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bacterial pathogenesis (how does the pathogen can cause disease in human -…
bacterial pathogenesis (how does the pathogen can cause disease in human
evasion and survival
modulation on the pathogen surface
Neissera menegitidis factor H binding protein
it will bind to factor H and inhibit the activation of the complement system(C3b)
streptococcus pyogens M protein
that mimics the cardiac myosin
the immune system
no recognition and no antibody
recognize it get confused and secrete antibodies against everything
autoimmune(rheumatic fever)
acute pharyngeal infection
release toxins that cause apoptosis
inhibition of phagocytosis
staphylococcus aureus protein A
can bind to the Fc of antibody and decreases phagocytosis
SpA bind to Fab of the B cell receptor and lead to apoptosis
adherence and attachment
it have many adherence factors
capsule
fimbriae
adhesin
teichoic and lipoteichoic acid
pilli
lipopolysaccaride
virulence factors
dose
infective
the amount of bacteria that is needed to
infect
50% of the animal
lethal
the amount of bacteria that is needed to
kill
50% of the animal
the infectious doses are different among bacteria
adhesion pili
klebsiella
invasion and biofilm formation
iron binding proteins
proteins that are secreted by pathogens to have high affinity for iron
siderophores
siderophore bind to ferric
lactoferrin
lactoferrin bind with ferric
heme binding proteins (homophore)
homophobe bind to Hg and come to bacteria
soluble Fe+2
by itself
lipopolysaccaride
in the surface helps to adhere to the host cells and colonization in H.pylori
virulent enzymes
excreted by bacteria extracellularly
nucleases
DNAse by the Staphylococcus and streptococcus to degrade the extracellular DNA that trap the bacteria
phospholipases
like clostridium perfringens and bacillus anthraces they can produce phospholipase that degrade phospholipid of the membrane and also helps in phagosomes
glycohydrolases
hylalurondiase S in s.aureus that can degrade the hylouronic acid that cement the cells
proteases
like collagensase that can degrade collagen in the connective tissue
coagulates and kinases
coagulase
form a clot surrounding the bacterium to prevent it from phagocytosis
kinase
digest the clot and spread the bacteria
streptokinase and staphylokinase
outer capsule
have hyaluronic acid
help in adherence
resist phagocytosis
toxins
exotoxins
usually the structure is of 2 parts A: effector B: receptor
majority is gram positive and some gram negative
they are specific on their action
heat labile(they can be altered by the temperature)
very small concentrations are lethal
diaphteria,tetanus and botulism
examples
A-B toxins
diaphteria
A-B
block protein synthesis
kill the cells
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cholera
A-5B
increase cAMP in intestine
movement of fluid into the lumen
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anthrax
2A-B
increase the expression of pro inflammatory mediators
swelling of the neck or neck glands
type 3 cytotoxins
they are toxins found in surface of bacteria that act like a syringe to inject the host cell
membrane damaging toxins
hemolysins and leuckocydens
lyse blood cells
form pores in membrane or disrupt the cell membrane
pore forming toxins
insert into the membrane and allow water to enter
the pore forming toxins will bind to the membrane receptors and form a pore
hetereogenous
streptomycin O
by group A streptococcus
lipases
lyse cells, eliminate defenses and provides nutrients for bacteria
exfoliative toxins(S.aureus)
hydrolyze the desmosomes
like s.aureus
hydrolyze the desomosmes that is in the epidermis
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extracellular matrix
collagenase
streptokinase
hyalurondiase
neurotoxins
clostridium tetani
prevent the relaxation of muscles
spastic paralysis
by preventing release of GABA
clostridium botilinum
prevent the contraction of muscles
flaccid paralysis
by blocking the release of ACH
enterotoxins
cause inflammation of GIT and fluid into the lumen and diarhea
clostridium difficile
vibrio cholera
superantigens
they are exotoxins that can trigger an excessive, non specific stimulation of immune cells to secrete cytokines
streptococcus pyogens
endotoxins
flagella
help in the motility of the bacteria
staphylococcus aureus
entry portal
skin
clostridium tetani
respiratory
mycobacterium tuberclosis
genital
neisseria gonorrhoeae
GIT
salmonella
it is specific