Necrotizing hepatitis associated with a reo-like virus infection in a parrot

A young African grey parrot was presented for necropsy following a 3-to-4-day illness consisting of lethargy, anorexia, and diarrhea. A disseminated necrotizing hepatopathy was evident upon histologic examination of the liver. Aggregates of approximately 70-nm-diameter viral particles having morphology consistent with the family Reoviridae were demonstrated by thin-section and negative-staining electron microscopy.     

Stimulation of swine growth by porcine growth hormone

Highly purified porcine growth hormone (pGH; USDA-B1) was administered by im injection (22 micrograms X kg body weight-1 X d-1) to rapidly growing Yorkshire barrows for 30 d. Growth hormone significantly increased growth rate (10%), feed efficiency (4%), cartilage growth and muscle mass. However, pGH did not affect carcass adipose tissue mass. Intramuscular lipid content of the longissimus was increased 50% by pGH administration. Plasma pGH concentration was elevated (7- to 11-fold) for 3 to 5 h post-injection. Chronic administration of pGH depressed pituitary GH content and concentration approximately 45%. No GH antibodies were detected in the plasma of GH-treated swine. Plasma somatomedin-C concentration was increased 55% by GH treatment 3 h post-injection. Plasma glucose and insulin concentrations were both significantly increased in GH-treated swine, suggesting that the animals had developed a state of insulin resistance. Plasma-free fatty acid concentration tended to be higher in GH-treated animals. Treatment of swine with pGH significantly decreased plasma blood urea nitrogen. Assessment of animal health during the trial and postmortem indicated that pGH administration did not have any adverse effects. In summary, treatment of young, rapidly growing swine with pGH stimulated growth performance without affecting animal health or inducing the production of GH antibodies.     

In vitro properties of diffuse cytoplasmic esterase-positive canine mononuclear leukocytes

Depletion of cytoplasmic esterase-positive canine peripheral blood monocytes from mononuclear cell suspensions was attempted using plastic adherence, carbonyl iron ingestion and/or Sephadex G-10 filtration. An esterase-positive, nonadherent, nonphagocytic subpopulation was identified and further characterized by the presence or absence of cell membrane receptors for the Fc portions of immunoglobulin and the activated third component of complement. The majority of these nonadherent cells lacked these receptors. The data suggests that canine peripheral blood monocytes are a heterogenous cell population.     

Cyclic nucleotides in hamster retina

The concentrations of cyclic 3':5'-adenosine monophosphate (cyclic AMP) and cyclic 3':5'-guanosine monophosphate (cyclic GMP) were determined in white light- and dim red light-adapted golden Syrian hamster retinas. Retinas from animals in dim red light had cyclic AMP concentrations of 9.29 +/- 2.94 pmol/mg of protein and cyclic GMP concentrations of 110.62 +/- 32.98 pmol/mg of protein. After white light adaptation, retinal cyclic AMP and cyclic GMP concentrations were reduced to 74% and 45% of the previous values, respectively. In another experiment with white light-adapted animals, the sex or method of immobilization of the animals (cervical dislocation vs sodium pentobarbital) had no significant effect on cyclic nucleotide values.     

Hematologic and biochemical abnormalities associated with induced extrahepatic bile duct obstruction in the cat

Bile duct obstruction was induced in 6 cats by surgical ligation and transection of the common bile duct. Clinical and laboratory changes were monitored weekly for 25 to 54 days. Clinical signs of obstruction were similar in all cats and included anorexia, pyrexia, lethargy, intermittent vomiting, weight loss, palpable gallbladder, hepatomegaly, and bleeding tendencies. Tissue jaundice and acholic feces were evident grossly as early as postsurgical day (PSD) 4 with a mean onset of jaundice at PSD 5.3 +/- 0.4. Hematologic changes were initially characterized by a mild neutrophilic leukocytosis that increased with the chronicity of bile duct obstruction. Regenerative anemia developed in 4 cats associated with gastrointestinal blood loss. Acute serum biochemical changes were characterized by a marked increase in the mean values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, and copper. Comparatively, only moderate increases in mean serum alkaline phosphatase activity were observed. Mean total bilirubin values increased remarkably at postsurgical week (PSW) 1, reaching a maximal value of 23.1 +/- 4.4 mg/dl at PSW 3 with 71.6 +/- 2.7% direct bilirubin. With chronicity of bile duct obstruction ranging from PSW 3 to PSW 7, the mean serum values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, serum alkaline phosphatase, and total and direct bilirubin stabilized and then declined, whereas the increased mean serum copper values persisted. At PSD 25 to 54, hepatic copper values and serum bile acids were markedly increased. Seemingly, clinicopathologic changes of induced cholestatic hepatic injury depended largely on the duration of biliary obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Death of an African elephant from probable toxemia attributed to chronic pulpitis

A 31-year-old captive male African elephant (Loxodonta africana) of 5,000-kg body weight died suddenly in ventral recumbency. Lesions seen at necropsy were bilateral purulent pulpitis and periodontitis of both tusks, serous atrophy of coronary groove fat, Grammocephalus cholangitis, myocardial and skeletal lipofuscinosis, and scattered segmental necrosis in the pectoral muscles. Nonhemolytic streptococci, Corynebacterium sp, Peptostreptococcus anaerobius, Fusobacterium nucleatum, and Bacteroides sp, were recovered from the exudate around one or both tusks. We postulated that the elephant died of hypoxia from prolonged ventral recumbency because of weakness and inability to rise secondary to toxemia from bilateral pulpitis and periodontitis.     

Nephrotoxicity of sodium arsenate in dogs

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.     

Dystrophy, degeneration and infiltration of the canine cornea

Three conditions of the cornea in the dog are described; a form of corneal dystrophy (central/paracentral lipid dystrophy, lipidosis, lipoidosis, cholesterolosis), degeneration (fatty and calcareous degeneration) and infiltration (arcus lipoides corneae, anterior embryotoxon, pre-senile arcus). The clinical appearance, together with histopathological and ultrastructural details, are recorded. The age, sex, breed incidence and possible hereditary factors are also included. Reference is made to previous reports in the veterinary literature and the three conditions are compared with similar conditions in man.     

TENESMUS AND STRANGURIA FROM A CYSTIC UTERINE REMNANT

A 14-year-old domestic short hair spayed female cat was examined for tenesmus and stranguria. The abdominal mass discovered was removed and found to be a cystic uterine remnant. Tenesmus and stranguria resolved following mass removal.     

Dorsal Laminectomy in the Horse II. Evaluation in the Normal Horse

Subtotal dorsal cervical laminectomy was performed on nine normal horses to evaluate positioning, refine the surgical technique, and assess the immediate and long-term effects of this procedure in the horse. Funkquist type B laminectomies were performed at various levels from C3-C4 to C6-C7. Absorbable gelatin sponge or autogenous nuchal fat was placed over the exposed dura mater. Surgery times varied from 2 to 3 hours, and all horses recovered without complication. Rapid primary intention wound healing occurred, with two horses showing neck pain. All remained neurologically normal. The horses were euthanized 6 weeks, 3 months, or 6 months postoperatively. Myelograms performed just prior to euthanasia demonstrated normal or expanded dye column widths. Necropsy revealed that all surgical sites had healed well. The laminectomy membrane was soft and pliable and could be easily separated from the underlying dura mater when fat was used as interpositional material. When gelatin sponge was used, the laminectomy membrane was firmly bonded to the dura. Spinal cords at the level of laminectomy appeared normal and moved freely within the vertebral canal. Histological evaluation of the laminectomy sites and associated spinal cord revealed no abnormalities attributable to the surgery. It was concluded that dorsal cervical laminectomy can be performed in horses without untoward sequelae. The procedure may be useful for the treatment of equine cervical compressive myelopathies.