cysticercosis

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cysticercosis

• Zhao zhixin
• zxzhao_at_21cn.com
• The 3rd affiliated hospital of
• Sun Yat-Sen University

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Key points

• Pathogenesis and its relationship to clinical
  presentations
• Clinical presentations
• Diagnosis(imaging studies and biopsy)
• Treatment (Anti parasitic therapy and Symptomatic
  therapy)

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Background

• an parasitic disease
• caused by the pork tapeworm, Taenia solium
• Infection occurs tapeworm larvae
• enter the body and form cysticerci
  (cysts)
• Encystment of larvae occur in almost any tissue
• the central nervous system (CNS) Involvement
• neurocysticercosis (NCC)
• the most important manifestation
• present with dramatic findings

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Pathogen

• Taenia solium, causes disease in both pigs and
  humans depending on its developmental stage.
• causes two forms of disease
• Taeniasis adult tapeworm infection caused by
  ingestion of the adult form. Taeniasis occurs
  only in the human host.
• Cysticercosis
• caused by cysticerci infection in various
  organ systems
• can occur in both porcine and human hosts.

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cysticercus

• Surrounded by fibrous capsule
• Containing an invaginated scolex
• Bladder-like, fluid filled cyst
• Multiple,0.5-2cm in size

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Pathogenesis and EPIDEMIOLOGY

• Life cycle of t.solium
• Where is the disease found?
• Contagion summary
• How NCC develop

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Cysticer- cosis
cysticerci
Oncospheres Intestine
Raw or undercook pork
Ingested by pig and human
Egg or gravid proglottides
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Where is the disease found?

• is found worldwide.
• rural, developing countries with poor hygiene
• Places where
• pigs are allowed to roam freely and eat
  human feces-
• allows the cycle to continue.

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Contagion summary(1)

• Sources of infection
• persons with Taeniasis
• Transmission ways
• not spread from person to person
  directly
• persons with Taeniasis will shed
  tapeworm eggs in their bowel movements

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Contagion summary(2)

• Infection can happen by
• By accidentally swallowing pork tapeworm eggs
• Through
• drinking contaminated water or food,
• by putting contaminated fingers to mouth

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Contagion summary(3)

• autoinfection
• A person who has Taeniasis can reinfect himself.
• internal autoinfection
• External autoinfection

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HOW NCC develop ?

• Cysticercus survive in the brain
• disarming host defence, remain for
  years
• protected by brain-barrier asymptomatic
• Once the parasite degenerate
• Inflammatory response
• 80cns parenchyma seizures
• numberous parenchyma cysticerki
  
• diffuse cerebral edema encephalitits
• 10-20 extraparenchymal
• ventricles hydracephalus
• encased in a granuloma
• resolves
• scarring and calcification.

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CLINICAL MANIFESTATIONS

• symptoms can be different
• depending on
• where infection with cysticerci occurs
• how many the cysts are there
• Most cases are asymptomatic.
• Incubation months5ys

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CLINICAL forms

• Subcutaneous and Muscular involvement
• NCC
• Cardiac involvement
• Ophthalmic involvement

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Subcutaneous and Muscular involvement

• 2/3 of patients have nodules.
• Number of nodules1-1000
• Subcutaneous tissues
• nodules on arms and chest.
• small, movable, painless
• Muscular involvement
• rarely painful
• seen as calcifications following muscle
  bundles in thighs or arms.
• Massive parasite burden limb muscular
  enlargement (pseudohypertrophy).

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CLINICAL MANIFESTATIONS

• Cardiac involvement
• 1-5 of patients
• typically asymptomatic
• abnormal rhythms or heart failure
  (rare)
• Ophthalmic involvement (1-3 ).
• Intraocular cysts
• solitary lesion
• freely float in the vitreous humor
• large parasitic burden
• Visual disturbance and visual loss

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NEUROCYSTICERCOSIS

• NCC frequently asymptomatic.
• Symptoms
• similar to those found with other
  intracranial mass lesions
• consistent with elevation of ICP.
• has gained increased recognition in the last 2
  decades

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NCC

• (1)Cerebral cysticercosis
• (2)Ventricular cysticercosis
• (3)Subarachnoid cysticercosis
• (4) mixed form not common

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NCC (1)Cerebral cysticercosis

• 50 - 80 of NCC.
• Epilepsy (seizures)
• Always the first and the only symptom.
• Caused by cysticerci located in the
• Cortex near to the motorium.
• characters
• Multiple focal and unstable
• Neurosis elevation of ICP
• headache , vomiting ,visual
  disturbances

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NCC (2)Ventricular cysticercosis

• 10 of brain cysticercosis
• Caused by acute obstruction of CSF circulation
• Manifests as valve syndrome
• Intermittent positional severe
• headache,vomiting ,shock.

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NCC (3)Subarachnoid cysticercosis

• 10 of brain cysticercosis
• ¾ have increased ICP.
• Chronic ,intermittent meningitis.
• CSF test inflammation change

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Focal neurologic deficits

• are unusual
• If positive
• suggest alternative diagnoses
• tuberculoma
• tumor

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Main Cysticercosis Diagnosis Tests

• lab test Antibody test
• imaging studies
• Soft tissue X-rays
• brain CT scans
• MRI of brain
• Procedures
• Lumbar puncture CSF tests
• Biopsy of the affective area
• subcutaneous nodule

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Laboratory studies

• Complete blood count (CBC)
• Serology
• Stool for ova and parasites
• Lab studies inferior to imaging in diagnosis
• but may play an adjunctive role.

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Complete blood count (CBC)

• Peripheral eosinophilia usually is not present
• but eosinophils may be 10-15 of white blood
  cells (WBCs).

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Serology-the most useful of lab tests.

• Sensitivity linked to number of parasitic
  lesions and the stage of lesions.
• false-negative result
• Single lesions
• calcification
• with parenchymal cysts
• False-positive
• other parasitic infections
• high percentage of false positive for
  patients from endemic area (?30)

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Antibody test on CSF

• performed on CSF
• Sensitivity may be increased
• it is only accurate when performed in
• patients with active meningeal disease.

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Stool for ova and parasites

• Positive If with simultaneous intestinal
  tapeworm infestation
• insensitive
• many samples needed over several days
• nonspecific for T solium species
• as the eggs appear similar to those of the
  beef tapeworm.

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Imaging Studies(1) Soft tissue x-ray

• show calcifications of inactive cysts.
• These may appear as oblong-shaped lesions.

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Imaging Studies(2)
CT scan

• recommended as the first-obtained imaging study.
• more widely available, less expensive, and has a
  faster imaging time than MRI.
• Obtain contrast and noncontrast studies.

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Imaging Studies(2) CT scan

• Noncontrast study show
• 1.cystic lesions, or calcifications of
  inactive disease
• the most common disease form at
  presentation
• 2.focal areas of edema in the acute phase
• 3. Findings indicate mass effect or
  hydrocephalus
• Contrast study may depict
• nonenhancing cystic lesions
• ring enhancement signifying
  inflammation

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Imaging Studies(3) MRI of brain

• MRI is recommended as an adjunctive diagnostic
  tool to CT scan.
• MRI may show a mural nodule within the cyst
  representing the larval scolex. This finding is
  pathognomonic.
• MRI may show cysticerci within the ventricular
  system, which are often missed by CT scan due to
  the similar appearance of CSF and cystic fluids.

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One Patients history

• This 42y male presented to the emergency room
  with acute seizure
• images from his head MRI show
• multiple low attenuation lesions
• many with mural nodules
• and multiple calcifications
• --consistent with active and chronic
  cysticercosis. 

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Lumbar puncture

• insensitive and nonspecific in the diagnosis.
• needed only to exclude other diagnoses.
• CSF is normal in many cases
• In the presence of significant inflammation
• lymphocytosis, increased protein, and/or
  
• decreased glucose levels
• eosinophilia
• With Special Wright or Giemsa
  stains
• a common but nonspecific finding

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Biopsy

• Biopsy specimens may be taken from
• subcutaneous nodules.
• Demonstration of organisms within
• nodular tissue is diagnostic of cystic
• Biopsy of CNS lesions is rarely necessary.

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diagnosis

• Signs and symptoms are nonspecific.
• most patients do not present with definitive
  evidence of infection.
• Diagnosis by combining
• Epidemiologic data
• clinical presentation
• and Lab?imaging or Biopsy studies

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diagnosis (1)Epidemiologic criteria

• Evidences of
• Eating raw food habit or eating rice meat
  history or history of pass noodle like white
  gravid proglottides.
• Individuals coming from or living in an endemic
  area
• Household contact with an individual infected
  with T solium

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(2)Absolute criteria

• Histological demonstration of the parasite from
  biopsy
• Direct visualization of subretinal parasites by
  funduscopic examination
• Cystic lesions showing the scolex on CT scans or
  MRIs

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(3)Major criteria

• Lesions highly suggestive of NCC on neuroimaging
  studies
• CT scan or MRI showing
• cystic lesions without scolex, enhancing
  lesions
• typical parenchymal brain calcifications
• antibodies
• positive demonstrated by immunoblot assay
• Treat response
• Resolution of intracranial cystic lesions
  after therapy with albendazole or praziquantel

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treatment

• Emergency Department Care
• Further Inpatient Care
• 1.Antiparasitic treatment
• 2.control therapy response
• 3.Symptomatic therapy
• 4.surgery therapy

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Emergency Department Care

• seizure activity
• supportive care
• monitor, and correct metabolic
  abnormalities
• Anticonvulsants are effective.
• evidence of increased ICP
• Steroids, osmotic agents, and/or
  diuretics
• Initiate proper diagnostic procedures
• blood work and imaging.
• Consult appropriate specialists
• neurosurgery, neurology,
  infectious diseases

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1.Antiparasitic treatment medications

• Anti parasitic therapy can only be done in the
  hospital
• Common used medicines
• Albendazole
• Praziquantel
• -- Broad-spectrum anthelmintic

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Albendazole

• Adult Dose
• 18-20 mg/kg/d , bid/tid, for 10days
• Pregnancy C - Safety for use during pregnancy has
  not been established.

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Praziquantel

• Adult Dose
• 20 mg/kg/d , tid , for 10days
• Pregnancy B - Usually safe but benefits must
  outweigh the risks.

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2.prevent inflammation after therapy
Corticosteroids

• A temporary increase in pericystic inflammation
  often is observed.
• it is often recommended
• be administered in combination with
  anthelmintic
• This practice is controversial
• should be tailored to the individual
  patient
• according to the number and location of
  cysticerci

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prevent inflammation after therapy

• 20 Manitol bid
• Dexamethasone0.75mg bid
• 1wk before till 1wk after the anti parasitic
  treatment course finished.
• 1w 10days 1w

Manitol and DXM
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3.Symptomatic therapy
Anticonvulsants

• Anticonvulsant therapy should proceed as in other
  epileptiform states
• Benzodiazepines first-line agents for active
  prolonged or repeated seizures.
• followed by a more definitive anticonvulsant such
  as phenytoin (Dilantin) .
• Barbiturates needed in more refractory cases.

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Surgical intervention first then
anthelmintic therapy

• Neurosurgical intervention
• in cases of obstructive hydrocephalus,
• ventricular cysticerci
• Ophthalmologic surgery
• in all cases of ocular cysticercosis
• --the inflammatory reaction associated with
  medical therapy may threaten vision.

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How can we prevent cysticercosis ?

• Control the sources of infection
• Control transmission ways
• Educate the populations
• Avoid eating raw or undercooked pork
• Wash hands after using the toilet and before
  handling food
• Wash and peel all raw vegetables and fruits
  before eating

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In conclusions

• 1. Cysticerci appear as multiple cyst
• 2. Presentations Commonly asymptomatic
• repeat seizures with different style
• multiple nodules in soft tissues
• are the most common seen
• 3. CT and MRI are the main diagnostic methods
• 4. Treatment with Albendazole and praziquantol

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thanks you!