Practical Veterinarian

Parasites of the Musculoskeletal System



• Worldwide distribution in a variety of mammals including pigs and humans; moderate significance to veterinary medicine but may be highly significant to public health.

Life Cycle

• Direct.

• Unique in that the adult and infective larvae occur within the same host with no intervening free-living stage.

• Adults live in the small intestine; females lay larvae that penetrate the wall of the intestine and enter venules and lymphatics; migrates via the circulatory system to skeletal muscles; preferred sites are diaphragmatic, intercostal, masseter, and tongue muscles; larvae enter myocytes, coil and grow, but do not molt; becomes infective L1 in approximately 15 days.

• Definitive host acquires infection by eating infected muscle tissue; larvae penetrate into the small intestinal mucosa, molt, and mature 36-40 hours postinfection; larviposition begins 5-6 days postinfection; adult infections are short-lived (4 — 6 weeks) and self-terminating.

• Sylvatic cycle involves wild carnivorous or omnivorous mammals and their prey species; domestic cycle occurs when prey species, such as rats, are ingested by pigs, dogs, or cats; human infections occur by ingesting undercooked or raw meat such as pork, pork products, horse, or bear meat.

Pathogenesis and Clinical Signs

• Larvae in the myocyte become encapsulated by a host-derived membrane in approximately 3 months; cysts may calcify as they age but some larvae will remain alive for 2 or more years.

• Infections of domestic animals are generally inap-parent; may be misdiagnosed.

• Infections in humans may be inapparent or fatal; symptoms may include abdominal pain, diarrhea, nausea, fever, myalgia, and malaise.



• Difficult; commercial enzyme immunoassays for use with serum, whole blood, or tissue fluids are available in the United States for testing pigs.


• Several samples of diaphragm (total of 1-5 gm) are pressed between glass slides and examined at approximately 40x for larvae; detects approximately 3 larvae per gram of muscle.

• Artificial digestion fluid can be used to break down muscle tissue to free larvae that can be seen in sediment with light microscopy.

Treatment and Control

• Generally do not treat domestic animals for infection.

• Control on-farm requires good hygiene; heat-treat (at least 60°C for 60 min) scraps fed to pigs; a new system of food safety to certify pigs as free of the parasite on-farm is being implemented in the United States.

• For humans, the best control is proper cooking of meat; larvae die around 57°C, so cooking of meat to an internal temperature of 77°C is recommended; freezing also kills larvae, but cuts must be <15 cm thick and frozen at -15°C for at least 20 days (freezing does not kill some of the other species of Trichinella such as T. nativa).



• Includes Taenia saginata (beef tapeworm) and T. solium (pork tapeworm) of humans; low to moderate significance to veterinary medicine, but highly significant to public health.

• Worldwide distribution although T. solium has become rare in Europe and North America.

Life Cycle

• Indirect.

• Intermediate host: cattle (T. saginata); domestic and wild swine, humans, occasionally dogs (T. solium).

• Metacestode: cysticercus.

Taenia saginata: gravid proglottids are passed in feces or migrate out of the anus; eggs are shed from proglottid; cattle become infected by ingesting eggs when feeding; oncospheres leave eggs, penetrate intestinal wall, and travel to cardiac and skeletal muscles via the circulatory system; cysticerci develop and become infective in 8-16 weeks; live up to 2 years; dead cysticerci may calcify; occasionally, may find cysticerci in brain, lungs, liver, and other sites; humans acquire infection by ingesting undercooked or raw beef; scavenging birds may disseminate eggs.

Taenia solium. similar to T. saginata; cysticerci may be found in striated muscle, heart, liver, lung, kidney, subcutaneous tissues, CNS; become infective in 10-12 weeks; may survive lifelong in the pig; humans are definitive host but can also become infected with cysticerci by release of eggs from gravid proglottids transferred to the stomach from the duodenum by reverse peristalsis or by ingestion of eggs; neurocysticercosis or ocular cysticercosis may result.

Pathogenesis and Clinical Signs

• Infection with both adult and metacestode stages is usually inapparent.

• In dogs, infections with cysticerci of T. solium may result in neurologic disorders and death as a result of localizing in the brain.

• In humans, infections with cysticerci of T. solium may interfere with vision or cause neurologic disorders and death.



• Can differentiate gravid proglottids of T. solium from those of T. saginata; however, it is unlikely the practitioner would be asked to do so.

• Serodiagnostic tests have been developed for pre-slaughter diagnosis of infections in pigs in countries outside the United States.


• Cysticercus of T. saginata is white, ovoid, fluid-filled, up to 1 cm in diameter; invaginated scolex does not have a rostellum or hooks; dead, calcifying cysticerci are difficult to identify.

• Cysticercus of T. solium is white, ovoid, fluid-filled, up to 1.8 cm in diameter; invaginated scolex has a rostellum and hooks; dead cysticerci can be recognized by the presence of hooks.

Treatment and Control

• Treatment of domestic animals for larval cestodes is generally not attempted.

• Control methods include proper hygiene to prevent contamination of feed and water with human feces.