10. Bacterial colonisation Flashcards

(51 cards)

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
what can gonorrhoea cause?
Infertility arthritis Proctitis
23
why are cases of gonorrhoea rising?
very drug resistant and super gonorrhoea cannot be treated Development of HIV prophylactic treatment means people are being less careful about other STIs
24
stages of gonococcal infections
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
what are the pro inflammatory cytokines?
TNFa and IFNy
26
what percentage of gonorrhoea cases can be asymptomatic?
10-30%
27
what virulence factors are involved in gonorrhoea pathogenesis?
Pili binding to integrins and possibly CD46 Opa porins - beta barrels LPS bind to glycoprotein receptors and complement and cause inflammation
28
what is different about enteric bacteria LPS?
no O-antigen repeats but shorter oligosaccharide region
29
what is the toxic part of LPS?
aceylated lipid A
30
how do you get diversity in LPS?
phase variation of LPS upto 14 types of different LPS
31
why do bacteria express lactoneotetraose?
to mimic host cells and avoid the immune system
32
what does siayl transferase do ?
transfers sialic acid from host membranes to the bacteria and add to lactoneotetraose?
33
when is siayl transferase expressed?
when the lactoneotetraose is present in the membrane
34
what are the complement inhibitor points?
C4b binding protein Factor H Vitronectin
35
what is the function of complement inhibitors?
they protect the host by preventing membrane attack complexes binding to host cells
36
how have bacteria like gonorrhoea evolved to use complement inhibitors?
they bind the inhibitors to protect themselves from the complement
37
how does gonorrhoea bind factor H?
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
what is unstable resistance?
resistance that can be phased on or off depending on the presence of a variable like galactose
39
what porins do gonorrhoea produce?
Por1A and Por1B trimeric outer membrane proteins
40
what is the function of porins in gonorrhoea?
nutrient uptake and invasion
41
how do porins cause apoptosis?
translocation from bacterial membrane to mitochondrial membrane activating the intrinsic apoptosis pathway
42
what is a positive about the porins?
it is a potential target for vaccines
43
how do the porins contribute to host mimicry?
Factor H can bind the porins preventing complement activation and no membrane attack complex formation
44
what is stable resistance?
the resistance is dependant is something that is nearly always expressed
45
what else binds to gonorrhoea porins to prevent classical activation of the complement?
Por1A and Por1B can bind C4 binding protein preventing membrane attack complex formation
46
what is a trade off for this resistance?
sialic acid coats bacteria in negative charge which can repel nutrients and other useful molecules cannot bind Opa
47
what are sialic acid binding lectins?
often on immune cells interactions can subvert neutrophil functions
48
what are the roles of LPS?
target receptors damage to host - lipid A toxin immune evasion - factor H