Influence of age, breed, and stage of pregnancy on hepatic ultrasonographic findings of cows was determined. In addition, the relation between body weight, height at the withers, milk production, and the measurements determined via ultrasonography was investigated. The liver of 186 cows was examined ultrasonographically. The cows comprised Swiss Braunvieh, Simmental, and Holstein breeds, and age ranged from 2.5 to 11.5 years. The ultrasonographic findings of the liver, gallbladder, caudal vena cava, and portal vein were described, and the position, size, thickness, and distal angle of the liver were determined. In addition, the position and diameter of the caudal vena cava and portal vein were determined. There was no significant difference between any of the variables determined and breed or age. Therefore, measurements for the 3 breeds and for the various ages were summarized into 1 group. There were significant correlations between body weight, milk production, and size and thickness of the liver. In 3 pregnant cows, the liver was examined ultrasonographically 8 times during the course of pregnancy. Positive correlation was detected between stage of pregnancy and diameter of the caudal vena cava. There was a negative correlation between stage of pregnancy and diameter of the portal vein. In 23 cows, the ultrasonographically determined measurements of the liver were compared with those determined at slaughter. Weight of the liver correlated well to thickness of the liver determined via ultrasonography.

Arterial blood samples were collected from 19 anesthetized pigs before and after hemorrhage was induced. Blood gas tensions and concentrations of sodium, potassium, chloride, lactate, and total protein were measured. Results indicated that hydrogen ion (H+) concentration calculated from a specific formula was a biased and imprecise estimate of measured H+ concentration. The bias was 5.45 nEq/L, with limits of agreement from -7.92 to 18.83 nEq/L. Because albumin is the fraction of plasma protein most important in acid-base balance, the agreement between predicted and measured H+ concentration was reevaluated, using an albumin charge estimate and a reference swine albumin-to-globulin ratio. This improved the ability of the formula to predict H+ concentration; the bias decreased to 1.33 nEq/L with limits of agreement from -12.16 to 9.49 nEq/L. The formula and a simplified approach for clinical application were biased and unacceptably imprecise estimators of lactate (L-) concentration. The formula approach underestimated L- concentration by 2.8 (-12.4, 6.7) mEq/L, whereas the simplified method overestimated L- concentration by 5.0 (-3.8, 13.9) mEq/L.

Maximal conduction velocities of compound action potentials evoked by stimuli of 2 times threshold in the caudal cutaneous sural (CCSN) and medial cutaneous antebrachial (MCAN) nerves were determined by averaging potentials evoked and recorded through percutaneous needle electrodes. Mean maximal conduction velocities of compound action potentials were: CCSN = 61.3 +/- 2.0 meters/second (m/s) and MCAN = 56.4 +/- 2.8 m/s. To confirm accuracy of our percutaneous recordings, compound action potentials were recorded through bipolar chlorided silver electrodes from the exposed surfaces of fascicles of the CCSN and the MCAN. The maximal conduction velocities of these potentials were in agreement with the conduction velocities of compound action potentials that were evoked and recorded through percutaneous needle electrodes. The specificity of stimulating and recording sites was verified by recording before and after section of the nerves. Stimuli from 3 to 5 times threshold evoked a second, longer latency, compound action potential that consisted of a variable number of components in the CCSN and MCAN. The configurations and conduction velocities of the shorter latency potentials were the same as those of the single compound action potentials evoked by stimuli of 2 times threshold. Mean conduction velocities of the longer latency potentials were: CCSN = 24.4 +/- 2.6 m/s and MCAN = 24.5 +/- 2.2 m/s. Needle electrode and direct stimulation of either the CCSN or the MCAN at 3 to 5 times threshold failed to evoke contractions of limb muscles. Therefore, action potentials that contributed to the evoked compound potentials recorded in these horses arose, most likely, from afferent nerve fibers.

A method for quantification of serum total IgE concentration in dogs by use of an ELISA containing monoclonal mouse anti-canine IgE was developed. Microtitration plates were coated with monoclonal mouse anti-canine IgE. Test sera and reference serum dilutions were added, followed by biotinylated monoclonal mouse anti-canine IgE. Avidin-alkaline phosphatase conjugate was added, and color development was measured spectrophotometrically, using a microtitration plate reader. Quantitative results were obtained by assigning to a reference serum a value of 100 IgE units/ml. Absorbance values of unknown samples were converted into IgE units by comparison with a standard curve generated by measurement of reference serum dilutions. Intra- and interassay coefficients of variation were 5 and 7%, respectively, and assay sensitivity was 1 U/ml. The assay was used to establish a normal range for total IgE concentrations in 30 healthy dogs. Total IgE concentration in healthy dogs followed a skewed distribution and ranged from < 1 to 91.2 U/ml, with a geometric mean value of 7.1 U/ml. The IgE concentration was remarkably stable in serum samples subjected to 25 freeze/ thaw cycles or incubation at approximately 25 C (room temperature) for up to 10 days. Comparison of total IgE concentrations in 23 serum samples assayed by use of double-overlay radial immunodiffusion and ELISA yielded correlation coefficient of 0.94. Comparison of the reference serum standard curve with serial dilutions of a purified IgE solution of known concentration yielded a range of values for the IgE unit of 0.7 to 2.0 micrograms.

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.

Sheep given powdered Ferula communis variety brevifolia at dosage of 2.5 g/kg of body weight/d for 15 days developed classical clinical signs of intoxication: anorexia, somnolence, apparent weakness, and hemorrhage. Marked reduction of vitamin K-dependent coagulation factors and prolongation of prothrombin time and activated partial thromboplastin time were consistent with presence of ferulenol, a toxic coumarinic factor in the plant. Changes induced in the coagulation system developed by the second day of plant administration and were normal within 4 days after dosing was stopped. There was no evidence of primary liver damage or platelet malfunction. Of 6 intoxicated sheep, 2 died with only minimal evidence of hemorrhage.

The effect of a dietary supplement, choreito, on in vitro struvite crystal growth in feline urine was evaluated. Adult specific-pathogen-free cats (4 females, 4 males) considered to be clinically normal on the basis of physical examination findings and normal results of CBC, serum biochemical analyses, and urinalyses obtained before the beginning of the study were used. Before 24-hour urine sample collections were made, cats were fed a commercial canned diet with 0 or 500 mg of choreito supplement/kg of body weight for at least 2 weeks in a cross-over design with 4 cats/treatment. Filtered urine samples were analyzed for urine pH, specific gravity, osmolality, and urine electrolytes. The struvite activity product was calculated, using a statistical software program that calculates urine saturation. Urine samples were placed in wells of cell culture plates, increasing concentrations of ammonium hydroxide were added to adjacent wells to stimulate struvite crystal growth, and the plates were incubated at 37 C. Crystal growth was assessed by determination of number of crystals and supersaturation index by direct visualization, using an inverted microscope. Supplementation of the diet with choreito (at this concentration) did not change urine pH, specific gravity, osmolality, urine electrolyte composition, or calculated struvite activity product. However, supplementation significantly (P < 0.05) reduced crystal number and supersaturation index. These results indicate that direct observation of struvite crystal formation in whole urine may more accurately predict the effects of treatments to prevent or treat struvite urolithiasis than do calculations based on electrolyte concentration that do not account for the effect of urine macromolecules. It also may mean that choreito consumption affects the concentration of inhibitors or promoters in urine. It was concluded that choreito significantly (P < 0.05) reduced growth of struvite crystals in feline urine, and thus may have a role in prevention of feline struvite urolithiasis. In vivo studies will be necessary to test this hypothesis.

Packed cell volume and plasma total protein (TP), serum albumin (Alb) and globulin (Glb), and plasma ionized calcium (PCa) concentrations, blood viscosity (BV), and plasma viscosity (PV) were measured in 42 horses at rest and after the cross country jumping phase of a horse trial competition. The BV and Pv were determined at 6 shear rates (230, 115, 46, 23, 11.5, 5.75 s 1), using a digital rotational cone and plate microviscometer. A paired t-test was used to determine differences between PCV, TP, Alb, Glb and PCa values at rest and after exercise. The PCV, TP, Alb, and Glb values increased (P < 0.05) in horses after exercise. The PCa concentration decreased (P < 0.05) in horses after exercise. Mean BV and Pv in the 42 horses at rest and after exercise were fitted to an asymptotic function. Significant (P < 0.05) correlation at aH shear rates was seen between BV at rest and PCV, TP, Alb, Glb, and PCa values at rest; and between BV after exercise and PCV, TP, Alb, Glb, and PCa values after exercise. Significant correlation was not seen between PV at rest and TP, Alb, Glb, and PCa at rest, or between PV after exercise and TP, Alb, Glb, and PCa concentrations after exercise at any shear rate.

Epidemiologic modeling of the likely herd-to-herd transmission of pseudorabies virus (PRV) was developed to assess the progress and potential for the PRV-eradication program in the United States. The herd-to-herd transmission of PRV over a 20-year period (1993 to 2012) in the United States was simulated under various scenarios, which included variable program-funding levels and variable prevalences. A transition model (Markov process model) was used to predict yearly changes in herd prevalence of PRV infection. Five mutually exclusive states of nature for herds were assumed: uninfected and not vaccinated; uninfected and vaccinated; known to be infected and not vaccinated; known to be infected and vaccinated; and infected, but not known to be infected. Three prevalences for states in the United States were assumed: higher prevalence, moderate prevalence, and lower prevalence. Three funding levels were assumed: no eradication program, continued funding at the current level, and increased funding of 25%. Estimates made by an expert panel for determining probabilities in the state-transition matrices were used. A model also was developed, and was considered to be the most optimistic scenario likely under increased funding of 25%. The most optimistic estimates of the probabilities that still lay within the range of estimates made by the expert panel were used for this model. Only the optimistic transmission matrices allowed for total eradication of PRV. Using the optimistic matrices, all states in the United States of America had moved into the moderate- or low-level risk status by the year 2000. The longest time taken to achieve eradication was for the state of Iowa, where eradication was not achieved until 2012.