Tissue Nematodes (Roundworms)

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Tissue Nematodes (Roundworms)

Tissue nematodes have life cycles similar to those of intestinal nematodes, consisting of five distinct stages including adult male and female worms and four larval stages. These organisms are distributed worldwide, predominantly in the tropics and subtropics. The organisms are transmitted by three routes: biting and subsequent blood-feeding arthropods (filarial worms), as discussed in Chapter 53; ingestion of small freshwater crustaceans; and ingestion of contaminated meat. In most cases, adult worms do not multiply and develop within the human host. Clinical symptoms are dependent on the number of infecting parasites, the tissue invaded, and the host’s general health and immune response. Diagnosis is typically by the microscopic visualization of the organisms in tissue when appropriate.

Trichinella Spiralis

General Characteristics

The family Trichinellidae contains 11 recognized species including Trichinella spiralis, Trichinella nativa, Trichinella nelsoni, T. murrelli, T. papuae, T. zimbabwensis, T. pseudospiralis, and T. britovi, all capable of causing trichinosis. However, T. spiralis is the most common human pathogen. The organism is unique in comparison to other helminths in that all stages of development, including the adult and larval stages, occur within a single host.


Trichinella occurs worldwide with the cycle maintained in several different mammalian species. The mammal serves as the definitive host for the adult worm and the intermediate host for the encysted larvae. Humans acquire the infection by eating undercooked meat that contains the infective encysted larvae. Although this is typically transmitted in pork, human cases have been associated with ingestion of bear, walrus, horsemeat, and other mammals.

The encysted larvae are ingested. When the undercooked meat is digested in the stomach, the larvae are resistant to the gastric pH and pass to the intestine, where they invade the mucosa. In about 1.5 days, the larvae mature and mate, and the female worm begins to release motile larvae. These larvae then migrate to the lymphatic system or mesenteric venules and become distributed throughout the body. The larvae then deposit in the striated muscle tissue, where they can continue development, coil, and encyst, becoming infective. The larvae encyst in the active striated muscle including the diaphragm, larynx, tongue, jaws, neck, ribs, biceps, and gastrocnemius. The generalized life cycle is depicted in Figure 52-1. The larvae may remain viable within the cyst for several years. The larvae eventually die and the encysted capsules become calcified.

Pathogenesis and Spectrum of Disease

Trichinosis is a disease of the muscle caused by infection with the encysted larval form of Trichinella spp. (Figure 52-2). The adult stages reside in the human intestine. The disease ranges from mild to severe dependent on the number of parasites present. The intestinal stage lasts approximately 1 week and typically includes mild symptoms of nausea, abdominal discomfort, diarrhea, and/or constipation. Diarrhea may last as long as 14 weeks with no apparent muscle involvement. The migration of the larvae results in an intense inflammatory response causing periorbital edema, fever, muscle pain or tenderness, headache, and myalgia. A marked peripheral eosinophilia is often present. If the parasitic infection is low, eosinophilia may be the only diagnostic sign evident. Occasionally, splinter hemorrhages may be present below the nails.

In addition to the typical infection of the active striated muscle as previously indicated, occasionally larvae will migrate into the brain, meninges, and myocardium. However, the larvae will not encyst in these tissues. Brain and meningeal infections will result in neurologic symptoms, and infection of the myocardium may result in myocarditis and dysrhythmias leading to sudden death.

Laboratory Diagnosis

Diagnosis may be difficult, because the symptoms may resemble a variety of flulike illnesses. A thorough patient history is required to assist the physician in diagnosing the condition in a timely fashion. Identification of encysted larvae through muscle biopsy provides definitive diagnosis. However, based on location, some tissues may be difficult to access and therefore the condition may not be diagnosed until the postmortem examination. Histologic examination of formalin-fixed or paraffin-imbedded tissue may be used to visualize encysted larvae. Occasionally, dependent on the length of infection, calcified larvae may be seen in x-rays.

Serologic diagnosis is sufficient in most cases. Patients will present with a specific antibody response in 3 to 5 weeks following acute illness. A negative serologic test followed by a positive seroconversion is considered definitive diagnosis.

Molecular species–specific polymerase chain reaction (PCR) has been developed. Various techniques including RFLP (restriction fragment length polymorphism) and RAPD (rapid amplification of polymorphic DNA) have been investigated. Currently, these methods are predominantly used in animal epidemiologic studies and have not been implemented within the diagnostic laboratory.

Toxocara Canis (Visceral Larva Migrans) and Toxocara Cati (Ocular Larva Migrans)

General Characteristics

Toxocara canis (intestinal ascarid of dogs) and Toxocara cati (intestinal ascarid of cats) are the cause of a human syndrome resulting from larval migration within the host.


Toxocariasis is a zoonotic disease with worldwide distribution. Humans become infected with the accidental ingestion of eggs (Figure 52-3). The definitive hosts, dogs (T. canis) and cats (T. cati), pass the larvae transplacentally or lactogenically to their offspring and pass unembryonated eggs in the feces. The eggs mature in 10 to 20 days, and then become infective. Once the eggs are ingested, the larvae are released in the small intestine, penetrate the mucosa, and migrate to the liver, lungs, or other body sites. The larvae migrate up the respiratory tract and are swallowed, returning to the intestinal tract where they mature into adult worms. The adult worms are unable to mature in a human host and therefore wander throughout the body causing the migratory syndromes.

Figure 52-3

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