Adults of the large roundworm, Ascaris suum, are found in the small intestine and transitorily in the large intestine during expulsion of the worms. 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/female) although shed intermittently; they can develop to the infective stage (eggs containing L3 larva) in 3–4 wk under optimal conditions. In temperate regions, the eggs stay dormant in winter (<15°C) and resume development when temperature rises 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 5–11 yr. 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 pass up the bronchial tree, are swallowed, and return to the small intestine by ~10–15 days after infection, where they mature into adult worms. The first eggs are passed ~6–7 wk after infection. Lifespan is ~6–9 mo. Earthworms and dung beetles can serve as paratenic hosts.
Distribution and Host Range:
A suum is found in pigs worldwide. Occasionally, nematodes may establish in sheep; however, ingestion of infective eggs while grazing generally results in pneumonia and liver lesions in sheep. Infections can also be seen in cattle and manifest as an acute, atypical interstitial pneumonia. Whether the human nematode Ascaris lumbricoides and A suum of pigs are the same is still debated. Current evidence indicates there is a single interbreeding population of Ascaris, and the populations occurring in pigs or people have only slight phenotypical and genotypical adaptive changes. Regardless, it is clear the pig ascarid is zoonotic, having been found in people from various areas of the world, particularly those in close contact with pigs. 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 (called “milk spots”) under the capsule and leading to condemnation of the liver at slaughter. These lesions become visible 7–10 days after infection and will regress within 1–4 wk; therefore, their presence indicates recent infection/reinfection. In resistant pigs, only a few larvae will reach the liver and the number of white spots will be low, despite continual reinfection. Therefore, the number of white spots and the liver condemnation rate are both poor measures of 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. 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.
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. Pigs are coprophagic; thus, low egg counts (<200 eggs/g) may indicate coprophagy rather than actual infection. A presumptive diagnosis can be made at necropsy 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 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.