Fasciolosis

PARASITES TREMATODES

Fasciolosis

The adult liver fluke, Fasciola hepatica, lives in the bile ducts of a wide range of animals, including sheep, cattle, rabits and, less often, horses. It can infect humans causing a painful abdominal disease. The intermediate host in the UK is a mud snail, Lymnaea truncatula. Significant economic losses occur in western parts of the British Isles. Deaths, clinical and subclinical disease in cattle is confined to a younger stock. Fasciolosis is a seasonal disease with more serious outbreaks occurring in some years than in others. A similar but slightly larger species, F. gigantica, occurs in wetter tropical regions.

Ovine Fasciolosis

Acute fasciolosis: sudden death; normally September-November; enlarged pale, friable, haemorrhagic liver with more than 1000 immature flukes in liver parenchyma. (In cattle, acute disease is rarely seen).

Sub-acute fasciolosis: rapid weight-loss over 1-2weeks; October-December; normochromic anaemia; enlarged liver with large haemorrhages; more than 500 flukes - 50:50 immature and adult.

Chronic fasciolosis: progressive weight-loss over weeks or months; January-March; anaemia normochronic, leads to hypochromic; hypoalbuminaemia, which leads to oedema; small distorted cirrhotic liver; enlarged bile ducts; more than 250 adult flukes. (In cattle, calcification of bile ducts leads to 'pipe-stem' liver).

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

Migration and Pathology

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.

Pathogenesis of 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.
• 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).
• Chronic damage to bile ducts leads to peribiliary fibrosis.

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

• 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:
  • migrating flukes → liver necrosis → anaerobic conditions → clostridial multiplication → toxin production → disease.

Adults in Bile Ducts

• Bile duct damage - adult flukes (2-5cms long) in bile ducts feed on epithelium and blood; chronic inflammatory responses → fibrosis of bile duct wall (and, in cattle, calcification).
• Bile duct damage - adult flukes feed on biliary epithelium (gamma glutamyl transpeptidase released by damaged cells) and blood, leading to ulceration and haemorrhage, which causes epithelial hyperplasia and increased mucosal permeability.
• Anaemia - 250 flukes can cause up to 50ml of blood loss daily → 10 times increase in rate of erythropoiesis → normochronic anaemia until iron stores are exhausted → hypochromic anaemia.
• Hypoalbuminaemia - anaemia (and other plasma proteins) lost into bile duct because of:

a) whole blood loss, and

b) increased epithelial permeability

→ catabolic rate incereased by 2.5times → increased nitrogen loss via urine.

• Depending on magnitude of nitrogen loss:

a) no obvious effect (although animal is still in abnormal physiological state)

b) reduced weight-gains and/or wool growth and/or milk production

c) loss of body tissue (i.e. weight-loss); hypoalbuminaemia → reduced plasma oncotic pressure → oedema.

Disease Manifestations

• Large numbers of metacercariae ingested over a short period of time leads to acute disease.
• Smaller numbers ingested over a longer period of time leads to chronic disease.
• Feed intake - fluke infections cause reduced food intake. Note: chronic fasciolosis occurs at a time of year when animals are on a low plane of nutrition. This combined with the reduced food intake causes significant effect on the development and severity of clinical and subclinical fasciolosis.
• Species susceptibility - the proportion of flukes that reach the bile ducts is determined mainly by the fibroplastic potential of the liver and the effectiveness of the protective immune responses (which are ineffective in sheep). Therefore, establishment rate: sheep>cattle>pig.