An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.

A double-antibody sandwich ELISA for detection of antibodies directed against the exotoxin of Corynebacterium pseudotuberculosis, the cause of caseous lymphadenitis (CL) in small ruminants, was developed. A concentrated exotoxin was used. For interpretation of ELISA results, these sera were tested: sequentially obtained sera of C pseudotuberculosis-inoculated goats and sheep that were monitored for 68 weeks; sequentially obtained sera from 80 goats of 3 flocks with CL; sera from 652 goats of 7 flocks without CL; sera from 160 sheep of 4 flocks without CL; and 2,265 caprine and 208 ovine sera submitted for diagnostic testing. Data regarding the infection status and history of 10,454 of the 23,302 animals were collected after testing; most of these were goats that had been part of a CL control program. Specificity and sensitivity of the ELISA were nearly 100%. Subsequently, 31,978 animals from which no data on infection status of flocks had been collected were then tested. It was concluded that the ELISA is a useful diagnostic test for CL eradication programs. Sera with doubtful or inconclusive ELISA results were examined by use of immunoblot analysis. Proteins from C pseudotuberculosis culture supernatant were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and blotted onto nitrocellulose. Six proteins with molecular mass of 68, 65, 39, 38, 31, and 29 kDa reacted with sera from goats and sheep with experimentally induced or naturally acquired infection. Immunoblot analysis was valuable in classifying sera with doubtful or inconclusive results by ELISA.

Liquid mercury strain gauges were implanted in the forelimb proximal sesamoidean ligaments (PSL) of 8 adult horses. The gauges measured PSL strain while horses were standing with or without external support. In 6 of the horses, the gauges also measured PSL strain in horses at a walk, with or without external support. Gauges were enclosed within sliding polypropylene tubes to prevent nonaxial deformation. Each gauge was placed in 1 arm of a low-resistance half-bridge circuit. To provide temperature compensation, a dummy gauge was placed in the adjacent arm of the bridge circuit and was implanted next to the active gauge in the surrounding fascial tissue. External support included fiberglass cast support (CAST), dorsal fetlock splint support (DFS), support wraps of 3 bandage materials (SW1, SW2, and SW3), and support wrap with caudal splint (SW4). The cast was applied, with the fetlock and foot in weightbearing position, from the proximal portion of the metacarpus distal to and including the foot. The DFS was applied by placing the cranial half of the fiberglass cast on the dorsal aspect of the instrumented limb. The SW1, SW2, and SW3 were applied in a figure-8 pattern around the fetlock, using 50% of the linear stretch capacity of the bandage material, with the horse standing squarely on all 4 limbs. The SW4 was applied identically to the other support wraps, with the exception of addition of a flexible caudal splint incorporated in the support wrap. Mean maximal strain while standing without external support for 8 horses was 6.0% (range, 3.8 to 7.5%). Mean maximal strain at a walk without external support for 6 horses was 5.9% (range, 4.1 to 8.2%). Only cast and DFS significantly reduced mean maximal strain while standing. Cast support reduced mean maximal strain while standing to a mean +/- SEM 1.4 +/- 0.2%, 77% reduction in total strain (P < 0.0001). Use of DFS reduced mean maximal strain while standing to a mean 4.2 +/- 0.3%, 30% reduction in total strain (P < 0.0001). The SW1, SW2, and SW3 did not significantly reduce mean maximal strain while standing (power > 0.8, delta = 20%). Conclusions cannot be made for reduction of mean maximal strain while standing with SW4 (power < 0.8, delta = 20%) because of low sample size. Only CAST and DFS significantly reduced mean maximal strain while walking. Cast support reduced mean maximal strain while walking to a mean 2.0 +/- 0.3%, 67% reduction in total strain (P < 0.0001). The DFS reduced mean maximal strain while walking to a mean 4.4 +/- 0.4%, 25% reduction in total strain (P < 0.008). The SW1, SW2, and SW3 did not significantly reduce mean maximal strain while walking (power > 0.8, delta = 20%). Conclusions cannot be made for reduction of mean maximal strain while walking with SW4 (power < 0.8, delta = 20%) because of low sample size.

Because hepatocyte-stimulating factor/interleukin 6 (IL-6) the principal inducer of acute-phase protein synthesis in the liver, quantification of its activity in blood provides an early and sensitive assessment of the acute-phase response. Circulating IL-6 activity was monitored in 4 adult horses for 72 hours after IV administration of endotoxin. In 4 experiments performed at weekly intervals and in randomized order, each horse was given endotoxin-1,000, 30, 1, and 0 ng/kg of body weight. Plasma IL-6 activity was quantified as the ability to promote growth of the IL-6-dependent B-cell hybridoma, B13.29 clone B9. Interleukin-6 activity (171 +/- 10.2 U/ml) was found in all pretreatment plasma samples and was significantly (P < 0.05) increased above baseline from 2 to 12 hours after 1,000 ng of endotoxin/kg was given and at 3 hours after 30 ng of endotoxin/kg was given. After 1,000- or 30-ng/kg dosage of endotoxin, peak plasma IL-6 activity (10,128 +/- 4,096 and 1,555 +/- 1,326 U/ml, respectively) was observed for 3 hours. The IL-6 response of endotoxin-treated horses began about 1 hour after tumor necrosis factor appeared in the circulation, and its course closely approximated the endotoxin-induced febrile reaction. Significant increase in plasma IL-6 activity was not detected in horses given 1 ng of endotoxin/kg or control buffer.

Communications between the femoropatellar, medial femorotibial, and lateral femorotibial joints were studied, using fresh equine cadaver specimens. A total of 90 specimens from 45 horses were used. Horses were randomly assigned to 3 groups with 15 horses/group. Each group was assigned an injection site (femoropatellar joint, medial femorotibial joint, or lateral femorotibial joint), and red latex was injected into the respective location of each joint in each group. Immediately after injection, the joints were flexed and extended 100 times. The stifles were frozen in slight flexion, then cut into 1-cm sagittal sections. The communications between the femoropatellar and medial and lateral femorotibial joints were determined. None of the specimens in this study had communication between afl 3 joint compartments. When the femoropatellar joint was injected, 18 of 30 joints (60%) communicated with the medial femorotibial joint, and 1 of 30 (3%) communicated with the lateral femorotibial joint. Injection of the medial femorotibial joint revealed 24 of 30 (80%) joints that communicated with the femoropatellar joint, and 1 of 30 (3%) that communicated with the lateral femorotibial joint. Injection of the lateral femorotibial joint resulted in communication with the femoropatellar joint in 1 of 30 (3%) joints. Communication did not exist between the medial and lateral femorotibial joints.

The effects of administration of a commercially available extract of Gingko biloba (EGB) on bromethalin-induced brain lipid peroxidation and cerebral edema in adult male Sprague-Dawley rats was determined. Gingko biloba extract was given (100 mg/kg) by gavage immediately after bromethalin (1.0 mg/kg) administration. Rats were euthanatized at 24 hours after dosing. Brain lipid peroxidation was determined by measurement of brain malonaldehyde-thiobarbituric acid chromophore (MDA-TBA) concentration, brain sodium concentration, and brain water content. Treatment of bromethalin-dosed rats (10/group) with EGB was associated with a statistically significant (P < 0.05) decrease in clinical sign severity, compared with bromethalin-dosed saline solution-treated rats. All rats given bromethalin and saline solution developed clinical signs of toxicosis including CNS depression, hind limb weakness, ataxia, paralysis, and coma. Some rats given bromethalin and EGB developed clinical signs, however, none developed hind limb paralysis. The brain MDA-TBA concentration (2.4 +/- 0.5 delta MDA-TBA concentration/mg of protein), percentage of water in brain tissue (80.3 +/- 0.30%), and brain sodium concentration (6.68 +/- 0.21 mg/g of dry weight) were significantly increased in rats given bromethalin and saline solution, compared with control rats given saline solution (1.0 +/- 0.1 delta MDA-TBA concentration/mg of protein; 78.1 +/- 0.33% water in brain tissue; 4.83 +/- 0.30 mg of brain Na+/g of dry weight) and rats given bromethalin and EGB (1.6 +/- 0.2 delta MDA-TBA concentration/mg of protein; 79.3 +/- 0.31% water in brain tissue; 5.37 +/- 0.34 mg of brain Na+/g of dry weight). The MDA-TBA concentration (1.2 +/- 0.2 delta MDA-TBA concentration/mg of protein), percentage of water in brain tissue (78.7 +/- 0.40%), and brain sodium concentration (4.93 +/- 0.26 mg/g of dry weight) increased slightly in control rats given EGB.

Neutrophil migration through bovine teat tissues into the teat cistern, after endotoxin infusion into the teat cistern, was determined in vivo by 2 experimental procedures, indium-111 labeling of blood neutrophils, and obtaining multiple biopsy specimens from the teat cistern tissues. In both experiments, the number of leukocytes in the teat cistern flushing samples was continuously measured. A lag phase of approximately 1 hour was required between endotoxin infusion into the teat cistern and the first observed neutrophil accumulation in the teat tissues. The rate of neutrophil accumulation in the teat tissues was highest between postinfusion (pI) hours 1 and 2, and the accumulation process ceased after PI hour 3. Neutrophils migrated toward the epithelium, and intraepithelial neutrophils were observed beginning approximately 2 hours after infusion, which coincided with the first influx of cells into the teat cistern. The cell influx into the teat cistern increased continuously up to PI hour 3, peaked between PI hours 3 and 5, and was close to preinfusion value at PI hour 22. Use of indium-111-labeled neutrophils in the study of the inflammatory process provides a reliable noninvasive method to quantify cell migration in vivo. Use of biopsies allows quantification of the number of cells in different tissue areas, but has the disadvantage of being invasive. These 2 procedures complement each other, and could be of use in future studies of the local inflammatory process.

Eighteen ponies were inoculated IV with Ehrlichia risticii-infected P388D1 mouse monocyte cells. Twenty-four hours after onset of fever (rectal temperature > 38.8 C), 9 ponies were treated with oxytetracycline (6.6 mg/kg of body weight, IV, q 24 h) for 5 days. The remaining 9 ponies served as infected nontreated controls. Mean scores of the following variables were not significantly different between groups on the day treatment was begun: rectal temperature, diarrhea, borborygmal sounds, feed intake, mental attitude, and evidence of a hyperresonant area in the abdomen. All ponies were observed for progression of clinical signs typical of ehrlichial colitis. Within 12 hours of initiation of treatment, only 1 treated pony had a rectal temperature > 38.8 C and most rectal temperatures were < 38.3 C. In contrast, only 2 control ponies had rectal temperatures < 38.8 C (mean rectal temperature values were significantly, P = 0.01, different between groups). In the treatment group, 4 ponies had no signs of depression after the first day of treatment, and only 1 had signs of depression after the second day of treatment (mean scores between groups were significantly different, P = 0.01). Feed intake remained normal in 4 treated ponies and improved in 4 of the remaining 5 after treatment began. Most of the control ponies had a progressive decrease in their feed intake during the observation period (mean scores between groups were significantly, P = 0.01, different). Three ponies in the control group and 2 ponies in the treatment group developed diarrhea before the treatment observation period began. Of the remaining 6 control ponies, 4 developed diarrhea after the treatment observation period began. None of the ponies in the treatment group developed diarrhea after treatment began. A profound decrease in borborygmal sounds, with silent periods lasting longer than 3 minutes, developed in 7 control ponies. Only 2 treatment ponies had borborygmi decreased to this level (mean scores between groups were significantly, P = 0.01, different). Three of 9 control group ponies developed severe disease and were euthanatized. All treatment-group ponies survived. In surviving ponies, clinical signs lasted 8 to 16 days (mean, 11.5) in the control group, but lasted only 1 to 7 days (mean, 4.5) in the treatment group (P = 0.01). Ponies from the treatment group did not develop clinical signs when reinoculated with Ehrlichia risticii at 4 and 8 months after original inoculation.

Atracurium besylate, a nondepolarizing neuromuscular blocking agent, was administered to 24 isoflurane-anesthetized domestic chickens. Birds were randomly assigned to 4 groups, and atracurium was administered at dosage of 0.15, 0.25, 0.35 or 0.45 mg/kg of body weight. The time of onset of twitch depression, the amount of maximal twitch depression, and the duration of muscular relaxation were recorded. After return to control twitch height, atracurium was further administered to achieve > 75% twitch depression. When twitch depression reached 75% during noninduced recovery, 0.5 mg of edrophonium/kg was administered to reverse the muscle relaxation. Throughout the experimental period, cardiovascular, arterial blood gas, and acid-base variables were monitored. The effective dosage of atracurium to result in 95% twitch depression in 50% of birds, (ED95/9595) was calculated, using probit analysis, to be 0.25 mg/kg, whereas the ED95/95 the dosage of atracurium to result in 95% twitch depression in 95% of birds, was calculated by probit analysis to be 0.46 mg/kg. The total duration of action at dosage of 0.25 mg/kg was 34.5 +/- 5.8 minutes; at the highest dosage (0.45 mg/kg), total duration increased to 47.8 +/- 10.3 minutes. The return to control twitch height was greatly hastened by administration of edrophonium. Small, but statistically significant changes in heart rate and systolic blood pressure, were associated with administration of atracurium and edrophonium. These changes would not be clinically relevant. In this study, atracurium was found to be safe and reliable for induction of muscle relaxation in isoflurane anesthetized chickens.

Superficial digital flexor tendinitis was induced in each forelimb of 8 horses by injecting 4,000 U of collagenase into the midmetacarpal region of the tendon. In each horse, each tendon was treated 24 and 96 hours after the collagenase injection with sc injections of sodium hyaluronate (treated limbs) or an equal volume of 0.9% NaCl solution (control limbs). Exercise was restricted for the first 3 weeks of the study, and a controlled exercise program was instituted for the remainder of the study. Horses were evaluated clinically for lameness, tendon swelling, and midmetacarpal limb circumference. Ultrasonographic examinations were performed regularly (11 examinations/horse) throughout the study, and all horses were euthanatized 12 weeks after collagenase injections. Tendons from 4 horses were harvested for biomechanical testing, and samples were obtained from tendons from the remaining 4 horses for biochemical analysis of collagen. Samples were obtained from all tendons for microscopic evaluation. Significant differences between treated and control tendons were not noticed in any of the variables examined in live horses, although trends toward less lameness in treated limbs and toward better healing on ultrasonographic examination in control limbs were recorded. Significant differences were not noticed in biomechanical or biochemical evaluations, and the only significant (P < 0.05) microscopic finding was more severe inflammation in tendons from treated limbs. This study did not reveal significant benefits of treatment with sodium hyaluronate outside a synovial sheath on tendon repair in collagenase-induced tendinitis.