Liver Disease in Farm Animals Flashcards
What is the lifecycle of Fasciola hepatica?
- Eggs –> Motile ciliated miracidia
- Minimum 9 days at 22-26oC
- Min day/night temp of 10oC for any development
- Miracidia must penetrate Galba truncatula (intermediate host) within 3 hours in order to survive
- Miracidia Þ Metacercaria
- Minimum 7 weeks (often more) within snail
- Min day/night temp of 10oC for any development
- 1 miracidia can produce 600 metacercariae
- Shed metacercaria encyst and become infective on blades of grass
- Metacercariae ingested by final host migrate across the gut wall and peritoneum, and penetrate the liver capsule
- Developing fluke migrate through the parenchyma (6-8 weeks) until they reach the small bile ducts
- Migrate into large bile ducts and mature over a further 4 weeks
- Mature fluke begin egg laying
- Minimum period of life cycle completion is 17-19 weeks
- Temperature only adequate in the UK between April and October
- Rainfall important
What is Galba truncatula?
What does it feed on?
What are its habitats?
- 5-10mm, 5-6 spirals
- Feeds on algae
- Like slightly acidic environment with slow moving water
- Habitats
- Ditch, pond and stream banks
- Boggy / marshy land
- Hoofmarks and wheel ruts following heavy rain or flooding
- Like warm and wet conditions
- Mean day/night temp of 10oC necessary for breeding
- Rainfall is the main influence on size of population
What pathology does Galba truncatula cause?
- Parenchymal destruction during migration
- Degree depends on numbers
- Numbers of eggs ingested depends on snail population
- Inflammation and fibrosis result
- Degree of fibrosis depend on level of damage
- Very rarely can damage large blood vessel leading to haemorrhage
- Anaerobic environment can activate Black disease (Infectious necrotic hepatitis)
- Fluke in bile ducts
- Anaemia (depending on numbers)
- Inflammation and fibrosis
- Anaemia (depending on numbers)
What does fasciola hepatica do to the parachyma?
- Parenchymal destruction during migration
- Degree depends on numbers
- Numbers of eggs ingested depends on snail population
- Inflammation and fibrosis result
- Degree of fibrosis depend on level of damage
What can fasciola hepatica sometimes damage in severe cases and what does this lead to?
Very rarely can damage large blood vessel leading to haemorrhage
With fasciola hepatica, what happens if you get fluke in the bile ducts?
- Anaemia (depending on numbers)
- Inflammation and fibrosis
What are the ACUTE clinical signs of fasciola hepatica in sheep?
- Late autumn / early winter
- Large numbers of migrating fluke in liver
- Anaemia – Pale mucus membranes / weak
- Hypoalbuminaemia
- Rapidly fatal, animals often found dead
What are the SUB-ACUTE clinical signs of fasciola hepatica in sheep?
- Late autumn / early winter
- Rapid condition loss
- Anaemia
- Oedema (Submandibular in sheep “Bottle Jaw”)
- Colic
What are the CHRONIC clinical signs of fasciola hepatica in sheep?
- Winter / Early spring
- Adult fluke sucking blood in bile ducts
- Poor condition
- Anaemia
- Hypoalbuminaemia
- Submandibular oedema
- Chronic scour
What are the ACUTE clinical signs of fasciola hepatica in cattle?
- Rare in cattle
- Fibrous nature of liver
- Acquired immunity does develop and provides protection (NB whilst antibody can be detected in sheep it appears to be non-protective)
What are the CHRONIC clinical signs of Galba truncatula in cattle?
- Similar presentation to sheep
- Brisket and ventral oedema also seen
What are the SUBCLINICAL clinical signs of fasciola hepatica in cattle?
- Increasingly recognised
- Poor performance (reduced growth rate / reduced yield / loss of condition / predisposes to other disease)
- Increased risk of Salmonella dublin?
What is the diagnosis of fasciola hepatica?
- Post mortem (Acute and Chronic disease)
- Fluke in parenchyma and bile ducts
- Elevation of liver enzymes
- AST and / or GLDH (Acute and chronic disease)
- yGT (Chronic disease. Bile duct damage)
- Faecal egg count
- Adults must be present, therefore chronic only
What is the clinical pathology of Fasciola hepatica - what are the biochemical tests used in farm animals?
- Aspartate aminotransferase (AST)
- Not liver specific, also produced from cardiac and skeletal muscle
- Gamma glutamyltransferase (γGT)
- Good indicator of bile duct damage
- Glutamate dyhydrogenase (GLDH)
- Liver specific, elevated in acute disease
- Sorbitol dehydrogenase (SDH)
- Liver specific, elevated in acute disease
- Bilirubin
- Conjugated increased with bile duct obstruction
- Unconjugated increased in haemolytic anaemia
What is the diagnosis on biochem tests for fasciola hpatica?
- Eosinophilia
- Indicative of parasitic infection
- Particularly useful in sub-clinically affected cattle
- Blood antibody ELISA
- NB Only indicates exposure (could be historic)
- Not protective in sheep
- Bulk Milk antibody ELISA
- Result indicates degree of (historic) exposure of the whole dairy herd
- NB Diagnosis in one animal may suggest all animals in the group will be affected
What is the treatment for fasciola hepatica?
- Triclabendazole
- Active against all stages (immature – adult)
- Resistance now starting to appear
- e.g. “Fasinex”, “Tribex” “Combinex” (with levamisole)
- Sheep and cattle by drench
- Nitroxynil
- Adults (minor effect on late immature fluke, label claim)
- e.g. “Trodax”
- Sheep and cattle by subcutaneous injection
- Closantel
- Adults/late immature stages
- e.g. “Flukiver”
- Sheep by drench
- Clorsulon
- Adult fluke only
- e.g. “Ivomec super” (with ivermectin)
- Cattle by subcutaneous injection
- Oxyclozanide
- Adult fluke only
- e.g. “Zanil” (licensed for lactating dairy cows, 3d w/d)
- e.g. “Levafas” and “Nilzan” (both with levamisole)
- Sheep and cattle by mouth
- Albendazole also has activity against adult fluke
What stages of fasciola hepatica is TRICLABENDAZOLE active against?
Resistance?
Which animals and route?
- Triclabendazole
- Active against all stages (immature – adult)
- Resistance now starting to appear
- e.g. “Fasinex”, “Tribex” “Combinex” (with levamisole)
- Sheep and cattle by drench
What stages of fasciola hepatica is NITROXYNIL active against?
Which animals and route?
- Nitroxynil
- Adults (minor effect on late immature fluke, label claim)
- e.g. “Trodax”
- Sheep and cattle by subcutaneous injection
What stages of fasciola hepatica is CLOSANTEL active against?
Which animals and route?
- Closantel
- Adults/late immature stages
- e.g. “Flukiver”
- Sheep by drench
What stages of fasciola hepatica is CLORSULON active against?
Which animals and route?
- Clorsulon
- Adult fluke only
- e.g. “Ivomec super” (with ivermectin)
- Cattle by subcutaneous injection
What stages of fasciola hepatica is OXYCLOZANIDE active against?
Which animals and route?
- Oxyclozanide
- Adult fluke only
- e.g. “Zanil” (licensed for lactating dairy cows, 3d w/d)
- e.g. “Levafas” and “Nilzan” (both with levamisole)
- Sheep and cattle by mouth
How can you prevent Galba truncatula?
- Limit snail habitats
- Drain affected land (Very expensive)
- Prevent access to snail habitats
- Manage poaching at pasture appropriately
- Fence off marshy areas (Possible if small areas)
- Remove stock from wet / boggy fields during high risk periods (Practically difficult)
- Application of molluscicides to pasture is theoretically possible but rarely practiced
- Prophylactic treatment
- Routine / regular treatment of all stock (most common method of control in fluke areas)
- Treat if and when there is evidence of disease
- Based on fluke “forecasts” - published local forecast based on temp and rain fall
Other than fasciola hepatica, name some other liver trematodes
- Fasciola gigantica
- Much larger (3.5 x 1cm)
- Common in tropical parts of the world
- Fasciola magna
- Predominantly N. America
- Fluke of moose and deer which can affect sheep, goats and occasionally cattle
- Dicrocoelium dendriticum
- Europe (not UK) and Asia
- Non-pathogenic unless very large infestation
- Two intermediate hosts (snails and ants)
What is the aetiology of liver abscessation?
- Bacteraemias from navel ill or other nidus of infection
- Rumentitis
- Foreign body penetration
- Traumatic reticulitis
- Iatrogenic (Biopsy)
- Usually T. pyogenes or Fusobacterium necrophorum
- Often well demarcated abscesses diffusely spread throughout the liver
What is this here?
Liver Abscessation
What is Rumenitis/rumen parakeratosis and what causes it?
- Common in barley beef animals fed 100% cereal diets +/- small quantities of forage
- Chronic low rumen pH results in inflammation of the rumen mucosa (rumenitis)
- Enlargement and hardening of the papillae
- Excessive keratinization of the mucosa including food material and bacteria
- Eventually rumen wall abscessation can occur which may extend into the liver
What are the clinical signs of liver abscessation?
- Poor performance / vague clinical signs
- Milk yield (dairy cows)
- Poor body condition (beef cows)
- Reduce growth rate / poor doing (barley beef animals)
- Common post mortem finding (therefore often “subclinical”)
What is the treatment for liver abscessation?
None
How can you prevent liver abscessation?
- Limit subclinical rumen acidosis
- Add small quantities of roughage to the diet
What are some complications of liver abscessation?
- Peritonitis
- Uncommon, cattle seem able to localise abdominal infections in many cases
- Endocarditis
- Bacteraemia from septic focus in liver localise on heart valves
- Caudal vena caval thrombosis syndrome
- Extension of infection into the caudal vena cava
- Septic foci seed out in lungs establishing local abscesses
- Erosion into major vessels can cause per-acute fatal haemorrhage
- Animals usually found dead in a huge pool of blood
What is occurring here?
Caudal vena caval thrombosis syndrome
What can ragwort poisoning cause?
A now uncommon plant toxicosis which can cause severe liver damage
What is the pathogenesis of ragowort poisoning?
- Pyrrolizidine alkaloids
- Toxic to hepatocytes
- Degree of liver damage depends on dose and duration of consumption
- Acute toxicity rare. Chronic damage from prolonged low dose exposure more common
- Often subclinical (NB Large function reserve)
What are some clinical signs of ragwort poisoning?
- Dull, depressed, weight loss, poor doing
- Jaundice
- Subcutaneous oedema
- Hypoalbuminaemia
- Sub-mandibular and ventral
- Colic and scour
- Photosensitization can occur
- Hepatic encephalopathy can occur
- Nervous signs including staggering, circling and blindness
What is the diagnosis of ragwort poisoning?
- History of exposure (examine pasture and conserved forage)
- Elevated liver enzymes in serum
- Histology following liver biopsy or PM
- Fine pericellular cirrhosis, hepatocytomegaly, bile duct proliferation
- Post mortem
- Characteristic shrunken, fibrosed, slate-grey or mottled liver
What is the treatment and prevention of ragwort poisoning?
- No treatment; symptomatic only
- Vital to prevent disease is other animals in the group (although may be too late)
Which animals and breeds are particularly sensitive to copper?
- Sheep are particularly sensitive to Cu toxicity
- North Ronaldsay, Charollais, Texel and Suffolk breeds, particularly so
- Sheep concentrates are specifically formulated with very low Cu levels.
- Now thought to be more common in cattle due to over supplementation in an attempt to avoid infertility caused Cu-responsive disorders
What is the pathogenesis of copper poisoning?
What are the clinical signs of acute and chronic copper poisoning?
- Acute
- Depression, colic, collapse and death
- Chronic
- Jaundice, anaemia, depression and anorexia, rumen stasis, colic and diarrhoea
- Recumbency and death over a few days
What is the diagnosis of copper poisoning?
- Clinical signs and history of exposure to copper or excess supplementation
- Post mortem
- Widespread jaundice
- Hepatomegaly and discolouration (yellow / orange)
- Necrotizing hepatopathy on histopathological examination
- Distended and discoloured (bronze/black) kidneys (esp. sheep)
- Plasma Cu >50mmol/L (Live animal)
- Liver Cu >8,000 mmol/Kg (PM or biopsy?)
- Kidney Cu >650 mmol/Kg (PM)
What is the treatment for copper poisoning?
- None if haemolytic crisis has occurred
- Remove from sources of Cu from diet
- Ammonium tetrathiomolybdate described but not licensed in UK/EU
- S/C three times daily for 5 days (3.4mg/Kg)
- Oral ammonium thiomolybdate (100-400mg/day) has been used in sheep
- Fluids and other supportive therapy
How can you prevent copper poisoning?
- Never feed cattle and pig concentrates to sheep
- Never graze sheep on pasture fertilised with pig manure
- Calculate and monitor Cu intake carefully, avoid over supplementation
- Medicated Feedstuffs Regulations
- Permit a max of 35ppm in dairy cow diets (~800mg Cu/cow/day
- Including higher levels in dairy cow concentrates is only allowed with a veterinary prescription
What uses does a liver biopsy have?
- Liver copper estimations
- Most reliable indicator of copper status?
- Diagnosis of fatty liver
- Histology in cases of liver disease (valuable animals only?)
What are the dangers of doing liver biopsys?
- Haemorrhage
- Infection
What site and technique do you use to perform a liver biopsy in farm animals?
- Site
- Right side, 11th rib space (13 ribs total)
- ~20cm below transverse process
- Technique
- Shave and aseptically prepare surgical site
- Local infiltration of small volumes (5ml) of local anaesthetic through all layers
- 1cm stab incision through skin
- Introduce biopsy needle through intercostal muscles towards left elbow
- Biopsy using standard technique
What is Fasciola hepatica?
How common is it?
- ‘Liver fluke’ in UK
- Hepatic parasite of ruminants
- Very common
- Prevalence increased over past 10 years
- Responsible for significant economic loss
- Does have zoonotic potential
What is the lifecycle of Fasciola hepatica?
What liver pathology does Fasciola hepatica cause?
- Juveniles migrate through liver until they locate the bile ducts where they mature
- Very severe disease can occur if many metacercariae are ingested over a short period of time (liver haemmorhage/anaemia)
- Usually small amounts are ingested over longer period of time, liver function compromised by fibrosis
