Six horses were subjected to 3 hours of low-flow ischemia and 3 hours of reperfusion of the large colon. After induction of anesthesia, the large colon was exteriorized through a ventral midline celiotomy. Colonic blood flow was measured continuously, using Doppler ultrasonic flow probes placed on the colonic arteries supplying the dorsal and ventral colons and was allowed to stabilize for 15 to 30 minutes after instrumentation. Low-flow ischemia was induced by reducing colonic arterial blood flow to 20% of baseline (BL) flow. Colonic mucosal, seromuscular, and full-thickness blood flow were determined on a tissue-weight basis by injecting colored microspheres proximally into the colonic artery supplying the ventral colon. Reference blood samples were obtained at a known flow rate from the colonic artery and vein at a site more distal to the site of injection. Left ventral colon biopsy specimens were harvested at BL, 3 hours of ischemia, and 15 minutes of reperfusion. Blood and tissue samples were digested and filtered to collect the microspheres, and dimethylformamide was added to release the colored dyes. Dye concentration in blood and tissue samples was measured by use of spectrophotometry, and tissue-blood flow was calculated. Data were analyzed, using two-way ANOVA for repeated measures; statistical significance was set at P < 0.05. Doppler blood flow decreased to approximately 20% of BL, whereas microsphere blood flow ranged between 13.7 and 15.5% of BL at 3 hours of ischemia. Doppler-determined blood flow increased immediately on restoration of blood flow, reached 183% of BL at 15 minutes of reperfusion, and remained at or above BL throughout 3 hours of reperfusion. This reactive hyperemia was also detected, using the colored microspheres; blood flow increased to 242 and 327% of BL at 15 minutes of reperfusion in the mucosal and seromuscular layers, respectively. Mucosal blood flow was not different from seromuscular blood flow at any time, indicating relatively equal distribution of blood flow between these 2 layers. As determined from the venous reference samples, there was no evidence of arteriovenous anastomoses.

The minimal inhibitory concentration (MIC) of cefixime, a new third-generation orally administered caphalosporin, was determined for reference and clinical isolates from dogs. The MIC of the drug for all but 1 of the 18 Enterobacteriaceae isolates tested, 1 Pasteurella canis, 1 Rhodococcus equi, 1 Streptococcus canis, and 1 Streptococcus group G isolate, was less than 1.0 micrograms/ml. The MIC for 9 Staphylococcus intermedius isolates ranged from 1.56 to 6.25 micrograms/ml and, for 8 Sta aureus isolates, the MIC values ranged from 1.56 to 12.5 micrograms/ml. Pseudomonas aeruginosa, Actinomyces sp, and a single Bordetella bronchiseptica isolate were considered resistant to cefixime. Cefixime was administered orally in 2 phases at a standard dosage of 5 mg/kg of body weight to clinically normal adult male and female dogs. In the first phase, the drug was given once as a capsule and once as a suspension. In the second phase, it was administered once per day for 6 consecutive days in capsule form. Serum drug concentration was determined by use of a microbiological assay, and the following kinetic values were estimated for each dog: area under the concentration-time curve, peak serum drug concentration (Cmax), time of Cmax, absorption half-life, and elimination half-life (t1/2el). The kinetic profile of the drug in serum after oral administration of a single dose of cefixime was similar, with mean Cmax values of 3.36 and 4.76 micrograms/ml after treatment with the capsule and suspension, respectively. Quick oral absorption is characteristic for cefixime in dogs; mean absorption half-life values of 1.3 and 0.58 hours for the capsule and suspension, respectively, were calculated. Drug elimination from serum was biphasic, with an initial mean t1/2el of 8.1 to 8.6 hours and a secondary mean t1/2el of 11.7 to 14.5 hours. In the trial involving once daily treatment for 6 days, serum drug concentration after the sixth dose was significantly (P < 0.05) higher than that after the first dose. indicating drug accumulation. Cefixime is extensively bound to canine serum proteins (82 to 92% at concentration ranging between 7.5 and 1.5 micrograms/ml). Concentration of cefixime was determined in the uterus, ovaries, and abdominal fat tissues 24 hours after single-dose treatment and 24 hours after the sixth treatment. Tissue drug distribution was limited after administration of the single dose, but improved after the sixth dose. The in vitro antibacterial activity of the drug and its pharmacokinetic properties warrant assessing its clinical and bacteriologic efficacy as a longterm once-daily orally administered treatment for common bacterial infections in dogs.

Objective: To determine whether standard manual frequency filters in the ON and OFF settings affected P-QRS-T voltages, discover whether recorded P-QRS-T voltages vary between commercial electrocardiographs, assess effects of frequency filters on base-line artifact, and evaluate ECG frequency content by high-fidelity recordings subjected to digital filters with variable frequencies. Design: Sequential 10-lead ECG were recorded in 30 cats, using 3 commercial electrocardiographs to assess effects of manual frequency filters on the P-QRS-T wave forms. Three clinically normal cats were evaluated for ECG frequency content. Animals: Thirty cats (13 with hypertrophic cardiomyopathy; 4 with restrictive cardiomyopathy; 3 hyperthyroid; 1 with ventricular septal defect; 1 with aortic stenosis; and 8 with no detectible cardiovascular disease). Three additional clinically normal cats were studied for effects of frequency filters on the ECG frequency content. Procedure: Ten-lead ECG were recorded on each cat by use of 3 commercial electrocardiographs sequentially. For each machine, a recording was made with manual filters ON, immediately followed by a recording with manual filters OFF. High-fidelity lead-II ECG recordings were made with filters set with their rolloff frequency at 0.1 Hz and 3.0 kHz; output voltage (0.2 mV/V) was fed to an analog-to-digital converter, then to attendant software, which sampled the signal at 6 kHz with a 12-bit sampler, and were digitally filtered at various corner frequencies. Results: Voltages recorded by all 3 electrocardiographs were greatest when filters were OFF (most prominent on R- and S-wave voltages). In all recorded leads, it-wave voltage was significantly greater when filters were OFF than ON. Comparison of voltages indicated significant (P < 0.05) differences between R-wave voltages recorded in all leads with manual filters ON, but not with filters OFF. With filters ON, each electrocardiograph produced a smaller percentage of recordings with moderate to severe baseline artifact than with filters OFF. R-Wave amplitudes of high-fidelity lead-II ECG were significantly decreased with digital filters set at corner frequencies < 150 Hz. Conclusion: Significant (P < 0.05) voltage attenuation was recorded by each of the 3 commercial electrocardiographs when frequency filters were ON, compared with OFF. Comparison of waveform voltages among electrocardiographs with filters ON indicated significant variation in R-wave amplitudes in all leads. With manual filters ON, each electrocardiograph recorded a smaller percentage of recordings with baseline artifact than with filters OFF. Substantial frequency components greater than or equal to 150 Hz are present in the feline ECG waveform. Thus, filters with frequencies < 150 Hz markedly attenuate the feline R wave. Clinical Relevance: Attenuation of feline ECG signals occurs with use of commercial electrocardiographs and varies greatly between manufacturers. This is attributable largely to internal manual frequency filters. These consequences may be important when applying standard feline reference values or when equivocal voltage measurements are recorded.

An ELISA for detection of Toxoplasma gondii-specific IgA in feline serum was developed. A group of cats (n = 7) was inoculated orally with T gondii bradyzoites. Toxoplasma gondii-specific serum IgM, IgG, and IgA responses were followed sequentially by use of the ELISA for 34 weeks. Serum IgA was detected later than IgM or IgG, and was detected in most cats on week 34 after inoculation. None of the cats was seropositive for IgA during the oocyst-shedding period. A group of client-owned cats with suspected clinical toxoplasmosis and a group of healthy cats were tested for T gondii-specific IgA in serum. A trend toward association of T gondii-specific IgA in serum of cats with ocular disease was observed.

The efficacy of 23 disinfectants (including the most commonly used chemical groups) and 6 quaternary ammonium compound based commercial formulations against Actinobacillus pleuropneumoniae serotype 1 (ATCC 4074) was studied. The organisms were tested in suspension and carrier tests with serum as the organic matter. Chloramine-T, hydrogen peroxide, glutaraldehyde, and mercurochrome alone, and a quatemary ammonium compound formulation containing 10% benzalkonium chloride, 2.5% glutaraldehyde, 6.8% glyoxal, and 6% formaldehyde were effective in all tests, regardless of the presence or absence of organic load. All but 2 of the nonformulated disinfectants (sodium hypochlorite and an iodophor) caused at least a 3-log10 reduction in colony-forming units in the suspension test. However, most of the disinfectants were not as effective in the carrier test as in the suspension test; this difference ranged from a 1- to 5-log10 reduction in colony-forming units. In addition, the presence of serum considerably reduced the disinfectant capacities of most of the compounds tested, particularly in the carrier test. These results indicate the importance of selecting suitable disinfectants for routine use on surfaces contaminated with this organism, especially in the presence of organic matter. Chloramine-T and the aforementioned commercial formulation were also tested directly under field conditions in pig nurseries, confirming their high effectiveness.

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (BL) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of BL. All horses were monitored for 6 hours after BL data were collected. Blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [SV]) for measurement of plasma endotoxin, 6-keto prostaglandin F1alpha (6-kPG), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (CV) serum samples. Data were analyzed, using two-was ANOVA, and post-hoc comparisons were made, using Dunnett's and Tukey's tests. Statistical significance was set at P < 0.05 Endotoxin was not detected in CV or SV plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at BL among groups for CV or SV 6-kPG, PGE2, or TXB2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group-2 horses. Colonic venous PGE2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 horses. There were no temporal alterations in SV PGE2 concentration. There was no difference in CV or SV TXB2 concentration among or within groups across time; however, there was a trend (P = 0.075) toward greater CV TXB2 concentration at 3.25 hours, compared with BL, in group-3 horses. Eicosanoid concentrations were significantly lower in SV, compared with CV plasma. Prostaglandin E2 and 6-kPG concentrations were approximately 3 to 8 and 5 to 10 times greater, respectively, in CV than in SV plasma. The increased concentrations of 6-kPG and PGE2 in CV plasma were likely attributable to their accumulation secondary to colonic ischemia. The increased values of these vasodilator eicosanoids may have a role in the reactive hyperemia observed during reperfusion. The increased 6-kPG concentration in SV plasma may represent spillover from the colonic vasculature, but more likely reflects systemic production.

A matched case-control study design was used to assess the effects of long-term administration of a prolonged release formulation of bovine somatotropin (sometribove) on clinical lameness and limb lesions in dairy cows. Cows treated with sometribove for at least 2 lactations (cases) and nontreated dairy cows matched by herd, parity, age, and stage of lactation (controls) in 8 herds were evaluated for clinical lameness (as assessed by gait abnormality) and limb lesions by 2 observers, using a standardized scoring procedure at a single herd visit. Although a high proportion of the study cows were clinically lame (43%), an association was not detected between chronic administration of sometribove and prevalent lameness. Of 21 types of limb lesions identified, 2 were positively associated and 2 were negatively associated with long-term sometribove use. Superficial laceration of the tarsus (odds ratio [OR] = 2.1) and superficial swelling of the metatarsophalangeal joint (OR = 4.5) were positively associated with sometribove treatment, whereas femoral lesions (OR = 0.2) and superficial lacerations of the femur (OR = 0.14) were negatively associated with sometribove treatment.

Fetal infectivity of Ehrlichia risticii was investigated in 19 ponies that were E risticii negative on the basis of results of an indirect fluorescent antibody (IFA) test. Thirteen pregnant ponies were infected by IV administration of E risticii between 90 and 180 days of gestation. Six pregnant ponies served as noninfected controls. Each infected pony had clinical signs of equine monocytic ehrlichiosis, was confirmed to be ehrlichemic, and developed an IFA titer to E risticii. Two infected ponies became recumbent, were unresponsive to supportive care, and were euthanatized. After recovery from clinical illness, the remaining ponies were observed throughout gestation for reproductive abnormalities. On abortion, each fetus was necropsied and tissue specimens from the liver, bone marrow, spleen, colon, and mesenteric lymph nodes were inoculated into canine monocyte cell cultures. Six infected ponies aborted at a mean 217 days of gestation, which was between postinoculation days 65 and 111. Five fetuses were recovered for evaluation, and E risticii was isolated from 4 of them. All 5 fetuses recovered had similar histologic findings, including enterocolitis, periportal hepatitis, and lymphoid hyperplasia with necrosis of the mesenteric lymph nodes and spleen. All fetuses tested negative for IgG to E risticii, although 3 had low IgM titer to E risticii. The remaining 5 infected ponies had normal parturition. Presuckle IFA titer to E risticii was measured in 4 of the term foals, and results for 3 were positive. Two foals from infected ponies were monitored for 6 months and daily gain in body weight was comparable to that of a control foal. None of the control ponies became ill or seroconverted during the clinical illness phase, and none aborted throughout gestation. Two control ponies seroconverted to E risticii 6 weeks before parturition. Results of this study indicate that E risticii is a primary abortifacient under experimental conditions.

Icterus condemnations compose a substantial proportion (41%) of total condemnations of bob veal, the class of veal composed of calves < 3 weeks old and weighing up to 68 kg. At postmortem examination, bob veal condemned because of icterus have generalized yellow discoloration of tissues, which is commonly associated with large, yellow liver (fatty liver), and a paucity of other gross pathologic changes. To establish that the generalized yellow discoloration was attributable to high tissue bilirubin concentrations and to examine the underlying mechanism(s) that might be responsible, blood samples and tissue specimens were obtained from clinically normal and icteric bob veal calves at slaughter. For comparison, blood samples were collected from clinically normal, 1- to 5-day-old Holstein calves being raised on local dairy farms. Hematologic and serum biochemical analyses were obtained for the 3 groups of calves (normal local, normal slaughter, and icteric slaughter), and tissues of slaughter calves were examined for histologic evidence of inflammatory or degenerative changes. Mean +/- SD total bilirubin concentration and creatine kinase (CK) activity in icteric bob veal (3.3 +/- 0.8 mg/dl; 869 +/- 788 U/L), normal bob veal (1.4 +/- 0.7 mg/dl; 486 +/- 890 U/L), and normal local calves (0.5 +/- 0.2 mg/dl; 156 +/- 158 U/L) were significantly different. When data for both normal and icteric bob veal calf groups were combined for analysis, total bilirubin concentration regressed significantly on hepatic lipid scores (P = 0.00003) and CK activity (P = 0.00049). Colostrum consumption was determined by measuring serum total protein concentration and serum gamma-glutamyltransferase activity. Bob veal calves that had not consumed colostrum had significantly higher total bilirubin (P = 0.00005) and CK (P = 0.0008) values. It was concluded that normal and icteric bob veal calves have significant increase in total bilirubin concentration, and icterus of bob veal calves is secondary to unconjugated hyperbilirubinemia. Lack of colostrum consumption was strongly correlated with icterus in bob veal calves.

During 2 separate studies, intracranial pressure (ICP) was measured in 13 healthy dogs (group A, n = 7; group B, n = 6), using a fiberoptic monitoring system implanted surgically in the right superficial cerebral cortex. Average ICP was measured for 15 minutes after a 15-minute postimplantation period of equilibration. Intracranial pressure was measured in group-A dogs at 2.0 and 1.3% end-tidal isoflurane concentrations. Mean +/- 1 SD ICP in group-A dogs at 2.0 and 1.3% end-tidal isoflurane concentrations was 11 +/- 2 and 11 +/- 3 mm of Hg, respectively. Dogs of group A were euthanatized immediately after measurements were obtained. Mean ICP +/- 1 SD in group-B dogs was 11 +/- 3 mm of Hg. After monitoring, but prior to euthanasia, group-B dogs underwent callosotomy, and were maintained for 30 days after surgery. The brain was removed from all dogs, formalin fixed, and examined grossly and microscopically for lesions associated with fiberoptic cable implantation. Variable degrees of hemorrhage and mechanical brain damage were seen focally around the catheter site in all brains from group-A dogs, especially when the cable entered through a sulcus. In 1 dog, local vacuolation was seen in the brain immediately adjacent to the tract associated with implantation of the fiberoptic catheter. In all other dogs, the additional cortex was histologically normal. Histologic lesions associated with cable implantation were not observed in group-B dogs.