Ascariasis is the infestation of swine by the roundworm, Ascaris suum, which can cause pneumonia, hepatitis, and ill thrift.
Ascariasis occurs worldwide in countries that raise significant numbers of swine. All ages are affected but ascariasis is more severe in young, growing pigs. It is the most prevalent and most economically important internal parasite of swine.
Migration of ascarid larvae occurs in several other animals, including man, but larvae usually do not develop to the adult stage in the intestine of these species. Migrating larvae occasionally infect lambs and calves and cause heavy losses from pulmonary lesions.
The ascarid of man, A. lumbricoides, was once believed to be the same parasite as A. suum. However, A. suum is now recognized as a separate species. Effective control of ascarid infection came only after the life cycle was elucidated and interventions based on that knowledge were used to prevent infection.
Mature ascarids are 15-40 cm long, thick bodied, round worms. A mature ascarid (prepatent period of seven to eight weeks) can lay almost two million eggs per day. Adults live in a pig for about six months before spontaneous expulsion begins but may survive a year or longer. Heavy infections can result in hundreds of ascarids in the intestine of a single pig.
Ascarid eggs are thick shelled, yellowish brown, almost spherical, 50-80 by 40-60 µm, and are coated with a sticky proteinaceous cover. The eggs are quite resistant to environmental degradation and disinfectants but can be destroyed by intensive steam cleaning or prolonged exposure to full sunlight.
A. suum eggs are extremely hardy and can survive for as long as 15 years in the environment. They remain viable in swine effluent water for at least 14 months. The eggs can be transported by infested pigs, insects, fomites, blowing dust, pig manure, and effluent. Eggs are often disseminated through the feces of purchased swine, including breeding stock.
Ascarid eggs are ingested and hatch in the intestine. The larvae penetrate the mucosa, and pass through the bloodstream to the liver, lungs and other sites. They reach the liver two to four days after ingestion and are present in lungs within ten days. Once arriving in the lung, they break into alveolae, are coughed up the airways to the pharynx and are re-swallowed. The larvae reach the intestine 14-20 days after being initially ingested as eggs and become mature approximately two months later. Ascarids are prolific egg-layers with a prepatent period of approximately eight weeks, at which time eggs begin to be passed in feces. Eggs require two to four weeks in the environment for maturation before they become infective.
Once a location is infested, ascariasis persists in the pig population despite all measures used to eliminate it. The extremely high number of eggs that are produced, the resistance of eggs to environmental degradation, and the multiple means in which they can be disseminated contribute to their persistence on infected farms.
Low levels of ascarid exposure will stimulate a protective immunity. The most severe consequences of ascarid infection occur when immunologically naïve pigs are placed into contaminated sites. Farrowing and nursery facilities often have a low prevalence of ascarid egg contamination such that young pigs will have had little or no exposure to the parasite. Hence, these animals are at risk of severe disease when subsequently placed in contaminated finishing barns.
Ascarids cause local inflammation in the intestine and compete with the host for nutrients. This adversely affects growth of pigs, especially those on marginal or poorly balanced diets. With heavy infections, the most significant effect of the disease is a result of the migrating larvae causing lesions in the liver and lungs, including scarring of liver and interstitial pneumonia.
In the lungs, larvae break out of capillaries into alveoli. This results in small hemorrhages and an inflammatory reaction that interferes with the clearance mechanism of airways and favors secondary bacterial infections. Larvae rarely are carried to ectopic sites, e.g. the retina or brain, which may cause signs of impaired vision or central nervous system (CNS) lesions.
Ascarids are known to produce immunosuppressive substances that affect the duration and severity of other swine diseases and also may influence the response of swine to vaccines. Although difficult to quantify, there is evidence that ascariasis increases the severity of acute erysipelas and mycoplasmal pneumonia.
Signs in young, growing pigs include unthriftiness, failure to gain weight, rough hair coat, pendulous abdomen, chronic paroxysmal coughing and occasionally, abdominal expiratory dyspnea (“thumping”).
Severe, sometimes fatal, respiratory disease may result in 7-14 days after naïve pigs (feeder pigs or breeding stock previously unexposed) are placed in facilities heavily contaminated with ascarid eggs. Affected pigs are afebrile, “thump,” are gaunt, and are often misdiagnosed as having bacterial or viral pneumonia. Other effects in heavily exposed gilts include delayed estrus, poor conception rate, pneumonia or death.
By 5-14 days after ingestion of infective eggs, there are small hemorrhages on and throughout the lungs. Larvae and inflammatory exudate obstruct smaller airways (verminous pneumonia). Often, there is a secondary suppurative bronchopneumonia. The pneumonia may be accompanied by emphysema that interferes with collapse of the lungs. Scarring in the liver first appears by 7-14 days after exposure as scattered, gray to white “milk spots” (0.2-1 cm) visible under the liver capsule that later expand, coalesce and can eventually resolve. In heavy infections, diffuse fibrosis may affect the entire liver and lead to its condemnation at slaughter. Minor areas of scarring can be repaired in 30 to 60 days, making diagnostic reliability of detecting an absence of liver lesions at slaughter dubious.
Diagnosis of chronic infestation (more than two months) can often be made by identifying eggs using fecal flotation examinations or by finding grossly visible ascarids in the small intestine. Since ascarids have some mobility, they sometimes can be found in the stomach or in the major bile and pancreatic ducts at necropsy. Obstruction of the bile duct sometimes leads to marked generalized icterus. Ascarids may not be present in animals recently “dewormed” but scarring in the liver or hemorrhages in the lung may still be apparent.
Diagnosis of acute infestations (less than two months) requires postmortem examination of a few typical pigs that have died or been sacrificed. Fecal flotations are not reliable during the first 6-8 weeks following infestation (prepatent period). Postmortem examination also permits the evaluation of concurrent diseases, including other sources of parasitism or causes of pneumonia. Diagnosis of early infestations is by observation of typical liver and lung lesions with confirmation by histopathology.
A complete knowledge of the life cycle of ascarids and the infestation status of a herd or group of pigs is required to make timely and economical deworming decisions.
Prevention of ascariasis is far better than treatment but may be difficult to achieve on many production sites. Swine raised in confinement with a good ascariasis control program usually have few ascarids. Some of the measures that confinement operators implement include: deworming the sows during gestation (usually about a week before farrowing); washing the sows to remove parasite eggs prior to putting them in sanitized farrowing crates; early weaning of two to four week old pigs (before ascarid eggs have become infective); and using all in/all out production systems with thorough cleaning between groups.
Often, pigs produced in sanitary confinement systems are free of ascarid infection until placed in contaminated grow/finish facilities. These pigs then may develop severe pneumonia as they ingest numerous eggs from the environment. Feeding a continuous dewormer (pyrantel) for the first 30 days is a control option in this situation. Pigs in such conditions should be dewormed at no greater than eight-week intervals to prevent additional egg contamination of the site.
In operations that utilize pasture or open lot housing, deworming the sows before moving them to clean pasture is a good practice. Pasture rotation will greatly reduce the exposure of swine to worm eggs, especially if the land is tilled when not pastured. Deworming programs need to be designed to fit the situation on each production site.
Anthelmintics should be selected on the basis of the entire spectrum of nematode species present on the farm, including ascarids. A monitoring system should be established and followed. Sometimes the parasite problem changes as a consequence of introduction of other kinds of parasites, facility changes, or climatic changes which may influence the number and variety of parasites. See the table Anthelmintics and Parasiticides for Swine