III - infection Flashcards by ahmad elmowag

what are microbial strategies used by pathogens for attachment

bind firmly to epithelial surface
produces IgA protease
inactivate IgA

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what are host defence for attachment of pathogens

microbes rinsed away by host secretions
produce secretory immunoglobulin (IgA)

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what is the host defence to pathogen invasion

host cell membrane poses barrier to intracellular microbe

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what is the microbial strategy for invasion

traverse host cell membrane; endure or trigger uptake by phagocyte and resist killing

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what is the microbial strategy for invasion to bypass host cell defences

fusion protein in viral envelope; inject proteins that trigger uptake and/or block intracellular killing

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what are microbial strategies for intracellular survival

block phagocyte chemotaxis
kills phagocyte before/after phagocytosis
inhibits phagocytosis and lysosome function
resist killing and multiply in the phagocyte

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what is the host defence to intracellular survival

restriction of Fe(III)

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what are microbial strategies for intracellular survival in response to iron restriction

scavenge iron in competition with the host

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how do microbes survive intracellularly in response to iron restriction

secrete siderophores - bind Fe(III) with extremely high affinity
imported into the cytosol where the captured iron is released

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what is the host defence to microbial extracellular survival

production of complements and antimicrobial peptides

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what are the microbial strategies for extracellular survival

alter their cell surfaces, inactivate complement; or bind complement non-productively

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what is the microbial mechanism for intracellular survival

release leucocidins, antiphagocytic haemolysins etc.
cell wall or capsule components to inhibit phagocytosis
inhibits 1 or 2 components needed for fusion of phagosome with lysosome
escape from phagosome into cytosol

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what is the host defensive response to molecular release of siderophores

production of reactive oxygen and nitrogen species

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what are the microbial strategies in response to host production of reactive O/N

avoids oxidative burst
removes reactive O and N species

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what are the mechanisms microbes employ to avoid oxidative burst and removal of reactive N/O species

divert vesicles bearing NADPH oxidase so they don’t fuse with the phagosome
production of enzymes (catalase, superoxidase dismutase) to inactivate reactive N/O

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what are the microbial mechanisms for extracellular survival, to go into ‘stealth mode’

sialyation of cell membrane or alteration in LPS structure
production of protease

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function of C3b receptor

microbial receptor that competes with that on a phagocyte
hinders production of membrane attack complex
aids in microbial extracellular survival

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what is another host defence to microbial extracellular survival

production of antimicrobial antibodies

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what are the microbial extracellular survival strategies in response to host production of antimicrobial antibodies

destroy antibodies
prevent induction of protective antibodies
express Fc receptors
prevent antibody binding - prevent immune recognition

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what are the microbial mechanisms for extracellular survival in response to antimicrobial antibodies

secretion of IgA protease
infection of lymphoid cells
bind antibody so that it is 180 degrees from normal
produce long LPS chain to keep antibodies/complements at ‘arms length’
acquire coating of host molecules - fibronectin

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what is a 3rd host defence to extracellular microbial survival

antimicrobial cell-mediated response

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what are the microbial strategies for extracellular survival in response to host antimicrobial cell-mediated response

invasion of T cells to inactivate or kill
switch on T/B cells non-productively

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what are the microbial mechanisms that allow invasion of T/B cells for extracellular survival

virus envelope component binds CD4 on T helper cell
polyclonal activation of B cells
polyclonal activation of T cells by release of T cell mitogens

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what is the host defence IV to prevent extracellular microbial survival

antimicrobial immune response

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what are microbial strategies for extracellular survival in response to host antimicrobial immune response

infects areas that are relatively inaccessible to antibodies/immune cells supress immune response vary microbial antigens

what are the host defences to prevent microbial shedding

apart from innate and acquired immunity, there is none

what are microbial strategies for shedding

stimulate host processes that increase chance of transmission via key routes: respiratory, faecal-oral or venereal blood via arthropods, needles, milk or saliva

effect of Vibrio cholerae

Diarrhoeal disease massive loss of water from intestinal epithelial cells

what does cholera toxin bind to and what happens

enterocyte GM1 receptors it is endocytosed

what occurs to endocytosed cholera toxin

is trafficked to the ER cholera A1 toxin is then released into the cytosol

function of cytosolic cholera toxin A1

diffuses towards the adenylate cyclase catalyses ADP ribosylation of the Gs alpha subunit using NAD

Gs alpha has intrinsic what, and what does ribosylation do to it

intrinsic GTPase activity ribosylation inhibits catalytic activity of hydrolysing GTP

what is the overall effect of ribosylation of Gs alpha subunit

increase in GTP increased adenylate cyclase activity increase in cAMP production

what e-coli cause noninflammatory diarrhoea

ETEC - enterotoxigenic E.coli EPEC - enteropathogenic E.coli

what E.coli cause inflammation

EIEC - enteroinvasive E.coli EAggEC - enteroaggregative E.coli EHEC - enterohaemorrhagic E.coli

what does ETEC do

attach to small intestinal mucosal elaborate one/both heat labile/stable toxins

what does EPEC do

attaches firmly to intestinal mucosa causes dissolution of brush border done by vesiculation of microvili

what does EIEC do

attach to colonic enterocytes penetrate via endocytic mechanism and replicate therein causes necrosis and large stripping of colonic mucosa and a dysentery

what does EAggEC do

damage and blunt colonic villi done by haemorrhagic necrosis

what does EHEC cause

diarrhoea haemorrhagic colitis haemolytic uraemic syndrome

what does EHEC destroy and what does it cause

RBC - haemolytic anaemia platelets - thrombocytopenia

what is the most common cause of acute renal failure in children

EHEC enterohaemorrhagic E.coli

what is the major toxin that EHEC produces

shiga-like toxins

what does EHEC adhere to

enterocytes in large intestine removes microvilli (efface)

what characteristic structural changes does EHEC cause onto a host cell

attaching-effacing lesions

how are pathogenicity islands acquired

via horizontal transfer from other bacteria

what is the major pathogenicity island in EHEC termed

locus of enterocyte effacement (LEE)

function of LEE

encodes proteins that form a specialised secretion system that injects EHEC into proteins into host cell as well as some of the injected proteins

what is EspA

filament extension in EHEC/EPEC

function of EspA

essential for host cell adherence transport of translocon and downstream effectors through the EspA filament to reach the host cell

structure of shiga-like toxins 1/2 (SLT)

have an enzymatic A subunit 5 identical B subunits

function of A subunits in SLT

inhibit protein synthesis cell is unable to recover

how specifically does the A subunit in SLT achieve its function

A subunit is a N-glycosidase depurinates adenosine 4324 in 28s rRNA

what do the B subunits in SLT bind to and where are they located

ceramide host cell receptors renal epithelial tissue CNS vascular endothelium

what are the stx1 and stx2 genes carried by

bacteriophage lysogens in EHEC cells

where does Stx production occur

in the intestine

how does bacteria cross the intestinal barrier

via M cells on Peyers patches in ileum cells in small intestine they are long polar fimbriae adhesins

where do bacteria enter, survive and produce Stx

lamina propria

what can helicobacter pylori be a causative agent for

peptic ulcers gastric cancer

what can helicobacter pylori protect against

protects against oesophageal cancer present in over 50% of the population

what is gram +/- bacteria based on and what are the differences

properties of their cell wall gram - - peptidoglycan surrounded by LPS gram + - no LPS layer, only thick layer of peptidoglycan

outline the steps required to stain both gram+/- bacteria in a culture

fixation crystal violet iodine treatment decolourisation counterstain

what is the function of crystal violet in staining

detects thick peptidoglycan and becomes trapped in the presence of iodine

function of ethanol in staining bacteria

stabilises/dehydrates crystal violet in gram + washes crystal violet and iodine out of gram -

name a counterstain

safranin

what is phytophora infestans

major fungal pathogen with broad host specificity (responsible for irish potato famine)