The cestodes, or tapeworms, are segmented worms that can be classified into two groups according to whether humans are the definitive or the intermediate host. The tapeworm attaches to intestinal mucosa via sucking cups or hooks located on the scolex. Proglottids (segments) form behind the scolex and constitute the bulk of the tapeworm.

Taeniasis Saginata and Taeniasis Asiatica

Microbiology Humans are the definitive host for Taenia saginata, the beef tapeworm, and T. asiatica, the swine tapeworm, which inhabit the upper jejunum. Eggs are excreted in feces and ingested by cattle or other herbivores (T. saginata) or pigs (T. asiatica); larvae encyst (cysticerci) in the striated muscles of these animals. When humans ingest raw or undercooked meat, the cysticerci mature into adult worms in ~2 months.

Clinical Manifestations Pts become aware of the infection by noting passage of motile proglottids in their feces. They may experience perianal discomfort, mild abdominal pain, nausea, change in appetite, weakness, and weight loss.

Diagnosis The diagnosis is made by detection of eggs or proglottids in the stool; eggs may be detected in the perianal area by the cellophane-tape test (as in pinworm infection). Eosinophilia and elevated IgE levels may occur.

Taeniasis Solium and Cysticercosis

Microbiology and Pathogenesis Humans are the definitive host and pigs the usual intermediate host for T. solium, the pork tapeworm.

• The disease has two forms, which depend on the form of parasite ingested.
  • - By ingesting undercooked pork containing cysticerci, humans develop intestinal tapeworms and a disease similar to taeniasis saginata.
  • - If humans ingest T. solium eggs (e.g., as a result of close contact with a tapeworm carrier or via autoinfection), they develop cysticercosis due to larvae penetrating the intestinal wall and migrating to many tissues.

Clinical Manifestations Intestinal infections are generally asymptomatic except for fecal passage of proglottids. The presentation of cysticercosis depends on the number and location of cysticerci as well as the extent of associated inflammatory responses or scarring.

• Cysticerci can be found anywhere in the body but most often are detected in the brain, skeletal muscle, SC tissue, or eye.
• Neurologic manifestations are most common and include seizures (due to inflammation surrounding cysticerci in the brain), hydrocephalus (from obstruction of CSF flow by cysticerci and accompanying inflammation or by arachnoiditis), and signs of increased intracranial pressure (e.g., headache, nausea, vomiting, changes in vision).

Diagnosis Intestinal infection is diagnosed by detection of eggs or proglottids in stool. A consensus conference has delineated criteria for the diagnosis of cysticercosis (Table 109-1). Findings on neuroimaging include cystic lesions with or without enhancement, one or more nodular calcifications, or focal enhancing lesions.

Echinococcosis

Microbiology and Epidemiology Humans are an intermediate host for Echinococcus larvae and acquire echinococcal disease by ingesting eggs spread by canine feces (for E. granulosus).

• After ingestion, embryos escape from the eggs, penetrate the intestinal mucosa, enter the portal circulation, and are carried to many organs but particularly the liver and lungs. Larvae develop into fluid-filled unilocular hydatid cysts within which daughter cysts develop, as do germinating cystic structures (brood capsules). Cysts expand over years.
• Echinococcosis is prevalent on all continents, particularly in areas where livestock is raised in association with dogs.
• E. multilocularis, found in Arctic or sub-Arctic regions, is similar to E. granulosus, but wild canines (e.g., foxes) are the definitive hosts and rodents are the intermediate hosts. The parasite is multilocular, and vesicles progressively invade host tissue.

Clinical Manifestations Expanding cysts exert the effects of space-occupying lesions, causing symptoms in the affected organ (usually liver and lung); the liver is involved in two-thirds of E. granulosus infections and ~100% of E. multilocularis infections.

• Pts with hepatic disease most commonly present with abdominal pain or a palpable mass in the RUQ. Compression of a bile duct may mimic biliary disease, and rupture or leakage from a hydatid cyst may cause fever, pruritus, urticaria, eosinophilia, or anaphylaxis.
• Pulmonary cysts may rupture into the bronchial tree or pleural cavity and cause cough, salty phlegm, chest pain, or hemoptysis.
• Rupture of cysts may result in multifocal dissemination.
• E. multilocularis disease may present as a hepatic tumor, with destruction of the liver and extension into adjoining (e.g., lungs, kidneys) or distant (e.g., brain, spleen) organs.

Diagnosis Radiographic imaging is important in detecting and evaluating echinococcal cysts.

• Daughter cysts within a larger cyst are pathognomonic of E. granulosus. Eggshell or mural calcification on CT is also indicative of E. granulosus infection.
• Serologic testing yields positive results in ~90% of pts with hepatic disease, but results can be negative in up to half of pts with lung cysts.
• Aspiration of cysts usually is not attempted because leakage of cyst fluid can cause dissemination or anaphylactic reactions.

Diphyllobothriasis

Diphyllobothrium latum, the longest tapeworm (up to 25 m), attaches to the ileal and occasionally the jejunal mucosa. Humans are infected by consumption of infected raw or smoked fish. Symptoms are rare and usually mild, but infection, particularly in Scandinavia, can cause vitamin B₁₂ deficiency because the tapeworm absorbs large amounts of vitamin B₁₂ and interferes with ileal B₁₂ absorption. Up to 2% of infected pts, especially the elderly, have megaloblastic anemia resembling pernicious anemia and can suffer neurologic sequelae due to B₁₂ deficiency. The diagnosis is made by detection of eggs in the stool. Praziquantel (5-10 mg/kg once) is highly effective.