Effects of increased dietary chloride and reduced sodium and potassium ion concentrations on coxofemoral joint conformation, as assessed by radiography, were examined in growing dogs. Dietary electrolyte balance was quantified by dietary anion gap (DAG), defined as Na+ + K+ - Cl- in milliequivalents per 100 g of food. Diets had anion gap ranging from 8 to 41 mEq/100 g of food. One hundred sixty-seven pups from 27 litters representing 5 breeds were studied during the period of rapid growth. The extent of subluxation of the femoral head was measured on radiographs, using the method of Norberg. On average, less subluxation of the femoral head (P < 0.05) was observed when diets with lower DAG were fed. Differences in DAG balance did not result in different rates of weight gain; therefore, the reduction in coxofemoral joint subluxation attributable to low DAG was unrelated to weight gain. Norberg angles measured at 30 weeks of age were highly correlated with coxofemoral joint status at 2 years of age, as measured by the Swedish diagnostic system and the scoring system of the Orthopedic Foundation for Animals (/r/ greater than or equal to 0.70, P < 0.0002, n = 24). This diet-related improvement in coxofemoral joint sub-luxation would be expected, on average, to delay or mitigate the characteristic clinical and radiographic signs of hip dysplasia in growing dogs.

A sensitive and specific DNA probe for detection and identification of bovine herpesvirus 4 (BHV-4) was developed. Cloned fragments from a library of HindIII fragments of the BHV-4 (DN-599) genome were labeled with 32P or digoxigenin and were tested for sentitivity and specificity in detecting viral DNA by dot-blot hybridization. Two probes were identified that detected 10 pg of purified viral DNA, and detected viral DNA in 0.001 microgram of total DNA extracted from BHV-4-infected cells. Both probes labeled with 32P and 1 labeled with digoxigenin detected viral DNA in samples prepared from cells infected with 2 prototype strains (DN-599 and Movar 33/63) and 4 field isolates of BHV-4. The DNA probes did not hybridize to total DNA prepared from uninfected bovine cells or from cells infected with BHV-1, BHV-2, alcelaphine herpesvirus 1, pseudorabies virus, or equine herpesvirus 1. One probe, labeled with digoxigenin, was tested further by dot-blot hybridization with infected cell lysates that were simply treated with sodium dodecyl sulfate and proteinase K prior to application to the membrane, avoiding extensive DNA purification procedures. This simplified procedure also resulted in specific detection of field isolates of BHV-4 and prototype strains of BHV-4.

The potential of a gonadotropin-releasing hormone (GnRH) agonist (goserelin acetate), delivered constantly for 28 days via a subcutaneous depot, to induce ovulation in seasonally anestrous mares, was investigated. Two experiments were conducted, in which a range of doses (30 to 240 micrograms/mare/d) was examined. Mares were selected on the basis of lack of substantial follicular development (follicle diameter < 20 mm determined ultrasonically) and low serum concentrations of luteinizing hormone (LH) and progesterone. Constant administration of the GnRH agonist-induced ovulation in anestrous mares, but a dose-response relation was not observed. Furthermore, with identical doses tested in consecutive or alternate years, considerable variation was observed in the ovulatory response. In general, ovulation in all treated mares was accompanied by increased circulating concentrations of LH and a decrease in follicle-stimulating hormone values. Ovulation was preceded by an increase in estradiol and LH concentrations. In mares in which ovulation did not occur, concentration of LH increased during agonist treatment, whereas that of follicle-stimulating hormone either increased or did not change. It was concluded that constant administration of GnRH agonists may induce ovulation in mares during seasonal anestrus; however, percentage of mares ovulating and the lack of reproducibility of effect indicate that this approach is inappropriate for use as a reliable method to manipulate breeding activity in commercial broodmares.

Single doses (2.2 mg/kg of body weight) of phenylbutazone (PBZ) were administered IV to 6 neonatal horses (5 to 17 hours old at time of dosing). Plasma concentrations of PBZ and its metabolite oxyphenbutazone were monitored serially for 120 hours after drug administration. Pharmacokinetic variables were calculated, using 1- and 2-compartment open models. Descriptive equations from the best model for each foal were then used to derive model-independent variables describing PBZ disposition. Median volume of distribution at steady-state was 0.274 L/kg (range, 0.190 to 0.401 L/kg). Median terminal half-life was 7.4 (6.4 to 22.1) hours, and median total plasma clearance of PBZ for foals in this study was 0.018 L/kg/h (range, 0.013 to 0.038 L/kg/h). Volume of distribution was larger, half-life was longer, and total clearance was lower, compared with similar values reported for administration of PBZ to adult horses.

An epidemiologic study of Pasteurella haemolytica serovar 1 (Ph1) in market-stressed feeder calves from 7 farms in eastern Tennessee was conducted. The nasal mucus of each calf was cultured sequentially at the farm of origin (day 0), at an auction market (day 133), and at a feedyard in Texas (days 141, 148, 155, and 169). Of the 103 calves tested, 77 were culture-positive, including 1 on day 0, 1 on day 133, 20 on day 141, 57 on day 148, 50 on day 155, and 14 on day 169. From the 143 Ph1 isolates, 20 enzyme profiles were determined by use of a commercial enzyme system that detects 19 enzymatic reactions; 4 antimicrobial susceptibility profiles were obtained, using the disk-diffusion method, which evaluated susceptibility to 11 antibacterial drugs. All isolates were positive for acid phosphatase and alkaline phosphatase, but were negative for alpha-galactosidase, alpha-mannosidase, beta-glucosidase, beta-glucuronidase, cystine aminopeptidase, N-acetyl-beta-glucosaminidase, and trypsin. Other positive enzyme reactions included: leucine aminopeptidase, 140 Ph1 isolates; phosphohydrolase, 90 isolates; alpha-fucosidase, 63 isolates; esterase (C4), 59 isolates; valine aminopeptidase, 30 isolates; esterase lipase (C8), 24 isolates; beta-galactosidase, 2 isolates; and alpha-glucosidase, chymotrypsin and lipase (C14), 1 isolate each. Thirty-four Ph1 profiles were identified, using combined enzyme and antimicrobial susceptibility profiles. The data indicate that the strains isolated during the feedyard period may have been determined more by farm of origin (P < 0.001) than by habitation with calves from other farms while in the feedyard. The combined enzyme and antimicrobial susceptibility profile method is a rapid and simple epidemiologic technique for tracking Ph1 strains in market-stressed feeder calves.

Nine CNS bovine herpesvirus type 1 (BHV-1) isolates, recovered from bovine brain samples submitted to the Texas Veterinary Medical Diagnostic Laboratories from 1974-1989, were compared by analyzing their DNA restriction endonuclease (RE) fragment migration pattern. Seven had pattern similar to that of the respiratory BHV-1 Cooper strain. The remaining 2 isolates, however, had variant patterns, similar to that of each other, but completely different from patterns for the other 7. The RE patterns of these 2 variants were similar to published RE patterns for 2 encephalitic or neuropathogenic BHV- 1 strains--the Australian N-569 strain and the Argentine A-663 strain. One of the Texas encephalitic variants (No. 30326) was isolated from the CNS of a calf that died during an epizootic of encephalitis in 1974. The other, designated TX-89, was isolated in 1989 from the CNS of a 7-month-old feedlot steer with acute fatal encephalitis. Microscopic lesions of encephalitis with neuronal degeneration and intranuclear inclusions were observed for 3 of the 9 isolates, the 2 variant isolates (No. 30326 and TX-89), and a respiratory isolate. The remaining 6 CNS isolates, all respiratory subtypes, were recovered from cattle that did not have clinical CNS disease or gross or microscopic CNS lesions; in 5 of these cattle, virus was recovered from at least 1 other organ (lungs) besides the CNS. We conclude that the CNS of calves can be naturally infected with 2 distinct BHV-1 subtypes, the respiratory and the encephalitic, and that the encephalitic subtype (subtype 3 or BHV-1.3) has been present in Texas cattle since at least 1974.

Observations were made in dorsal and sagittal planes of the ultrasonographic mean gray scale of the flexor tendons and ligaments of the metacarpal regions of 5 Thoroughbred geldings, during weight bearing and nonweight bearing. In images made when the horses were nonweight bearing, the mean gray scale of the superficial and deep digital flexor tendons and accessory ligament was significantly reduced, but that of the interosseous medius muscle (suspensory ligament) was not. When relaxed, collagen fiber bundles in the tendons and ligaments acted as diffuse, rather than specular, reflectors of ultrasonic waves leading to localized regions of hypoechogenicity and a consequent reduction in mean gray scale. The suspensory ligament, however, remained under tension during nonweight bearing and so mean gray scale was not reduced. Analyses of the ultrasonographic mean gray scale have the potential to provide quantitative data relating to the changes in echogenicity that develop in injured equine tendons and ligaments.

A field study involving 325 calves from 17 dairy herds in Saskatchewan was conducted to determine the risk of enzootic pneumonia and to assess its association with a number of factors. Two different case definitions of pneumonia were used in the analyses: the first was based on producers' treatment risk (CASE1) and the second was based on semimonthly clinical examinations of calves by the research veterinarian (CASE2). The risk of pneumonia based on CASE1 was 39% and on CASE2 was 29%. The measure of agreement between CASE1 and CASE2 at the calf level of analysis was poor (kappa = 0.24, SE = 0.02) and at the herd level of analysis was moderate (kappa = 0.40, SE = 0.12). The mortality risk from pneumonia was 1.8% and a variety of infectious organisms were isolated from pneumonic lungs. Twenty-seven percent of the calves had inadequate (total IgG < or = 800 mg/dL) levels of passively acquired antibodies as measured by radial immunodiffusion. The proportion of seropositive titers in calves within the first two weeks of age was 94% to parainfluenza 3 virus (PI3V) and bovine respiratory syncytial virus (BRSV), 73% to Pasteurella haemolytica (Ph), 68% to bovine viral diarrhea virus (BVDV), 67% to infectious bovine rhinotracheitis virus (IBRV), 46% to Mycoplasma dispar (Md), 44% to Haemophilus somnus (Hs), and 21% to Mycoplasma bovis (Mb). At the calf level of analysis and after adjusting for clustering, there was a negative association (p = 0.10) between the diagnosis of pneumonia based on CASE2 and total IgG levels and Ph titers (rPh).

Two experiments were undertaken to evaluate whether porcine reproductive and respiratory syndrome (PRRS) virus was able to cross the placenta and infect midgestation fetuses following intranasal inoculation of sows and whether PRRS virus directly infected fetuses following in utero inoculation. In experiment 1, eight sows between 45 and 50 days of gestation were intranasally inoculated with PRRS virus (ATCC VR-2332), and four control sows were inoculated with uninfected cell culture lysate. Virus inoculated sows were viremic on postinoculation (PI) days 1, 3, 5, 7 and 9, shed virus in their feces and nasal secretions, and became leukopenic. Sixty-nine of 71 fetuses from principal sows euthanized on PI day 7, 14 or 21 were alive at necropsy and no virus was isolated from any of the fetuses. Two principal sows that farrowed 65 and 67 days PI delivered 25 live piglets and three stillborn fetuses. The PRRS virus was isolated from two live piglets in one litter. In experiment 2, laparotomies were performed on five sows between 40 and 45 days of gestation and fetuses were inoculated in utero with either PRRS virus alone, PRRS virus plus a swine serum containing PRRS antibodies, or uninfected cell culture lysate. Three sows were euthanized on PI day 4 and two sows on PI day 11. Viral replication occurred in fetuses inoculated with virus alone and was enhanced in fetuses inoculated with virus plus antibody. No virus was isolated from control fetuses. The results indicate that sows and fetuses are susceptible to PRRS virus infection in mid-gestation, that viral replication is enhanced by the addition of serum with PRRS virus antibody, and that the virus does not readily cross the placental barrier during mid-gestation.

The relationship between histologic lesions in endometrial biopsy specimens and susceptibility to chronic uterine infection (CUI) in mares was investigated. Mares were allotted to 4 groups on the basis of degree of endometrial lesions. Mares in group 1 (n = 6) had no pathologic changes, mares in group 2 (n = 5) had only mild pathologic changes, group-3 mares (n = 7) had moderate changes, and group-4 mares (n = 7) had severe inflammatory and fibrotic endometrial changes. Susceptibility to CUI was determined by the inflammatory response to intrauterine inoculation of 5 X 10(6) Streptococcus zooepidemicus. The inoculum was given on the third day of behavioral estrus and in the presence of a follicle > 30 mm. Mares with > 1 neutrophil/5 high-magnification (400 X) microscopic fields and > 20 colonies of S zooepidemicus at 96 hours after inoculation were considered to be susceptible to CUI. There was a significant association between biopsy grade and susceptibility to CUI among the groups. Histologically normal endometrium was associated with resistance to CUI, and severe histopathologic changes in the endometrium were associated with susceptibility to CUI. Mild to moderate endometrial lesions did not correlate consistently with susceptibility or resistance to CUI.