Cysticercosis
- Staci A. Fischer, M.D.
Basic Information
Definition
Cysticercosis is an infection caused by the tissue deposition of larval forms of the pork tapeworm Taenia solium. T. solium cysts, or cysticerci, may accumulate in any human tissue, including the eyes, spinal cord, skin, muscle, heart, and brain. Central nervous system (CNS) involvement is common and is known as neurocysticercosis. Humans most commonly acquire cysticercosis via fecal-oral transmission from human tapeworm carriers or via ingestion of larval cysts in infected pork or tapeworm eggs in contaminated water or soil. Larvae in the gastrointestinal tract migrate hematogenously to tissues, where they encyst, forming cysticerci.
Synonyms
Cysticerciasis
Taeniasis
Pork tapeworm
| ICD-10CM CODES | |
| B69 | Cysticercosis |
| B69.0 | Cysticercosis of central nervous system |
| B69.1 | Cysticercosis of eye |
| B69.81 | Myositis in cysticercosis |
| B69.89 | Cysticercosis of other sites |
| B69.9 | Cysticercosis, unspecified |
Epidemiology & Demographics
- soliuminfection is worldwide in distribution. Tapeworm infection and cysticercosis are endemic in developing countries where pigs are raised as a food source, including developing countries of Central America, South America, and parts of Africa and Asia.
Serologic studies from endemic areas of Latin America have demonstrated seroprevalence rates of 4% to 24% in native populations.
Neurocysticercosis is most common in the United States in states with large immigrant populations from countries where the disease is endemic.
Physical Findings & Clinical Presentation
After ingestion of T. solium eggs or cysts, humans may remain asymptomatic for years.
Cysticerci in muscles and skin may form subcutaneous nodules without erythema, warmth, or tenderness, mimicking lipomas or subcutaneous cysts.
Neurocysticercosis, the presence of cysts within the brain parenchyma, is usually asymptomatic. Symptoms develop due to the inflammatory response to degeneration of cysts, which can result in focal encephalitis, vasculitis, chronic meningitis, and cranial nerve palsies.
Seizures are the most common manifestation of neurocysticercosis, occurring in 70% to 90% of symptomatic cases. Headache and focal neurologic deficits can also occur.
Up to 40% of patients with epilepsy in endemic areas have neurocysticercosis.
In 10% to 20% of cases of neurocysticercosis, cysts lodge within the ventricular system and result in obstructive hydrocephalus, causing acute intracranial hypertension. Symptoms are caused by the presence of the parasite itself, ependymal inflammation, and/or fibrosis, each of which blocks the circulation of cerebrospinal fluid (CSF). Death may occur from progressive hydrocephalus, cerebral edema, or intractable seizures.
Ocular cysticercosis occurs in less than 5% of infections and is generally asymptomatic. Inflammation in response to degenerating cysticerci may result in chorioretinitis, vasculitis, or retinal detachment, threatening vision.
Etiology
- soliumhas a complex two-host life cycle.
Humans are the only definitive host and harbor the adult worm in the intestine (taeniasis). However, both humans and pigs can serve as intermediate hosts and harbor the larvae or cysticerci.
Diagnosis
Differential Diagnosis
Epilepsy of unknown etiology
Migraine
CNS vasculitis
Primary neoplasia of CNS
Chronic CNS infections, including toxoplasmosis, coccidioidomycosis, tuberculosis, and cryptococcosis
Brain abscess
CNS involvement with sarcoidosis or systemic lupus erythematosus
Workup
Comprehensive clinical history: obtain information on current and previous travel and residence, including geographic area, sanitary conditions, and consumption of undercooked pork.
Laboratory Tests
Serum antibody detection by enzyme-linked immunoelectrotransfer blot (EITB) assay has a sensitivity of 98% and a specificity of 100% in patients with more than one cyst but has less predictive value in patients with a single cyst, in which up to 38% can be falsely negative. The same assay can be performed in CSF, with lower sensitivity. Antibodies detected by EITB can persist for years after successful therapy, limiting the usefulness of this assay in following patients after treatment. In endemic regions, a negative test result is useful in ruling out disease but a positive result is a marker of exposure, not necessarily symptomatic infection.
Circulating cysticercus antigens can be detected in blood and CSF, providing a marker of viable organisms, even when CNS lesions are calcified and presumed to be inactive. This method may be particularly useful in monitoring patients after therapy. Antigen levels usually fall within 3 months of successful treatment.
Polymerase chain reaction (PCR) detection of T. solium DNA has been developed, with a reported sensitivity of 96.7%, but it is not widely available.
Definitive diagnosis is based on the histopathologic demonstration of cysticerci in the tissue involved. Fine-needle aspiration cytology may be useful in diagnosing infection.
Peripheral eosinophilia is usually absent.
Stool examination for ova and proglottids of T. solium is insensitive and not specific for the diagnosis of cysticercosis.
CSF examination in neurocysticercosis is usually unremarkable, but may demonstrate pleocytosis, with lymphocytic or eosinophilic predominance, low glucose, and elevated protein.
Imaging Studies
Plain radiographs of the extremities may reveal calcified cysts in patients with soft tissue or muscle involvement.
High-resolution ultrasound may be useful in detecting subcutaneous cysts containing scoleces.
For diagnosis of neurocysticercosis, CT and MRI are most commonly used.
Brain CT (Fig. 1) has a sensitivity and specificity of 95% and can identify living cysticerci, which appear as hypodense lesions, as well as degenerating cysts, which appear as isodense or hyperdense lesions with surrounding edema. CT is the best method for detecting calcification associated with prior infection, which suggests inactivity.
Neurocysticercosis.
This 40-year-old Bolivian man presented with left-hand weakness. A, B, Noncontrast head computed tomography (CT) scan, brain windows. C, CT scan with contrast moments later; compare this with (B). A slice through the same level of the brain before contrast administration. Hypodense lesions are present, with surrounding hypodensity (dark gray) representing edema. Scattered calcifications are also seen, which are a common feature of old neurocysticercosis lesions. Administration of intravenous contrast leads to ring enhancement, a feature of many infectious and inflammatory conditions, including neurocysticercosis, brain abscess, and toxoplasmosis.
From Broder JS: Diagnostic imaging for the emergency physician, Philadelphia, 2011, Saunders.
Brain MRI is the most accurate technique to assess the extent of infection, location, and evolutionary stage of the parasites. MRI provides detailed images of living and degenerating cysts, perilesional edema, as well as small cysts or those located in the ventricles, brainstem, and cerebellum. However, MRI has a low sensitivity for detecting calcified lesions, which are the most common neuroimaging finding in endemic populations.
Treatment
Acute General Rx
Asymptomatic cysticercosis:
There is no evidence that administering antiparasitic therapy is beneficial.
Symptomatic neurocysticercosis:
The goals of treatment are to control seizures and mass effect from cysticercal lesions, control intracranial hypertension, and reduce the size of active cysts.
Treatment decisions in neurocysticercosis should be individualized. Initial measures should focus on the symptomatic management, considering antiparasitic therapy when appropriate.
Patients with active lesions, with evidence of surrounding edema and/or inflammation, generally warrant treatment with antiparasitics, corticosteroids, and anticonvulsants.
1.
Patients who have seizures or are considered at risk for recurrent seizures based on imaging should be treated with anticonvulsants.
2.
Corticosteroids may decrease inflammation and edema and should be given whenever antiparasitic therapy is given.
3.
Antiparasitic therapy is indicated in the treatment of symptomatic patients with multiple viable brain parenchymal cysticerci. Despite treatment, only 30% to 50% of lesions resolve within 6 months.
4.
Calcified cysticerci are generally inactive and do not warrant antiparasitic treatment.
5.
Antiparasitic therapy is often unnecessary in patients with single cysts, which are usually self-limited and resolve spontaneously within 6 months.
Antiparasitic therapy:
Patients with viable parenchymal or subarachnoid cysts should be treated with albendazole 15 mg/kg/day PO divided twice daily for 7 days or praziquantel 50 mg/kg/day divided three times daily for 28 days. Albendazole is preferred, since praziquantel management is more complicated due to an interaction with anticonvulsants such as phenytoin. Patients should receive prednisolone (2 mg/kg/day) or dexamethasone (0.15 mg/kg/day) orally before initiation of antiparasitic therapy. Antiparasitics should be used cautiously in patients with massive cysticercal infection of the brain parenchyma (≥50 cysts) or cysticercal encephalitis. These patients should be managed initially with corticosteroids, and perhaps mannitol, to control intracranial hypertension. Once the inflammation and edema have resolved by MRI, antiparasitics can be administered.
Albendazole is considered to be the drug of choice due to slightly better efficacy, greater availability, fewer drug interactions, and lower cost.
Combination therapy with praziquantel (50 mg/kg/day) and albendazole (15 mg/kg/day) with dexamethasone (0.1 mg/kg/day) has been demonstrated to be more efficacious than albendazole and steroids alone for cyst resolution; seizures persisted despite treatment in many cases, so antiepileptic therapy is indicated.
Surgical therapy:
Surgery may be indicated in patients with obstructive hydrocephalus or giant cysts with associated intracranial hypertension.
Minimally invasive neurosurgery (neuroendoscopy) for cyst removal and ventricular shunt formation has greatly improved the management of intraventricular neurocysticercosis.
Extraparenchymal neurocysticercosis, including ocular, subarachnoid, and intraventricular disease, carries a poor prognosis and requires a more aggressive approach. When feasible, complete surgical excision of lesions remains the definitive therapy.
Chronic Rx
Prolonged antiparasitic therapy does not improve outcomes in neurocysticercosis and may delay calcification of lesions. Antiepileptic medications should be continued for 2 years or 6 to 12 months after CT/MRI resolution of viable cysts, before tapering. In some cases, antiepileptic therapy needs to be continued indefinitely.
Rare patients with neurocysticercosis develop chronic or recurrent perilesional inflammation, requiring long-term, high-dose steroid therapy. Methotrexate has been reported to be of use as a steroid-sparing agent in this setting.
Disposition
In seizure-free, stable neurocysticercosis, outpatient management is appropriate.
Patients with seizures should be restricted from driving.
Referral
Infectious diseases consultation.
Neurology consultation in patients with seizures.
Neurosurgical consultation if extraparenchymal neurocysticercosis or obstructive hydrocephalus is present.
Prevention
- Eradication of taeniasis/cysticercosis is possible with implementation of meat inspection, improvement of pig husbandry, and improvement of socioeconomic conditions in endemic areas.
- A porcine vaccine against soliumhas been developed and successfully implemented in Peru, Mexico, and Australia.
- There is currently no human vaccine to prevent tapeworm infection or cysticercosis.
Patient & Family Education
- Pork should be inspected for the presence of cysticerci, which are visible in raw meat.
- Pork must be well cooked.
- Proper disposal of human excreta and handwashing are of utmost importance to break the transmission cycle in households.
Suggested Readings
- Z.V. Alonso, et al.: Parasite antigen in serum predicts the presence of viable brain parasites on patients with apparently calcified cysticercosis only. Clin Infect Dis. 57:e154 2013 23788241
- P.T. Cantey, et al.: Neglected parasitic infections in the United States: cysticercosis. Am J Trop Med Hyg. 90:805 2014 24808248
- H. Carabin, et al.: Taenia solium cysticercosis and taeniosis: achievements from the past 10 years and the way forward. PLoS Negl Trop Dis. 11 (4):e0005478 2017 28426664
- Centers for Disease Control and Prevention: Parasites—cysticercosis . https://www.cdc.gov/parasites/cysticercosis/
- N. Deckers, P. Dorny: Immunodiagnosis of Taenia solium taeniosis/cysticercosis. Trends Parasitol. 26:137 2010 20083438
- H.H. Garcia, et al.: Cysticercosis of the central nervous system: how should it be managed?. Curr Opin Infect Dis. 24:423 2011 21788891
- H.H. Garcia, et al.: Efficacy of combined antiparasitic therapy with praziquantel and albendazole for neurocysticercosis: a double-blind, randomized controlled trial. Lancet Infect Dis. 14:687 2014 24999157
- H.H. Garcia, et al.: Cysticidal efficacy of combined treatment with praziquantel and albendazole for parenchymal brain cysticercosis. Clinical Infect Dis. 62:1375 2016
- P. Goyal, et al.: A cytological study of palpable superficial nodules of parasitic origin: a study of 41 cases. Patholog Res Int. 373472:2014 2014
- D. Meena, et al.: Isolated intramuscular cysticercosis: clinicopathological features, diagnosis and management—a review. J Clin Orthop Trauma. 7 (Suppl 2):243 2016 28053392
- L. Michelet, et al.: Human neurocysticercosis: comparison of different diagnostic tests using cerebrospinal fluid. J Clin Microbiol. 49 (1):195 2011 21068283
- L.M. Moyano, et al.: Neurocysticercosis as a cause of epilepsy and seizures in two community-based studies in a cysticercosis-endemic region in Peru. PLOS Negl Trop Dis. 8:e2692 2014 24551255
- V. Rajshekhar: Surgical management of neurocysticercosis. Int J Surg. 8:100 2010 20045747
Related Content
Cysticercosis (Patient Information)