Coughing young stock and parasitic respiratory disease

Question 1

What is integrated parasite management?

Answer 1

• a system where multiple approaches for control are utilised taking into consideration economic factors, epidemiology, resistance status, the production system and management structures in place
• 3 categories: identifying risk (temporal and geographical), treating appropriately (right animals at the right time), avoiding resistance (maintain ‘in refugee’ parasite population

Question 2

Trickle challenge vs clinical dz (parasitology principles)

Answer 2

• a trickle or low infectious challenge over time allows immunity to develop without clinical signs of disease
• a high, abrupt infectious challenge over a short period of time exceeds the ‘threshold’ and causes clinical/sub-clnical dz
• avoiding all challenge means animals are naive and susceptible to infection
• worm control programme is about reducing the worm burden

Question 3

Assessing environmental risk

Answer 3

Is the pasture likely to have infective stages of the parasite on it?
Has the climate recently been favourable for the parasite being considered?

Question 4

Husk

Answer 4

= lungworm
= parasitic bronchitis
= verminous pneumonia

Question 5

Cattle lungworm

Answer 5

Dictyocaulus vivparus
- seen more in dairy herds than sucklers
- mainly affects cattle but is also seen in other ruminants e.g. deer

Question 6

Sheep lungworm

Answer 6

Dictyocaulus filaria/muellerius capillaris most common

Question 7

Life cycle of lungworm

Answer 7

• direct
• L1 passed in faeces
• Develops into infective L3 (takes <1 week in optimal conditions, but can take several weeks when cooler)
• Rain, vectors and Pilobolus fungus aid dispersion of L3 from dung.
• L3 ingested, migrate to lungs, develop into adults which produce eggs.
• Eggs hatch and L1 larvae coughed up and swallowed.
• PPP=3-4 weeks, very fecund and L1-L3 development fast = high infection levels can develop quickly.
• Carrier animals (inhibited L4) and L3 overwintering on forage are both sources of infection.
• Larvae can survive >1y on pasture if cold and wet (warm and dry = shorter larval survival times)
• Cattle can get infection either from carrier animals (lungworm overwinters in animal, commonly as L4) or from forage (lungworm overwinters on forage, commonly as L3).

Question 8

Risk factors for lungworm

Answer 8

• Wetter/western area
• Late summer/Autumn
• High stocking densities
• First season grazers/naïve animals

Question 9

Lungworm epidemiology

Answer 9

• seasonal patterns vary year to year and farm to farm
• less predictable than PGE and fluke

Question 10

Lungworm pathogenesis

Answer 10

• Ingested L3 become more active in the presence of bile.
• Cross small intestine into lymphatic system and mesenteric lymph nodes then to thoracic duct and circulation to the lungs.
• Reaches the lungs within 1w post-infection
• Colonise alveoli then bronchioles, ending up as adults at the base of the trachea.
• Promotes inflammation, eosinophil rich mucus and parasite debris.
• Alveolar epithelialisation = cells incapable of gaseous exchange.
• Alveolar epithelialisation is irreversible which may result in apparent ‘tx failure’
• Loss of ciliated epithelium = more prone to other respiratory infections.

Question 11

Lungworm - clinical presentation for carrier animals

Answer 11

• Few adverse effects for individual

Question 12

Lungworm - clinical presentation for subclinical disease

Answer 12

• Weight loss (£50-100/animal)
• Milk drop (£3/cow/day)

Question 13

Lungworm - clinical presentation for clinical disease

Answer 13

• coughing: may be mild and brought on by exercise through to persistent and present at rest
• dyspnoea/tachypnoea: may have abducted elbows and outstretched neck. may auscultate squeaks and crackles over posterior lung lobes
• mortality: sudden death may occur within 24-48h
• pyrexia: mild, occasionally seen

Question 14

Lungworm: clinical presentation - 4 phases

Answer 14

• penetration phase
• pre-patent phase
• patent phase
• post-patent phase

Question 15

Lungworm: clinical presentation - penetration phase

Answer 15

• Days 1-7 post infection
• Larvae penetrate body of host and migrate to lungs

Question 16

Lungworm: clinical presentation - prepatent phase

Answer 16

• Days 8-25 post infection
• Larvae develop in the lungs
• Can see clinical signs during this phase

Question 17

Lungworm: clinical presentation - patent phase

Answer 17

• Days 26-60 post infection
• Worms mature and produce eggs

Question 18

Lungworm: clinical presentation - post-patent phase

Answer 18

• Days 61-90 post infection
• Recovery phase once adult worms have been expelled
• Post-patent parasitic bronchitis can cause severe clinical signs/death (death in apparently recovering animals a few weeks later, thought to be due to dissolution and aspiration of dead/dying parasite material)
  (- after recovery residual lesions may persist for months, and some lung damage may be permanent)

Question 19

Lungworm: clinical presentation - Re-infection syndrome

Answer 19

Immunity to D.viviparus has 2 main components:
- Reduction in number of larvae reaching the lungs
(short duration – approx. 4 months)
- Destruction of adult worms that have reached the lungs
(longer duration – approx. 2 years)

Immunity can wane during housing. If cattle are turned out onto heavily contaminated pasture large numbers reach the lungs, as the short duration immunity has waned. Longer duration immunity in the lungs kills large numbers of these mature worms causing acute illness.

Sterile immunity is unlikely, so even ‘immune’ cattle will commonly shed small numbers of larvae onto pasture. This can ‘boost’ immunity within a herd as it maintains a trickle level of infection. Pasture unlikely to be heavily contaminated at turnout.

Question 20

Lungworm diagnosis

Answer 20

• Clinical signs and grazing history (risk factors)
• Detection of L1 in faeces (Baermann technique)
  – If negative could cattle be in the pre or post patent phase, or could it be re-infection syndrome?
• Examination of sputum for eggs/larvae – detects patent infections slightly earlier than faecal samples.
• Bulk milk or blood ELISA (antibody)
  – Sensitivity of ELISA for patent infections is low
  – Seroconversion can take 4-6 weeks
  – Bulk milk useful for routine monitoring of dairy herds
• Post-mortem
  – Cut along bronchial tree
  – Adult worms seen in bronchi and bronchioles

Question 21

Lungworm Treatment and control

Answer 21

Wormers
- Group 1 – Benzimidazoles – no persistent action (last 24h)
- Group 2 – Levamisole – no persistent action (last 24h)
- Group 3 – Macrocyclic lactones – persistent action
- Oral drenches may cause more stress to administer than injectable/pour-on which is important to note for animals in respiratory distress

Also consider:
- Route of administration
- Advise farmers that treatment may worsen clinical signs
- Effect on PGE (parasitic gastroenteritis)
- Timing of treatment
– In response to clinical signs
– Strategic e.g. early season dose to reduce pasture contamination/rumen boluses. NB need to allow enough exposure to promote immune response.
– Housing: tx at housing can prevent carriers overwintering L4

Supportive treatment
- NSAIDs
- Antibiotics if pyrexic.

Grazing strategies
- Delay turnout – keep stock in until late April/May to reduce larval levels that have overwintered
- Rotational grazing – Outbreaks are less predictable than parasitic gastroenteritis, so this is harder to utilise (will cover in relation to PGE)

Vaccination
- e.g. Huskvac
- Calves >8w old get 2 doses 4 weeks apart at least 2w pre turnout.
- Can give booster doses in following years, but if there is low level natural infection (e.g. carrier animals) this will naturally boost immunity.
- Don’t mix naïve and vaccinated animals (as vaccinated animals can become carriers), and don’t worm within 2 weeks of vaccinating.
- Do not use vaccine in herds with no history of lungworm.
- Vaccine is a drench so can be tricky to administer, but is the safest way to provide immunity for lungworm to a herd