The large roundworm of pigs (Ascaris suum) is the most common and widespread parasite of swine. Larval migration through the liver results in focal hepatitis (milk spots) and condemnation of the liver at slaughter but no clinical signs. Migration through the lungs causes pulmonary lesions that can lead to pneumonia, particularly in animals co-infected with other viral or bacterial pathogens. Small intestinal stages compete with the host for nutrition, resulting in poor feed conversion and slower weight gains. Infections usually stimulate immunity, which results in older animals having fewer nematodes and excreting fewer eggs than younger ones. Infections can be detected via fecal flotations during the patent period but postmortem examination is required for detection of prepatent infections. Numerous anthelmintics are available for use against the intestinal stages, but control programs must incorporate strict sanitation as well.
Adults of the large roundworm of pigs (Ascaris suum) live in the small intestine. Males are up to 25 cm and females up to 40 cm long, whitish, and quite thick. Large numbers of eggs are produced (as many as 200,000 to 1 million/day per female), although they are shed intermittently; they can develop to the infective stage (eggs containing third-stage [L3] larva) in 3–4 weeks under optimal conditions.
In temperate geographic areas, the eggs stay dormant in winter (< 10–15°C) and resume development when temperatures rise in spring. The eggs are highly resistant to chemical agents; however, conditions with low humidity, heat, or direct sunlight decrease their survival time. Under optimal conditions, eggs may survive for 6–9 years.
When the eggs are ingested, the larvae hatch in the intestine, penetrate the wall, and enter the portal circulation. After a short period in the liver, they are carried by the circulation to the lungs, where they pass through the capillaries into the alveolar spaces. Approximately 9–10 days after ingestion, the larvae migrate to the lungs, pass up the bronchial tree, then are coughed up and swallowed. They return to the small intestine by approximately 10–15 days after infection, where they mature into adult worms. The first eggs are passed approximately 6–7 weeks after infection. Lifespan is approximately 6–9 months. Earthworms and dung beetles can serve as paratenic hosts.
Distribution and Host Range of Ascaris suum in Pigs
Ascaris suum is found in pigs worldwide. Occasionally, the nematodes may establish infection in sheep. Ingestion of infective eggs while grazing generally results in pneumonia and liver lesions. Infections can also occur in cattle and manifest as an acute, atypical interstitial pneumonia. Whether the nematode Ascaris lumbricoides of humans and A suum of pigs are the same is debated. Evidence indicates they are likely genetically independent populations. However, in areas where A lumbricoides is absent, ascarid infections in humans are mainly due to pig-derived Ascaris. Furthermore, in areas where both parasites occur, cross-infections have been documented. Thus, the pig ascarid is zoonotic, having been identified in humans from various areas of the world, particularly those in close contact with pigs. Visceral larva migrans due to migrating larvae has been described.
Clinical Findings of Ascaris suum in Pigs
Courtesy of Dr. Bruce Lawhorn.
Adult worms of A suum may appreciably decrease the growth rate of young pigs; in rare cases, the worms may cause mechanical obstruction of the intestine. Migration of larvae through the liver causes hemorrhage, fibrosis, and accumulation of lymphocytes seen as white spots (called milk spots) under the capsule, leading to condemnation of the liver at slaughter. These lesions become visible 7–10 days after infection and will regress within 1–4 weeks; therefore, their presence indicates recent infection or reinfection.
In resistant pigs, only a few larvae reach the liver and the number of white spots is low, despite continual reinfection. Therefore, the number of white spots and the liver condemnation rate are both poor measures of the severity of herd infection. In heavy infections, the larvae can cause pulmonary edema and consolidation, as well as exacerbate swine influenza and endemic pneumonia. Heavily infected susceptible pigs show abdominal breathing, commonly referred to as thumps. In addition to the respiratory clinical signs, marked unthriftiness and weight loss may occur. Infection generally induces development of acquired resistance to reinfection, and prevalence is highest in young growing pigs. If the treatment rate is very low and the level of herd immunity is also low, prevalence may be highest in breeding animals.
Diagnosis of Ascaris suum in Pigs
Standard fecal flotation methods (patent infections)
Postmortem examination (prepatent infections)
During the patent period, diagnosis of A suum in pigs can be made by demonstrating the typical eggs (golden brown, thick pitted outer wall, 50–70 × 40–60 mcm) by fecal analysis or by observation of large worms in feces. Pigs are coprophagic; thus, low egg counts (< 200 eggs/g) may indicate coprophagy rather than actual infection. A presumptive diagnosis can be made at postmortem examination based on demonstration of the typical milk spots; however, other migrating parasites (eg, larvae of Toxocara canis, Stephanurus dentatus) may cause similar lesions. Worms may be demonstrated in the lungs (small immature worms) and the small intestine (large immature or adult worms) at postmortem examination.
Treatment of Ascaris suum in Pigs
Anthelmintics
Supportive treatment as needed
Many anthelmintics have been used to remove adult ascarids from pigs. Piperazine preparations have low toxicity and are moderately priced. The benzimidazoles and probenzimidazoles, dichlorvos, ivermectin, doramectin, and pyrantel are effective and have a broader spectrum of activity than piperazine. Hygromycin is active against ascarids when administered as a low-level additive to the feed. Less information is available concerning the control of migratory stages; pyrantel and fenbendazole show some activity. Supportive treatment, including treatment for secondary bacterial invaders, may be necessary during the respiratory phase of infection.
Prevention is more effective than treatment but may be difficult to achieve. Good ascariasis control in confinement systems may include deworming sows approximately 1 week before farrowing; washing sows to remove any adherent ascarid eggs before moving to sanitized farrowing crates; early weaning (2–4 weeks of age, before eggs become infective); and using all-in/all-out production systems with thorough cleaning between groups. Pigs that are free from ascarids are at risk of developing severe pneumonia if placed into contaminated grower/finisher facilities. If so, feeding a continuous dewormer for the first 30 days is an option. Pigs in these situations should be dewormed at no greater than 8-week intervals to prevent additional contamination of the facility.
In pasture or open lot housing systems, deworming sows before moving to a pasture that has not been grazed in several years (ie, a clean pasture) is often recommended. Pasture rotation will also help decrease swine contact with ascarid eggs, especially if pastures are tilled between uses.
Key Points
Ascariasis, the infection of pigs with the swine roundworm A suum, occurs worldwide, wherever swine are raised.
Clinical signs, including chronic coughing, unthriftiness, and failure to gain weight, tend to be more prevalent in young, growing pigs.
Severe, sometimes fatal, respiratory disease can occur, particularly in naive animals placed in heavily contaminated facilities.
Chronic infections (>2 months) can be detected using fecal flotations to find the eggs; diagnosis of acute (< 2 months) infections requires postmortem examination.
Control should not depend solely on anthelmintics but must also incorporate appropriate sanitation.
For More Information
Iowa State University College of Veterinary Medicine Swine Disease Manual: Ascariasis
