MORNING REPORT:

CYSTICERCOSIS

Palak Parikh
December 12, 2008
EPIDEMIOLOGY
 Found in approximately 50 million people
worldwide (probably an underestimate)
 Endemic in several countries in Central and
South America, sub-Saharan Africa, India,
and Asia
 Prevalence in this country often higher in
rural areas
 221 deaths identified in the US from 1990-
2002 (62% had emigrated from Mexico)
CYSTICERCOSIS TRANSMISSION
 Caused by the larval stage of Taenia solium,
the pork tapeworm
 Humans develop by ingestion of T. solium
eggs; they can spread infection by:
 Egg-containing feces contaminating water
supplies in endemic areas
 Contaminating food directly, as eggs are sticky
and can often be found under the fingernails of
tapeworm carriers.
 LIFE CYCLE
 Once eggs ingested, embryos
are released in the small
intestine and invade the bowel
wall.
 They then disseminate
hematogenously to other tissues
and develop into cysticerci over
3 weeks to 2 months.
 Cysticerci – liquid-filled vesicles
consisting of a membranous
wall and a nodule containing the
invaginated scolex.
 Scolex – head armed with
suckers and hooks and a
rudimentary body.
PATHOGENESIS
 Cysticerci initially viable but do not cause much inflammation in
surrounding tissues – asymptomatic infection
 Host develops immune tolerance to cysticerci, which remain in
this stage for several years.
 Postulated mechanisms of tolerance:
 Taenia elaborate substances that inhibit or divert complement
pathways away from parasite
 Humoral antibodies do not kill mature taenia.
 Poorly defined factors may interfere with lymphocyte
proliferation and macrophage function, inhibiting normal cellular
immune defenses.
 Clinical manifestations occur when inflammatory response
develops around degenerating cysticercus.
SYMPTOMATIC DISEASE
 Divided into:
 Neurocysticercosis
 Extraneural cysticercosis
NEUROCYSTICERCOSIS
 80% of infections are asymptomatic
 Symptoms mainly due to mass effect, inflammatory
response, or obstruction of foramina and ventricular
system of brain.
 Most common symptoms:
 Seizures
 Focal neurological signs
 Intracranial hypertension
 Peak estimated to occur 3-5 years after infection
NEUROCYSTICERCOSIS
 Increased risk of seizures with a single calcific granuloma.
 Risk of seizures highest when lesions are degenerating and are
surrounded by inflammation.
 Encephalitis and diffuse brain edema most common in children
and young females.
 1-3% of cases involve the spinal cord, with thoracic lesions the
most common.
NEUROCYSTICEROSIS IN
ENDEMIC COUNTRIES
 Most common cause of adult-onset seizures
 Risk of seizures in seropositive individuals 2-
3 times higher than seronegative controls.
 Punctate calcifications most frequent finding
on neuroimaging of brain.
EXTRANEURAL CYSTICERCOSIS
 Typically involves:
 Eyes – in 1-3% of all infections
 Muscle
 Subcutaneous tissue – nodules most common
in patients from Asia and Africa than from
Latin America
DIAGNOSIS
 Serologic testing
 Peripheral eosinophilia only if cyst is leaking
 CT scan or MRI
 Pathognomonic Lesion: Scolex – mural nodule
within a cyst
 Brain biopsy (only in symptomatic patients
with equivocal serology and radiologic tests)
SEROLOGIC TESTING
 ELISA
 Complement fixation (CF)
 Radioimmunoassay
 Enzyme linked immunoelectrotransfer blot
(EITB) assay – test of choice
EITB ASSAY
 Enzyme-linked immunoelectrotransfer blot assay
 Test of choice for detecting anticysticercal antibodies
 Uses affinity-purified glycoprotein antigens
 Higher sensitivity (83-100%) and specificity (93-98%)
than ELISA
 Can be performed on serum or CSF but has a higher
sensitivity on serum.
 Detected 94% of pathologically confirmed NCC with 2 or
more lesions compared to only 28% with a single lesion
in one study.
CT VS MRI
 MRI preferred since it is more sensitive in detecting:
small lesions
 brainstem or intraventricular lesions
 perilesional edema around calcific lesions
 scolex
 degenerative changes in the parasite
 CT scan cheaper and better at detecting:
 small areas of calcifications.
 cysticercal infestation of extraocular muscles.

* Perform CT scan first followed by MRI in patients with

inconclusive findings or in those with negative CT scans where
strong clinical suspicion persists.
PERUVIAN STUDY
 25 patients w/ calcified intraparenchymal
brain lesions underwent non-contrast CT
scan of thighs
 13 (52%) had 1 or more muscle calcifications
consistent with extraneural cysticercosis
 These patients had plain x-rays of thighs.
 Only 6 of 13 had visible calcifications on x-ray
POTENTIAL TREATMENTS
 Albendazole (15 mg/kg/day) X 15 days +
corticosteroids (30-40 mg prednisolone or 12-16 mg
dexamethasone daily) – per UpToDate
 Praziquantel (50 mg/kg/day) X 15 days +
corticosteroids (30-40 mg prednisolone or 12-16 mg
dexamethasone daily) – per UpToDate
 Corticosteroids alone
 Anticonvulsants in patients who present with seizures
or are at high risk for seizures
 Surgery
 ALBENDAZOLE VS
PRAZIQUANTEL
 Albendazole
 Destroys 75-90% of parenchymal brain cysts
 Does not interact with anticonvulsants
 Levels not adversely affected w/ co-administration of corticosteroids

 Praziquantel
 Destroys 60-70% of cysts 3 months after administration
 Decreased efficacy compared to Albendazole
 Available for oral administration
 Does not cross the blood-brain barrier well, so CSF levels only approx 20%
of plasma levels.
 Involves cytochrome P-450 hepatic metabolism, which is induced by
corticosteroids, phenytoin, and phenobarbital

 No blinded randomized controlled trials comparing albendazole to

praziquantel.

Because of the above, praziquantel is generally considered second-line

therapy.
TREATMENT
 One randomized, double-blind, placebo-controlled trial
 120 pts with living cysticerci in the brain and seizures treated
with antiepileptic drugs
 Randomized to either albendazole (800 mg qd) and
dexamethasone (6 mg qd X 10 days) or double placebo
 Followed for 30 months or until they were seizure-free for 6
months after tapering of antiepileptic drugs
 Results:
 Resolution of intracranial cystic lesions more common in
treatment arm
 Number of patients experiencing generalized seizures declined
in the treatment arm
 No significant change between the two groups in patients
experiencing partial seizures
NEUROCYSTICERCOSIS
 Treatment in those with:  No Treatment in those
 5-50 cysts (both with:
antiparasitic and  Asymptomatic
steroids) nonviable
 Steroids alone in neurocysticercosis
patients w/ > 50 cysts  Calcified cysts
 Single viable cysts
 Fewer than 5 cysts
ANTICONVULSANTS
 Recommended for patients who present with
seizures
 Should be stopped if patient remains seizure-free
during therapy to see if the patient remains
asymptomatic
 Should be reinitiated chronically if the patient has
recurrent seizures
 Should be considered in patients w/ multiple cysts
who have no history of seizure activity
SURGICAL INTERVENTION
 Used in some patients with intracranial hypertension
 Shunting improves hydrocephalus, although recurrent
blockages of shunts common
 Surgical intervention recommended for cysts:
 Located in the 4th ventricle
 Attached to middle cerebral artery
 Compressing the optic chiasm
 Located in the spine
TREATMENT OF EXTRANEURAL
CYSTICERCOSIS
 None if pt asymptomatic
 Surgical excision for intraocular disease
 Medical therapy for involvement of
extraocular muscles or optic nerve.
 NSAIDs for patients w/ symptomatic
subcutaneous or intramuscular lesions.
 Excision of solitary lesions if NSAIDs fail or
not tolerated.
BEFORE INITIATING MEDS…
 Apply PPD.
 Consider treating with a single dose of
ivermectin before beginning corticosteroids,
as many patients have risk factors for
strongyloidiasis.
 Consult ophthalmology to rule out ocular
cysticercosis.
PATIENT MONITORING
 Intermittent surveillance w/ imaging until
cyst(s) resolve(s).
 Perhaps every 3-6 months if patient improving
or earlier if patient symptomatic.
 Reimaging of brain 2 months after completion
of treatment
 Consider antiparasitic therapy if cysts
growing off therapy
POSSIBLE PREVENTION
 Human Tapeworm Infections
 Inspection of pork for cysticerci
 Freezing or adequately cooking meat to destroy cysticerci
 Administering antiparasitic agents to pigs
 Infection in Pigs
 Confining animals and not allowing them to roam freely
 Improved sanitary conditions
 Egg Transmission to Humans
 Good personal hygiene and hand washing prior to food
preparation
 Identifying human carriers of tapeworms
 Mass community programs to treat tapeworm carriers.
 Possible Vaccine – porcine vaccine currently in the works
TAKE HOME POINTS
 Cysticercosis caused by the larval stage of Taenia solium, the
pork tapeworm
 Pay special attention if pt from Central and South America, sub-
Saharan Africa, India, and Asia, as neurocysticercosis is the
most common cause of adult-onset seizures in these endemic
areas.
 Order Head CT first to diagnose neurocysticercosis; if negative
and suspicion still high, order Brain MRI.
 EITB test of choice for serology.
 Place PPD before starting treatment.
 Obtain Ophthalmology consult before starting treatment.
 Albendazole and Dexamethasone comprise first-line treatment
for symptomatic cysticercosis. Consider concurrent
anticonvulsants if pt presents with seizures.
REFERENCES
 aapredbook.aappublications.org
 UpToDate.
 www.dpd.cdc.gov
 www.e-radiology.net
 www.parasite-diagnosis.ch
 www.stanford.edu/class/cysticercosis/sympto
ms