Dictyocaulus viviparus can cause disease at several stages of its development in cattle: pre-patent - when larvae are newly arrived in the lungs cause tissue damage; patent - when adults present in the airways obstruct air flow, and when eggs, first-stage larvae, and exudates aspirated into the bronchioles and alveoli cause tissue damage, including metaplasia of the alveolar epithelium; and post-patent - when many of the adult parasites have been shed as a result of immune-mediated expulsion (a common occurrence with this parasite) and there is a hypersensitivity-like reaction in the alveoli. Typical clinical signs for all stages of infection include dyspnoea, coughing (often with the head down), and drooling. Morbidity can be high and there may be some mortality, particularly in animals affected by the post-adult hypersensitivity reaction.
The closest relatives of D. viviparus are the lungworms D. filiaria of sheep and D. arnfieldi of equids, both of which have similar life cycles.
Adult D. viviparus measure up to approximately 5.5 cm (males) and 8.0 cm (females) in length. The males have a distinct copulatory bursa and short, thick spicules. Adult parasites are usually identified on the basis of their location on the host – they are the only adult nematodes found in the trachea and bronchi of cattle.
The first-stage larvae of D. viviparus (the stage passed in feces) measure approximately 400 to 450 µ in length, and have a granular intestine and a bluntly pointed tail.
Host range and geographic distribution
Life cycle - direct
Life Cycle: Dictyocaulus viviparus
Dictyocaulus viviparus seems to require access to pasture for successful transmission. The basic annual epidemiological cycle for D. viviparus is similar to that for the GI trichostrongyles of cattle. At the start of the grazing season in most areas of Canada the pastures are probably free of larvae, but inhibited pre-adult larvae and adult parasites may be present in yearlings and adult cattle. These serve as the source of infective larvae for the calves, which develop patent infections, and sometimes clinical disease. Infected wildlife (for example, deer and elk) may (or may not) be reservoirs of D. viviparus for cattle.
The epidemiology of D. viviparus has two special features. First, a dry summer may result in crusting of the surfaces of fecal masses on the pasture and persistence of viable infective larvae in the centres on the masses. Rain in the fall may soften the crusts and release the larvae on to the herbage. Second, infective larvae in the fecal masses may migrate on to the sporangia of the fungus Pilobolus, and when the sporangium bursts, these larvae are propelled up to three metres into the herbage.
Pathology and clinical signs
Many cattle with low-level D. viviparus infections show no adverse effects. The presence and severity of clinical disease seems to depend on the rate of ingestion of infective larvae. Heavier infections, especially those acquired over a short time period, can cause severe lung pathology and clinical signs, These result from the damage caused by pre-adult larvae migrating in the lungs, the irritation caused by the adults in the airways, and by the aspiration deep into the lungs of mucus, and of eggs and larvae.
Among the significant pathological changes produced by the parasites, beginning towards the end of the pre-patent period and persisting in some animals into the post-patent period, are changes in the structure and function of the alveolar epithelium and the deposition of a hyaline membrane over the alveolar surfaces. Both these lesions can significantly interfere with gaseous exchange.
Clinical signs of lungworm infection can appear before the infection becomes patent and, as a result of parasite-induced damage to the respiratory epithelium, can persist in some animals after the adult parasites have died and been expelled. Clinical signs include difficulty breathing, coughing, noisy lung sounds, emphysema and rapid loss of condition. In Canada, clinical lungworm disease is most often seen in young animals towards the end of their first grazing season.
Treatment and control
Additional information on the products mentioned is available from the Compendium of Veterinary Products (Twelfth Edition, 2011), or from the manufacturers.
Successful control of lungworm in cattle depends on an awareness of the clinical signs, and prompt treatment of all the animals at risk, generally considered as those sharing grazing with the sick animals. Moving treated cattle to a "clean" pasture (one though to be free of infective larvae) after treatment is also very important.
In Europe, but not in North America, an oral vaccine is commercially available containing irradiated third stage larvae, which undergo development in cattle sufficient to generate a protective immunity, but which do not cause significant pathology and do not mature to adults. The vaccine is usually given in the spring, before turn-out to pasture.