Revision Liver Trematodes

Question 1

Outline different types of Fascioliidae?

Answer 1

Fasciola hepatica (30 mm)

Fasciola gigantica (75 mm)

Fascioloides magna (100 mm)

+ many others

Question 2

Outline the general fluke lifecycle?

Answer 2

Question 3

Outline fascioloidosis in different hosts?

Answer 3

Cattle/Camelids : Pathogenicity usually low, but liver may still be condemned at slaughter. (eggs not passed) [dead-end host]

Sheep/goats : Few pathogens can cause a very serious disease due to the extent of migration. (eggs not passed) [aberrant host]

Deer : Adults become encapsulated, usually no pathology. (Eggs are passed)

Patent infection in deer suggests; the true host.

Question 4

Discuss immune response to trematodes in goats?

Answer 4

• Immune response in goats
• Increase in blood eosinophils.
• Increased eosinophil and plasma cell infiltrate in tissues in which flukes have migrated.
• Serum IgG specific for the E/S products of F. magna detected in sheep and goats.

Otherwise very few immunological studies done with this species.

Question 5

How are liver trematodes diagnosed?

Answer 5

• Eggs in faeces via McMaster. However, in some cases none will be seen e.g. Fascioloides in sheep and cattle.
• ELISA (available for some trematodes). Plasma enzymes which signal liver or bile duct damage e.g gamma- glutamyltransferase(GGT)
• Generally on condemnation of liver or following necropsy.

Question 6

Outline treatment for fluke diseases?

Answer 6

Question 7

Discuss fasciola gigantica?

Answer 7

• Chronic fascioliosis in cattle, Buffalo less susceptible.
• Acute often fatal disease in sheep.
• Severe economic loss in weight gain and milk throughout Africa and Asia.
• Life cycle the same as F. hepatica but snail species may be different.

Question 8

Discuss buffalo and fasciola?

Answer 8

• Pre-patent period in cattle has been reported at 64 days but in buffalo this is about 95 days.

(longer incubation period)

• Although infection rate in both cattle and buffalo is similar pathology in cattle is greater.

(less pathology)

• Eosinophilia delayed in buffalo compared to cattle which may account for a more rapid pathological effect in cattle.

(less immune response)

Question 9

Look at this Dicrocoelium dendriticum?

Answer 9

(Lancet/small/lesser fluke) 6 mm –1.0 cm

Question 10

What is the lifecycle of Dicrocoelium dendriticum?

Answer 10

Question 11

Discuss what Dicrocoelium dendriticum does in the host?

Answer 11

In the host (usually ruminant)

• Usually sub-clinical but can cause disease during very heavy infections.
• If clinical then usually sheep rather than cattle.
• Does not penetrate the liver capsule, tissue or gut wall as with F. hepatica.
• Anaemia, oedema, liver fibrosis and hepatic damage may occur in heavy infection.
• Little is known about the immune response, antibody responses have been seen against adult protein secretions.

Question 12

Discuss epidemiological factors of Dicrocoelium dendriticum?

Answer 12

• Eggs quite resistant (can survive many months on pasture).
• May lead to exposure of land snails and ants to large number of eggs.
• Wild life may act as reservoirs.
• Resistance to Flukicides.

Question 13

Discuss fasciola hepatica?

Answer 13

Fasciola hepatica

• Known as ‘Liver fluke’
• Hepatic parasite of ruminants
• Extremely common in the UK
• Prevalence increasing with time
• Spread of disease to previously unaffected areas
• Responsible for significant economic loss
• Does have public health implications

Question 14

Discuss the lifecycle of fasciola hepatica?

Answer 14

F. hepatica has a definitive ruminant mammalian host and an intermediate molluscan host

Question 15

How is Fasciola hepatica diagnosed?

Answer 15

• Gold standard is the faecal egg count (FEC)
• Standard sedimentation technique followed by examination under microscope.
• Eggs are 140 μm x 80 μm in size.
• Additionally clinical exam can reveal some signs of infection, e.g. Body score, diarrhoea
• Serum concentrations of liver enzymes AST, GGT, GLDH are indicative of infection.
• Differential blood count -eosinophilia
• Progress in antibody based diagnostics –Bio-X diagnostics ELISA kit –Cathepsin L1 based kits

Question 17

What is the clinical presentation of fasciola hepatic infection?

Answer 17

Acute, Sub-acute, Chronic.

Dependent on a number of factors:

• Dose of metacercariae
• Rate of uptake of metacercariae
• Final worm burdens
• Animals are routinely treated?
• Parasites are drug resistant or not?
• Animal condition at onset of infection.

Question 18

How does acute fasciola hepatica infection present?

Answer 18

• Sudden death between Aug-Oct (time required to pick up large enough number of metacercariae from pasture.
• Signs of liver damage including haemorrhage.
• Non-clinical diagnosis –liver damage + many larvae bile ducts and gall bladder (liver enzymes in plasma/ albumin and globulin conc.)
• Also think about epidemiology. Rainy/dry year

Question 19

How does sub-acute fasciola hepatica infection present?

Answer 19

• Rapid loss of body condition
• Poor fleece condition
• Depression
• In-appetance
• Inability to stand
• Non-clinical diagnosis by liver enzymes/protein conc. in plasma and immature flukes in bile duct and gall bladder (again need to consider epidemiology)
• Death may occur in Autumn but fatal sub-acute fasciolosis usually occurs in Winter.

Question 20

How does chronic fasciolosis present?

Answer 20

• Very poor body and fleece condition
• Bottle jaw may be apparent
• Death may occur during lambing
• Non-clinical diagnosis -eggs in faeces and adult flukes in bile duct

Question 21

Describe liver pathology in F hepatic infection?

Answer 21

• Juveniles migrate through liver until they locate the bile ducts where they mature
• Severe disease occurs when many ME are ingested over a short period of time resulting in liver haemorrhage/anaemia
• Usually small amounts are ingested over longer period of time, liver function compromised by fibrosis

Question 22

Discuss infectious necrotic hepatitis (black disease)?

Answer 22

• Occurs in cattle and sheep.
• Animal ingests spores of Clostridium novyi in soil.
• Non-pathogenic in oxygen rich environment
• Within the liver, bacteria multiply rapidly in area of necrosis caused by migrating flukes
• Bacteria produce tissue toxins which cause severe damage to liver
• Usually no signs-animal suddenly dies
• This can lead to misdiagnosis as acute fasciolosis

Question 23

What is the treatment of F. hepatica?

Answer 23

• If fluke is present treat with triclabendazole in Sept/Oct & again in Jan if FEC is positive.
• Treat against adult only stages in May/June preventing pasture contamination.
• Do not use the same treatment at Sept/Oct, Jan, or May/June.
• Treat additionally if particularly wet years.
• Isolate & treat all new animals bought from outside.
• Inefficient/wasteful use of triclabendazole means drug resistance is a major concern in Ireland & UK.
• Fence off wet areas (e.g. pasture running to rivers and streams)
• Increase soil drainage.
• Control of wildlife reservoirs of Fasciola –where possible & legal!

Question 24

What is the epidemiology of F. hepatica?

Answer 24

• In Europe almost exclusive snail host is Lymnaea truncatula (common pond snail)
• In other countries other Lymnaea species are important.
• Snail habitat crucial to spread therefore wet conditions ideal.
• Climate change and drug resistance believed to be important in UK spread.