6,502
edits
Changes
Jump to navigation
Jump to search
→Pathology
===Pathology===
===Pathology===
====Acute Fascioliasis====
====Acute Fascioliasis====
*'''Liver pathology'''
**Flukes
develop from 0.1mm-1cm within the liver parenchyma causing trauma,
necrotic tracts, and haemorrhages
**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.)
*'''Black
disease (Infectious Necrotic Hepatitis)'''
**caused by a toxin
produced by ''Clostridium novyi'' type B.
**It is commonly
associated with liver fluke infestation because migrating flukes → liver
necrosis → anaerobic conditions → clostridial multiplication → toxin
production → disease
The acute disease is a less common type of Fasciola hepatica, and generally occurs 2-6 weeks after large ingestion of metacercariae. The young liver flukes migrate through the liver parenchyma causing severe haemorrhaging, due to the damage to the [[Liver - Anatomy & Physiology|liver]] vasculature.
The acute disease is a less common type of Fasciola hepatica, and generally occurs 2-6 weeks after large ingestion of metacercariae. The young liver flukes migrate through the liver parenchyma causing severe haemorrhaging, due to the damage to the [[Liver - Anatomy & Physiology|liver]] vasculature.
====Chronic Fascioliasis====
====Chronic Fascioliasis====
*'''Bile duct damage'''
**Adult flukes (2-5cm long) in bile ducts feed on epithelium and blood
**Chronic inflammatory responses → fibrosis of bile duct wall (and, in cattle, calcification)
**Gamma glutamyl transpeptidase released by damaged cells
**Ulceration and haemorrhage of bile duct → epithelial hyperplasia and increased mucosal permeability
*'''Anaemia'''
**250 flukes → up to 50ml of blood loss daily → 10 times increase in rate of erythropoiesis → normochronic anaemia until iron stores are exhausted → hypochromic anaemia.
*'''Hypoalbuminaemia'''
**Albumin (and other plasma proteins) lost into bile duct because of
#Whole blood loss
#Increased epithelial permeability
** → Increased catabolic rate by 2.5x → increased nitrogen loss via urine
**The effects seen depend on the magnitude of nitrogen loss
#There is no obvious effect (although animal is still in abnormal physiological state)
#Reduced weight-gain and/or wool growth and/or milk production
#Loss of body tissue (i.e. weight-loss); hypoalbuminaemia → reduced plasma oncotic pressure → oedema
This is usually seen in late winter, early spring and is currently the most common fascoloiasis seen. It occurs around 4-5 months after ingestion of the metacercariae. Hypochromic and macrocytic anaemia and hypoalbuminaemia are common, as the adult flukes are capable of sucking up to 0.5ml of blood each day. In heavy infections, this can prove to be a severe loss.
This is usually seen in late winter, early spring and is currently the most common fascoloiasis seen. It occurs around 4-5 months after ingestion of the metacercariae. Hypochromic and macrocytic anaemia and hypoalbuminaemia are common, as the adult flukes are capable of sucking up to 0.5ml of blood each day. In heavy infections, this can prove to be a severe loss.
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
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
*The prepatent period is 10-12 weeks
==Treatment==
==Treatment==