During the spring of the first year of a vaccine study, 57 of 238 calves (24%), in which modified-live Pasteurella haemolytica vaccine (MLV) was injected twice, developed 1 or more abscesses. Abscesses were not observed after multiple visual examinations of 437 calves given killed P. haemolytica bacterin or placebo injections of similar adjuvants used in the vaccine and bacterin. Calves that developed abscesses after the second injection of MLV weighed significantly (P < 0.05) less (on the basis of body weight adjusted for weaning weight) at the second injection than did those that did not develop abscesses. Compared with calves given MLV that did not develop observable abscesses, calves developing abscesses after the second injection of MLV weighed 11.0 and 14.2 kg less, respectively, at 56 days and 112 days after injection, and they had 11.0 kg less gain at 56 days after injection. Abscess prevalence tended to be highest on certain days or at certain locations used for cattle processing, and the prevalence of abscesses increased in cattle processed later on a given day. Abscesses were not observed in 2 other groups of similarly treated calves vaccinated in the autumn or in the subsequent spring.

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.

A commercially available radioimmunoassay kit for measurement of human osteocalcin was validated for use in horses. For accurate measurement of equine serum osteocalcin, blood samples may be collected at a temperature between 20 and 25 C, then centrifuged within 90 minutes; serum may be stored at - 20 C in plastic tubes for up to 26 weeks. Serum may be thawed and refrozen up to 5 times without significant change in measured equine serum osteocalcin concentration. Assay sensitivity was 0.16 ng/ ml. Recovery of bovine osteocalcin standard added to equine serum was linear. Intra-assay coefficient of variation (x 100) for 2 equine serum pools was 6.9 (mean +/- SD, 13.9 +/- 1.0 ng/ml) and 7.5 (10.6 +/- 0.8 ng/ml) %. Interassay coefficient of variation for 3 equine serum pools measured in 12 assays was 12.5 (16.1 +/- 2.0 ng/ml), 12.7 (11.5 +/- 1.5 ng/ml), and 24.6 (3.0 +/- 0.7 ng/ml) %. Dilutional parallelism was documented by assaying pooled equine serum at 4 dilutions and correcting the mean result for dilution. Significant change was not observed in equine serum osteocalcin concentration for various time-of-day blood sample collections in horses housed under continuous lighting.

To assess the role of enterotoxigenic (ETEC), verotoxigenic (VTEC), and necrotoxigenic (NTEC) Escherichia coli in cattle with diarrhea, 1,524 colonies of E coli isolated from 197 calves with diarrhea and from 112 healthy controls were investigated for production of heat-labile and heat-stable enterotoxins, verotoxins, and cytotoxic necrotizing factors (CNF1 and CNF2). The ETEC were isolated from only 2 (1%) calves with diarrhea and from 5 (4%) healthy controls. In contrast, VTEC and NTEC that produced CNF2 were frequently identified. The VTEC were isolated from 18 (9%) calves with diarrhea and from 21 (19%) healthy cattle (P < 0.05), whereas NTEC that produced CNF2 were detected in 39 (20%) ill calves and in 38 (34%) controls (P < 0.01). Therefore, VTEC and NTEC that produced CNF2 were isolated significantly more frequently from healthy than diseased calves. Serogroups to which VTEC belonged differed considerably from the O groups involved with NTEC. Although, VTEC belonged to 18 serogroups, only 4 (O26, O103, O113, and O157) accounted for 56% (25 of 45) of verotoxigenic strains. The NTEC that produced CNF2 belonged to 26 serogroups; however, 64% (69 of 108) were from 6 serogroups (O1, O3, O15, O55, O88, and O123). Our results are compatible with cattle being a reservoir of VTEC that are pathogenic for human beings and with ETEC being an unusual cause of bovine colibacillosis in Galicia (northwestern Spain). Furthermore, results of this study indicate that VTEC and NTEC that produced CNF2 may be part of the normal intestinal flora of cattle.

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.

Cats with cardiomyopathy, especially dilated cardiomyopathy associated with taurine deficiency, often develop systemic thrombi. To investigate the relation of taurine deficiency to formation and persistence of thrombi, cats were made taurine-deficient by consumption of a casein-based taurine-deficient diet, then were evaluated for anticoagulant and pro-fibrinolytic activities and platelet function. The cats served as their own controls in the taurine-replete state; then, values were compared for the taurine-deficient state. Plasma (P < 0.01), blood (P < 0.05), and platelet (P < 0.05) taurine concentrations were decreased markedly after cats consumed the taurine-deficient diet for 6 weeks, compared with baseline concentrations before diet. Compared with the taurine-replete state, taurine deficiency induced significantly (P < 0.05) increased mean antithrombin III activity, no significant change in plasminogen and fibrinolytic activities, and similar clot retraction/lysis test results. Decreased (P < 0.01) adenosine diphosphate (ADP)-induced platelet aggregation and [14C]serotonin release, and slightly increased (P < 0.05) collagen-induced platelet [14C]serotonin release, but unchanged collagen-induced platelet aggregation were observed in taurine-deficient cats, compared with taurine-replete cats. Changes in antithrombin III activity most likely reflected hepatocellular acute-phase reaction, which indicates that taurine deficiency may induce a stress-responsive state. Results of platelet function testing indicate that taurine may modulate platelet responsiveness to physiologic agonists, but not in a consistent manner. That platelets from the taurine-deficient cats had decreased responsiveness to ADP, but increased responsiveness to collagen is surprising, because irreversible aggregation is mediated by release of granule-associated ADP after sufficient initial stimulus. All cats had normal clot retraction in dilute blood, which indicated adequate platelet numbers and function; however, clots failed to lyse in vitro. To the authors knowledge, this observation, at present, lacks adequate explanation. Development of marked taurine deficiency and altered in vitro results of anticoagulant activities and some platelet function tests did not result in clinical manifestations in our cats. Results of our study do not conclusively document a pathophysiologic role of taurine depletion in the formation or persistence of thrombi.

Cows and calves from a 1,600-cow drylot dairy were screened for IgG antibodies to Salmonella dublin lipopolysaccharide (LPS), using an indirect ELISA. The ELISA was performed on milk samples from lactating cows and on sera from nonlactating cows and calves. Fecal samples were collected from calves and nonlactating cows for culture of Salmonella spp. All seropositive cattle were retested by culture and ELISA 5 times at monthly intervals or until antibody concentration decreased. None of the cattle remained culture-positive and seronegative. Prior to and during the sample collection period, approximately 30% of calves < 8 weeks old died of S dublin infection. Vaccination of cows with a killed S dublin/S typhimurium vaccine at cessation of lactation was a routine management practice. The ELISA-determined Igg response to vaccination had decreased by 50 days after vaccination. Eight cows and 5 calves that maintained a high serologic response to S dublin were purchased and moved to a research facility for 6 months of intensive monitoring. Lactating cows were milked twice daily, and culture of milk and feces for Salmonella spp was performed 5 times/wk. Serum IgG antibodies to S dublin LPS were measured weekly, using ELISA. At the end of 6 months, all 13 cattle were necropsied and tissues were obtained for culture of Salmonella spp. All 8 cows and 5 calves maintained persistently high ELISA titer for the 6 months of testing, and shed S dublin in the milk and/or feces during the same period. On this basis, they were termed S dublin carriers. Salmonella dublin was isolated from mammary tissue of 2 calves at necropsy, indicating that bacteremia may be a mode of mammary infection by S dublin. Results of the study indicated serologic testing can be used successfully on a large dairy to identify S dublin carrier cattle. Using initial milk screening, 42 of 1,268 lactating cows were identified as suspect, requiring repeated serologic testing. One nonlactating cow, 7 of the 42 suspect lactating cows, and 5 of the 222 calves maintained an Igg response, and were found to be S dublin carriers. Carrier cows shed S dublin in 3.35% of fecal samples and 2.51% of milk samples, and carrier calves shed S dublin in 17.26% of fecal samples.

Thirty young ponies were examined endoscopically for evidence of gastric ulceration. Seven ponies had noninduced gastric ulcers present at the initial examination and were eliminated from the study. In an attempt to induce gastric ulcers experimentally, flunixin meglumine (1.1 mg/kg of body weight, IM, q 8 h) was administered for 7 days to the 23 ponies with endoscopically normal gastric mucosa. During the 7 days of flunixin administration, 11 ponies developed gastric ulcers that were appropriate for study. The 11 ponies were randomly allotted to 2 groups. Group-A (n = 5) and group-B (n = 6) ponies received ranitidine (4.4 mg/kg, PO, q 8 h) and corn syrup, respectively, until ulcers healed or for a maximum of 40 days. General anesthesia was induced every 3 to 5 days for visual evaluation of ulcer healing by use of a video endoscope. The earliest complete healing of gastric lesions observed in a corn syrup-treated pony was at 17 days. At 40 days, 3 of 5 and 3 of 6 ponies of the ranitidine and corn syrup-treated groups, respectively, had healed ulcers. Results of this study indicate that: noninduced gastric ulcers may be common in young ponies, flunixin meglumine may be effective in inducing gastric ulcers for gastric healing studies in young ponies, and ranitidine (4.4 mg/kg, q 8 h) is not significantly effective in accelerating healing of experimentally induced gastric ulcers in ponies under conditions of this study.

Stimulatory effects of 6 zymosan preparations on luminol-dependent chemiluminescence (CL) responses of isolated bovine neutrophils were compared. Unopsonized zymosan particles and zymosan particles opsonized with bovine IgG1, IgG2, fresh serum, or serum from which zymosan-specific antibodies, but not complement, had been removed (C3- serum) induced strong CL responses, with nearly equal maximal peaks in the presence of extracellular Ca2+ and Mg2+, whereas the response to fetal bovine serumopsonized zymosan particles was markedly low. Removal of extracellular divalent cations almost completely blocked the CL reaction triggered by unopsonized, IgG1-opsonized, C3-opsonized, and fetal bovine serum-opsonized zymosan particles. By contrast, no change in the respiratory burst activity induced by serum-opsonized zymosan and only partial reduction in the response to IgG2-opsonized zymosan were seen under these conditions. Further experiments were performed with 4 zymosan preparations on neutrophils isolated from 2 calves with a genetic deficiency of CD11/CD18 membrane antigens. The unopsonized zymosan-induced CL reaction was absent in these cells. A reduced, but clear, response was observed with C3-opsonized zymosan. Unexpectedly, in the absence of extracellular Ca2+ and Mg2+ , serum-opsonized zymosan failed to generate the respiratory burst, whereas response to IgG2-opsonized zymosan was normal in the CDll/CD18-deficient neutrophils. These findings indicate that unopsonized zymosan may act in a divalent cation-dependent manner at the receptor for C3bi in bovine neutrophils, as it has been shown to do in the human system. In addition, it seems that IgG2-Fc receptors capable of signaling the respiratory burst in the absence of extracellular Ca2+ and Mg2+ exist on bovine neutrophils.