D. F. Kelly

A Lymphomatoid Granulomatosis of the Lungs in Young Dogs

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.

Pathology of acute respiratory distress in the dog associated with paraquat poisoning

Abstract The morbid anatomical, histological and ultrastructural changes in the lungs of 10 dogs with acute respiratory distress are described. The duration of signs varied from 12 h to 7 days. The early phase of respiratory distress was associated with pulmonary haemorrhage and oedema, focal necrosis of bronchiolar epithelium, alveolar collapse and loss of both type I and type II pneumonocytes. In the later stages there was intra-alveolar fibrosis, bronchiolar epithelial regeneration and alveolar epithelialization by immature type II pneumonocytes. Paraquat was recovered from 4 of the dogs and the similarity between the clinical and pathological features within the group, and to paraquat poisoning in other species, suggested that this compound was probably responsible for the lesions in all 10 dogs. Histological changes also included necrosis of the adrenal zona glomerulosa, renal tubular necrosis, focal myocardial necrosis and medial fibrinoid necrosis of coronary arteries, a change not hitherto described in association with paraquat poisoning. The lesions are discussed in relation to their possible functional role in the development of clinical signs, and are compared with the lesions of paraquat poisoning which have been described in man and laboratory animals.

Histology of Salivary Gland Infarction in the Dog

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.

Experimental pyelonephritis in the cat. 1. Gross and histological changes.

Abstract Young adult cats were given an intravenous injection of Escherichia coli after ligation of one ureter lasting 24 or 48 h. Ten cats injected with a human strain of E. coli (between 2·3 and 35·23 × 10 8 per kg) developed mild pyrexia. Some of the cats examined between 1 and 16 months later had a mild focal non-progressive pyelonephritis in the obstructed kidney. Injection of a feline strain E. coli (between 0·83 and 6·4 × 10 8 per kg) produced an acute bacteraemic illness and 6 of 10 cats died between 1 and 11 days after infection. Cats that survived the acute illness had extensive pyelonephritis and scarring in the obstructed kidney when examined between 17 days and 5 months after infection. The experiments indicate that, after temporary ligation of one ureter, intravenous injection of E. coli is followed by establishment of infection in the obstructed kidney. Renal infection with a feline strain of E. coli can progress to a stage of patchy pyelonephritis that resembles the naturally occurring lesion in the cat.

Megaloesophagus and associated gastric heterotopia in the cat.

Two young adult male Siamese cats had heterotopic gastric mucosa in the dilated and inflamed oesophagi. Normally differentiated gastric mucosal glands were present and there was severe ulceration in one cat. It is uncertain whether the gastric heterotopia was a reparative change after oesophagitis or whether it represented a coincidental anatomical anomaly.

Experimental pyelonephritis in the cat 2. Ultrastructural observations

Abstract An ultrastructural study was made of the renal cortical lesions in cats with pyelonephritis produced by experimental Escherichia coli infection and temporary renal obstruction. The most striking changes were interstitial fibrosis, thickening and folding of the tubular basement membrane, and atrophy of renal tubular epithelium. Interstitial inflammatory cells were mainly lymphocytes and plasma cells. Release of renal tubular lipid into the interstitium occurred commonly but did not appear to provoke additional cellular response. Glomerular changes included segmental sclerosis, wrinkling and collapse of basement membrane, thickening and fragmentation of Bowmans capsule, and periglomerular fibrosis. The changes described are similar to those which occur in a variety of human and animal nephropathies and represent non-specific responses to injury.

Experimental pyelonephritis in the cat: 3. Collagen alterations in renal fibrosis.

Chronic pyelonephritis was induced in young adult cats by the intravenous injection of a human or a feline strain of Escherichia coli after ligation of one ureter for 24 or 48 h. In the 3 cats infected with the feline strain, scarred kidneys from the obstructed side were removed at necropsy 3, 4 and 5 months later. Collagen was extracted from pyelonephritic and normal kidney tissue with dilute acetic acid and limited proteolysis with pepsin. Scarred kidneys gave higher yields of both acid-soluble collagen (normal = 0.57 +/- 0.12 mg per g tissue; scarred = 0.88 +/- 0.10 mg per g tissue) and pepsin-solubilized collagen (normal = 9.69 +/- 1.79 mg per g tissue; scarred = 20.02 +/- 2.84 mg per g tissue). There was no significant increase in the collagen yield from the kidneys of the 2 cats in which mild focal lesions were found 14 and 16 months after infection with the human strain of E. coli. Pepsin released collagens were separated by fractional salt precipitation and identified by agarose gel chromatography and polyacrylamide gel electrophoresis. Normal kidney was shown to contain collagen of Types I, IV and V (AB). The Type IV collagen extracted consisted of a mixture of 4 major pepsin-resistant chains of apparent molecular weights of 150 000, 115 000, 85 000 and 60 000. The collagen extracted from scarred kidneys was predominantly Type I, only trace amounts of Type IV and V components being present. These findings suggest that basement membrane collagens of the kidney are selectively degraded during the atrophy and scarring of chronic feline pyelonephritis and are preferentially replaced by interstitial Type I collagen.