Parasites of the Urogenital System

By | 2011-11-05



• Distributed in domestic and wild pigs in tropical and subtropical regions; locally significant in pigs raised in outdoor situations.

• Common name: kidney worm.

Life Cycle

• Direct; indirect with paratenic host.

• Eggs passed in urine; L1 develops and hatches; infective L3 develops in approximately 4 days; paratenic host becomes infected by ingesting infective L3.

• Pig acquires infection through either the percutaneous route, ingestion of infective L3 directiy or in paratenic host, or transplacental transmission; ingested larvae penetrate the stomach wall, molt to L4, and migrate to liver via portal circulation; percutaneous larvae molt to L4 in skin and migrate to liver via the lungs and systemic circulation; larvae migrate in the liver for 3-9 months, molt, and penetrate the liver capsule to migrate to the perirenal tissues and wall of the ureters where they mature.

• Prepatent period is 9-16 months; may live 3 or more years.

Pathogenesis and Clinical Signs

• Migrating larvae are more pathogenic than adults with the liver most severely affected; hypertrophy, cirrhosis, and thrombosis of hepatic vessels may occur; larvae may also migrate to ectopic sites where they are encapsulated.

• Adults are enclosed in fibrous cysts connected by channels to ureters or renal pelvis; adults may cause peritonitis, urethritis, and cystitis.

• Clinical signs may include inappetence, decreased weight gain or weight loss, emaciation, ascites; death is rare.



• Can find trichostrongyle-type eggs in urine sediment.

• Eggs are ellipsoidal, broad, thin-shelled, 90-120 x 43-70 um, containing morula with 32-64 cells.


• Adults are pinkish, stout, 2-4.5 cm in length; found in capsules in perirenal fat, ureter walls, and adjacent tissues.

Treatment and Control

• See Table Partial List of Nematodical Anthelmintics for Pigs for treatment.

• Because of the long prepatent period, can run gilts through a single breeding cycle before egg shedding begins; this progressively eradicates the source of infection.


• Distributed in southern Europe, North and South America in mink, marten, polecat, weasels, canids, cats; occasionally reported in cattle, pigs, and humans.

• Common name: giant kidney worm.

Life Cycle

• Indirect.

• Intermediate host: aquatic oligochete.

• Paratenic host: frogs and fish (e.g., bullhead, pike).

• Eggs are passed in the urine; L1 develops within the egg in approximately 1 month; oligochete ingests egg containing Lx; develops to infective L3 in 2-4 months.

• Definitive host becomes infected by ingesting infected oligochete or, more likely, through ingestion of paratenic host; larvae penetrate stomach wall, migrate through the liver and body cavity to the kidney, molt, and mature to adults.

• Prepatent period: 3.5-6 months.

Pathogenesis and Clinical Signs

• Larval migration through the stomach cause hemorrhages, inflammation, and fibrosis; migration through the liver causes necrotic tracks that fibrose; if females remain in the abdominal cavity, they may release large numbers of unfertilized eggs causing peritonitis; infection of the kidney causes atrophy and fibrosis; hydronephrosis may or may not occur.

• Infection may be inapparent; clinical signs may include abdominal and lumbar pain, inappetence, vomiting, hematuria, uremia, and polydipsia.



• Eggs may be found in urine sediment.

• Eggs are barrel-shaped, with thick, yellow-brown, pitted shell except at poles that are clear (“bipolar plugs”), 71-84 x 46-52 urn.


• Worms are red, very large — females are up to 1 m in length and 1 cm in width; found in the abdominal cavity or kidney.

Treatment and Control

• Treatment consists of surgical removal of the parasite and affected kidney, if necessary.

• Prevent predation and scavenging whenever possible.


• Probably worldwide in distribution in a variety of carnivores and omnivores; low significance.

Life Cycle

• Indirect; known for P. plica only.

• Eggs are passed in the feces; infective L1 develops in approximately 2 weeks and hatches after ingestion by earthworms; larval development beyond L1 does not occur.

• Definitive host acquires infection by ingesting infected earthworms.

• Prepatent period is approximately 2 months.

Pathogenesis and Clinical Signs

• Generally not pathogenic.



• Eggs may be found in urine sediment or on fecal flotation of urine-contaminated feces.

• Eggs are typical capillarid type, clear to yellow, approximately 65 x 25 um, with flattened bipolar plugs on each end.


• Adults live in the urinary bladder; adult worms are hairlike and are generally missed during gross necropsy; rather, they may be found on histologic sections.

Treatment and Control

Fenbendazole at 50 mg per kg daily for 3 days and ivermectin at 0.2 mg per kg once have been successful in dogs.



• Worldwide distribution in cattle; moderate significance.

Life Cycle

• Direct.

• Transmitted by coitus; in cows, parasites first multiply in secretions of the vagina (2 weeks), then the uterus; in bulls, parasites colonize the secretions of the epithelial lining of the penis, prepuce, and distal urethra; prevalence increases in bulls >4 years old.

Pathogenesis and Clinical Signs

• Bulls: infection is inapparent; remains infected for life.

• Cows: causes vaginitis and endometritis; clinical signs include early embryonic death, abortion, pyometra, fetal maceration, or infertility; infection is self-limiting with clearance occurring within 20 weeks of primary infection and 10 weeks of secondary infection.



• Examination of wet mounts and/or stained smears of bull smegma, vaginal secretions or washings, or aborted material for organisms; may want to culture material to increase numbers; because nonpathogenic trichomonads live in the intestinal tract, must be careful not to contaminate sample with feces.

• Organisms are pear-shaped, 10-25 x 3-15 um, with three anterior flagella, undulating membrane, and trailing posterior flagellum.

• A single positive test is adequate to diagnose herd infections but three or more negative tests are necessary to ensure individual bulls are not infected.

Treatment and Control

• Generally do not treat cattle for infection.

• Control measures: replace older bulls with younger bulls; do not borrow or lease bulls; culture all newly purchased bulls regardless of age and bulls 2 weeks after the breeding season — cull those that are positive; use artificial insemination whenever possible using semen from a facility that tests for the parasite; vaccinate cows and heifers if the threat of exposure is unavoidable.