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1,225 bytes added ,  22:44, 22 December 2008
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=== Migration and Pathology ===
 
=== Migration and Pathology ===
 
==== Migration ====
 
==== Migration ====
Metacercariae excyst = immature flukes in small intestine = migrate across peritoneal cavity
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Metacercariae excyst, so immature flukes are present in the small intestine. They then migrate across the peritoneal cavity (takes approximately 1week) to the liver. They meander through the liver parenchyma for 6-7weeks, becoming more destructive as they grow, and then enter bile ducts. The prepatent period is 10-12weeks.
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==== Pathogenesis of Fasciolosis ====
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*'''Liver pathology''' - in parenchyma, flukes develop from 0.1mm-1cm, which causes trauma (glutamate dehydrogenase (GDH) released by damaged cells), necrotic tracts, and haemorrhages, leading to acute disease.
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*Acute damage to liver causes post-necrotic scarring, which in turn causes shrinkage of affected tissues and hypertrophy of normal tissue (this causes the typical appearance of the liver in chronic disease).
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*Chronic damage to bile ducts leads to peribiliary fibrosis.
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(Note: other complex events also occur, including disruption of haemodynamics, monolobular fibrosis, egg-granulomas etc.)
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*'''Black disease (Infectious Necrotic Hepatitis)''' - is caused by a toxin produced by ''Clostridium novyi'' type B. It is commonly associated with liver fluke infestation because:
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**migrating flukes cause → liver necrosis, causing anaerobic conditions, and therefore clostridial multiplication, which leads to toxin production, causing disease.
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