1.10. Bacterial Pathogenesis 1 Flashcards

1
Q

pathogenicity

A

Capacity to cause disease

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

Organism needs to be able to:

A
  1. Transmit-(communicability) from one host/reservoir to another
  2. Survive-in the new host
  3. Infect-ability to breach the new host’s defences
  4. Be virulent-ability of a pathogen to harm a host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Opportunistic Pathogens

A
  • Rarely cause disease in immune-competent individuals
  • If immunological/ anatomic defences are compromised, these bacteria can cause disease
  • Often normal flora
  • Become pathogenic in the absence of normal defence mechanisms ±removal of competing bacteria (e.g. broad spectrum antibiotics)
  • E.g. Coagulase Negative Staphylococci (CNS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

natural history of HIV-1 infection

A
  1. thrush
  2. oral hairy leukoplakia
  3. tuberculosis
  4. pneumcystis carnii pneumonia
  5. Histoplasmosis
  6. Coccidloidmycosis
  7. Cryptococcosis
  8. Toxoplasmosis
  9. Atypical herpes simplex virus disease
  10. crytosporidiosis
  11. Cytomagalovirus disease
  12. Mycobacterium avium complex disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Primary Pathogens

A
  • Able to cause disease in healthy immuno-competent individuals
  • BUT may more readily cause disease in individuals with impaired defences
  • E.g. Streptococcus pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Virulence

A
  • Usually a multitude of factors acting in a co-ordinated fashion to produce disease
  • Genetically determined/ expressed
  • Single virulence factor rarely sufficient to cause disease
  • Not all strains of a particular bacterial species are equally pathogenic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why does a bacterium need virulence factors:

A
  • Colonisation: adhesion factors
  • Invasion: allow uptake of bacteria into cells
  • Survival and multiplication
  • Avoidance of host defence mechanisms-capsules, M protein, resist phagocytosis
  • Toxin production-endotoxins, exotoxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Establishing infection

A

•Pathogen entry: skin, respiratory tract, gastro-intestinal tract, urinary/genital tract
•Some pathogens require specific contact
-e.g. Treponema pallidum (syphilis)
-Requires direct skin to skin contact
-Humans are the only host-they will die in the environment
•Source of infection: individuals with clinical diseaseor carriers
-Carrier: individuals in whom symptoms may be absent or relatively mild because the disease process is at an early stage or because of partial immunity to the pathogen (e.g. Typhoid Mary)
•Other pathogens may be able to infect humansand animals-e.g. Salmonella spp, Shigellaspp, Campylobacter spp
-Source of infection: contaminated food or water in the environment
•Animals:
-Reservoir of infection (animals are infected, but do not get sick)
-Source of environmental contaminatio

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

colonisation definition

A

the establishment of a stable population of bacteria in the host

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

what does colonisation require?

A

•Requires adhesion to a mucosal surface•This allows for a focus of infection to develop, which may lead to localised infection/systemic spread•Adhesion involves surface interaction between host cell receptors and adhesinson bacterial surface•Presence or absence of cell receptors contribute to tissue specificity of infection

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

what are the consequences of adhesion?

A
  • Induces changes in bacterial expression

* Induces intracellular signalling pathways

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

what are the types of adhesins?

A
  1. fimbrial adhesins

2. non-fimbrial adhesins

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

fimbrial adhesins

A
  • Thin, rigid, rod like structure
  • Mediate attachment to cell
  • Found in GP and GN bacteria
  • E.g. E.coli colonization factor antigen I and II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

non-fimbrial adhesins

A

•Protein or polysaccharide structures that are on the bacteria cell or excreted
•Found in GP and GN bacteria
•E.g. Teichoic acid-CNS
Flagella –Vibriocholerae

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

Binding to Fibronectin

A
  • A complex human glycoprotein found in plasma, associated with mucosal surfaces and promotes adhesion functions
  • Many bacteria use fibronectinfor adhesion purposes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Invasion

A
  • Some bacteria are able to cause disease after colonisation
  • Most bacteria need to invade cells/tissue
  • Some bacteria which are able to survive within the host cell: Mycobacteria, Salmonella, Shigella, E.coli, Listeria, Neisseria species
17
Q

Cell invasion

A
  • Ability to avoid humoral defence mechanisms
  • Provide a niche rich in nutrients
  • Provide protection from other bacteria
18
Q

Uptake into host cells

A
  • Usually use phagocytic entry mechanisms
  • Some organisms remain in the superficial cell layers e.g. Shigella spp.
  • Others invade into deeper tissue e.g. Salmonella spp.
19
Q

Role of cell receptors

A
  • Availability of specific receptors defines the types of host cells involved
  • Specific host receptors have been identified for some organisms
  • E.g. M. tuberculosis –complement receptors on phagocytes
20
Q

Avoid host defence

A
  • Humoral immune responses
  • Cell mediated immune response
  • Complement
  • Lysozyme
  • Iron chelators-transferrin, lactoferrin
21
Q

Capsule

A
Aids in avoiding phagocytosis
examples: 
Neisseria meningitidis, 
Haemophilus influenzae,
Streptococcus pneumoniae
22
Q

Streptococcal M Protein

A

Not a capsule but avoids phagocytosis in a similar manner
example:
Streptococcus pyogenes

23
Q

Resistance to killing by phagocytic cells

A
  1. Prevention of phagosome-lysosome fusion (Mycobacterium tuberculosis)
  2. Able to prevent oxygen-dependent killing (Salmonella Typhi)
  3. Production of catalase to negate effect of toxin radicals (Staphylococcus aureus)
  4. Inhibits phagosome-lysosome fusion (Legionella pneumophila)
24
Q

Antigenic Variation

A
Change of antigen or DNA sequence to avoid an immune response against that antigen (immune system unable to recognise)
example: 
Neisseria meningitidis
-PorA amino acid mutations
-Switch off expression of capsule
25
Q

IgA Proteases

A

A protease that specifically cleaves IgA at mucosal surfaces
example:
Meningitis causing pathogens

26
Q

Serum Resistance

A

Resist lysis as a result of deposition of complement on the bacterial surface
example:
O1 polysaccharide
Sialic acid capsule in E.coliK1

27
Q

Iron Acquisition

A

Scavenge iron from mammalian iron-binding proteins
example:
Staphylococcus aureus-specific receptors for transferrin and lactoferrin

28
Q

list the virulence factors that avoid host defence

A
  1. capsule
  2. streptococcal M Protein
  3. resistance to killing by phagocytic cells
  4. antigenic variation
  5. IgA proteases
  6. Serum resistance
  7. Iron Acquisition
29
Q

toxins

A

Exert their pathogenic effect on a target cell/interact with cells of the immune system to release cytokines that cause pathophysiological effect

30
Q

Endotoxins

A
  • Lipopolysaccharide
  • Component of outer membrane of GN bacteria
  • Released from the bacterial surface via vesicles
  • Causes endotoxic/septic shock
  • Activate macrophages, thus inducing a range of cytokines
31
Q

Exotoxins

A
  • Diffusible proteins secreted into the external medium
  • GP and GN bacteria
  • Vary in molecular structure, function, mechanism of secretion and immunological properties
  • Type 1:
  • Membrane acting
  • Bind surface receptor and stimulate transmembranesignals
  • Type 2:
  • Membrane damaging
  • Form pores and disrupt lipid bilayers
  • Type 3:
  • Intracellular effect
  • Modify intracellular target molecule
32
Q

list some effects of bacterial exotoxins

A
  1. lethal action
  2. pyrogenic effect
  3. action on GIT
  4. action on skin
  5. cytolytic effects
  6. inhibition of metabolic activity
33
Q

Lethal Action

A

Effect on neuromuscular junction

e.g. Clostridium botulinum toxin A

34
Q

Pyrogenic Effect

A

Increased body temperature and polyclonal T cell activation
e.g. Staphylococcal Toxic Shock
Syndrome Toxin -1

35
Q

Action on GIT

A

Secretion ofwater and electrolytes

e.g. Cholera and E.colienterotoxin

36
Q

Action on skin

A

Necrosis

e.g. Clostridium perfringens toxins

37
Q

Cytolyticeffects

A

Lysis of blood cells

e.g. StreptolysinO and S (S. pyogenes)

38
Q

Inhibition of metabolic activity

A

Protein synthesis

e.g. Diphtheria toxin