Musculature from 198 Canadian cattle with suspected lesions of eosinophilic myositis were examined histologically and by pepsin digestion. Sera from 51 of the 198 animals were also examined by enzyme-linked immunosorbent assay (ELISA) for anti-Trichinella antibodies. Viable larvae of Trichinella were not recovered from any of the cattle but one animal from Ontario tested positive for anti-Trichinella antibodies. Histologically, focal and/or diffuse eosinophilic myositis lesions were observed in 149 (75.2%) of the animals studied. Other conditions identified were sarcocystiosis, abscesses, cysticercosis, steatosis, fibrosis, granuloma, lymphosarcoma and necrosis. Sarcocystiosis was identified in 105 of the 198 animals in both normal and affected musculature. The study indicates that trichinosis is not a primary cause of eosinophilic myositis in cattle.

Eight bovine hearts with lesions of eosinophilic myositis (EM) and 2 bovine hearts without EM lesions were collected at slaughter. Blood samples from these 10 hearts, and the heart of a newborn calf also were collected. Histologically, Sarcocystis cruzi was identified in the 8 hearts with EM lesions and the 2 hearts without EM lesions, but not in the heart of the newborn calf. Serum was harvested from the 10 blood samples and was used in homologous, modified, passive cutaneous anaphylaxis test. Antigen was prepared from S cruzi bradyzoites isolated from the 2 hearts without EM lesions. Serum samples from the 8 cattle with EM lesions reacted positively to S cruzi antigen. When heat-inactivated IgE in serum (56 C for 4 hours) was used, all passive cutaneous anaphylaxis responses were considered negative. Using ELISA, serum IgE concentrations from the 10 cattle with and without EM lesions were 2.2 to 9 U/ml. As determined by radial immunodiffusion, IgM concentrations were 80 to 215 mg/dl. Immunoglobulin G concentrations were 420 to 2,050 mg/dl, but most were less than or equal to 1,700 mg/dl. Immunoglobin A concentrations were 0 to 62 mg/dl; 1 steer with EM lesions had 0 mg/dl. Double-gel immunodiffusion confirmed the presence of Sarcocystis-specific precipitating antibodies. Sera from the 10 cattle with and without EM lesions formed at least 1 precipitin band.

Sarcocystis cruzi sarcocysts were isolated from eosinophilic myositis (Em)-affected and nonaffected bovine hearts. Isolates were ruptured and used to prepare a bradyzoite antigen extract from each heart. The nonaffected heart from one newborn calf contained no apparent sarcocysts when examined histologically and was used to prepare Sarcocystis-negative control antigen. Blood samples were taken from the heart approximately 20 minutes after slaughter. Serum was obtained and evaluated, using a radioimmunoassay to measure Sarcocystis-specific IgG and IgE titers. Sarcocystis cruzi extract from a heart without EM lesions was used for antigen in the radioimmunoassay. Sarcocystis-specific IgG titer ranged between 1:1,280 and 1:2,560 in EM-affected cattle and was 1:640 in nonaffected cattle. Sarcocystis-specific IgE titer ranged between 1:640 and 1:1,280 in Em-affected and nonaffected cattle. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and protein (western) immunoblot analysis were used to compare antigen extracts and serum samples from EM-affected vs nonaffected cattle. Twenty protein bands, ranging from approximately 22 to 215 kD, were detected consistently on bradyzoite blots probed with anti-bovine IgG after incubation with serum samples. Seven of these bands, 37, 44, 53, 57, 94, 113, and 215 kD, were also detected consistently on bradyzoite blots probed with monoclonal anti-bovine IgE. One additional band, 61 kD, was detected consistently on bradyzoite blots probed for IgE, but was seldom recognized when probed for IgG. Sixteen protein bands were evident in silver-stained gels of S cruzi-negative, newborn calf antigen, but none were recognized by antisera on western blots. Consistent differences were not found among antigen extracts or among serum from EM-affected vs nonaffected cattle on silver-stained gels or western blots.

Wick catheters were used to measure intracompartmental pressures of the extensor carpi radialis muscles and long heads of the triceps brachii muscles of 7 horses maintained under halothane anesthesia during controlled ventilation. Horses were positioned in left lateral recumbency on a water bed for 4 hours. Using a crossover design, 6 of the 7 horses were subjected to normotensive and hypotensive anesthesia on separate occasions. Hypotension was achieved by increasing the inspired halothane concentration. Hematologic and biochemical measurements were determined at designated intervals before, during and for 7 days after each anesthetic episode. Under hypotensive conditions, 2 horses developed severe, generalized myositis and were euthanatized. Three of the 5 other horses developed swelling of the downside masseter muscle, 4 demonstrated mild extensor deficits of the downside forelimb, and 1 had a severe extensor deficit of the uppermost hind limb. As a group, the hypotensive horses had markedly increased activities of serum enzymes (creatine kinase, aspartate transaminase, and blood lactate) and abnormalities in calcium-phosphorus homeostasis. Lameness or enzyme alterations were not observed in normotensive horses. Altough the intracompartmental pressure values were markedly increased in the muscle bellies of the compressed limbs of all horses, there was a statistically significant difference in intracompartmental pressures between the downside or compressed muscle compartments of the extensor carpi radialis of hypotensive and normotensive horses. High concentrations of halothane may predispose anesthetized horses to postanesthetic myositis, even when protective padding is used. Intracompartmental muscle pressure, as measured by the wick catheter, may not be a reliable predictor of equine postanesthetic lameness.