Pork Tape Worm Disease : Clinical Aspects

PORK TAPEWORM DISEASE

EPIDEMIOLOGY

Although infected swine are still occasionally found in the United States, most human disease is found in immigrants from endemic areas. Although this infection is widely dis-tributed throughout the world, it is particularly common in south and southeast Asia, Africa, Latin America, and Eastern Europe.

PORK TAPE WORM DISEASE :  CLINICAL ASPECTS

MANIFESTATIONS

The signs and symptoms of infection with the adult worm are similar to those of taeniasis saginata. Clinical manifestations are totally different when humans serve as intermediate hosts. Cysticerci develop in the subcutaneous tissues, muscles, heart, lungs, liver, brain, and eye. As long as the number is small and the cysticerci remain viable, tissue reaction is moderate and the patient asymptomatic. The death of the larva, however, stimulates a marked inflammatory reaction, fever, muscle pains, and eosinophilia.

 The most important and dramatic clinical presentation of cysticercosis results from lesions in the central nervous system (CNS). During the acute invasive stage, patients experience fever, headache, and eosinophilia. In heavy infections, a meningoencephalitic syndrome with cerebrospinal fluid (CSF) eosinophilic pleocytosis may be present. Es-tablished cysts can be found in the cerebrum, ventricles, subarachnoid space, spinal cord, or eye. Cerebral cysts are usually small, often measuring 2 cm or less in diameter; racemose lesions may be threefold larger. These parenchymal infections can induce fo-cal neurologic abnormalities, personality changes, intellectual impairment and/or seizures; in many endemic areas, cysticercosis is the leading cause of epilepsy. Sub-arachnoid lesions and cysticerci located within the fourth ventricle may obstruct the flow of CSF, producing increased intracranial pressure with its associated headache, vomit-ing, visual disturbances, or psychiatric abnormalities. Multiple racemose lesions have a predilection for the basal cisterns, particularly in young women, from whence they rapidly spread around the base of the brain and cerebrum with catastrophic result. Spinal involvement produces cord compression or meningeal inflammation. Eye lesions incite pain and visual disturbances.

DIAGNOSIS

Infection with the adult worm is diagnosed as described for T. saginata. Cysticercosis is suspected when an individual who has been in an endemic area presents with neurologic manifestations or subcutaneous nodules. Roentgenograms of the soft tissues often reveal dead, calcified cysticerci. Viable lesions may be detected as low-density masses by com-puted tomography (CT) or magnetic resonance imaging (MRI). Brain cysticerci typically are 5 to 10 mm in diameter. Subarachnoid lesions are often larger, may be lob-ulated, and are often “isodense,” making them difficult to visualize radiographically. The diagnosis is confirmed by demonstrating the larva in a biopsy sample of a subcutaneous nodule or specific antibodies in the circulating blood. Serum and CSF enzyme im-munoassays and Western blot testing for specific anticysticercal antibodies have a sensi-tivity of 80 to 95%. The presence of IgG antibodies alone may reflect the presence of past or inactive disease.

TREATMENT AND PREVENTION

Infection with the adult worm is approached in the manner described for T. saginata. Be-cause the mortality rate in patients with symptomatic neurocysticercosis approaches 50%, aggressive management is warranted. Patients with parenchymal lesions usually respond to prolonged treatment with praziquantel or albendazole. Concomitant corticosteroid administration helps minimize the inflammatory response to dying cysticerci. Intraven-tricular subarachnoid and eye lesions appear relatively refractory to chemotherapy; surgery, CSF shunts, and corticosteroids may help ameliorate symptoms.