Serum amyloid A and haptoglobin levels in bovine amyloidosis

Serum amyloid A (SAA) and haptoglobin (Hp) levels were determined in 25 cows suffering from amyloidosis. SAA levels in cows with amyloidosis ranged between < 0.3 and 225.8 microg/ml, with a median level of 105.1 microg/ml, and Hp levels ranged between < 20 and 1860 microg/ml, with a median level of 950 microg/ml. These levels were significantly higher than the levels observed in healthy cows (SAA levels ranged from < 0.3 to 13.5 microg/ml, with median of 1.4 microg/ml, and Hp levels were undetectable in all cases), but were not significantly different from the levels observed in control cows with chronic inflammation. There was a significant correlation between SAA and Hp levels in cows with chronic inflammation , but not in cows with amyloidosis. It was concluded that the serum SAA levels in cows with amyloidosis might be changed by some factor other than inflammation.     

Ultrastructural and enzyme histochemical aspects of amyloidosis in the bovine renal medulla.

Electron micrsocopic studies of bovine kidneys with amyloidosis showed macrophage-like cells in the interstitial amyloid that were either disseminated or in small groups. They had rather uniform protracted vacuoles filled with parallel fibrils. Similar vacuoles were also found in some reticular interstitial cells. In some samples electron-dense vacuoles and vacuoles containing fibrils were seen. Protracted lysosomal enzyme activity was seen in macrophage-like cells and reticular interstitial cells; these areas of activity showed green birefringence with Congo red. The vacuoles were thought to be lysosomes, and the parallel amyloid fibrils could be a consequence of intracellular formation or of phagocytosis.     

Familial renal amyloidosis in Abyssinian cats

Medullary and glomerular amyloidosis, papillary necrosis, and secondary interstitial disease were diagnosed in eight related adult Abyssinian cats from two catteries. The lesions were similar to those in two unrelated mongrel cats with renal amyloidosis. Ultrastructurally, the patterns of amyloid deposition were as described in other species, although medullary deposition predominated. Potassium permanganate oxidation blocked Congo red staining of the deposits suggesting that they contained amyloid A protein (secondary amyloid). The disease may be a model of familial secondary amyloidosis and offers an opportunity to study the pathogenesis of both amyloid deposition and papillary necrosis. The histochemical characteristics of feline renal amyloid require careful attention to technique. Section thickness affects Congo red affinity and both dichroism as well as birefringence should be considered when interpreting staining reactions. Thioflavine-T may be the preferred stain for identification of small deposits of amyloid. Variation in section thickness markedly affected the degree of potassium permanganate oxidation.     

Immunohistochemical distribution of amyloid deposits in 25 cows diagnosed with systemic AA amyloidosis

The distribution of amyloid deposits was histopathologically and immunohistochemically examined in 25 cows aged 5 to 10 years that had been diagnosed with systemic AA amyloidosis. This examination revealed that amyloid deposits were also present in the hypophysis, ovary, uterus, mammary gland and skeletal muscle, in addition to the liver, kidney, spleen, pancreas, thyroid gland, adrenal gland, gastrointestinal mucosa, heart, lung and lymph nodes. The examined cows tended to have chronic inflammations, including chronic mastitis (six cases) or chronic pneumonia (four cases), which is thought of as a causative agent of AA amyloidosis. In contrast, five cases did not exhibit any chronic inflammation.     

Familial renal amyloidosis in Chinese Shar Pei dogs

Renal amyloidosis was diagnosed in 14 young Chinese Shar Pei dogs, all of which were related. Clinical signs were those of renal failure and included vomiting, anorexia, lethargy, polydipsia, polyuria, weight loss, and dehydration. Some dogs had a history of intermittent fever and joint swelling. Laboratory findings also were compatible with renal failure and included azotemia, hyperphosphatemia, low total CO2 content in serum, isosthenuria, proteinuria, and hypercholesterolemia. All dogs had medullary deposition of amyloid, and 9 of 14 (64%) had glomerular involvement. The remaining renal lesions were typical of end-stage renal disease. In some dogs, amyloid deposits were found in other tissues (eg, liver, spleen, stomach, small intestine, myocardium, lymph node, prostate gland, thyroid gland, and pancreas). Amyloid deposits were sensitive to potassium permanganate oxidation, suggesting the presence of amyloid protein AA.     

Diagnosis of bovine neosporosis

The protozoan parasite Neospora caninum is a major cause of abortion in cattle. The diagnosis of neosporosis-associated mortality and abortion in cattle is difficult. In the present paper we review histologic, serologic, immunohistochemical, and molecular methods for dignosis of bovine neosporosis. Although not a routine method of diagnosis, methods to isolate viable N. caninum from bovine tissues are also reviewed.     

Diagnosis of bovine tuberculosis

Extract

In any scheme for the eradication of bovine tuberculosis, the aim is to do so as efficiently as possible. There are a number of tests which can be used on the living animal which attempt to classify it as “tuberculous” or “non-tuberculous”. The fate of the animal probably depends on the result. Unfortunately, none of these tests is perfect. It is important, then, to know the relative merits of these tests and. how they should be used.     

Dubious effect of dimethylsulphoxide (DMSO) therapy on amyloid deposits and amyloidosis

Data from the literature on DMSO therapy for amyloidosis in laboratory animals and man are reviewed and found to be inconclusive. In hamsters with casein-induced amyloidosis, as well as in dogs with spontaneous amyloidosis, therapeutic experiments with DMSO were performed. In these investigations no effect of DMSO on amyloid and amyloidosis was found.Research funded by the Netherlands League Against Rheumatism.     

Hepatic AA amyloidosis in a cat: cytologic and histologic identification of AA amyloid in macrophages

A 3‐year‐old, spayed female, Domestic Shorthair cat presented with anorexia, lethargy, vomiting, probable hemoabdomen, and multiple masses on the right lateral liver lobe. Clinicopathologic and imaging abnormalities included anemia, azotemia, icterus, and hepatomegaly with hypoechoic masses. On cytologic evaluation of a fine‐needle aspiration of a liver mass there was abundant extracellular pink‐ to purple‐colored material between hepatocytes. The amorphous material was stained with direct fast scarlet (DFS), and green birefringent areas were observed under polarized light, confirming the presence of amyloid. A unique finding on the cytologic smear were macrophages containing amorphous and fibrillar amyloid‐like protein. Histopathologic examination using H&E and Congo red staining confirmed amyloid deposits within the space of Disse, along the sinusoids, portal tracts, blood vessel walls, and within the cytoplasm of macrophages. Immunohistochemical staining with anti‐AA amyloid antibodies further confirmed the presence of AA amyloid. To the author's knowledge, this is the first report of the cytologic finding of AA amyloid protein within macrophages and DFS stain detection of amyloid on a cytologic smear.