Nutritional siderosis in the bovine

Hartley, W. J.; Mullins, John J.; Lawson, B. M.

doi:10.1080/00480169.1959.33341

Cited by 24 publications

(10 citation statements)

References 8 publications

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“…In addition to the hepatic lesion described in the first report, all animals of the second study had myocardial necrosis, lymphoid depletion and fibrosis in diverse lymph nodes. Besides hereditary iron storage disease in Salers cattle, there is only a single report of nutritional hepatic siderosis and fibrosis in cattle from New Zealand (Hartley et al, 1959). These, however, appear to be caused by increased iron uptake, since affected animals lived on iron-rich pastures and had a water supply with high levels of iron.…”

Section: Haemochromatosis Of Salers Cattle: Overlapping Clinical Butmentioning

confidence: 97%

The Pathology of Comparative Animal Models of Human Haemochromatosis

Klopfleisch

Olias

2012

Journal of Comparative Pathology

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Section: Haemochromatosis Of Salers Cattle: Overlapping Clinical Butmentioning

confidence: 97%

The Pathology of Comparative Animal Models of Human Haemochromatosis

Klopfleisch

Olias

2012

Journal of Comparative Pathology

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“…In mammals and birds this is essential for the maintenance and transport of oxygen around the tissues (Butler, 1983;Dewar, 1986). Parenteral iron can be toxic but because the uptake of iron from ingested sources is generally limited, acute intoxication is not usually seen unless intestinal absorption is promoted above normal levels (Hartley et al, 1959). Chronic ingestion of large amounts of absorbable iron in the diet can lead to the storage of iron in the liver in many vertebrate species, including humans (MacDonald, 1972;Nhonoli, 1973;Borch-Ionson & Nilssen, 1987;BorchIohnson et al, 1989;Spelman et al, 1989;.…”

Section: Introductionmentioning

confidence: 94%

Iron storage diseases in birds

Cork¹

2000

Avian Pathology

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Parenteral iron is toxic to many species but, because the uptake of iron from the diet is regulated in the intestine, acute intoxication is not seen under natural conditions. Chronic ingestion of large amounts of absorbable iron in the diet can lead to the storage of iron in the liver in many species, including humans. The excess iron is stored within hepatocytes as haemosiderin and can be quantitatively assessed by liver biopsy or at necropsy using special stains such as Perls iron stain and/or biochemical tests. Iron may also be found within the Kupffer cells in the liver and the macrophage cells of the spleen especially where concurrent diseases are present such as haemolytic anaemia, septicaemia, neoplasia and starvation. Iron accumulation in the liver, also known as haemosiderosis, may not always be associated with clinical disease although in severe cases hepatic damage may occur. It is probable that concurrent disease conditions are largely responsible for the degree and nature of the pathological changes described in most cases of haemosiderosis. In some human individuals there may be a genetic predisposition to iron storage disease, haemochromatosis, associated with poor regulation of iron uptake across the intestine. In severe cases iron pigment will be found in the liver, spleen, gut wall, kidney and heart with subsequent development of ascites, heart failure and multisystem pathology. Clinical disease associated with accumulation of iron in the liver, and other tissues, has been reported in many species of bird although it is most commonly reported in Indian hill mynas ( Gracula religiosa ) and toucans ( Ramphastos sp ). It is likely that the tolerance to the build up of tissue iron varies in individual species of bird and that the predominant predisposing factors may differ, even within closely related taxonomic groups.

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“…25,34,68,80 Chronic dietary iron overload occurs in some mammalian species fed iron-rich forage or incorrectly formulated diets or as a seasonal phenomenon, but this dietary overload has been reported only once in cattle. 6,37,41,54 Iron overload in avian species such as mynah birds (Gracula sp.) has features of hemochromatosis.…”

Section: Discussionmentioning

confidence: 99%

“…A report from New Zealand documented subclinical disease in Aberdeen Angus cattle that was detected at slaughter and was characterized by hepatic siderosis, perilobular hepatic fibrosis, and osteoporosis. 41 Two forms of iron overload are recognized: hemosiderosis and hemochromatosis. Hemosiderosis (secondary iron overload) occurs under various clinical conditions and is characterized by accumulation of iron in the reticuloendothelial system and little or no tissue injury.…”

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confidence: 99%

Hepatic Failure and Hemochromatosis of Salers and Salers-cross Cattle

et al. 2001

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Abstract. Hemochromatosis is rare in domestic mammals. Five clinical cases and one preclinical case of hemochromatosis were diagnosed in Salers and Salers-cross cattle. Clinical disease developed between 9 and 22 months of age. Animals were healthy until weaning but then lost weight, developed rough hair coats, and lost incisor teeth. In two animals, hemochromatosis was identified by liver biopsy, biochemical evidence of hepatic injury, and/or elevated transferrin saturation values. At necropsy, carcasses were thin, with firm dark brown livers and lymph nodes, soft bones, and brown-colored small bowel. The principal histologic changes were hepatocellular siderosis and periportal, bridging, and perivenular fibrosis. Siderocalcinosis involved collagen, elastin, reticulin, and basement membrane components in liver, lymph nodes, spleen, duodenum, and kidney. Hepatic iron concentrations in clinically affected cattle were 1,500-10,500 g/g wet weight (reference range for cattle ϭ Ͻ300 g/ g). Ultrastructurally, the heaviest intrahepatic deposition was in hepatocytes, which contained large intracytoplasmic siderosomes. Iron deposition in bone was associated with osteopenia. Genetic analysis indicated a common ancestral bull in the pedigrees of five of six affected cattle; no pedigree was available for the remaining animal. Four dams of five affected animals were phenotypically normal and had histologically normal livers. Test mating of four cows to the ancestral bull resulted in a female calf that developed clinicopathologic and histologic evidence of preclinical hemochromatosis by 40 days of age. It was not possible to establish the pattern of inheritance because of the small number of pedigrees from affected cattle.

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Nutritional siderosis in the bovine

Cited by 24 publications

References 8 publications

The Pathology of Comparative Animal Models of Human Haemochromatosis

The Pathology of Comparative Animal Models of Human Haemochromatosis

Iron storage diseases in birds

Hepatic Failure and Hemochromatosis of Salers and Salers-cross Cattle

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