PARASITE INFECTION IN

CENTRAL NERVOUS SYSTEM

PARASITOLOGY DEPARTMENT
MEDICAL FACULTY OF USU
CESTODE
INFECTION
NEUROSISTISERKOSIS
FREE LIVING
AMOEBA
GRANULOMATOUS AMEBIC ENCEPHALITIS (GAE)
PRIMARY AMEBIC MENINGOENCEPHALITIS (PAM)
AMOEBA
INFECTION
SPOROZOA
INFECTION
CEREBRAL TOXOPLASMOSIS
CEREBRAL MALARIA
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NEUROCYCTICERCOSIS
GENERAL
Caused by infestation Taenia Solium Larvae
There is no pathognomonic clinical feature or a
typical Neurocysticercosis syndrome (Takayanagui
OM et al., Parasitol Int. 55) OM et al., Parasitol Int. 55)
The life cycle of this parasite have been known in
19 century and the clinical manifestation was
identified in mid-20 century
The development of diagnostic resulted in the
increasing reported cases of neusrocycticercosis
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NEUROCYCTICERCOSIS
EPIDEMIOLOGY
World wide distribution
with high prevalent ,
such as: Mexico, North
America and South,
India, Africa and China. India, Africa and China.
In Indonesia, Bali and
Papua have many
cases reported.
Human is the definitive
host
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NEUROCYCTICERCOSIS
PATHOGENESE
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NEUROCYCTICERCOSIS
PATHOGENESE
Route of infection from
Taenia solium:
Raw meat consumption
(contamination by
T.soliumlarvae)
Auto infection: Auto infection:
regurgitation and the eggs
swallowed
Fecal-oral route ingested
ova from a tape worm
carriers
Larvae (cysticercus cellulosa)
in brain can be developed
from eggs.
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NEUROCYCTICERCOSIS
PATHOGENESE
Neurologic symptoms arise when the cysticersus
cellulose dies and the human mounts an associated
inflammatory response.
Cyst produces enzyme Paramiosin, taniestatin Cyst produces enzyme Paramiosin, taniestatin
(inhibitor protease serin) that binding C1q and
blocking its classic pathway or alternative.
Cyst wall is covered by Polysaccharide sulfa
activating complement to avoid the parasite,
interfering with leukocyte chemo taxis and block
the cytokine production.
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Neurocysticercosis
Diagnosis
Major Criteria:
CT-scan; cysticercus 0.5 2 cm
Specific antibody anti cysticercal (Enzyme linked
immuno transfer blot/ EITB): (+)
Minor Criteria:
Clinical symptom: seizure, Intracranial Pressure increase
Intra cerebral Calsification pungtata
Subcutaneous nodule
Diagnose: 2 major criteria or 1 major & 2 minor
criteria
Neurocysticercosis
Prevention
Personal hygiene and environment
No consumption half cooked meat
Community Education
Pig Vaccination Pig Vaccination
Free Living Amoeba Infection
Primary Amebic Meningoencephalitis (PAM)
Is caused by Naegleria fowleri
Thermophilic, tolerating temp
40-45C.
Sources for Naegleria:
Soil
Sewage sludge
Nasal & throat swabs
Water: tap water, lakes,
stream, ponds, swimming
pools, thermal spring.
Free Living Amoeba Infection
Primary Amebic Meningoencephalitis (PAM)
Transmission
on of contaminated dust is possible
Nasal instillation
Organism enters hosts nasal cavity & infects the Organism enters hosts nasal cavity & infects the
mucous membranes and the paranasal sinuses.
Then the trophozoites penetrate the cribriformplate
and follow the olfactory nerve to the brain where they
multiply & may be isolated from the CSF
Transmission via inhalation
Free Living Amoeba Infection
Primary Amebic Meningoencephalitis (PAM)
Diagnosis
Usually pt dies before diagnosis made
High index of suspicion is vital
Motile trophozoites seen in CSF Motile trophozoites seen in CSF
Large lobopodia, single nucleus which contains a
prominent central karyosome, surrounded by a halo
CSF culture on NNA overlay with E. coli
At autopsy ~ brain biopsy shows trophozoites only &
no cysts
Amoeba does not en-cyst in tissue
Free Living Amoeba Infection
Primary Amebic Meningoencephalitis (PAM)
Treatment and prevention
Most cases fatal
Early & aggrassive tx with IV
and intrathecal Amphotericin and intrathecal Amphotericin
B may possibly cure disease
No easy control of Naegleria
as they are ubiquitous in
nature
Guidelines from the Australian
health commission ~ keep
head above water
Free Living Amoeba Infection
Granulomatous Amebic Encephalitis
Is caused by Acanthamoeba sp.
CNS infection acquired
hematogenously by the
inhalation,aspiration of
trophozoites and cysts, resulting trophozoites and cysts, resulting
in pneumonitis, or through skin
and mucosal ulceration with
direct vascular invasion
This usually happens with the
immunosuppressant patient.
Free Living Amoeba Infection
Granulomatous Amebic Encephalitis
In brain invasion moves from deeper areas to the
surface
Trophozoites and cysts can be found in CNS
lesions lesions
Slow progression of disease (wks to mths)
Clinical picture that of space occupying lesions
Headache, nausea, vomitting related to
formation of granuloma
Later localizing neurological signs such as
hemiparesis, personality changes, confusion
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Cerebral Malaria
General
Is caused by Plasmodium falciparum
Mortality rate is high for malaria cases due to cerebral
malaria (15% adult & 20% children)
Early stage: Schizont in hepar will rupture in day 4after Early stage: Schizont in hepar will rupture in day 4after
infection.
In microscopic examination can be seen only ring and
gametocyte stage.
Trophozoite and schizont will disappear in peripheral
blood (24 hours) and stay in internal organ capillary
Incubation periode : 9-14 days
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Cerebral Malaria
pathogeneses
Complex, at times confusing & conflicting
hypothesis
Lack of satisfactory model hampered
understanding
Several hypothesis
Hemodynamic
Immunologic
Metabolic
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Congestion & pigmentation
Cerebral Malaria
pathogeneses
Hemodynamic change: (cytoadherence)
Infectious erythrocyte binding to normal erythrocyte,
thrombocyte, and capillary endothelial .
This condition will produce rosette form and
coagulation in blood vessels coagulation in blood vessels
Obstruction to microcirculation-tissue anoxia
Modulated by cytokine
Binding place is known knob that consist of Protein
(PfEMP-1 / P.falc. Eryth. Membrane protein)
Brain capillary endothelium and thrombocyte receptor
(ICAM-1) will be increased by TNF- Increased
Nitric oxide (NO) production brain sequel
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Cerebral Malaria
pathogeneses
Immunologic :
Th1 produce pro-inflammation cytokine
activated macrophage and destructed infectious
blood cell
In P.falciparum; Over production of IL-1 and TNF In P.falciparum; Over production of IL-1 and TNF
can increase cytoadherence erythrocyte with parasite
in vascular endothelium NO sequel in
cerebral (neurotransmission barrier)
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Cerebral Malaria
pathogeneses
Metabolic change
Abnormal membrane cell erthrocyte
Parasite Nutrition Parasite Nutrition
Tissue Hypoxia
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Expressed adhesins e.gPfMP-1
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Rosetting
Hakim SL 2002
Sludging
Sequestration
Cerebral Malaria
pathogeneses
Immunological hypothesis
Important in certain severe manifestations
Acute glomerulonephritis
Black water fever: auto-immune disorder Black water fever: auto-immune disorder
Lack of sequestration in some cases: ? vasculitis
due to hyper-allergic reaction
However, no evidence of inflammatory cells
infiltration
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CEREBRAL TOXOPLASMOSIS
Etio : Toxoplasma gondii
Cerebral toxoplasmosis is one of
the most common opportunistic
neurological infections in neurological infections in
AIDS patients.
It is also directly related to the
prevalenceof anti-T. gondii
antibodies in the general
population
PATHOGENESIS
Cerebral toxoplasmosis usually represents
reactivation of chronic infection
Reactivation possibly results from the rupture
of a cyst
Normally the bradyzoites destroyed by the Normally the bradyzoites destroyed by the
hosts immune responses
In immunosuppressed patient rupture of
cyst may result in renewed multiplication
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