated with 250 (n = 23) or 375 mg (n = 21) of benzathine cloxacillin, or mineral oil (n = 20) on days 1 and 4. For phase II, affected calves (n = 16; Angus crossbred, 3 to 9 months of age) from herd 2 were treated with benzathine cloxacillin (250 mg). Eight of these calves were retreated on day 4. After treatment, all calves were examined every 72 hours for 16 days. For examinations, a clinical score was assigned to each eye, and the surface areas of photographed corneal ulcers were measured. The ocular secretions were collected and examined culturally for Moraxella bovis. On days 7, 10, and 13, the calves treated with benzathine cloxacillin had significantly (P less than 0.05) lower lesion scores, compared with the controls. The percentage of day-1 area measurements on posttreatment days 4, 7, and 10 were significantly larger in the controls than in the treated calves. The mean healing times of corneal lesions in the 2 antibiotic treatment groups were significantly (P less than 0.05) shorter than in the controls. In the treated calves, the healing times of corneal ulcers less than or equal to 0.05 cm in diameter on day 1 were significantly (P less than 0.05) shorter than the healing times of larger lesions. The healing times of the corneal ulcers in the Angus crossbred calves were significantly (P less than 0.05) longer than the healing times of the Holsteins. The controls had the greatest number of nonhealed corneal ulcers on day 16. The number of calves that remained infected with M bovis on days 4, 7, 10, and 13 was significantly less in both groups of treated calves than in the controls. The scores, surface area measurements, healing times, and the M bovis isolation frequency in the calves of the 250-mg and 375-mg and 1- and 2-dose treatment groups were not significantly different. The minimal inhibitory concentrations (MIC) of penicillin, cloxacillin, and ampicillin in the day-16 isolates from benzathine cloxacillin-treated herd-2 calves were greater than in isolates from corresponding calves on observation day 1; however, twofold increases of the respective MIC of pretreatment and day-16 specimens were not observed. The highest MIC of ampicillin, cloxacillin, gentamicin, oxytetracycline, and penicillin were 0.5, 8.0, 0.5, 2, and 1 migrogram/ml, respectively, for isolates collected during the final study week.

Colostral volume and IgG and IgM concentrations were determined in 6 multiparous mares at foaling and then every 2 hours from 16 to 20 hours after parturition. Serum IgG and IgM concentrations at foaling also were determined in each mare. The rate of mammary secretion was 292 +/- 26 ml/h (range, 202 to 389 ml/h), and the colostral volume was 5.1 +/- 0.5 L (range, 3.2 to 7.0 L). The colostral IgG and IgM contents were 440 +/- 106 g (range, 199 to 855 g) and 3.1 +/- 0.9 g (range, 0.7 g to 7.1 g), respectively. There was no significant correlation between serum and initial colostral IgG and IgM concentration or between serum and total colostral IgG or IgM values. The colostral IgG and IgM concentrations at foaling correlated well with the total colostral IgG and IgM contents, respectively. The initial 250 ml of colostrum contained 10 +/- 1.4% (range, 6.0 to 13.9%) and 6 +/- 1.0% (range, 2.4 to 8.5%) of the total IgG and IgM contents, respectively, and the initial 500 ml of colostrum contained 20 +/- 2.7% (range 12.0 to 27.1%) and 14 +/- 1.2% (8.2 to 17%) of the total colostral IgG and IgM contents, respectively.

Sulfadiazine (SDZ)/trimethoprim (TMP; 30 mg of SDZ/TMP/kg of body weight) was given IV to the same 6 male calves at 1, 7, and 42 days of age and to 2 additional calves at 7 days of age. Serum concentrations of SDZ and TMP were best represented by a 2-compartment open model, but in 42-day-old calves, CSF concentrations of both drugs were best represented by a 1-compartment open model with first-order input. Between 1 and 42 days of age, the elimination half-life (t1/2(beta)) of SDZ decreased from 5.7 to 3.6 hours, and total body clearance (CLtot) increased from 1.43 to 1.88 ml/min/kg; the area under the curve (AUCo leads to x) decreased from 291.5 to 225.4 mg/L.h. The distribution coefficient (Vd(area)/kg of body weight) decreased with age, changing from 0.72 to 0.59 L/kg, between 1 and 42 days of age. Therapeutic concentrations of SDZ in serum (greater than 2 micrograms/ml) were maintained for 24 hours in 1-day-old calves and for about 15 hours in 7- and 42-day-old calves. The elimination rate of TMP increased about 9-fold; t1/2(beta) was 8.4, 2.1, and 0.9 hours, respectively, at 1, 7, and 42 days of age. Other values also reflected an increase in TMP elimination rate with age: CLtot increased from 2.8 to 12 to 28.9 ml/min/kg, k13 increased from 0.336 to 0.654 to 1.664/h and AUC(0 to infinity) decreased from 32.8 to 7.9 to 3.1 mg/L/h, respectively. Therapeutic concentrations (greater than 0.1 microgram/ml) were maintained for 15 hours, 8 hours, and about 6 hours in 1-, 7-, and 42-day-old calves, respectively. Penetration of SDZ and TMP into the CSF in 42-day-old calves was substantial; ratios of AUC(CSF)/AUCserum were 0.60 and 0.69, respectively. Therapeutic concentrations of drugs in CSF were maintained if serum concentrations were above therapeutic concentrations; elimination rates of both drugs from the CSF equaled those of serum. Sulfadiazine was excreted mainly unchanged; the percentage of dose excreted unchanged in 24 hours increased from 22.1 to 47.8 to 50.8% in 1-, 7-, and 42-day-old calves, respectively, paralleling the increase in CLtot. Trimethoprim was extensively biotransformed; the percentage of dose excreted unchanged in the urine in 24 hours decreased from 12.8 to 8.7 to 3.5%. Sulfadiazine and TMP were concentrated in the urine, and therapeutic concentrations of both drugs in urine were maintained for greater than 24 hours in calves of all ages.

The in vitro and in vivo binding of a monoclonal antibody (MAB) that recognizes a tumor-associated carbohydrate antigen was studied in dogs. Monoclonal antibody 155H.7 was raised in response to innoculation of mice with beta-galactose(1-3)betaN-acetylgalactosamine conjugated to human serum albumin. Avidin-biotin-complex immunohistochemical staining of cryostat sections of normal and neoplastic canine tissue specimens revealed heterogenous binding of MAB 155H.7 to the cells of many canine mammary and lung carcinomas and homogenous staining of may sarcomas, including osteogenic sarcoma. In addition, there was variable staining of a variety of normal tissues including some ductual epithelium, peripheral nerve fibers, and some endothelial cells and fibroblasts. Immunoscintigraphy with 131I-labeled MAB 155H.7 was used to study the in vitro distribution of the antibody. The 131I-labeled MAB 155.H.7 was administered to 1 clinically normal dog, 7 dogs with osteogenic sarcoma, 1 dog with undifferentiated sarcoma, and 2 dogs with mammary tumor. Scintigraphy revealed concentration of radioactivity in 8 of 10 tumor sites within 24 hours after MAB administration. The ratio of 131I in tumor sites to 131I in the surrounding normal tissues, compared with the similar ratio of 99mTc-labeled erythrocytes ranged from 1.1 to 4.3 in tumor vs normal tissue with a mean value of 2, confirming tumor localization of the radiolabeled MAB in excess of that associated with enhanced tumor vascularization.

Anaplasma marginale was propagated in a tick cell line derived from Dermacentor variabilis embryos. The rickettsial organism was identified and monitored in culture by transmission electron microscopy and the indirect immunofluorescence technique, using specific monoclonal antibodies. Inoculation of the embryonic tick cell line with midguts of infected adult ticks (culture 1), nymphal ticks (culture 2) and adult ticks that were infected as nymphs and dissected as adults (culture 3) resulted in 3 continuous cultures of A marginale. Culture 1 had been maintained through 22 passages over a 11-month period; cultures 2 and 3 had been maintained for 18 passages over a 9-month period. Growth of A marginale in the cell line began in the area of the nuclear membrane at approximately 4 days after inoculation or transfer. Thereafter, the organisms were observed in inclusions scattered throughout the cytoplasm of the host cells. Maximal growth of the organism occurred at 7 to 14 days, after which numbers of inclusions rapidly decreased to minimal or undetectable levels. The organism began new cycles of growth with each 1:5 to 1:10 split and transfer of the host cells. Electron microscopy of recently infected cells revealed a morphology of the organism that closely resembled that observed in marginal bodies of infected erythrocytes. After several passages, A marginale organisms had a varied morphology and resembled the organism described in midgut cells of naturally infected ticks. Substitution of adult bovine serum for fetal bovine serum and adjustment of the pH of the medium from 6.9 to 7.4 resulted in several-fold increases in amount of growth and reduced the period required to reach maximal growth to a predictable time of 5 to 7 days. The importance and potential of this method of continuous laboratory propagation of A marginale are discussed.

The virulence of 2 porcine group-A rotavirus isolates was compared. Forty hysterotomy-derived 3-day-old gnotobiotic pigs were inoculated orally with 2 ml of intestinal homogenate containing either the Ohio State University (OSU) or the South Dakota State University (SDSU) strain of porcine rotavirus or were inoculated with medium only. Clinical signs of disease, body weight, distribution of viral antigen, fecal excretion of virus, and histologic lesions (observed by light and scanning electron microscopy) were determined. Morphometric measurements of villi and crypts were made. In pigs inoculated with OSU or SDSU strains, diarrhea began at postinoculation hours (PIH) 19 to 48 and PIH 24 to 54, respectively. None of the virus-infected pigs died as a consequence of infection and all had similar clinical signs of disease, body weight changes and virus-shedding patterns, regardless of the strain of rotavirus with which they were infected. Microscopic findings in the small intestine of virus-infected pigs were similar, except that the SDSU strain caused more severe villus atrophy and villus fusion in the duodenum at PIH 72 and 168 than was associated with the OSU strain. Viral antigen in the small intestine of pigs infected with either virus was observed by use of immunofluorescence at PIH 24 and 72, but was seldom seen at PIH 168.

In 2 studies, the effects of dietary aflatoxin (AF) and deoxynivalenol (DON) were evaluated in growing crossbred barrows. The first study consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 2.5 mg of DON/kg of feed, 0.75 mg of AF/kg of feed, and 2.5 mg of DON + 0.75 mg of AF/kg of feed. Pigs were fed their respective diets for 21 days. Treatment with DON caused decreases in weight gains, but no other treatment-related differences could be attributed to diets. In a second study, the experimental design consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 3 mg of DON/kg of feed, 3 mg of AF/kg of feed, and 3 mg of DON + 3 mg of AF/kg of feed fed ad libitum for 28 days. The pigs were observed twice daily for clinical signs, hematologic and serum biochemical measurements were made weekly, and body weights and feed consumption were determined weekly. Body weight gains were significantly depressed by the AF and the AF + DON treatments for days 7, 14, 21, and 28. Body weights and body weight gains were only slightly reduced in the DON treatment. Changes in serum enzymatic activities of alkaline phosphatase, aspartate transaminase, creatine kinase, and gamma-glutamyl transferase were noticed in pigs given treatments with AF alone and those given AF + DON. Total iron binding capacity and serum total protein, albumin, cholesterol, BUN, and glucose concentrations were decreased, whereas prothrombin and activated thromboplastin times were increased by AF and AF + DON treatments. Lesions in the AF-treated groups were compatible with a diagnosis of aflatoxicosis. The control and DON-treated pigs had no abnormalities. These data provide a description of the effects of dietary AF and DON, singly and in combination, in growing barrows.

Pharmacologic effects of alpha-methylfentanyl and 3-methylfentanyl, analogs of fentanyl, were investigated in mares. The ability of an 125I-labeled fentanyl radioimmunoassay (125I-RIA) to detect these methylated fentanyl analogs in individual and pooled urine samples from horses was evaluated. Also, the ability of 7 fentanyl antibodies to react with fentanyl and fentanyl derivatives (sufentanil, alfentanil, and carfentanil) was investigated. Mares were studied in a locomotor test to determine the amount of stimulation methylated fentanyl analogs might induce. Two mares each were given alpha-methylfentanyl at 1, 2, 4, 8, or 13 microgram/kg of body weight, IV, or 3-methylfentanyl at 0.4, 0.7, or 1 microgram/kg IV. The cross-reactivity of sufentanil, alfentanil, carfentanil, alpha-methylfentanyl, and 3-methylfentanyl with 7 fentanyl antibodies was studied, using the 125I-RIA. All fentanyl analogs, with the exception of alfentanil, cross-reacted well with a C1 antibody raised to fentanyl. Less satisfactory cross-reactivity was determined with 6 other antibodies raised to fentanyl derivatives. When the C1 antibody was combined with an iodinated analog to fentanyl, good detectability of alpha-methylfentanyl and 3-methylfentanyl, in terms of fentanyl equivalents, was obtained from urine samples of dosed mares. The ability of the 125I-RIA to detect methylated fentanyl analogs in forensic urine samples pooled in groups of up to 20 samples was evaluated. When these methylated analogs were administered to mares in doses that induced measurable locomotor stimulation, the analog's presence was readily detected in individual or pooled samples.