Plasma alpha-tocopherol (vitamin E) values weremonitored serially in 9 foals sired by a stallion with equine degenerative myeloencephalopathy (EDM) and in 5 age-matched control foals (sired by a clinically normal stallion) raised in the same environment for the first year of life. Clinical evaluation determined that 8 of the 9 foals sired by the stallion with EDM had neurologic deficits consistent with the disease on one or more occasions during the study period, whereas control foals had normal gait. From 6 weeks to 10 months of age, plasma alpha-tocopherol values in foals with signs of EDM were significantly (P < 0.001) lower than those in control foals. An oral vitamin E absorption test was performed, and results for 8 of the affected horses and the affected stallion were compared with results for 4 of the monitored control horses and 4 additional control horses. Significant differences were not evident in any of the absorption indices. On the basis of data from this study and supported by reported prophylactic and therapeutic benefits of supplemented vitamin E, low plasma concentration of vitamin E is concluded to be a factor in the development of EDM in the first year of life of hereditarily predisposed foals. It was also concluded that the significantly lower alpha-tocopherol values seen in the foals in this study did not reflect a primary gastrointestinal tract absorption problem.

The hemodynamic effects of 1.5 minimal alveolar concentration of halothane alone (1.6% end-tidal) and 1.5 minimal alveolar concentration of halothane (1.1% end-tidal concentration) combined with epidurally administered morphine were compared during controlled ventilation in 10 dogs used on 2 occasions and randomly allocated to 2 groups. Arterial blood pressure, cardiac index, stroke volume, left ventricular work, and pulmonary arterial pressure were significantly (P < 0.05) higher in dogs of the morphine-treated group before administration of morphine. After epidural administration of morphine (0.1 mg/kg of body weight diluted in 0.26 ml of saline solution/kg), hemodynamic changes were not observed, and the aforementioned variables remained significantly (P < 0.05) higher than values in dogs of the halothane only group. Compared with halothane (1.6%) alone, the reduction in halothane end-tidal concentration (1.1%) associated with epidurally administered morphine is beneficial in maintaining hemodynamic function.

Gentamicin sulfate-induced nephrotoxicosis was compared in 2 groups of horses fed different rations. Four horses were fed only alfalfa hay, and 4 other horses were fed only whole oats. Seven days after initiation of the diet, all horses were given gentamicin IV (5 mg/kg of body weight) every 12 hours for 22 days. Urinary gamma-glutamyltransferase to urinary creatinine (UGGT:UCr) ratio was calculated daily, and serum concentration of gentamicin was measured at 1 and 12 hours after drug administration. Results indicated that horses fed oats had greater renal tubular damage than did horses fed alfalfa. Mean UGGT:UCr for horses fed alfalfa was 47.1 +/- 18.8 and was 100.0 +/- 19.0 for horses fed oats (P = 0.007). The UGGT:UCr in horses fed oats was > 100 for a total of 54 days; horses fed alfalfa had UGGT:UCr > 100 for only 7 days. Two horses not given gentamicin were fed only oats and 2 were fed only alfalfa. These horses had mean UGGT:UCr of 17.6 +/- 2.2 and 30.5 +/- 3.0, respectively. Mean peak and trough concentrations of gentamicin were statistically different for horses fed oats and those fed alfalfa (peak 23.16 +/- 1.87 and 14.07 +/- 1.79 microgram/ml, respectively [P = 0.0001], and trough, 1.81 +/- 0.69 and 0.71 +/- 0.70 microgram/ml, respectively [P = 0.02701)]. Mean half-lives of gentamicin (estimated from peak and trough concentrations) for horses fed alfalfa (2.58 +/- 0.26 hours) and horses fed oats (2.88 +/- 0.27 hours) were not significantly different. Horses fed only oats had greater degree of gentamicin-induced nephrotoxicosis than did those fed only alfalfa.

The purpose of this study was to document the effect of calfhood vaccination for Mycobacterium paratuberculosis on a serologic ELISA. Fifteen calves vaccinated with a killed paratuberculosis vaccine and 5 unvaccinated control calves were tested from the first through the fifteenth month of life. Age of vaccination ranged from 5 to 40 days. Blood samples were collected prior to vaccination and periodically thereafter. Serum antibody was analyzed by use of the ELISA. All calves were Elisa-negative prior to vaccination. Thirteen of 15 vaccinated calves became ELISA-positive between 2 and 6 months after vaccination. The unvaccinated cohort remained Elisa-negative. Widespread use of vaccine may interfere with diagnosis of paratuberculosis and with control programs that are based on serologic tests that measure humoral antibody.

Pathophysiologic effects of Ostertagia ostertagi infection and their prevention by strategic anthelmintic treatments were studied in 3 groups each of 6 steer calves. Group-1 calves were noninfected controls. Group-2 calves were inoculated with 100,000 third-stage larvae on the 1st and 28th days of the experiment and grazed on pasture initially free of contamination. Group-3 calves were on a similar regimen as those in group 2, but were also treated with ivermectin 9 days after each larval inoculation. Group-2 calves had increased plasma pepsinogen and gastrin values and decreased weight gains, and total serum protein and albumin concentrations from the 2nd week of infection onward. They were anemic at 10 to 12 weeks and had lower carcass and meat quality at slaughter. Strategic anthelmintic treatments were effective in preventing these effects and calves in groups 1 and 3 had similar performances. On the basis of our findings, high pepsinogen values were related to worm burdens, whereas high gastrin concentrations were related to gastric lesions.

A technique for detection of bovine viral diarrhea virus (BVDV) from circulating blood leukocytes, using the polymerase chain reaction, is described. The published nucleotide sequences of 2 strains of BVDV and that of hog cholera virus were aligned and the information was used to design oligonucleotides coding for 2 regions of amino acid homology. The oligonucleotides were a mixed population including all possible codons for the conserved amino acids. These degenerate oligonucleotides were used in the polymerase chain reaction to detect viral RNA in cells infected in vitro, or in circulating blood leukocytes from infected animals. Virus was detected in over 60 samples from diverse isolates. The detection of BVDV by the polymerase chain reaction is a rapid, sensitive, and specific technique, which represents an improvement over existing technology.

Ten foals of various breeds were deprived of colostrum from birth to 36 hours of age, then were allotted to 2 groups. Foals of group 1 (n = 6) were given 20 g (200 ml) of purified equine IgG IV in a 10% solution, and foals of group 2 (n = 4) were given 30 g (300 ml) of the same preparation. Total administration time for each 10 g of IgG in 100 ml was approximately 10 minutes. Serum IgG concentration in foals was assessed prior to, between 24 and 48 hours, and at 7 and 14 days after IgG administration. Between 24 and 48 hours after IgG administration, mean serum IgG concentration in group-1 foals was 425 mg/dl (range, 350 to 480 mg/dl). Mean body weight for this group of foals was 50.3 kg (range, 43.3 to 54.7 kg). For group-2 foals, mean serum IgG concentration was 768 mg/dl (range, 640 to 920 mg/dl) between 24 and 48 hours after administration of IgG. Foals of this group had mean body weight of 43.2 kg (range, 36.5 to 47.5 kg). Serum IgG concentration in group-2 foals at 24 to 48 hours was significantly (P = 0.005) greater than that in group-1 foals. Mean total IgG recovery at 24 to 48 hours, calculated on the basis of 94.5 ml of plasma volume/kg of body weight, was approximately 100%. Values of IgG measured in all foals 1 and 2 weeks after administration of the IgG concentrate were equivalent to values expected after normal decay of passively acquired IgG. Mild, adverse reactions occurred in 3 of the treated (1 group-1 foal and 2 group-2 foals).

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were Liven each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, IV; xylazine, 2.2 mg/kg, IM; detomidine, 0.01 mg/kg, IV; detomidine, 0.02 mg/kg, IV; and detomidine, 0.04 mg/kg, IM. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following IV administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, IV administration of 0.02 mg of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, + dP/dt and - dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The PCV was significantly reduced by all treatments. Respiratory rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 IV treatments only.

Axial length and corneal curvature were determined by use of A-scan ultrasonography and keratometry on both eyes of dogs of various breeds, sizes, and ages. Mean axial length was 20.43 +/- 1.48 mm; axial length was not related to age or sex, but was significantly greater (P = 0.047) in dogs of larger breeds. Mean corneal curvature was 39.94 +/- 2.61 diopters. Dogs of large breeds had significantly (P < 0.001) flatter corneas. Mild, roughly symmetric astigmatism was detected in a majority of dogs. Use of mean values in a theoretic artificial intraocular lens power equation suggests that aphakic dogs require an implant of approximately 40 diopters to achieve emmetropia.

The effects of single IV injections of sodium bicarbonate (0.5 mEq/kg of body weight, 1 mEq/kg, 2 mEq/kg, and 4 mEq/kg) on serum osmolality, serum sodium, chloride, and potassium concentrations, and venous blood gas tensions in 6 healthy cats were monitored for 180 minutes. Serum osmolality increased and remained significantly (P less than 0.05) increased for 120 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium was increased significantly (P less than 0.05) for 30 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium decreased and remained significantly (P less than 0.05) decreased for 120 minutes in cats given 1 g of 20% mannitol/kg, and serum osmolality was significantly (P less than 0.05) decreased at 30 and 60 minutes. Serum chloride decreased significantly (P less than 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and was significantly decreased for 30 minutes in cats given 2 mEq and 4 mEq of sodium bicarbonate/kg. Serum chloride decreased and remained significantly (P less than 0.05) decreased for 30 minutes in cats given 1 g of 20% mannitol/kg. Serum sodium and serum osmolality did not change significantly (P less than 0.05) in cats given 4 ml of 0.9% sodium chloride/kg. Serum potassium decreased significantly (P less than 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and for 120 minutes in cats given 2 mEq/kg or 4 mEq/kg. There was a significantly (P less than 0.05) greater decrease in serum potassium that lasted for 30 minutes after giving sodium bicarbonate at the dosage of 4 mEq/kg, compared with other dosages given. Serum potassium did not change significantly in cats given 1 g of 20% mannitol/kg, but was significantly (P less than 0.05) decreased 10 minutes following 4 ml of 0.9% sodium chloride/kg. Sodium bicarbonate infusion significantly (P less than 0.05) increased venous blood pH and plasma bicarbonate concentration in all cats. The magnitude and duration of these changes were significantly greater following administration of sodium bicarbonate at dosages of 2 mEq/kg and 4 mEq/kg. Significant (P less than 0.05) increases in PCO2 were associated only with the highest dosage of sodium bicarbonate (4 mEq/kg). Base excess increased significantly (P less than 0.05) in all cats following sodium bicarbonate infusion. There were significantly (P less than 0.05) greater increases in base excess lasting 30 minutes following administration of sodium bicarbonate at dosages of 2 mEq/kg and 4 mEq/kg. Significant (P less than 0.05) changes in venous blood pH, PCO2, or bicarbonate were not observed in cats given 4 ml of 0.9% sodium chloride/kg, or in cats given 1 g of 20% mannitol/kg. Base excess was significantly (P less than 0.05) increased for 10 minutes in cats given 1 g of 20% mannitol/kg. As expected, 4 mEq of sodium bicarbonate/kg induced the most time- and dosage-related effects. Caution should be used when administering sodium bicarbonate IV to cats at dosages greater than 2 mEq/kg, because of the potential for important acid-base and electrolyte changes.