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T solium is transmitted to pigs that ingest human feces Humans can be either the definitive host (after consuming undercooked pork, leading to tapeworm infection) or the intermediate host (after consuming food contaminated with human feces containing T solium eggs, leading to cysticercosis, which is discussed under invasive tapeworm infections) As with the beef tapeworm, infection with T solium adult worms is generally asymptomatic, but gastrointestinal symptoms may occur Infection is generally recognized after passage of proglottids Autoinfection with eggs can progress to cysticercosis
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Infection with D latum follows ingestion of undercooked freshwater fish, most commonly in temperate regions Eggs from human feces are taken up by crustaceans, these are eaten by fish, which are then infectious to humans Infection with multiple worms over many years can occur Infections are most commonly asymptomatic, but nonspecific gastrointestinal symptoms, including diarrhea, may occur Diagnosis usually follows passage of proglottids Prolonged heavy infection can lead to megaloblastic anemia and neuropathy from vitamin B12 deficiency, which is due to infection-induced dissociation of the vitamin from intrinsic factor and to utilization of the vitamin by worms
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INVASIVE CESTODE INFECTIONS 1 Cysticercosis
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Exposure to T solium through fecal contamination of food Seizures, headache, and other findings of a focal CNS lesion Brain imaging shows cysts; positive serologic tests
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H nana is the only tapeworm that can be transmitted between humans Infections are common in warm areas, especially with poor hygiene and institutionalized populations Infec-
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have shown that corticosteroids alone are as effective as specific therapy plus corticosteroids for controlling seizures, and some reports have shown exacerbation of disease after antihelminthic therapy Considering active lesions, disease with a high likelihood of progression, such as intraventricular cysts, may benefit from therapy At the other end of the spectrum, inactive calcified lesions probably do not benefit from therapy Overall, it remains difficult to determine when treatment is indicated When treatment is deemed appropriate, standard therapy consists of albendazole (10 15 mg/kg/d for 8 days) or praziquantel (50 mg/kg/d for 15 30 days) Albendazole is probably the preferred therapy, as corticosteroids appear to lower circulating praziquantel levels, but increase albendazole levels Increasing the dosage of albendazole to 30 mg/kg/d may improve outcomes Corticosteroids are usually administered concurrently but dosing is not standardized Patients should be observed for evidence of localized inflammatory responses Anticonvulsant therapy is provided if needed, and shunting is performed if required for elevated intracranial pressure Surgical removal of cysts may be helpful for some difficult cases of neurocysticercosis and for symptomatic non-neurologic disease
Del Brutto OH et al Meta-analysis: Cysticidal drugs for neurocysticercosis: albendazole and praziquantel Ann Intern Med 2006 Jul 4;145(1):43 51 [PMID: 16818928] Garcia HH et al; Cysticercosis Working Group in Peru Neurocysticercosis: updated concepts about an old disease Lancet Neurol 2005 Oct;4(10):653 61 [PMID: 16168934] Garcia HH et al New concepts in the diagnosis and management of neurocysticercosis (Taenia solium) Am J Trop Med Hyg 2005 Jan;72(1):3 9 [PMID: 15728858] Gongora-Rivera F et al Albendazole trial at 15 or 30 mg/kg/day for subarachnoid and intraventricular cysticercosis Neurology 2006 Feb 14;66(3):436 8 [PMID: 16382035] Hawk MW et al Neurocysticercosis: a review Surg Neurol 2005 Feb;63(2):123 32 [PMID: 15680651] Nash TE et al Treatment of neurocysticercosis: current status and future research needs Neurology 2006 Oct 10;67(7):1120 7 [PMID: 17030744] Yancey LS et al Cysticercosis: recent advances in diagnosis and management of neurocysticercosis Curr Infect Dis Rep 2005 Jan;7(1):39 47 [PMID: 15610670]
General Considerations
Cysticercosis is due to tissue infection with cysts of T solium that develop after humans ingest food contaminated with eggs from human feces, thus acting as an intermediate host for the parasite Prevalence is high where the parasite is endemic, in particular Mexico, Central and South America, the Philippines, and Southeast Asia An estimated 20 million persons are infected with cysticerci yearly, leading to about 400,000 persons with neurologic symptoms and 50,000 deaths Antibody prevalence rates up to 10% are recognized in some endemic areas, and the infection is one of the most important causes of seizures in the developing world and in immigrants to the United States from endemic countries
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