III - infection Flashcards
what are microbial strategies used by pathogens for attachment
bind firmly to epithelial surface
produces IgA protease
inactivate IgA
what are host defence for attachment of pathogens
microbes rinsed away by host secretions
produce secretory immunoglobulin (IgA)
what is the host defence to pathogen invasion
host cell membrane poses barrier to intracellular microbe
what is the microbial strategy for invasion
traverse host cell membrane; endure or trigger uptake by phagocyte and resist killing
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
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
what is the host defence to intracellular survival
restriction of Fe(III)
what are microbial strategies for intracellular survival in response to iron restriction
scavenge iron in competition with the host
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
what is the host defence to microbial extracellular survival
production of complements and antimicrobial peptides
what are the microbial strategies for extracellular survival
alter their cell surfaces, inactivate complement; or bind complement non-productively
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
what is the host defensive response to molecular release of siderophores
production of reactive oxygen and nitrogen species
what are the microbial strategies in response to host production of reactive O/N
avoids oxidative burst
removes reactive O and N species
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
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
function of C3b receptor
microbial receptor that competes with that on a phagocyte
hinders production of membrane attack complex
aids in microbial extracellular survival
what is another host defence to microbial extracellular survival
production of antimicrobial antibodies
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
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
what is a 3rd host defence to extracellular microbial survival
antimicrobial cell-mediated response
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
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
what is the host defence IV to prevent extracellular microbial survival
antimicrobial immune response
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)