Kidney Worm Infection

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Infection of swine with the nematode worm Stephanurus dentatus.


Stephanurus dentatus infection occurs only in swine. All age groups, including fetuses, are susceptible. Pigs raised in tropical or subtropical areas on moist, shaded pastures are most often infected. In the United States, endemically affected areas include the area south of a line from the Carolinas westward to southern Missouri. However, the disease has occurred in feral and domestic swine in Canada and in other northern locations where southeastern pigs have been transported.

Historical information

Stephanurus dentatus infections once were common in several southern and southeastern states. However, good control of the parasite was realized once its life cycle was determined. A shift to raising a larger numbers of pigs in the Midwestern US, an area less favorable for S. dentatus, helped reduced incidence of infection. Indoor housing, confinement rearing and more effective parasiticides have further improved control.


Adult kidney worms are 20-45 mm long and about 2 mm in diameter. They have a black and white mottling related to internal organs and their contents. Their life cycle is lengthy. Patency seldom is reached in less than 9-12 months and is usually only achieved in swine that reach breeding age. The mature parasites produce ova for at least three years.

The ova are thin walled, morulated, and measure 120 by 70 um. Ova are passed in the host’s urine. In a warm, moist, shaded environment, ova hatch in one to two days and larvae are infective in three to five days. Under favorable conditions, the larvae can survive for several months.


Invasion by larvae can occur prenatally across the placenta, by skin penetration, ingestion in feed or, perhaps, by ingestion of earthworms. Ingestion probably is the most common route of infection.

Larvae go through five developmental stages (L1-L5) to reach maturity. Ingested L3 larvae migrate from the small or large intestine to various sites. Many travel via mesenteric lymphatics or by portal venous blood to the liver where they migrate extensively for two to four months. The larvae then penetrate the liver capsule, cross the peritoneal cavity and encyst in their definitive site: the perirenal fat or near ureters. Here they establish fistulous connections with the renal pelvis or ureters. When mature, they discharge their ova into the urine. Occasionally the parasites can be found within the kidney.

When infection by the L3 occurs transcutaneously, larvae first migrate to the lungs, then ascend the trachea to the pharynx, and finally are swallowed to reach the intestine. They then follow the same route followed by ingested larvae.

Development to patency usually takes at least 9-12 months after ingestion of larvae. Prenatal infections can result in patency in less than five months but this route of infection seems only to occur infrequently. Most swine are marketed before patency can occur.


Severe damage is caused by the migrating larvae. During migration through the portal vein, they often produce a severe phlebitis. Prolonged migration in the liver, prior to patency of the parasite, can cause severe interstitial hepatitis with extensive fibrosis. In slaughter age swine, hepatic fibrosis and abscessation can be extensive and lead to liver condemnation. Because larvae migrate widely, lesions are produced at many different sites.

Clinical signs

An unthrifty appearance, slow growth, poor feed conversion and occasional deaths in the herd are common signs. Other signs are usually seen only sporadically and reflect localization of larvae in aberrant sites. Posterior ataxia or paralysis occurs occasionally in pigs when larvae migrate in or along the spinal cord.


Lesions depend somewhat on the stage of parasitism observed. Often the most obvious lesion is a gray to white, cirrhotic liver which may contain small abscesses. Lesions usually are more severe than those caused by the larvae of Ascaris suum. Additional lesions may include swelling of mesenteric lymph nodes, phlebitis in the portal vein with occasional thrombi, and small abscesses in the pancreas or lung. Other less common lesions include peritonitis (sometimes with intussusception of the intestine), pleuritis, and localized abscesses or abscess-like lesions in the spleen, lumbar muscles, retroperitoneum or spinal cord. Adult worms are most often found in or near the kidney, in walls of the ureters, or in the perirenal fat.


Diagnosis is usually made at necropsy by observation of the abscesses and parasites at sites of localization. The extensively-scarred, enlarged liver seen with severe infestations is rather unique in swine and may suggest the diagnosis, especially in areas where the parasite is endemic. Diagnosis can be made in the live animal or at necropsy by identifying ova in the urine. The first urine passed in the morning often contains many ova.


Control is possible through a breeding program that utilizes only gilts and young boars. These are slaughtered after producing one litter. This usually precludes their living long enough for ova of S. dentatus to be passed in their urine. Eradication has been achieved on some production sites by this and management changes that preclude swine coming into contact with the parasite on pasture. Placing feeding and watering equipment on concrete in a sunny, well-drained location is a simple management practice that has value.

Confinement housing usually eliminates losses from kidney worms.

Treating sows a few weeks prior to farrowing will usually prevent transplacental transmission of the parasite to fetuses. For treatment, see the table, Anthelmintics and Parasiticides.