Experiments were conducted to evaluate the effect of restricted feeding of a starter diet to suckling pigs (creep feeding) in a model of postweaning colibacillosis. The hypothesis that restricted creep feeding primes an intestinal allergic reaction to starter diet ingested after weaning was tested. Twenty-eight suckling pigs were fed a starter diet for 3 h/d on days 7, 8, and 9 after birth (creep-fed). Twenty-six suckling pigs were not fed the diet until 3 weeks of age (not creep-fed), when all pigs were weaned and given the starter diet. One day after weaning, 24 creep-fed and 22 not creep-fed pigs were inoculated with K88+ enterotoxigenic Escherichia coli, and 4 pigs in each group were kept as noninoculated controls. Among inoculated pigs (principals), 10 creep-fed and 12 not creep-fed pigs were found to be genetically resistant to K88+ E coli and remained healthy during the 6-day postinoculation period, as did the noninoculated controls. Eighteen (10 creep-fed and 8 not creep-fed) of the 24 genetically susceptible principals developed diarrhea after inoculation. There were no significant differences in the incidence and severity of diarrhea, amount of body weight loss, and mortality between creep-fed and not creep-fed susceptible principal pigs. Histologic examination of intestine from control pigs and principals that survived for 6 days after infection did not reveal any substantial morphologic difference between creep-fed and not creep-fed groups. In conclusion, creep feeding was not required for the production of diarrhea in this model. Creep feeding did not induce morphologic changes characteristic of an allergic reaction in the small intestine.

Streptococcal species isolated from dairy cows with clinical mastitis were obtained from mastitis research workers in Florida, Louisiana, New York, Vermont, Washington, and West Virginia. Seventy-one streptococcal isolates were tested, including 39 strains of Streptococcus agalactiae, 21 strains of S dysgalactiae, and 11 strains of S uberis. The minimal inhibitory concentration of erythromycin, lincomycin, oxytetracycline, penicillin, spectinomycin, streptomycin, and tetracycline was determined for each isolate. Differences were not detected among strains with respect to geographic origin. None of the strains was resistant to penicillin. Lincomycin was the next most effective antimicrobial, with only 2 resistant strains of each streptococcal species. There were no differences among the streptococcal species with respect to resistance to either penicillin or lincomycin. Streptococcus uberis was more likely to be resistant to erythromycin than were S agalactiae and S dysgalactiae (P < 0.02). Streptococcus agalactiae and S uberis had similar distributions for resistance to oxytetracycline, tetracycline, spectinomycin, and streptomycin. Strains of S dysgalactiae were more likely to have intermediate resistance to oxytetracycline and streptomycin than were strains of S agalactiae and S uberis, which were highly resistant to oxytetracycline and streptomycin (P < 0.001). Differences were not detected among the streptococcal species with respect to resistance to spectinomycin. Resistance to multiple antimicrobials was observed in all streptococcal species tested. Although S dysgalactiae appeared to have a greater percentage of strains (73%) that were resistant to multiple antimicrobials than did S agalactiae (31%) or S uberis (45%), differences were not statistically significant.

Concentrations of total, free, and esterified carnitine were determined in plasma, liver, and skeletal muscle from cats with idiopathic hepatic lipidosis and compared with values from healthy cats. The mean concentrations of plasma, liver, and skeletal muscle total carnitine; plasma and skeletal muscle free carnitine; and plasma and liver esterified carnitine were greater (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. The mean for the ratio of free/total carnitine in plasma and liver was lower (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. These data suggest that carnitine deficiency does not contribute to the pathogenesis of feline idiopathic hepatic lipidosis.

The pharmacokinetics of flunixin were studied in 6 adult lactating cattle after administration of single IV and IM doses at 1.1 mg/kg of body weight. A crossover design was used, with route of first administration in each cow determined randomly. Plasma and milk concentrations of total flunixin were determined by use of high-pressure liquid chromatography, using an assay with a lower limit of detection of 50 ng of flunixin/ml. The pharmacokinetics of flunixin were best described by a 2-compartment, open model. After IV administration, mean plasma flunixin concentrations rapidly decreased from initial concentrations of > 10 micrograms/ml to nondetectable concentrations at 12 hours after administration. The distribution phase was short (t1/2 alpha, harmonic mean = 0.16 hours) and the elimination phase was more prolonged (t1/2 beta, harmonic mean = 3.14 hours). Mean +/- SD clearance after IV administration was 2.51 +/- 0.96 ml/kg/min. After IM administration, the harmonic mean for the elimination phase (t1/2 beta) was prolonged at 5.20 hours. Bioavailability after IM dosing gave a mean +/- SD (n = 5) of 76.0 +/- 28.0%. Adult lactating cows (n = 6) were challenge inoculated with endotoxin as a model of acute coliform mastitis. After multiple administration (total of 7 doses; first IV, remainder IM) of 1.1 mg/kg doses of flunixin at 8-hour intervals, plasma flunixin concentrations were approximately 1 microgram/ml at 2 hours after each dosing and 0.5 microgram/ml just prior to each dosing. Flunixin was not detected in milk at any sampling during the study. Flunixin concentrations necessary to induce therapeutic effects in cattle are unknown. Results of our study indicate that administration of 1.1 mg/kg doses of flunixin meglumine at 8-hour intervals would produce plasma concentrations similar to those demonstrated to be effective clinically in treatment of equine musculoskeletal disorders and colic.

Clorazepate dipotassium was administered orally to 8 healthy dogs at a dosage of 2 mg/kg of body weight, q 12 h, for 21 days. Serum disposition of nordiazepam, the principle metabolite of clorazepate, was determined after the first and last dose of clorazepate. Disposition variables were analyzed by use of model-independent pharmacokinetics by the predictive equations method and the trapezoidal rule method. Complete blood counts, serum chemical analyses, and urinalyses were performed before administration of clorazepate and at 10 and 21 days after administration of clorazepate. Maximal nordiazepam concentrations ranged from 446 to 1,542 ng/ml (814 +/- 334 ng/ml), at 59 to 180 minutes (97.9 +/- 42.0 minutes) after a single oral dose of clorazepate. Maximal nordiazepam concentrations ranged from 927 to 1,460 ng/ml (1,308 +/- 187.6 ng/ml), at 120 to 239 minutes (153 +/- 57.9 minutes) after multiple oral doses of clorazepate. Serum disposition was significantly altered after multiple doses of clorazepate. Using data determined by the predictive equations method, the mean residence time after multiple doses (712 +/- 214 minutes) was longer (P less than 0.05) than after a single dose (527 +/- 95.8 minutes). Oral volume of distribution after multiple doses of clorazepate (1.76 +/- 0.647 L/kg) was smaller (P less than 0.02) than after a single dose (3.18 +/- 1.52 L/kg). Oral clearance after multiple doses of clorazepate (3.09 +/- 0.726 milliliter/min/kg) was less (P less than 0.001) than after a singledose (6.54 +/- 2.15 ml/min/kg). Absorption half-life after multiple doses (72 minutes) was longer (P less than 0.01) than after a single dose (33 minutes). The elimination half-life after a single dose (284 minutes) was not significantly different after multiple doses (355 minutes). Significant changes (P less than 0.05) in serum chemical values after multiple doses of clorazepate included decreased concentrations of albumin, total protein, and calcium and increased concentrations of urea nitrogen and glucose. Serum activities of alkaline phosphatase and alanine transaminase increased after multiple doses of clorazepate. Significant changes (P less than 0.05) in the hemogram included increased total WBC count, segmented neutrophils, lymphocytes, and eosinophils. Urine pH after multiple doses (5.88 +/- 0.641) was lower (P less than 0.01) than after a single dose (7.44 +/- 1.29). All changes in laboratory values remained within our reference ranges. Mild sedation and ataxia developed in only 1 dog after the first dose of clorazepate. These effects were transient and did not redevelop with additional dosing. An oral clorazepate dosage of 2 microgram/kg, q 12 h, maintains serum nordiazepam concentrations considered to be therapeutic in human beings (500 to 1,900 ng/ml).

Alveolar macrophages were collected at necropsy from pigs inoculated with Mycoplasma hyopneumoniae or Actinobacillus pleuropneumoniae or both and were tested for phagocytic capabilities, using in vitro techniques. Macrophages from noninoculated littermates were used as controls. Alveolar macrophages from pigs inoculated with either M hyopneumoniae or A pleuropneumoniae had significantly (P < 0.05 to P < 0.0025) higher phagocytic capacity than that of noninoculated controls. Macrophages from A pleuropneumoniae-inoculated pigs were comparatively more stimulated than were those from M hyopneumoniae-inoculated pigs. Pigs inoculated with M hyopneumoniae and then challenge-exposed with A pleuropneumoniae 2 and 4 weeks later had greatly reduced phagocytosis. Infection with M hyopneumoniae or A pleuropneumoniae caused stimulation of alveolar macrophage functions, and M hyopneumoniae infections may have suppressed phagocytic responses when pigs were challenge-exposed with a secondary pathogen (A pleuropneumoniae). This potential suppression may represent a prediposition of the host by M hyopneumoniae to secondary bacterial infections.

A study was conducted to develop valid estimates of lymphocyte count (LC; cells per microliter) of individual, clinically normal dairy cattle. Estimated weighted regression was used on repeated measures of individual LC to examine 6 models predicting LC as a function of age in cattle not infected with bovine leukemia virus. The generalized growth curve model of analysis of variance was used to estimate intercepts, slopes, and prediction limits for the models and to compare the LC-to-age relationship between Holstein and Guernsey breeds. The best-fitting model (P = 0.0001) with the narrowest prediction interval was LC = 4,414.4 - 84.6X, where X = (age - 48) if age less than or equal to 48 months, and X = 0 if age > 48 months, and 163.6 and 8.1 are the SE of the estimates, respectively. Upper one-sided 95%-predicted normal LC tended to be higher than estimates derived from traditional hematologic keys that use confidence limits of mean LC. Difference was not found in the LC-to-age relationship between the Holstein and Guernsey cattle (P = 0.67). Results of this study provided estimates of normal LC that are more specific in diagnosing lymphocytosis in individual cattle.

A fully age-structured deterministic model of the population biology of a pseudorabies epizootic in a farrow-to-finish operation was used to examine the disease-related change in productivity following the initial disease episode. A strategy involving continual sow vaccination was compared with various strategies involving the vaccination of growing pigs, as well as sows. The model suggests that vaccinating growing pigs, in addition to the breeding herd, results in only a relatively small improvement in long-term productivity following a pseudorabies epizootic.

Oscillatory potentials (OP) and electroretinograms (ERG) were recorded from clinically normal dogs after 5, 10, 15, 20, 30, 40, 50, and 60 minutes of dark adaptation. At the end of the adaptation period, OP were characterized by 5 distinct positive peaks, O1 through O5, with mean latencies of 14.46, 20.24, 27.38, 35.31, and 44.85 ms, respectively, and with mean amplitudes ranging from 7.20 to 34.84 microvolt. After 60 minutes of dark adaptation, the ERG had a mean a-wave latency of 12.03 ms and a mean b-wave amplitude of 109.29 microvolt. Peaks O3 and O4, which partially mask the summit of the b-wave, had mean latencies of 28.66 and 36.83 ms, respectively. The mean amplitude of the b-wave measured to the peak of O3 was 240.06 microvolt and 230.73 microvolt when measured to peak O4. Changes in the OP during dark adaptation consisted of significant (P less than 0.05) increases in the latencies of O1, O2, and O3, and significant increases in the amplitudes of O1, O3, O4, and O5. Concurrent ERG changes consisted of significant increases in the amplitudes of the a-wave and b-wave measured from O3 and O4, and significant increases in the latencies of peaks O3 and O4 on the b-wave.

Pharmacokinetic variables of etomidate were determined after IV administration of etomidate (3.0 mg/kg of body weight). Blood samples were collected for 6 hours. Disposition of this carboxylated imidazole best conformed to a 2- (n = 2) and a 3- compartment (n = 4) open pharmacokinetic model. The pharmacokinetic values were calculated for the overall best-fitted model, characterized as a mixed 2- and 3-compartmental model. The first and most rapid distribution half-life was 0.05 hour and a second distribution half-life was 0.35 hour. Elimination half-life was 2.89 hours, apparent volume of distribution was 11.87 +/- 4.64 L/kg, apparent volume of distribution at steady state was 4.88 +/- 2.25 L/kg, apparent volume of the central compartment was 1.17 +/- 0.70 L/kg, and total clearance was 2.47 +/- 0.78 L/kg/h.