Lungworms are parasitic nematodes primarily of the superfamilies Trichostrongyloidea and Metastrongyloidea that infest the lungs and respiratory tract of various vertebrate hosts, primarily mammals, causing inflammatory conditions such as verminous bronchitis and pneumonia. These helminths reside in the bronchi, bronchioles, and lung parenchyma, where they mature, reproduce, and elicit immune responses that damage host tissues.[1][2]They affect a diverse array of animals, including livestock such as cattle, sheep, goats, and pigs; companion animals like dogs and cats; and wildlife including foxes, coyotes, and pinnipeds. Notable species include Dictyocaulus viviparus in cattle, which can cause severe outbreaks in temperate regions; Angiostrongylus vasorum and Crenosoma vulpis in dogs, leading to cardiovascular and respiratory issues; and Aelurostrongylus abstrusus in cats, often resulting in chronic respiratory disease.Life cycles vary: direct cycles occur in some Dictyocaulus species, where larvae develop in the environment and are ingested directly, while others, like A. vasorum and A. abstrusus, require intermediate hosts such as snails or slugs, or paratenic hosts like rodents and birds.[1][2][3][4][5]Infections typically present with clinical signs including persistent coughing, dyspnea, wheezing, exercise intolerance, and weight loss, often exacerbated by secondary bacterial or viral infections. In livestock, lungworm disease poses significant economic challenges through reduced productivity, such as decreased milk yield and weight gain in ruminants; in companion animals, it can lead to life-threatening complications if untreated, though many cases are subclinical.Prevalence is higher in humid, temperate climates worldwide, with emerging concerns about zoonotic potential in species like Angiostrongylus cantonensis, which can cause eosinophilic meningitis in humans, with recent spread in regions such as the United States as of 2025.[1][3][4][5][6]
Overview and Classification
Definition and Characteristics
Lungworms are parasitic nematodes belonging to the order Strongylida, particularly the superfamily Metastrongyloidea, that primarily infest the lungs and airways of vertebrate hosts, resulting in respiratory conditions such as verminous bronchitis and pneumonia.[7][1] These parasites are characterized by their elongated, thread-like bodies, which enable them to navigate and reside within the bronchial tree.[1] They exhibit dioecious reproduction, with distinct male and female adults, and their infective stage is typically the first-stage larva (L1), which is resilient in the external environment before host invasion.[8]Biologically, lungworms are adapted to the pulmonary environment, where adults lodge in the bronchi and bronchioles, causing mechanical damage through migration and eliciting host inflammatory responses that lead to tissue injury and impaired gas exchange.[1] For certain species, such as Angiostrongylus cantonensis in aberrant hosts like humans, larval migration can result in eosinophilic meningitis, highlighting their pathological versatility beyond primary respiratory effects.[9]The disease burden imposed by lungworms includes substantial economic losses in agriculture, such as reduced milk yield and weight gain in infected ruminants, with outbreak costs estimated at €170–300 per affected animal in dairy herds.[10][11] Furthermore, certain species carry zoonotic potential, posing public health risks through accidental humaninfection and contributing to emerging infectious diseases.[9] Major groups include members of the Metastrongyloidea and Trichostrongyloidea superfamilies.[1]
Taxonomy and Major Groups
Lungworms are parasitic nematodes classified within the phylum Nematoda, class Chromadorea, and order Strongylida. This order encompasses a diverse array of gastrointestinal and respiratory parasites, with lungworms primarily belonging to the superfamilies Trichostrongyloidea and Metastrongyloidea, though some are found in Trichuroidea. The Trichostrongyloidea includes genera with direct life cycles, such as Dictyocaulus, which parasitizes the bronchi of ruminants (e.g., D. viviparus in cattle and deer, D. filaria in sheep and goats) and equids (D. arnfieldi in horses and donkeys). In contrast, the Metastrongyloidea predominantly features indirect life cycles involving intermediate hosts like mollusks or arthropods, encompassing genera such as Angiostrongylus (e.g., A. vasorum in canids and felids, A. cantonensis in rodents and occasionally humans), Aelurostrongylus (A. abstrusus in cats), Metastrongylus (e.g., M. apri in pigs), and Crenosoma (C. vulpis in dogs). Additionally, the family Protostrongylidae within Metastrongyloidea includes lesser-known species like those in Varestrongylus and Protostrongylus, which infect the lungs of wild ungulates such as caribou (Varestrongylus eleguneniensis), moose (V. alces), and sheep (P. rufescens), often with complex indirect cycles utilizing gastropod intermediates.[1][12][13][14][15]The evolutionary history of lungworms reflects adaptations from ancestral gut-dwelling parasites in the Strongylida, which likely originated from free-living rhabditid nematodes during the late Devonian or early Carboniferous periods. Multigene phylogenetic analyses using ribosomal DNA markers (e.g., 18S and 28S rRNA genes) indicate that the Metastrongylina suborder, comprising most lungworms, forms a monophyletic clade specialized for pulmonary habitats in mammalian hosts, diverging from gastrointestinal lineages through shifts in predilection sites and enhanced host specificity. These genetic markers reveal host-parasite co-evolution, with clades showing strict associations to particular host groups, such as ungulates or carnivores, driven by selective pressures for respiratory migration and immune evasion. Transitional forms, like rhabdiasoid nematodes, illustrate intermediate stages between intestinal and lung parasitism, underscoring the gradual pulmonary specialization.[16]
Species and Hosts
Lungworms in Domestic Animals
Lungworms represent a significant parasitic concern in domestic animals, particularly in livestock, equines, and companion animals like dogs and cats, where they primarily affect the respiratory system through host-specific infections. These nematodes belong to various genera within the superfamily Metastrongyloidea, with transmission often occurring via direct ingestion of infective larvae in contaminated pasture for ruminants or indirectly through intermediate hosts such as snails and slugs for canids and felids.[1][17]In cattle, Dictyocaulus viviparus, commonly known as the bovine lungworm, is the primary species responsible for infections, leading to conditions like husk disease; it exhibits high host specificity to ruminants and is acquired through grazing on pastures contaminated with infective third-stage larvae. Prevalence in European cattle herds varies but can reach 20-30% in temperate regions such as northern Germany, with young calves under one year being at highest risk due to immature immunity and increased outdoor exposure.[18][19]Sheep and goats are commonly infected by Muellerius capillaris, a protostrongylid lungworm that resides in the lung parenchyma and is highly prevalent worldwide, particularly in small ruminants kept on pasture; infections occur indirectly via ingestion of larvae-encysted mollusks like snails. Studies report prevalences of 30-60% in goat populations in regions like Europe and the Middle East, with higher rates in young animals and those with access to damp environments that favor intermediate hosts.[1][19][20]Domestic pigs are affected by Metastrongylus spp., including M. apri, M. elongatus, M. pudendotectus, and M. salmi, which inhabit the bronchi and bronchioles; transmission occurs indirectly through ingestion of infective larvae in earthworms as intermediate hosts. These lungworms are common in outdoor or free-range pigs worldwide, with prevalences up to 50-80% reported in some European and North American herds, though less common in intensive systems due to reduced earthworm exposure.[1][21]Equines, including horses and donkeys, are affected by Dictyocaulus arnfieldi, which shows strong host preference for donkeys but can spill over to horses through shared grazing; donkeys serve as reservoirs, with infections acquired by ingesting free-living larvae on pasture. Prevalence is notably higher in donkeys, around 30% in the UK, compared to lower rates (under 10%) in horses, influenced by co-grazing practices and age, with younger equines more susceptible.[22][23]In dogs, Angiostrongylus vasorum, often called French heartworm, is an emerging metastrongylid parasite targeting the pulmonary arteries and right ventricle, transmitted indirectly through predation on gastropod intermediates or paratenic hosts like frogs; it displays specificity to canids but is increasingly reported in domestic dogs across Europe. Prevalence in European dog populations ranges from 1-5%, with higher risks in young dogs and those in rural or outdoor settings in endemic areas like the UK and France. While most domestic lungworms pose low zoonotic risk, A. vasorum has garnered attention for its expanding range, though human infections remain unconfirmed.[24][25][26]Cats are primarily hosts to Aelurostrongylus abstrusus, the feline lungworm, which inhabits the bronchioles and alveolar spaces and is acquired via ingestion of infected intermediate hosts such as birds, rodents, or mollusks; it exhibits high specificity to felids. This cosmopolitan parasite shows prevalences of 1-10% in outdoor cats across Europe, with elevated rates in hunting-prone or free-roaming populations in temperate climates.[27][28][29]
Lungworms in Wildlife and Humans
Lungworms pose significant risks in wildlife ecosystems, serving as reservoirs for zoonotic transmission to humans. Angiostrongylus cantonensis, commonly known as the rat lungworm, uses rats as its definitive hosts, where adult worms reside in the pulmonary arteries and produce larvae that are shed in feces.[30] In Florida, recent detections in 2025 highlight its expansion into novel wildlife hosts, including the endangered Florida burrowing owl (Athene cunicularia floridana), indicating urban adaptation and potential for broader ecological impact.[31] Other metastrongylid lungworms, such as Metastrongylus spp., infect wild pigs (Sus scrofa), with prevalence rates exceeding 70% in some populations, leading to respiratory compromise and increased mortality in piglets.[32] Similarly, Parelaphostrongylus spp., including P. tenuis (brainworm), parasitize cervids like white-tailed deer (Odocoileus virginianus), elk (Cervus canadensis), and moose (Alces alces), where larvae migrate through neural tissues, though definitive hosts often remain asymptomatic.[33] These wildlife reservoirs facilitate environmental contamination with infective larvae, amplifying spillover risks.Human infections with lungworms are predominantly accidental and zoonotic, with A. cantonensisaccounting for the majority of cases through neuroangiostrongyliasis, a form of eosinophilic meningitis resulting from larval migration into the central nervous system.[30] Rare abdominal infections occur with Angiostrongylus costaricensis, which typically targets rodents but has caused documented enteritis in humans via larval invasion of intestinal walls, with over 190 cases reported across the Americas since its discovery.[34] Globally, more than 7,000 human cases of A. cantonensisinfection have been recorded, concentrated in Southeast Asia and the Pacific Islands, with rising trends driven by urbanization and habitat changes.[35]Transmission to humans occurs primarily through inadvertent ingestion of third-stage larvae in intermediate hosts like snails and slugs, or on contaminated fresh produce such as unwashed vegetables.[36] Paratenic hosts, including freshwater prawns and frogs, can also harbor larvae, though direct consumption of undercooked mollusks remains the dominant route. In 2025, the parasite's spread to Italy was confirmed in rats and gastropods near Naples, marking its establishment in the Mediterranean and raising concerns for European travelers.[35] Concurrently, climate-driven increases in Australia, linked to higher rainfall and temperatures favoring snail proliferation, have spurred a surge in infections, with canine cases peaking at 32 in 2022 in eastern regions and human risks escalating.[37] These developments underscore the role of environmental factors in amplifying zoonotic potential from wildlife.
Lifecycle and Transmission
General Lifecycle Stages
Lungworms primarily of the superfamily Metastrongyloidea, though notable species like Dictyocaulus viviparus belong to Trichostrongyloidea, exhibit a lifecycle characterized by larval stages that alternate between the host's respiratory tract and the external environment. For many lungworms such as Dictyocaulus spp., adult worms reside in the bronchi and bronchioles of the lungs, where females lay larvated eggs containing first-stage larvae (L1). These eggs typically hatch into L1 larvae either directly in the bronchi or, after being coughed up, swallowed, and passed in the feces. For others like Angiostrongylus vasorum, adults inhabit the pulmonary arteries, producing eggs that lodge in lung capillaries and hatch into L1 larvae there. The L1 larvae are then excreted in the host's dung, initiating environmental development.[1]In the external environment, the L1 larvae molt through second-stage (L2) to third-stage infective larvae (L3), which are ensheathed and capable of infecting new hosts. These L3 develop on pasture or in feces under suitable conditions, often aided by dispersal mechanisms such as rainfall or fungi like Pilobolus spp. Upon ingestion by a suitable host—via contaminated forage or water—the L3 penetrate the intestinal mucosa and migrate through the lymphatic system or bloodstream to the lungs, where they penetrate the alveoli, mature into adults, and establish patency. The migration and maturation process generally takes 3-6 weeks, with the prepatent period varying by species, such as approximately 25 days for Dictyocaulus viviparus in cattle.[1][38][39]Lifecycle patterns differ between direct and indirect types. Direct cycles, common in species such as Dictyocaulus spp., involve no intermediate hosts, with L3 developing freely in the environment and infecting grazing animals directly from contaminated pasture. In contrast, indirect cycles in Metastrongyloidea, like Angiostrongylus vasorum in dogs, require intermediate hosts such as gastropods (slugs or snails) or arthropods, where L3 develop before transmission to the definitive host, sometimes via paratenic hosts like rodents or birds. The overall duration from infection to egg-laying (patency) is typically 4-8 weeks across species.[1][3]Environmental factors critically influence larval viability and transmission. Infective L3 larvae thrive and survive longest—up to several months—in cool, moist conditions, such as overwintering on pasture, but development accelerates in warm, humid settings (5-7 days to L3). Conversely, exposure to heat, dryness, or extreme cold leads to rapid mortality, often within 2-3 weeks in summer conditions, limiting outbreaks to favorable climates or seasons.[1][38][40]
Transmission Routes and Variations
Lungworms are primarily transmitted through the oral ingestion of third-stage larvae (L3), which occurs via direct or indirect routes depending on the species. In direct cycles, such as that of Dictyocaulus viviparus in cattle, infective L3 larvae develop on contaminated pastures from eggs and first-stage larvae (L1) excreted in feces, and are ingested during grazing without requiring an intermediate host.[39][41] Indirect cycles, common in metastrongyloid lungworms like Angiostrongylus vasorum and Aelurostrongylus abstrusus, involve development of L1 to L3 within intermediate hosts before ingestion by the definitive host.[24][1] Transplacental transmission is rare and documented in select species, such as Protostrongylus spp. in sheep and certain cetacean lungworms, where larvae cross the placenta to infect fetuses.[42][43]Transmission variations reflect host-specific adaptations and environmental interactions. For D. viviparus, pasture contamination drives seasonal outbreaks in first-grazing cattle through direct larval uptake from herbage.[44] In contrast, A. vasorum in dogs spreads via ingestion of L3-laden gastropods or paratenic hosts like frogs and birds, often in damp habitats favoring snail proliferation.[26] Human infections with Angiostrongylus cantonensis typically result from consuming raw mollusks, contaminated vegetables bearing slug/snail slime, or paratenic hosts such as freshwater prawns, highlighting inadvertent dietary exposure in endemic areas.[36][45]Gastropods, including snails and slugs, serve as primary intermediate hosts for most metastrongyloidea lungworms, where L1 larvae ingested from feces molt to infective L3 within their tissues.[46] Paratenic hosts, such as amphibians (e.g., frogs), reptiles, birds, rodents, and crustaceans, transport L3 without further development, amplifying transmission by bridging ecological gaps between intermediate and definitive hosts.[1]Several factors modulate transmission dynamics. Seasonality peaks in late summer to autumn for D. viviparus in cattle, aligning with optimal larval development on pastures during warmer, moist conditions.[47] Herd-level immunity develops in cattle after initial exposure in the first grazing season, reducing susceptibility in subsequent years, though introducing immunologically naive replacements can lower thresholds and trigger outbreaks.[41][48] Climate change exacerbates transmission by extending larval viability through warmer temperatures, as studies indicate higher survival and faster development of D. viviparus L3 above 1.4°C, potentially shifting outbreak timing earlier in regions like northern Europe.[49][50]
Clinical Manifestations
Symptoms in Animals
Lungworm infections in animals primarily manifest through respiratory signs, which arise from the presence of adult worms in the bronchi and bronchioles, as well as the migration and hatching of larvae in pulmonary tissues. Common symptoms include coughing, dyspnea, and nasal discharge, which can become severe in cases of heavy infection burdens. For instance, in cattle infected with Dictyocaulus viviparus, the condition known as "husk" or parasitic bronchitis leads to pronounced coughing, serous to mucopurulent nasal discharge, tachypnea, abdominal breathing, and pyrexia, often exacerbated during the patent phase when adult worms are shedding larvae.[51][47]Systemic effects of lungworm infections extend beyond the respiratory tract, contributing to overall debilitation and increased susceptibility to secondary complications. Infected animals frequently experience weight loss, reduced feed intake, and diminished productivity, such as lower milk yield in dairy cattle.[52] Heavy infestations can predispose hosts to secondary bacterial pneumonia by damaging airway epithelium and impairing mucociliary clearance, allowing opportunistic pathogens to colonize the lungs.[53] In dogs harboring Angiostrongylus vasorum, systemic involvement is particularly notable, with bleeding disorders manifesting as epistaxis, hemoptysis, petechiae, ecchymoses, or more severe hemorrhages into body cavities, alongside neurological signs like paresis, ataxia, seizures, or acute lumbar pain.[54][55]Symptoms vary by host species and parasite, reflecting differences in lifecycle adaptation and host immunity. In horses infected with Dictyocaulus arnfieldi, clinical presentation typically involves a chronic, dry cough and occasional mucoid nasal discharge, often without detectable first-stage larvae (L1) in feces due to the non-patent nature of the infection in this host.[56][57] Conversely, cats with Aelurostrongylus abstrusus infections may remain asymptomatic or exhibit only mild respiratory signs, such as occasional coughing, sneezing, dyspnea, or mucopurulent nasal discharge, particularly in low-burden cases; severe manifestations like open-mouth breathing or weight loss occur infrequently and are linked to higher worm loads or concurrent stressors.[58][59]The pathophysiology of these symptoms is driven by larval migration and the presence of adult worms in the respiratory system. Following ingestion of infective third-stage larvae (L3), the parasites penetrate the intestinal wall and migrate via lymphatic or vascular routes to the lungs, where developing larvae elicit hemorrhage, eosinophilicinflammation, and granuloma formation through tissue disruption and immune activation.[60][61] Hatching eggs and first-stage larvae further provoke alveolar and bronchial inflammation, while adult nematodes physically obstruct airways, exacerbate mucus production, and promote fibrotic changes, culminating in impaired gas exchange and the observed clinical signs.[62]
Symptoms in Humans
Human infections with lungworms, particularly the zoonotic nematode Angiostrongylus cantonensis, primarily manifest as neuroangiostrongyliasis, characterized by eosinophilic meningitis due to larval migration in the central nervous system. The most common symptoms include severe headache, neck stiffness, paresthesia (often described as tingling or burning sensations), vomiting, and low-grade fever, typically appearing 1-3 weeks after ingestion of infective larvae.[63] These neurological symptoms arise from the inflammatory response to the parasites in the meninges and brain tissue, mimicking bacterial meningitis but distinguished by peripheral eosinophilia.[64]The incubation period for A. cantonensisinfection averages 1-3 weeks but can range from 1 day to more than 6 weeks, depending on the larval load and host factors.[63] Symptoms generally persist for 2-8 weeks, with most cases resolving spontaneously, though severe infections may progress to encephalitis, cranial nerve palsies, or ocular involvement, such as larval migration into the eye leading to vision impairment.[65] Potential long-term complications include persistent neurological deficits, such as chronic headaches or sensory disturbances.[64]Rare human infections with the lungworm Eucoleus aerophilus (syn. Capillaria aerophila) have been reported, primarily causing respiratory symptoms such as coughing, fever, bronchitis, dyspnea, and blood in the saliva, often accompanied by peripheral eosinophilia. These cases are typically mild but can mimic chronic bronchitis or other pulmonary conditions.[66]In recent years, particularly through 2025, there have been increased reports of pediatric cases in eastern Australia, attributed to climate-driven proliferation of intermediate snail hosts facilitated by warmer temperatures and higher rainfall.[67] Children may experience more pronounced symptoms, including higher rates of fever and cranial nerve involvement compared to adults.[68]
Diagnosis
Methods in Veterinary Medicine
Diagnosis of lungworm infections in animals typically follows the observation of respiratory symptoms, such as coughing and dyspnea, and relies on a combination of parasitological, imaging, and molecular techniques to detect larvae, adults, or associated pathological changes.[1]Fecal examination remains a cornerstone of veterinary diagnosis for lungworms, particularly for detecting first-stage larvae (L1). The Baermann funnel technique is the gold standard for identifying L1 larvae of Dictyocaulus viviparus in ruminants, as it exploits the larvae's migratory behavior through a warm water medium to concentrate them for microscopic examination.[1][39] For cases with low larval burdens, such as in Aelurostrongylus abstrusus infections in cats, fecal flotation with centrifugation or sedimentation can enhance sensitivity, while real-time PCR on fecal samples provides species-specific identification and quantification, especially useful for mixed infections.[69][54]Imaging modalities aid in visualizing lung pathology and confirming the presence of adult worms. Thoracic radiography often reveals alveolar or interstitial patterns indicative of lung consolidation or verminous pneumonia in affected animals, while ultrasound can detect pleural effusions or dilated pulmonary arteries in canineAngiostrongylus vasorum cases.[1][70]Bronchoscopy or endoscopy is particularly valuable for direct visualization of adult worms or nodular lesions in the trachea and bronchi, as seen in Oslerus osleri infections in dogs.[71][72]Serological and molecular assays complement fecal and imaging methods, especially for prepatent infections. Antigen-detection tests, such as the Angio Detect™ kit, offer rapid in-clinic diagnosis of A. vasorum in dogs with 97.1% sensitivity and 98.9% specificity by identifying circulating antigens in serum.[73] Additionally, multiplex quantitative PCR assays enable molecular identification of multiple lungworm species, including A. vasorum and Crenosoma vulpis, in fecal or bronchoalveolar lavage samples, facilitating early detection in mixed infections.[74][54]Diagnostic challenges arise from the biology of lungworms, including intermittent larval shedding in feces, which can lead to false-negative results even with repeated sampling.[75] Early-stage infections prior to patency further increase the risk of missed diagnoses, necessitating integrated approaches combining multiple tests for reliable confirmation.[27][76]
Methods in Human Medicine
Diagnosis of human angiostrongyliasis, caused primarily by Angiostrongylus cantonensis, relies on a combination of clinical history, laboratory tests, and imaging, as definitive identification of larvae in cerebrospinal fluid (CSF) is rare due to low parasite numbers.[77] A presumptive diagnosis is often made in patients presenting with symptoms of eosinophilic meningitis, such as headache and neck stiffness, alongside a history of travel to or residence in endemic areas like Southeast Asia, the Pacific Islands, or parts of the Americas, and consumption of raw or undercooked mollusks (e.g., snails or slugs) or contaminated produce.[78] This exposure history is crucial, as it supports suspicion in up to 80-90% of confirmed cases in outbreak settings.[64]Cerebrospinal fluid analysis via lumbar puncture is the cornerstone of diagnosis, typically revealing eosinophilic pleocytosis with greater than 10% eosinophils, alongside elevated protein levels (often 50-500 mg/dL) and normal or mildly low glucose.[77] Eosinophilia in CSF, present in over 90% of cases, distinguishes angiostrongyliasis from bacterial or viral meningitis.[78] Polymerase chain reaction (PCR) testing of CSF for A. cantonensis DNA provides confirmatory evidence, with real-time PCR assays achieving sensitivities of 80-100% in eosinophilic meningitis patients when larvae are present.[79] Larvae or characteristic tracks may occasionally be visualized microscopically in CSF, though this occurs in fewer than 5% of cases.[64]Serological tests, performed on blood or CSF, detect antibodies against A. cantonensis antigens and serve as a non-invasive adjunct, particularly useful in early or mild infections where CSF eosinophilia may be absent.[80] Enzyme-linked immunosorbent assay (ELISA) and Western blot targeting 29- or 31-kDa antigens offer high specificity (95-100%) and sensitivity (up to 90%), with ELISA being the most widely available.[81] These assays are especially valuable in non-endemic regions for imported cases.[82]Imaging modalities like magnetic resonance imaging (MRI) or computed tomography (CT) support diagnosis by revealing non-specific signs of meningitis, such as leptomeningeal enhancement, brainstem involvement, or hydrocephalus in severe cases, but they do not confirm etiology.[64] MRI is preferred for its sensitivity in detecting meningeal inflammation, showing linear or nodular enhancements in 70-80% of symptomatic patients.[83]As of 2025, advancements in molecular diagnostics include a more sensitive real-time PCRassay for A. cantonensis DNA in CSF, enabling earlier detection and reducing reliance on invasive sampling in resource-limited settings; preliminary studies also explore PCR adaptation for blood samples to improve non-invasive options, though CSF remains the gold standard.[84][85]Rare human infections with other lungworms, such as Eucoleus aerophilus, which causes pulmonary capillariasis, are diagnosed primarily through coproscopic examination of feces or sputum for characteristic eggs, often using flotation or sedimentation techniques; molecular confirmation via PCR may be used in suspected cases, though human reports remain sporadic and require differentiation from animal-derived infections.[86]
Antiparasitic treatments for lungworm infections primarily involve anthelmintic drugs tailored to the host species and the specific lungworm involved, such as Dictyocaulus viviparus in ruminants or Angiostrongylus vasorum in dogs.[1] In veterinary medicine, macrocyclic lactones like ivermectin and moxidectin are commonly used for treating Dictyocaulus infections in cattle, with ivermectin administered at 0.2 mg/kg orally or subcutaneously achieving high efficacy against adult and larval stages.[87] Similarly, moxidectin at a single subcutaneous dose of 0.2 mg/kg provides over 95% reduction in lungworm burdens in cattle, demonstrating persistent efficacy for up to several weeks post-treatment.[88] For ruminants, benzimidazoles such as fenbendazole (5-10 mg/kg orally as a single dose) and levamisole (7.5 mg/kg orally or subcutaneously) are effective alternatives against Dictyocaulus species, particularly in sheep and goats where they target both gastrointestinal and pulmonary nematodes.[89][90]In companion animals, milbemycin oxime is used for Angiostrongylus vasorum in dogs; for treatment, it is administered at 0.5 mg/kg orally weekly for 4 weeks to eliminate adults and larvae, while monthly dosing prevents infection by reducing immature adult stages with efficacy rates exceeding 85% in experimental models.[87][54] For cats infected with Aelurostrongylus abstrusus, milbemycin oxime at 0.5 mg/kg orally, often combined with praziquantel, effectively eliminates larvae and adults, with repeated dosing recommended for heavy infections.[87][58] Species-specific considerations are critical; for instance, while ivermectin is highly effective against Dictyocaulus arnfieldi in horses at 0.2 mg/kg orally, its use may yield lower efficacy in some equine populations, prompting preference for moxidectin at 0.4 mg/kg orally.[87][91]For human infections, primarily caused by Angiostrongylus cantonensis, anthelmintics like albendazole (400 mg twice daily for 2-3 weeks) or mebendazole (100 mg twice daily for 5 days) are available but controversial due to the risk of severe inflammation from dying larvae, often requiring concurrent corticosteroids; treatment is not always recommended for mild or asymptomatic cases.[92]Anthelmintic resistance in lungworms, particularly to macrocyclic lactones in livestockspecies like Dictyocaulus viviparus, is emerging and monitored through fecal egg count reduction tests, with reports of inefficacy noted as of 2024. Recent studies (as of 2024) have reported potential resistance to ivermectin and moxidectin in D. viviparus, emphasizing the need for efficacy testing before routine use.[93][94][95]
Supportive and Adjunctive Therapies
Supportive and adjunctive therapies for lungworm infections focus on managing complications such as inflammation from larval migration, secondary bacterial infections, and respiratory distress, rather than directly targeting the parasites. In veterinary medicine, these interventions are often tailored to the severity of clinical signs in affected animals, including dogs and livestock. For instance, corticosteroids like prednisone or dexamethasone are administered to reduce inflammation associated with larval migration in the lungs and other tissues. In dogs infected with Angiostrongylus vasorum, immunosuppressive doses of corticosteroids, such as prednisolone at approximately 1 mg/kg body weight daily for 14 days, have been used to mitigate severe pulmonary hemorrhage or neurological involvement.[72][54]Additional supportive care in animals includes oxygen therapy for those exhibiting significant respiratory compromise, such as hypoxemia due to pneumonia or bronchial obstruction. Antibiotics are employed to address secondary bacterial infections, particularly in cases of pneumonia complicating the primary parasitic infestation, while bronchodilators may aid in alleviating bronchospasm. In livestock, such as cattle infected with Dictyocaulus viviparus, non-steroidal anti-inflammatory drugs (NSAIDs) and antibiotics provide symptomatic relief during outbreaks, alongside nutritional support to aid recovery in severely affected animals, which may involve supplemental feeding to counteract weight loss and maintain immune function. Post-treatment monitoring is essential, involving serial fecal examinations using techniques like the Baermann method to confirm larval clearance, typically repeated 2-4 weeks after initiating therapy, along with clinical assessments for resolution of symptoms.[3][96][1][97]In humans, primarily affected by Angiostrongylus cantonensis causing eosinophilic meningitis, adjunctive therapies emphasize symptom control and prevention of neurological sequelae. High-dose corticosteroids, such as prednisolone at 60 mg daily for 1-2 weeks, are recommended to reduce inflammation and headache severity, particularly in patients with moderate to severe symptoms. Analgesics like acetaminophen are used for pain management, while serial lumbar punctures serve to relieve elevated cerebrospinal fluid (CSF) pressure and provide diagnostic confirmation through cytological analysis. For cases with low parasite burden, routine anthelmintic use is often avoided to prevent paradoxical worsening of inflammation from dying larvae, favoring supportive measures alone.[98][99]
Prevention and Control
Strategies for Animals
Prophylactic measures against lungworm infections in domestic animals primarily rely on strategic anthelmintic treatments to reduce larval burdens and prevent clinical disease. In cattle, pour-on formulations of ivermectin are commonly administered at turnout or early in the grazing season, with persistent activity providing protection against Dictyocaulus viviparus for up to 28 days, often followed by one or two additional doses during the season to cover high-risk periods.[1][100] Similarly, other macrocyclic lactones like doramectin or moxidectin offer extended efficacy, allowing for targeted dosing rather than routine monthly applications to minimize resistance risks.[101] Pasture management complements these treatments through rotational grazing, where livestock are moved to clean pastures every one to four weeks to dilute infective larvae and break the lifecycle, with shorter intervals recommended for lungworm control; this is particularly effective in first-season calves.[102][103]Biosecurity protocols are essential to prevent introduction of infected animals into herds or flocks. Quarantine of new livestock for 21 to 30 days, combined with broad-spectrum anthelmintic treatment upon arrival, helps eliminate potential carriers of lungworm larvae before integration.[104][105] For species like dogs susceptible to Angiostrongylus vasorum, controlling intermediate hosts such as snails in communal areas like parks involves removing moist debris, applying barriers, and regular environmental sanitation to reduce exposure opportunities.[3][106]Ongoing monitoring through seasonal fecal examinations enables early detection in high-risk groups, such as young grazing cattle. The Baermann technique is the standard method to identify first-stage larvae in fresh fecal samples, recommended for herds with a history of infection during spring and autumn peaks.[41][1]Vaccination provides another layer of prevention, particularly in Europe where the irradiated larval vaccine Dictol (also known as Huskvac) is used for D. viviparus in calves; it involves two oral doses four weeks apart, administered before turnout to induce protective immunity without causing disease.[107]In equine facilities, integrated pest management has emerged as a key strategy, incorporating fecal egg count-directed deworming with ivermectin or moxidectin alongside separated pastures to curb transmission of Dictyocaulus arnfieldi linked to mixed grazing with donkeys.[108][109]
Public Health and Zoonotic Prevention
Public health measures to mitigate human exposure to zoonotic lungworms, particularly Angiostrongylus cantonensis (rat lungworm), focus on interrupting transmission from environmental reservoirs to prevent neuroangiostrongyliasis, a form of eosinophilic meningitis in humans.[110] These strategies emphasize personal protective behaviors, community-level interventions, and regulatory oversight, as humans acquire the infection accidentally by ingesting larvae in contaminated food or water rather than through direct person-to-person spread.[64]Food safety practices are foundational to prevention, with recommendations to avoid consuming raw or undercooked intermediate hosts such as snails, slugs, freshwater shrimp, land crabs, prawns, frogs, or monitor lizards, which may harbor infective larvae.[111] Produce, especially leafy greens and salads, should be thoroughly washed under running potable water to remove potential snail slime containing larvae, and cooking or freezing such items is advised to kill parasites.[64] In endemic areas like Southeast Asia and the Pacific, travelers and residents are urged to refrain from eating raw intermediate hosts or unwashed produce from local markets.[112]Vector control efforts target the reduction of snail, slug, and rodent populations in human environments to limit parasite circulation. Effective methods include using traps, barriers, and pesticide baits around homes, gardens, and water sources, as well as rodent-proofing structures to prevent access.[65] Public campaigns in high-risk regions, such as Hawaii's $1 million initiative launched in 2017, promote community-wide snail and rat reduction through education on habitat modification and integrated pest management, significantly raising awareness and reducing exposure risks.[113] Similar efforts in Australia, including fact sheets from New South WalesHealth, encourage residents to eliminate mollusks from yards and report sightings to local authorities.[114]Surveillance systems play a critical role in early detection and response, with confirmed cases of neuroangiostrongyliasis required to be reported to public health authorities for investigation and contact tracing.[64] In Hawaii, the Department of Health maintains active monitoring, documenting three cases in 2025 (as of October 2025) and seven in 2024, and disseminates educational materials like posters and rack cards at airports and community sites to track and contain outbreaks.[115]Travel advisories from health organizations warn visitors to Southeast Asia and the Pacific Basin to adhere to food hygiene practices, highlighting the parasite's endemicity in these regions.[112]As of 2025, prevention strategies increasingly incorporate climate adaptation due to warming temperatures expanding suitable habitats for A. cantonensis vectors, particularly in urban settings. Guidelines for urban gardening, such as those promoted in Hawaii through school and community networks, recommend elevating plants, using mulch barriers against slugs, and regular inspections to minimize mollusk habitats amid rising humidity and rainfall.[37][116]For other zoonotic lungworms like Eucoleus aerophilus (formerly Capillaria aerophila), which can cause respiratory infections in humans through ingestion of eggs from contaminated soil, water, or undercooked meat from infected animals, prevention includes thorough handwashing after soil contact, proper cooking of wild game or petmeat, and regular deworming of companion animals to reduce environmental contamination.[1][117]
Epidemiology
Global Distribution and Prevalence
Lungworm infections exhibit distinct geographic patterns influenced by host distribution and environmental conditions. Dictyocaulus viviparus, the primary lungworm affecting cattle, is widespread in temperate regions of Europe and North America, where prevalence in cattle herds varies widely, often exceeding 40% in first-season grazers depending on grazing practices and climate.[44] In contrast, Angiostrongylus vasorum, a metastrongylid lungworm in dogs, has established foci across Europe, with serological prevalence in canine populations varying from 1% to 5% in endemic areas such as the United Kingdom, Spain, and Portugal.[25] These patterns reflect the parasite's reliance on intermediate hosts like slugs and snails, which thrive in moist, temperate environments.Zoonotic lungworm species, particularly Angiostrongylus cantonensis (rat lungworm), are concentrated in hotspots within the Asia-Pacific region, where human incidence can reach up to 2-3 cases per 100,000 population annually in endemic areas of Thailand.[118] Prevalence remains low in the Americas and Africa, with sporadic reports linked to introduced populations rather than established endemic cycles.[64]Among animal hosts, lungworm infections are notably high in young ruminants within grazing systems, where prevalence often surpasses 50% during the first grazing season due to direct life cycle transmission via contaminated pasture. In companion animals, prevalence is more variable, typically ranging from 1% to 5% in dog populations across Europe, influenced by access to outdoor environments and proximity to wildlife reservoirs like foxes.[119]Key factors shaping global distribution include favorable temperate climates that enhance larval survival and development in free-living stages, as seen with Dictyocaulus species in cooler, humid zones.[120] Additionally, globalization through animal trade and movement facilitates parasite spread, enabling establishment in new regions beyond native ranges.[121]
Recent Trends and Emerging Issues
In recent years, the epidemiology of lungworm infections has shown notable shifts, particularly with the expansion of Angiostrongylus cantonensis, the rat lungworm, into new regions of Europe. In 2025, detections of A. cantonensis were reported in rats and gastropods from the Campania region in southern Italy, indicating a broadening distribution across the European mainland following prior findings in Spain.[35] This emergence highlights the parasite's potential for zoonotic transmission through contaminated produce or environmental exposure, prompting calls for enhanced monitoring in Mediterranean areas.Climate change is influencing lungworm dynamics by altering environmental conditions favorable to larval survival. A 2025 study from the University of Sydney linked warmer temperatures and increased rainfall in eastern Australia to extended viability of A. cantonensis larvae in intermediate hosts like snails and slugs, correlating with a surge in neural angiostrongyliasis cases in dogs and humans.[37] These climatic drivers have heightened transmission risks, particularly during wet seasons, and are projected to expand endemic zones in subtropical regions.In veterinary contexts, challenges with Dictyocaulus viviparus, the bovine lungworm, include rare instances of anthelmintic resistance. Reports from 2024 documented inefficacy of macrocyclic lactones like ivermectin and moxidectin in treating infections in dairy calves, suggesting emerging resistance that could complicate control in livestock.[122] Concurrently, upticks in lungworm outbreaks among housed cattle have been attributed to changes in management practices, such as prolonged indoor housing of youngstock and altered grazing patterns, which increase reinfection risks even in non-pastured herds.[123]Addressing these trends requires improved global surveillance to track parasite spread and resistance patterns. In regions like eastern Australia, human cases of rat lungworm disease have risen notably, driven by environmental factors, emphasizing the need for integrated zoonotic monitoring systems to mitigate public health threats.[124]