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| Measurement of serum glutamate dehydrogenase (GLDH) and/or glutamyl transpeptidase (GGT) levels may prove useful. GLDH is an enzyme released by damaged hepatic cells and becomes elevated within the first few weeks of infection. GGT indicates damage to the epithelial cells lining the bile ducts and rises later in disease, although high levels are maintained for longer. Fluke serology is possible by means of a reliable ELISA test that identifies anti-fluke antibodies in the serum or in milk. | | Measurement of serum glutamate dehydrogenase (GLDH) and/or glutamyl transpeptidase (GGT) levels may prove useful. GLDH is an enzyme released by damaged hepatic cells and becomes elevated within the first few weeks of infection. GGT indicates damage to the epithelial cells lining the bile ducts and rises later in disease, although high levels are maintained for longer. Fluke serology is possible by means of a reliable ELISA test that identifies anti-fluke antibodies in the serum or in milk. |
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| + | ===Biopsy=== |
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| + | Biopsy or histopathology may reveal necrotic areas of liver, haemorrhage, hyperplastic bile ducts or indeed the presence of ''[[Fasciola hepatica]]'' within the section. |
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| ===Pathology=== | | ===Pathology=== |
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| [[Image:Fasciola hepatica - bile duct.jpg|150px|thumb|right|Bile duct fibrosis due to chronic ''Fasciola hepatica'' infestation. Source: Wikimedia Commons; author: Flukeman]] | | [[Image:Fasciola hepatica - bile duct.jpg|150px|thumb|right|Bile duct fibrosis due to chronic ''Fasciola hepatica'' infestation. Source: Wikimedia Commons; author: Flukeman]] |
| + | The pathology of fasciolosis is similar in both sheep and cattle, although the species have a different incidence of acute and chronic disease, as described above. |
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| + | In acute fasciolosis, immature flukes grow and migrate within the liver parenchyma, causing necrotic tracts and haemorrhage. On post-mortem, the liver is enlarged and a fibrinous peritonitis may be be present. Fibrin takes are often particularly apparent on the ventral lobe. Histologically, tracts are seen as areas of degenerate hepatocytes and haemorrhage, which may later become infiltrated with eosinophils and lymphocytes. In the long term, these areas will become fibrosed. In sub-acute fasciolosis, the liver again is enlarged on post-mortem, and haemorrhagic tracts can be seen. |
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− | In acute fasciolosis, immature flukes grow and migrate within the liver parenchyma, causing necrotic tracts and haemorrhage. On post-mortem, the liver is enlarged and a fibrinous peritonitis may be be present. Fibrin takes are often particularly apparent on the ventral lobe. Histologically, tracts are seen as areas of degenerate hepatocytes and haemorrhage, which may later become infiltrated with eosinophils and lymphocytes. In the long term, these areas will become fibrosed.
| + | Chronic fasciolosis is associated with damage to the bile ducts by adult flukes. On post-mortem, the liver is distorted by areas of fibrosis caused by the migration of the original immature flukes. The bile ducts are dilated, and flukes may be expressed from within. The gall bladder may also be enlarged. The walls of the bile ducts may be ulcerated and haemorrhagic with areas of epithelial hyperplasia. The walls eventually become fibrosed and may calcify in cattle. Calcified bile ducts can be seen protruding from the liver surface - this is known as "pipe stem liver". |
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− | Subactute Fascioliasis
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− | This is caused by ingestion of metacercariae over a longer period of time. Some may have migrated to the bile ducts, causing [[cholangitis]], whilst other metacercariae are migrating through the liver causing lesions similar to those present in acute fascioliasis. The infected host may present with severe haemorrhagic anaemia, with [[hypoalbuminaemia]], rapid loss of body condition, reduced appetite, pale mucous membranes, and submandibular oedema may also be present. On post-mortem, an enlarged liver is common and haemorrhagic tracts are usually visible on the liver surface. If left untreated, it is often fatal. This form of fascioliasis occurs around 6-10 weeks after ingestion of the metacercariae by the host, and like acute fascioliasis occurs in late autumn and winter.
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− | Chronic Fascioliasis
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− | *'''Bile duct damage'''
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− | **Adult flukes (2-5cm long) in bile ducts feed on epithelium and blood
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− | **Chronic inflammatory responses → fibrosis of bile duct wall (and, in cattle, calcification)
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− | **Gamma glutamyl transpeptidase released by damaged cells
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− | **Ulceration and haemorrhage of bile duct → epithelial hyperplasia and increased mucosal permeability
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− | Infected animals may present with progressive loss of body condtion, reduced appeptite, which along with hypoalbuminaemia can result in an gaunt animal. Other common signs include pale mucous membranes, and submandibular oedema, more commonly known as 'bottle jaw.' On biopsy the liver will have an irregular shape, distorted shape with areas of fibrous tissue replacing the cells damaged by the migrating flukes. The bile ducts appear dilated, and dark, and it is often possible to express numerous numbers of adult flukes from within the ducts. Pathology is similar in both sheep and cattle, expect in cattle you may see calcification of the bile ducts, and enlargement of the gall bladder. The calcified bile ducts are often seen protruding from the liver surface, which is known as 'pipe stem liver.'
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| ==Treatment== | | ==Treatment== |