Cutaneous mastocytosis in a dog.
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Animals↗
Biomedical subjects
D J Meuten
Publications and source records attributed to D J Meuten.
Ischemic necrosis of cartilage in spontaneous and experimental lesions of osteochondrosis.
This study was designed to examine the association of spontaneous lesions of osteochondrosis with vascular supply to epiphyseal cartilage, and to determine whether similar lesions could be experimentally reproduced by selective interruption of cartilage canal blood supply. The vascular supply to the articular-epiphyseal cartilage complex of the distal end of the femur was studied in 27 microfil- or barium-injected and cleared specimens and 24 serially sectioned microangiographic specimens from 27 clinically normal female swine (3.6 to 71.0 kg). Blood vessels supplying the articular-epiphyseal cartilage complex were consistently restricted to the epiphyseal region and the number of vessels decreased as the pigs increased in weight (p less than 0.001). Spontaneous lesions of osteochondrosis (i.e., cartilage necrosis) were initially seen in the first areas of epiphyseal cartilage to become avascular and were associated with necrotic blood vessels. The number and size of foci of necrotic cartilage increased as the pigs increased in weight (p less than 0.001). Blood supply to epiphyseal cartilage from cartilage canal vessels was surgically interrupted in a highly vascular area of the medial femoral condyle in eight additional 23-kg female swine. This procedure resulted in necrosis of blood vessels within cartilage canals followed by necrosis of surrounding cartilage, lesions that appeared to be identical to early spontaneous lesions of osteochondrosis. These results suggest that the viability of epiphyseal cartilage in the articular-epiphyseal cartilage complex is highly dependent on an adequate blood supply from cartilage canal vessels, and strongly implicates a defect in blood supply in the pathogenesis of osteochondrosis.
Animals↗
Short-chain fatty acids induce reversible injury of porcine colon.
Carbohydrate malabsorption frequently results in an increased net production of organic acids by colonic microorganisms and an acidification of colonic contents. Colonic structure and function during and following mucosal exposure to acetate at various H ion concentrations was examined under both in vivo and in vitro conditions. An acetic acid dose and time-dependent injury of the surface epithelium sequentially resulted in (1) degeneration and extrusion of enterocytes and increased ion permeability (pH 5.0); (2) formation of subepithelial blisters and increased mucosal permeability to mannitol (pH 4.0), and (3) sloughing of surface epithelium and the abolition of active NaCl absorption (pH 3.0). Both acetate and lactate at pH 4.0 produced significantly greater injury than similarly acidified NaCl. Crypt cell structure and Cl secretory function were preserved, however, and migration of viable cells from adjacent crypts rapidly covered the denuded surface within 30-60 min of recovery. Normal structure and function were nearly restored in 2 hr. These results suggest that colonic mucosal injury is possible under conditions that may be present during carbohydrate malabsorption syndromes. They also provide evidence that the process of surface reepithelialization may be of central importance in the defense and repair of the colonic mucosa during such acid-induced injury.
Acetates↗
Bone fragility in a kitten: an osteogenesis imperfecta-like syndrome.
A 12-year-old kitten was found to have bone fragility. Previously described causes of bone fragility in domestic cats were excluded on the basis of serum biochemical profile and radiographic histologic examinations. The findings in this kitten correlated most closely with osteogenesis imperfecta, a syndrome documented in human beings and cattle.
Animals↗
Villous atrophy, crypt hyperplasia, cellular infiltration, and impaired glucose-Na absorption in enteric cryptosporidiosis of pigs.
Intestinal morphology and fluid and electrolyte transport were examined in a neonatal porcine model of cryptosporidiosis. Sections of jejunum, ileum, and colon were obtained for morphometric analysis on days 3, 6, 9, and 12 postinfection, and in vivo perfusion studies of jejunum and ileum were conducted on days 3 and 4 postinfection. The most severe morphologic lesion was seen in the ileum on day 3, and consisted of villous atrophy, crypt hyperplasia, and cellular infiltration. Villous surface area was reduced from 2.1 +/- 0.4 x 10(5) microns2 in control ileum to 0.8 +/- 0.1 x 10(5) microns2 in infected ileum, a result associated with enterocytes that were fewer in number and reduced in cross-sectional area. Conversely, the number of inflammatory cells in the lamina propria of the villus increased from 456 +/- 116 in control to 1014 +/- 187 in infected villus without a significant change in the volume of the lamina propria. At the height of infection, there was an approximate 1:2 ratio of both organisms and inflammatory cells to villous enterocytes. In contrast, organisms were not observed in the crypts, and the concentration of inflammatory cells in crypt lamina propria was unaltered. Disappearance of organisms and polymorphonuclear cells from the ileum was associated with restoration of normal structure and was complete by day 12. Although organisms were seen in the colon, the general architecture was not severely affected. On days 3 and 4 postinfection, there was a complete impairment of the glucose-stimulated Na and water absorption in both jejunum and ileum of infected pigs; however, absorption of electrolytes and water from a basic Ringer's solution, in the absence of glucose, was not significantly affected. These results are consistent with a malabsorptive diarrheal disease associated with the morphological damage and are very similar to those seen in enteric viral disease in pigs, except that the upper intestine is more severely affected in the latter.
Animals↗
Degeneration of cartilage canal vessels associated with lesions of osteochondrosis in swine.
Articular-epiphyseal cartilage complexes from the distal femur and humerus of five 3-month-old pigs were collected and preserved using either a conventional or a ruthenium hexammine trichloride (RHT)-supplemented fixation technique. Lesions were similar regardless of the fixation technique. Areas of necrosis were in epiphyseal but not articular cartilage from both sites of all pigs. Cartilage canals were confined to epiphyseal cartilage and contained vessels which had endothelial cells in varying stages of degeneration and necrosis. Areas of necrotic cartilage often were adjacent to or surrounded degenerate cartilage canals. Lipid emboli (up to 40.0 micron in diameter) were infrequently located in vessels within cartilage canals. Associated with the lipid emboli were leukocytes, erythrocytes, necrotic cell remnants, and flocculent material. Restriction of necrosis to epiphyseal cartilage and the association of these necrotic areas with degenerating vessels in cartilage canals strongly implicate a defect in cartilage canal blood supply in the pathogenesis of osteochondrosis. The RHT fixation technique resulted in excellent cellular detail at the light microscopic level, but ultrastructurally there was marked vacuolation of chondrocytes and matrix. The conventional technique caused shrinkage of all chondrocytes, resulting in a wide halo of pericellular matrix surrounding each cell.
Animals↗
Evaluation of red blood cell fragility in Pygmy goats.
Red blood cells from 6 Pygmy goats were determined to be significantly (P less than 0.01) more susceptible to osmotic lysis and mechanical stress than were RBC from 6 Toggenburg goats. Differences in RBC size and shape and adenosine 5'-triphosphate concentration between the 2 breeds were not significant. The differences observed in the in vitro tests may be attributable to differences in RBC membrane composition.
Adenosine Triphosphate↗
Effect of reduced growth rate on the prevalence and severity of osteochondrosis in gilts.
Ninety-six recently weaned gilts were assigned to 3 groups. Group-1 gilts were fed a corn-soybean meal diet ad libitum and were killed when they weighed 110 kg. Gilts in groups 2 and 3 were fed 70% of the feed consumed by group-1 gilts. Group-2 gilts were killed when they weighed 110 kg, and group-3 gilts were killed at the same age as group-1 gilts. At slaughter, the right pelvic and thoracic limbs from all gilts were removed, and the distal end of each femur and humerus was sectioned serially at 5-mm intervals. Articular-epiphyseal cartilage complexes from these sites were examined grossly, radiographically, and histologically. Effects of treatment (ad libitum vs limited energy intake) and average daily gain on the prevalence and severity of lesions were analyzed statistically, using chi 2 analysis, a categoric-modeling technique, analysis of variance, and correlation coefficients. Of humeri and femora, 49 and 70%, respectively, had lesions of osteochondrosis, and 86% of the gilts had a lesion at one or both sites. Group-2 gilts (killed at 110 kg, but approx 70 days older than group-1 gilts) had significantly lower prevalence (P = 0.009) and severity (P = 0.002) of osteochondrosis of the distal end of the femur than did gilts in groups 1 and 3. When each group was evaluated individually, gilts that had a higher average daily gain had an increased prevalence and severity of lesions.
Animal Feed↗
Toxicity of palmitoyl glycerol to mice: depression of thyroid function.
Mice given propylthiouracil, a thyroid inhibitor, and fed a diet containing a nontoxic level of rac-1(3)-palmitoyl glycerol showed the hypothermia and mortality expected for a toxic dose, but did not show these signs when linoleate or oleate was added to the diet. Loss of radioiodine from the whole animal and thyroid gland was slower when mice were fed the toxic palmitoyl glycerol diet than when fed the same diet containing 4% safflower oil. However, mice fed the two diets did not differ in the extent of the incorporation of radioiodine, and essentially all was bound to protein in each case. Follicular thyroid cells from mice fed the potentially toxic diet that contained unsaturated fat were normal in appearance. Conversely, cells from mice fed the toxic diet were smaller and more densely stained, showing evidence of glycoprotein inside the cell. These findings show that the thyroid gland is affected by the palmitoyl glycerol diet. However, the thyroid is not the only organ affected, because giving either thyroxine or triiodothyronine had no effect on the toxicity of palmitoyl glycerol.
Animals↗
Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings.
An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
Animals↗
Cultivation of Rhinosporidium seeberi in vitro: interaction with epithelial cells.
Rhinosporidium seeberi, a fungus that is associated with polyp-like tumors in animals and man, was successfully cultivated. This organism stimulated proliferation of epithelial cells in vitro, producing polyp-like structures. Spores produced in culture required a period of aging or development, or both, before they were capable of reinitiating the growth cycle.
Animals↗
The ultrastructure of osteochondrosis of the articular-epiphyseal cartilage complex in growing swine.
Osteochondrosis of the articular-epiphyseal cartilage complex (A-E complex) is a significant clinical disease in swine. It has been suggested that osteochondrosis is the underlying cause of osteochondritis dissecans in humans. The purpose of this investigation was to characterize the ultrastructural changes in the earliest macroscopically visible lesion of the epiphyseal cartilage in osteochondrosis of the A-E complex in swine. Osteochondritic epiphyseal cartilage from the distal femora and humeri of growing crossbred boars was collected, embedded in plastic, and studied light and electron microscopically. The predominant lesion was chondronecrosis, characterized by chondrocyte death and loss of matrical proteoglycan. Transition from normal to abnormal cartilage was abrupt. Lipid accumulated in chondrocytes within and adjacent to lesions, but not in chondrocytes distant from lesions. Intracellular lipid accumulation was an important feature of the lesion and may play a role in its initiation. It is hypothesized that intracellular lipid accumulation results from hypoxia/anoxia and may precede matrix degeneration, which precedes cell death.
Animals↗
Nasal rhinosporidiosis in the dog.
Rhinosporidiosis was diagnosed in six dogs from the southeastern United States. All six dogs had unilateral nasal polyps with multiple small white sporangia visible beneath the surface. Microscopically, the polyps consisted of organisms and fibrovascular tissue with a surface of columnar or squamous epithelium. Juvenile sporangia were unilamellar, 15-75 microns in diameter, nucleated, and accounted for about 65% of sporangia seen. Approximately 5% of the sporangia were in intermediate stages of maturation, were bilamellar, 100-150 microns in diameter, and contained immature endospores. Mature sporangia comprised about 30% of the total, were usually unilamellar, 100-400 microns in diameter, and contained a mixture of immature and mature endospores. The inner layer of the wall of the intermediate sporangia and the single wall of the mature sporangia were argyrophilic and carminophilic. Ultrastructurally, the earliest stage contained a nucleus and many ribosomes, lipid droplets, and phagolysosomes. Maturing sporangia contained discrete membrane-bound, round clevage products. These structures subsequently matured to spores, each of which had a wall and contained a nucleus and many lipid droplets. The organism from one dog was cultured and grown in vitro for 7 months and is the first successful cultivation of Rhinosporidium seeberi.
Animals↗
Idiopathic hyperaldosteronism in a dog.
Idiopathic hyperaldosteronism was diagnosed in an 8-year-old castrated male Yorkshire Terrier, based on increased concentration of plasma aldosterone, hypertension, hypernatremia, decreased natriuresis, hypokalemia, and hyperkaluria. Unilateral adrenalectomy was performed after visualization of a nodule on the right adrenal gland. Hyperplasia of the zona glomerulosa and increased postoperative aldosterone concentrations supported the diagnosis of idiopathic hyperaldosteronism.
Adrenal Glands↗
Necropsy procedure.
The purpose of this article is to provide guidelines for the necropsy of a calf with diarrhea. Figures and tables are designed to help this procedure. With proper tools and a systematic approach, the entire necropsy should take only 20 to 30 minutes. The efficient and thorough completion of a necropsy often improves the relationship between owner and veterinarian.
Abdomen↗
Canine laryngeal rhabdomyoma.
Three canine laryngeal tumors were diagnosed as oncocytomas by light microscopy, but were determined to be rhabdomyomas following ultrastructural and immunocytochemical examination. Tumors consisted of large eosinophilic cells interspersed with smaller dark cells. Large tumor cells had a granular, intensely eosinophilic cytoplasm. Scattered through the tumors were a few elongated cells with cytoplasmic cross striations and multiple nuclei. Tumor cells from all three dogs contained numerous mitochondria and bundles of myofibrils with electron-dense Z-lines typical of striated muscle cells. Intracellular myoglobin and desmin were detected in the tumors by immunocytochemistry. Comparisons are made with a previous report of canine laryngeal oncocytomas.
Adenoma↗
Canine Rocky Mountain spotted fever: a kennel epizootic.
Within a period of 5 consecutive days after the initial observation of illness was made, 7 of 12 Siberian Husky dogs developed clinical signs of Rickettsia rickettsii infection. One dog died and was necropsied. Clinical signs of infection consisted of lethargy, anorexia, ocular and nasal discharges, and neurologic disorder (incoordination and rolling). Scleral blood vessel injection, fever, lymphadenomegaly, splenomegaly, and increased bronchovesicular lung sounds were prominent findings. Clinical laboratory test results identified decreased platelet numbers, variable neutrophil counts, increased serum alkaline phosphatase activity, hyponatremia, hypokalemia, and bilirubinuria. Diagnosis of Rocky Mountain spotted fever was confirmed by serologic evaluation of acute and convalescent sera, using the micro-immunofluorescence technique, and R rickettsii antigen was determined by demonstration of intracellular rickettsial organisms in vascular endothelial cells of brain and lung (stained with carbol-basic fuchsin and aqueous malachite green) and by demonstration of spotted fever-group rickettsiae in tissues by direct fluorescent antibody technique. Near-simultaneous naturally occurring tick-borne infection of 7 dogs with R rickettsii documents an unreported occurrence.
Animals↗
Hepatic necrosis associated with use of halothane in a dog.
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Anesthesia, General↗