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Biomed 2 - Season finale > III - infection > Flashcards

III - infection Flashcards

1
Q

what are microbial strategies used by pathogens for attachment

A

bind firmly to epithelial surface
produces IgA protease
inactivate IgA

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2
Q

what are host defence for attachment of pathogens

A

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

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3
Q

what is the host defence to pathogen invasion

A

host cell membrane poses barrier to intracellular microbe

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4
Q

what is the microbial strategy for invasion

A

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

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5
Q

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

A

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

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6
Q

what are microbial strategies for intracellular survival

A

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

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7
Q

what is the host defence to intracellular survival

A

restriction of Fe(III)

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8
Q

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

A

scavenge iron in competition with the host

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9
Q

how do microbes survive intracellularly in response to iron restriction

A

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

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10
Q

what is the host defence to microbial extracellular survival

A

production of complements and antimicrobial peptides

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11
Q

what are the microbial strategies for extracellular survival

A

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

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12
Q

what is the microbial mechanism for intracellular survival

A

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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13
Q

what is the host defensive response to molecular release of siderophores

A

production of reactive oxygen and nitrogen species

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14
Q

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

A

avoids oxidative burst
removes reactive O and N species

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15
Q

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

A

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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16
Q

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

A

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

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17
Q

function of C3b receptor

A

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

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18
Q

what is another host defence to microbial extracellular survival

A

production of antimicrobial antibodies

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19
Q

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

A

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

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20
Q

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

A

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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21
Q

what is a 3rd host defence to extracellular microbial survival

A

antimicrobial cell-mediated response

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22
Q

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

A

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

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23
Q

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

A

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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24
Q

what is the host defence IV to prevent extracellular microbial survival

A

antimicrobial immune response

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25
Q

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

A

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

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26
Q

what are the host defences to prevent microbial shedding

A

apart from innate and acquired immunity,
there is none

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27
Q

what are microbial strategies for shedding

A

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

28
Q

effect of Vibrio cholerae

A

Diarrhoeal disease
massive loss of water from intestinal epithelial cells

29
Q

what does cholera toxin bind to and what happens

A

enterocyte GM1 receptors
it is endocytosed

30
Q

what occurs to endocytosed cholera toxin

A

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

31
Q

function of cytosolic cholera toxin A1

A

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

32
Q

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

A

intrinsic GTPase activity
ribosylation inhibits catalytic activity of hydrolysing GTP

33
Q

what is the overall effect of ribosylation of Gs alpha subunit

A

increase in GTP
increased adenylate cyclase activity
increase in cAMP production

34
Q

what e-coli cause noninflammatory diarrhoea

A

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

35
Q

what E.coli cause inflammation

A

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

36
Q

what does ETEC do

A

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

37
Q

what does EPEC do

A

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

38
Q

what does EIEC do

A

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

39
Q

what does EAggEC do

A

damage and blunt colonic villi
done by haemorrhagic necrosis

40
Q

what does EHEC cause

A

diarrhoea
haemorrhagic colitis
haemolytic uraemic syndrome

41
Q

what does EHEC destroy and what does it cause

A

RBC - haemolytic anaemia
platelets - thrombocytopenia

42
Q

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

A

EHEC
enterohaemorrhagic E.coli

43
Q

what is the major toxin that EHEC produces

A

shiga-like toxins

44
Q

what does EHEC adhere to

A

enterocytes in large intestine
removes microvilli (efface)

45
Q

what characteristic structural changes does EHEC cause onto a host cell

A

attaching-effacing lesions

46
Q

how are pathogenicity islands acquired

A

via horizontal transfer from other bacteria

47
Q

what is the major pathogenicity island in EHEC termed

A

locus of enterocyte effacement (LEE)

48
Q

function of LEE

A

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

49
Q

what is EspA

A

filament extension in EHEC/EPEC

50
Q

function of EspA

A

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

51
Q

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

A

have an enzymatic A subunit
5 identical B subunits

52
Q

function of A subunits in SLT

A

inhibit protein synthesis
cell is unable to recover

53
Q

how specifically does the A subunit in SLT achieve its function

A

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

54
Q

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

A

ceramide host cell receptors
renal epithelial tissue
CNS
vascular endothelium

55
Q

what are the stx1 and stx2 genes carried by

A

bacteriophage lysogens in EHEC cells

56
Q

where does Stx production occur

A

in the intestine

57
Q

how does bacteria cross the intestinal barrier

A

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

58
Q

where do bacteria enter, survive and produce Stx

A

lamina propria

59
Q

what can helicobacter pylori be a causative agent for

A

peptic ulcers
gastric cancer

60
Q

what can helicobacter pylori protect against

A

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

61
Q

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

A

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

62
Q

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

A

fixation
crystal violet
iodine treatment
decolourisation
counterstain

63
Q

what is the function of crystal violet in staining

A

detects thick peptidoglycan and becomes trapped in the presence of iodine

64
Q

function of ethanol in staining bacteria

A

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

65
Q

name a counterstain

A

safranin

66
Q

what is phytophora infestans

A

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

Biomed 2 - Season finale (24 decks)

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