01 Thursday October 2020
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Overview of Lungworm Infection


An infection of the lower respiratory tract, usually resulting in bronchitis or pneumonia, can be caused by any of several parasitic nematodes, including Dictyocaulus viviparus in cattle and D eckerti in deer; D arnfieldi in donkeys and horses; D filaria, Protostrongylus rufescens, and Muellerius capillaris in sheep and goats; Metastrongylus apri in pigs; Oslerus osleri in dogs; and Aelurostrongylus abstrusus and Capillaria aerophila in cats. Other lungworm infections occur but are less common.

The first 3 lungworms listed above belong to the superfamily Trichostrongyloidea and have direct life cycles; the others belong to the Metastrongyloidea and, except for O osleri and C aerophila, have indirect life cycles.

Some nematodes that inhabit the right ventricle and pulmonary circulation, eg, Angiostrongylus vasorum and Dirofilaria immitis, both found in dogs in certain areas of the world, may be associated with pulmonary disease. Clinical signs relating to a cardiac or a pulmonary syndrome or to a combination of both may occur.


Diseases caused by the 3 Dictyocaulus spp are of most economic importance. The cattle lungworm D viviparus is common in northwest Europe and is the cause of severe outbreaks of “husk” or “hoose” in young (and more recently, older) grazing cattle. The lungworm of goats and sheep, D filaria, is comparatively less pathogenic but does cause losses, especially in Mediterranean countries, although it is also recognized as a pathogen in Australia, Europe, and North America. D arnfieldi can cause severe coughing in horses and, because patency is unusual in horses (but not in donkeys), differential diagnosis with disease due to other respiratory diseases can be difficult. M capillaris is prevalent worldwide and, while usually nonpathogenic in sheep, can cause severe signs in goats. Other lungworm infections cause occasional sporadic infections in various animal species in many countries.

Dictyocaulus spp

Adult females in the bronchi lay larvated eggs that hatch either in the bronchi (D viviparus), or in host feces (D arnfieldi) after being coughed up and swallowed. The larvae can become infective in feces on pasture after a minimum of 1 wk in warm, moist conditions, but typically in summer in temperate northern climates will require 2–3 wk. Once infective, the larvae can be further dispersed from fecal pats mechanically or in the case of D viviparus by the sporangia of the fungus Pilobolus. A proportion of infective larvae survive on pasture throughout the winter until the following year but, in very cold conditions, most become nonviable. The principal source of new infections each year is from infected carrier animals, with overwintered larvae providing a secondary but not unimportant contribution in some countries. In the case of D arnfieldi, donkeys are the prime source of pasture contamination for horses. Because D viviparus infection in cattle is the most economically important, it has been most investigated, and many of the observations from it are applicable to other species. Clinical disease usually develops on first exposure to sufficient infective larvae; the severity of disease and stimulation of an immune response is related to the number of larvae ingested. In cattle and sheep, this usually occurs during their first season at pasture; however, an increase in the number of older cattle affected has been reported and is attributed to the efficiency of some prophylactic anthelmintic regimens, which prevent exposure at an earlier age. Because transmission of infection to horses requires infected donkeys, first infections can occur at any age in that species. Once infected, adults generally become immune to further disease, but a proportion contract subclinical infections during which they act as a source of further larval contamination. Occasionally, when previously infected adults or groups that have not been exposed to reinfection for >1 yr, and in which immunity may have waned, are exposed to an overwhelming level of infection, clinical disease may recur. In areas of Europe in which cattle are housed during winter and first grazing season calves turned out in late April or May, the first infections can be seen between mid June and late July, but most severe infections develop in previously unexposed calves after multiplication of a second generation of infective larvae on pasture between August and early October.

Other Species

Because other lungworm species either require an intermediate host or are found in nonherd animals, disease caused by them is more sporadic. Metastrongylus apri in pigs requires an earthworm as intermediate host; thus, infection is confined to pigs with access to pasture and may become more common as a result of organic farming methods. Muellerius capillaris and Protostrongylus rufescens in sheep and goats require slugs or snails as intermediate hosts, which must be eaten for infection to occur. Aelurostrongylus abstrusus is normally transferred to cats after ingestion of a paratenic host such as a bird or rodent that has previously eaten the slug or snail. Adults of Oslerus osleri live in nodules in the trachea of dogs, and larvated eggs laid by adults hatch there. Pups become infected from saliva or feces of an infected dog, in the former case by being licked by their dams. Capillaria aerophila in cats has a direct cycle, with infective eggs being ingested with food or water.


The pathogenic effect of lungworms depends on their location within the respiratory tract, the number of infective larvae ingested, and the animal's immune state. During the prepatent phase of Dictyocaulus viviparus infection, the main lesion is blockage of bronchioles by an infiltrate of eosinophils in response to the developing larvae; this results in obstruction of the airways and collapse of alveoli distal to the block. Clinical signs are moderate unless large numbers of larvae are present, in which case the animal may die in the prepatent phase with severe interstitial emphysema.

In the patent phase, the adults in the segmental and lobar bronchi cause a bronchitis, with eosinophils, plasma cells, and lymphocytes in the bronchial wall; a cellular exudate, frothy mucus, and adult nematodes are found in the lumen. The bronchial irritation causes marked coughing, and the entire reaction leads to increased airway resistance. A major component of the patent stage is development of a chronic, nonsuppurative, eosinophilic, granulomatous pneumonia in response to eggs and first-stage larvae aspirated into alveoli and bronchioles. This is usually in the caudal lobes of the lungs and is severe when widespread; in combination with the bronchitis, death may result. Interstitial emphysema, pulmonary edema, and secondary bacterial infection are complications that increase the likelihood of death. Survivors may suffer considerable weight loss.

If the animal survives until the end of patency (2–3 mo for D viviparus), most or even all of the adult worms are expelled, and the cellular exudate resolves over the ensuing 4 wk. Most recover unless secondary infection develops in the damaged lungs during the postpatent phase. In a few animals, clinical signs are exacerbated in the postpatent phase due to development of a diffuse, proliferative alveolitis characterized by hyperplasia of the type II alveolar epithelial cells. The cause is unknown, but it is observed much less often in cattle treated with anthelmintics with a persistent action against D viviparus such as the macrocyclic lactones ivermectin, doramectin, eprinomectin, and moxidectin.

D filaria is similar to D viviparus, but interstitial emphysema is not a common complication. Bronchial lesions predominate in D arnfieldi infections; when an alveolar reaction occurs, as in donkeys or foals, there are lobular areas of overinflation due to intermittent obstruction of small bronchi.

The pathogenic effect of the other lungworms has a similar basis, but frequently such severe clinical signs are not produced, perhaps because of a more restricted localization in the lungs and less severe infections. The patent phase and the associated lesions last >4 mo for some lungworms (M apri and A abstrusus) but can be >2 yr (M capillaris). The lesions in pigs with M apri are a combination of localized bronchitis and bronchiolitis with overinflation of related alveoli, usually at the edges of the caudal lobes. In pigs, hypertrophy and hyperplasia of bronchiolar and alveolar duct smooth muscle with marked mucous cell hyperplasia are striking features. Near the end of the patent period (as adult worms are killed), gray-green lymphoid nodules (2–4 mm) are formed; fragments of dead worms may be seen microscopically in these nodules composed of lymphocytes and plasma cells surrounding a central zone of eosinophils.

In M capillaris and P rufescens infections, chronic, eosinophilic, granulomatous pneumonia seems to predominate; the reaction is in the bronchioles and alveoli that contain the parasites, their eggs, or larvae. They are surrounded by macrophages, giant cells, eosinophils, and other immunoinflammatory cells, which produce gray or beige plaques (1–2 cm) subpleurally in the dorsal border of the caudal lung lobes. Small (1–2 mm), greenish, nodular lesions may also develop. The effect of these lesions in sheep is minor, perhaps because of the predominantly subpleural location. This infection represents the lower end of the pathogenic spectrum for lungworms.

In cats, A abstrusus produces nodular areas of granulomatous pneumonia in the caudal lobes that, if sufficiently generalized, can be clinically significant and occasionally fatal; a notable feature is the hypertrophy and hyperplasia of the smooth muscle in the media of pulmonary arteries and arterioles. The nodules of O osleri, found in the mucous membrane of the trachea and large bronchi, can produce extreme airway irritation and persistent coughing. Capillaria aerophila infection causes chronic tracheitis and bronchitis.

In adult animals not previously exposed to infection, the lesions and pathogenesis are the same as in young animals. However, in adults with some degree of immunity, reexposure to the parasite (eg, husk in adult cattle) can result in different lesions. Despite the immune response, many larvae reach the lungs before they are killed in the terminal bronchioles and alveoli. Larvae that are not killed in the terminal bronchioles may reach the bronchi and cause a bronchitis characterized by marked eosinophilic infiltration of the bronchial walls and greenish yellow exudate in the lumen comprising eosinophils, other inflammatory cells, and parasitic debris. The reaction associated with this process can lead to severe clinical signs if the nodules are numerous and the eosinophilic bronchitis extensive; this is responsible for the reinfection phenomenon.

Clinical Findings

Signs of lungworm infection range from moderate coughing with slightly increased respiratory rates to severe persistent coughing and respiratory distress and even failure. Reduced weight gains, reduced milk yields, and weight loss accompany many infections in cattle, sheep, and goats. Patent subclinical infections can occur in all species.

The most consistent signs in cattle are tachypnea and coughing. Initially, rapid, shallow breathing is accompanied by a cough that is exacerbated by exercise. Respiratory difficulty may ensue, and heavily infected animals stand with their heads stretched forward and mouths open, and drool. The animals become anorectic and rapidly lose condition. Lung sounds are particularly prominent at the bronchial bifurcation. In adult dairy cattle, milk yield drops severely, and abnormal lung sounds are heard over the caudal lobes. The reinfection phenomenon in adult dairy cattle is usually seen in the fall; although less severe than in initial infections, the signs are widespread coughing and tachypnea and a marked drop in milk yield.

The signs in sheep and goats infected with D filaria are similar to those in cattle. Pulmonary signs usually are not associated with M capillaris or P rufescens in sheep, but the former can affect goats similarly to D filaria. D arnfieldi is associated with coughing, tachypnea, and unthriftiness in older horses, but few if any signs in foals or donkeys.

The main clinical sign of M apri in pigs is a persistent cough that may become paroxysmal.

Coughing and dyspnea occur in cats and dogs with A abstrusus and O osleri infections, respectively. Fatalities are relatively uncommon with these lungworms, although they do occur in kittens.


Diagnosis is based on clinical signs, epidemiology, presence of first-stage larvae in feces, and necropsy of animals in the same herd or flock. Bronchoscopy and radiography may be helpful. Larvae are not found in the feces of animals in the prepatent or postpatent phases and usually not in the reinfection phenomenon. ELISA tests are available in some laboratories. The test is mainly of use in detecting cattle that have not been exposed rather than as a differential diagnosis tool in acute respiratory disease. In the early stages of an outbreak, larvae may be few in number. First-stage larvae or larvated eggs can be recovered using most fecal flotation techniques with the appropriate salt solutions. Bronchial lavage can reveal D arnfieldi infections in horses. A convenient method for recovering larvae is a modification of the Baermann technique in which large fecal samples (25–30 g) are wrapped in tissue paper or cheese cloth and suspended or placed in water contained in a beaker. The water at the bottom of the beaker is examined for larvae after 4 hr; in heavy infections, larvae may be present within 30 min.

In domestic pets and horses, because of the relative infrequency of infection, diagnosis may be made only after failure of antibiotic therapy to ameliorate the condition. Adults of Dictyocaulus spp and M apri are readily visible in the bronchi during the patent phases of infection. However, examination of smears from bronchial mucus or histologic sections from lesions may be necessary to confirm the diagnosis during other stages of lungworm infection (and also for other lungworms).


Bronchoscopy can be used to detect nodules of O osleri or to collect tracheal washings (dogs and horses) to examine for eggs, larvae, and eosinophils.


Necropsy should include examination of the trachea, particularly at the bifurcation, for O osleri and the lesions they induce.


Several drugs are useful. The benzimidazoles (fenbendazole, oxfendazole, and albendazole) and macrocyclic lactones (ivermectin, doramectin, eprinomectin, and moxidectin) are frequently used in cattle and are effective against all stages of D viviparus. These drugs are also effective against lungworms in sheep, horses, and pigs. Levamisole is used in cattle, sheep, and goats, but treatment may need to be repeated 2 wk later because it is less effective against larvae during the early stages. Fenbendazole and milbemycin have been used successfully in cats for A abstrusus. O osleri in dogs is a problem, but there is evidence that fenbendazole and albendazole are effective if treatment is prolonged. C aerophila in cats is similarly difficult to treat, but three 5-day cycles of levamisole at 9-day intervals have been reported to be successful.

Table 1


Recommended Treatments for Lungworms a




Dictyocaulus viviparus


Ivermectin, doramectin, moxidectin, eprinomectin, fenbendazole, albendazole, levamisole

D filaria

Sheep, goat

Ivermectin, doramectin, moxidectin, eprinomectin, fenbendazole, albendazole, levamisole

D arnfieldi

Horse, donkey

Ivermectin, moxidectin

Metastrongylus apri


Ivermectin, moxidectin, doramectin

Aelurostrongylus abstrusus


Fenbendazole, milbemycin, selamectinb

Oslerus osleri


Fenbendazole, albendazole

Capillaria aerophila


Levamisole, selamectinb

a In severe cases NSAID may also be helpful.

b Anecdotal evidence for efficacy but no published evidence or label recommendations.

Animals at pasture should be moved inside for treatment, and supportive therapy may be needed for complications that can arise in all species.


Lungworm infections in herds or flocks are controlled primarily by vaccination or anthelmintics. Oral vaccines are available in Europe for D viviparus (northeastern areas) and D filaria (southeast). Two doses of irradiated infective larvae are given 4 wk apart at least 2 wk before the start of grazing or exposure to probable infection. Used properly, they prevent clinical disease, but some vaccinated animals may become mildly infected to the extent that larvae are excreted to perpetuate further infection.

Anthelmintic prophylaxis has become feasible with the advent of anthelmintics with prolonged activity (eg, ivermectin, doramectin, moxidectin, eprinomectin). With persistent anthelmintics, 2 or 3 treatments during the grazing season, the timing of which depends on local grazing practice and epidemiology, are effective and may, by disrupting developing infections, stimulate immunity to the parasite. The use of multiple treatments may delay exposure to D viviparus until the animal is adult, when infection (albeit usually less severe) can occur. However, these methods have become popular in that GI parasites are controlled simultaneously.

Other more sporadic infections can be controlled more easily by management, eg, avoidance of grazing horses with donkeys, indoor husbandry of pigs, and by not mixing sheep and goats on the same grazing.