Endotoxin concentrations in the blood following intravenous injection and effect on prostaglandin F2 alpha release, calcium and bile acids in goats

Injection of endotoxin from Salmonella typhimurium in male goats resulted in a biphasic release pattern of PGF2 alpha, as determined by 15-ketodihydro-PGF2 alpha concentrations in plasma. A small initial peak at 30 minutes was followed by a second peak one hour after injection. The rectal temperature increased three to five hours after endotoxin injection and calcium concentrations started to decrease soon after injection; a significant decrease was seen from 105 minutes. Endotoxin concentrations varied among the animals but had a tendency to increase three hours after injection, simultaneously with a decrease in bile acid concentrations three hours after injection. The decrease in bile acids indicated alimentary stasis. Therefore, the raised endotoxin levels could be of endogenous origin. This study also shows that the prostaglandin metabolite is a very reliable parameter for estimating the effect of endotoxin.     

A computer-derived protocol using recursive partitioning to aid in estimating prognosis of horses with abdominal pain in referral hospitals

In order to determine which variables are useful and accurate in estimating prognosis in horses with abdominal pain, data were analyzed from 231 horses presented at a veterinary teaching hospital. Using multiple stepwise discriminant analysis in a recursive partition model, we obtained a decision protocol that identified survivors and nonsurvivors. The prevalence of survivors was 61% in this population. The sensitivity, specificity, and positive and negative predictive values of this model were 71, 83, 87 and 65%, respectively. This decision protocol was validated by Jackknife classification and also by evaluation with a referral population of 100 horses in which the prevalence of survivors was 83%. This led to sensitivity, specificity, and positive and negative predictive values of 83, 78, 94 and 50%, respectively.     

Detection of Ehrlichia risticii using an avidin-biotin-immunoperoxidase staining system

An indirect immunoperoxidase procedure using a specific anti-Ehrlichia risticii monoclonal antibody and an avidin-biotin-peroxidase staining method was used to detect E. risticii antigen in infected P388D1 murine monocytes. Several different methods of cytological fixation were used, including acetone (15 min), 95% ethanol (15 min), Bouin's fixative (5 hr), and 10% buffered neutral formalin (24 hr). The E. risticii organisms were labeled effectively and identified in cells fixed with acetone and ethanol. However, infected P388D1 cells fixed in 10% formalin or Bouin's fixative required enzymatic digestion with 1.0% trypsin for 15 min at 37 C before positive results were evident. This indirect immunoperoxidase avidin-biotin staining procedure proved to be a sensitive assay for the detection of intracellular E. risticii and may be an effective diagnostic procedure for formalin-fixed paraffin-embedded tissue.     

Urethral obstruction in a male llama

An 8-year-old sexually intact male llama was euthanatized because of obstruction of the penile portion of the urethra and rupture of the urinary bladder. Clinical signs of obstruction included anorexia, lethargy, teeth grinding, straining to defecate, inability to urinate, and tense abdomen. Laboratory findings included anemia, leukocytosis with left shift, high serum urea nitrogen, creatinine, and phosphorus concentrations, and low serum chloride concentration. Necropsy revealed ruptured urinary bladder and acute fibrinous peritonitis. A firm, gray, nonmineralized urethral plug occluded the penile portion of the urethra for a distance of 14 cm in the midpenile region, distal to the sigmoid flexure of the penis. The urinary bladder mucosa and the urethra had microscopic evidence of chronic inflammation. Escherichia coli, Klebsiella sp, and alpha-streptococci were isolated from the urethral plug.     

Combinations of high-moisture harvested sorghum grain and dry-rolled corn: effects on site and extent of digestion in beef heifers

To determine the effects of blends of high-moisture harvested sorghum grain (HMS) and dry-rolled corn (DRC) on site and extent of digestion, high-grain diets were fed to Angus-Hereford heifers (315 kg) in a 5 x 5 latin square. The grain portion consisted of ratios (HMS:DRC) of 0:100, 25:75, 50:50, 75:25 and 100:0. Heifers were equipped with ruminal, duodenal and ileal T-type cannulas. Digestibilities of OM (P less than .05) and non-ammonia nitrogen (NAN; P less than .01) in the total tract declined linearly as HMS replaced DRC. Chyme flow (liters/d) through the duodenum increased linearly (P less than .01), and true ruminal OM disappearance tended to decline linearly (P less than .10) as HMS replaced DRC. A quadratic response (P less than .05) in extent of starch disappearance (g/d) in the rumen was noted; blends were lower than either individual grain. Ruminal escape of feed N tended to be quadratic (P less than .10); values for individual grain types were greater than blends. Microbial efficiency increased linearly (P less than .05) as HMS replaced DRC. Extent of starch digestion in the rumen averaged 82.7% compared to only 2.9% in the small intestine and 5.7% in the large intestine. Altering the ratio of HMS to DRC appeared to have more effect on ruminal fermentation than on digestion in the small intestine; most starch and nitrogen responses were quadratic. Increases in ruminal pH and chyme flow, potentially caused by increased salivary flow, may cause non-linear changes in the solubility of proteins in HMS and DRC, when fed as blends, altering the digestibility of protein and starch from values predicted from the individual grains.     

Ionophores alter hepatic concentrations of intermediary carbohydrate metabolites in steers

The effects of ionophores on liver weight and function were determined in finishing steers (n = 24; avg weight 440 kg). Steers were group-fed one of three treatments (control, lasalocid or monensin at 33 mg/kg feed) for 46 d prior to slaughter. Three days prior to slaughter, blood was collected for the determination of serum Ca and Mg. At slaughter, the liver was removed, weighed, sampled, frozen in liquid nitrogen and subsequently analyzed for concentrations of carbohydrate metabolites and minerals. Liver weight (5.9 kg) was unaffected by treatment. Serum and hepatic Ca and Mg were not affected by ionophore treatment. Hepatic glycogen levels in steers fed ionophores were unaffected by treatment. Fructose 1,6-bisphosphate was 21% lower (P less than .10) in hepatic tissue of steers fed ionophores, whereas dihydroxyacetone phosphate was 15 to 37% greater in hepatic tissue of steers fed monensin (P less than .20) or lasalocid (P less than .10). Glyceraldehyde 3-phosphate was elevated more extensively by lasalocid than by monensin with increases of 72 (P less than .05) and 132% (P less than .001), respectively, over controls. Glycerol 3-phosphate levels were 37% (P less than .05) and 12% (NS) greater with these ionophores. Hepatic levels of pyruvate were elevated 12 (NS) to 36% (P less than .17) for monensin and lasalocid. Fructose 2,6-bisphosphate levels were 25% lower (P less than .25) in hepatic tissue of steers fed ionophores than in hepatic tissue from control steers. Other metabolites of carbohydrate metabolism in hepatic tissue were not altered appreciably. Changes in levels of intermediary metabolites of carbohydrate metabolism suggest alterations in hepatic carbohydrate metabolism favoring gluconeogenesis in steers fed ionophores.     

Formulation with CpG ODN enhances antibody responses to an equine influenza virus vaccine

Previous studies have shown that protection against equine influenza virus (EIV) is partially mediated by virus-specific IgGa and IgGb. In this study we tested whether addition of a CpG ODN formulation to a commercial killed virus vaccine would enhance EIV-specific IgGa and IgGb antibody responses, and improve protection against an experimental EIV challenge. Thirty na?ve horses were assigned to one of three groups and vaccinated as follows: 10 were given vaccine (Encevac TC4, Intervet Inc.) alone, 10 were given vaccine plus 0.25 mg CpG ODN 2007 formulated with 30% Emulsigen (CpG/Em), and 10 controls were given saline. All horses were challenged with live virus 12 weeks after the final vaccination. Antibody responses were tested by single radial hemolysis (SRH) and ELISA, and protection was evaluated by determination of temperature, coughing, and clinical scores. Killed virus vaccine combined with CpG/Em induced significantly greater serologic responses than did the vaccine alone. All antibody isotypes tested increased after the addition of CpG/Em, although no shift in relative antibody isotypes concentrations was detected. Vaccination significantly improved protection against challenge but the differences between the two vaccine groups were not statistically significant. This study is the first demonstration that CpG/Em enhances antigen-specific antibody responses in horses and supports its potential to be used as an adjuvant for vaccines against equine infections.     

Single nucleotide polymorphism identification, linkage and radiation hybrid mapping of the porcine pituitary adenylate cyclase-activating polypeptide type I receptor gene to chromosome 18

Pituitary adenylate cyclase‐activating polypeptide (PACAP) is a neuropeptide with diverse biological actions. Type I PACAP receptors (PACAPR) are specific for PACAP, whereas type II and III PACAPRs are less restricted. To localize and analyse the variation of this gene, a 559‐bp long intronic fragment of the porcine PACAPR gene was amplified by polymerase chain reaction and sequenced in samples from five different pig breeds. One single nucleotide polymorphism was identified and its allele frequency was determined in all five breeds. Linkage analysis in a Berkshire × Yorkshire reference family placed the PACAPR gene on chromosome 18, between SW787 and S0062 (SW787– 8.1 cM –PACAPR– 3.0 cM –S0062). Radiation hybrid mapping confirmed that the PACAPR gene was linked to SW1682 on chromosome 18 (28.8 cR₃₀₀₀; LOD = 10.4).