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PARASITE INFECTION INCENTRAL NERVOUS SYSTEM
PARASITOLOGY DEPARTMENTMEDICAL FACULTY OF USU
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NEUROCYSTICERCOSIS
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NEUROCYSTICERCOSISGeneral
Caused by the infestation ofTaenia solium
larvae There is no pathognomonic clinical feature or a
typical neurocysticercosis syndrome
a ayanagu e a ., The life cycle of this parasite has been known
in 19th century and the clinical manifestationwas identified in mid 20th century.
The development of diagnostic resulted in theincreasing reported cases ofneusrocycticercosis.
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NEUROCYCTICERCOSISEpidemiology
World wide distribution
with high prevalence ,such as: Mexico, NorthAmerica and South,
n a, r ca an na. In Indonesia, Bali and
Papua have many
cases reported. Human is the definitive
host
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NEUROCYCTICERCOSISLife Cycle
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NEUROCYCTICERCOSISPathogeneses
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NEUROCYCTICERCOSISPathogenesis
Route of :
Raw meat consumption(contamination by Tsolium larvae)
Auto infection:
regurgitation answallowing the eggs
Fecal-oral route ovaingestion from thetapeworm carriers
Larvae (cysticercuscellulose) in brain can bedeveloped from eggs.
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NEUROCYCTICERCOSISPathogenesis
Neurologic symptom arises when the cysticercus
cellulose dies and the host (human) mounts an
associated inflammatory response.
(inhibitor protease serin) enzymes that bind C1qand blocking its classic pathway or alternative.
Cyst wall is covered by polysaccharide sulfaactivating complement to avoid the parasite
interfering .
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FREE LIVING AMOEBA
INFECTION
Primary Amoebic Meningoencephalitis (PAM)
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Primary Amebic Meningoencephalitis
General
Etiology: Naegleria fowleri
Thermophilic, toleratingtemp 40-45C.
Sources:
Soil
Sewage sludge
Nasal & throat swabs
Water: tap water, lakes,stream, ponds,swimming pool, thermalspring.
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Primary Amebic Meningoencephalitis
Transmission
Transmission via inhalation
Contaminated dust
Nasal instillation
mucous membranes and the paranasal sinuses.
Then the trophozoites penetrate the cribriformplate and follow the olfactory nerve to the brain
where they multiply and may be isolated from theCSF
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Primary Amebic Meningoencephalitis
Diagnosis
Usually patient dies before diagnosis is made
High index of suspicion is vital
Motile trophozoites seen in CSF
Lar e lobo odia sin le 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 and
no cysts Amoeba does not encyst in tissue
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FREE LIVING AMOEBA
INFECTION
Granulomatous Amoebic Encephalitis (GAE)
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Granulomatous Amoebic Encephalitis
General
Etiology: Acanthamoeba sp.
CNS infection is acquiredhematogenously byinhalation, aspiration of
trop ozoites an cysts,resulting in pneumonitis, orthrough skin and mucosalulceration with direct
vascular invasion. This usually happens in
immunosuppressant
patient.
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Granulomatous Amoebic Encephalitis
Pathogenesis
In brain invasion moves from deeper areas to the
surface Trophozoites and cysts can be found in CNS
lessions
Slow progression of disease (weeks to months) Clinical picture is that of space occupying lesions
Headache, nausea, vomiting related to
formation of granuloma Later localizing neurological signs such as
hemiparesis, personality changes, confusion
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CEREBRAL MALARIA
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Cerebral MalariaGeneral
Etiology: Plasmodium falciparum.
Mortality rate is high for malaria cases due to cerebralmalaria (15% adult & 20% children).
Earl sta e: schizont in liver will ru ture in da s after
infection. Microscopic examination: only ring and gametocyte
stages.
Trophozoite and schizont will disappear in peripheralblood (24 hours) and stay in internal organ capillary.
Incubation periode : 9-14 days.
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Cerebral MalariaPathogenesis
Complex, at times confusing & conflicting
hypothesis Lack of satisfactory model hampered
understanding
Several hypothesis: Sludging
Permeability
Mechanical Immunological
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Congestion & pigmentation
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Cerebral MalariaPathogeneses
Sludging hypothesis
Parasitised cells in cerebral capillaries
Large late trophozoites & schizont (rosetting)
Permeability hypothesis
Cerebral edema is common at autopsy
Cytokines: increase permeability of capillaries
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Cerebral MalariaPathogenesis
Mechanical: cyto-adherence
Popular hypothesis with lots of molecular
biology inputs
Intimate apposition of endothelial cells andinfected RBC
Receptor-ligands interaction
Modulated by cytokines
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Expressed adhesins e.g. PfMP-1
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Cerebral MalariaPathogeneses
Immunological hypothesis Important in certain severe manifestations
Acute glomerulonephritis
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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
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Cerebral ToxoplasmosisGeneral Etiology : Toxoplasma gondii
Cerebral toxoplasmosis isone of the most commono ortunistic neurolo ical
infections in AIDS patients. It is also directly related to
the prevalence of anti-T
gondiiantibodies in thegeneral population
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Cerebral ToxoplasmosisPathogenesis
Cerebral toxoplasmosis usually represents
reactivation of chronic infection.
Reactivation possibly results from the rupture
o a cyst. Normally the bradyzoites destroyed by the
hosts immune responses.
In immunosuppressive patient, rupture ofcyst may result in renewed multiplication.
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THANK YOU
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