Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

oral cavity - BDS 1 > Mechanisms of infection :) > Flashcards

Mechanisms of infection :) Flashcards

1
Q

what are pathogens

A

disease causing organisms that are fully virulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do pathgens show

A

clonality
reproduction -asexual
each cell has a similar capability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are opportunistic pathogens

A

possess soem virulence factors

often commensals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

aim of pathgen

A

reproduction and maintenance of its genes in envrionemtn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are seroconverts

A

those who can make antibodies agains the pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

routes of transmission

A 
aerosols
foetal oral spread
venereal spread
vector vertebrate reservoir
vector vertebae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

vertical transmission

A

between generations e.g. through placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is an infectious dose

A

have to have enough bacteria that will survive to infect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

requirement for infection

A

adhere to susceptible cell
grow in/on host
evade host defenses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

examples of bacterial appendages

A

pilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are bacterial capsules made of

A

polysaccharides

bind to artificial surfaces and tooth pellicles (important in biofilm formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what can bacteria bind to

A

surface proteins/glycoprotiens

e.g. HIV binds to CD4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

biofilm formation

A

primary colonisation of surface

secondary colonisation by extracellular polysaccharide and cell interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the gradients within the plaque community

A

towards edge more active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what can aid colonisation

A

motility i.e. flagellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what can flagellum help with

A

penetrate mucous blanket
penetrate intercellular junctions
colonisation of catheters

17
Q

formation of pedestals

A

1) Bacteria sticks to cell
2) retracts the cells
3) needles stick out
4) send proteins out through the needles
5) form a hole to send more proteins
6) proteins sit in the membrane
7) Then the bacteria can sit in the membrane
8) Sends in more protein, causes actin polymerisation (cytoskeleton)
9) Pellicle is formed

18
Q

how can bacteria manituplate the host

A

manipulate the endocytosis system of cells
bind receptors using pili
pedestal formed in intestinal brush border
then inject cell effectors using section needles

19
Q

invasion of cell steps

A

1) Attaches
2) Sends needle inside cytoskeleton
3) Uses the vesicle to go inside
4) pH changes
5) triggers organism to send out another needle
6) Manipulates vesicle to make home for itself
7) Then divides

20
Q

summary of colonisation

A
  • Transmission by aerosol, direct contact, wound/infect
  • Attachment by fimbriae, polysaccharide, protein adhesion
  • Motility aids colonisation
  • Invade by subversion of endocytosis system
21
Q

complement involved in invasion

A

deposits on surface
become activated by antigens
makes membrane attack complement
bacterial cell then burst

22
Q

evasion of complemtn

A

gram -
LPS forms a brush border preventing proteins getting to the cell membrane
gram +
capsules able to stop deposition on surface of the cell

23
Q

normal IgA fuction

A 
non complement activated cell
M cell detects pathogen
- T cell and B cell activation to make IgA colecuels
IgA molecules are then sent out
protect from adhesion

soem bacteria are able to chop up IgA

24
Q

subverting phagocytosis

A 
toxis
evade phagocytosis (capsule exclusion)
avoid killing within a phagosome
25
Q

how do toxins evade defences

A

toxins can target leucoidins

kills phagocytes

26
Q

how can you avoid killing within a phagosome

A

escape from phagosome
resist lytic enzymes
inhibit generation of superoxide or degrafde them

27
Q

what does tuberculosis do

A

evades killing
surpasses immune responcec
multiplies in macrophages

28
Q

subverting t cells

A

incapacitate t cells

- infects and destroys CD4 and T cells

29
Q

secret agent methods of evasion

A 
surface antigen variation
molecular mimicry 
infection of privleged sites
decoys:smokescreens
degrade or inhibit complement
30
Q

surface antigen variation

A

change antigens to evade immune system

31
Q

molecular mimicry

A

coat with host protein

incorporation of silica acid into LPS on surface

32
Q

infection of privileged sites

A

not easily detected in areas with less immune cells

33
Q

decoys/smokescreen

A

bacteria may send out false messages

bind to antibodies/antigens to occupying them to give more time to run away

34
Q

degraded inhibit complement

A

intercept codes and misinformation

give more time for colonisation, adhesion or infection

35
Q

force fields

A

organisms produce urease
acts as protective cloud during transit to gastric mucin layer
take the urea and chop it up into amminoia and CO2

oral cavity - BDS 1 (66 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions