Sheep had viremias that were first detected on day 3 (+/- 1) after infection with several strains of bluetongue virus (BTV) representing United States serotypes 10, 11, 13, and 17. Diphasic peaks of infectivity were attained on days 6 and 10 (+/- 2). Interferon (IFN) was first detected in serum samples on day 5 (+/- 1), and reached greatest concentrations on day 6 (+/- 2), which coincided with the first viremic peak; IFN concentrations then decreased toward zero by day 10 (+/- 2). Interferon peak concentrations induced approximately a 90% decrease in virus titer. The decrease in IFN concentrations by day 9 (+/- 2) corresponded with the second viremic peak on day 10 (+/- 2). Onset of the decrease in detectable concentrations of virus after the second peak of viremia corresponded to the initial detection of serum antibody to BTV by day 10 (+/- 2). Virus titer decreased and antibody production increased until approximately days 21 to 28, when the titers plateaued and virus was not detected. Febrile responses peaked on day 7 (+/- 1) during the peak viremic period. The WBC count was depressed at the time the virus titer increased, but returned to normal values while the sheep were still viremic. Diphasic viremias in BTV-infected sheep were attributed to induction of high concentrations of IFN concurrent with the first virus titer peak, followed by production of antibody to specific BTV strains and a subsequent reduction in viremia at the second virus titer peak.

Enzyme-linked immunosorbent assay screening of antibody produced against aflatoxin was accomplished by a new and simple procedure. To demonstrate the new indirect ELISA technique used, antibody against aflatoxin M1 was produced in female BALB/CJ mice by immunization with an aflatoxin M1-bovine serum albumin conjugate. Instead of coating test-plate wells with purified antibody (direct ELISA) or synthesizing a second protein-aflatoxin conjugate (aflatoxin M1-poly-L-lysine) to coat test-plate wells, wells were coated with the readily available aflatoxin M1-bovine serum albumin and aflatoxin B1-bovine vine serum albumin. This method, applicable for any aflatoxin conjugated by the common cyclopentano-carboxymethoxyl-oxime technique, eliminates the more time-consuming and technically difficult portions of earlier direct and indirect ELISA. The new technique can be valuable in continued efforts toward development of new and improved immunoassays against aflatoxin metabolites.

Pulmonary lavage samples were collected from 90- to 130-day-old calves before and 6 days after aerosol inoculation with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI3) virus. Alveolar lining material was separated from lavage fluids by high-speed centrifugation and phospholipids were extracted from alveolar lining material and analyzed by high-performance liquid chromatography. Phosphatidylcholine and phosphatidylethanolamine were 74.2 +/- 6.5% and 13.3 +/- 2.8%, respectively, of the total phospholipid content in the surfactant obtained from calves before virus inoculation. Other phospholipids were represented by substantially lower percentages. Infection with either of the 2 viruses caused a significant (P < 0.05) decrease in the percentage of phosphatidylcholine to 66.0 +/- 8.0% and 65.1 +/- 10.8% in the calves inoculated with BHV-1 and PI3 virus, respectively. A significant (P < 0.05) increase in the percentage of phosphatidylethanolamine to 18.1 +/- 2.2% and 17.8 +/- 4.5% developed in calves inoculated with BHV-1 and PI3 virus, respectively. Infection with BHV-1 also induced an increase (not significant) in the percentage of phosphatidylinositol from 5.5 +/- 2.8% to 7.8 +/- 2.2%. A similar, but not significant, increase in the percentage of phosphatidylinositol was also seen in the calves inoculated with PI3 virus. Less substantial changes in the percentage of other phospholipids were detected after virus infection.

The Escherichia coli heat-stable enterotoxin (STb) is the most prevalent toxin associated with diarrheagenic E coli isolates of porcine origin. Unequivocal biological activity of this toxin has been observed only in swine intestine. In this study, when endogenous protease activity was blocked with soybean trypsin inhibitor, intestinal secretion was stimulated by STb in jejunal loops of rats, mice, calves, and rabbits. Compared with pigs, rats, mice, and calves, rabbits were relatively insensitive to STb. These data demonstrate that the activity of STb is not a species-specific toxic activity; there is species variation in sensitivity to STb, and some common laboratory animals may have potential to be used to measure biological activity Of STb.

Thirty-six of 50 young equids examined at necropsy for gross pathologic and histopathologic evidence of osteochondrosis were determined to have lesions characteristic of this disorder in the distal joints of the tarsus. Abnormalities ranged from retained endochondral cores underlying undisturbed articular cartilage surfaces to clefts, subchondral osseous cyst-like lesions, and cartilage ulceration. Our findings supported the conclusion that osteochondrosis may cause spavin in the juvenile equid.

It has been shown that zearalenone disrupts early pregnancy in swine without altering intrauterine content of estradiol 17 beta or progesterone, embryo migration, or estradiol-17 beta thesis by blastocysts. However, serum concentrations of progesterone were reduced 2 to 3 weeks after mating in gilts that ingested zearalenone. Therefore, progesterone was administered to gilts during early pregnancy to determine whether it could counteract the detrimental actions of zearalenone on embryonic development. Thirty-two crossbred gilts (Hampshire X Chester White X Yorkshire X Duroc) were assigned randomly to a 2 X 2 factorial arrangement of treatments: zearalenone (Z); zearalenone plus progesterone (ZP); progesterone (P); or control (C). From postmating days 4 to 15, Z- and ZP-treated gilts were fed 1 mg of Z/kg of body weight, and P-treated and C gilts were fed ethanol as vehicle in a corn-soybean diet. On postmating days 3 to 15, P- and ZP-treated gilts were injected IM with 100 mg of progesterone, and C and Z-treated gilts were injected with progesterone carrier (15% ethanol, 15% benzyl alcohol, 70% propylene glycol). Blood was collected from gilts by puncture of the jugular vein daily from days 3 to 15, on alternate days from days 17 to 31, and then twice weekly until the end of the experiment. Fetal development was assessed in Z and ZP-treated gilts on postmating day 47.6 +/- 2.9 by cesarean section and in P-treated and c gilts at slaughter on postmating days 51.2 +/- 3.2. Serum concentrations of progesterone in P-treated gilts were greater on days 7 to 8, 10 to 15, 17, and 19 than in C gilts. Serum concentrations of progesterone were greater on days 8, 10, and 12 in ZP-treated than in C gilts. However, serum concentrations of progesterone were lower in ZP-treated gilts than in C gilts on postmating days 19 to 31. Serum concentrations of progesterone were lower in Z-treated gilts than C gilts on postmating days 15, 17, and 19. At slaughter or cesarean section, viable fetuses were not found in Z-treated gilts, but 80% of the C and P-treated gilts had viable fetuses. All Z-treated gilts were classified as pseudopregnant because uteri were turgid and the ovaries had functional corpora lutea. Uteri of ZP-treated gilts appeared normal. Corpora lutea of pregnancy had regressed by postmating day 35 in 7 of 8 ZP-treated gilts. Crown-to-rump length was similar between P-treated and C gilts (94 vs 92 mm). Fetal weight was similar between P-treated and C gilts (70 vs 62 g). These data demonstrate that 100 mg of progesterone/d failed to counteract the adverse effects of 1 mg of Z/kg of body weight on early pregnancy in primiparous gilts.

Pharmacokinetic determinants of spiramycin and its distribution into the respiratory tract were studied in 2 groups of calves, 4 to 10 weeks old. Group-A calves (n = 4) were used to determine pharmacokinetic variables of spiramycin after IV (15 and 30 mg/kg of body weight) and oral administrations of the drug (30 mg/kg) and to measure distribution of spiramycin into nasal and bronchial secretions. Group-B calves (n = 4) were used to determine distribution of spiramycin into lung tissue and bronchial mucosa. Spiramycin disposition was best described by use of an open 3-compartment model. Mean (+/- SD) elimination half-life was 28.7 +/- 12.3 hours, and steady-state volume of distribution was 23.5 +/- 6.0 L/kg. Bioavailability after oral administration was 4 +/- 3%. High and persistent concentrations of spiramycin were achieved in the respiratory tract tissues and fluids. Tissue-to-plasma concentration ratio was 58 for lung tissue and 18 for bronchial mucosa at 3 hours after spiramycin administration and 137 and 49, respectively at 24 hours. Secretion-toplasma concentration ratio was 4 for nasal secretions and 7 for bronchial secretions, and remained almost constant with time. Thus, spiramycin penetrates well into the respiratory tract, although the value in bronchial secretions is lower than that in lung tissues and bronchial mucosa. Calculations indicate that a loading dose of 45 mg/kg, administered IV, followed by a maintenance dose of 20 mg/kg, IV, once daily is required to maintain active concentrations of spiramycin against bovine pathogens in bronchial secretions.

A comparison of immune variables following lung sensitization with live Pasteurella haemolytica serotype 1 (Ph1)-impregnated agar beads was done in 2 separate trials. The Ph1 immune variables studied were blood bactericidal activity, serum bacteriolysis, total classical complement, and indirect hemagglutination antibody. Each trial had 16 male weanling goats: 6 controls and 10 principals. In trial 1, each goat was surgically catheterized through the trachea, then the material was deposited in a bronchus. The controls received only agar beads and the principals received agar beads impregnated with live Ph1. These goats were studied for 32 days, euthanatized, and necropsied. In trial 2, the controls were each transthoracically injected with agar beads into the left lung and the principals were similarly injected with agar beads impregnated with live Ph1. These goats were studied for 35 days, then challenge exposed transthoracically by injection of Ph1 in saline solution (1.2 X 10(7) CFU/ml) into the right lung. Four days later, they were euthanatized and necropsied. The volume of lung consolidated tissue was an excellent measure of Ph1 immunity. Principal goats generated solid protective immunity to subsequent challenge exposure because minimal or no lung consolidation was observed, whereas large volumes of lung consolidation were seen in the controls. The principal goats in trial 1 gave a weak serum indirect hemagglutination Ph1 antibody response, which was attributed to the bronchial method of depositing the Ph1. The corresponding response of the control group remained negative. The Ph1 agar beads (1 X 10(6) CFU in 0.5 ml) protected the bacteria from immediate phagocytosis and lysis as indicated by the induced pneumonic deaths of 2 principals 5 days later. Also, live Ph1 were isolated on day 32 during necropsy of respiratory tracts of 3 principals. At necropsy, no Ph1 isolates were found in the controls. Bacteriolytic activity was not induced against Ph1 in either control or principal groups in this trial. the study, but antibody titers of the principals increased to a geometric mean of 1:250 seven days after lung injection (1 X 10(5) CFU in 0.5 ml). Serum bacteriolytic titers on day 0 indicated that both principals and controls could be subgrouped to high or low subgroups on the basis of their bacteriolytic activity. The bacteriolytic activities of the controls remained unchanged during the experiment, and neither control subgroup was protected from Ph1 challenge exposure. Bacteriolytic activities of the high and low principal subgroups responded differently to Ph1 agar bead lung injection, but both principal subgroups were protected from lung challenge exposure. The low principal subgroup generated high titers of indirect hemagglutination Ph1 antibody, whereas, the high principal subgroup generated lower antibody titers. Total complement, serum bacteriolytic, and blood bactericidal profiles were similar in the principal group with high bacteriolytic activity. The immune factors that protected 2 principal subgroups did not appear to be associated with Ph1 serum bacteriolysis.

Recordings of averaged brain stem auditory-evoked potentials were obtained from 13 Beagle pups of both genders to document the postnatal development of the response from age 1 to 76 days. Responses were recorded between needle electrodes placed on the vertex and the ipsilateral ear, with ground at the interorbital line. Recordings were performed without sedation. Low-amplitude responses to high-intensity stimuli could be recorded from animals prior to opening of the ear canals. Peak latencies did not change after day 20 for peak I, day 30 for peaks II and III, and day 40 for peak V. As a result, the interpeak latencies between peaks I and III did not change after day 30, but continued to decrease until day 40 for peaks III-V and I-V. Peak amplitudes reached plateau values by day 20 (peak I) or day 30 (peaks II, III, and V). All of the measured latency and amplitude values had significant (P <0.001) linear regression lines of latency vs age and amplitude vs age. The brain stem auditory-evoked potential thresholds were mature by day 20.

Acidemia stimulates renal ammonia production and excretion. This adaptive response allows increased H+ secretion and generation of new bicarbonate. To determine whether a relationship existed between urine ammonium (NH4+) concentration and excretion and urine anion gap (Na+ + K+ - Cl-), ammonium chloride (NH4Cl) was administered per OS for 5 days to induce systemic acidemia in 12 healthy Beagles. During NH4Cl administration, a strong, statistically significant (P < 0.0001) relationship was apparent between urine NH4+ concentration measured in millimoles per liter and urine anion gap. Regression equation: urine [NH4+] = 8.2 - 0.416 X urine anion gap; r = -0.897. A statistically significant (P = 0.0001) relationship existed between urine NH4+ excretion measured in millimoles per kilogram of body weight per day and urine anion gap. Regression equation: urine NH4+ excretion = 0.74 - 0.38 X urine anion gap; r = -0.768. As urine NH4+ concentration or excretion increased, urine anion gap became more negative. Before NH4Cl administration (no systemic acidemia), a weak, but statistically significant (P = 0.015) relationship was observed between urine NH4+ concentration and urine anion gap. Regression equation: urine [NH4+] = 65.2 - 0.141 X urine anion gap; r = -0.41. However, a relationship was not evident between urine NH4+ excretion and urine anion gap before NH4Cl administration. Hence, urine anion gap is a reliable index of urine NH4+ concentration and excretion only in dogs with metabolic acidosis. In human beings with distal renal tubular acidosis, NH4+ excretion is inappropriately low and results in a positive urine anion gap. Therefore, as a reliable index of NH4+ excretion, urine anion gap may represent an easy and rapid method to aid in the diagnosis of distal renal tubular acidosis in dogs.