Cysticercosis and Taeniasis
- Taeniasis is an intestinal infection with the adult tapeworm, either Taenia saginata (from cattle) or Taenia solium (from pigs). Infected individuals often have mild or no symptoms. One dose of oral antiparasitic therapy is very effective in eradicating the parasite.
- T solium infection can lead to cysticercosis. Cysticercosis is a tissue infection with the larval stage (or cysticercus) of the pork tapeworm.
- Humans are the definitive hosts for both adult Taenia tapeworms. Eggs released in human stool contaminate the soil and infect pigs and cattle. Porcine cysticercosis is highly endemic in Latin America, sub-Saharan Africa, and South and Southeast Asia.
- Neurocysticercosis is the most severe form of cysticercosis. It is caused by cysts in the central nervous system and is a major cause of epilepsy (adult onset and, less commonly, childhood onset), in endemic areas. Seizures, headaches and hydrocephalus are the most common manifestations.
- Cases of neurocysticercosis are becoming more common in Europe, the U. S. and Canada because of increased migration and travel.
- Health care providers should understand the symptoms, diagnosis and treatment of this potentially serious condition.
- Consultation with specialists in infectious diseases, neurology and ophthalmology is recommended before initiating antiparasitic therapy.
Taeniasis is caused by intestinal infection with the adult tapeworm: Taenia saginata (from cattle) or Taenia solium (from pigs). Taenia saginata asiatica causes taeniasis in Asia. T. solium takes two distinct forms in the human host:
- Taeniasis: Tapeworm infection of the gut lumen.
- Cysticercosis: Infection of tissues with larval cysts (cysticerci).
Taenia: Life cycle
Taeniasis is acquired by inadvertently ingesting the cysticerci in undercooked pork (T. solium) or beef (T. saginata). Cysticerci can develop into adult worms, living in the intestine and, if untreated, reach a length of 2 to 8 meters. Six to eight weeks after ingestion, gastrointestinal tract symptoms can occur, such as nausea, diarrhea or constipation and abdominal pain, but many patients remain asymptomatic.
The adult tapeworm releases egg-bearing gravid proglottids (segments) which may look like a white elastic band protruding from the anus or be seen migrating from the anus or in feces. Left untreated a tapeworm can live and produce proglottids for decades.1
Diagnosis of taeniasis (adult tapeworm infection) is based on the presence of proglottids or ova in the patient’s feces or perianal region. Because ova and proglottids are shed intermittently, the sensitivity of stool microscopy for ova is only 26%. Yield is increased if 3 stool samples are submitted on different days. The ova of T. solium and T. saginata are microscopically indistinguishable. Species identification of the parasite is based on the different structures of gravid proglottids and scolex.2
Treatment with oral praziquantel or niclosamide is highly effective for eradicating infection with the adult tapeworm. Praziquantel (5 mg/kg to10 mg/kg, one dose) should be taken with liquids during a meal. Consultation with a paediatric infectious disease specialist is advisable because neither agent is licensed or commercially available in Canada. An application to Health Canada’s Special Access Programme (SAP) is required.
Cysticercosis: Life cycle
T. solium taeniasis (from pork) is of greater public health concern than T. saginata because, left untreated, it can cause cysticercosis, a serious parasitic disease.1
Cysticercosis in humans is acquired by ingesting eggs of the pork tapeworm (T. solium). Unlike taeniasis, it is not from ingestion of undercooked meat. Eggs are found only in human feces, and a carrier can shed eggs into the environment in stool or transmit them on unwashed hands and fingernails, to other people or to pigs, who are infected when they swallow contaminated soil, water or food.1 These eggs can live for 2 months in water, soil or vegetation.3
Once ingested, the eggs hatch in the small intestine and the larvae migrate to various tissues throughout the body, where they form cysts. This is called cysticercosis. If the cysts are in the brain, the condition is called neurocysticercosis, the most severe form of the disease.
Between 50 and 100 million people worldwide are thought to be infected with cysticercosis. Cysticercosis is highly endemic in Latin America, sub-Saharan Africa and South and Southeast Asia, as well as parts of Korea, China, Indonesia and Papua New Guinea.2
In the developing world, neurocysticercosis is a common infection of the human central nervous system (CNS) and the most frequent preventable cause of epilepsy. Increasing migration from and travel to disease-endemic regions, means that neurocysticercosis is being seen more often in industrialized countries.
Typical cases in the U.S. have been immigrants, from Latin America and Asia who became infected in their home country,2 or who acquired cysticercosis from a close contact in the U.S. who is carrying T. solium intestinal stage infection.
There are limited Canadian data. In 2012, Del Brutto performed a MEDLINE and manual search of case reports and case series of patients with cysticercosis diagnosed in Canada. A total of 21 articles reporting 60 patients were found, of which 40 (67%) were diagnosed in the past two decades. Immigrants accounted for 96% of the 28 cases for whom citizenship information was available.4 It is possible that at least some of the patients may have acquired the disease in Canada from a household contact harbouring the adult T. solium in the intestine.3
Although cysticercosis is rare, health care providers should be especially aware of symptoms, diagnosis and treatment for this potentially serious condition.
Cysticercosis: Clinical clues
The time between infection and onset of symptoms is variable and people infected with cysticercosis can remain asymptomatic for years.
Clinical manifestations are also variable and depend on the location of the cysticerci and the host’s inflammatory response.2
Most symptoms are caused by inflammation around a degenerating or dying cyst, although calcified (dead) cysts can also serve as a seizure focus and enlarging, viable (live) cysts can cause symptoms due to mass effect. Symptoms and signs are listed in Table 1 and described below.
Table 1. Symptoms and signs of cysticercosis
|More common||Less common|
The infection location that most often, and seriously, prompts medical consultation is the brain. Some patients, including children, experience severe headache (resembling a tension headache or migraine) as their only symptom.2
Epilepsy is present in 70% to 90% of symptomatic patients. Onset typically occurs from 5 to 40 years of age, but seizures have been noted in infants. Seizures are usually focal with secondary generalization, although they can also be focal or generalized.2
Neurocysticercosis can present with signs or symptoms of raised intracranial pressure and altered mental status. Diffuse cerebral edema caused by multiple inflamed cysticerci is known as cysticercal encephalitis.2 Intracranial hypertension, the presence of large basilar or supratentorial cysts or a large numbers of cysts, or cerebral infarction, can all be life-threatening.5
Less frequent manifestations include obstructive hydrocephalus, chronic meningitis, cranial nerve abnormalities and behavioural disturbances. Infected children may develop learning disabilities.
Cysts in the spinal column can cause gait disturbance, pain or transverse myelitis.
Subcutaneous cysticerci produce palpable though painless, mobile cystic lesions that resolve in months to years.6 Subcutaneous disease is more common in Asia and Africa than in the West.2 Skeletal muscle involvement may result in pseudohypertrophy, or weakness with massive infection, or in cigar-shaped calcifications which can be seen on radiographs even without musculoskeletal symptoms.6 Ocular involvement, most commonly involving the retina or vitreous, can reduce visual acuity or cause other visual field defects.7
In a patient with multiple cysticerci, different clinical presentations (eg, brain parenchymal lesaions causing seizures, intraventricular cysts causing hydrocephalus, spinal cord lesions, ocular lesions) can be seen at the same time.
Neurocysticercosis is more difficult to diagnose than many other parasitic infections because parasite eggs may not be present in the patient’s stool and clinical presentations are nonspecific. While enhancing lesions are typical of neurocysticercosis, similar lesions can be seen with tuberculosis, brain abscesses and tumors.2
Consider a diagnosis of neurocysticercosis if your patient:3
- Has a household contact with T. solium infection
- Comes from a region where cysticercosis is endemic
- Travels repeatedly to a disease-endemic region
- Experiences a new onset seizure (more common in adults than in children)
- Presents with cystic lesions, solitary enhancing lesions or has punctate calcifications observed on neuroimaging studies
- Has intracranial cystic lesions that resolve after treatment with albendazole or praziquantel
Tests used to detect cysticercosis include doing a biopsy of subcutaneous cysts, immunodiagnosis (finding antibodies or parasite antigens in serum samples) and imaging (radiography, computed tomography [CT] and magnetic resonance imaging [MRI]).1
A diagnosis of neurocysticercosis usually requires both CNS imaging and serological testing. A careful history should always be taken, with focus on residence or extended travel in disease endemic countries and the consumption of food prepared by someone who has lived in a high-risk area.8 Advice on taking a history with newcomer families, including the use of interpreters, is available in this resource.
CNS imaging with CT or MRI can be diagnostic if a scolex (the tapeworm’s attachment or holdfast organ, which can have a ‘hole-with-dot’ appearance) is seen on the image.9 An inflammatory reaction to cyst degeneration and resultant edema may appear as a contrast-enhanced ring around the cyst. In children, lesions typically are found within the cortex.2
Serological testing is needed to confirm the diagnosis when neuroimaging indicates the possibility of neurocysticercosis. Antibody assays that detect specific antibody to larval T. solium in serum and cerebrospinal fluid (CSF) are the tests of choice. The enzyme-linked immunoblot transfer assay is the serological test preferred by the U.S. Centres for Disease Control and Prevention because of its sensitivity and specificity. In general, antibody tests are more sensitive with serum specimens than with CSF specimens.10 The antibody may persist after treatment.2 Serological testing is less useful when there is a solitary lesion, a finding more common in children, and in people from the Indian subcontinent.5
Actually seeing a parasite during an ophthalmoscopic examination or in a tissue sample are rare but definitive diagnostics for neurocysticercosis.2 Polymerase chain reaction testing (PCR) on biopsy tissue also can be used, but such tissue is not often available.
It is possible to have adult T. solium tapeworm infection (taeniasis) and cysticercosis at the same time, and cysticercosis can represent a spectrum of diseases that differ in optimal management.2 The decision to treat with an anthelmintic (an agent destructive to worms) will depend on the location, number and stage of cysticerci, and on clinical manifestations (especially whether encephalopathy or hydrocephalus is present). Finding of a single lesion in an asymptomatic patient does not necessarily need antiparasitic treatment.
Initiation of anthelmintic chemotherapy is not urgent and can be planned while initial medical care is focused on symptom control (eg, starting antiseizure medication or neurosurgical intervention for hydrocephalus).5
Because life-threatening side effects can occur with antiparasitic therapy, consulting with specialists in infectious diseases, neurology and ophthalmology (to rule out intraocular cysticerci) before initiating such treatment is critical.
Two antiparasitic drugs – albendazole and praziquantel – are available in Canada through Health Canada’s Special Access Programme.
Both cysticidal drugs damage the parasite and release antigens.3 The perilesional inflammation induced by treatment with either drug can worsen a patient’s condition initially or even cause death depending on the location of viable cysts.5
For the patient’s treatment team, some general principles apply:8
- Anthelmintic therapy is generally indicated for symptomatic patients with multiple lesions (non-calcified) cysticerci.
- Anthelmintic therapy does not benefit patients with dead worms and calcified cysts.
- Concomitant administration of steroids that cross the blood–brain barrier (e.g., dexamethasone) is often indicated to suppress the inflammatory response induced by destroying live cysticerci.
- Conventional anticonvulsive therapy is the mainstay for managing neurocysticercosis-associated seizure disorders.
Albendazole is preferred to praziquante, because it has fewer drug-to-drug interactions with anticonvulsants. Phenytoin and carbamazepine may decrease praziquantel’s effects.11
The current expert consensus is that patients with multiple cysticerci usually should be treated with a course of an antiparasitic agent (albendazole, 15 mg/kg/day divided in 2 doses orally [maximum 800 mg/day] for 8 to 30 days, with duration dictated by the number and location of cysts) or praziquantel (100 mg/kg/day divided in 3 doses for one day, then 50 mg/kg/day divided in 3 doses for 29 days).10 For CNS disease with multiple lesions, administer steroids and anticonvulsants before starting the first dose. The duration of steroids is determined by the infectious diseases specialist or neurosurgeon, but is typically in the range of 5 to 30 days to minimize the inflammatory response. Anticonvulsants may be required for a long duration.
Corticosteroids have also been used in conjunction with surgery or with albendazole or praziquantel to treat arachnoiditis, vasculitis or cerebral edema.10,11
Intraventricular cysts are usually treated by surgical removal, preferably by endoscopy. Anthelmintics are relatively contraindicated, because the resulting inflammatory response can precipitate obstructive hydrocephalus. If cysticerci cannot be removed easily, hydrocephalus should be corrected by placing intraventricular shunts. Adjunctive chemotherapy with anti-parasitic agents and corticosteroids may decrease the rate of subsequent shunt failure.2
Cysticercosis of the eye, spine or subcutaneous tissue is usually treated by removing the cysticerci surgically. Albendazole or praziquantel should not be used to treat ocular or spinal cysts, even in conjunction with corticosteroids. Inflammation may cause permanent damage.
Seizures can recur for months or years. The decisions to discontinue an anticonvulsive regimen is made on a case by case basis. However, anticonvulsant therapy is recommended until there is neuroradiological evidence of resolution and seizures have not occurred for 1 to 2 years. The presence of calcified cysts may require the long-term use of anticonvulsants.
The proportion of patients who fully recover from cysticercosis, with or without treatment, is unknown.1
The prognosis of neurocysticercosis is extremely variable. Symptomatic patients with single lesions generally do well, are often seizure- free, and may be able to discontinue anticonvulsant therapy within 1 to 2 years. Patients with numerous subarachnoid cysticerci often require repeated courses of therapy and multiple surgeries.2 Mortality is low in patients with parenchymal cysts without hydrocephalus.
Preventing the transmission of eggs from person to person is key to controlling this disease. Here are some practical steps:
- Identification and treatment of tapeworm carriers is an important Public Health measure that can prevent further cases.8
- Identify and treat individuals with taeniasis.
- Screen individuals with cysticercosis and their close contacts for taeniasis.
- Food preparers can reduce the risk of transmitting enteric diseases, including neurocysticercosis, through good handwashing practices.
- Travelers to areas with poor sanitation should be particularly careful to avoid foods that might be contaminated by human feces such as uncooked vegetables and fruits that cannot be peeled.
Development of an effective vaccine against cysticercosis may provide the best potential tool for eradication of the disease.12
- WHO, Neglected tropical diseases: Cysticercosis/Taeniasis.
- Cherry J, Demmler-Harrison GJ, et al (eds.) Feigin and Cherry’s Textbook of Paediatric Infectious Diseases, 7th edn. Elsevier/Saunders, 2014:3030-40.
- Burneo JG, Plener I, Garcia HH. Neurocysticercosis in a patient in Canada. CMAJ 2009; 180(6):639-42.
- Del Brutto OH. A review of cases of human cysticercosis in Canada. Can J Neurol Sci 2012; 39(3):319-22.
- Krilov LR, Cantey PT, Burke AP. Cysticerosis among parasitic infections targeted by CDC. AAP News 2012;33(10):20.
- Public Health Agency of Canada. Taenia solium pathogen safety data sheet – Infectious Substances.
- Garcia HH, Del Brutto OH; Cysticercosis Working Group in Peru. Neurocysticercosis: Updated concepts about an old disease. Lancet Neurol 2005;4(10): 653-61.
- Centers for Disease Control and Prevention – Parasites – Cysticercosis: Resources for Health Professionals.
- Del Brutto OH. Neurocysticercosis: A review. ScientificWorld Journal 2012;159821, doi:10.1100/2012/159821
- American Academy of Pediatrics. Tapeworm Diseases: Taeniasis and Cysticercosis. In: Pickering LK, Baker CJ, Kimberlin DW, et al (eds.). Red Book: 201 Report of the Committee on Infectious Diseases. Elk Grove Village, IL: AAP, 2012:703-5, 858-9.
- McMillan J, Carlton KL, Siberry GK, et al. The Harriet Lane Handbook of Pediatric Antimicrobial Therapy, 2nd edn. Elsevier, 2014:111-12,378 -9,
- Nash TE, Mahanty S, Garcia HH. Neurocysticercosis - More than a neglected disease. PLoS Negl Trop Dis 2013;7(4): e1964.
- Heather Onyett, MD
Last updated: July, 2014