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&

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A parasite may live in or on thetissues of its host w/o causingevident harm.

However, in a mayority of cases, the

PATHOGENESIS

damage.

The lesion may be localized at the sitewhere the parasite has becomeestablished, or it may extend to distantparts of the hosts body.

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Thepathogenic

nutrition robbing

lytic necrosis

effects ofparasite toxin production

interaction of the hostimmune/

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, , , .

: ( : ) ( : , ) ( : ) ( : )

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, / .

.

.

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/

. . :

/ / ,

& ( : ,)

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. /

, & .

& & .

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/

.. . :

. ,

& .

, , &

.

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.

, .

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.

/ .

.

.11/18/2010 11DEWI M D

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11/18/2010 12

.

.

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& .

.

,

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Acquired Immunity to Parasite

An acquired immune response is stimulated bya spesific foreign substance called an Ag &circularly an Ag is any substance that willstimulate an immune response.

Different protozoa & helminths vary greatly in

t e r structura oc em ca propert es, ecycles & pathogenic mechanisms acquiredimmune responses.

The principal defense mechanism againstprotozoa that survive within macrophagee isCMI, particularly macrophage activation byTH1 cell-derived cytokines.

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/

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Worm infections elicit Th2 protective immune responses.Protozoan infections elicit Th1 protective immune responses.

Parasiteantigen

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/

.

.

,

. .

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Mediated by Ag-specific T

cells; cell-mediatedimmunity (CMI)

Th1 driven; cytokines

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IFN- , TNF, IL-12Effectors: activatedmacrophages andmonocytes, (some cytotoxicCD8+ T cells)

Granulomas, tuberculin-type reactions (Filariasis)

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/

Malaria Blackwater Feverhemolysis of erythrocytes

Malaria excess anemia; bothinfected and uninfectederythrocytes opsonized andphagocytosed

Chagas disease :cardiomyopathy, megacolon,megaesophagus

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,

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IgE and Eosinophils

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Destruction of Large Parasites by ADCC

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. .

.

.

.

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. :

,

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( ,

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