VL3: Bacterial pathogenicity and surface structures Flashcards Preview

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Flashcards in VL3: Bacterial pathogenicity and surface structures Deck (29)
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1
Q

How can commensal B become pathogenic (3)?

A
  • Proliferation (higher nb than normal)
  • Entry into normally sterile sites (e.g. blood, lungs, bladder)
  • host immunity reduced
2
Q

How does an organism cause disease? (briefly explain 2 ways)

A
  • toxins or lytic enzymes (e.g. v.cholerae: cholera toxin)
  • colonization (usually gastrointestinal or respiratory tract) and/or invasion of tissues
  • > often is the actual disease caused by the immune response (e.g. salmonella endotoxin (LPS))
3
Q

Describe the general courses a disease can take with examples

A
  1. active (incubation, illness, convalesence) (e.g. influenza)
  2. chronic (incubation, illness…) illness persists Malaria HIV
  3. Latent (incubation, illness, convalescence // latent period // illness may recur) tuberculosis
4
Q

3 Ways of spreading disese

A
  1. Direct (human to human (air, sexually)
  2. vector (arthropodes) e.g. malaria, borrelia
  3. food, water e.g. v. cholerae
5
Q

Summary of Kochs postulate

A

shows that an organism is pathogenic

  1. path in all diseased individuals (and not healthy people)
  2. isolate pathogen -> grow in culture
  3. reinfection causes disease (problem: immunity, dose)
  4. reisolate pathogen from reinfected person
6
Q

What is the difference between primary and opportunistic pathogens ? (+ examples)

A

Primary pathogens are always pathogenic (rabies virus, malaria plasmodium, tuberculosis mycobacterium)

opportunistic pathogens are only pathogenic in susceptible people (candida, pseudomonas aeruginosa) present everywhere not usually pathogenic, only at some places in body, skin infections after burn injuries or lungs in CF

7
Q

2 differences in host range in diffrent bacteria

A

ex. only in humans (helicobacter pylori, typically vertical transfer, mom child)

broad host range, e.coli salmonella

8
Q

What is virulence and how is it defined?

A

The relative ability of a pathogen to cause disease

defined as mortality rate (LD50) of ability to invade host tissue (no experiments)
defined as ability to invade host tissue

9
Q

Does the infectious dose correlate with virulence?

A

No
B with pathogenic mechanisms that depend on secreted molecules (distant action) need a higher dose for infection than b with local action

10
Q

5 examples for major virulence factors

A
capsules
endotoxins
exotoxins
immunoglobulin proteases
enzymes that damage host tissue
11
Q

Name some strategies for infection prevention and treatment

A

vaccines
antimicrobial drugs

hygiene
nutrition
sanitation
isolation

12
Q

How do B establish infections? (6 steps)

A
Entry into the body
Colonization
Avoiding immune respose
Adhesion
Invasion
Surviving within host cells
13
Q

How do microbes invade the body?

A

Skin- through lesions or vectors (bites)

many B have ways to get through epithelia (cells specialized for engulfment or transport in various body openings)

14
Q

3 methods to promote colonization

A

(requires ability to obtain food and evade immune mechanisms)

  • sIgA proteases (prevents trapping of B in mucin)
  • Iron acquisition (sideophores, direct uptake of host iron-carrying prot,Low level toxin production ( host cell lysis releases iron) , iron abistinece
  • Synthesis of nutrient scavenging systems
15
Q

3 methods to avoid the immune system

A
  • antigenic variation of surface structurs (e.g. pilins Neisseria gonorrhoeae)
  • using a coat of host proteins
  • avoiding phagocytosis and complement activation (capusles and lps alterations)
16
Q

Brief description of adhesion

A

necessary first step for invasion of host tissue but not necessary for all infections (uropathogenic e.coli)

adhesins bind to specific molecules on cell surface like pili or fimbriae
Why pili?
-pili can help to increase volume where bacteria search for cells
-they maintain a separation between bacterial cell and eukaryotic cell

17
Q

Why and how do B invade host cells?

A

how?

  • uptake by phagocytic cells
  • induction of uptake in non-phagocytic cells (epitelial)

why?

  • nutrition
  • to hide from immune system
18
Q

Strategies to survive within pahgocytes

A
  • Listeria, Shigella get out of phagosome
  • Salmonella prevents fusion with lysosome
  • mycobacterium, prevents acidification

induce defense systems (deal with ROS nitrogen radicals, low pH, nutrient limitations ect)

example tuberculosis:
in pagosome: mildly acidic, (tries to prevent phagosome maturation?)
IFN-y –> maturation phagosome-lysosome: stress more acidic, lysosomal hydrolases, ubiquitin derived peptides…
tuberculosis survives by resisting acidification with serine protease, magnesium transporter and pore forming outer membrane protein

19
Q

4 types of cell envolpes, 2 types of appendages

A

Cell Envelopes:

  • capsules: for adheerece, resistance to engulfment, storage
  • cell wall: potection against lysis or rupture of the cell
  • outer membrane: with LPS (endotoxin)
  • endospores: protected resting state

Appendages:

  • Flagella- organelles for motility
  • Pili: for attachment or adherece to surfaces; sex pilus used during some genetic exchange processes
20
Q

What is a cell wall? What is is made out of? what is good for?

A

sturcutre that surrounds cell protoplast
almost all B have a cell wall (except mycoplasma)

peptidoglycan (PG) (repeating units of NAG and NAM linked by peptide bridges(L-ala, D-glu, DAP, D-ala)

  • semi rigid, gives cell its shape
  • protection from rupture and osmotic stress

PG: Peptidoglycan
NAG: n-acetylglucosamine
NAM: n-acetylmuramic acid

21
Q

What is the difference between Gram + and - cell walls?

A

Gram positive (mostly cocci (staphylococci, streptococci, pneumococci, enterococci), some bacilli (bacillus, clostridia, coynebacteria)
-thick PG (10-100nm)
-90% of CW
-Single membrane
cell wall is a thick homogenous monolayer

Gram-negative (mostly bacillis (e.coli, v.cholerae, salonella, h.pylori)
-thin PG (2nm)
-20% of CW
-Inner membrane, outer membrane
-periplasmic space,
-LPS
cell wall is thin heterogeneous multilayer

22
Q

How do penecillin and lysozyme work?

A

Penicillin works by preventing formation of a interpeptide bond in PG cell walls
lysozyme breaks glycoside bond between NAG and NAM

PG: Peptidoglycan
NAG: n-acetylglucosamine
NAM: n-acetylmuramic acid

Murein is a polymer of the peptidoglycan subunit

23
Q

What are teichoic acids good for?

A

Teichoic acids are thought to stabilize the gram positive cell wall and may be used in adherence

24
Q

Name two important properties of outer membrane of gram negative cell walls

A
  1. protects the cells from permeability of substances (including penicillin and lysozyme)
  2. location of lipopolysaccarides (endotoxin) which is toxic for animals
25
Q

What are capsules?

A

capsules are composed of polysaccharides deposited outside the cell wall
discrete layers enclosing a cell or group of cells –> easiliy visible under under microscope

26
Q

Name 5 functions of capsules

A
  1. Protection against phagotrophic engulfment
  2. Mediate adherence to surfaces
  3. Protection against drying
  4. Reserves of nutrients
  5. Biofilms for protection against antimicrobial agents and immune system
27
Q

Briefly describe endospore formation

A
  • Vegetative cell
  • DNA becomes more dense
  • Asymmetric cell division
  • endospore septum grows around protoplast
  • forespore formation
  • exosporium synthesis (primordial cortex is formed between the 2 membranes, dehydration)
  • Ca2+ incorporation, further dehydration, ext
  • Maturation –> development of resistance to heat and chemicals
  • Lysis of cell and release of endospore
28
Q

Name some Properties of endospores

A
  • resting dormant cells, show no sign of life (due to lack of water)
  • unique surface layers not found in vegetative cells (like exosporium, cortex)
  • highly resistant to heat, acids, bases, dyes, irradiation, disingectants, antibiotics…
  • Not a mechanism of reproduction
  • survival in deleterios environments
  • one vegetative cell develops into one endospore
29
Q

3 examples of medically improtant endospore forming B

A
  • Bacillus anthracis –> anthrax
  • Clostridium tetani –> tetanus
  • Clostridium botulinum –> botulism