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Cysticercosis (Outside the Central Nervous System)

Epidemiology and Pathology

Man acquires cysticercosis by ingesting food, water, or feces containing eggs of T. solium (Figs. 7.6, 7.7). Autoinfection can occur from contaminated hands or, less commonly, by regurgitating proglottids of an adult tapeworm from the gut into the stomach during a bout of nausea; this may occur spontaneously or in association with antihelminthic therapy. Oncospheres (larvae) released from their shells in the gut penetrate the mucosa and spread throughout the body, developing into cysticerci, most commonly in the voluntary muscles and brain, but also in the orbits, heart muscle, liver, and lung. Oncospheres may invade the eye and be seen clearly moving in the anterior or posterior chamber. Infections vary from a single cysticercus to many hundreds (Fig. 7.8), and may be limited to one organ or be generalized.

Fig. 7.6. Immature stages of human tapeworms: Sparganum (top); Hymenolepis and Taenia cysticerci (middle); Echinococcus larva (bottom left); Coenurus larva (bottom right). (From Medical Parasitology, U.S. Navy).


Fig. 7.7. (A) T. solium eggs with paired booklets within the embryos. x410. (B) T. solium egg which has erupted after expelling its larva. x 410.


Fig. 7.8. (A) Multiple cysticerci of T. solium digested free from cattle muscle. (Courtesy of Dr. Herman Zaiman) (B) Encysted cysticercus with its scolex. Note the characteristic oval shape. x4. (C) Section through cysticercus of T. saginata. The cysticercus is a bladder (1) containing a scolex (2) formed by invagination of the proliferating wall. x 10. AFIP 68-5273.

The resting cysticercus grows to a stable size of 1-2 cm within 3-4 months. Intact cysticerci provoke mild inflammation and fibrosis that "walls them off." As long as the parasite remains alive, equilibrium is maintained between the living cysticercus and the host tissue; when it dies, antigens escape and provoke a more violent inflammatory reaction which includes suppuration, chronic inflammation, and eventually a foreign body granulomatous reaction to the tegument, hooklets, and calcareous corpuscles. Finally, after a few months, the lesion resolves as a calcified scar. Such calcification may not affect the cyst capsule or its contents, and the shape may be maintained unless pressure causes collapse, flattening the calcified cyst into a spindle shape. The life of the cyst may vary within wide limits, and both dead calcified cysts and living parasites may coexist in the same individual and even in the same organ. The parasites usually die in 3-6 years, although they may live longer. In body tissues, it takes several months to 3 years to develop calcification, but within the brain calcification is less common and takes even longer to develop.

Laboratory Diagnosis

A positive pathological diagnosis is made when the cysticercus is excised and identified microscopically. However, the radiological appearance is usually so characteristic that it provides a reliable way of establishing the diagnosis. In cerebral cysticercosis, the cerebrospinal fluid (CSF) may show a significant eosinophilia with lymphocytosis and raised protein albumin; these changes are nonspecific. ELISA can reveal antigens in the CSF and in serum, but false negatives can occur in HIV-positive individuals. Enzyme-linked immunoelectrotransfer blot (EITB) exhibits higher specificity and sensitivity than ELISA.

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Copyright: Palmer and Reeder

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