Threadworm Infection (Strongyloidosis)
Parasitism of swine by Strongyloides ransomi.
Infection with S. ransomi occurs only in swine. The parasite has a cosmopolitan distribution and is of importance in warmer countries or areas. It does not occur frequently in most areas of the United States. Although infection occurs in all age groups, including fetuses, pathogenicity usually is confined to nursing piglets.
Most references to threadworm infection in swine are from the 1960s and 1970s. There are few recent publications. This suggests that current losses attributable to the parasite in the US are relatively minor. Environmental requirements of the parasite apparently restrict its spread.
Only asexual females of Strongyloides ransomi are important in parasitism of swine. Free-living generations can produce progeny that are free living (heterogonic cycle) or progeny that are parasitic (homogonic cycle). Free-living generations can alternate with parasitic generations.
The asexual females are almost microscopic, about 3.3-4.5 mm long, and live in the mucosa of the anterior small intestine, usually the duodenum. The ova are thin shelled, larvated and are passed in the host’s feces. Infective larvae hatch in one to two days. They require warmth and moisture for survival and are usually eliminated by desiccation, sunshine and good sanitary practices.
Three mechanisms tend to assure survival of the parasite. These include the ability of S. ransomi to survive for some time in a non-parasitic form, four possible routes of transmission, and the ability to achieve patency in piglets in only a few days.
Parasitic larvae invade the host either by penetration of the skin (percutaneous), ingestion in feed (oral), ingestion in colostrum (transcolostral), or through direct invasion of developing fetuses (transplacental/perinatal). In all cases, the asexual female reaches the mucosa of the small intestine where many ova are produced and passed in feces of the host.
Larvae sequestered in muscle or in the mammary fat of sows are mobilized in the periparturient period and transmitted to piglets in colostrum. This is the most common route of transmission to neonatal piglets. Larvae in colostrum arrive at the intestinal mucosa without migration. Larvae also are transmitted directly to fetuses, presumably during the periparturient period.
Larvae that penetrate the skin enter the blood stream and are carried to the lungs. After breaking out into alveoli and tracheal migration to the pharynx, they are swallowed and reach the small intestine. Larvae taken into the mouth penetrate the mucous membranes of the oral cavity and, after a similar migration, reach the small intestine.
Adults that develop in the small intestine irritate the intestine, with the severity depending upon the number of parasites. The parasites cause a blunting and atrophy of intestinal villi. These alterations result in leakage of proteins into the gut and failure of the intestine to effectively absorb nutrients and fluids. The alterations lead to anemia, diarrhea, dehydration and emaciation. Migration of larvae through the lungs causes small hemorrhages as well as thickening and inflammation of alveolar septa that impair respiration.
In mild infections there are few or no signs. In severe infections of neonatal piglets, there is anemia, diarrhea, dehydration, emaciation and deaths. Most mortality occurs in piglets less than two weeks old. Diarrhea, dehydration and unthriftiness can occur in pigs up to three months old.
These are not readily apparent on gross examination. On microscopic examination of the small intestine, there is villous atrophy and blunting. Adult parasites can be seen in tunnels in the epithelium of glandular crypts of the mucosa. In the lung there is inflammation and thickening of alveolar walls, scattered hemorrhages, and perhaps migrating larvae. Neither hemorrhages nor larvae are numerous.
Diarrhea in nursing pigs may suggest the possibility of infection with S. ransomi. However, all other common causes of diarrhea must be excluded first, especially infections with rotavirus, Escherichia coli, Clostridium perfringens and C. difficile, and coccidiosis. Strongyloides ransomi can often be identified in mucosal scrapings or histologic sections. The thin-shelled larvated ova can be identified by laboratory fecal examination but must be differentiated from larvated ova of lungworms (Metastrongylus spp).
Avoidance of pastures with an environment favorable to the parasite will reduce exposure of sows and piglets. Indoor housing and confinement rearing, combined with maintenance of good sanitation, will reduce the likelihood of threadworm infection. Avermectins given to the sow a week or two prior to farrowing will control transmission of larvae to fetuses. For additional options, see the table, Anthelmintics and Parasiticides.