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Lungworm Infection in Animals

(Verminous Bronchitis, Verminous Pneumonia)


Lora Rickard Ballweber

, DVM, DACVM, DEVPC, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University

Reviewed/Revised Oct 2021 | Modified Nov 2022
Topic Resources

Lungworm infection, also known as verminous bronchitis or verminous pneumonia, is an inflammatory disease of the lower respiratory tract caused by a variety of nematodes. Coughing and dyspnea are the most common clinical signs, which can be exacerbated by concomitant bacterial or viral infections. The Baermann technique is used to detect first-stage larvae in fecal samples. In some countries, an ELISA test is available to detect antibodies against Dictyocaulus viviparus; however, interpretation is hampered by persistent titers. Treatment and control of bovine lungworm is achieved primarily via strategic use of anthelmintics, although an orally administered vaccine is available in some countries.

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, llamas, and alpacas

  • D filaria in goats, sheep, llamas, and alpacas

  • D eckerti and D cervi in deer

  • D arnfieldi in donkeys and horses

  • Protostrongylus rufescens and Muellerius capillaris in sheep and goats

  • Metastrongylus apri, M pudendotectus, and M salmi in pigs

  • Oslerus osleri, Crenosoma vulpis, and Eucoleus aerophilus in dogs

  • Aelurostrongylus abstrusus and E aerophilus in cats

Other lungworm infections occur but are less common.

Species of Dictyocaulus belong to the superfamily Trichostrongyloidea and have direct life cycles. E aerophilus belongs to the Trichuroidea and is thought to have a direct life cycle. Other species belong to the Metastrongyloidea superfamily and, except for O osleri, have indirect life cycles. Some nematodes that inhabit the right ventricle and pulmonary circulation, eg, Angiostrongylus vasorum and Dirofilaria immitis, which affect both dogs and cats in certain areas of the world, may be associated with pulmonary disease. Clinical signs relate to a cardiac or pulmonary disease, or a combination of both may occur.

Epidemiology of Lungworm Infection in Animals

Dictyocaulus spp infection of ruminants is the lungworm infection of greatest economic importance. D viviparus infection of cattle occurs in temperate areas with high rainfall or intense irrigation and is the cause of severe outbreaks of parasitic bronchitis (also called husk in Britain, hoose in Ireland) in cattle of all ages.

The lungworm of goats and sheep, D filaria, is comparatively less pathogenic; however, it does cause losses, especially in Mediterranean countries, and it is also recognized as a pathogen in Australia, Europe, and North America. D filaria and D viviparus are less pathogenic in alpacas and llamas, although severe infections can cause coughing, dyspnea, depression, and loss of condition.

D arnfieldi can cause severe coughing in horses and, because patency is unusual in adult horses (but not in donkeys), differential diagnosis with disease due to other respiratory infections can be difficult. M capillaris is prevalent worldwide and, although usually nonpathogenic in sheep, can cause severe clinical signs in goats. Other lungworm infections cause sporadic infections in various animal species in many geographic areas.

Dictyocaulus spp

Adult females in the bronchi of host animals lay larvated eggs that hatch either in the bronchi (D viviparus, D filaria) or quickly in host feces (D arnfieldi) after being coughed up and swallowed. The infective third-stage larvae can develop on pasture within 5–7 days in warm, moist conditions, although typically in summer in temperate northern climates it takes 2–3 weeks. Once larvae are infective, transmission depends primarily on mechanical dispersal away from the fecal pats. Dispersal mechanisms include rain or, in the case of D viviparus and possibly D arnfieldi, during discharge of the sporangia of the fungus Pilobolus. A proportion of infective larvae survive on pasture throughout the winter until the following year, although 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 contribution in some geographic areas. In the case of D arnfieldi, patent infections rarely occur in adult horses (however, they may occur in foals and yearlings), so donkeys are the prime source of pasture contamination for horses. Clinical disease in ruminants usually develops after 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, clinical disease usually occurs during their first season at pasture; however, an increase in the number of older cattle affected has been reported. This is attributed to the efficiency of some prophylactic anthelmintic regimens, which eliminate infection and prevent development of a protective immune response. Introducing nonimmune animals onto contaminated pastures can also result in severe infections. Horses may be infected at any age.

Once infected, adult ruminants generally become immune to further disease; however, some maintain subclinical infections and are a source of further pasture contamination. Occasionally, exposure to an overwhelming number of larvae may cause clinical disease to recur in previously infected adults or groups that have not been exposed to reinfection for >1 year, and in which immunity may have waned. 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 occur between mid June and late July; however, most severe infections generally occur in previously unexposed calves after development of the second generation of infective larvae on pasture between August and early October.

Other Species

Metastrongylus spp in pigs require an earthworm intermediate host; thus, infection occurs only in pigs with access to the outdoors and may become more common in previously less endemic areas as a result of free-range production methods. M capillaris and P rufescens in sheep and goats require slugs or snails as intermediate hosts, which must be eaten for infection to occur. C vulpis is acquired by dogs via ingestion of an infected terrestrial snail or slug intermediate host. A abstrusus is normally acquired by cats after ingestion of a paratenic host such as a bird or rodent that has previously eaten the infected slug or snail intermediate host. Adults of O osleri live in nodules in the trachea of dogs, and larvated eggs laid by adults hatch there. Larvae migrate up the bronchial tree and may pass in the feces; however, these are not active, are often dead or degenerating, and are not an important route of transmission. Infection in domestic dogs is mainly via saliva as the dam cleans its pups. E aerophilus in dogs likely has a direct cycle, with larvated eggs being ingested with food or water.

Pathogenesis of Lungworm Infection in Animals

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. For D viviparus, during the prepatent phase of 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 ingested, in which case the animal may die in the prepatent phase with severe interstitial emphysema and pulmonary edema.

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 lose considerable weight.

If the animal survives until the end of patency (2–3 months for D viviparus), most or all of the adult worms are expelled, and the cellular exudate resolves over the ensuing 4 weeks. Most animals 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; however, it occurs 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.

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 D viviparus 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 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 syndrome.

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; frequently, however, 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 months for some lungworms (M apri and A abstrusus) but can last >2 years (M capillaris). The lesions in pigs with metastrongylosis are a combination of localized bronchitis and bronchiolitis with overinflation of related alveoli, usually at the tips and midway along the diaphragmatic lobes. Associated with the mass of nematodes in the lumen is hypertrophy and hyperplasia of bronchiolar and alveolar duct smooth muscle with marked mucous cell hyperplasia. Near the end of the patent period (as adult worms are killed), gray-green lymphoid nodules (2–4 mm in diameter) 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 in diameter) subpleurally in the dorsal border of the caudal lung lobes. Small (1–2 mm in diameter), 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 that, if sufficiently generalized, can be clinically important and occasionally fatal; a notable feature is the hypertrophy and hyperplasia of the smooth muscle in the media of pulmonary arteries and arterioles, which seems to be irreversible. The nodules of O osleri, found in the mucous membrane of the trachea and large bronchi, can produce extreme airway irritation and persistent coughing. In small breeds of dogs, C vulpis infections result in chronic bronchitis and bronchiolitis. E aerophilus infections in dogs may result in chronic tracheobronchitis Kennel Cough Kennel cough results from inflammation of the trachea. It is a mild, self-limiting disease but may progress to bronchopneumonia in puppies or to chronic bronchitis in debilitated adult or aged... read more .

Clinical Findings of Lungworm Infection in Animals

Clinical 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 production, and weight loss accompany many infections in cattle, sheep, and goats. Patent subclinical infections can occur in all species.

The most consistent clinical 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 production drops severely, and abnormal lung sounds are audible over the caudal lobes. The reinfection phenomenon in adult dairy cattle usually occurs in the fall; although less severe than in initial infections, the clinical signs are widespread coughing and tachypnea and a marked drop in milk production.

The clinical signs in llamas, alpacas, 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; however, the former can affect goats similarly to D filaria. D arnfieldi is associated with coughing, tachypnea, and unthriftiness in older horses and has few if any clinical signs in foals or donkeys.

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

Coughing and dyspnea occur with A abstrusus infections in cats and O osleri or C vulpis infections in dogs. Small-breed dogs and puppies tend to display clinical signs more often with O osleri due to the nodules reducing the already small diameter of the respiratory tract. E aerophilus infections in dogs are usually well tolerated; however, they may cause a persistent cough with bronchovesicular sounds on auscultation. Fatalities are relatively uncommon with these lungworms, although they do occur in young, debilitated, or immunosuppressed cats with A abstrusus.

Diagnosis of Lungworm Infection in Animals

  • Baermann technique the method of choice

  • ELISA to detect antibodies against D viviparus in serum or bulk milk tank samples

  • Baermann technique and ELISA prone to false negatives


On endemic farms, diagnosis of bovine lungworm should be uncomplicated if both clinical signs and epidemiology features of the disease are taken into account. On nonendemic farms. other causes of these clinical signs are usually investigated first ( See table: Some Primary Differential Diagnoses for Bovine Lungworm Disease Some Primary Differential Diagnoses for Bovine Lungworm Disease Some Primary Differential Diagnoses for Bovine Lungworm Disease ). Diagnosis of ruminant lungworm infection is based on appropriate clinical signs during high-risk times of the year, the presence of first-stage larvae in feces, and/or postmortem examination of animals in the same herd or flock. Bronchoscopy and radiography may be helpful.

ELISA tests are available in some countries to detect antibodies against D viviparus, but antibodies are of limited diagnostic value because:

  • they can still be detected for a few months after host elimination of the worms in primary infections, and

  • low or no antibody response will occur on reinfection

Furthermore, the sensitivity of the bulk milk tank ELISA is currently too low for reliable herd-level diagnosis, although strategies to overcome these deficits are being investigated.

Larvae are not found in the feces of animals in the prepatent or postpatent phases and usually not in the reinfection phenomenon (D viviparus). First-stage larvae or larvated eggs (D arnfieldi) can be recovered using most fecal flotation techniques with the appropriate flotation solutions; however, larvae will crenate if allowed to sit for much time on the slide before examination, making identification difficult. The Baermann technique is still the method of choice for larval recovery. A convenient modification places large fecal samples (25–30 g for ruminants) wrapped in tissue paper or cheesecloth and suspended in water contained in a beaker. The water at the bottom of the beaker is examined for larvae after 4 hours; in heavy infections, larvae may be present within 30 minutes. Samples must be kept refrigerated and processed rapidly because 80% of D viviparus larvae will die within 48 hours at room temperature and 20% will die within 24 hours of sampling even when refrigerated. Bronchial lavage can reveal larvae and/or larvated eggs and is, probably, underused; it is the primary detection method for D arnfieldi infections in horses.

In companion animals, detection of first-stage larvae in the feces, either on flotation or with the Baermann technique, is still the diagnostic technique of choice. However, in dogs, cats, and horses, because of the relative infrequency of infection in many geographic areas, lungworms may not be considered until after failure of antimicrobial treatment to ameliorate the presumed bacterial 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.

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

Treatment of Lungworm Infection in Animals

  • Broad-spectrum anthelmintics

  • Antimicrobials for secondary bacterial infections

  • Anti-inflammatory drugs as needed


Several anthelmintics are useful to treat lungworms ( see Table: Anthelmintic Treatments for Lungworms a Anthelmintic Treatments for Lungworms a Anthelmintic Treatments for Lungworms <sup >a</sup> ). 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. Topical formulations containing moxidectin, selamectin, or emodepside and oral fenbendazole have been used successfully in cats for A abstrusus. Treating O osleri in dogs is difficult; however, there is evidence that fenbendazole and ivermectin are effective if treatment is prolonged (fenbendazole). E aerophilus in dogs and cats is similarly difficult to treat; however, success has been reported with ivermectin, fenbendazole, or selamectin.

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

Control of Lungworm Infection in Animals

Lungworm infections in herds or flocks are controlled primarily by vaccination or anthelmintics. Oral vaccines are available in Europe for D viviparus. Two doses of irradiated infective larvae are administered 4 weeks apart, with the second dose given at least 2 weeks before the start of grazing or exposure to probable infection. Used properly, they prevent clinical disease; however, some vaccinated animals may become mildly infected to the extent that larvae are excreted, adding to pasture contamination and further infections.

Anthelmintic prophylaxis has become the mainstay of bovine lungworm control and has the added benefit of controlling GI nematodes as well in areas where anthelmintic resistance of GI nematodes has not become problematic. With persistent anthelmintics (eg, ivermectin, doramectin, moxidectin, eprinomectin), two or three 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, however, may delay immunity to D viviparus until the animal is an adult, when infection (albeit usually less severe) can occur.

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

Key Points

  • Bovine lungworm disease occurs most often in temperate areas with high rainfall or intense irrigation.

  • Clinical disease is most evident in young, nonimmune stock (< 12 months) or in previously naive yearling or adult cattle.

  • Of the three major species of small ruminant lungworms, M capillaris appears to be the most common.

  • Cats and dogs with access to outdoor environments are at greatest risk of acquiring lungworms.

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