Lungworm Infection

Lungworm infection is a parasitic respiratory disease affecting multiple farm animal species caused by nematode parasites that reside in the airways and lung tissue of their hosts. The condition is characterized by inflammation of the bronchi and bronchioles, excessive mucus production, and varying degrees of pneumonia resulting from both the physical presence of the parasites and the host's immune response to their presence. Lungworm infections represent significant health and economic concerns in grazing livestock systems worldwide, causing reduced growth rates, decreased milk production, and in severe cases, death from respiratory failure. The disease is particularly problematic in temperate climates with adequate moisture to support larval development and survival on pastures.

Multiple species of lungworm affect farm animals, with host specificity varying among parasite species. In cattle, Dictyocaulus viviparus is the primary pathogen causing the condition commonly known as husk or hoose. Sheep and goats are affected by Dictyocaulus filaria and Muellerius capillaris, among others, with the latter causing chronic infections that are often subclinical. Pigs can harbor Metastrongylus species, though these infections are now relatively uncommon in modern production systems. Llamas and alpacas may be infected by species affecting small ruminants. Each host-parasite combination has unique epidemiological characteristics and clinical presentations that influence diagnosis and treatment approaches.

The economic and welfare impact of lungworm infection on livestock operations can be substantial, particularly in naive animals experiencing their first grazing season. Clinical disease causes immediate losses through mortality in severe cases and reduced productivity in surviving animals. Subclinical infections, where parasite burdens are insufficient to cause obvious disease, still impair growth rates and feed efficiency, resulting in insidious economic losses that may go unrecognized. The costs of treatment and prevention programs add to the economic burden, though these are typically far outweighed by the losses prevented. From a welfare perspective, lungworm infection causes significant respiratory distress and suffering in affected animals.

Lungworm infection is highly treatable when recognized promptly, and effective prevention strategies exist for most production systems. Anthelmintic drugs effective against lungworms are widely available and generally provide rapid clinical improvement when administered early in the disease course. However, treatment of advanced cases may be complicated by secondary bacterial pneumonia and permanent lung damage that persist despite elimination of the parasites. Prevention through strategic anthelmintic use, pasture management, and in some regions vaccination provides the most effective approach to controlling lungworm in livestock populations. Understanding the parasite life cycle and epidemiology is essential for implementing effective control programs.

The primary cause of lungworm infection in farm animals is ingestion of infective third-stage larvae from contaminated pastures, followed by migration of the parasites to the lungs where they mature and reproduce. In cattle, the causative organism Dictyocaulus viviparus has a direct life cycle without intermediate hosts. Adult worms in the bronchi produce eggs that are coughed up, swallowed, and passed in feces containing first-stage larvae. These larvae develop through two molts on pasture to reach the infective third stage over approximately one week under optimal conditions. When ingested by grazing cattle, larvae penetrate the intestinal wall, migrate through lymphatics to the lungs, and develop to adults within approximately three to four weeks. The entire cycle from egg to reproducing adult takes roughly five to six weeks.

Genetic and breed predisposition to lungworm infection is minimal, as all cattle breeds are susceptible to infection when exposed. However, previous exposure resulting in acquired immunity significantly influences disease severity. Animals that have never encountered lungworm, including first-season grazers and adults from lungworm-free herds, lack protective immunity and may develop severe clinical disease when exposed to contaminated pastures. Cattle that survive infection develop strong immunity that provides protection against subsequent challenges, though this immunity wanes without continued low-level exposure. The channel island breeds, particularly Jerseys, have been suggested to show increased susceptibility, though this observation may reflect management differences rather than true genetic factors.

Environmental and management factors are the primary determinants of lungworm infection risk in grazing livestock systems. Warm, moist conditions favor larval development and survival on pastures, making disease most common during late summer and autumn in temperate regions. Overstocking and continuous grazing concentrate infective larvae on pastures, increasing exposure risk. Pastures grazed by infected animals in previous years may harbor overwintered larvae that initiate infections in spring. Introduction of naive animals to contaminated pastures creates conditions for severe outbreaks. In contrast, hot dry weather and freezing temperatures reduce larval survival and decrease transmission risk.

Several risk factors increase the likelihood of clinical lungworm disease in individual animals and herds. First-season grazers are at highest risk due to lack of acquired immunity. Mixed grazing with older carrier animals that shed low numbers of larvae creates ongoing exposure. Nutritional stress and concurrent diseases that compromise immune function increase susceptibility to clinical disease. High stocking rates increase both pasture contamination and exposure levels. Grazing patterns that concentrate animals on areas with high larval density, such as around water sources or supplemental feeding areas, increase infection intensity.

The pathophysiology of lungworm infection involves multiple mechanisms of disease causation. Initial larval migration through the lungs causes hemorrhage and inflammation in the lung parenchyma. As larvae reach the airways and mature, they cause bronchitis with epithelial damage and excess mucus production that obstructs airflow. The host immune response to parasite antigens contributes significantly to pathology through inflammatory reactions. Dead and dying parasites, whether from natural death or treatment, can trigger acute inflammatory responses that temporarily worsen clinical signs. Secondary bacterial infection of damaged airways commonly complicates lungworm infection, particularly in severe cases. In chronic infections, lung damage may include emphysema, fibrosis, and permanent airway changes.

Early warning signs of lungworm infection in farm animals are often subtle and may be missed without careful observation. In cattle, the earliest indication is typically an increased respiratory rate noticed when animals are at rest or during mild exertion. A soft, occasional cough may be heard, particularly when animals are moved or during the cooler parts of the day. Affected animals may show slightly reduced appetite and begin to lag behind the group during movement. Growth rates may decline before obvious clinical signs appear, representing the subclinical production losses associated with developing infections. Alert herdsmen may notice animals breathing more deeply than normal or standing with slightly extended necks.

As infection progresses, symptoms become more obvious and species-specific patterns emerge. Cattle with significant lungworm burdens develop a characteristic harsh, frequent cough that is easily heard across the pasture. Respiratory distress becomes apparent, with animals showing increased respiratory rate and effort. Affected cattle may stand with their heads lowered and necks extended, mouth breathing in severe cases. Sheep and goats with Dictyocaulus infection show similar respiratory signs, while those with Muellerius typically have milder clinical presentations unless burdens are heavy. Pigs with lungworm infection show coughing, particularly during movement, and may develop a thumping respiratory pattern in severe cases.

Behavioral changes accompany the respiratory signs of lungworm infection and provide additional indicators of disease. Affected animals reduce grazing time and may be observed resting more than herdmates. They typically position themselves at the rear of moving groups and may resist handling due to respiratory compromise. Feed intake decreases progressively, and animals lose interest in supplemental feeds they previously consumed eagerly. In dairy cattle, milk production declines and animals may be reluctant to enter the milking parlor or walk up ramps. Social behavior changes as affected animals isolate themselves and spend less time engaging in normal herd interactions.

Physical examination findings in lungworm-infected animals vary with infection intensity and stage. Body condition typically declines, with loss of muscle mass and fat cover despite adequate forage availability. The hair coat may become rough and dull in chronically affected animals. Auscultation of the chest reveals increased breath sounds, wheezes, and crackles over affected lung regions, particularly in the caudodorsal fields where adult worms concentrate. Heart rate may be elevated secondary to hypoxia and stress. Rectal temperature is often normal or only mildly elevated unless secondary bacterial infection has developed. Mucous membranes may appear pale in chronically affected animals or slightly cyanotic in those with severe respiratory compromise.

Symptom progression in untreated lungworm infection follows a generally predictable pattern tied to the parasite life cycle and accumulating lung damage. Following initial infection, clinical signs develop over two to four weeks as larvae migrate and mature in the lungs. Signs may transiently worsen around the time of patency when adult worms begin egg production and trigger intensified immune responses. Without treatment, continued pasture contamination and reinfection cause progressive worsening over weeks to months. Animals may eventually reach a state of equilibrium with chronic low-grade disease, or may deteriorate to the point of death from respiratory failure, particularly if secondary bacterial pneumonia develops.

Emergency symptoms requiring immediate veterinary intervention include severe respiratory distress with open-mouth breathing, reluctance or inability to move, cyanosis of visible mucous membranes indicating oxygen deprivation, and collapse. Animals showing these signs may have very heavy worm burdens, severe secondary pneumonia, or acute hypersensitivity reactions. Sudden death can occur in heavily infected animals, particularly following stress such as handling or transport. Pregnant animals with severe lungworm infection may abort or deliver weak calves. Animals showing signs of septicemia, including high fever, depression, and rapid deterioration, require immediate aggressive treatment for bacterial complications.

Clinical examination by a licensed veterinarian forms the foundation of lungworm diagnosis in farm animals and should consider both individual and herd-level findings. The examination begins with assessment of the grazing history and management factors that influence lungworm risk. Individual animals are evaluated for respiratory signs including increased respiratory rate, cough, and abnormal breath sounds on auscultation. The presence of harsh breath sounds and wheezes, particularly in the caudodorsal lung fields, supports a diagnosis of lungworm infection. Simultaneous evaluation of multiple animals in an affected group helps establish whether respiratory disease is widespread or limited to individuals, with widespread disease in first-season grazers highly suggestive of lungworm.

Diagnostic tests are essential for confirming lungworm infection and differentiating it from other causes of respiratory disease in grazing livestock. Fecal examination using the Baermann technique detects first-stage larvae shed by infected animals and is the primary diagnostic method for patent infections. However, larvae are not present in feces during the prepatent period or in some immune-mediated respiratory reactions, so negative results do not rule out lungworm involvement. Blood tests may reveal eosinophilia, particularly during larval migration phases, though this finding is variable and nonspecific. Antibody tests are available for D. viviparus in cattle and can detect both current and past exposure. Bronchoalveolar lavage may reveal larvae or characteristic inflammatory cells and can be valuable when fecal testing is negative.

Differential diagnosis for lungworm infection includes numerous other causes of respiratory disease in grazing ruminants that must be considered and ruled out. Infectious bovine rhinotracheitis and other viral respiratory infections may cause similar clinical signs. Bacterial pneumonia from various pathogens, including Mannheimia haemolytica and Pasteurella multocida, can produce respiratory signs overlapping with lungworm disease. Fog fever and other acute bovine pulmonary edema and emphysema syndromes occur in adult cattle on lush pastures. Aspiration pneumonia from various causes should be considered. In sheep, maedi-visna virus causes chronic progressive pneumonia that may be confused with parasitic disease.

Herd-level diagnostics provide valuable information for understanding lungworm epidemiology within a production system and guiding control strategies. Bulk tank milk testing for antibodies to D. viviparus can indicate herd exposure levels in dairy operations. Strategic fecal sampling of multiple animals in at-risk groups helps assess infection prevalence and intensity. Pasture larval counts, while technically demanding, can quantify environmental contamination and guide grazing decisions. Necropsy examination of animals that die provides definitive diagnosis through recovery of adult worms from airways and assessment of lung pathology. Review of production records, including growth rates in youngstock and milk production in dairy cattle, may reveal performance impacts suggesting subclinical infection.

Emergency and immediate treatment for animals with severe respiratory distress due to lungworm infection focuses on stabilization while addressing both the parasitic and any secondary bacterial components of disease. Animals in acute distress should be disturbed as little as possible and provided a quiet, well-ventilated environment to reduce respiratory demands. Broad-spectrum antibiotics are typically administered immediately to address secondary bacterial pneumonia, which is common in severe cases. Anti-inflammatory drugs, including corticosteroids in critical situations, may help reduce inflammation and improve breathing. Anthelmintic treatment, while essential, may initially worsen clinical signs as dying parasites trigger acute inflammatory responses, so treated animals require close monitoring in the hours following treatment.

Medical management of lungworm infection centers on anthelmintic therapy to eliminate the parasites causing disease. Multiple drug classes are effective against lungworms in cattle, including macrocyclic lactones such as ivermectin, doramectin, eprinomectin, and moxidectin, as well as benzimidazoles including fenbendazole and albendazole. Levamisole also has efficacy against lungworms. Drug selection should consider species, route of administration, withdrawal times for meat and milk, and convenience for the producer. Pour-on formulations provide ease of application but may have different efficacy profiles than injectable products. All withdrawal times must be strictly observed in food-producing animals, with documentation of treatment dates and products used.

Supportive care complements anthelmintic therapy and is particularly important in severe cases where lung damage may persist despite parasite elimination. Affected animals should be removed from contaminated pastures and provided clean, dry, well-ventilated housing. High-quality, easily digestible feed supports recovery and provides energy for tissue repair. Fresh clean water should be readily available. Stress should be minimized, with affected animals protected from extreme weather and not mixed with unfamiliar animals or forced to compete for resources. Monitoring should continue for several days following treatment, as some animals may initially worsen due to reactions to dying parasites before showing improvement.

Herd treatment protocols become important when lungworm infection affects multiple animals or when the goal is to prevent disease in exposed but currently healthy individuals. Mass treatment of at-risk groups using pour-on anthelmintics or in-feed medications allows efficient administration to large numbers of animals. Strategic treatment timed to prevent clinical disease while allowing development of natural immunity provides the best long-term control in endemic situations. Treatment should be combined with movement to clean pastures where possible to prevent immediate reinfection. In outbreak situations, treating all animals in affected groups regardless of clinical status helps reduce pasture contamination and protects those still in the prepatent period.

Treatment decisions for lungworm infection must balance immediate animal needs with long-term herd health goals and economic considerations. In valuable individual animals showing clinical signs, prompt treatment is clearly indicated to resolve disease and prevent permanent lung damage. Decisions regarding treatment of subclinically infected animals or those at risk of infection should consider the costs of treatment against expected losses from disease, as well as the impact of treatment on immunity development. Repeated frequent treatment may prevent the development of protective immunity, creating perpetually susceptible animals that require ongoing intervention. In some systems, allowing controlled exposure followed by treatment creates populations with robust natural immunity.

Producers must observe all relevant withdrawal times when treating food-producing animals for lungworm infection. Withdrawal periods vary by drug, formulation, dose, and species, and may be significantly longer than label recommendations in some jurisdictions or for certain markets. Milk from treated dairy cattle must be discarded for the appropriate period, representing an additional economic cost of treatment. Animals may not be slaughtered for human consumption until withdrawal times have elapsed, which may complicate marketing decisions for beef and market lamb operations. Accurate treatment records are essential for ensuring food safety compliance and should include date of treatment, product used, dosage, route of administration, and earliest slaughter or milk release date.

Recovery timeline for animals treated for lungworm infection varies based on the severity of disease at the time of treatment and the extent of lung damage that has occurred. Mild cases caught early in the disease process typically show clinical improvement within two to three days of anthelmintic treatment, with coughing decreasing and respiratory rate normalizing. Moderate cases require one to two weeks for significant clinical improvement, though full resolution of respiratory signs may take several weeks. Severe cases with extensive lung damage may show only partial recovery, with residual respiratory compromise persisting long-term. Animals that have developed secondary bacterial pneumonia require longer recovery periods and may have permanent lung scarring.

Post-treatment care and monitoring are essential components of successful recovery from lungworm infection. Treated animals should be moved to clean or low-risk pastures to prevent immediate reinfection before lung healing is complete. Continued observation for signs of relapse or incomplete treatment response should extend for at least two weeks. Body weight and condition should be monitored, with steady gains indicating successful recovery. Repeat fecal examinations can confirm elimination of infection if initial testing was positive. Animals that fail to show improvement within one week of treatment should be reevaluated for persistent infection, anthelmintic resistance, or complications such as bacterial pneumonia.

Prognosis for animals with lungworm infection depends on multiple factors including timing of treatment, severity of initial disease, and presence of complications. Animals treated during the prepatent period before significant lung damage has occurred have excellent prognoses for complete recovery. Those with moderate disease at treatment time typically recover well with appropriate therapy, though some residual decrease in lung function may persist. Animals with severe disease, particularly those with secondary bacterial pneumonia or emphysema, have more guarded prognoses and may never return to full productivity. Death can occur despite treatment in animals with overwhelming infection or severe hypersensitivity reactions to dying parasites.

Return to production considerations for recovered animals should account for both residual health effects and the development of protective immunity. Cattle that have recovered from lungworm infection typically develop strong immunity that provides protection against subsequent challenge, potentially making them more valuable for grazing high-risk pastures in future seasons. However, animals with permanent lung damage may not tolerate the demands of high production and may be candidates for early culling. Dairy cattle returning to production after treatment should be monitored for any persistent decrease in milk yield. Breeding animals with history of severe lungworm infection should be evaluated for any lasting reproductive impacts before being retained in the herd.

Vaccination protocols provide the most effective prevention of lungworm infection in cattle in regions where the disease is endemic. An oral vaccine containing irradiated D. viviparus larvae is available and stimulates protective immunity without causing clinical disease. The vaccine is administered in two doses several weeks apart, ideally before first turnout to pasture. Vaccinated animals must have low-level field exposure to maintain their immunity, so the vaccine is most appropriate for systems where cattle will graze potentially contaminated pastures. Animals kept entirely indoors or on guaranteed lungworm-free pastures do not require vaccination but will remain susceptible to disease if their circumstances change.

Biosecurity measures help prevent introduction of lungworm infection to clean farms and reduce transmission within affected operations. Purchased cattle should have known grazing history and ideally come from lungworm-free or well-controlled herds. New arrivals should be quarantined and, in high-risk situations, treated with effective anthelmintics before introduction to the main herd. Grazing management that separates susceptible animals from potentially contaminated pastures reduces exposure risk. Avoiding shared grazing with cattle from unknown sources prevents introduction of infection from carrier animals. In sheep and goat operations, similar principles apply, though vaccination is not available for small ruminant lungworms.

Strategic anthelmintic use provides an alternative or complementary approach to lungworm prevention, particularly where vaccination is not available or practical. Treatment timing should be based on local epidemiology and weather patterns that influence larval development and transmission. In temperate regions, mid-grazing season treatment often targets the period when larval challenge peaks while still allowing some exposure for immunity development. The move-and-treat strategy involves treating animals and immediately moving them to clean pastures, breaking the transmission cycle. Anthelmintic choice should consider efficacy against local parasite populations and the potential for resistance development with repeated use of the same drug class.

Management practices significantly influence lungworm transmission and should be optimized as part of comprehensive prevention programs. Rotational grazing systems that allow pastures to rest reduce larval accumulation and survival. Mixed or sequential grazing with different species can reduce parasite burdens on pastures, as most lungworm species are host-specific. Avoiding overgrazing that forces animals to graze close to fecal deposits reduces infection intensity. Provision of clean water sources away from potentially contaminated areas decreases exposure during drinking. Adequate nutrition supports immune function and enhances the ability of animals to resist and recover from infection.

Pasture management and monitoring support lungworm prevention by reducing environmental contamination and providing early warning of infection pressure. Pastures known to have harbored infected animals in previous years should be considered potentially contaminated, as overwintered larvae can survive and initiate new infections. Resting such pastures over winter and into spring allows natural die-off of larvae before grazing. Regular fecal monitoring of grazing cattle, particularly first-season grazers, allows early detection of infection before clinical disease develops. Integration of pasture history, weather conditions, animal immune status, and monitoring results guides optimal timing and intensity of control measures.

Daily management and monitoring requirements for operations where lungworm is a concern include regular observation of grazing animals for signs of respiratory disease. Personnel responsible for livestock should be trained to recognize early coughing, increased respiratory effort, and behavioral changes that might indicate developing infection. First-season grazers warrant particularly close attention due to their high susceptibility. Daily or twice-daily observation during high-risk periods allows prompt intervention before disease becomes severe. Monitoring should include assessment of grazing behavior, with reduced grazing time being an early indicator of respiratory compromise.

Housing and environmental management influence lungworm risk and recovery in affected animals. Indoor housing eliminates exposure to pasture-borne larvae and is the definitive method of preventing infection, though it may not be practical or economically feasible in all systems. When animals must be brought indoors for treatment or recovery, housing should provide excellent ventilation to support respiratory function while protecting from drafts and extreme temperatures. Bedding should be kept clean and dry to minimize respiratory irritants. Stocking density should allow adequate space per animal and prevent stress from overcrowding. Recovered animals being returned to grazing should go to clean or low-contamination pastures when possible.

Herd health programs addressing lungworm should be developed in consultation with a veterinarian familiar with local conditions and parasite epidemiology. Programs should define the approach to prevention, whether through vaccination, strategic treatment, pasture management, or combinations of these methods. Protocols for monitoring infection status should be established, including schedules for fecal testing during the grazing season. Response plans for clinical disease should be in place before outbreaks occur, ensuring rapid access to appropriate treatments. Regular review of program effectiveness through production monitoring and health outcome tracking allows continuous improvement.

Record keeping for lungworm management should track information relevant to both individual animal care and herd-level epidemiology. Treatment records should document dates, products, dosages, and withdrawal times for all animals receiving anthelmintics. Grazing records should note which pastures have been used by which groups of animals, supporting assessment of contamination risk. Health observations including respiratory disease episodes should be recorded to identify patterns over time. Production data such as growth rates and milk yields provide objective measures of subclinical impacts. Integration of these records with weather data helps identify conditions associated with increased disease risk.

Economic considerations should guide investment in lungworm prevention and control programs. The costs of prevention measures including vaccination, anthelmintic treatments, and pasture management must be weighed against the potential losses from clinical and subclinical disease. In endemic areas with susceptible animals, the return on investment in prevention is typically strongly positive. However, overreliance on anthelmintic treatments can be economically and parasitologically counterproductive if it prevents immunity development or promotes drug resistance. Cost-benefit analysis should consider both direct costs and returns as well as longer-term factors such as herd immunity status and pasture contamination levels.

High-risk breeds and species for severe lungworm infection are primarily those lacking prior exposure and protective immunity rather than those with true genetic susceptibility differences. First-season grazing cattle of any breed are highly susceptible to clinical disease when exposed to contaminated pastures. Adult cattle that have been housed continuously or grazed on lungworm-free land throughout their lives remain fully susceptible to infection if their circumstances change. Among cattle breeds, some observations suggest Channel Island breeds including Jerseys and Guernseys may show increased susceptibility or severity of disease, though this has not been definitively established and may reflect management differences rather than genetics. Generally, breed is less important than exposure history in determining lungworm disease risk.

Production type influences lungworm risk through its effects on management practices and exposure patterns. Dairy operations where cattle graze potentially contaminated pastures face significant risk, particularly if replacement heifers are raised on the same land as the milking herd. Beef cattle systems with continuous grazing of the same pastures year after year may develop high contamination levels. Sheep and goat operations vary in risk depending on stocking rates, pasture management, and presence of Muellerius capillaris which can maintain chronic infections without obvious clinical disease. Intensive indoor production systems eliminate lungworm risk through prevention of exposure but create populations that are fully susceptible if management changes.

Genetic selection and testing for lungworm resistance is not currently practical as a primary prevention strategy, though general selection for improved health and immune function may provide some benefit. Some research has identified genetic markers associated with resistance to gastrointestinal parasites in sheep, and similar variation may exist for lungworm susceptibility, but this has not been developed into practical selection tools. The strong acquired immunity that develops following natural exposure means that exposure history is far more important than genetics in determining disease susceptibility. Selection of animals from herds with effective lungworm control programs ensures that purchased stock have been managed to minimize both disease impact and parasite introduction risk.

Commonly co-occurring conditions with lungworm infection include other parasitic infections that share transmission routes and management risk factors. Gastrointestinal nematode infections frequently accompany lungworm in grazing cattle, sheep, and goats, as both are acquired through pasture exposure. Liver fluke infection may be present on the same farms where lungworm occurs, particularly in wet grazing areas. Secondary bacterial pneumonia is a common and important complication of lungworm infection, with damaged airways and accumulated mucus providing ideal conditions for bacterial colonization. Concurrent viral respiratory infections may predispose animals to more severe lungworm disease or develop as opportunistic complications.

Conditions with similar symptoms that must be differentiated from lungworm infection span infectious, parasitic, and noninfectious causes of respiratory disease in livestock. Infectious bovine rhinotracheitis and other viral respiratory infections cause coughing and respiratory distress that may resemble lungworm disease. Bacterial pneumonias from various causes produce overlapping clinical signs. In adult cattle, fog fever and other acute bovine pulmonary edema and emphysema syndromes can cause sudden severe respiratory distress. Hypersensitivity pneumonitis from mold exposure occurs in housed cattle and may mimic parasitic disease. In sheep, maedi-visna causes chronic progressive respiratory disease that must be distinguished from parasitic bronchitis.

Complications and sequelae of lungworm infection can significantly impact long-term health and productivity even after the parasitic infection has been eliminated. Secondary bacterial pneumonia is the most common and serious complication, causing additional lung damage and potentially fatal septicemia. Pulmonary emphysema may develop in severe cases, creating permanent respiratory compromise. Fibrosis and scarring of lung tissue from healed infections reduce functional capacity and predispose to future respiratory problems. Hypersensitivity reactions to lungworm antigens can cause reinfection syndrome in previously exposed cattle, producing severe acute respiratory disease even with relatively low worm burdens. Chronic poor performance and reduced productivity may persist in animals that have recovered from severe infection.