Bovis ISSN 2398-2993

Lungworm: the disease

Synonym(s): Parasitic bronchitis

Contributor(s): Mike Taylor , Andrew Forbes

Introduction

  • Cause: Dictyocaulus viviparus.
  • Signs: lungworm infection causes bronchitis and pneumonia characterized by widespread coughing, tachypnea and dyspnea.  Heavy infections can result in death.
  • Diagnosis: history, clinical signs, identification of first stage (L1) in feces.
  • Treatment: anthelmintics – macrocyclic lactones (ivermectin, doramectin, eprinomectin, moxidectin), benzimidazoles (eg fenbendazole, albendazole),  imidazothiazoles (levamisole) antibiotics if pyrexic, anti-inflammatories, hydration therapy if dehydrated.
  • Prognosis: guarded prognosis. Mild infections usually recover with early treatment intervention but severe losses may occur in disease outbreaks. Infections in lactating cows can lead to significant drop in milk yields.

Pathogenesis

Etiology

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.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Holzhauer M, van Schaik G, Saatkamp H W & Ploeger H W (2011) Lungworm outbreaks in adult dairy cows: estimating economic losses and lessons to be learned. Veterinary Record 169, 494 PubMed.
  • Eysker M, Claessens E W, Lam T J G M, Moons M J & Pijpers A (1994) The prevalence of patent lungworm infections in herds of dairy cows in the Netherlands. Veterinary Parasitology 53, 263-267 PubMed.
  • Eysker M (1991) Direct measurement of dispersal of Dictyocaulus viviparus in sporangia of Pilobolus species. Research in Veterinary Science 50, 29-32 PubMed.
  • Eysker M (1991) Direct measurement of dispersal of Dictyocaulus viviparus in sporangia of Pilobolus species. Research in Veterinary Science 50, 29-32 PubMed.
  • Eysker M & van Miltenburg L (1988) Epidemiological patterns of gastrointestinal and lung helminth infections in grazing calves in the Netherlands. Veterinary Parasitology 41, 127-135 PubMed.
  • Jørgensen R J (1981) Studies on the lungworm Dictyocaulus viviparus (Bloch, 1792) and its epidemiology in young cattle with a description of an attempt to prevent parasitic bronchitis. Acta Veterinaria Scandinavica 76, 1–77.
  • Parker W H (1963) Lungworm infection in cattle-Control and Treatment. Journal of the American Veterinary Medical Association 142, 743-750 PubMed.
  • Jarrett W F H, McIntyre W I M, Jennings F W, Mulligan W & Urquhart G M (1960) Immunological studies on Dictyocaulus viviparus infection Immunity produced by the administration of irradiated larvae. Immunology 3, 145-151 PubMed.
  • Michel J F (1959) Recent progress in the study of parasitic bronchitis. Journal of the Royal Agricultural Society of England 120, 28-44.
  • Michael J K, Mackenzie A (1965) Duration of the acquired resistance of calves to infection with Dicytocaulus viviparus. Research in vet sci 6, 344-395 PubMed.
  • Jarrett W F H, McIntyre W L M & Urquhart G M (1957) Husk in Cattle. A review of a year’s work. Veterinary Record 66, 665-692.
  • Jarrett W F H, McIntyre W I M, Jennings F W & Mulligan W (1957) The natural history of parasitic bronchitis with notes on prophylaxisand treatment. Veterinary Record 69, 1329-1336.
  • Michel J F & Rose J H (1954) Some observations on the free living stages of the cattle lungworm in relation to their natural environment. Journal of Comparative Pathology and Therapeutics 64, 195-205 PubMed.
  • Soliman K N (1953) Migration route of Dictyocaulus viviparus and D. filaria infective larvae to the lungs. Journal of Comparative Pathology 63, 75-84 PubMed.

Other sources of information

  • Taylor M A, Coop R L & Wall R L (2016) Chapter 8 - Parasites of Cattle: Dictyocaulus viviparus. In: Veterinary Parasitology. 4th edn. John Wiley & Sons, Chichester, West Sussex, UK, pp 380-382.
  • Van Dijk (2004) The epidemiology and control of dictyocaulosis in cattle. Cattle Practice 12 (2), 133-143.
  • David G (1999) Strategies for the control of parasitic bronchitis in cattle. In Practice 21, 62-68.
  • Control of Worms Sustainably (COWS) Control of lungworm in cattle. www.cattleparasites.org.uk.


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