parasite infection in central nervous system rev

7/28/2019 Parasite Infection in Central Nervous System Rev.

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PARASITE INFECTION INCENTRAL NERVOUS SYSTEM

PARASITOLOGY DEPARTMENTMEDICAL FACULTY OF USU


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1/26/2009DEWI M.DARLAN 3

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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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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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


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

-

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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parasite infection in central nervous system rev

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