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.

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.

A nuclear imaging technique of the stomach, using technetium pertechnetate (99mTcO4), was evaluated in healthy dogs. The stomach was first insufflated with room air, then filled with barium sulfate to induce mild distention, outlining the gastric wall. Six dogs were imaged twice: initially without use of drugs that might affect gastric secretion of 99mTcO4, then after pretreatment with cimetidine and glycopyrrolate. These scans established the appearance of the normal (control) stomach and compared the quality of the image in the same dogs not pretreated, then pretreated with cimetidine and glycopyrrolate before administration of 99mTcO4. Avascular defects were then surgically created on the greater curvature of the stomach of the same 6 dogs, and gastroscintigraphy was performed in similar manner. Significant (P < 0.05) quantitative differences were detected in the gastric images for scans of the avascular area, compared with various control scans. Qualitative assessment had overall accuracy of 90.28%. Results of the study reported here indicate that nuclear imaging can be a valuable diagnostic technique for detecting ischemic areas in the gastric wall of dogs.

Techniques for the measurement of breath hydrogen excretion have been evaluated in dogs and the breath hydrogen test has been shown to be useful for clinical diagnosis and as a research tool. A simple method was developed for collection of expired air and measurement of breath hydrogen concentrations in cats, which enabled demonstration of carbohydrate malassimilation. Breath hydrogen concentrations were measured in healthy cats after food was withheld and after xylose and lactulose administration. Breath samples were collected by use of an open flow system with the cat confined in an acrylic plastic chamber. Breath hydrogen excretion did not exceed 0.53 ml of hydrogen/h in cats not fed. Breath hydrogen concentrations after the ingestion of xylose, a pentose sugar given orally at 0.75 g/kg of body weight, were not significantly higher from those of cats not fed. After ingestion of 3.35 g of lactulose, a nonabsorbable disaccharide, breath hydrogen excretion increased and breath hydrogen concentrations were significantly higher by 45 minutes (P < 0.05) and 60 minutes (P < 0.01) from breath hydrogen concentrations measured in cats not fed and after xylose administration. Administration of lactulose at an increased dosage resulted in further significant (P < 0.01) increases in breath hydrogen excretion. In this study, mouth-to-cecum transit times were variable. A mean +/- SEM mouth-to-cecum transit time of 86 +/- 6 minutes was calculated from measurement of breath hydrogen excretion after oral administration of 3.35 g of lactulose. Measurements of breath hydrogen concentrations after breath collection by open-flow and closed-flow sampling systems were highly correlated and both variables followed log-normal distributions. The dilution of expired air by the open flow sampling system was not excessive and the results of this correlation study suggested that differences in the assimilation of xylose in healthy cats and dogs may well exist.

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.

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.

Classical hemolytic complement (C) of calves was analyzed during a protocol designed to imitate the usual market handling of feeder calves from the southeastern United States. Serum C concentrations of the calves (n = 100 X 4 years) were evaluated on their farm of origin, on arrival at an auction market, on arrival at a feedyard, and during their first 4 weeks in the feedyard. Complement concentrations (measured in CH50 units) were typically lowest at the farm of origin and highest when the calves entered the auction market 28 to 133 days later. Serum C concentrations decreased after the calves encountered the severe stresses of being in the auction market for 7 days, 24-hour truck transport (1,932 km) to the feedyard, and the first 7 days in the feedyard. The C concentrations recovered after 21 to 28 days in the feedyard. Steers had significantly (P less than or equal to 0.05) lower C concentrations than did heifers in 3 of 4 years at the farm of origin, and in 2 of 4 years at the auction market. Morbid calves had significantly (P less than or equal to 0.05) lower C values than did healthy calves on day 7 in the feedyard in 3 of 4 years. There were significant differences in C concentrations of calves from different farms of origin in each of the 4 years. There was no significant difference in C concentrations of calves that were vaccinated vs those not vaccinated with Pasteurella haemolytica.

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.

Erythrocyte insulin receptor binding measurements were evaluated in 8 dogs with spontaneous hyperadrenocorticism. These dogs had normal serum glucose concentration, with normal to high serum insulin concentration (range, 45 to 1,400 pmol/L; normal, 40 to 170 pmol/L). Dogs with hyperadrenocorticism had significant (P < 0.01) decrease in mean +/- SEM percentage of maximal binding for erythrocyte insulin receptors (2.25 +/- 0.21%), compared with results in 11 clinically normal pet dogs (4.29 +/- 0.42%). The decrease in erythrocyte receptor binding was attributed to significant (P < 0.01) decrease inhigh-affinity receptor sites in dogs with hyperadrenocorticism (14.5 +/- 2.8), compared with clinically normal dogs (31.2 +/- 4.3). Significant differences in receptor affinity were not apparent between the 2 groups. Percentage of maximal binding for erythrocyte insulin receptors for dogs with hyperadrenocorticism was inversely correlated with serum insulin concentration (r = - 0.85, P < 0.01). Results indicate that the observed decrease in erythrocyte insulin receptor binding could contribute to insulin resistance and hyperinsulinemia associated with hyperadrenocorticism. Alternatively, decreased binding of insulin receptors in animals with hyperadrenocorticism may result from down-regulation secondary to hyperinsulinemia itself caused by insulin resistance at a postreceptor site (decreasedresponsiveness).