Ultrastructure of the kidney in amyloidosis of rabbits.
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Biomedical subjects
Publications and source records attributed to V M Lucke.
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12 marmosets of 3 different species died of hepatitis during a period of 5 months. The lesions closely resembled those of virus hepatitis in man but material from these animals and from in-contact marmosets failed to reveal the presence of hepatitis A. This together with certain aspects of the epidemiology of the disease suggests that the outbreak was not caused by a virus of human origin but possibly by a virus indigenous to the marmoset or tamarin.
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In an outbreak of type C botulism in a group of captive primates, six squirrel monkeys, six white throated capuchin monkeys and two weeper capuchin monkeys succumbed rapidly and died. Clostridium botulinum type C toxin was detected in the remains of the chopped chicken feed and in nine of 11 blood samples and one of three stomach contents samples from the affected animals.
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Clinical signs in three young dogs with primary lung neoplasms included cough, weight loss and anorexia. Chest radiographs taken in the terminal stages of the disease showed nodular and diffuse consolidation of the lungs typical of primary neoplasms. Macroscopically the lungs were infiltrated by firm, pale tissue; similar tissue replaced the enlarged bronchial lymph nodes. In two dogs similar deposits were found also in the liver and spleen. The infiltrates were composed of atypical, polymorphous lymphoreticular cells. Invasion of pulmonary blood vessels and of bronchi and bronchioles was striking. The lesions closely resembled those of lymphomatoid granulomatosis, a rare human disease of unknown cause.
Salivary gland infarction was found in two adult dogs. The main changes were ischaemic necrosis, capsular fibrosis and regenerative hyperplasia of surviving ductal epithelium. Necrosis of arterial tunica media and thrombosis were found only in the infarcted parts of the salivary glands. The lesions appeared to be confined to the salivary glands; no cause of the infarction was found.
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An 18 month old cat had a 6 month history of abnormal high stepping gait, ataxia, muscle twitching and loss of sensory perception. The clinical course was interrupted by several episodes of temporary remission. The essential pathological features were those of a polyradiculoneuritis with segmental demyelination, focal mononuclear cell infiltration and hypertrophic onion-bulb formations. The condition is compared with chronic relapsing polyradiculoneuritis in the dog and in man.
Two examples of renal papillary necrosis in the tiger are described. The necrosis was characterised by large zones of liquefaction with minimal inflammation and was associated with pronouced scarring in the cortex. Both animals had been vomiting terminally and were severely dehydrated. It is suggested that papillary necrosis was precipitated by the reduced renal perfusion associated with dehydration in kidneys in which the medullary blood supply was already compromised by chronic cortical scarring. Comparisons are made between the lesions described in these tigers and those reported in the domestic cat, man and other domestic animals.
Thirty-three cases of canine renal carcinoma reported between 1907 and 1972 are reviewed, and clinical and pathological features of nine other cases seen in Bristol between 1966 and 1975 are described. Clinical features frequently include nonspecific signs of anorexia and weight loss. The age range of affected dogs varies from 3 to 15 years, with a mean of 7.1 years. Male dogs appear to be affected more frequently than females, but there is no breed predilection. The clinical behaviour of canine renal carcinoma is variable, with 4 years the longest survival time after nephrectomy. The primary tumours characteristically are large and unilateral and occupy most of one pole of a kidney. Metastatic spread can involve a wide range of organs, the commonest being lymph nodes and lung. Solid, tubular and papillary patterns are common. Clear cell carcinoma is uncommon.
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