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Lect 27: Host Pathogen Interactions - Coggle Diagram
Lect 27: Host Pathogen Interactions
Pathogen Colonization
Getting into the body
Penetrate skin
diff, unless cuts/bites
Penetrate mucous mem
epithelial cell ruffling
uptake by M cells
microfold cells
function
sample bac/antigens in gut to macrophages/dendritic cells underneath M cell
like scout in army
transcytosis
tissue under M cell called MALT
Mucosal Associated Lymphoid Tissue
Direct phagocytosis by macphages
extend dendritic cell to uptake from lumen
3 routes for infection
extracellular
goal
avoid host detection
pathogen stay in blood or tissue
:red_cross: in host cells
Avoid Phagocytosis
C5a peptidase
prevent PMN recruitment
leukocidin
kill phagocyte
capsules
block PAMP so phagocyte TLR doesn't find them
Fc receptor
bind Fc part of Ig
present "self" antigen to body
Avoid Complement
C3b
bind to bac surface to activate alternate complement pathway
recruits other proteins to form convertase to kill bac
MAC
Neutrophil
Inflammation
Avoided using a receptor to bind factor H
Patho "steal" host factor H by making a fake on
Avoid Ab
protease
antigenic variation
Pilus Cassette switching
change pilli to avoid being recog by Ab
Sialic acid capsule
mimic self antigen
Intracellular in circulating cells
macrophages
pathogen want to be seen by host
must be able tos urvive in macrophage
can use macrophage mvmt to spread in host
methods
break out of phagosome and live in cytoplasm
prevent pagosome/ lysosome fusion
Live in phagolysosome and don't get digested
must get in macrophage before it is activated
engulfed quickly
Intracellular in non-circulating cells
epithelial cells
infection localized
spread epithelial cell to cell
Host rely on Tc/NK cells to kill infected epi cells
Pathogen Goal is to avoid them
Methods
pilli with adhesin bind to host receptors
specific binding
receptors normal for other purpose
fimbriae
How get in epi cells
effectors enhance pathogen binding and uptake
membrane ruffling
rearrange host cells cytoskeleton
Type 3 secretion system
How spread
polymerizing host actin cytoskeletal protein
actin "rockets"
Pathogen Evolution
Types
Primary
cause disease in normal host
have virulence factors
Opportunistic
normal flora
cause disease in immunocompromised
Subclinical
too few
below infectious dose
no virulent
Clinical
cause
signs
apparent upon examination
symptoms
effects only patients notices
Localized
immediate area of infection
disseminated/systemic
affect other locations too/ whole body
Common blood related
Does a virulent want to cause sympotms?
NO
balanced pathogenicity
pathogen want to remain in body
until can replicate and spread to new host
Courses of Infection
smaller reservoir hidden from immune system
How do we know organism cause disease?
Koch Postulates
Are all infectious diseases caused by organisms?
:red_cross:
Infection
more organisms = more signs and symptoms
killing org cures disease
antimicorbials
Intoxication
toxin produced by org cause disease
org X need to be present
as long as toxic get into body
food poisoning
Ab no effect on disease
Treat with anti-toxin
Immunogenic
mediated by cytokine release
Imm Sys response kill bac
Also cause tissue damage
inflammation
Does presence of microbe always indicate disease
:red_cross:
Native Flora
Imp part of immune system
esp gut microbiome
Hygiene Hypothesis
decr native flora
decr T reg
incr in autoimmune diseases
What makes something a pathogen vs oppurtunist?
Virulence Factors
prod by pathogenic strains
enhance invasion/colonization of host
AKA IC factors
genes for v.f. passed b/w bac cells as ...
pathogenicity island (PAI)
ex of horizontal gene transfer
advantage?
Higher change to be all transfered rather than having each v.f. separate
