Thoracic compliance measurements by use of readily available equipment were determined to be practical and safe in dogs. Twenty healthy dogs (age 1 to 16 years, weight 2.3 to 49.5 kg) were anesthetized for routine procedures such as dentistry or neutering. The animals were first hyperventilated to reduce pulmonary atelectasis, to check for leakage at the endotracheal tube cuff, and to induce mild hypocarbia, thus minimizing voluntary respiratory efforts. Total thoracic compliance measurements were calculated as the difference between exhaled volumes at static inspiratory pressures of 15 and 20 cm of H2O, divided by the pressure difference, and expressed as a function of body weight. The procedure was easy, took 5 to 10 minutes, and caused no recognizable ill effects in any of the dogs studied. Mean total thoracic compliance was 42.25 +/- 32 ml/cm of H2O. There was a significant correlation with weight, but no significant relationship was seen between compliance and age, or gender. The mean weight-adjusted total thoracic compliance was 1.85 +/- 0.56 ml/cm of H2O/kg. In studies in a small group of dogs with documented respiratory tract disease, 4 of 7 had a mean compliance > 2 SD below the normal range. Thus, this test may become part of the routine workup of any animal being anesthetized for procedures such as bronchoscopy to evaluate respiratory tract disease. Routine monitoring of animals on ventilators could provide early warning of complications such as pneumonia, pleural effusion, or pulmonary edema.

Six healthy Holstein calves were anesthetized with isoflurane in O2 and instrumented for hemodynamic studies. A saphenous artery was catheterized for measurement of blood pressure and withdrawal of blood for determination of the partial pressure of carbon dioxide (Paco2), oxygen (Pao2), and arterial pH (pHa). Respiration was controlled throughout the study. The ECG and EEG were monitored continuously. A thermodilution catheter was passed via the right jugular vein into the pulmonary artery for determination of cardiac output and measurement of central venous pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. Base-line values (time 0) were recorded following recovery from isoflurane. Tiletamine-zolazepam (4 mg/kg)-xylazine (0.1 mg/kg) were administered IV immediately after recording baseline values. Values were again recorded at 5, 10, 20, 30, 40, 50, and 60 minutes after injection. Changes in left ventricular stroke work index, Paco2, and pHa were insignificant. Arterial blood pressure and systemic vascular resistance increased above baseline at 5 minutes and then gradually decreased below baseline at 40 minutes, demonstrating a biphasic response. Values for pulmonary capillary wedge pressure, pulmonary arterial pressure, central venous pressure, and Pao2 were increased above baseline from 5 to 60 minutes. Stroke volume, stroke index, and right ventricular stroke work index were increased from 20 or 30 minutes to 60 minutes. Pulmonary vascular resistance increased at 10 minutes, returned to baseline at 20 minutes, and was increased again at 60 minutes. Heart rate, cardiac output, cardiac index, and rate pressure product were decreased at 5 minutes, and with the exception of cardiac output, remained so for 60 minutes. Cardiac output returned to the baseline value at 30 minutes. All calves recovered without complications. We concluded that tiletamine-zolazepam (4 mg/kg IV)-xylazine (0.1 mg/kg IV) is a safe and useful anesthetic regimen for use in calves.

Conventionally raised Chinese Meishan and European Large White pigs were intragastrically challenge exposed with 2. 1 X 10(10) enterotoxigenic Escherichia coli strains bearing colonization factor K88, 987P, F41, or F41 plus K99. In response to challenge exposure with the K88-positive (K88+) organisms, 96% of Large White pigs died within 48 hours, whereas none of the Meishan pigs died. Both breeds of pigs had similar susceptibility to strains bearing 987P or F41. Lastly, Meishan pigs were found to be more susceptible than Large White pigs to a strain expressing K99 and F41. In pigs with diarrhea, challenge-exposure strains intensively colonized the jejunum (10(8) to 10(10) bacteria/g of tissue) and, to less extent, the duodenum (except K88+ strain, which comprised 10(8)/g). In most cases, jejunal concentrations of the challenge-exposure strains were substantially lower in pigs that did not have diarrhea. Half the resistant Meishan pigs eliminated the K88+ strain from the intestines. Colostral antibody titer that agglutinated challenge-exposure strains did not differ between Meishan and Large White gilts. Results indicate that resistance of pigs to the K88+ strain did not extend to enterotoxigenic strains bearing other well-known factors. They indicate, in addition, that genetic resistance to K88+ strains described in pigs in Europe may exist in pigs in China.

Forty 3- to 17-week old domestic ferrets, including 2 gnotobiotes, were inoculated orally and/or rectally with 10(6), to 10(9) colony-forming units of 1 or more of 4 strains of Campylobacter jejuni, 3 of mink and 1 of human origin. Feeding or gavage of any of the 4 strains, in milk or broth, with or without preinoculation sodium bicarbonate treatment to neutralize stomach acid, induced colonization in 38/40 ferrets; diarrhea lasted 2 to 4 days in conventional kits, 6 days in gnotobiotes. Bacteremia was detected in 4 of 18 tested, 2 to 5 days after inoculation. Two strains caused no more severe disease or prolonged colonization after 3 serial IV passages in kits than they did before passage. Multiple inoculations with a given strain resulted in progressively briefer colonization and milder disease, but subsequent inoculation with a different strain induced colonization and gastrointestinal disease similar to a primary infection. Five kits inoculated rectally after 4 previous homologous inoculations were resistant to colonization as well as to disease. Agglutinin titers of ferrets inoculated orally or rectally once were low or undetectable, but increased in response to repeated inoculation. Pretreatment with a 1% formalin enema caused mild colon irritation without clinical or histologic evidence of proliferative colitis in ferrets concurrently inoculated orally and/or rectally, whether or not they had preexisting antibodies to any strain of C jejuni. Histologic examination of tissues revealed leukocytic infiltration of intestinal lamina propria in 29 of 35 infected kits and 5 of 8 noninfected controls, and cryptosporidiosis in 5 infected kits plus 1 control. Examination of silver-stained sections of intestine from 15 infected ferrets revealed Campylobacter-like organisms on the surface of, but never inside, epithelial cells. The lack of characteristic gross or histologic lesions suggested that C jejuni is not, by itself, responsible for proliferative colitis in ferrets.

To evaluate underlying causes of calcium oxalate urolithiasis, 24-hour excretion of urine metabolites was measured in 6 Miniature Schnauzers that formed calcium oxalate (CaOx) uroliths during periods when they were fed a standard diet and during periods when food was withheld. Serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D also were evaluated. Serum calcium concentrations were normal in all 6 affected Miniature Schnauzers; however, during diet consumption, mean 24-hour urinary excretion of calcium was significantly (P = 0.025) higher than calcium excretion when food was withheld. In 1 dog, urinary calcium excretion was lower during the period of food consumption, compared with the period when food was withheld. Compared with clinically normal Beagles, Miniature Schnauzers that formed CaOx uroliths excreted significantly greater quantities of calcium when food was consumed (P = 0.0004) and when food was withheld (P = 0.001). Miniature Schnauzers that formed CaOx uroliths excreted significantly less oxalate than clinically normal Beagles during fed (P = 0.028) and nonfed (P = 0.004) conditions. Affected Miniature Schnauzers also excreted abnormally high quantities of uric acid. Excretion of citrate was not different between Miniature Schnauzers with CaOx urolithiasis and clinically normal Beagles. In 5 of 6 Miniature Schnauzers with CaOx urolithiasis, concentrations of serum parathyroid hormone were similar to values from age- and gender-matched Miniature Schnauzers without uroliths. The concentration of serum parathyroid hormone in 1 dog was > 4 times the mean concentration of clinically normal Miniature Schnauzers. Mean serum concentrations of 1,25-dihydroxyvitamin D in Miniature Schnauzers with calcium oxalate urolithiasis were similar to concentrations of clinically normal Miniature Schnauzers.

Bilateral, midshaft metacarpal osteotomies were performed in 11 sheep and bilateral, midshaft radial osteotomies were performed in 7 sheep. The lesions were repaired with bone plates. One of each pair of plates was luted with polymethylmethacrylate and all screws were tightened uniformly with a torque screwdriver. Sheep were allowed unrestricted exercise after surgery. At 8 weeks, 10 of 11 sheep with metacarpal osteotomies were sound and both osteotomies were healing. Seven were lame on the limb with the unluted plate during the first 3 weeks; 4 were never lame on either limb. The screws of the unluted plates were significantly (P < 0.01) looser at 8 weeks than those in the luted plates. All of the sheep with radial osteotomies were lame in the limb with the unluted plate. Four of 7 sheep had overt loosening of the unluted plates. One sheep only had mild screw loosening with continued alignment of the osteotomy. Two of 7 sheep fractured the radius with the luted plate; these 2 sheep were lame in the limb with the unluted plate and were using the limb with the luted plate vigorously. Excluding the 2 sheep with fractures, all had substantially more screw loosening in the unluted plate. Histologically, there were no discernible differences in the vascularity or porosity of the bone under the luted vs the unluted plates. The only adverse consequence of the luting technique was introduction of a small amount of polymethylmethacrylate into the osteotomy gap in 5 bones.

One hundred four heartworm-free Beagles < 1 year old were studied to determine the efficacy of ivermectin chewable tablets and of 2 other ivermectin tablet formulations against heartworm larvae. At 30 days after SC inoculation of dogs with infective Dirofilaria immitis larvae, all ivermectin formulations were given orally at dosage of 6 microgram/kg of body weight. The ivermectin chewable tablets also were given orally at dosage of 2 and 6 microgram/kg at 30 and 45 days, respectively, after injection of larvae. Replicates of 6 or 8 dogs in each study were formed on the basis of gender and body weight and, within replicates, were randomly allocated to treatment groups. At 30 days after injection of larvae, the additional dogs (in replicates of 8) were assigned to the control group and to the group given ivermectin chewable tablets at dosage of 6 microgram/kg. All dogs were housed individually. Necropsy was performed approximately 5 or 6 months after larvae were administered. In both trials, all control dogs had heartworms at necropsy (University of Illinois-geometric mean, 35.0; Florida-geometric mean, 26.1). In both trials, the ivermectin chewable tablet (6 microgram/kg) and both tablet formulations (6 microgram/kg) given at 30 days after larval injection, and the chewable formulation (6 microgram/kg) given at 45 days after larval injection were 100% effective (P < 0.01) in preventing development of induced infection with D immitis. Of 8 dogs at the University of Illinois that were given ivermectin chewable tablets (2 microgram/kg) at 30 days after larval injection, 6 had heartworms (geometric mean, 2.25; efficacy, 93.6%; P < 0.01) and 5 of 7 dogs treated similarly in Florida had heartworms (geometric mean, 4.4; efficacy, 83.3%; P < 0.05). Drug-related adverse reactions were not observed in either trial.

Cellular oncogenes of genomic DNA in 6 canine primary mammary tumors were screened by Southern blot analysis, using 7 oncogene probes. A canine genomic oncogene related to the human c-yes-1 oncogene was detected as abnormal bands in solid carcinoma genomic DNA digested with Ecori, HindIII, HindIII-EcoRI, or HindIII-BamHI. Comparison was made between other tumor specimens and control specimens obtained from 4 clinically normal dogs-1 mixed breed and 3 Shiba Inu dogs (the same breed as the dog from which the solid carcinoma was obtained). These abnormal bands were 0. 1 to 1 kilobase shorter than the normal gene. However, digestion of genomic DNA obtained from normal WBC of this dog also produced all of the abnormal bands as observed in digested DNA from the solid carcinoma tissue. Therefore, in this dog, the genomic DNA of all somatic cells from the ontogenic stage still had the abnormal sequences related to the human c-yes-1 oncogene, and it is possible that this abnormal structure may have some role (eg, as an initiator) in tumorigenesis or the progression of this tumor.

An epidemiologic survey was performed to determine the incidence of torovirus infections in 2 disease entities of cattle: diarrhea of replacement calves up to 2 months old, and winter dysentery of adult cattle. Samples were obtained from 187 diarrheal and 115 healthy calves from 15 farms, as well as 149 diarrheal and 67 healthy cows from 27 farms with or without winter dysentery. Enzyme-linked immunosorbent assays for detection of torovirus, rotavirus, and coronavirus antigen in feces, and of torovirus and coronavirus antibodies in serum were used to monitor infections in these groups. Torovirus was detected in 9 of the 15 farms in the study, and in 6% of calves with diarrhea, which was significantly higher than in healthy calves (2%). Seroconversion to torovirus was found significantly more often after winter dysentery episodes than on farms without a disease history; coronavirus seroconversion was less common.

Actinobacillus (Haemophilus) pleuropneumoniae plasmids were characterized and classified. They were isolated from A pleuropneumoniae strains different in serotype, year isolated, or location from which isolated. Six of 8 plasmids encoded streptomycin (Sm) and sulfonamide (Su) resistance (SmSu). One of the other plasmids, pVM105, encoded ampicillin (Ap) resistance and another, pHMO, encoded no drug resistance. All SmSu plasmids were transferred to Escherichia coli strains by transformation. Among them, pABO and pMS260 were 8.1 kb and incompatible with each other; they were stable in E coli. The other SmSu plasmids, pHM1, pVM104, pVM106, and pKD25, were 4.3 kb and did not replicate stably in E coli. The former SmSu plasmids were mobilized in E coli strains by a plasmid RP4, which belonged to incompatibility (Inc) group P, but the latter plasmids were not. Further, each 8.1-kb SmSu plasmid and each 4.3-kb plasmid had the same respective restriction pattern. These results indicated that there were at least 2 types of SmSu plasmids in A pleuropneumoniae. The 2 types were classified in 2 groups: Hl(pMS260 and pABO) and H2(pHM1, pVM104, pVM106, and pKD25). The Hl and H2 plasmids belonged to a different Inc groups, and H2 plasmids belonged to a different Inc group from that of pHMO and pVM105.