Transcript Document

cysticercosis
Zhao zhixin
[email protected]
The 3rd affiliated hospital of
Sun Yat-Sen University
Key points

Pathogenesis and its relationship to
clinical presentations

Clinical presentations

Diagnosis(imaging studies and biopsy)

Treatment (Anti parasitic therapy and
Symptomatic therapy)
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
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.
cysticercus

Surrounded by fibrous capsule

Containing an invaginated scolex

Bladder-like, fluid –filled cyst

Multiple,0.5-2cm in size
Pathogenesis
and EPIDEMIOLOGY
Life cycle of t.solium
 Where is the disease found?


Contagion summary

How NCC develop
cysticerci
cosis
Oncospheres
Intestine
Cysticer-
Raw or undercook
pork
Ingested by pig and
human
Egg or gravid proglottides
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 fecesallows the cycle to continue.

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
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
Contagion summary(3):
autoinfection:
 A person who has Taeniasis can reinfect
himself.

internal autoinfection
External autoinfection
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
80%cns parenchyma
seizures
numberous parenchyma cysticerki
diffuse cerebral edema encephalitits
10-20% extraparenchymal:
ventricles
hydracephalus
encased in a granuloma
resolves
scarring and calcification.
CLINICAL
MANIFESTATIONS
 symptoms
can be different
depending on
where infection with cysticerci occurs
how many the cysts are there
 Most

cases are asymptomatic.
Incubation: months~5ys
CLINICAL forms

Subcutaneous and Muscular
involvement

NCC

Cardiac involvement

Ophthalmic involvement
Subcutaneous and Muscular
involvement:
2/3 of patients have nodules.
 Number of nodules:1-1000
 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).

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
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
NCC
(1)Cerebral cysticercosis
(2)Ventricular cysticercosis
(3)Subarachnoid cysticercosis
(4) mixed form: not common
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
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.
NCC:
(3)Subarachnoid cysticercosis

10% of brain cysticercosis

¾ have increased ICP.
Chronic ,intermittent meningitis.

CSF test: inflammation change
Focal neurologic deficits

are unusual

If positive:
suggest alternative diagnoses
tuberculoma
tumor
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
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.
Complete blood count (CBC):

Peripheral eosinophilia usually is not
present

but eosinophils may be 10-15% of white
blood cells (WBCs).
Serology-the most useful of lab tests.
o
o
o
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%)
Antibody test on CSF

performed on CSF:
Sensitivity may be increased

it is only accurate when performed in
patients with active meningeal disease.
Stool for ova and parasites
o
o
o
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.
Imaging Studies(1)
Soft tissue x-ray
show calcifications of inactive cysts.
 These may appear as oblong-shaped
lesions.

Imaging Studies(2)
CT scan
o
recommended as the first-obtained
imaging study.
o
more widely available, less expensive,
and has a faster imaging time than MRI.
o
Obtain contrast and noncontrast studies.
Imaging Studies(2)
CT scan
o
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
o
Contrast study may depict
nonenhancing cystic lesions
ring enhancement signifying inflammation
Imaging Studies(3)
MRI of brain
o
o
o
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.
One Patient’s 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.
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
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.
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

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
(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
(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
treatment

Emergency Department Care

Further Inpatient Care
1.Antiparasitic treatment
2.control therapy response
3.Symptomatic therapy
4.surgery therapy
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
1.Antiparasitic treatment
medications

Anti parasitic therapy can only be
done in the hospital

Common used medicines
Albendazole
Praziquantel
-- Broad-spectrum anthelmintic
Albendazole

Adult Dose
18-20 mg/kg/d , bid/tid, for 10days

Pregnancy C - Safety for use during
pregnancy has not been established.
Praziquantel

Adult Dose
20 mg/kg/d , tid , for 10days

Pregnancy B - Usually safe but
benefits must outweigh the risks.
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
prevent inflammation after therapy
20% Manitol: bid
Dexamethasone:0.75mg bid
 1wk before till 1wk after the anti
parasitic treatment course finished.
1w
10days
1w

Manitol and DXM
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.
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.

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
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