Cysticercosis

9 Interesting Facts of Cysticercosis

1. Cysticercosis is infection caused by the larval stage of Taenia solium (pork tapeworm); most common and serious manifestations occur when cysticerci (larval stage) invade the central nervous system, causing neurocysticercosis
2. Manifestations depend on number, location, size, and stage of lesion (viable, degenerative, calcified), and host inflammatory response to degenerating cysts; months or years may lapse between initial infection and symptom onset
3. Symptomatic disease usually results from intracerebral lesions (eg, seizures, mass effect), intraventricular cysts (eg, hydrocephalus), subarachnoid lesions (eg, chronic arachnoiditis), and spinal cord lesions (eg, cord compression)
4. Disease is most prevalent in conditions of poor sanitation where free-roaming pigs and humans coexist; areas of endemicity include Latin America, Asia, India, and sub-Saharan Africa
5. Humans develop adult intestinal tapeworm infestation (taeniasis) after ingestion of poorly cooked, contaminated pork; ingestion of Taenia solium eggs (larval form) excreted in feces of human adult tapeworm carrier may result in cysticercosis
6. Diagnosis is based on neuroimaging (both MRI and CT) and serologic testing
7. Treatment is individualized and largely tailored to anatomic location of infection; focus initial treatment on symptom control (eg, treatment of seizures, treatment of hydrocephalus), then consider use of antiparasitic agents
8. Pharmacotherapeutic regimen of choice is albendazole for 2 or fewer viable cysts and albendazole-praziquantel when more than 2 viable cysts are present, in the absence of contraindications
9. Concomitant use of corticosteroids is recommended when anthelmintic drugs are prescribed

Pitfalls

• Eating undercooked pork does not result in cysticercosis; however, ingestion of infected pork may result in taeniasis (human pork tapeworm carrier state); later, fecal-oral autoinoculation of eggs excreted in feces may result in both human cysticercosis and taeniasis in the same patient
• Anthelmintic treatment often results in rebound inflammatory response with the death of the cysticerci parasite; manifestations may temporarily worsen with initiation of treatment
• Initial priority is treatment and control of symptoms, rather than immediate initiation of cysticidal pharmacotherapy; control seizures and intracranial hypertension before initiation of specific antiparasitic therapy, when indicated
• Avoid treatment of neurocysticercosis with cysticidal drugs solely based on symptoms without definitive neuroimaging and full characterization of infection; empiric treatment without fully defining extent and location of cysts may result in harm (eg, precipitous rise in intracranial pressure, optic nerve entrapment with loss of vision)

• Cysticercosis is infection caused by the larval stage of Taenia solium (pork tapeworm); most common and serious manifestations occur when cysticerci (larvae) invade the central nervous system, causing neurocysticercosis 
• Manifestations of neurocysticercosis depend on number, location, size, and stage of lesion (ie, vesicular, degenerative, or calcified), and host inflammatory response to degenerating cysts; seizures, headache, and obstructive hydrocephalus are the most common presenting manifestations 
• Cysticercosis not involving the central nervous system is often asymptomatic; most common sites of involvement include muscle, skin, subcutaneous tissue, and eyes
• Technically, cysticercosis is a general term describing an infection with a number of parasite tapeworms that have a cysticercus anatomic form of larvae; however, it has come to be understood as infection associated specifically with Taenia solium larvae

Classification

• Based on life cycle stage of pork tapeworm when ingested, site of infection, and subsequent manifestations
  • Taeniasis: ingestion of larval cysts (cysticerci) resulting in gastrointestinal infection with adult tapeworm 
    • Infection is acquired by ingestion of raw or undercooked pork containing cysticerci
    • Infection is limited to the gastrointestinal tract and most pork tapeworm carriers are asymptomatic; some patients may report passing of white ribbons (proglottids) in stool
    • Eggs produced by adult pork tapeworm are excreted in fecal material; cysticercosis may develop if eggs are ingested
  • Cysticercosis: ingestion of eggs excreted in feces of pork tapeworm carrier that results in tissue infection with larval cysts (cysticerci) 
    • Asymptomatic infection (most cases)
      • Most cysts outside of the central nervous system remain asymptomatic 
    • Neurocysticercosis
      • Taenia solium cysts within the central nervous system
      • Most common symptomatic presentation
    • Cysticercosis not involving the central nervous system
      • Often involves subcutaneous tissue, muscle (including heart), and eye (anterior chamber, extraocular muscles)
• Based on life cycle stage of neurocysticercosis lesion
  • Vesicular stage (viable)
    • Initial stage in which live parasite evades immune system response; inflammation (eg, edema, contrast enhancement) surrounding lesion is absent
    • Characterized by membrane-bound cyst with clear center surrounding parasite head (scolex) 
    • Cysts may survive in this quiescent phase for months to years before beginning to degenerate 
  • Degenerative stages
    • Stages characterized by host immune response to parasite. Pericystic inflammation develops as cysts degenerate; symptoms are most frequently noted during this phase
    • Colloidal stage
      • Progressive cellular response eventually leads to increased local inflammation and density of cyst contents; cyst borders become poorly defined 
      • Turbidity develops in cyst fluid and scolex begins to deteriorate; fluid gradually becomes more opaque 
    • Granular-nodular stage
      • Eventual cyst collapse results in a small, nodular, granulomatous lesion 
      • Scolex is almost completely degenerated 
  • Calcified stage
    • Eventual resorption of necrotic larvae results in a residual calcified scar (in most cases) or no residual lesion
    • Intermittent perilesional edema may develop and corresponding clinical symptoms may flare 
• Based on location of neurocysticercosis lesion
  • Parenchymal
    • Intracerebral lesions are the most common site of central nervous system infection 
    • Tend to develop in areas of gray-white interface 
    • Symptomatic patients typically present with seizures, headache, or manifestations secondary to mass effect 
    • Cysticercotic encephalitis is a rare form of disease caused by massive number of parenchymal cysts; numerous dying parenchymal cysts result in diffuse cerebral edema with corresponding spike in intracranial pressure 
  • Extraparenchymal
    • Subarachnoid neurocysticercosis
      • Most common extraparenchymal site is subarachnoid space and associated meninges 
      • Typically develop in sylvian fissure; cysts may involve interhemispheric spaces and basal cisterns 
      • Arachnoiditis may result from exuberant inflammatory response; stroke and vasculitis may occur 
      • Cysts may form large vesicular clusters (racemose cysticercosis) that may impose mass effect on neighboring structures 
      • A variety of cranial nerve deficits may develop when basal cisterns are involved; optic nerve compression may lead to visual impairment 
      • Hydrocephalus may develop from a number of mechanisms including arachnoiditis-associated meningeal fibrosis and mechanical obstruction of cerebrospinal fluid flow, owing to high parasite burden in subarachnoid space 
    • Intraventricular neurocysticercosis
      • Cysticerci within ventricular space; growth of lesion (size) is limited by ventricular space
      • Frequently results in obstructive hydrocephalus secondary to obstruction of cerebrospinal fluid flow and ventriculitis; Bruns syndrome is caused by intermittent, ball-valve obstruction of 3rd or 4th ventricle associated with postural changes
      • 4th ventricle is most commonly involved followed by lateral ventricles 
      • Lesions may eventually involute and resolve spontaneously, particularly when lesion is adherent to ventricular wall and involving the lateral ventricles
    • Spinal neurocysticercosis
      • Cysticerci within the spinal subarachnoid space or intramedullary cysticerci within the spinal cord 
      • Rare (less than about 5% of disease); frequently presents with concomitant cranial involvement 
      • Usually develops after dissemination through communicating cerebrospinal fluid pathways secondary to disease involving subarachnoid space, particularly involving basal cisterns 
      • Most patients are asymptomatic; may present as cord compression syndrome, meningitis, or lumbar arachnoiditis 
      • When symptomatic, back pain, radicular pain, and urinary dysfunction are the most common presenting features
    • Ocular neurocysticercosis
      • Cysticerci involving retina
      • May result in retinal detachment or iridocyclitis
  • Mixed
    • Patients with both parenchymal and extraparenchymal lesions

Diagnosis

Clinical Presentation

History

• Symptoms of systemic illness (eg, fever, weight loss, regional adenopathy) are typically absent 
• Neurocysticercosis
  • Infection is often chronic and manifestations may develop months to years after infection 
    • Onset of manifestations is most common between 3 and 5 years after infection 
    • Symptoms often develop during cyst degeneration stages, when immune system response results in inflammation 
    • Occasionally patients with parenchymal disease develop symptoms a few months after infection; encephalitis is an acute manifestation
  • Manifestations depend on size, number, location, and stage of cysticerci lesion 
    • Active symptoms may refer to more than 1 anatomic site; presence of multiple cysticerci in the central nervous system is much more common than a solitary lesion 
    • Cysticerci may be present at different life cycle stages in a given patient when multiple lesions are present
  • Most common presenting patterns
    • Seizures
      • Most characteristic manifestation of parenchymal lesions
      • Seminology (pattern of movements) usually correlates with the anatomic region the lesion occupies; seizure duration is highly variable
      • Todd paralysis (transient focal neurologic deficits) may occur after repeated focal seizures 
      • May occur in any stage of lesion; most common in degenerating cysts and rare in viable, noninflamed cysts 
    • Headache
      • May represent an isolated symptom, postictal phenomenon, symptom of intracranial hypertension, or arachnoiditis; may occur with parenchymal, cisternal, or ventricular disease
      • May be bilateral or hemicranial, mimicking migraine or tension headache 
      • Pain associated with a parenchymal degenerating cyst or a calcified cyst undergoing perilesional edema is often localized to the side and quadrant of underlying lesion
    • Intracranial hypertension
      • Obstruction of cerebrospinal fluid flow may result from a number of underlying mechanisms (eg, external compression, internal obstruction of cerebrospinal fluid pathways, diffuse edema)
      • Symptoms may include vomiting, headache, dizziness, mental status changes (eg, drowsiness, confusion), syncope, and diplopia (secondary to papilledema or lateral rectus palsy)
      • Often symptoms are worse in the morning after lying recumbent for hours
      • Symptom onset may be abrupt, intermittent, or gradual
    • Focal neurologic deficits
      • May result from mass effect secondary to large cyst or cyst clusters in subarachnoid space or perilesional edema
      • Specific symptom complex (eg, diplopia, weakness, visual impairment) reflects anatomic location of cyst
• Cysticercosis involving the eye but not the central nervous system
  • May present with visual disturbances and eye pain
• Subcutaneous cysticerci
  • Typically presents with nonpainful subcutaneous nodules or remains asymptomatic
  • Most frequent locations are arms and chest 
• Muscular cysticerci
  • Usually asymptomatic 
  • Often suspected in appropriate clinical context when discrete calcified nodules are incidentally noted within musculature on plain radiographs obtained for other clinical indications

Physical examination

• Neurocysticercosis
  • Seizures
    • Often begin as focal; may secondarily generalize
  • Intracranial hypertension
    • Hypertension, bradycardia, and papilledema are suggestive
  • Focal neurologic deficits
    • Variable cranial nerve palsies
  • Visual deficits from cysticerci in subretinal space
• Cysticercosis involving the eye but not the central nervous system
  • Intraocular cysts may be free floating in vitreous, resulting in visual impairments 
  • Retro-ocular cysts may present with proptosis 
  • Extraocular involvement may result in ptosis 
• Subcutaneous cysticerci
  • Nontender, mobile, subcutaneous nodules 

Causes

• Taenia solium can result in varying clinical manifestations depending on parasite life cycle stage at time of infection
  • Human cysticercosis is caused by (accidental) ingestion of human feces contaminated with ova of Taenia solium eggs 
    • Close contact with a human carrier of intestinal tapeworm is a risk factor for infection; autoinfection is possible 
      • Develops after ingestion of Taenia solium eggs through fecal-oral transmission 
      • Ingested tapeworm eggs hatch in digestive system and liberate oncospheres; oncospheres invade intestinal mucosa, enter bloodstream, then distribute to tissues (eg, eyes, skin, muscle, central nervous system); oncospheres develop through metacestode stages, evolving to cysticerci
      • Human cysticercosis does not develop after ingestion of infected pork with cysts
    • Most cysts are destroyed by human immune system or not able to develop; cysts deposited inside the blood-brain barrier may evade host immune system and persist in the central nervous system for years (neurocysticercosis)
    • Cyst growth and subsequent accompanying inflammation ultimately result in clinical manifestations
    • Low-burden disease is likely a result of environmental exposure; high-burden cyst load is likely secondary to close personal contact with carrier
  • Porcine cysticercosis
    • Pigs acquire infection by ingesting Taenia solium eggs or proglottids (segment of tapeworm body containing eggs), usually by means of scavenging through material contaminated by infected human fecal material
    • Eggs hatch in the digestive system and liberate oncospheres (larval stage) that invade mucosa and disseminate to tissue via the blood stream; cystic larvae develop in muscle and other tissue of pigs (porcine cysticercosis)
    • Humans consuming poorly cooked, infected pork may develop taeniasis (adult intestinal tapeworm infestation)
  • Human tapeworm infection (taeniasis)
    • Develops after ingesting poorly cooked, contaminated pork
    • Humans are only known definitive host (ie, tapeworm completes its life cycle and exists in adult form, capable of producing eggs, only in the human intestine) 
    • Intestinal infection is typically asymptomatic; mild gastrointestinal symptoms may occur and tapeworm segments may be rarely seen as white ribbons (proglottids) passed in stool 
    • Eggs are excreted in human stools; ingestion of eggs results in cysticercosis
    • Both humans and pigs serve as intermediate hosts (ie, hosts in which tapeworm eggs can develop only up to the metacestode larval stage)
      • Pigs that ingest eggs excreted in contaminated human stool develop porcine cysticercosis
      • Humans that ingest eggs excreted from contaminated human stool develop human cysticercosis

Risk factors and/or associations

Age

• Peak incidence occurs among patients aged 25 to 35 years 

Other risk factors/associations

• Residence in endemic region
  • Regions of endemicity include Latin America, Caribbean, sub-Saharan Africa, Southeast Asia, India, China, Indonesia, and Nepal 
    • Regional differences are noted among patients with symptomatic disease 
      • Neurocysticercosis in India is most frequently characterized by a single parenchymal lesion
      • Neurocysticercosis in Latin America is often characterized by multiple cysticerci in parenchyma, ventricles, or subarachnoid space
  • Affects at least 10% to 20% of villagers in areas of endemicity (based on population prevalence of brain calcifications) 
  • Cumulative infection risk increases in areas of endemicity with increasing age, frequent consumption of pork, and poor household hygiene 
• Immigration from and travel to area of endemicity
  • Increasing incidence noted in high-income countries (eg, United States, Canada) and throughout Europe is largely attributed to increasing rates of immigration 
• Contact with tapeworm carrier 
• Consumption of food prepared by person who has previous residence in high-risk area 
• Residence or travel in area with lack of adequate sanitation and clean water 
• Personal history of tapeworm infection is noted in only a small minority with cysticercosis 

Diagnostic Procedures

Primary diagnostic tools

• Accurate diagnosis of neurocysticercosis is often challenging 
  • Heterogeneity of clinical presentation may complicate diagnostic process 
  • Diagnostic criteria incorporate clinical history, epidemiologic factors, neuroimaging results, and immunologic evidence to classify disease as either definitive or probable 
• Suspect diagnosis based on compatible clinical presentation (eg, seizures, hydrocephalus) in appropriate clinical context, such as: 
  • Residence in, immigration from, or travel to area of endemicity (eg, Latin America, Caribbean, sub-Saharan Africa, Southeast Asia, India, China, Indonesia, Nepal)
  • Consumption of food handled by person from high-risk area
  • Contact with Taenia solium carrier or household member diagnosed with cysticercosis
  • Many cases are suspected after neuroimaging obtained to assess symptoms (eg, headaches, seizures) reveals lesion(s) suggestive of neurocysticercosis
• Obtain brain MRI, head CT, and enzyme-linked immunoelectrotransfer blot for all suspected cases 
• Establish diagnosis and stage lesions based on neuroimaging
  • Obtain both CT and MRI in all patients with suspected neurocysticercosis, when possible
  • Combined information from both CT and MRI most accurately define number, location, size, and stage of lesion(s)
• Obtain serologic testing in patients with suspected neurocysticercosis
  • Diagnosis may be confirmed by serology in patients with suggestive findings 
  • Enzyme-linked immunoelectrotransfer blot is test of choice 
  • Serology is particularly helpful when findings on neuroimaging are consistent but not definitively diagnostic for disease
• Other testing platforms are only available in very select laboratories (eg, NIH) 
  • Cestode antigen test (performed with serum and cerebrospinal fluid)
  • Cestode DNA testing (performed with serum, urine, and cerebrospinal fluid)
• Diagnosis may be supported by identification of Taenia solium carrier in household based on stool microscopy 
  • Stool testing among family members is only indicated when epidemiology suggests possibility (eg, recent immigration, recent travel)
  • It is extremely rare to find taeniasis in a patient with cysticercosis, owing to long incubation period for both types of involvement; therefore, stool testing is not routine for patients diagnosed with cysticercosis
• Additional testing indicated at time of initial diagnosis
  • Ophthalmologic examination is required to exclude ocular disease before treatment with anthelmintic drugs
  • MRI of spine in all patients diagnosed with subarachnoid disease; up to 60% of patients with subarachnoid disease have spinal involvement 
  • Screen for latent tuberculosis and strongyloidiasis in patients likely to require prolonged steroid regimens
  • Screen household members of patients for tapeworm carriage if it is likely they acquired disease in a nonendemic area
• Testing indicated for patients with cysticercosis diagnosed outside of the central nervous system is not standardized and official recommendations are lacking
  • In Western countries, most experts regard imaging the central nervous system prudent with or without symptoms suggestive of central nervous system involvement
  • In endemic countries, imaging is often obtained only when symptoms suggest central nervous system involvement

Laboratory

• LLGP (lentil-lectin purified glycoprotein) enzyme-linked immunoelectrotransfer blot assay
  • Western blot assay using LLGP antigens is only available at the CDC and a few commercial laboratories in the United States 
  • Preferred serologic assay owing to lack of cross-reactivity with other infections and improved test characteristics compared with other serologic platforms 
    • Avoid commercially available ELISA antibody detection test because of inferior test characteristics 
  • 98% sensitive for diagnosis in patients with 2 or more brain cysts; sensitivity is much lower (less than 50%) in patients with a single lesion or only calcified cysticerci 
    • A negative test result does not definitively exclude diagnosis when clinical suspicion is high; however, negative test result in patient with 2 or more lesions should prompt a work-up for alternative diagnosis 
  • Serum or cerebrospinal fluid samples may be used; test characteristics appear to be similar in both serum and cerebrospinal fluid samples (although some sources identify improved sensitivity in serum compared with cerebrospinal fluid samples) 
  • Presence of Taenia solium antibodies does not definitively indicate either active disease or central nervous system involvement 
    • Positive test result may occur from presence of infection outside the central nervous system, exposure without established infection, previous infections that have resolved spontaneously, and passive transfer from mother to fetus 
      • Presence of antibodies does not inform location of infection 
      • Antibodies may persist in serum for long periods after clearing of parasite 
    • Overall, up to 20% of patients living in endemic regions exhibit specific antibody reactions owing to viable neurocysticercosis or alternate causes for positive results 
• Stool microscopy for ova and parasites
  • May be used to identify eggs and proglottids (body segments harboring eggs) of pork tapeworm carriers
  • Sensitivity is low owing to threshold of egg number needed in sample to be visible with microscopy
  • Specificity for identification of proglottids is considered high with experienced examiners; all Taenia solium ova are indistinguishable

Imaging

• Characteristic findings
  • Staging of lesion by neuroimaging characteristics
    • Viable (live) vesicular cyst
      • Well-defined, round cystic structure with liquid contents; signal of liquid is isointense to cerebrospinal fluid 
      • Parenchymal cysts usually measure 0.5 to 2 cm in diameter 
      • Absent or very minimal perilesional inflammation (enhancement and edema) 
      • Scolex may be visualized as a high-density nodule within cyst (dot in hole sign) 
    • Degenerating (involuting) cyst
      • Colloidal stage
        • Much less defined than viable cysts with poorly defined cyst borders 
        • Cystic fluid is isointense on CT and MRI
        • Often perilesional edema surrounds cyst as noted by contrast-enhanced CT and contrast-enhanced T1-weighted MRI
        • Scolex is no longer visible
      • Granular-nodular stage
        • Cyst involution results in a small nodular lesion
        • CT and MRI demonstrate contrast enhancement
    • Calcified (dead) cyst
      • Usually appears as nonenhancing hyperdense nodules on CT imaging
      • MRI is less sensitive for detecting calcification; perilesional enhancement may persist for some time after evidence of complete calcification on CT
      • Intermittent worsening of perilesional edema and reappearance of perilesional enhancement may occur in this phase in association with corresponding symptom flares (eg, recurrent seizures)
  • General imaging considerations
    • Presence of multiple unilocular cysts in the central nervous system is far more common than a solitary cyst 
    • Definitive identification of scolex is a pathognomonic sign 
    • Parenchymal lesions are round and usually between 5 and 20 mm in diameter 
      • Lesions with diameter greater than 20 mm, irregular borders, or accompanying midline shift are more likely to have other causes 
      • Lesions with thick irregular borders usually represent tumor and not neurocysticercosis
    • Perilesional or diffuse edema suggest presence of active host immune response; focal contrast enhancement suggests blood-brain barrier dysfunction 
    • Imaging may demonstrate other complications (eg, hydrocephalus, stroke) 
    • Starry-sky appearance is classic description of multiple parenchymal cysts at various evolutionary stages 
    • Large cysts may develop air fluid levels mimicking brain abscess; multiple cysts in close proximity may resemble multiseptated cyst 
• Specific imaging modality considerations
  • MRI
    • Advantages over CT
      • Improved visualization of small lesions, lesions close to skull, and extraparenchymal lesions (eg, posterior fossa, subarachnoid, basal cistern, intraventricular, spinal cord) 
      • Better defines degree of parenchymal inflammation or periventricular effusion in patients with hydrocephalus 
      • Better defines evolutionary stage of lesion and more sensitive for detection of scolex 
      • Better detects basilar arachnoiditis 
    • Because cyst fluid and cerebrospinal fluid have similar densities, the ability to visualize cysts in the intraventricular space and subarachnoid space is less optimal than in other locations (eg, parenchymal and spinal spaces) 
  • CT
    • Primary advantages over MRI include improved detection of calcification and availability 
• Special imaging considerations based on lesion location
  • Cysts located in subarachnoid or ventricular spaces
    • Specialized MRI imaging techniques often best define subarachnoid and intraventricular disease (eg, FIESTA and FIESTA-C [Fast Imaging Employing Steady state Acquisition], BFFE [Balanced Fast Echo], TrueFISP [True Fast Imaging with Steady state Precision], CISS [Constructive Interference Steady State]) 
    • Subarachnoid space lesions
      • Lesions may grow to occupy large spaces, especially in the sylvian fissures and basal cisterns
      • Often less well-defined than cysts in other locations and may distort normal anatomy because of tendency to accommodate to available space
      • Cysts located in basal subarachnoid space are often associated with concomitant spinal lesions; therefore, spinal MRI is indicated 
    • Intraventricular space lesions
      • May be challenging to diagnose with CT, particularly when coexisting parenchymal lesions are absent, because lesions are isodense and isointense to cerebrospinal fluid
      • Ventricular deformity, distention, and hydrocephalus may be the only suggestive findings on CT

Other diagnostic tools

• Diagnostic criteria for neurocysticercosis (revised 2017 version)
  • Diagnosis based on degree of certainty
    • Definitive diagnosis is defined by any of the following:
      • 1 absolute criterion
      • 2 major neuroimaging criteria plus any clinical/exposure criteria
      • 1 major and 1 confirmative neuroimaging criteria plus any clinical/exposure criteria
      • 1 major neuroimaging criteria plus 2 clinical/exposure criteria (including at least 1 major clinical/exposure criterion), together with the exclusion of other pathologies producing similar neuroimaging findings
    • Probable diagnosis is defined by either:
      • 1 major neuroimaging criteria plus any 2 clinical/exposure criteria, or
      • 1 minor neuroimaging criteria plus at least 1 major clinical/exposure criteria
  • Criteria
    • Absolute criteria (unequivocal evidence of cysticerci infection of the central nervous system)
      • Histologic demonstration of parasite from biopsy of brain or spinal cord lesion
      • Visualization of subretinal cysticercus
      • Conclusive demonstration of a scolex within a cystic lesion on neuroimaging studies (by an experienced examiner)
    • Neuroimaging criteria
      • Major criteria
        • Cystic lesions without a discernible scolex
        • Enhancing lesions
        • Multilobulated cystic lesions in subarachnoid space
        • Typical parenchymal brain calcifications
      • Confirmative criteria
        • Cystic lesion resolution after cysticidal drug therapy
        • Spontaneous resolution of single, small enhancing lesion
        • Ventricular cyst migration documented on sequential neuroimaging studies
      • Minor criteria
        • Obstructive hydrocephalus (symmetrical or asymmetrical) or abnormal enhancement of basal leptomeninges
    • Clinical/exposure criteria
      • Major clinical/exposure
        • Detection of specific anticysticercal antibodies or cysticercal antigens by well-standardized immunodiagnostic tests
        • Cysticercosis outside central nervous system
        • Evidence of household contact with Taenia solium infection
      • Minor clinical/exposure
        • Clinical manifestations suggestive of neurocysticercosis
        • Persons coming from or living in an area where cysticercosis is endemic
  • Test characteristics of diagnostic criteria include sensitivity of about 94% and specificity of 81% 

Differential Diagnosis

Most common

• Central nervous system tumor
  • Solitary lesion or metastasis to brain may present with similar symptoms (eg, seizures, headache, increased intracranial pressure) and findings on neuroimaging
  • Symptoms of systemic illness (eg, fever, weight loss, regional lymphadenopathy) are usually present in patients with tumors but are absent in most patients with cysticercosis
  • In most cases, findings on neuroimaging can differentiate; when in question, solitary lesions pose a particular diagnostic challenge because negative result on enzyme-linked immunoelectrotransfer blot assay does not definitively exclude diagnosis of cysticercosis
  • Histopathologic confirmation of diagnosis may be required when diagnosis remains in question
• Brain abscess
  • May present similarly with headache, seizures, focal neurologic symptoms, and a solitary ring-enhancing lesion
  • Symptoms of systemic illness (eg, fever) are usually present in patients with abscess but are absent in patients with cysticercosis
  • Exclusion of neurocysticercosis may be difficult. Sensitivity of enzyme-linked immunoelectrotransfer blot assay is less than 50% for patients with a solitary lesion; therefore, a positive result helps to suggest cysticercosis, but a negative result cannot exclude the disease
  • Diagnostic confirmation may require culture of aspirate from lesion when diagnosis remains in question
• Intracranial fungal granuloma
  • Mycotic granuloma may present with similar manifestations (eg, headache, focal neurologic signs) and findings on neuroimaging (single or multiple enhancing lesions)
  • Infection is most common in patients with HIV infection and immunocompromise
  • In many cases, findings on neuroimaging can differentiate; when in question, solitary lesions pose a particular diagnostic challenge because negative result on enzyme-linked immunoelectrotransfer blot assay does not definitively exclude diagnosis of cysticercosis
  • Definitive diagnosis may require resection with histopathologic examination and fungal culture
• Intracranial tuberculoma
  • May present with similar manifestations (eg, headache, focal neurologic signs, seizure) and findings on neuroimaging (single or multiple enhancing lesions)
  • Regional adenopathy, fever, night sweats, and weight loss suggest tuberculosis; HIV infection is a common comorbidity 
  • May be difficult to differentiate, particularly without an additional focus on tuberculosis infection (eg, negative chest radiograph findings)
  • Definitive diagnosis may require biopsy with histopathologic examination, culture, and/or nucleic acid amplification testing
• Intracranial toxoplasmosis
  • May present similarly with fever, seizures, confusion, focal neurologic defects, or single or multiple ring-enhancing lesions on neuroimaging
  • Infection is most common in patients with HIV infection and immunocompromise
  • May be distinguished by polymerase chain reaction or histochemical staining of cerebrospinal fluid, or by histopathology of biopsied tissue

Treatment Goals

• Manage symptoms (eg, seizures, intracranial hypertension, headache)
• Treat infection with antiparasitic pharmacotherapy, when indicated and in the absence of contraindications
• Control inflammation

Disposition

Admission criteria

Criteria for ICU admission

• Increased intracranial pressure, status epilepticus, paralysis awaiting response to high-dose steroids, giant cysts, and encephalitis may require ICU level of care

Recommendations for specialist referral

• Manage neurocysticercosis in consultation with neurologist and/or neurosurgeon and infectious disease or tropical medicine specialist with experience treating disease 
• Refer for formal ophthalmologic examination at time of diagnosis to exclude presence of intraocular cysticercosis before treatment with anthelmintic pharmacotherapy 
• Notify local public health authorities of cysticercosis and taeniasis diagnosis to investigate need for further identification and treatment of tapeworm carriers; cysticercosis and taeniasis are reportable in some states and regions in the United States 

Treatment Options

Review complete disease profile before establishing an individualized treatment plan

• Number of cysts, central nervous system anatomic location(s), stage of cyst degeneration, and host immune response to infection all affect treatment plan 
• Screen all patients with formal ophthalmologic examination to exclude ocular cysticercosis before treatment with anthelmintics 

First step is treatment of presenting symptoms

• Treat pain with analgesics as indicated based on general practice and standard of care 
• Treat seizures in standard fashion according to established guidelines before, during, and after anthelmintic treatment 
  • Lack of clear consensus regarding choice and optimal duration of antiepileptic drug treatment 
  • Guide choice of antiepileptic drug based on local availability, drug interactions, and potential adverse effects 
• Control intracranial hypertension with steroids, acetazolamide, mannitol, and/or surgical interventions in consultation with neurosurgeon before beginning anthelmintic drugs; manage hydrocephalus with neurosurgical shunting 

Second step is tailored disease-specific treatment, when indicated

• Antiinflammatory treatment
  • Corticosteroid treatment is indicated in all patients treated with antiparasitic (cysticidal) drugs
    • Inflammation occurs as part of natural course of infection during cyst degeneration and may be precipitated by antiparasitic pharmacotherapy 
    • Exacerbation of neurologic symptoms is common during treatment, secondary to death of parasite and ensuing local inflammatory reaction 
      • Inflammatory reaction may be severe with the presence of many cysts, large lesions, and lesions located in delicate areas of the brain
      • Ideally, begin corticosteroids at least a few days before beginning cysticidal pharmacotherapy; continue for about a week after completing course of cysticidal pharmacotherapy 
    • Optimal dose, duration, and taper of corticosteroid is not definitively established
  • Corticosteroid treatment alone (without concomitant antiparasitic therapy) may be used for patients at high risk of vigorous central nervous system inflammatory reaction (eg, heavy parasite load, diffuse infection) 
  • Screen patients requiring prolonged corticosteroid therapy for strongyloidiasis and latent tuberculosis; empiric ivermectin treatment for strongyloidiasis is recommended by some in lieu of screening 
  • Consider adding H₂ blocker or proton pump inhibitor to prevent gastritis in patients requiring prolonged corticosteroid therapy 
  • Tapering dose is recommended rather than abrupt withdrawal to avoid rebound inflammation at time of corticosteroid discontinuation 
  • Methotrexate and etanercept may be used as potential steroid-sparing agents in patients requiring long-term antiinflammatory treatment; however, clinical data are limited and precise indications have yet to be defined 
  • Some antiepileptics (eg, phenytoin, phenobarbital) may result in induction of corticosteroid metabolism 
• Cysticidal treatment
  • Use is somewhat controversial; however, most experts and guidelines recommend use for the following: 
    • Viable and early degenerating (colloidal) parenchymal cysts in absence of contraindications
    • Subarachnoid extraparenchymal cysts in absence of contraindications
  • Cysticidal drugs are ineffective against granular and calcified cysts 
  • Drug of choice is albendazole; second line drug is praziquantel
    • Single-drug therapy with albendazole is preferred with 1 or 2 cysts; dual therapy (albendazole-praziquantel) is used when more than 2 cysts are present 
    • Albendazole
      • Albendazole has superior antiparasitic efficacy, better cerebrospinal fluid penetration, and fewer interactions with commonly coadministered drugs than praziquantel 
      • Take with fatty meal to improve absorption; dexamethasone increases plasma levels 
      • Obtain lung function tests and CBC with differential before starting therapy and every 2 weeks during treatment
      • May be associated with reproductive risk. Obtain pregnancy testing before prescribing to patients of reproductive potential. Advise patients to use effective birth control during treatment and for 3 days after final dose
    • Praziquantel
      • Concomitant use of cimetidine may blunt first-pass metabolism; extensive first-pass metabolism is induced by some antiepileptic drugs and corticosteroids, resulting in reduced serum concentrations 
  • Anthelmintic treatment contraindications
    • Untreated increased intracranial pressure 
    • High preexisting risk of developing hydrocephalus (eg, subarachnoid disease, cysticercotic encephalitis) 
    • Ocular cysticercosis 
    • Presence of only nonviable, calcified lesions 
    • Use only with extreme caution in patients with high parasite load and extensive infection (eg, racemose neurocysticercosis, severe extraparenchymal disease) 
  • Data are lacking to guide preferred treatment strategy for patients with disease failing first course of antiparasitic medication
    • Some experts suggest longer course of albendazole or combined course of albendazole plus praziquantel 
• Treatment strategy based on location of disease
  • Parenchymal disease
    • Usually treated with corticosteroids and anthelmintics
    • Antiepileptics are required for patients with seizures; prophylactic antiepileptics are used by many experts for a period before, during, and after treatment
    • Most experts recommend retreatment of viable lesions that persist for 6 to 12 months after initial course of therapy 
  • Subarachnoid disease
    • Usually treated first by management of hydrocephalus, then with a prolonged course of corticosteroids and anthelmintics (2-12 months) followed by a prolonged, slow corticosteroid taper
    • Some patients may require surgical debulking 
  • Intraventricular disease
    • Preferably treated by cyst removal (endoscopic or open microsurgical approach); usually feasible when cyst is not adherent to wall of ventricle 
      • Avoid preoperative antiparasitic pharmacotherapy; perioperative corticosteroids are often recommended 
    • Shunting followed by corticosteroid and anthelmintic therapy is used when cyst cannot be safely removed because it is adherent to wall of ventricle (bleeding risk is too great with adherent cysts) or significantly inflamed 
  • Spinal disease
    • Treat with medical and/or surgical therapy based on individualized treatment plan
  • Ocular disease
    • Surgical excision of cysticerci is treatment of choice
    • Anthelmintic drugs are usually avoided to prevent exacerbating inflammation
  • Symptomatic cysts outside of central nervous system
    • Optimal approach is surgical resection; anthelmintic treatment may be recommended for symptomatic cysts when surgical removal is not feasible

Drug therapy

• Corticosteroids (optimal dosing has not been established)
  • Dexamethasone
    • Dexamethasone Oral tablet; Children, Adolescents: 0.1 mg/kg/day to 0.2 mg/kg/day PO divided into 3 or 4 daily doses (Max: 16 mg/day), followed by a gradual taper to avoid rebound symptoms.
    • Dexamethasone Oral tablet; Adults: 6 to 8 mg/day divided into 3 daily doses for 28 days, followed by slow tapering off over 2 to 8 weeks to avoid rebound symptoms. Higher doses may be required (up to 16 mg/day).
  • Prednisolone
    • Prednisolone Oral solution; Children, Adolescents, and Adults: 1 mg/kg/day PO divided 1 to 2 times daily. Maximum dosage not well defined, use clinical judgement. Individualize doses based on the condition and response of the patient.     
  • Prednisone
    • Prednisone Oral tablet; Children, Adolescents, and Adults: 1 to 2 mg/kg/day PO divided 1 to 2 times daily.  Maximum dosage not well defined, use clinical judgement. Individualize doses based on the condition and response of the patient.     
• Antiparasitics
  • Albendazole
    • Cysticercosis
      • Albendazole Oral tablet; Children and Adolescents: 15 mg/kg/day PO given in 2 divided doses (Max: 800 mg/day) for 8 to 30 days; can repeat as necessary.
      • Albendazole Oral tablet; Adults: 15 mg/kg/day PO given in 2 divided doses (Max: 800 mg/day) for 8 to 30 days; can repeat as necessary.
    • Neurocysticercosis
      • Albendazole Oral tablet; Children and Adolescents: 15 mg/kg/day PO given in 2 divided doses up to 1,200 mg/day for 10 days for 1 to 2 viable parenchymal lesions, up to 1,200 mg/day in combination with praziquantel for more than 2 viable parenchymal lesions, and up to 800 mg/day for 1 to 2 weeks for degenerating intraparenchymal neurocysticercosis. Retreatment may be necessary for lesions persisting for 6 months after the end of therapy. FDA-approved Max: 800 mg/day for 8 to 30 days. Initiate adjunctive corticosteroid therapy prior to antiparasitic drugs.
      • Albendazole Oral tablet; Adults: 15 mg/kg/day PO given in 2 divided doses up to 1,200 mg/day for 10 days for 1 to 2 viable parenchymal lesions, up to 1,200 mg/day in combination with praziquantel for more than 2 viable parenchymal lesions, and up to 800 mg/day for 1 to 2 weeks for degenerating intraparenchymal neurocysticercosis. Retreatment may be necessary for lesions persisting for 6 months after the end of therapy. FDA-approved Max: 800 mg/day for 8 to 30 days. Initiate adjunctive corticosteroid therapy prior to antiparasitic drugs.
    • Subarachnoid extraparenchymal cysts
      • Albendazole Oral tablet; Children and Adolescents: 15 mg/kg/day PO given in 2 divided doses up to 1200 mg/day for 1 month with high-dose steroids. Treatment for up to 12 months may be required.
      • Albendazole Oral tablet; Adults: 15 mg/kg/day PO given in 2 divided doses up to 1200 mg/day for 1 month with high-dose steroids. Treatment for up to 12 months may be required.
  • Praziquantel
    • Cysticercosis
      • Praziquantel Oral tablet; Children and Adolescents: 50 mg/kg/day PO given in 3 divided doses.
      • Praziquantel Oral tablet; Adults: 50 mg/kg/day PO given in 3 divided doses.
    • Neurocysticercosis
      • Praziquantel Oral tablet; Children and Adolescents: 50 mg/kg/day PO given in 3 divided doses plus albendazole for 10 to 14 days in patients with more than 2 viable parenchymal lesions. Initiate adjunctive corticosteroid therapy prior to antiparasitic drugs. 
      • Praziquantel Oral tablet; Adults: 50 mg/kg/day PO given in 3 divided doses plus albendazole for 10 to 14 days in patients with more than 2 viable parenchymal lesions. Initiate adjunctive corticosteroid therapy prior to antiparasitic drugs.
    • Taeniasis without cysticercosis (for carrier state only)
      • Praziquantel Oral tablet; Children 4 years and older and Adolescents: 5 to 10 mg/kg PO as single dose.
      • Praziquantel Oral tablet; Adults: 5 to 10 mg/kg PO as single dose.
      • After treatment, stools should be collected for 3 days to search for tapeworm proglottids for species identification. Stools should be reexamined for Taenia eggs 1 and 3 months after treatment to confirm the infection is cleared 

Nondrug and supportive care

• Surgical procedures
  • Neurosurgical methods may be employed to control hydrocephalus
    • May include fenestration of anterior wall of third ventricle, ventriculoperitoneal shunt placement, and/or excision of large lesions or lesion conglomerates 
    • Shunt dysfunction and infection is fairly common after shunt placement; corticosteroids are often used to diminish risk of shunt malfunction
  • Neurosurgical procedures may be indicated to remove lesions; indications may include:
    • Excision of large lesions associated with mass effect and encroachment on vital structures 
    • Endoscopic removal of intraventricular cysts is preferred approach, when feasible 
• Disease is reportable in some states; contact state health department to determine reporting requirements 
• Prevention of disease transmission depends on prevention of fecal-oral transmission of eggs from carriers with taeniasis 
  • Identify and adequately treat pork tapeworm carriers
    • Targeted groups for screening (stool sample examination)
      • Food handlers and child care workers emigrating from areas of endemicity 
      • Household members of patients diagnosed with cysticercosis, particularly patients with history consistent with possible recent exposure (eg, immigration, travel to endemic area) 
    • Treatment is single dose of praziquantel or niclosamide (not available in the United States) 
    • Ensure eradication with follow-up stool screening examinations at 1 and 3 months after treatment 
  • Educate and promote good hand washing practices among food handlers 

Special populations

• Pregnant patients
  • Preferred approach is deferment of anthelmintic therapy until after pregnancy 
  • Albendazole is contraindicated in pregnancy 
  • Some antiepileptics (eg, valproic acid, phenobarbital) are contraindicated in pregnancy owing to teratogenicity
  • Avoid using methotrexate as an antiinflammatory drug owing to teratogenicity 

Monitoring

• Monitor clinically during antiparasitic therapy because increased neurologic symptoms (eg, seizures, worsening of hydrocephalus) are common 
  • Some specific monitoring parameters based on location of disease include:
    • Intraparenchymal neurocysticercosis
      • Follow up clinically 2 to 4 weeks after initial diagnosis to assess for recurrent seizures and new or worsening disease manifestations
      • Guidelines suggest follow-up MRI every 6 months until resolution of the cystic component; other experts suggest follow-up at about 2 to 4 weeks after stopping therapy to assess need for additional treatment
    • Subarachnoid neurocysticercosis
      • Follow-up MRI every 3 months to monitor treatment response
      • Some experts monitor cerebrospinal fluid parameters (eg, cestode antigen, cestode DNA, WBC counts)
    • Repeated course of drug treatment is recommended by most experts for viable cysts persisting 6 months after initial course of drug treatment 
    • Some experts recommend continuing therapy until all cysts have resolved on MRI, serum and/or cerebrospinal fluid antigen testing is negative, and cerebrospinal fluid pleocytosis is improved 
• Patients requiring albendazole for more than 14 days
  • Monitor for hepatotoxicity (transaminase level greater than 5 times upper reference limit) and leukopenia (absolute neutropenia); development of either condition is a relative contraindication to continued use
  • Optimal frequency of monitoring is not definitively established; guidelines suggest weekly monitoring during the first month of treatment
• Patients requiring anticonvulsants
  • Consider weaning off of antiepileptic medications in consultation with neurologist
    • In general, guidelines recommend considering taper and discontinuation in patients after resolution of lesion on neuroimaging and seizure-free period (6 months for single lesion; 1 to 2 years for multiple lesions)
  • Monitor clinically and with periodic laboratory testing to assess for adverse medication effects according to established guidelines; most antiepileptic medications do not require routine monitoring of drug concentrations
  • Obtain CT before considering discontinuation of antiepileptics to assess for presence of seizure risk factors (eg, calcified lesions with increased enhancement, perilesional edema) 
• Patients receiving chronic corticosteroids
  • Monitor clinically for known adverse effects (eg, opportunistic infection, altered mood, Cushing syndrome, gastritis) 
  • Monitor blood glucose when receiving for more than 2 weeks 
  • Routine prophylaxis for pneumocystis infection, gastritis, and osteoporosis may be indicated

Complications

• Worsening neurologic symptoms with initiation of anthelmintic therapy
  • Increased frequency of seizures, worsening neurologic deficits, and increased risk for development of hydrocephalus are associated with antiparasitic therapy
  • Degenerating cysts may cause increased perilesional edema, thus worsening clinical signs and symptoms with treatment
• Seizure disorder
  • About one-third of patients with 1 seizure related to disease will experience a second seizure 
  • Parenchymal neurocysticercosis accounts for almost 30% of recurrent symptomatic seizures in endemic regions 
  • Exacerbation of perilesional edema is often related to recurrence of seizure activity in patients years after treatment, particularly those with residual calcification
  • Natural history of seizures in patients with parenchymal disease is fairly unpredictable 
  • Risk factors for seizure recurrence may include presence of a calcified lesion, perilesional edema, frequent seizures, status epilepticus at presentation, breakthrough seizures, and poor adherence to antiepileptic drugs 
  • Many patients may be eventually weaned off anticonvulsant medications after a seizure-free interval after anthelmintic treatment; discontinuation of anticonvulsants is often individualized in consultation with neurologist 
• Todd paralysis
  • Transient neurologic deficits may take hours to a few days to resolve 
• Obstructive hydrocephalus
  • Most commonly develops with extraparenchymal disease
  • May result from a number of mechanisms
    • External compression of cerebrospinal fluid pathways from cystic mass
    • Internal blockage of cerebrospinal fluid pathways from intraventricular cyst
    • Acute arachnoiditis in patients with subarachnoid disease and residual arachnoiditis in patients with chronic disease
    • Large cystic masses occupying sylvian fissure or interhemispheric spaces
  • Bruns syndrome
    • Transient obstruction of cerebrospinal fluid secondary to mobile ventricular cysts, precipitated by positional changes 
  • Shunt complications
    • Shunt malfunction (blockage) and shunt infection are common in patients requiring mechanical shunting 
• Cysticercotic encephalitis
  • Acute, encephalitislike reaction with diffuse cerebral edema secondary to massive cyst burden after ingestion of very large number of ova 
  • Rare, life-threatening condition that most frequently affects young female patients and children 
• Stroke
  • Obstruction of vasculature by cysticerci and inflammatory exudates may lead to vasculitis and stroke 
  • Small lacunar infarcts are not uncommon; larger vessel stroke may occur but is much less frequent 
• Cognitive alterations
  • Depression is extremely common among patients with disease 
  • Learning disabilities and cognitive deficits have been described 
• Headache syndromes
  • Extremely common among patients with disease
• Arachnoiditis
  • May develop secondary to massive inflammatory response in patients with subarachnoid disease 
• Ventriculitis
  • May develop secondary to inflammatory response in patients with intraventricular disease 
• Cranial nerve deficits
  • Cranial nerve palsies may develop with compression and entrapment of nerves; optic nerve involvement results in visual impairment 
• Visual loss
  • May result from damage to retinal tissue secondary to ocular cysticercosis, papilledema, or compression of optic chiasm 
• Spinal neurocysticercosis
  • Dissemination to spinal meninges may occur with subarachnoid disease, particularly if involving the basal cisterns 
  • Presents with motor (eg, weakness, incontinence) and sensory (eg, paresthesias, radicular pain) dysfunction related to level of involvement at which lesion occurs; transverse myelitis–like presentation may occur 
• Ocular neurocysticercosis
  • May be complicated by retinal detachment, iridocyclitis, chronic uveitis, and visual loss
• Cardiac cysticercosis
  • Cardiac cysticerci are sometimes noted at autopsy in patients with cysticercosis
  • Most patients remain asymptomatic; conduction abnormalities and heart failure are much less common manifestations
• Death
  • Giant subarachnoid cysts may be life-threatening; surgical decompression and high-dose corticosteroids may help improve survival
  • Intraventricular neurocysticercosis may lead to acute onset hydrocephalus and possible sudden death 

Prognosis

• Most patients have low-burden disease involving parenchyma and experience reasonably good long-term outcomes with appropriate treatment of disease
• Parenchymal neurocysticercosis
  • Infections are considered benign overall with good long-term prognosis, provided symptomatic care is adequate 
    • Exceptions
      • Cyst burden of greater than 50 lesions is associated with a less favorable prognosis 
      • Cysticercotic encephalitis is associated with a very poor prognosis 
  • Many lesions resolve spontaneously with or without treatment over a course of months to years 
  • Use of antiparasitic therapy reduces likelihood of seizure recurrence, decreases risk of disease progression, and hastens time to resolution 
  • Efficacy for first course of antiparasitic treatment is between 60% to 80% for cyst destruction and 30% to 40% for complete resolution of all lesions 
  • Mortality is typically limited to seizure-related deaths in patients with parenchymal disease 
• Extraparenchymal neurocysticercosis
  • Often not benign and carries less favorable prognosis than parenchymal disease; morbidity and mortality is much higher than noted in parenchymal disease, mainly owing to development of intracranial hypertension 
    • Parasite loads tend to be greater; growth of cysticerci is less restricted and more irregular than noted in parenchymal disease 
  • Subarachnoid neurocysticercosis
    • Disease is progressive and associated with significant mortality; mortality may approach 20% in well-equipped centers
    • Efficacy data for first course of antiparasitic treatment are limited; overall, efficacy is lower than that noted in patients with disease limited to parenchyma and recurrence of disease is common
  • Intraventricular neurocysticercosis
    • Patients surviving acute phase of disease have a fair prognosis with appropriate care 

Screening

At-risk populations

• Screen household members of patients diagnosed with cysticercosis, particularly those who probably acquired disease in a nonendemic area 
• Consider screening persons at high risk for carrier state (eg, those emigrating from areas of endemicity) 

Screening tests

• Screening tests are not optimal
  • Questioning patient about history of proglottids (white ribbons) in stool may be most sensitive test
  • Screen stool specimen by microscopy for taeniasis (carrier state) is most readily available laboratory test; however, sensitivity is low 
  • Immunologic noncommercial test is available in some endemic regions; DNA-based test is not commercially available

Prevention

• Primary prevention measures
  • Human cysticercosis is caused by (accidental) ingestion of human feces contaminated with ova of Taenia solium eggs
  • Prevention of disease transmission depends on prevention of fecal-oral transmission of eggs from carriers with taeniasis
    • Use safe water supply when in endemic regions
    • Consume food safe from contamination when in endemic regions; avoid eating undercooked vegetables and fruit that cannot be peeled 
  • Avoid eating raw or undercooked pork in effort to avoid development of taeniasis (human tapeworm infection; carrier state) 
• Eradication of Taenia solium has proven difficult
  • Solutions intended to interrupt transmission include the following:
    • Improved sanitation and clean water supply
    • Improved meat inspection and condemnation of infected pork 
    • Increased education in endemic regions regarding cycle of disease (eg, pen pigs instead of allowing free-roaming pigs, any efforts to prevent pigs from contacting human waste, avoiding use of human waste as fertilizer)
    • Identify and treat human carriers; praziquantel is recommended to eradicate carrier state in the United States
    • Develop programs for vaccinating pigs and anthelmintic therapy for pigs in affected farms
    • Improve disease surveillance
  • One elimination program based in Peru consisting of multiple rounds of human deworming with niclosamide, antiparasitic treatment of pigs with oxfendazole, and pig vaccination (with TSOL18 vaccine) interrupted active transmission in nearly all villagers (104 of 117); effects persisted for at least 1 year without further intervention 

Seek Additional Information

CDC: Parasites – Cysticercosis. Resource for Health Professionals. CDC website. Reviewed May 21, 2020. Accessed August 18, 2020. https://www.cdc.gov/parasites/cysticercosis/health_professionals/index.html  Cross Reference