Brainscape's Knowledge GenomeTM

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


See full index

Fundamentals of P > Microbial Immune Evasion Mechanisms > Flashcards

Microbial Immune Evasion Mechanisms Flashcards

1
Q

Explain the concept of Balanced Pathogenicity

A

Properties of the microbe
(Pathogenic mechanisms):

Adhesins
Toxins
Capsule
Etc.

VS

Properties of the host
(Defensive mechanisms):

Natural barriers
Defensive cells
Complement
Immune response

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

Virulence Factors - describe 3 effects

A

Promote colonisation and adhesion

  • To establish infection
    e. g. adhesins

Evade host defences

Promote tissue damage

  • Growth, Transmission?
    e. g. toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Roles of Complement

A 
induces inflammatory response
	promotes chemotaxis
	↑ phagocytosis by opsonisation
	↑vascular permeability
	mast cell degranulation
	lysis of cell membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Intracellular pathogens:- example

A

Intracellular pathogens:-
e.g. Mycobacterium tuberculosis
Listeria
Salmonella

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

Intracellular pathogens:- hidden from?

A

hidden from serum killing, complement, antibodies

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

Phagocytosis - functions

A

kill cell - leucocidins - Staphs
prevent opsonisation - protein A (binds Fc portion of IgG) - Staphs

block contact - capsules -meningococcus, Hib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

intracellular pathogens:- function

A

Promote own uptake (safe)
- CR3; mannose lectin receptors

Prepares cell for invasion - Shigella

  • ve P-L fusion
  • M. tuberculosis

Escape P-L to cytoplasm - Listeria

Resist oxidative killing
- produce catalases/peroxidases

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

Describe phagocytosis

A
  1. Directs phagocytosis
    via CR3 – no ROI
  2. Actin rearrangement - +ve engulfment
  3. Type 3 secretion systems – prepares cell
  4. Resists digestion and ROIs
    in PLs - SOD, catalase
  5. Escape into cytoplasm
    e. g. Listeria
  6. Inhibits PL fusion
    maintains early endosome
    Blocks acidification
    e.g. mycobacteria
  7. Controls antigen
    presentation
    Stops CTLs or
    Pφ activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effect of production of Fc receptors by microbes

A

Microbial antigen bind to antibody leading to elimination

However when microbial Fc receptors bind antibodies leads to binding specific + non-specific antibody by Fc portion

Access to surface antigen
by specific antibody blocked

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

Concealment of antigen - describe

A

Adaptive immunity

  • hide inside cells
  • privileged sites
  • block MHC antigen presentation = Herpes -ve TAP protein
  • surface uptake of host molecules e.g. CMV and beta2microglobulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Effect of immunosuppression

A

Immunosuppression

- e.g. ↓ MHC, ↓ receptors, apoptosis, cytokine switch IgA proteases

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

Streptococcus pneumoniae - pathogenic mechanisms

A

Colonisation of nasopharynx
(adhesins; receptor NAc-hex-gal, sIgA proteases) = Otitis media
(inflammation)

Inhalation into lungs

By-passes defences: surfactants sIgA proteases; pneumolysin

Reaches lung

=

Escapes phagocytosis
(capsules)

Inflammation -Lung damage
(teichoic acids; pneumolysin)

Damage to endothelial cells
(inflammation; pneumolysin)

=

pneumonia

Bacteraemia

Meningitis + septicaemia
(Inflammation and toxic shock)

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

Viral Immune Evasion - describe

A
  1. Latency - VZV, herpes simplex
  2. ↓ antigenic presentation by binding to TAP
    - Inhibits peptide transfer to MHC
    - Herpes simplex
  3. ↓MCH expression - Cytomegalovirus (CMV)
  4. Mutation of epitopes
    B cells - neutralisation escape
    T cells - CD8+ escape mutants of HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Intracellular pathogens - requires

A

Intracellular pathogens - requires adaptive cell mediated immunity

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

Ophthalmic Zoster - presentation

A

During chicken pox VZ V becomes latent in nerve ganglia

In shingles, reactivates years later

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

Ophthalmic Zoster - define

A

Shingles involving the eye. Symptoms = include a rash of the forehead with swelling of the eyelid.

There may also be eye pain, eye redness, and light sensitivity.

17
Q

Explain infection of next generation susceptibles

A

Microbes infects
susceptibles

Microbe remains
latent

Microbes reactivates (zoster)
and infects next generation
of susceptibles

18
Q

Explain immunological state of nerves

A

Nerves –
immunologically privileged site
Poor protective immunity for reactivation

19
Q

Phenotype changes - list

A

Phenotype changes - colony morphology, virulence, serotype loose flagella, change surface sugars

20
Q

Antigenic Diversity/ polymorphisms - define with an example

A

Antigenic Diversity/ polymorphisms

  • genetically stable and alternative forms of antigens in a population of microbes
    e. g. serotypes of Strep.pneumoniae
21
Q

Antigenic Variation - define

A

Antigenic Variation
- successive expression of alternative forms of an antigen
in a specific clone or its progeny

22
Q

Define phase variation - when does it occur

A
  • Phase variation - ON/OFF of an antigen at low frequency

Occurs:

  • during course of infection in an individual host
  • during spread of microbe through a community
23
Q

Gonorrhoea – a sexually transmitted disease = define

A

Inflammatory and pyogenic infection of anterior urethra
Infects mucosal surfaces with columnar epithelium
- urethra, cervix, rectum, pharynx, conjunctiva

24
Q

Gonorrhoea – a sexually transmitted disease = effects

A

dysuria, redness, swelling, pain on urination, destruction of mucosa

prostatitis, orchitis, strictures, ovaritis, fistulas, PID, proctitis, sterility

Disseminated infections → arthritis, endocarditis, meningitis

25
Q

Neisseria gonorrhoeae - characteristics

A

Surface components interact with host cells
Components vary at high frequency in a population of bacteria
Variation to avoid immune response

26
Q

Neisseria gonorrhoeae - list cell surface components

A 
Pilus
Capsule
Inner membrane
Outer membrane
Opa
27
Q

Neisseria gonorrhoeae - cell surface structures can undergo what

A

All of these structures can undergo either:
Phase variation i.e. an ON-OFF switch (capsule, Opa’s)
Antigenic variation e.g. pilins (or both phase and antigenic)

28
Q

Epidemics cause

A

Antigenic drift

– mutation + selection

29
Q

Pandemics cause

A

Antigenic shift

- gene reassortment

30
Q

What effects do bacterium have on the body

A

Superantigens and inappropriate immune
activation

Induction/inhibition of apoptosis

Inhibition of antigen presentation

Prevents opsonin binding
C3a and C5a proteases
Anti-inflammatory
and anti chemoattractant

Inhibits opsonisation

Inhibit complement
activation

Ig binding proteins
e.g. protein A

sIgA proteases

Survival inside macrophages

Induction/inhibition of apoptosis

31
Q

What effects do viruses have on the body

A

MHC mimics – block killing by NK cells

Downregulate MHC

Block antigen processing by TAP

Induce immune suppression
↓CMI, ↓CD4+

Host Mimicry

Cytokine mimics and binding proteins

Hide inside cells

Survival inside cells

Induction/inhibition of apoptosis

Blockage of cell cycle
progression

CTL escape mutants –
quasi species swarms

Latency reactivation
e.g. VZV, Herpes simplex

Rapid growth and transmission prior to adaptive immunity e.g. colds

Fundamentals of P (62 decks)

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