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Taenia solium, the pork tapeworm, is endemic in most developing countries. The adult tapeworm only lives in the small intestine of humans, who get infected eating poorly cooked pork with cystic larvae. Tapeworm carriers expel microscopic tapeworm eggs and occasionally tapeworm segments with the stools. In areas with poor sanitation, pigs ingest stools from the environment and become infected with larvae.1 Humans can also get infected with cysticercosis by fecal-oral contamination, clustering around the houses where a tapeworm carrier lives. In this issue, O’Neal and colleagues report two cases of neurocysticercosis in a family of refugees from Burma who moved to a refugee camp in Thailand and then to the United States.2 In this report, the occurrence of multiple cases in a family demonstrates the focal nature of cysticercosis transmission, suggesting that the detection of a confirmed cysticercosis case should prompt the evaluation of other household members for both symptomatic cysticercosis and intestinal taeniasis. It also adds to reports from other countries published in the journal and elsewhere (including a case report in an immigrant from Laos3 and a series of neurocysticercosis cases in Israeli travelers4), reflecting the wide areas of endemicity of the disease.2–8

Diagnosis

  1. Top of page
  2. Diagnosis
  3. Geographic Distribution
  4. Antiparasitic and Adjuvant Treatment
  5. Prevention and Control
  6. Declaration of Interests
  7. References

Despite many advances in the diagnosis of cysticercosis in the past two decades, the primary diagnosis is still obtained by neuroimaging [either computed tomography (CT) or magnetic resonance imaging (MRI)], poorly available and economically difficult to obtain in rural endemic areas (or immigrant camps). The requirement for imaging arises from the need to know the number, size, and stage of parasites, as well as the degree and extent of the inflammatory response of the host and other findings which could require immediate management (ie, obstructive hydrocephalus), or be of risk if antiparasitic treatment is instituted (fourth ventricle cysts, massive infections, or ocular cysts).1 Serology plays a confirmatory role with the enzyme-linked immunoelectrotransfer blot (EITB) assay using purified glycoprotein antigens from the parasite as the assay of choice.9 Serum antigen-detection assays may provide useful information on the presence or persistence of living parasites for case characterization and follow-up purposes.10 Sensitivity of the EITB in cases with two or more brain lesions approaches 100%, while the sensitivity of antigen-detection enzyme-linked immunoabsorbent assay (ELISA) in intraparenchymal neurocysticercosis seems somewhat lower. Individuals with a single brain degenerating cysticercus may easily (∼30%–40%) test negative for antigens or antibodies.9,10 Polymerase chain reaction (PCR) in cerebrospinal fluid (CSF) has been reported of use for diagnosis.11,12 Confirmatory studies should better define its performance, particularly in intraparenchymal neurocysticercosis where most diagnostic dilemmas occur. Characterization of the specific degree, location, and stage of CNS involvement is key in guiding the medical or surgical management of neurocysticercosis.

Geographic Distribution

  1. Top of page
  2. Diagnosis
  3. Geographic Distribution
  4. Antiparasitic and Adjuvant Treatment
  5. Prevention and Control
  6. Declaration of Interests
  7. References

Cysticercosis is also seen in industrialized countries with some frequency, mostly as a result of migration from endemic countries, or less frequently in travelers as recently reviewed by Leshem and colleagues.4 Usually perceived as a disease of Hispanics, endemic areas involve most of Africa, parts of China, the Indian subcontinent, and sizable parts of Asia. Still, many physicians in North America and Europe are not familiar with cysticercosis. As shown by the Burma refugees' report, migration to areas with easy access to neuroimaging can highlight endemic areas not previously known. This information on endemicity is required to drive diagnostic suspicion, particularly in cases of late onset epilepsy or intracranial hypertension in immigrants from endemic regions, whose accumulated exposure and likely disease prevalence would be much higher than the occasional traveler.

Antiparasitic and Adjuvant Treatment

  1. Top of page
  2. Diagnosis
  3. Geographic Distribution
  4. Antiparasitic and Adjuvant Treatment
  5. Prevention and Control
  6. Declaration of Interests
  7. References

Treatment of symptomatic neurocysticercosis involves symptomatic measures to control seizures, headache, intracranial hypertension or other symptoms, and antiparasitic agents to destroy live parasites.1,13,14 The use of antiparasitic agents has been questioned because of the resulting inflammation and exacerbation of symptoms as a treatment-associated paradoxical reaction when the parasites degenerate. Antiparasitic treatment of neurocysticercosis should be performed under hospital conditions and after excluding ocular cysticercosis or other conditions which could be associated with increased risks if given antiparasitic treatment (eg, in acute hydrocephalus due to ventricular cysts, particularly those in the third or fourth ventricles, or diffuse brain edema in massive infections). Antiparasitic treatment uses 1 to 2 weeks of albendazole at 15 mg/kg/d, or 2 weeks of praziquantel at 50 mg/kg/d, although shorter regimens of albendaozle may be considered. Albendazole is preferred because it is cheaper and available in most countries, and appears to be slightly more efficacious. A first course of antiparasitic therapy is expected to kill approximately 60% to 70% of cysts, resolving all live parasites in only 40% of patients. Corticosteroids are routinely added as concomitant therapy to modulate the inflammation which results from parasite damage and antigen exposure followed by the immune response of the host, and thus patients should be screened for tuberculosis or strongyloidiasis.15,16

Standard doses of antiparasitic treatment as used for geohelminths can also trigger neurological symptoms in latent neurocysticercosis, as reported and discussed in a few instances.2,17–19 Thus, most experts recommend niclosamide (2 g, p.o., single dose) as the treatment of choice for intestinal T solium taeniasis because it is not absorbed from the intestinal lumen. How frequently neurological side effects occur is open to argument. Massive albendazole or praziquantel chemotherapy programs have rarely reported neurological side effects. However, these programs are performed in field conditions, where follow-up is much poorer than that in hospitalized patients, and tend to use passive rather than active adverse event surveillance so underreporting is clearly possible. The likelihood of moderate to severe neurological adverse events is likely restricted to individuals harboring live brain cysts, which in endemic villages are a small minority of those infected (the vast majority of asymptomatic neurocysticercosis-infected individuals in endemic regions have calcified brain lesions only). In any case, caution and appropriate surveillance should be taken when using antiparasitic medication in individuals coming from cysticercosis-endemic regions.

Neurocysticercosis-associated seizures usually respond well to standard treatment with first-line antiepileptic drugs. After a seizure-free period of 2 to 3 years, antiepileptic therapy can be discontinued but the risk of seizure relapse is significant. In relapses, the antiepileptic drug should be reinstated and continued for much longer. Some authors advocate early withdrawal of antiepileptic drugs after the resolution of a single intraparenchymal lesion, but no controlled data is yet available to support this claim.

Prevention and Control

  1. Top of page
  2. Diagnosis
  3. Geographic Distribution
  4. Antiparasitic and Adjuvant Treatment
  5. Prevention and Control
  6. Declaration of Interests
  7. References

Taenia solium cysticercosis is claimed to be eradicable, on the basis of several characteristics which include having a single and easily targetable definitive host (human), only one intermediate host of importance in transmission (pig), the availability of accurate diagnostics including CT, MRI, and serology, and effective etiological treatments including albendazole, praziquantel, and niclosamide. Multiple interventions have been tried to control cysticercosis by interrupting transmission in endemic regions, mostly based on mass human chemotherapy with praziquantel or niclosamide. In recent years, our group in Peru performed a wide-scale elimination program which used repeated courses of mass human chemotherapy with niclosamide, mass porcine chemotherapy with oxfendazole,20 porcine vaccination with the Australian effective vaccine TSOL18,21 and case confirmation of taeniasis with coproantigen detection,22 with very promising results.23 Currently, active surveillance is being applied into the areas intervened more than 1 year ago, to assess if the effect of the intervention persists over time, and to identify factors related to persistence or reintroduction of active transmission. Proof of concept and sustainment of elimination would represent a first step in a long way toward eradication. Meanwhile, in nonendemic countries, more awareness on the infection (either taeniasis or cysticercosis) and the disease (neurocysticercosis) are required, particularly for clinicians attending to immigrant populations.

Declaration of Interests

  1. Top of page
  2. Diagnosis
  3. Geographic Distribution
  4. Antiparasitic and Adjuvant Treatment
  5. Prevention and Control
  6. Declaration of Interests
  7. References

H. H. G. is supported by a Wellcome Trust International Senior Research Fellowship in Public health and Tropical Medicine. Otherwise he has no conflicts of interest to declare.

References

  1. Top of page
  2. Diagnosis
  3. Geographic Distribution
  4. Antiparasitic and Adjuvant Treatment
  5. Prevention and Control
  6. Declaration of Interests
  7. References