Ectopic mineralization and nutritional hyperparathyroidism in boars.

The influence of a high phosphorus (1.5%) and high calcium (2.2%) diet on ectopic mineralization in boars was examined over a four month period. The high phosphorus diet caused metastatic mineralization in the left atrial endocardium in 84% of animals and in the pulmonary and diaphragmatic pleura in 21 and 58% of animals, respectively. Mineralization, that apparently commenced as deposits of extraneous calcium and progressed by metastatic deposition, occurred also in the lamina propria mucosae of the respiratory airways and in the lamina muscularis mucosae of fundic stomach. Hyperplasia of osteoclasts and microfractures in costochondral junction, morphological features of activated parathyroid cells and a significant drop in serum phosphorus during the fourth month in boars fed high phosphorus, suggest that nutritional hyperparathyroidism was experimentally induced. No systemic bone disease developed. Feeding a high calcium diet resulted in 20% incidence of discrete lesions in the left atrial endocardium and no pleural involvement. Also, lesions in respiratory airways and fundic stomach were mild. The fact that high phosphorus but not high calcium increased the incidence and extent of ectopic mineralization suggests that hyperparathyroidism under normocalcemic conditions might be involved in the pathogenesis of these lesions.     

Primary hyperparathyroidism in dogs and cats

The most common cause of primary hyperparathyroidism in dogs and cats is a solitary adenoma involving an extracapsular parathyroid gland. The prognosis is excellent if the affected parathyroid gland is removed. Nonsurgical methods are discussed, although there are no current data to support any benefit over conventional surgery. The common postoperative complication to consider is hypocalcemia. Hypocalcemia can be successfully managed in these animals if it is anticipated and treated promptly.     

Experimental parvovirus infection in dogs.

Five eight week old dogs were inoculated orally and intranasally with cell culture origin canine parvovirus. Three dogs became depressed and anorectic and developed a mild (one dog) to severe diarrhea five days postinfection. The remaining dogs had subclinical infections but developed a lymphopenia followed by a transient lymphocytosis. The ill dogs developed mild (one dog) to severe neutropenia and a moderate lymphopenia. One died nine days postinfection. Recovery was associated with cessation of viral excretion and with lymphocytosis and antibody production. Two of three dogs challenged intragastrically developed mild clinical signs and a moderate panleukopenia four to eight days postinfection. The pathological changes of the experimental disease were very similar to that of spontaneous disease. Bone marrow changes included a severe granulocytic and mild erythroid depletion. The pathogenesis of canine parvovirus infection is discussed.     

Fractures secondary to nutritional bone disease in dogs: a review of 38 cases

The pattern of bone fractures secondary to nutritional bone disease in 38 dogs was analysed using a radiographic survey. The majority of fractures were either caused by a fall (28.95%) or showed no history of direct trauma (31.58%). Mongrels were more commonly affected by pathological fractures, followed by Dobermanns and German Shepherds. Significantly more (P < 0.05) fractures were found in dogs aged less than 6 months (64.71%). The incidence of such fractures was significantly higher in males than in females (M:F = 2.70:1.00). General radiological signs included a generalized decrease in cortical density, thinning of cortices and widening of metaphyses/epiphyses in most of the animals. Fractures were found significantly more frequently (P < 0.01) in the femur (81.58%) than in any other bone. Of the different types of fracture, complete oblique and incomplete fractures were most common.     

Secondary phosphorus poisoning in dogs

Subsequent to a possum (Trichosurus vulpecula) poisoning operation purportedly using 1% phosphorus baits, six dogs with access to poisoned possums died of phosphorus poisoning. Two dogs survived, following treatment with oral copper sulphate and parenteral vitamin K. Clinical signs included depression, jaundice, vomiting and bloody diarrhoea. Post-mortem lesions included large areas of subcutaneous, interstitial and intermuscular haemorrhage, subserosal haemorrhage and liver degeneration. Free phosphorus was detected in the ingesta of three of the dogs which died up to 7 days after the last of the poison was laid. Analysis of two batches of baits used showed P levels of 1.17% and 1.24%.     

Astrocytomas in young dogs

Primary brain tumors are not commonly reported in young dogs; however, they are the second most common cancer in children. Astrocytomas are the majority of these tumors. This report presents three cases of astrocytomas in young dogs, indicating a possible higher incidence than what is currently held. When suspected, it is recommended that biopsy or surgical excision be performed to further characterize and grade the tumor and, if appropriate, guide treatment.     

Secondary myelofibrosis in three dogs

Myelofibrosis was diagnosed in 3 dogs. In each dog, there was evidence of concurrent bone marrow necrosis, suggesting that the myelofibrosis was a secondary change. This suggestion was supported by a lack of dysplastic changes in hematopoietic cells. Bone marrow necrosis in 2 of the dogs may have been the result of widespread malignancy. Reversal of the myelofibrosis in 1 dog suggested that myelofibrosis is not always a terminal disorder.