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Pituitary pars intermedia dysfunction is a slowly progressive disorder that afflicts most breeds of horses. Because it shares features with human Cushing disease, it has been referred to as equine Cushing disease. A variety of tests of pituitary-adrenocortical function were performed on horses with evidence of pituitary pars intermediate dysfunction, and results were compared with those in healthy control horses. Diurnal variations in plasma cortisol concentration were not statistically different between control horses and those with pituitary pars intermedia dysfunction. An ACTH stimulation (1 U of natural ACTH gel/kg of body weight, IM) test or a combined dexamethasone suppression test (10 mg, IM) and ACTH stimulation (100 mg of synthetic ACTH, IV) test also failed to distinguish horses with pituitary pars intermedia dysfunction from control horses. A significant (P < 0.001) dose-related suppression of cortisol concentration in response to increasing doses (5, 10, 20, and 40 micrograms/kg) of dexamethasone was observed in control horses but not in those with pituitary pars intermedia dysfunction. On the basis of plasma cortisol concentration, the dexamethasone suppression test, using 40 micrograms/kg, whether initiated at 5 PM with sample collection at 15 (8 AM) and 19 (12 PM) hours after dexamethasone administration, or initiated at 12 AM with sample collection at 8 (8 AM), 12 (12 PM), 16 (4 PM), 20 (8 PM), and 24 (12 AM) hours after dexamethasone administration, reliably distinguished between control horses and those with pituitary pars intermedia dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma amino acid patterns were studied in 6 clinically normal adult horses during the course of hepatic disease induced by feeding them plants containing pyrrolizidine alkaloids. At death, there were significant (P less than 0.01) increases in glutamine, proline, tyrosine, asparagine, lysine, histidine, alanine, phenylalanine, methionine, aspartic acid, and ornithine values. There were no significant changes in glycine, valine, isoleucine tryptophan, and arginine values. There were significant (P less than 0.01) decreases in citrulline. Ammonia increased 4-fold. Alpha-Aminoadipic acid and alpha-aminobutyric acid were not detectable in the plasma of clinically normal horses, but were in the plasma of horses with severe hepatic disease. The ratio of branched chain amino acids (isoleucine + leucine + valine) to phenylalanine plus tyrosine progressively decreased from a normal of +/- 0.5 to 1.3 +/- 0.3 (mean +/- SD) just prior to death. The relative changes in plasma amino acid pattern in horses with hepatic diseases seem similar to those changes occurring in man and other animals with hepatic disease.

An indirect method of blood pressure measurement was evaluated in 169 dogs, including 114 that were hospitalized because of a variety of diseases, 10 clinically normal dogs presented for neutering, and 45 privately owned, clinically normal dogs. Measurements correlated well with values obtained by simultaneous direct arterial puncture. Normotension was considered to be 130 to 180 mm of Hg, systolic, and 60 to 95 mm of Hg, diastolic. As a group, 20 dogs with advanced renal disease had significant (P less than 0.001) hypertension, compared with the groups of clinically normal dogs. Of 94 dogs with a variety of diseases exclusive of renal disease, 10 had hypertension and 2 had hypotension.

The physical findings, clinical signs, age, breed and sex distributions, and laboratory data of 117 dogs with untreated Cushing's syndrome were reviewed. Poodles, Dachshunds, and Boxers of all ages were found to be at increased risk, as were dogs of all breeds greater than or equal to 6 years old. Polydipsia, polyuria, progressive bilaterally symmetric alopecia, and abdominal distention were the most frequently observed clinical signs and physical findings. Lymphopenia, eosinopenia, above normal values of serum alkaline phosphatase, serum cholesterol, and sulfobromphthalein dye retention, and below normal urine specific gravity were the most frequent abnormalities found in the laboratory data. About 50% of the dogs had urinary tract infections. Final diagnosis was established on the basis of abnormally high plasma corticosteroid values in response to an intramuscular injection of adrenocorticotropic hormone.

A chronic mucocutaneous disease was diagnosed in 3 dogs. Clinically, the disease was characterized by erosions and ulcerations of the oral mucosa, various mucocutaneous junctions, and the skin. Histologically, there was acantholysis or a separation of the epithelial cells from one another, resulting in the formation of clefts and bullae. Based on clinical and laboratory findings, the disease seemed to be the canine equivalent of pemphigus vulgaris (PV) in man.

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.

Case records of horses with equine ehrlichiosis (Ehrlichia equi) at the University of California Veterinary Medical Teaching Hospital and Ackerman Creek Large Animal Clinic were analyzed for evaluation of clinical signs, time of onset, hematologic values, response to treatment, and recovery. Equine ehrlichiosis was found to be seasonal in horses in the foothills of northern California, with higher incidence than reported previously. The horses developed fever, anorexia, depression, limb edema, icterus, and ataxia. Hematologic changes were leukopenia, thrombocytopenia, icterus, anemia, and inclusion bodies in the neutrophils and eosinophils. Diagnosis was made by observing the characteristic inclusion bodies, using a standard Wright's stain. Mortality was low, although complications of opportunistic secondary infection and injury due to ataxia did develop. Treatment with tetracycline resulted in prompt clinical improvement within 24 hours. Chronic cases were not detected. Equine ehrlichiosis should be differentiated from diseases with similar clinical signs including encephalitis, liver disease, purpura hemorrhagica, equine infectious anemia, and equine viral arteritis.

Nine adult horses were fed alfalfa hay cubes containing approximately 10% Senecio vulgaris until all horses had consumed approximately the same amount of toxic components of S vulgaris, pyrrolizidine alkaloids (PA). The amount of PA consumed was determined by the amount that induced clinical signs of PA toxicosis in 3 horses. The 6 other horses were given similar amounts per kilogram of body weight. An initial decrease of feed intake was observed when horses' diets were changed from alfalfa cubes to alfalfa/Senecio cubes, and feed intake was decreased further over 89 to 98 days. From 50 to 159 days, body weight decreased in all horses. Liver disease was induced in all 9 horses after they ate an average of 233 +/- 9.2 mg of PA/kg of body weight. Eight horses died or were euthanatized. Treatment with branched chain amino acids had no effect on mortality, but appeared to reduce neurologic problems. Clinical signs of PA-induced liver disease included ataxia, head pressing, and decreased feed intake. Other clinical signs of toxicosis were observed individual horses, but did not develop in most horses. Megalocytic hepatopathy developed. Liver abnormalities proceeded as PA was consumed and were severe in 8 of 9 horses before clinical signs of toxicosis appeared. Sulfobromophthalein sodium clearance did not decrease until PA-induced liver disease was advanced. Bile acid (BA) concentrations increased to greater than or equal to 50 mumol/L, in the 8 horses that died. One horse had hepatopathy and increased BA concentration, but survived. In this horse, BA concentration peaked at 33 mumol/L and then decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.