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The Oregon State University Colleges of Veterinary Medicine and Agricultural Sciences instituted the Endophyte Service Laboratory to aid in diagnosing toxicity problems associated with cool-season grasses in livestock. The endophyte (Neotyphodium coenophalum) present in tall fescue (Festuca arundinacea) produces ergopeptine alkaloids, of which ergovaline is the molecule used to determine exposure and toxicity thresholds for the vasoconstrictive conditions "fescue foot" and "summer slump". Another vasoconstrictive syndrome, "ergotism," is caused by a parasitic fungus, Claviceps purpurea, and its primary toxin, ergotamine. "Ryegrass staggers" is a neurological condition that affects livestock consuming endophyte (Neotyphodium lolii)-infected perennial ryegrass (Lolium perenne) with high levels of lolitrem B. HPLC-fluorescent analytical methods for these mycotoxins are described and were used to determine threshold levels of toxicity for ergovaline and lolitrem B in cattle, sheep, horses, and camels. In addition, six clinical cases in cattle are presented to illustrate diagnosis of these three diseases.

Neoplasms affecting the central and peripheral nervous systems of wild animals are extremely rare. Described are clinical signs and pathologic and immunohistochemical findings in an adult female raccoon (Procyon lotor) with an astrocytoma that involved medulla, cervical spinal cord, and roots of the cervical spinal nerves. Microscopically, the neoplastic cells revealed some pleomorphism but generally had fusiform morphology and showed moderate numbers of mitotic figures. Glial fibrillary acidic protein was demonstrated within the neoplastic cells by immunohistochemistry. This appears to be the only reported case of astrocytoma that involved multiple anatomic sites in the central nervous system of this raccoon.

The essential oil extracts of western juniper oil (Juniperus occidentalis) and Port-Orford-cedar oil (Chamaecyparis lawsoniana) were evaluated for possible dermal toxic effects on mice and rabbits. Mice were tested for their response to both extracts utilizing a local lymph node assay. Western juniper oil extract at 0.5% and 5% concentrations did not show a stimulation index (SI) greater than normal (3.0); however, a 50% concentration did show a positive response at 3.3. Port-Orford-cedar oil extract did not show a positive response at concentrations of 0.5%, 5% or 50%. An acute dermal irritation study using rabbits had a primary irritation index (PII) of 3.3 with 100% Port-Orford-cedar oil extract. This was reduced to a PII of 0.625 when diluted 1:1 with olive oil. Undiluted western juniper oil extract had a PII score of 2.7. While a 5.0% solution had a PII score of 0.3, a 0.5% solution of western juniper oil was a non-irritant. It would appear that animals bedded on wood shavings have contact with essential oils at concentrations far less than the 2% maximum by weight obtained by steam distillation extraction. These concentrations did not elicit a hypersensitivity response.

Fescue foot, summer syndrome, reproductive problems, and ryegrass staggers are all diseases of livestock related to endophyte toxins in pasture grasses. Range finding experiments and case studies of fescue foot relative to ergovaline toxin found in endophyte infected tall fescue and lolitrem B present in endophyte infected perennial ryegrass were conducted. Within 42 d of initiating a feeding trial with chopped tall fescue straw containing 825 ppb ergovaline and at environmental temperatures of 15.9 C clinical signs of fescue foot were seen in cattle. Sheep on tall fescue pastures in November consuming feed with 540 ppb ergovaline and at environmental temperatures of 7.8 C developed fescue foot in 21 d while sheep on the adjacent field in the previous 2 mo with environmental temperatures of 16.6 C and 12.8 C and 458 ppb ergovaline in the pasture grasses did not. In a field outbreak of fescue foot affecting 42/425 feeder lambs in November, the ergovaline of sample pasture grasses had a mean concentration of 813 ppb. Perennial ryegrass staggers was seen in 42/237 feeder lambs when mean lolitrem B in the sampled grass was 2,135 ppb. Overgrazing both tall fescue and ryegrass fields increased probability of clinical disease since the highest levels of toxin were found in the crowns and basal leaf sheaths of tall fescue and perennial ryegrass respectively. Based on these findings, ergovaline dietary levels of 400 to 750 ppb to cattle and 500 to 800 ppb to sheep and lolitrem B levels of 1,800 to 2,000 ppb in feed for both species are approximated threshold values for disease. Cold environmental temperatures are equally important to toxin concentrations in precipitating fescue foot disease.

An adult female sea otter housed for 5 years in an outdoor habitat in an aquarium developed signs of neurologic disease. Bilateral caudal paresis was evident initially and other neurologic signs consistent with CNS disease developed rapidly. Diagnostic work-up included CBC, serum biochemical analyses, determination of serum antibody titers, radiography of the vertebral column, CSF analysis, muscle biopsy, computed tomography of the brain, and assays for mercury, lead, and thiamine. A tentative diagnosis of encephalitis caused by a Sarcocystis neurona-like organism was made on the basis of detection of CSF antibodies by use of Western blot analysis. Response to treatment was not satisfactory and the sea otter was euthanatized. Immunohistochemical staining revealed S neurona-like organisms within foci of inflammation in the brain and spinal cord. This report provides evidence that, for sea otters, there may be a mode of transmission of an S neurona-like organism that does not involve opossums.

Neurological disorders have been reported from parts of Africa with protein-deficient populations and attributed to cyanide (CN-) exposure from prolonged dietary use of cassava, a cyanophoric plant. Cyanide is normally metabolized to thiocyanate (SCN-) by the sulfur-dependent enzyme rhodanese. However, in protein-deficient subjects where sulfur amino acids (SAA) are low, CN may conceivably be converted to cyanate (OCN-), which is known to cause neurodegenerative disease in humans and animals. This study investigates the fate of potassium cyanide administered orally to rats maintained for up to 4 weeks on either a balanced diet (BD) or a diet lacking the SAAs, L-cystine and L-methionine. In both groups, there was a time-dependent increase in plasma cyanate, with exponential OCN- increases in SAA-deficient rats. A strongly positive linear relationship between blood CN- and plasma OCN- concentrations was observed in these animals. These data are consistent with the hypothesis that cyanate is an important mediator of chronic cyanide neurotoxicity during protein-calorie deficiency. The potential role of thiocyanate in cassava-associated konzo is discussed in relationship to the etiology of the comparable pattern of motor-system disease (spastic paraparesis) seen in lathyrism.

Components of the equine nervous system are described including classical anatomy and newer sensory innervation maps that are useful for localizing lesions to and within the nervous system. The key components in a neurological examination that help differentiate primary neurologic disease from musculoskeletal disorders are explained. Gait deficits associated with neurologic dysfunction are listed as well as diagnostic aids and an overview of differential diagnoses.

Sodium cyanate, a neurotoxic chemical in rodents, primates and humans, is implicated in neurodegenerative disorders in protein-deficient populations subsisting in parts of Africa on the cyanogenic plant cassava. The molecular and cellular mechanisms of cyanate neurotoxicity are not understood. This study investigates the effect of sodium cyanate on glutathione (GSH) homeostasis in rodent brain and liver in vitro and in vivo. GSH levels in mouse brain were rapidly, time- and dose-dependently decreased following intraperitoneal administration of 100, 200 or 300 mg/kg sodium cyanate. By contrast, GSH disulfide (GSSG) levels were increased and GSH/GSSG ratios were decreased in a dose-dependent manner in rat brain. Sodium cyanate depleted GSH levels in all regions of mouse brain. Brain glutathione reductase activity was dose-dependently inhibited, while glutathione peroxidase activity was not affected by sodium cyanate. The disruption of GSH homeotasis, as evidenced by reduced tissue GSH/GSSG ratios, likely results from cyanate-induced inhibition of glutathione reductase activity. The results of this study suggest that cyanate neurotoxicity, and perhaps cassava-associated neurodegenerative diseases, are mediated in part by disruption of glutathione homeostasis in neural tissue., (Copyright 1999 Elsevier Science B.V.)

Nutritional status is an important factor in modulating the metabolic fate of xenobiotics. Sulfur amino acid (SAA) deficiency has been proposed as a risk factor for human neurological diseases among protein-poor populations subsisting on the cyanophoric plant cassava. Female Sprague-Dawley rats were used to develop and define a model of SAA deficiency for use in future studies examining cassava-related neurotoxicity. Rats were kept in metabolic cages for 7-21 d and fed a balanced diet (BD) of known composition or a comparable diet selectively deficient in methionine and cystine (SAA-free diet). Animals fed the SAA-free diet failed to thrive, lost body weight, excreted porphyrinic materials, and showed a steep and persistent reduction of urinary inorganic sulfate. In contrast, animals on the BD gained body weight and maintained baseline output of urinary inorganic sulfate. Urinary thiocyanate excretion did not differ between groups, but plasma thiocyanate concentrations reached double that in SAA-deficient rats. Increased plasma thiocyanate suggests mobilization of sulfur amino acids from endogenous sources. Liver glutathione and blood cyanide concentrations were similar in animals on the BD and the SAA-deficient diet. In summary, a diet free of methionine and cystine results in increased retention of inorganic sulfur as thiocyanate and a near absence of inorganic sulfur excretion in urine.

Otitis media/interna in the equine most commonly is a chronic, insidious infection with the unique sequella of temporohyoid osteoarthropathy in some horses. Head shaking may be the only clinical sign of the early stages of this disease. The arthritic condition often leads to fusion of the temporohyoid joint with resultant stress fractures of the petrous temporal bone. When this occurs, the horse presents as an acute neurologic case with clinical signs of vestibular and facial nerve dysfunction. Diagnosis, treatment, and prognosis are discussed. Recognition of this syndrome is important because many of these horses can be treated successfully and can return to normal function.

Objective: To determine seroprevalence of antibodies to Sarcocystis neurona in neurologically normal horses residing in 4 regions of Oregon and to describe the effects of age, gender, breed, and housing on seroprevalence within each region., Design: Prevalence survey., Sample Population: Serum samples from 334 horses systematically selected by practicing veterinarians., Procedure: Antibodies to S neurona were measured in sera, using a western blot. Information including age, gender, breed, housing, geographic location, and duration of residence was obtained for each horse. Data were analyzed, using descriptive statistics., Results: 45% (149/334) of horses evaluated were seropositive for antibodies to S neurona with significant differences in the percentage of seropositive horses from different regions of the state. Seroprevalances of antibodies to S neurona in horses in regions I and II, west of the Cascade Range, were 65 and 60%, respectively; whereas seroprevalances in central and eastern Oregon, regions III and IV, were 43 and 22%, respectively. Seroprevalence consistently increased with age of horse for each region. Gender, breed, and housing were not associated with significant differences in seroprevalence of antibodies to S neurona in the overall sample population, or in comparisons of samples obtained from horses within a particular region, or among samples obtained from horses residing in different regions., Clinical Implications: The high seroprevalence of antibodies to S neurona in neurologically normal horses indicates that analysis of serum alone would not be useful for definitive diagnosis of equine protozoal myeloencephalitis in horses in Oregon.

A group of 6- to 8-month-old calves developed head tremors, stiff gait, and staggering after consuming ryegrass straw that contained 3,711 micrograms of lolitrem-B/ kg. Signs were consistent with ryegrass staggers syndrome. At necropsy, all calves examined had atypical interstitial pneumonia, with marked emphysema and bullae. Infectious organisms and pneumotoxins were not identified. Experimentally, feeding the same ryegrass straw to age-matched calves induced similar neurologic signs, but did not result in pneumonic lesions. The high concentration of lolitrem-B in the straw or other, undefined factors, such as feed changes, may have contributed to the atypical interstitial pneumonia in the naturally exposed calves.

Megaesophagus was diagnosed in 15 llamas on the basis of survey and contrast radiography. Age of onset ranged from 13 months to 9.5 years. Clinical signs varied, with salivation being the most common; regurgitation or dysphagia were noted in only 33% of the cases. Duration of the disorder ranged from 1 week to 5 years. Organophosphate toxicity was the cause of megaesophagus in 1 llama. While most cases were of unknown etiology, the 3 with histological abnormalities included 1 with vagal neuropathy and 2 with a degenerative myopathy of esophageal muscles. The causes in most were undetermined.

Electromyography of the esophageal musculature of a cow that had been regurgitating and losing weight after correction of an esophageal obstruction was suggestive of unilateral denervation. Radiography before and after oral administration of barium sulfate revealed a dilated terminal portion of the thoracic esophagus, suggestive of a focal motility problem. Electromyography was performed on the esophageal musculature by positioning the electrode through the rumen fistula and into the thoracic esophagus and by positioning the electrode percutaneously with the aid of a tube placed in the cervical esophagus. Numerous fibrillation potentials and sharp epsilon-positive waves were detected in the muscles of the left side of the distal portions of the cervical and thoracic esophagus. During hospitalization, the cow was given alfalfa pellets, ground corn, and sodium bicarbonate through the rumen fistula 3 times each day for several weeks to maintain body weight.

An in vitro assay was used to examine biotransformation of toxic Senecio jacobaea pyrrolizidine alkaloids (PA) in ovine, bovine, and caprine rumen contents. Pyrrolizidine alkaloids were analysed by high performance liquid chromatography, and the rates of the alkaloid biotransformation were determined. The microbiological "Most Probable Numbers" technique was also used, in combination with thin-layer chromatography, to estimate relative numbers of rumen PA-biotransforming bacteria in the same samples. Pyrrolizidine alkaloids were biotransformed at average rates of 2.9 micrograms/ml/h (bovine), 25.6 micrograms/ml/h (caprine), and 19.2 micrograms/ml/h (ovine). Estimates of numbers of PA-biotransforming bacteria were 1.1 x 10(7) bacteria/ml rumen contents (bovine), 2.4 x 10(7) bacteria/ml (caprine), and 3.0 x 10(7) bacteria/ml (ovine). This project is among the first to quantitate rates of PA biotransformation in rumen contents and to identify caprine and bovine, in addition to ovine, rumen PA-biotransforming activity, as well as to estimate the actual numbers of PA-biotransforming bacteria in rumen contents.

Recent evidence concerning the pathogenesis of equine degenerative myeloencephalopathy indicated that low blood alpha-tocopherol values are a factor in the disease process. Variables that could be introduced by a veterinarian procuring, transporting, or storing samples were evaluated for effects on alpha-tocopherol concentration in equine blood. These variables included temperature; light; exposure to the rubber stopper of the evacuated blood collection tube; hemolysis; duration of freezing time, with and without nitrogen blanketing; and repeated freeze/thaw cycles. It was found that hemolysis caused the greatest change in high-performance liquid chromatography-measured serum alpha-tocopherol values, with mean decrease of 33% (P < 0.001). Lesser, but significant (P < 0.01) changes in serum alpha-tocopherol values were an approximate 10% decrease when refrigerated blood was left in contact with the red rubber stopper of the blood collection tube for 72 hours and an approximate 5% increase when blood was stored at 20 to 25 C (room temperature) for 72 hours. Repeated freeze/thaw cycles resulted in a significant (P < 0.05) 3% decrease in alpha-tocopherol values in heparinized plasma by the third thawing cycle. Freezer storage for a 3-month period without nitrogen blanketing resulted in slight (2%) decrease in mean serum alpha-tocopherol values, whereas values in serum stored for an identical period under nitrogen blanketing did not change. A significant (P < 0.001) mean decrease (10.3%) in alpha-tocopherol values was associated with freezer (-16 C) storage of nitrogen blanketed serum for 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

The ability of ovine ruminal fluid to metabolize pyrrolizidine alkaloid (PA) from Senecio jacobaea under anaerobic conditions was evaluated. Four fistulated sheep fed PA served as individual sources of ruminal fluid, which was incubated in a defined minimal salts medium under two different anaerobic conditions, denitrifying and methanogenic. Anaerobic cultures amended with ovine ruminal fluids (20%), PA (100 micrograms/ml), and a defined minimal salts medium were monitored for a period of several days. These cultures revealed that while PA was not depleted in sterile, autoclaved controls or under denitrifying conditions, it was metabolized during periods of active methanogenesis under methanogenic conditions. In addition, samples of ruminal fluid were separated by differential centrifugation under anaerobic conditions, and the resultant supernatants were tested for their ability to metabolize PA as compared with those of the respective uncentrifuged control fluids. Uncentrifuged controls exhibited a PA depletion rate of -4.04 +/- 0.17 micrograms of PA per ml per h. Supernatants 1 (centrifuged at 41 x g for 2 min), 2 (centrifuged at 166 x g for 5 min), and 3 (centrifuged at 1,500 x g for 10 min) exhibited significantly slower depletion rates, with slopes of data representing -1.64 +/- 0.16, -1.44 +/- 0.16, and -1.48 +/- 0.16 micrograms of PA metabolized per ml per h, respectively, demonstrating no statistically significant difference among the supernatant cultures. Microscopic evaluations revealed that protozoa were present in the control whole ruminal fluid and to a lesser extent in supernatant 1, while supernatants 2 and 3 contained only bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Ingestion of pyrrolizidine alkaloids, naturally occurring plant toxins, causes illness and death in a number of animal species. Senecio jacobaea pyrrolizidine alkaloids cause significant economic losses due to livestock poisoning, particularly in the Pacific Northwest. Some sheep are resistant to pyrrolizidine alkaloid poisoning, because ovine ruminal biotransformation detoxifies free pyrrolizidine alkaloids in digesta. Antibacterial agents modify ruminal fermentation. Pretreatment with antibacterial agents may account for some animal variability in resistance to pyrrolizidine alkaloid toxicosis, and antibacterial agents can also be used for characterizing ruminal pyrrolizidine alkaloid-biotransforming microflora. The objective of this study was to evaluate the effects of antibacterial agents on biotransformation of a predominant S. jacobaea pyrrolizidine alkaloid, jacobine, in ovine ruminal contents. Ovine ruminal jacobine biotransformation was tested in vitro with 20 independent antibacterial agents. Low amounts of rifampin and erythromycin prevented jacobine biotransformation. Chlortetracycline, lasalocid, monensin, penicillin G, and tetracycline were slightly less effective at inhibiting jacobine biotransformation. Bacitracin, crystal violet, kanamycin, and neomycin were moderately inhibitory against jacobine biotransformation. Brilliant green, chloramphenicol, gramicidin, nalidixic acid, polymyxin B SO4, sodium azide, streptomycin, sulfisoxazole, and vancomycin had little to no effect on jacobine biotransformation. The antibiotics that were most effective at inhibiting biotransformation were those that are active against gram-positive bacteria. Therefore, gram-positive bacteria are most likely critical members of the jacobine-biotransforming consortia.

Plasma alpha-tocopherol (vitamin E) values were monitored 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 less than 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.

An oral vitamin E absorption test used in human beings was modified for use in horses. The most appropriate techniques with which to measure gastrointestinal tract absorption of vitamin E (alpha-tocopherol) in horses were developed. Vitamin E was administered orally, and serum values of alpha-tocopherol were measured by use of high-performance liquid chromatography at 0, 3, 6, 9, 12, and 24 hours after vitamin E administration. Variables included comparison of 2 dosages (45 and 90 IU/kg of body weight), routes of administration, and absorption dynamics of 3 preparations of dl-alpha-tocopherol. Absorption of the 2 doses of dl-alpha-tocopherol acetate indicated a dose response; the area under the curve at 24 hours (AUC24) was 4.3 micrograms.h/ml for the 45-IU/kg dose and 32.2 micrograms.h/ml (P less than 0.01) for the 90-IU/kg dose. Maximal absorption was apparent when vitamin E was naturally consumed in grain, compared with administration of identical preparations by stomach tube or paste. In the same horses, dl-alpha-tocopherol and dl-alpha-tocopherol acetate plus polyethylene glycol had statistically similar absorption curves and both had significantly greater AUC24, compared with dl-alpha-tocopherol acetate; values for the 3 compounds were 23.6, 25.8, and 12.6 micrograms.h/ml, respectively. The AUC24 varied between individual horses, but time of peak value was consistently observed between 6 and 9 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

A clinical, viral, hematologic , and genetic study was conducted over a 4-year period on a family of Appaloosas with high incidence of clinical ataxia and pathologic features of equine degenerative myeloencephalopathy. Marginal to deficient serum vitamin E (alpha-tocopherol) and blood selenium values were the only other consistent antemortem abnormalities in the affected horses. Members of this family were all descendants of a clinically normal mare and were raised in 3 separate environments with variable quality of feed. All horses had access to pasture grasses. Normal chromosomal karyotypes were found in 11 affected and/or related horses examined. Equine herpesvirus type 2 was isolated from 4 of the horses, but evidence for a role of this virus in the pathogenesis of the disease was not found. The role of antioxidant deficiency in the pathogenesis of neurologic dysfunction in this equine family and in others reported to be affected with equine degenerative myeloencephalopathy remains speculative.

Severe necrotizing myelitis secondary to localization and reactivation of Toxoplasma gondii within the spinal cord of a domestic shorthair cat was diagnosed by use of light and electron microscopy and immunohistochemistry. The cat also was infected with feline immunodeficiency virus. This case may have useful comparative features to T gondii infections in human patients with acquired immunodeficiency syndrome.

Several factors, including age, sex, race number, post position, and race class, were evaluated for relationships to prerace percentage body weight loss and performance in all Greyhounds racing during August 1983 in Oregon. The incidence of percentage body weight loss greater than or equal to 2.5% was low (5%). Race number had a direct effect on weight loss; the later the dogs raced, the more weight loss they experienced. Female dogs were 3 times more likely to lose greater than 2.4% of body weight than males. All dogs experiencing greater than 2.4% body weight loss were 2 times more likely to finish in the first 3 places when racing in the first 5 races overall. In addition, males losing greater than 2.4% of body weight performed better than females when racing together in the final 6 races. Males appeared to be better performers than females, as they were twice as likely to be in class A races. However, once in the race, males and females performed equally.

Blood samples were collected on nonracing days from 57 racing Greyhounds at 2 weeks, 8 weeks, 13 weeks, and 16 weeks after the beginning of the racing season. Hematologic and biochemical tests were performed to detect marked changes induced by stress of racing. In general, these Greyhounds were healthy. Rhabdomyolysis was detected in one dog. In several other dogs, possible subclinical muscle injury was identified by increased serum creatine kinase activities. Mean serum Ca concentrations tended to decrease during the racing season. None of the tests was a good predictor of racing performance. Mean values for several hematologic and biochemical tests were different from those of other breeds of dogs.

A model for chronic perfusion of the liver of ruminants was developed. This allowed for investigation of the pathophysiology of pyrrolizidine alkaloids (PA) in two species. This model has general application to toxicological studies for both acute or chronic perfusion, as well as, metabolic studies utilizing sheep, cattle or goats. Catheterization of the portal vein via the right ruminal vein was done to separate the ruminal effects of toxin metabolism and absorption from the direct effects of PA on liver tissue. The selection of this vessel insured the equal distribution of infused substances throughout all lobes of the liver. A left flank laparotomy surgical approach was used. A dacron patch glued to the catheter at vein entry site eliminated a number of common catheter problems. Catheters were used for infusion of up to 2 L/daily for 20 d to 7 mo.

Cervical dorsal spondylosis with spinal cord compression in a black swan (Cygnus atratus) was confirmed radiographically and morphologically. Clinically ataxia was associated. Noninflammatory, degenerative changes of the synovial joint cartilage were associated with the spondylosis.

Fluctuations of serum vitamin E (alpha-tocopherol), cholesterol, and total lipids were monitored in 12 horses at 3-hour intervals for 72 hours. Mean coefficients of variation were 12, 5, and 15%, respectively. Statistical analyses were used to conclude that instrumentation error was accountable for only a small portion of the vitamin E variation. Results indicated that a single serum sample assay is an unsatisfactory indicator of vitamin E status in horses. These data have clinical application in the evaluation of horses suspected to be affected with equine degenerative myeloencephalopathy. The large variance of serum total lipids and the lack of correlation of it with serum vitamin E over time preclude the use of vitamin E/serum total lipids ratio in assessing vitamin E status.

The histologic and histochemical features of palatine muscles from 53 horses were studied; 25 of the horses were racehorses that had upper airway obstruction associated with dorsal displacement of the soft palate and 28 of the horses did not have any respiratory disorders and served as controls. Pathologic features observed included myonecrosis, phagocytosis, mononuclear cell infiltration of perimysial connective tissue, alkaline phosphatase-positive myofibers, and myofibers with cytoarchitectural changes that included irregular staining of the intermyofibrillar sarcoplasm and sarcoplasmic masses. These histopathologic features were judged to be indicative of myositis. Those features were found in both control horses and horses with dorsal displacement of the soft palate; however, their prevalence was higher in horses with dorsal displacement of the soft palate. For the control horses as well as the horses with dorsal displacement of the soft palate, the inflammatory changes were more prevalent in older horses. The finding of myositis suggests that palatal muscle weakness may contribute to the development of dorsal displacement of the soft palate; however, the myositis might have been secondary to trauma associated with displacement of the soft palate. We could not distinguish between these 2 possibilities. A large number of horses with dorsal displacement of the soft palate also had concurrent pharyngeal lymphoid hyperplasia. Extension of the mucosal inflammatory changes associated with pharyngeal lymphoid hyperplasia into the underlying palatine muscle might have accounted for the myositis.

Normal nerve conduction velocity values in 10 ponies were determined for sensory nerve fibers in the median and ulnar nerves. A percutaneous signal-averaging technique was developed and used. Medial and lateral palmar digital nerves on the abaxial surface of the proximal sesamoid bones were used as the sites for percutaneous stimulation, whereas recording sites included the medial and lateral palmar nerves just distal to the carpus and the median and ulnar nerves in the middle of the radius. Sensory nerve conduction velocities can be evaluated simply and clinically in the limbs of horses, using percutaneous signal-averaging techniques.

Neutralizing antibodies against equine herpesvirus 1 were measured in serum and cerebrospinal fluid of 16 horses and ponies from a closed herd both before and after vaccination with modified live equine herpesvirus 1. These titers were also measured in 22 neurologically normal and 15 neurologically abnormal horses at a teaching hospital. Animals from the closed herd had prevaccination serum titers up to 1:8 and postvaccination serum titers up to 1:128. Horses from the teaching hospital had serum titers up to 1:64. Cerebrospinal fluid titers were not detected in the vaccinated horses or the neurologically normal horses but a low titer (1:8) was noted in one neurologically abnormal horse. This titer probably resulted from hemorrhage into the cerebrospinal fluid following trauma.

Normal sensory nerve conduction velocity (SNCV) values in 8 ponies and 8 horses were compared by use of a percutaneous signal-averaging technique. Nerve fibers evaluated included those in the medial and lateral palmar and plantar digital nerves. Mean SNCV values were significantly slower (P less than 0.0002) for horses, compared with those values for ponies. Animal height and nerve segment length were inversely related to SNCV consistently. The SNCV values were affected by surface skin temperature by a factor of approximately 1.2 m/s change for 1 degree C change in temperatures from 35 C. The ability to calculate warning limits to define those SNCV values in normal and abnormal ranges were developed from these data for both ponies and horses.

Methodology for the neurologic examination in the equine species is described. Information is organized to assist the reader in defining neurologic deficits and in localizing lesions to the major subdivisions within the central or peripheral nervous system. Numerous examples of deficits are presented to assist the reader in recognition of common neurologic disease states.

Dimethyl sulfoxide (DMSO) was administered IV to 6 Thoroughbred horses at 2 dosages: 1.0 g/kg and 0.1 g/kg. The pharmacokinetics seemed linear, with biological half-lives of 8.6 +/- 0.3 hours and 9.8 +/- 2.2 hours for the 1.0 g/kg and 0.1 g/kg dosages, respectively. This was further substantiated by mean residence times of 9.8 +/- 0.44 hours and 13.8 +/- 4.25 hours, areas under the curve of 12.55 +/- 1.42 mg/ml/hr and 1.63 +/- 0.49 mg/ml/hr, and the clearances of 0.081 +/- 0.009 L/kg/hr and 0.066 +/- 0.022 L/kg/hr for the large and small dosages, respectively. At 12 hours after 1.0 g/kg was administered, 26.6% of the DMSO dose was excreted unchanged into the urine; at 12 hours after 0.1 g/kg was administered, 25.3% of the DMSO dose was excreted unchanged into the urine. It was predicted that 29.4% and 40.6% of the total DMSO dose would be excreted into the urine for the 1.0 g/kg and 0.1 g/kg dosages, respectively. A 10% DMSO concentration in normal saline solution was safe to give as rapid IV infusion. Slow administration is recommended for more concentrated solutions. Based on the half-life, DMSO should be administered 2 times a day IV for the treatment of increased intracranial pressure and/or cerebral edema in horses.

The structure of sarcocysts in a horse is presented. Light microscopic examination revealed that the maximum cyst dimensions were 136 X 990 micrometers and the cyst walls were striated and 1 to 3 micrometers thick. Electron microscopic examination revealed that the "cyst wall" was formed by villuslike protrusions of the parasitophorous vacuole's primary wall. A unique feature was the presence and arrangement of microtubules within the parasitophorous vacuole. Thirty-four to 55 microtubules extended from the apical tips and sides of each villus and passed through the ground matrix to form junctions with the outer pellicle membrane of bradyzoites and metrocytes located at the margins of the cyst. The average dimensions of the bradyzoites were 3.2 X 14.2 micrometers.

The cutaneous innervation of the thoracic limb was investigated in 18 barbiturate-anesthetized horses, using electrophysiologic techniques. The cutaneous area (CA) innervated by each cutaneous nerve was delineated in at least 4 horses by stroking the hairs with a small watercolor brush while recording from the nerve. Mapping of adjacent CA revealed areas of considerable overlap. The part of a CA of a given nerve supplied only by that nerve is referred to as its autonomous zone (AZ). In contrast to the standard textbook illustrations cutaneous branches of the axillary, radial, musculocutaneous, and ulnar nerves overlapped extensively in the antebrachium. Clinically testable AZ were found in the antebrachium for the caudal cutaneous antebrachial nerve of the ulnar nerve and in the carpus and manus for the cutaneous branches of the median, ulnar, and musculocutaneous nerves; AZ were not found for the cutaneous branches of the radial and axillary nerves.

Phenylbutazone was administered to six Thoroughbred horses in a cross-over study in which the horses received cimetidine pretreatment or no cimetidine pretreatment. Blood samples were collected at various times for 48 h after phenylbutazone administration and the plasma was analysed for phenylbutazone. Cimetidine pretreatment elevated phenylbutazone plasma concentrations during the first 8 h after phenylbutazone administration. The absorption rate, maximum phenylbutazone plasma concentrations and AUC were significantly greater with cimetidine pretreatment. The half-life of phenylbutazone did not change with cimetidine pretreatment; however, lower plasma concentrations of the metabolite gamma-hydroxyphenylbutazone were observed with cimetidine pretreatments. Plasma concentrations of the metabolite oxyphenbutazone were unchanged with cimetidine pretreatment compared to control values. Twenty-four-hour plasma concentrations of phenylbutazone were not different from control values with cimetidine pretreatment. This study suggests that concurrent treatment with cimetidine and phenylbutazone 24 h before race time does not result in elevations of plasma phenylbutazone concentrations above control values.

A chronic progressive neurologic disease was observed and monitored for 18 months in a young, tamed Bengal tiger. Clinical, serologic, and neuropathologic evidence of canine distemper virus infection was seen. Clinical signs included convulsions, myoclonus, and slowly progressive ataxia. Marked increases in neutralizing antibodies against canine distemper virus were seen in the serum and cerebrospinal fluid. Neuropathologic findings were nonsuppurative meningoencephalomyelitis, with perivascular cuffing, demyelination, and inclusion bodies typical of canine distemper virus. It was concluded that, in light of this case and an earlier report of canine distemper in lion cubs, vaccination of this subgroup of carnivores with a killed vaccine may be beneficial if exposure to other animals susceptible to canine distemper is anticipated.

Dimethyl sulfoxide (DMSO) had been postulated to be a 'masking agent' when used concurrently with therapeutic or prohibited drugs in racing animals. Eight drugs (flunixin, furosemide, caffeine, apomorphine, phenylbutazone, lidocaine, cocaine, and acepromazine maleate) were administered to six horses singly and with concurrent intravenous DMSO. Urine samples were analyzed for the presence of the drugs and/or their metabolites by thin layer chromatography. Direct comparison of thin layer chromatograms of extracts of positive urine samples with and without DMSO verified that DMSO did not interfere with the detection of these drugs.

Acute onset of vestibulocochlear and facial nerve dysfunction due to a stress fracture of the petrous part of the temporal bone was diagnosed in 3 horses. The fracture was secondary to chronic inflammatory changes in the petrous part of the temporal bone and the proximal stylohyoid bone, with fusion of the temporohyoid joint. Bacterial meningoencephalitis was a complicating factor. Treatment resulted in reduction of severity of clinical signs in 2 of the 3 cases, but residual compensated vestibular deficits persisted.