82789
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Mindmap von tanitia.dooley, aktualisiert more than 1 year ago
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Erstellt von tanitia.dooley
vor etwa 11 Jahre
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Immunity to parasites
- EUKARYOTIC live either ECTOPARASITES (outside
host)/ENDOPARASITES (inside host),
MICROPARASITES-usually transmitted by insect vectors/
ingestion e.g..Malaria. MACROPARASITES-have complex
life styles with several host species eg. Intestinal worms
- Humoral responses important for EXTRACELLULAR
parasites- can be Ab, Ab+complement, Ab+effector cells
- Humoral responses important for EXTRACELLULAR
parasites- can be Ab, Ab+complement, Ab+effector cells
- Malaria
- Transmitted: female Anopheles mosquitoes
- Sporozoites injected into host circ- find way to
liver-infect liver cells- form
merozoite-replicate-rupture-merozoites released-can
affect another liver cell/ RBC penetration- can
rupture/ asexual reproduction-develop into
gametocytes-uptake during blood meal by mosquito
and find way to salivary glands
- Sporozoites injected into host circ- find way to
liver-infect liver cells- form
merozoite-replicate-rupture-merozoites released-can
affect another liver cell/ RBC penetration- can
rupture/ asexual reproduction-develop into
gametocytes-uptake during blood meal by mosquito
and find way to salivary glands
- Plasmodium Falciparum
- Immunity gradually builds up
(years)-fades in absence of
exposure. Immune response may
fail to control infection=death
(naive individuals eg children who
never been exposed before).
Immunity is strain specific- many
strains circulate in human popn.
- T cell dependent mech- CD8+
responses & macrophage
activation against liver stages/
CD4+ against erythrocyte
stages (TH1&2)/ Ab
dependent- block erythrocyte
invasion- Ab to merozoite-
agglutinate merozoite &
infected cells=killed in spleen
- EVASION STRATEGIES- intracellular for most of mammalian
life cycle/ erythrocytes lack MHC-cant present parasite Ags/
Sporozoites-invade hepatocytes quickly & shed surface coat
if Abs bind during this time/ Merozoites-surface Ags highly
polymorphic-some can undergo temporal antigen
variation/cytoadherance molecules-expressed by infected
erythrocytes enable sequestration in capillary & avoid
passage through spleen-one of main causes of death if stick
to blood capillary in brain
- EVASION STRATEGIES- intracellular for most of mammalian
life cycle/ erythrocytes lack MHC-cant present parasite Ags/
Sporozoites-invade hepatocytes quickly & shed surface coat
if Abs bind during this time/ Merozoites-surface Ags highly
polymorphic-some can undergo temporal antigen
variation/cytoadherance molecules-expressed by infected
erythrocytes enable sequestration in capillary & avoid
passage through spleen-one of main causes of death if stick
to blood capillary in brain
- T cell dependent mech- CD8+
responses & macrophage
activation against liver stages/
CD4+ against erythrocyte
stages (TH1&2)/ Ab
dependent- block erythrocyte
invasion- Ab to merozoite-
agglutinate merozoite &
infected cells=killed in spleen
- Immunity gradually builds up
(years)-fades in absence of
exposure. Immune response may
fail to control infection=death
(naive individuals eg children who
never been exposed before).
Immunity is strain specific- many
strains circulate in human popn.
- Plasmodium vivax
- Transmitted: female Anopheles mosquitoes
- Sleeping sickness/
African trypanosomiasis
- Transmitted: Tsetse fly
- Trypanosoma brucei
- fly=blood meal=injects metacyclic trypomastigotes-transformed to bloodstream
trypomastigotes & carried to other sites-multiply by binary fission in blood, lymph
& spinal fluid (diagnostic stage)-trypomastigotes in blood-Tstes has blood
meal=transform into pro cyclic trypomastigotes in flys midgut-multiply by binary
fission-leave midgut-transform into epimastigoted-multiply in salivary
glans-transform into metacyclic trypomastigotes...
- Immunity: not effective in humans-fatal if not treated. Trypanosomes
are extracellular (tissue spaces, blood, CNS)-infection characterised
by FLUCTUATING PARASITAEMIA (can control it but not
eradicate). Can be killed by Ab mechs-binding of IgM to
surface=agglutination, Ab-mediated phagocytosis, direct lysis via
classical pathway. As infection progresses=spread to CNS-causes
symptoms of sleeping sickness
- EVASION: have single dominant surface Ag (Variant surface
glycoprotein (VSG)) which masks all other surface antigens,
protects aganst lysis via alt complement-each expresses one VSG
from repitore of ~1000 each immunologically distinct-individual
trypanosomes switch expression from one to another at a rate of
1/100 cell divisions= fluctuating parasitaemia. Can be killed by
Ab-mediated mechs but takes time during which new antigenic
variants will appear-not protective
- EVASION: have single dominant surface Ag (Variant surface
glycoprotein (VSG)) which masks all other surface antigens,
protects aganst lysis via alt complement-each expresses one VSG
from repitore of ~1000 each immunologically distinct-individual
trypanosomes switch expression from one to another at a rate of
1/100 cell divisions= fluctuating parasitaemia. Can be killed by
Ab-mediated mechs but takes time during which new antigenic
variants will appear-not protective
- Immunity: not effective in humans-fatal if not treated. Trypanosomes
are extracellular (tissue spaces, blood, CNS)-infection characterised
by FLUCTUATING PARASITAEMIA (can control it but not
eradicate). Can be killed by Ab mechs-binding of IgM to
surface=agglutination, Ab-mediated phagocytosis, direct lysis via
classical pathway. As infection progresses=spread to CNS-causes
symptoms of sleeping sickness
- Transmitted: Tsetse fly
- Chaga's disease
- T. cruzi
- Transmitted:
kissing bugs
- When scratch, metacyclic trypomastigotes from faeces enter body-turn
into amastigotes-find way to muscle/neural tissue-form a amistogote net
(causes the problem)= chronic infections=neurological disorders
(dementia, damage to heart muscle, dilation of digestive tract)
- Immunity: has 2 phases: ACUTE (weeks/months)-trypanosomes in
bloodstream, fatal in ~10% of children-immune response able to supress
parasitaemia but not elimination-cell-mediated & Ab-dependent but killing
mech unclear/ CHRONIC-~30% patients (lasts years with an indeterminate
phase with no symptoms)-infection for life=damage to heart, oesophagus &
colon caused by autoimmunity due to cross-reacting T.cruzi Ags
- Immunity: has 2 phases: ACUTE (weeks/months)-trypanosomes in
bloodstream, fatal in ~10% of children-immune response able to supress
parasitaemia but not elimination-cell-mediated & Ab-dependent but killing
mech unclear/ CHRONIC-~30% patients (lasts years with an indeterminate
phase with no symptoms)-infection for life=damage to heart, oesophagus &
colon caused by autoimmunity due to cross-reacting T.cruzi Ags
- EVASION: complement
resistant-express parasite coded
decay acceleration factor (DAF).
Host cell invasion by induced
phagocytosis by cells that are not
normally phagocytic (muscle,
nerves-limited antimicrobial
capacity). Parasites taken up by
macrophages etc can escape from
phagosome into the host cell
cytoplasm avoiding lysosomal
attack. Expresses antigens which
mimic the host-inhibiting immune
recognition (autoimmunity). Infection
induces production of IL-10 &
TGF-beta=inhibits macrophage
activation=immunosupression
- T. cruzi
- Leishmania major
- Transmitted: Sandfly
- Sandfly takes blood meal-promastigotes
phagocytosed by macrophages-transform
into amastigotes inside-multiply in cells of
various tissues
- IMMUNITY: leads to small lesion in skin @ site (usually increased
to ~1-2cm then resolves-cure in months=scar tissue). Individuals
that cure primary=memory response. Parasites killed by TH1-Ag
presentation & production of IL-12 by dendritic cells stimulate
production of IFN-gamma by CD4+ T cells-IFN-gamma induces NO
synthase & NO production by host macrophages
- EVASION: intracellular adapted to live in phagolysosomal compartment
of host macrophages-survive at low pH & surface glycolipids make them
resistant to lysosomal enzymes. Macrophages cant kill them unless
stimulated by IFN-gamma & TNFalpha-the parasite multiplies during this
'silent stage' while immune response developing. In some cases infection
stimulates early production of IL-4 by TH2=non-protective=decreased
TNFalpha & IFNy=infections last longer/fail to resolve=chronic/multiple
skin lesions
- EVASION: intracellular adapted to live in phagolysosomal compartment
of host macrophages-survive at low pH & surface glycolipids make them
resistant to lysosomal enzymes. Macrophages cant kill them unless
stimulated by IFN-gamma & TNFalpha-the parasite multiplies during this
'silent stage' while immune response developing. In some cases infection
stimulates early production of IL-4 by TH2=non-protective=decreased
TNFalpha & IFNy=infections last longer/fail to resolve=chronic/multiple
skin lesions
- IMMUNITY: leads to small lesion in skin @ site (usually increased
to ~1-2cm then resolves-cure in months=scar tissue). Individuals
that cure primary=memory response. Parasites killed by TH1-Ag
presentation & production of IL-12 by dendritic cells stimulate
production of IFN-gamma by CD4+ T cells-IFN-gamma induces NO
synthase & NO production by host macrophages
- Transmitted: Sandfly
- Schistosomiasis (Bilharzia)
- Snails- worms live inside
body secreting eggs- caused
by trematodes from genus: 4
main species (S. mansion)
- IMMUNITY: takes years, TH2 response-production of Abs to
secretions/excretions of worms & eggs released. Eventually when
protective can act against infection by subsequent larvae-killed by
ADCC via IgE/eosinophils and IgG/macrophages disrupting the
tegument & killing worms. Response to eggs-elicit granulomas &
damage/gross changes to liver-main cause of morbidity/mortality
- EVASION: larvae in skin shed their surface coat shortly after penetration & absorb host Ags (A & B blood
groups, Ig, complement, MHC)=disguise the worm from detection. Immune responses that kill larvae not
affective against disguised adult worm-concomitant immunity. Release of soluble Ags & formation of
immune complexes=reduces Ab binding to worm surface & causes blockade of cytotoxic cells
- EVASION: larvae in skin shed their surface coat shortly after penetration & absorb host Ags (A & B blood
groups, Ig, complement, MHC)=disguise the worm from detection. Immune responses that kill larvae not
affective against disguised adult worm-concomitant immunity. Release of soluble Ags & formation of
immune complexes=reduces Ab binding to worm surface & causes blockade of cytotoxic cells
- Snails- worms live inside
body secreting eggs- caused
by trematodes from genus: 4
main species (S. mansion)
- Lymphatic filariasis
- TRANSMITTED:
mosquito bite
- Wucheria bancrofti
- Wucheria bancrofti
- Variable clinical symptoms-some no signs,
high no.s of microfilariae but little disease/few
microfilariae but severe pathology. Microfilaria
killing via ADCC by eosinophils, macrophages,
neutrophils, IgE most important Ab. Requires
TH1 & TH2. Obstruction of lymphatics by adult
worms causes gross pathology
- EVASION: nematode worm has thick cuticle-difficult to
kill. Worms produce antioxidant enzymes & protease
inhibitors to neutralise cytotoxic killing mechs. Individual
microfilaria show reduced TH1 responsiveness caused
by lack of Ag specific cells & increased TGF-b & IL-10,
also have reduced B cell responses. Worms express
homologues of TGFb & Macrophage inhibitory factor
(MIF) which may interfere with host immune response
- EVASION: nematode worm has thick cuticle-difficult to
kill. Worms produce antioxidant enzymes & protease
inhibitors to neutralise cytotoxic killing mechs. Individual
microfilaria show reduced TH1 responsiveness caused
by lack of Ag specific cells & increased TGF-b & IL-10,
also have reduced B cell responses. Worms express
homologues of TGFb & Macrophage inhibitory factor
(MIF) which may interfere with host immune response
- TRANSMITTED:
mosquito bite
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