Adults of the large roundworm, Ascaris suum, are found in the small intestine and transitorily in the large intestine during expulsion of the worms. They are ∼15–40 cm long, whitish, and quite thick. Large numbers of eggs are produced (as many as 200,000 to 1 million/day/female); they can develop to the infective stage (eggs containing L3 larva) in 3–4 wk under optimal conditions. In temperate regions, they stay dormant in winter (<15°C) and resume development when temperature rise in the spring. The eggs are highly resistant to chemical agents, but conditions with low humidity, heat, or direct sunlight reduce their survival significantly. Under optimal conditions, eggs may survive for 5–10 yr. When the eggs are ingested, the larvae hatch in the intestine, penetrate the large intestinal wall, and enter the portal circulation. After a period in the liver, they are carried by the circulation to the lungs, where they pass through the capillaries into the alveolar spaces. About 9–10 days after ingestion, the larvae pass up the bronchial tree to return to the GI tract. On arrival in the small intestine, most larvae are expelled; remaining larvae develop into mature adult worms. The first eggs are passed 6–7 wk after infection.
Distribution and Host Range
A suum is found in pigs worldwide. The worms may also establish in neonatal lambs and calves, in which adult worms are located in the bile duct. A suum is zoonotic, and adults are commonly found in preschool children in contact with swine herds. Visceral larva migrans due to migrating larvae has been described.
Adult worms may significantly reduce the growth rate of young pigs; in rare cases, they may cause mechanical obstruction of the intestine. Migration of larvae through the liver causes hemorrhage, fibrosis, and accumulation of lymphocytes seen as “white spots” under the capsule and leading to condemnation of the liver at slaughter. White spots heal within 1–4 wk; therefore, their presence indicates recent reinfection. In resistant pigs, only a few larvae will reach the liver and the number of white spots will be low, despite continuous reinfection. Therefore, the number of white spots and the liver condemnation rate are both poor measures for the herd infection level. In heavy infections, the larvae can cause pulmonary edema and consolidation as well as exacerbate swine influenza and endemic pneumonia. Heavily exposed susceptible pigs show abdominal breathing, commonly referred to as “thumps.” In addition to the respiratory signs, marked unthriftiness and weight loss may be seen. The infection generally induces the development of acquired resistance to reinfection, and the prevalence is highest in young growing pigs. If the treatment rate is very low, the level of herd immunity is also low, and prevalence may be highest in breeding animals.
During the patent period, diagnosis can be made by demonstrating the typical eggs (golden brown, thick pitted outer wall, 50–70 × 40–60 μm) by fecal analysis or by observation of large worms in feces. A presumptive diagnosis can be made based on demonstration of liver white spots; however, other migrating parasites (eg, larvae of Toxocara canis) may cause similar lesions. Worms may be demonstrated in the lungs (small immatures) and the small intestine (large immatures, adults) at necropsy.
Supportive therapy, including treatment for secondary bacterial invaders, may be necessary during the respiratory phase of infection. Many drugs have been used to remove adult ascarids. Piperazine preparations have low toxicity and are moderately priced. The benzimidazoles and probenzimidazoles, dichlorvos, ivermectin, levamisole, 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 activity.
Last full review/revision March 2012 by Allan Roepstorff, DSc, PhD, MSc