Changes

  NOTE: Calcification of bile duct in cattle → 'pipe-stem' liver

  NOTE: Calcification of bile duct in cattle → 'pipe-stem' liver

'''Sub-clinical effects''':

'''Sub-clinical effects'''

*In sheep, fleece weight and fibre quality are affected even by small fluke burdens. There is some evidence that reproductive performance (number of lambs born and growth-rate of lambs) is inversely influenced, but this has not been well documented.

*In sheep, fleece weight and fibre quality are affected even by small fluke burdens. There is some evidence that reproductive performance (number of lambs born and growth-rate of lambs) is inversely influenced, but this has not been well documented.

*Liver conemnations cause economic losses at slaughter. (Note: in beef cattle - sub-clinical infection leads to longer finishing times to slaugter weight, reduced carcass value).

*Liver condemnations cause economic losses at slaughter  

*In dairy cows - reduced milk yield (and quality).

*Longer finishing times to slaughter weight and reduced carcass value in beef cattle

*Reduced milk yield and quality in dairy cows

 

=== Migration and pathology ===

=== Migration and Pathology ===

==== Migration ====

==== Migration ====

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.

Metacercariae excyst → immature flukes present in the small intestine → migrate across the peritoneal cavity (about 1 week) → to the liver → migrate through the liver parenchyma for 6-7 weeks becoming more destructive as they grow → enter bile ducts

 

*The prepatent period is 10-12 weeks

==== Pathogenesis of Fasciolosis ====

==== Pathogenesis of acute fasciolosis ====

*'''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.

*'''Liver pathology'''

*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).

**Flukes develop from 0.1mm-1cm within the liver parenchyma causing trauma, necrotic tracts, and haemorrhages

*Chronic damage to bile ducts leads to peribiliary fibrosis.

**Glutamate dehydrogenase (GDH) is released by damaged cells

*Acute damage to liver causes post-necrotic scarring → shrinkage of affected tissues and hypertrophy of normal tissue → the typical appearance of the liver in chronic disease

*Chronic damage to bile ducts → peribiliary fibrosis

(Note: other complex events also occur, including disruption of haemodynamics, monolobular fibrosis, egg-granulomas etc.)

(Note: other complex events also occur, including disruption of haemodynamics, monolobular fibrosis, egg-granulomas etc.)