Lungworm: the disease

Etiology

• Parasitic bronchitis is caused by the nematode, Dictyocaulus viviparus Dictyocaulus viviparus.

Predisposing factors

General

• The disease typically affects young cattle during their first grazing season on permanent pastures.
• Clinical symptoms are caused by the ingestion of large numbers of infective larvae by non-immune cattle.
• Wet summers and heavy stocking densities predispose to disease outbreaks, which generally occur in late summer and early autumn.
• Wet weather conditions also promote the release of infective (L3) larvae from the fecal pats.
• Conversely, dry weather may lead to low exposure to infective (L3) larvae leading to a lack of build- up of protective immunity.
• A strong immunity to D. viviparus Dictyocaulus viviparus begins to develop within 10 days of exposure to infective larvae.
• Immunity initially manifests as resistance to the establishment of larval infections but then declines after around 3 months in the absence of continued larval challenge.
• However, immunity to the development and survival of adult worms is longer lasting resulting in the excretion of few larvae in the feces.
• It therefore seems that re-infection and presence of adult worms in the lungs is necessary to maintain a strong immunity.

Pathophysiology

• Lungworm infection is characterized by bronchitis and pneumonia divided into three phases.
  • During the pre-patent phase, larvae appear within the alveoli causing alveolitis.
    • This is followed by bronchiolitis and finally bronchitis as the larvae become immature adults and move up the bronchi.
  • The patent phase is associated with a parasitic bronchitis characterized by the presence of large numbers of adult worms in the bronchi and a parasitic pneumonia with dark red collapsed areas around infected bronchi.
  • The post-patent phase is normally the recovery phase after the adult lungworms have been expelled.
    • The bronchi are still inflamed and residual lesions such as bronchial and peribronchial fibrosis may persist for several weeks or months.
    • In some heavily infected animals, there may be a flare up of clinical signs which may be fatal.
    • The lung is pink and rubbery due to epithelialization of the lung with type 2 pneumocytes accompanied by interstitial emphysema and pulmonary edema.

Timecourse

• The prepatent phase is from 1-3 weeks p.i.
• The patent phase, when L1 are present in the feces occurs between 3-9 weeks p.i.
• The post-patent phase is between 2-3 months p.i.

Epidemiology

• The epidemiology is more complex, and infections are less predictable than seen with gastrointestinal nematodes.
• Generally only calves in their first grazing season are clinically affected, since on farms where the disease is endemic older animals have a strong acquired immunity.
• Adult cattle can be affected with lungworm if they have not had sufficient exposure to lungworm larvae in previous years to allow adequate immunity to develop and are subsequently grazed on heavily contaminated pastures.
• ‘Re-infection husk’ may occur on heavily infected pastures, when the immune system is overwhelmed by large numbers of migrating larvae in the lungs.
• Lungworm infection is predominantly a problem in areas such as northern Europe that have a mild climate, a high rainfall, and abundant permanent grass.
• Outbreaks of disease occur in late summer to early autumn after calves have been at grass for 2-5 months.
• It is thought that initial ingestion of overwintered larvae in spring involves so few worms that neither clinical signs nor immunity is produced but leads to sufficient numbers of L3 on pasture later in the year to produce clinical disease if conditions are right.
• High summer rainfall helps dispersion of larvae by breaking the fecal pats.
• Dispersion also occurs via fungal spores produced by the fungus, Pilobolus, which grows on the surface of the fecal pats.
• Infection can persist from one season to the next, as either overwintered L3 on pasture, or in carrier animals.