Sustainable Control of Fluke and Lungworm

Question 1

1. Parasite causing fasciolosis / liver fluke?
2. What spp. does it affect?
3. IH in UK?
4. Where is this infection an important zoonosis?

Answer 1

1. Fasciola hepatica.
2. Cattle and sheep (Also horses, rabbits, other grazers and humans).
3. Galba truncatula (mud snail).
4. E.g. Egypt and Peru.

Question 2

Fasciola hepatica increases susceptibility to what other diseases?

Answer 2

Black disease.
- Necrotising hepatitis due to Clostridium novyi.
- Secondary to liver fluke damage.
- Sudden death.
- In cattle, sheep and goats.
Salmonella Dublin.
Evidence suggests bovine TB diagnostic test compromised in fluke-infected cattle.

Question 4

Life cycle of Fasciola hepatica?

Answer 4

Eggs in environment > to miracidium > enter snail > sporocyst > Redia > Cercaria > Leave the snail > Cercaria encyst (metacercaria) on herbage > Metacercaria ingested by sheep/cattle while grazing > Juvenile and adult fluke in sheep and cattle > defaecate eggs out.

Question 5

1. PPP of Fasciola hepatica in DH (sheep/cattle)?
2. Galba trunculata shell.
3. Optimum temperatures for galba trunculata development.
4. Define aestivation.

Answer 5

1. 10-12wks.
2. Height = 5 - 10mm.
   Width = 2.5 - 6mm.
3. 15 - 22C optimal.
   Stops at <5C.
4. Prolonged torpor or dormancy.

Question 6

Galba trunculata habitat.

Answer 6

Prefers mud to free water.
Around natural springs.
Banks of rivers and ditches.
Boggy ground w/ clumps of rushes.
Temporary pools e.g. wheel ruts, poached ground.

Question 7

Where in the UK is Fasciolosis most common and why?

Answer 7

Western parts of England and Scotland, Wales and Ireland.
Because the area need to be boggy for the snails.
Cattle and sheep grazing around wetlands are particularly at risk.

Question 8

Seasonal effect on Galba Trunculata populations?

Answer 8

Snail size is increased in wetter months of optimal temperatures e.g. April and August.

Question 9

How does re-infection occur in autumn?

Answer 9

They become infected by infected carrier animals or overwintered eggs, then cercariae develop in the snails, and then there are fresh metacercariae on pasture as a result in autumn.

Question 10

Winter infection of snails with Fasciola hepatica.

Answer 10

Snail infected from carrier animals or overwintered eggs in the summer and Rediae and sporocyst develop. No maturation over the winter. Then in spring, cercariae develop in the snail, resulting in fresh metacercariae on pasture.

Question 11

1. Chronic fasciolosis in cattle caused by?
2. Subclinical fasciolosis in cattle caused by?
3. Acute fasciolosis in sheep caused by?
4. Subacute fasciolosis in sheep caused by?
5. Chronic fasciolosis in sheep caused by?
6. Subclinical fasciolosis in sheep caused by?

Answer 11

1. Lots of adult fluke in bile ducts.
2. Fewer adult fluke in the bile ducts.
3. Lots of immature fluke in the liver parenchyma.
4. Fewer immature fluke in liver parenchyma and some adults in the bile ducts..
5. Many adult fluke in the bile ducts.
6. Fewer adult fluke in the bile ducts.

Question 12

Clinical signs of bovine fasciolosis?

Answer 12

Chronic condition.
Weight loss.
Anaemia.
Sub-mandibular oedema.
- Severe cases.
- “Bottle jaw”.
Poor growth.
Reduced milk yield.
Young cattle after first autumn at grass.
Immunity in older cattle (not sheep).
Late autumn, winter.

Question 13

Acute ovine fasciolosis clinical signs?

Answer 13

Animals found dead.
Usually in the autumn.
Others in flock may have:-
– Anaemia (pale ocular MMs).
– Dyspnoea.
– Swollen livers.
– Abdominal pain.

Question 14

Subacute ovine fasciolosis clinical signs.

Answer 14

Rapid weight loss over 1-2wks.
Anaemia.
Enlarged liver.
Abdominal pain (resent palpation).
Deaths.
Autumn to early winter.

Question 15

Chronic ovine fasciolosis clinical signs.

Answer 15

Progressive loss of condition.
Severe anaemia.
Submandibular oedema.
In severe cases:-
- Emaciation.
- Ascites.
- Death.
Late winter, early spring.

Question 16

Diagnosis of fasciolosis.

Answer 16

History on farm.
Time of year.
Presence of suitable snail habitat.
Clinical examination.
Lab tests.

Question 17

How can faeces be examined for fasciola eggs.

Answer 17

Only for patent infections i.e. adult fluke/chronic infections
Convention McMaster nematode egg count method using saturated saline NOT EFFECTIVE.
- Specifically request fluke egg count.
- Specific sedimentation methods.
- Flotation using ZnSO4,
Mini-FLOTAC.
FLUKEFINDER.
Intermittent emptying of gall bladder –> very variable egg counts.
Test more than one faecal sample.
Composite faecal samples reduce testing costs.

Question 18

Biochemical and immunological tests for fluke.

Answer 18

Biochem = liver damage – non-specific.
Glutamate dehydrogenase (GLDH).
– Levels increase from 2-3wks after infection.
– Helpful in acute infection.
Gamma glutamyl transpeptidase (GGT).

Immunological.
– Milk ELISA –> bulk tank milk.
– Serum ELISA.
– Coproantigen ELISA.

Question 19

How can we control snails?

Answer 19

Fencing off risky areas (unpopular w/ farmers).
Drainage (Discouraged to protect biodiversity.
UK Governament’s new Environmental Land Management scheme.
– Farmers’ subsidy for environmental management, rather than production.
– New wetlands, new snail habitat?

Question 20

How is climate change impacting the infection of animals w/ fasciola hepatica?

Answer 20

Summers becoming wetter.
Areas that were not previously affected are being affected (N.E. England, East Anglia).
Major threat to sheep and cattle in the UK.
A significant problem impacting on health, welfare and productivity.

Question 21

Preventative treatment of Fasciola hepatica.
1. When?
2. Target of treatment?
3. Agent?
4.

Answer 21

1. Late summer/autumn for sheep (typically October).
   At winter housing for cattle.
   Esp. important after wet summers.
2. Larvae migrating through liver parenchyma, so agent must be effective against immature fluke.
3. Triclabendazole - effective against all ages of Fasciola (incl. immature fluke from 1-2wks of age) (but some concerns about resistance).
   Closantel – reasonable activity against immature fluke. – From 3-4wks of age but more so at >5wks.
   Nitroxynil – effective from 6-7wks.

Question 22

Further treatments of fasciola hepatica.

Answer 22

Usually necessary against adult fluke developing during winter and thereafter:-
– January.
– May – in high-risk areas.
– September –> if clinical signs.
Avoid use of triclabendazole at these times to prevent resistance, by restricting use to when essential to kill immature fluke.
Use an agent effective against adult fluke.
– Clorsulon – only suitable for cattle.
– Oxyclosanide.
– Albendazole.

Question 23

Treatment of fasciolosis in dairy cattle.

Answer 23

Fasciola hepatica has significant impact on dairy cow productivity in the UK.
No product licenced for use in lactating dairy cattle.
Triclabendazole permitted in dry period, ~50-day milk withdrawal.

Question 24

1. Where is Triclabendazole resistance in sheep reported?
2. Where is Triclabendazole resistance in cattle reported?
3. How can Triclabendazole resistance be managed?

Answer 24

1. Scotland, Wales, N. Ireland and Eire, Australia and New Zealand.
2. The Netherlands, Australia and South America.
3. Avoid use unless essential.
   Quarantine treatment of newly introduced stock.
   - Other fasciolicides control triclabendazole resistant fluke.
   - Cannot stop spread completely – deer and rabbits are hosts.
   Change fasciolicide if resistance suspected.
   - BUT none have same range of activity against immature fluke.
   Try reduce reliance on fasciolicides BUT snail ctrl also problematic.
   Vaccination – lots of ongoing work, none yet available.

Question 25

1. What parasite causes bovine lungworm?
2. AKA?
3. % morbidity?
4. Mortality?
5. Financial cost?
6. Commonly diagnosed by?

Answer 25

1. Dictyocaulus viviparus.
2. Parasitic bronchitis, “Husk”, “Hoose”.
3. > 50%.
4. Variable.
5. Can be in £10,000s.
6. APHA.

Question 26

1. Where is bovine lungworm most commonly?
2. Immunity?
3. How long until patent phase after exposure?

Answer 26

1. Temperate regions w/ high rainfall.
2. Acquired immunity strong following infection (or vac).
3. 26-60 days.

Question 27

Season of infection of bovine lungworm.

Answer 27

Disease outbreaks: June - November.
Most common: July - September.
Disease is usually not apparent until cows at grass for 2-5mnths following spring turnout.

Question 28

Four possible stages of disease of parasitic bronchitis.

Answer 28

Acute – prepatent phase, days 8-25.
– Exudate in airways, alveolitis, bronchiolitis and bronchitis.
– No larvae in faeces.

Subacute – patent phase, days 26-60.
– 100s-1000s of adults in bronchi.
– Parasitic pneumonia –> aspiration of eggs and L1.
Larvae in faeces.

Post-patent phase, days 61-90.
– Lung fibrosis and epithelialisation.
– Secondary bacterial infection.
– No larvae in the faeces.

Re-infection syndrome.
– Previous exposed animals with lapsed immunity.
– Hypersensitivity reaction.

Question 29

Phases of acquired immunity to bovine lungworm.

Answer 29

1: Resistance to colonisation of lungs by larvae.
– Weakens rapidly (3-6mths) if no further exposure occurs.
– Similar to GI mucosal immune responses – short lived.

2: Destruction and elimination of larvae/adults from lungs.
– Lasts longer (>2yrs).
– Systemic immune responses tend to be longer lasting.

Question 30

Issues w/ immunity to bovine lungworm.

Answer 30

Immunity not lifelong, requires boosting, esp. phase 1.
Heavy challenge can lead to “Re-infection syndrome” in animals exposed >6mths previously (previous grazing season).m
– No phase 1 immune response, so larvae get to lungs.
– When numerous larvae reach lungs and are killed by phase 2 host response (8-10 days after change in pasture), ‘hypersensitivity’ can result.

Question 31

How do we diagnose bovine lungworm?

Answer 31

• Grazing at pasture, time of year, coughing.
• Larvae in faeces – Baermann apparatus.
  – only after day 23.
• Ab-ELISA (APHA).
  – only after day 23.
• PM exam.
  relatively few larvae to cause disease

Question 32

When does lungworm outbreak in calves occur?

Answer 32

When rate of ingestion of pasture w/ sufficient disease-causing L3 exceeds level of developing immunity.
– Weather conditions favourable for development of L3.
– Calves grazing pastures contaminated by older cattle.
– Concurrent respiratory disease may exacerbate.

Question 33

1. What calves are at greater risk? – why?
2. What calves are at lower risk? – why?
3. What makes lungworm unpredictable?

Answer 33

1. Those born in autumn and weaned in summer. – Significant numbers of infective L3 on pasture when they start to graze and they would not yet have had much exposure –> naive.
2. Spring born calves – Exposed to small numbers of L3 at an earlier age, so have greater immunity by time they ingest significant numbers of L3. Mild coughing not uncommon.
3. Climate change and variable seasonal weather patterns.