Taenia Infection 

Updated: Jul 24, 2018
Author: Supatida Tengsupakul, MD; Chief Editor: Russell W Steele, MD 

Overview

Background

Of the 32 recognized species of Taenia, only Taenia solium (pork tapeworm) and Taenia saginata (beef tapeworm) are medically important. However, recent epidemiologic studies in Southeast Asia have identified a third Taenia species in humans, known as Taenia asiatica.[1, 2] Taeniasis is an infection due to an adult tapeworm in the intestine. Humans acquire taeniasis from ingestion of undercooked pork containing cysticerci. Cysticercosis is the development of extraintestinal encysted larval forms of T. solium in various organs. Humans develop cysticercosis from ingestion of T. solium egg excreted by themselves (autoinfection), or by a human tapeworm carrier which means humans can have cysticercosis even though they do not eat pork. (see Cysticercosis). The CNS is involved in 60-90% of cases; this condition is termed neurocysticercosis (NCC). For more information, see Neurocysticercosis.

Differentiating between T. solium and T. saginata infections is important because infection with T. solium can cause neurocysticercosis, which is one of the leading cause of deaths from food-borne illnesses, resulting in a total of 2.8 million disability-adjusted life-years (DALYs) according to the World Health Organization (WHO).[3] Cysticercosis caused by T. saginata is rare; T. saginata has far lower impact on human health than T. solium. Both infections are endemic in Southeast Asia, Africa, Europe, and Central and South America. Infection in children usually goes unrecognized.[4]  WHO developed a roadmap for control and eradication of T. solium taeniasis/cysticercosis to be implemented in selected countries by 2020.[3]

Pathophysiology

Humans are the definitive host. Adult tapeworms live in the human small intestine. Humans pass gravid eggs in feces; these mature eggs contaminate pastures and barnyards, where cattle and pigs ingest them. Upon reaching the alimentary canal of infected animals, the embryos are released, penetrate the gut wall, and enter the circulation. The embryos filter from the circulation and encyst in muscular tissue. Larvae (ie, cysticerci) become infectious within 2-3 months. Humans develop a tapeworm infection by eating raw or undercooked beef or pork containing cysticerci. The cysticercus becomes activated, attaches to the wall of the small intestine by the scolex, and becomes a mature tapeworm. This maturation process takes 10-12 weeks for T. saginata and 5-12 weeks for T. solium. A single tapeworm produces an average of 50,000 eggs per day and may live up to 25 years.

Pigs are the intermediate host for T. solium and T. asiatica. The larvae of T. solium has predilection to infect the muscles and brain of pigs, however, the larvae of T. asiatica tends to infect pig viscera especially pig liver. Cows are the intermediate host for T. saginata with the larvae predominantly found in the muscle.

Humans can also act as an intermediate host for T. solium. Cysticercosis results from human ingestion of T. solium eggs through fecal contamination, reverse peristalsis of gravid proglottids, or autoinfection. The cysticerci may develop in any organ, and their effects depend entirely on the location of the cysticerci.

A coenurus is the larval stage of Taenia multiceps, Taenia serialis, and Taenia brauni. Adult tapeworms develop in dogs or other canids that ingest coenurus larvae in the tissues of various intermediate hosts. These hosts include sheep, goats, hares, rabbits, and other herbivores for T multiceps; hares, rabbits, and other rodents for T. serialis; and gerbils for T. brauni. Each protoscolex within a coenurus can mature into an adult tapeworm after ingestion by a canid host. Adult worms produce eggs, which are passed in feces; these eggs are morphologically similar to taeniid eggs. Ingestion of eggs by an appropriate intermediate host or by humans leads to development of coenurus. Coenuri are cysts that contain many protoscolices attached in rows on the internal membrane of the cyst.

Epidemiology

Frequency

United States

Cysticercosis is primarily an imported disease. Approximately 1000 cases are diagnosed each year. Most occur in persons who have immigrated, primarily from Latin America.[5] Cysticercosis has also developed following close contact with recently immigrated, infected individuals. Although some patients with NCC are born in the United States, many have traveled to rural areas in countries where the condition is endemic. Locally acquired infections have been confirmed in Los Angeles, New York, Chicago, Oregon,[6, 7] and elsewhere. Although T. saginata infection occurs worldwide, prevalence in the United States is less than 1% because most US cattle are free of the parasite.

A study analyzed in-patient records using the Nationwide Inpatient Sample for 1998-2011 to estimate cysticercosis-related hospitalizations and patient/institutional characteristics in the United States. The study reported that there were an estimated 33,060 cysticercosis-related hospitalizations nationwide, representing a hospitalization rate of 8.03 per million population. The study further reported that the highest proportion of cases were male (54.8%), Hispanic (62.0%), aged 18-44 (58.8%), and occurred in the West (45.1%). An estimated 459 deaths occurred, representing an in-hospital case-fatality rate of 1.4%.[8]

International

Approximately 50 million people worldwide are infected by T. saginata or T. solium. Approximately 50,000 people die annually of cysticercosis. T. saginata is common in cattle-breeding regions. Areas with the highest (ie, >10%) prevalence are central Asia, the Near East, and central and eastern Africa.[9, 10, 11] Areas with low (ie, 1%) prevalence are Southeast Asia, Europe, and Central and South America.

T. solium is endemic in Central and South America, Southeast Asia,[12, 13, 14] India, the Philippines, Africa,[15] Eastern Europe, and China. Areas of highest prevalence include Latin America and Africa. In some regions of Mexico, prevalence may reach 3.6% of the general population.

A study of school aged children from 27 schools in China showed overall prevalence of T. solium cysticercosis to be 6%. In three schools the prevalence was 15% or more. Risk factors for cysticercosis included pig ownership, feeding pigs with human feces, and worms in their feces. Schools with higher prevalence had more students with households that have free range pigs and practice open defecation.[16]

T. multiceps has been reported in the Americas and parts of Europe and Africa.

T. serialis infections occur in the United States and Canada.

T. brauni has been reported in Africa.

Mortality/Morbidity

Most intestinal taeniid infections are asymptomatic. When symptoms occur, they are usually mild and involve abdominal pain, anorexia, weight loss, or malaise. Cysticercosis causes a mass effect in various vital organs (eg, brain, eye, heart). The mortality rate for cysticercosis is low and is generally caused by complications such as encephalitis, increased intracranial pressure secondary to edema and/or hydrocephalus, and stroke.

Race

All races are equally affected.

Sex

Both genders are equally affected.

Age

All ages are susceptible to infection. The age at which raw meat consumption begins is the primary determinant. T. solium taeniasis has been reported in children older than 2 years in certain rural communities of Mexico.

 

Presentation

History

Taeniasis

Most individuals with taeniasis are either asymptomatic or have mild-to-moderate complaints.

The most common complaint is passage (active or passive) of proglottids, which is associated with slight discomfort. Other symptoms include the following:

  • Colicky abdominal pain (more common in children)

  • Nausea

  • Weakness

  • Loss of appetite

  • Increased appetite

  • Headache

  • Constipation

  • Dizziness

  • Diarrhea

  • Pruritus ani

  • Hyperexcitability

Abdominal pain and nausea are reportedly more common in the morning and are characteristically relieved by eating small amounts of food. Children are more symptomatic than adults and often manifest change of appetite, both increased and decreased. Symptoms in infants are more pronounced and consist of vomiting, diarrhea, fever, weight loss, and irritability.

The most common serious complication of adult tapeworm infection is appendicitis. Other reported complications include obstruction of bile ducts, pancreatic duct and tapeworm growth in ectopic locations (eg, middle ear, adenoid tissue, uterine cavity). A mild eosinophilia of 5-15% may occur in 5-45% of patients; higher levels are rare. Taenia infection has been reported mimicking Crohn's disease.[17]

Cysticercosis and neurocysticercosis (NCC)[18]

In cysticercosis, the cysticerci are most often located in subcutaneous and intermuscular tissues, followed by the eye and then the brain. The CNS is involved in 60-90% of patients (ie, NCC). Most patients have more than one cyst; as many as 200 cysts have been reported.

NCC symptoms include 3 characteristic syndromes: convulsions and/or seizures, intracranial hypertension, and psychiatric disturbances, which may occur separately or simultaneously.[19] Onset can be insidious (eg, elevated intracranial pressure) or abrupt (eg, floating cysticerci suddenly block cerebrospinal fluid [CSF]). See the following:

  • Convulsions and/or seizures: Seizures are caused by the localization of cysticerci in brain parenchyma. Children most often present with seizures, which are focal with acute onset. Cysticercosis is the most common cause of epilepsy in endemic areas[20] and is the sole manifestation in as many as one third of patients.[21]

  • Intracranial hypertension: This is caused by obstruction of CSF by intraventricular brain cysts. Symptoms include headache, nausea, vomiting, vertigo, and papilledema.

  • Psychiatric disturbances: Although changes in personality and mental status occur more often in adults than in children, behavioral changes and learning disabilities were reported in a study of 25 affected children.[22]

NCC must be differentiated from severe cysticercal meningitis, a syndrome reminiscent of bacterial, tuberculous, or amebic meningitis.[23]

Other possible infections

  • Ocular cysticercosis: The subretinal space, vitreous, and conjunctiva are the most frequent sites of infection. Common manifestations of infection include severe pain and blurred or lost vision.

  • Muscular and dermatologic cysticercosis: Cysticerci in muscles often are associated with NCC. Any muscle mass may be involved and appear as acute myositis. However, most patients are asymptomatic. Subcutaneous nodules may be evident.

  • Coenurosis: Clinical manifestations are determined by the site of the coenurus larvae. Patients with cerebral coenurosis can present with seizure or intracranial hypertension. Ocular coenurosis manifests as a red and painful eye.

Physical

Most children with intestinal taeniasis appear healthy. Physical findings may include the following:

  • Weight loss, caused by loss of appetite, is more pronounced in infants than in adults.

  • Subcutaneous nodules are less common in children than in adults.

  • Neurologic abnormalities in some children with NCC may manifest as hemiparesis, sensory disturbances, and papilledema.

  • Intraocular larva may be evident.

  • Muscular pseudohypertrophy may occur.

Causes

Taeniasis is caused by ingesting inadequately cooked beef or pork that contains the larvae or cysticerci of T. saginata or T. solium respectively. Cysticercosis, which is caused by ingesting eggs of T. solium, occurs when larvae are deposited in skeletal muscle, brain, eyes, and other organs. Taeniasis is endemic in countries where both T. saginata and T. solium are common and public hygiene is poor.

T. asiatica, a species of Taenia recently identified in many Southeast Asian countries, resembles T. saginata at morphology of adult worms and larvae but different at the molecular level, and its ingestion in inadequately cooked pork or pork viscera, especially pork liver, causes an intestinal infection. This close relationship with T. saginata has led to the assumption that it does not cause human cysticercosis because human cysticercosis is caused almost exclusively by T. solium.

Coenurosis results when humans accidentally ingest mature T. multiceps or T. serialis eggs, usually in contaminated fruits or vegetables. Approximately 100 cases of coenurosis have been reported, primarily in tropical Africa, with the remainder in North and South America and South Africa. Interestingly, the cases in central Africa rarely involved the CNS, whereas more than 75% of the cases elsewhere had CNS involvement. Larvae of these species may be inoculated directly into a child's conjunctiva and skin as the child plays on contaminated ground.

 

DDx

 

Workup

Laboratory Studies

Intestinal taeniasis

CBC count detects mild eosinophilia.

Examine 3 stool samples (direct and concentrated stool preparations) collected on 3 different days from patients and contacts.

  • Determination of species on the basis of ova examination is difficult because the eggs of T. solium and T. saginata are identical.

  • Examining the gravid proglottids helps identify the species; count the main uterine branches (7-16 branches for T. solium, 14-32 branches for T. saginata and 11-32 branches for T. asiatica).[24]

  • Examining the scolex helps differentiate the species because a T. solium scolex has 4 suckers and an armed rostellum and hooks but T. saginata scolex does not have rostellum and hook. T. asiatica has rostellum without a hook.[24]

Serology

Copro-Ag ELISA can be used to detect T. solium tapeworm carrier with sensitivity of 84.5% and specificity of 92%.[25]

Molecular analysis

  • Copro-PCR has been used to detect T. solium carrier with sensitivity of 82.7% and specificity of 99%. [25]
  • Multiplex loop-mediated isothermal amplification (multiplex LAMP) targeting mitochondrial cytochrome c oxidase subunit 1 ( cox 1) gene couple with dot enzyme-linked immunosorbent assay (dot-ELISA) help identify human Taenia species ( T. solium, T. saginata and T. asiatica). This technique is easy to perform and interpret and does not require expensive equipment which make it feasible to perform in resource-limited settings. [26]  Unfortunately, these molecular methods are not commercially available.

Endoscopy/capsule endoscopy can help diagnose taenia infection.[27, 17]

Neurocysticercosis (NCC)

Examine stool samples as described above.

Perform a lumbar puncture.[28]

  • CSF findings are abnormal in 50-90% of patients with NCC (but may be normal in children with single-lesion disease).

  • Protein levels are usually elevated (but may be normal in children with single-lesion disease).

  • Glucose levels are usually mildly to moderately depressed (but may be normal in children with single-lesion disease).

  • A predominantly mononuclear pleocytosis is common.

  • Cell counts rarely exceed 300/μL.

Eosinophils in the CSF are a common but nonspecific finding. Giemsa or Wright stains should be performed to detect their presence.

An enzyme-linked immunotransfer blot (EITB) assay is the test of choice to confirm the diagnosis of NCC indicated by clinical and radiologic findings. Test specificity is 100% and sensitivity is 90% with more than 2 lesions; sensitivity declines to 50-70% with a solitary lesion. Therefore, EITB assay may have limited value for children because most present with a single lesion. A serum immunoblot assay is more sensitive than the assay using CSF, thus obtaining CSF solely for that purpose is unnecessary.

Although an enzyme-linked immunosorbent assay (ELISA) can be performed on both CSF and serum, CSF provides better reliability. ELISA may provide either false-positive or false-negative results. ELISA provides a reported sensitivity of 75%. ELISA can aid in diagnosis in patients with few CNS lesions and relatively mild disease. Newer serologic methods may allow improved diagnostic testing.[29]

Imaging Studies

Radiography

Plain films of the chest, neck, arms, and thighs can depict calcified cysticerci, although calcification takes approximately 3 years, and sometimes longer, to occur.

A central calcified scolex surrounded by a calcified cyst wall is pathognomonic.

CT

Perform CT scanning in all children presenting with new-onset focal seizures.

Although CT scanning is superior to MRI to detect intracerebral calcification, calcification occurs less frequently in children than in adults.

CT scanning reveals both cysts and granulomata. Cysts, which may be single or multiple, are approximately 5-20 mm in diameter. Most children (ie, 75%) have a single cyst, usually located in the cortex or at the junction of gray and white matter.

CT scanning can also detect edema associated with dead worms. The dead worms appear as spherical hypodensities, often with the parasite's protoscolex appearing as an eccentric dot of calcium (ie, mural nodule).

CT scanning with contrast shows a ring-enhancing image. Later obliteration of the cyst may produce a solid-enhanced image.

MRI

MRI is superior to CT scanning in detecting intraventricular and subarachnoid cysts.

MRI may reveal a mural nodule within the cyst, which is pathognomonic for NCC.

MRI with parallel imaging may facilitate detection of cysts.[30]

See the Neurocysticercosis Case from the Gorgas Course in Clinical Tropical Medicine and the image below for typical lesions revealed using CT scanning and MRI.

Brain MRI that reveals a cystic lesion containing Brain MRI that reveals a cystic lesion containing a dead parasite with surrounding vasogenic edema on fluid-attenuated inversion recovery (FLAIR) imaging. MRI is of a 16-year-old Guatemalan adolescent with first-time afebrile seizure and normal EEG, cerebrospinal fluid (CSF), and examination findings.

Other Tests

Ocular cysticercosis

Funduscopic examination may show freely floating cysticerci in the anterior chamber and vitreous chamber and may provide visual identification of the movements and morphology of larval forms. Larvae may be found adhering to subretinal tissues.

Subretinal cysts are associated with vasculitis and edema.

Cysts in vitreous are associated with chorioretinitis and retinal detachment.

Procedures

Excise or perform biopsy of subcutaneous nodules.

For skeletal cysticercosis, perform a biopsy or excision of the nodule and histologic examination of the cysticerci.

For neurocysticercosis, perform a lumbar puncture (see Lab Studies).

Histologic Findings

Mature cysticerci are ellipsoidal, translucent, fluid-filled cysts, 1-2 cm in diameter. Younger cysticerci are smaller. A single dense white body can be seen through the membrane. The spiral canal of the cyst wall, which has a wavy appearance in most tissue preparations, is most frequently observed in biopsy specimens. The wall, which is 100-200 micrometers wide, is characterized by an internal parenchymal layer of longitudinal and circular muscle, a middle layer of pseudoepithelial cells, and an outer cuticular layer composed of a dentate membrane with a microvillus projection that interfaces with host tissues. The scolex region is thickened and more organized. Cross sections of the scolex appear as several layers of folded smooth muscles, which may contain parts of the suckers or hooklets.

The parasite is surrounded by an adventitia of host tissue reaction. A scant local cellular reaction that consists of some eosinophils and macrophages surrounds live cysticerci; dead cysticerci are surrounded by a dense inflammatory infiltrate that consists of the entire spectrum of inflammatory cells, including multinucleated giant macrophages.

 

Treatment

Medical Care

Most patients with intestinal Taenia infection are asymptomatic or mildly symptomatic. If adult tapeworms are detected in the stools, anthelmintic therapy (praziquantel or niclosamide) usually suffices. Treating individual with Taeniasis is important because it may prevent cases of cysticercosis.[24] Asymptomatic cysticercosis requires no treatment. However, an asymptomatic individual may not truly be asymptomatic. Cysticercosis can have a long incubation period up to 16 years before developing symptoms.[31] Treating other conditions with albendazole or praziquantel can result in adverse outcomes in undiagnosed cysticercosis individuals due to an inflammatory response from the dying parasite.[24]

Treatment for symptomatic neurocysticercosis (NCC) is controversial and challenging.[32] If anthelmintic therapy is chosen, albendazole[33] , praziquantel, or both[34, 35] are the drug of choice. Because these agents provoke an anti-inflammatory response in the CNS, glucocorticosteroids should be used in conjunction with antihelmintic therapy.

Ocular, ventricular, and spinal lesions may require surgical treatment because treatment with anthelmintic drugs can provoke irreversible drug-induced inflammation.

Surgical Care

Surgery may be needed if intestinal taeniid infection causes complications such as acute surgical abdomen, appendicitis, or obstructed bile or pancreatic ducts.

Surgical intervention may also be required for cysticercosis and NCC (see Cysticercosis, Neurocysticercosis),[36]  and in some case of intraventricular cysticercosis, removal of the cyst can successfully treat the condition without the need of antihelmintic therapy.[31]

Surgical excision of ocular cysticercosis is the preferred method of treatment.

Consultations

Consult with an infectious disease specialist for help with a questionable diagnosis, help eradicating the organism, and information on public health issues.

Consult a neurologist and a neurosurgeon for the management of NCC manifestations.

Consult an ophthalmologist for cases involving ocular cysticercosis.

Diet

Other than adequately cooking pork and beef products to prevent reinfection, taeniid infections require no specific diet.

Activity

No activity restrictions are necessary.

Prevention

Prevention and control of T. solium infection as recommended by WHO[3]

  • Mass drug administration for taeniasis
  • Identification and treatment of taeniasis cases
  • Health education, including hygiene and food safety
  • Improved sanitation
  • Improved cultivation and production of pig 
  • Anthelmintic treatment of pigs (oxfendazole)
  • Vaccination of pigs (TSOL18 vaccine)
  • Improved meat inspection and processing of meat products
 

Guidelines

Guidelines Summary

COHEMI (COordinating resources to assess and improve HEalth status of MIgrants from LatinAmerica) project published guidelines for screening, diagnosis and management of T. solium taeniasis and cysticercosis in 2017.[24]

1. Who should be screened for cysticercosis?

Subjects at high risk for cysticercosis including:

  • Confirmed T. solium taeniasis 
  • Household and daily contacts of confirmed T. solium taeniasis cases
  • Family members of a cysticercosis patient
  • Subjects with possible exposure in an endemic country before undergoing treatment with antiparasitic drugs such as praziquantel or albendazole 

High-risk subjects should be screened for symptoms (headache, seizure) and signs (subcutaneous nodules) suggestive of neurocysticercosis and have brain imaging studies such as CT scan or MRI if indicated. 

2. Who should be screened for T. solium taeniasis?

  • Patients with cysticercosis and live parenchymal cyst or enhancing lesions
  • Household and daily contacts of patients with cysticercosis, especially if a recent/local transmission is suspected such as cysticercosis in children, cysticercosis in patients who never travel to endemic countries, patients with viable cysticerci
  • Patients with history of proglottids expulsion within the last year 

3. How to diagnose T. solium taeniasis?

  • History of proglottids expulsion within the past year, with visualization of proglottids in stool sample
  • Microscopic and macroscopic examination of stool samples collected on three different days showing proglottids or eggs
  • Taenia species identification should always be performed, especially in subjects exposed to T. solium in highly endemic countries (Latin America, Asia and Africa) by examining scolex, proglottids and uterine branches

4. Treatment of T. solium taeniasis 

  • Single dose of praziquantel or niclosamide
  • Confirm the efficacy of treatment with history of proglottids expulsion after 1 week of treatment, microscopic and macroscopic examination of stool samples 1 month and 3 months later and if available, obtain CoAg-ELISA at 1 month and 3 months later. If any of these tests become positive, the treatment should be repeated

Diagnosis and treatment of cysticercosis, see Neurocysticercosis.

 

Medication

Anthelmintics

Class Summary

Treatment of both tapeworm infections is similar; praziquantel is considered the drug of choice. Niclosamide can also be used. Both are administered as single-dose therapy. A new drug, tribendimidine, is being studied in China. With T solium infection, start treatment immediately because of the possibility of cysticercosis via autoinfection.

Praziquantel (Biltricide)

Praziquantel is the DOC for Taenia infection. It increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature.

Niclosamide (Niclocide)

Niclosamide acts by causing necrosis of the head and adjoining segments of the tapeworm. The worm loses hold and is eliminated in pieces or intact with feces. It is available as a 500-mg tablet. It should be chewed to fine pulp before swallowing with a little water or crushed in liquid and then swallowed.

Albendazole (Albenza)

Albendazole decreases ATP production in the worm, causing energy depletion, immobilization, and, finally, death. To avoid inflammatory an response in the CNS, the patient must also be started on anticonvulsants and high-dose glucocorticosteroids.

Glucocorticoids

Class Summary

These agents are useful in cases of primary increased intracranial pressure or cases resulting from anthelmintic-induced cyst death and resultant inflammation.

Dexamethasone (Decadron)

Dexamethasone is an adrenocortical steroid. It decreases inflammation by suppressing the migration of PMNs and reducing capillary permeability.

 

Follow-up

Further Outpatient Care

Following treatment, patients should carefully examine stools for proglottid elimination during the next 5 weeks for T solium infection and for 3 months for T saginata infection.

Confirm the efficacy of treatment of T. solium taeniasis with history of proglottids expulsion after 1 week of treatment, microscopic and macroscopic examination of stool samples 1 month and 3 months later and if available, obtain CoAg-ELISA at 1 month and 3 months later. If any of these tests become positive, the treatment should be repeated.[24]

Further Inpatient Care

Admit the patient if complications such as intestinal obstruction arise because of intestinal taeniid infection.

See Cysticercosis and Neurocysticercosis for information on further inpatient care for these diseases.

Deterrence/Prevention

Individuals should avoid eating inadequately cooked beef or pork.

Examine the stools of potentially infected individuals for taeniid infection and provide treatment if test results are positive.

Practice good hand hygiene.

Complications

See the list below:

  • Appendicitis

  • Cholecystitis

  • Pancreatitis

  • Intestinal obstruction

  • Tubo-ovarian abscess (rare)

  • Systemic cysticercosis[37]

Prognosis

Treatment with praziquantel reportedly provides cure rates of 99-100%.

Patient Education

Educate patients and families about routes of infection and preventive measures.

Teach patients and families proper sanitary and personal hygiene measures.