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Infection and immunity > 10. Bacterial colonisation > Flashcards

10. Bacterial colonisation Flashcards

1
Q

mutualism

A

both parties benefit

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2
Q

mutualism example

A

gut bacteria breaking down nutrients

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3
Q

commensalism

A

one party benefits the other is neutrally effected

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4
Q

commensalism example

A

skin flora

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5
Q

parasitism

A

one party benefits the other is harmed

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6
Q

parasitism example

A

bacterial pathogens

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7
Q

what are the 3 relationships between bacteria and humans?

A

mutualism, commensalism and parasitism

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8
Q

what steps are essential for colonisation?

A

adhesion
local spread
growth
evasion of host defences
exit from host - transmission
damage to host

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9
Q

what are the colonisation steps unique to pathogens?

A

damage to host

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10
Q

how are capsules used for adhesion?

A

sticky so stick to the host cell

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11
Q

how are slime layers used for adhesion?

A

sticking

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12
Q

how are flagella used for adhesion?

A

to drive deeper into tissues and through mucus layers

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13
Q

how are pili/fimbriae used for adhesion?

A

get through mucus layers
no gram -ve and +ve

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14
Q

how are lipoteichoic acids and carbohydrates used for adhesion?

A

attach to cell host cells

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15
Q

how are bacterial outer membrane proteins used for adhesion?

A

stick to ECM protein like fibronectin and fibrinogen

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16
Q

what do bacteria bind to on host cells?

A

surface receptors
ECM proteins
secreted proteins and carbohydrates
calcified components
implants and prostheses

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17
Q

Why are epithelial cells a big target for bacteria?

A

Because of the massive mucosal epithelium surface area

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18
Q

why are fibroblasts targetted by bacteria?

A

they are in the sub dermal layer and help with wound healing and tissue repair

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18
Q

what are the cell types targetted by bacteria?

A

epithelial cells
fibroblasts
phagocytic cells
Endothelial cells

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18
Q

why are phagocytic cells targetted by bacteria?

A

to disrupt their function to continue disease progression

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19
Q

why are endothelial cells targetted by bacteria?

A

target blood vessels for distribution and sepsis

19
Q

how do humans Initially defend against bacteria?

A

lysozymes in the saliva
mucus to wash away pathogens
acidic environments like the stomach

20
Q

what causes the most pain in a bacterial infection?

A

the inflammation response of the immune system

21
Q

where can you get gonorrhoea?

A

sexual organs
throat
blood stream
skin

22
Q

what can gonorrhoea cause?

A

Infertility
arthritis
Proctitis

23
Q

why are cases of gonorrhoea rising?

A

very drug resistant and super gonorrhoea cannot be treated
Development of HIV prophylactic treatment means people are being less careful about other STIs

24
Q

stages of gonococcal infections

A
  1. Initial exposure at the epithelium
  2. at the basal surface and interact with macrophages
  3. activation of pro-inflammatory cytokines leading to chronic inflammation
  4. Tissue damage
  5. cell damage - dead and dying epithelium and neutrophilsh
25
Q

what are the pro inflammatory cytokines?

A

TNFa and IFNy

26
Q

what percentage of gonorrhoea cases can be asymptomatic?

A

10-30%

27
Q

what virulence factors are involved in gonorrhoea pathogenesis?

A

Pili binding to integrins and possibly CD46
Opa porins - beta barrels
LPS bind to glycoprotein receptors and complement and cause inflammation

28
Q

what is different about enteric bacteria LPS?

A

no O-antigen repeats but shorter oligosaccharide region

29
Q

what is the toxic part of LPS?

A

aceylated lipid A

30
Q

how do you get diversity in LPS?

A

phase variation of LPS
upto 14 types of different LPS

31
Q

why do bacteria express lactoneotetraose?

A

to mimic host cells and avoid the immune system

32
Q

what does siayl transferase do ?

A

transfers sialic acid from host membranes to the bacteria and add to lactoneotetraose?

33
Q

when is siayl transferase expressed?

A

when the lactoneotetraose is present in the membrane

34
Q

what are the complement inhibitor points?

A

C4b binding protein
Factor H
Vitronectin

35
Q

what is the function of complement inhibitors?

A

they protect the host by preventing membrane attack complexes binding to host cells

36
Q

how have bacteria like gonorrhoea evolved to use complement inhibitors?

A

they bind the inhibitors to protect themselves from the complement

37
Q

how does gonorrhoea bind factor H?

A

can express the galactose needed to bind host sialic acid so the body thinks it is a host cell
this means factor H will bind to it and prevent membrane attack complexes forming on the gonorrhoea bacteria

38
Q

what is unstable resistance?

A

resistance that can be phased on or off depending on the presence of a variable like galactose

39
Q

what porins do gonorrhoea produce?

A

Por1A and Por1B
trimeric outer membrane proteins

40
Q

what is the function of porins in gonorrhoea?

A

nutrient uptake and invasion

41
Q

how do porins cause apoptosis?

A

translocation from bacterial membrane to mitochondrial membrane
activating the intrinsic apoptosis pathway

42
Q

what is a positive about the porins?

A

it is a potential target for vaccines

43
Q

how do the porins contribute to host mimicry?

A

Factor H can bind the porins preventing complement activation and no membrane attack complex formation

44
Q

what is stable resistance?

A

the resistance is dependant is something that is nearly always expressed

45
Q

what else binds to gonorrhoea porins to prevent classical activation of the complement?

A

Por1A and Por1B can bind C4 binding protein preventing membrane attack complex formation

46
Q

what is a trade off for this resistance?

A

sialic acid coats bacteria in negative charge which can repel nutrients and other useful molecules
cannot bind Opa

47
Q

what are sialic acid binding lectins?

A

often on immune cells
interactions can subvert neutrophil functions

48
Q

what are the roles of LPS?

A

target receptors
damage to host - lipid A toxin
immune evasion - factor H

Infection and immunity (22 decks)

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