Non-parasitic liver disease

Question 1

Ddx for non-parasitic liver disease

Answer 1

• Copper toxicity
• Neoplasia
• Liver abscess
• Hepatic necrosis
• Cholecystitis
• Cirrhosis
• Tuberculosis
• Fatty liver syndrome

Question 2

Copper toxicity

Answer 2

• massive liver damage
• may be acute or chronic
• much more common cause of death than copper deficiency in sheep
• chronic copper toxicity:
  – only ‘spills over’ to hypercupraemia when the storage capacity of the liver is exceeded
  – will then present as acute toxicity
• acute copper toxicity:
  – seen after inadvertent over-administration
  – usually found recumbent or dead
  – Normal blood Cu = 50-200µg/dl
  -> In an acute crisis see 10-20 fold increase
  – In this acute phase, liver levels may be normal as they have released their excess into the bloodstream

Question 3

Neoplasia

Answer 3

• rare but not unheard of, esp in older cattle
• lymphosarcoma and adenocarcinoma are seen

Question 4

Liver abscess

Answer 4

• A. pyogenes or Fusobacterium necrophorum - originate in rumen
• Often follow rumen trauma, such as grain overload
• often present with cranial abdominal pain: but the pain can’t be explained i.e. no ruminal bloat, normal on rectal exam, possibly slightly pyrexic, no DA
• more common in high yielding dairy cows fed mixed ration
• phosphate levels higher in jugular blood than in tail vein blood

Question 5

Hepatic necrosis

Answer 5

• Fusobacterium invasion
• Sometimes with jaundice
• End-stage of liver abscess (caused by the same bacterium)

Question 6

Cholecystitis

Answer 6

• rare and hard to diagnose
• more likely to result in jaundice than direct liver damage

Question 7

Cirrhosis

Answer 7

• nearly always a result of fluke in cattle
  – basically means chronic subacute liver fluke infestation
• also ragwort poisoning, associated with encephalopathy and tenesmus
  – distinguish for lead by blood parameters and possible photosensitisation with ragwort

Question 8

Tuberculosis

Answer 8

• very rare manifestation

Question 9

Fatty liver syndrome

Answer 9

• usually due to dietary imbalance pre-partum

Question 10

Diagnosis of chronic copper toxicity

Answer 10

• Jaundice seen – of sclera and skin
• Urine – black in colour (as copper exceeds renal threshold and so is excreted out in urine)
• Liver – bronze coloured
• Kidneys – gun-metal appearance

Clinpath shows:
- anaemia
- haemaglobinaemia
- increased liver enzymes
- azotaemia

Urinalysis:
- haemoglobinuria
- isothenuria

Combination of azotaemia and isothenuria indicates acute renal failure.

Question 11

Chronic copper toxicity presentation

Answer 11

– anorexic
- depressed
- diarrhoea
- abdominal pain
- weakness
- found dead

Question 12

Cirrhosis presentation

Answer 12

• Often present in early lactation when metabolic demands are highest
• Often present as constipated rather than Diarrhoea
• Can also see other clinical syndromes associated with the damage caused by the fluke including endocarditis, salmonellosis

Question 13

Ragwort poisoning

Answer 13

• pyrrolizidine alkaloids found in this plant, Senecio jacobaea or tansy ragwort
• usually cattle aren’t attracted to graze on it
• major problem if gathered up with hay

Question 14

Ragwort poisoning - pathogenesis

Answer 14

• Direct hepatocellular damage by the alkaloids
• Speed of destruction and consequences depend on dose and duration
• Acute poisoning therefore rare as the functional reserve of the liver means that a lot can be destroyed before clinical signs are seen
• Slow, chronic ingestion is more common

Question 15

Ragwort poisoning – clinical signs

Answer 15

• Weight loss
• Mild to moderate jaundice
• Photosensitisation
  – through the alkaloid complexes being metabolised to photodynamic compounds in the liver
• Diarrhoea and low grade colic
• Hypoalbuminaemia may occur, with associated oedema
• Possible hepatic encephalopathy as ammonia levels rise around the brain
  – see head pressing, stupor, blindness, staggering

Question 16

Ragwort poisoning – treatment and prevention

Answer 16

• Adjust diet
  – Sheep can be less susceptible, so may even be able to tolerate ragwort at pasture in low doses
• Pull the plants before they flower and seed
• Do not make hay or silage from affected fields
• Treatment of clinically sick animals is unrewarding
  – They have overcome their hepatic threshold

Question 17

Liver abscess - pathogenesis

Answer 17

• damage to rumen through grain overload
  -> acidosis
  -> rumenitis
  -> bacterial translocation / bacteria enter blood stream
  -> bacteria enters portal blood system
  -> bacterial emboli break off in the liver and form abscesses

Question 18

Liver abscess – sequalae

Answer 18

• Complications can be very serious
• Rupture into the abdominal cavity causing massive peritonitis
• Rupture into a major vessel causing major haemorrhage, shock and sudden death
• Vena cava thrombosis.
  – This usually settles where the vena cava passes through the diaphragm resulting in reduced venous return to the heart -> ascites
  – May result in pulmonary thromboembolism with pulmonary abscessation
  -> This will give a painful cough and dyspnoea, probably with haemorrhage

Question 19

Liver abscess – treatment and prevention

Answer 19

• Treatment is unrewarding
• Prevention through avoiding acidotic ruminal conditions
  – Feed enough roughage
  – Do not over-feed grain
• Stimulate the rumen to ruminate, cudding to happen and so the brilliant buffering effect of saliva to be maximised