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Farm Animal Final Year > Liver Disease in Farm Animals > Flashcards

Liver Disease in Farm Animals Flashcards

1
Q

What is the lifecycle of Fasciola hepatica?

A
  • 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
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2
Q

What is Galba truncatula?

What does it feed on?

What are its habitats?

A
  • 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
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3
Q

What pathology does Galba truncatula cause?

A
  • 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
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4
Q

What does fasciola hepatica do to the parachyma?

A
  • 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
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5
Q

What can fasciola hepatica sometimes damage in severe cases and what does this lead to?

A

Very rarely can damage large blood vessel leading to haemorrhage

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6
Q

With fasciola hepatica, what happens if you get fluke in the bile ducts?

A
  • Anaemia (depending on numbers)
  • Inflammation and fibrosis
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7
Q

What are the ACUTE clinical signs of fasciola hepatica in sheep?

A
  • Late autumn / early winter
  • Large numbers of migrating fluke in liver
  • Anaemia – Pale mucus membranes / weak
  • Hypoalbuminaemia
  • Rapidly fatal, animals often found dead
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8
Q

What are the SUB-ACUTE clinical signs of fasciola hepatica in sheep?

A
  • Late autumn / early winter
  • Rapid condition loss
  • Anaemia
  • Oedema (Submandibular in sheep “Bottle Jaw”)
  • Colic
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9
Q

What are the CHRONIC clinical signs of fasciola hepatica in sheep?

A
  • Winter / Early spring
  • Adult fluke sucking blood in bile ducts
  • Poor condition
  • Anaemia
  • Hypoalbuminaemia
  • Submandibular oedema
  • Chronic scour
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10
Q

What are the ACUTE clinical signs of fasciola hepatica in cattle?

A
  • 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)
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11
Q

What are the CHRONIC clinical signs of Galba truncatula in cattle?

A
  • Similar presentation to sheep
  • Brisket and ventral oedema also seen
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12
Q

What are the SUBCLINICAL clinical signs of fasciola hepatica in cattle?

A
  • Increasingly recognised
  • Poor performance (reduced growth rate / reduced yield / loss of condition / predisposes to other disease)
  • Increased risk of Salmonella dublin?
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13
Q

What is the diagnosis of fasciola hepatica?

A
  • 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
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14
Q

What is the clinical pathology of Fasciola hepatica - what are the biochemical tests used in farm animals?

A
  • 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
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15
Q

What is the diagnosis on biochem tests for fasciola hpatica?

A
  • 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
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16
Q

What is the treatment for fasciola hepatica?

A
  • 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
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17
Q

What stages of fasciola hepatica is TRICLABENDAZOLE active against?

Resistance?

Which animals and route?

A
  • Triclabendazole
  • Active against all stages (immature – adult)
  • Resistance now starting to appear
  • e.g. “Fasinex”, “Tribex” “Combinex” (with levamisole)
  • Sheep and cattle by drench
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18
Q

What stages of fasciola hepatica is NITROXYNIL active against?

Which animals and route?

A
  • Nitroxynil
  • Adults (minor effect on late immature fluke, label claim)
  • e.g. “Trodax”
  • Sheep and cattle by subcutaneous injection
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19
Q

What stages of fasciola hepatica is CLOSANTEL active against?

Which animals and route?

A
  • Closantel
  • Adults/late immature stages
  • e.g. “Flukiver”
  • Sheep by drench
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20
Q

What stages of fasciola hepatica is CLORSULON active against?

Which animals and route?

A
  • Clorsulon
  • Adult fluke only
  • e.g. “Ivomec super” (with ivermectin)
  • Cattle by subcutaneous injection
21
Q

What stages of fasciola hepatica is OXYCLOZANIDE active against?

Which animals and route?

A
  • 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
22
Q

How can you prevent Galba truncatula?

A
  • 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
  1. Routine / regular treatment of all stock (most common method of control in fluke areas)
  2. Treat if and when there is evidence of disease
  3. Based on fluke “forecasts” - published local forecast based on temp and rain fall
23
Q

Other than fasciola hepatica, name some other liver trematodes

A
  • 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)
24
Q

What is the aetiology of liver abscessation?

A
  • 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
25
Q

What is this here?

A

Liver Abscessation

26
Q

What is Rumenitis/rumen parakeratosis and what causes it?

A
  • 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
27
Q

What are the clinical signs of liver abscessation?

A
  • 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”)
28
Q

What is the treatment for liver abscessation?

A

None

29
Q

How can you prevent liver abscessation?

A
  • Limit subclinical rumen acidosis
  • Add small quantities of roughage to the diet
30
Q
A
31
Q

What are some complications of liver abscessation?

A
  • 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
32
Q

What is occurring here?

A

Caudal vena caval thrombosis syndrome

33
Q

What can ragwort poisoning cause?

A

A now uncommon plant toxicosis which can cause severe liver damage

34
Q

What is the pathogenesis of ragowort poisoning?

A
  • 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)
35
Q

What are some clinical signs of ragwort poisoning?

A
  • 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
36
Q

What is the diagnosis of ragwort poisoning?

A
  • 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
37
Q

What is the treatment and prevention of ragwort poisoning?

A
  • No treatment; symptomatic only
  • Vital to prevent disease is other animals in the group (although may be too late)
38
Q

Which animals and breeds are particularly sensitive to copper?

A
  • 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
39
Q

What is the pathogenesis of copper poisoning?

A
40
Q

What are the clinical signs of acute and chronic copper poisoning?

A
  • Acute
  • Depression, colic, collapse and death
  • Chronic
  • Jaundice, anaemia, depression and anorexia, rumen stasis, colic and diarrhoea
  • Recumbency and death over a few days
41
Q

What is the diagnosis of copper poisoning?

A
  • 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)
42
Q

What is the treatment for copper poisoning?

A
  • 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
43
Q

How can you prevent copper poisoning?

A
  • 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
44
Q

What uses does a liver biopsy have?

A
  • Liver copper estimations
  • Most reliable indicator of copper status?
  • Diagnosis of fatty liver
  • Histology in cases of liver disease (valuable animals only?)
45
Q

What are the dangers of doing liver biopsys?

A
  • Haemorrhage
  • Infection
46
Q

What site and technique do you use to perform a liver biopsy in farm animals?

A
  • 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
47
Q

What is Fasciola hepatica?

How common is it?

A
  • ‘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
48
Q

What is the lifecycle of Fasciola hepatica?

A
49
Q

What liver pathology does Fasciola hepatica cause?

A
  • 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

Farm Animal Final Year (131 decks)

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