Parasitic Bronchitis - Cattle

Caused by Dictyocaulus viviparus

Epidemiology of Parasitic Bronchitis

Our knowledge of the epidemiology of disease is far from complete, i.e. there are still outbreaks of parasitic bronchitis that we are unable to explain.

Disease is carried on from one year to the next by

• Low numbers of L3 overwintering on pasture
• Carrier animals (30% yearlings and 5% cows in an endemic area)

Sequence of events that leads up to an outbreak of clinical disease is as follows

• A few calves in a group pick up overwintered L3 from pasture after turnout, leading to patent infections
• L1 develop to L3 in dungpat
• Translation of L3 onto the pasture largely by fungus (Pilobilus species)
• Remainder of calves infected. The infection may cycle 1, 2 or more times before sufficient L3 accumulate on pasture to cause disease (July – September)
• Large proportion of ingested larvae become inhibited in lungs of calves overwinter, leading to pasture contamination following spring turnout, i.e. “carrier animals”.

Immunity

• Rapidly acquired following heavy exposure to infection (within a few weeks)
• Minimal age resistance (i.e. older stock susceptible if not previously exposed)

Pathogenesis of Parasitic Bronchitis

Primary Infection

Penetration Phase (week 1)

• Larvae migrate to the lungs; no clinical signs.

Prepatent Phase (weeks 1-3)

• Development and migration of larvae → bronchiolitis → eosinophilic exudate → blocks passage of air → alveolar collapse distal to blockage → clinical signs (tachypnoea, coughing depending on the number of worms)

Patent Phase (weeks 4-8)

• Worms mature and become egg-producing. Main lesions are
  • Bronchitis (due to adult worms)
  • Parasitic pneumonia (due to aspiration of eggs and larvae → cellular infiltration of polymorphs, macrophages and “foreign body” giant cells)

Postpatent Phase (weeks 8-12)

• Period at the end of disease when the majority of worms are expelled. In 25% of cases, clinical signs flare up as a result of alveolar epithelialisation, which may be accompanied by interstitial emphysema and pulmonary oedema, or secondary bacterial infection

Reinfection Syndrome

• Immune cattle only show clinical signs if exposed to a massive challenge
• Pathogenesis; large numbers of larvae reach bronchioles → killed by immune response
• Pathology; parasite granulomata (grey-green, 5mm diameter; macrophages, giant cells, eosinophils) and eosinophilic plugs in bronchioles

Diagnosis of Parasitic Bronchitis (Calves)

• Seasonal incidence
• Previous grazing history
• Clinical signs
• Faecal examination for larvae
  • Baerman technique; examine both healthy and sick cattle
  • Carrier animals may be important in the epidemiology of disease, e.g. in an endemic area 30% yearlings and 5% cows harbour patent infections, as do vaccinated animals

NOTE: All lungworm-positive faecal samples are potentially significant

• Post mortem examination
  • Recovery of worms from lungs; “Inderbitzen” or lung perfusion technique. Worms flushed out of lungs by pumping water through pulmonary arteries. Water and worms passed out of trachea collected over sieve

NOTE: Only 200-300 worms are required to cause clinical disease c.f. >40,000 Ostertagia

Diagnosis of Parasitic Bronchitis (Adult Cattle)

• Seasonal incidence
• Previous grazing history
• Clinical signs
• Faecal examination
  • Baerman technique; examine healthy and sick cattle, but often no larvae in faeces
• Blood and Milk examination (ELISA)
  • Variable results (depending upon Ag used)
  • Herd results better than individual results
• Grass examination for larvae around dung pats
• Response to anthelmintic treatment

Control of Parasitic Bronchitis

Vaccination – “Huskvac” (Intervet, original vaccine = “Dictol”)

• First-season calves, >2months old, reared indoors
• Attenuated oral vaccine (each dose, 1,000 X-irradiated Dictyocaulus viviparus L3)
• Vaccinate 6 weeks and 2 weeks pre-turnout

NOTE: Never mix vaccinated and non-vaccinated animals

• Result:
  • Effective at preventing disease
  • Not 100% effective at preventing infection, i.e. even vaccinated calves may pass a few larvae → boost immunity in vaccinated calves, but could cause disease in non-vaccinated animals
• Breakdown in protection can occur due to:
  • Overwhelming challenge
  • Improper storage or administration of vaccine
  • Concurrent disease
  • Mixing vaccinated and non-vaccinated calves
• Strategic anthelmintic programmes for preventing parasitic bronchitis:
  • Ivermectin 3, 8 and 13 week post-turnout treatment

NOTE: Residual activity of 28 days against lungworm

• No anthelmintic cover if challenge encountered either:
  • early (0-3 weeks) or
  • late (after 17 weeks) in grazing season.