Figure 198.1 Cysticerci in subcutaneous location (A), on brain computed tomography (CT) showing innumerable cysticerci (starry-night appearance) (B), and calcifications in soft tissues (C). (Courtesy of Dr. S. K. Gaekwed.) Bradley’s Neurology in Clinical Practice, 4th edn. Butterworth-Heinemann; 2004.
Neurocysticercosis is often asymptomatic; in such cases, indications for treatment must be considered carefully. Symptomatic cases can be active or inactive (calcified). Therapy can be via specific anthelmintic treatment, surgery, corticosteroids, or symptomatic treatment. The choice of treatment has to be individually tailored. Anthelmintic therapy with praziquantel or albendazole is indicated in active cysticercosis with several parenchymal cysts or with clinical signs of vasculitis, encephalitis, and arachnoiditis. Traditionally, praziquantel is given orally in a daily dose of 50 mg/kg for 14 days, but a shorter regimen with a higher dose has been proposed. Albendazole is given orally in a daily dose of 15 mg/kg for 8 days. For parenchymal brain cysticerci, the efficacy is about 60% for praziquantel and 85% for albendazole. Damage to cysticerci, caused by both drugs, may result in a local inflammatory reaction and edema, which necessitates a concomitant additional corticosteroid or antihistamine drug therapy.
Surgical extirpation is indicated for single parenchymal, intraventricular, spinal, and ocular cysticerci and with focal symptoms (e.g., cranial nerve dysfunction). A ventricular shunt is indicated in hydrocephalus. Corticosteroids and immunosuppressants may control vasculitis and encephalitis. Antiepileptic drugs are used mainly in inactive cysticercosis with granulomatous or calcified lesions. The global disability and mortality from neurocysticercosis are still considerable but its control measures are introduced only locally.
Hymenolepis nana infections
Hymenolepis nana, the dwarf tapeworm, 15 to 40 mm long, lives only up to 3 months in human small intestine. Some of the tapeworm eggs are expelled with feces and constitute a source of autoinfection or infection for other people. The other eggs hatch in the human intestine and develop within a month into cysticercoids in intestinal villi and later into the next generation of adult tapeworms in the same host.
Such a cycle facilitates spread of infection in close communities (day-care centers, schools, psychiatric institutions) as well as permits intensive infections of thousands of tapeworms, especially in malnourished or immunodeficient individuals. Usually a specific immunity develops and regulates the intensity and duration of infection, which occurs mainly in children and often clears spontaneously in adolescence. Hymenolepiasis is very common in regions with a hot, dry climate; it is rare in countries with appropriate sanitation.
Intensive infections may cause diarrhea, abdominal pains, and general symptoms such as weight loss, pallor, and weakness. Diagnosis is made by finding characteristic H. nana eggs in feces. Treatment with a single dose of praziquantel, 15 to 25 mg/kg, is highly effective; in intensive infections treatment must be repeated after 3 weeks. Niclosamide is much less effective and requires repeated courses of 7 days with the daily dose of 2 g for adult patients. Successful treatment has to be confirmed by negative fecal examination every 2 weeks for 2 months after therapy.
Other intestinal cestodes
Diphyllobothriasis, caused by Diphyllobothrium latum, Diphyllobothrium dendriticum, and Diphyllobothrium pacificum, still occurs around unpolluted large lakes in moderate climates (the Great Lakes in the United States and Canada and lakes in Finland and Switzerland) and along the Pacific Coast in South America. An uncommon clinical complication of diphyllobothriasis is vitamin B12 deficiency. Diagnosis is made by finding characteristic eggs during fecal examination. Treatment is a single dose of praziquantel, 15 to 25 mg/kg. Evaluation of successful therapy is by repeated fecal examination some months after.
Hymenolepis diminuta
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