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Foundations Of Medicine > 11.2 Bacterial Pathogenicity, Growth and Antibiotics > Flashcards

11.2 Bacterial Pathogenicity, Growth and Antibiotics Flashcards

1
Q

Which surfaces of a host do commensal bacteria colonise?

A

All of them

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2
Q

What are two benefits to the host of commensal bacteria?

A
  • Protection against pathogen
  • Metabolic benefits (e.g. folate production by bifidobacterium)
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3
Q

How do commensal bacteria usually protect against pathogens?

A

Via competition for colonisation sites

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4
Q

What are some instances where opportunistic pathogens may infect a host?

A
  • Trauma/tissue damage
  • Infection/immunological insult
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5
Q

What is a pathogen?

A

An organism whose growth inflicts damage upon its host as a by-product of its nutrient gathering strategy

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6
Q

Describe indirect pathogenic damage

A
  • Disturbs metabolic balance/nutrient acquisition
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7
Q

Describe direct pathogenic damage

A
  • Bacteria secretes toxins
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8
Q

Pathogenesis

A

Mechanism of disease

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9
Q

Virulence

A

Capacity to cause disease/severity of symptoms

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10
Q

Two categories of structural and functional features of pathogens

A
  • Promote competition
  • Damage host and cause symptoms
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11
Q

What are the four phases of the pathogenic cycle?

A
  • Transmission
  • Colonisation
  • Proliferation
  • Evasion
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12
Q

List some disease transmission routes

A
  • Direct contact
  • Indirect contact
  • Aerosol/respiratory
  • Zoonotic
  • Food-borne
  • Faecal-oral
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13
Q

What is the infectious dose 50 of a bacteria?

A

The number of organisms required to infect 50% of individuals

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14
Q

What is inoculum size?

A

Amount of a pathogen an individual is actually exposed to

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15
Q

Give an example of an extracellular enzyme secreted by bacteria which have a role in pathogenesis

A

Beta haemolysin

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16
Q

What are the two types of bacterial toxins?

A
  • Exotoxins (made and secreted during growth)
  • Endotoxins (structural components that have toxic activity)
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17
Q

Which type of bacterial toxins are more toxic at low doses?

A

Exotoxins (e.g. neurotoxin, enterotoxin, hepatotoxin etc.)

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18
Q

What are the two broad groups of exotoxins

A
  • Cytolysins (cause lysis of cells)
  • Two component toxins (A-B) remember Christopher Wong -> disrupt cellular processes
19
Q

When are endotoxins released? What influence does this have on medication?

A
  • Released upon death of bacteria
  • This means that too much antibiotics can be detrimental, since it leads to a whole bunch of dead bacteria
20
Q

What are the three outcomes of infection?

A
  • Clearance
  • Asymptomatic carriage
  • Symptomatic disease (potential long term impacts/death)
21
Q

What factors affect the outcome of an infection?

A
  • Immune status
  • Prior exposure
  • Diet
  • Microbiome
22
Q

What structures can antibiotic resistant genes be found in?

A
  • Bacterial chromosomes
  • Plasmids
  • Mobile genetic elements (integrons and transposons; move into chromosomes or plasmids)
23
Q

Describe transformation as a mechanism of antibiotic resistance propagation

A
  • Transfer of plasmid DNA or a fragment of free DNA from a lysed cell to a living cell
24
Q

What is genetic transduction? how common is this in spreading antibiotic resistance?>

A
  • Transfer of genes between bacteria via bacteriophages
  • Rarely involved in antibiotic resistance transfer
25
Other than antibiotic resistance, what other genetic information might be carried on an R plasmid?
- Sugar metabolism - Heavy metal resistance - Resistance to osmotic stress
26
How does the spread of resistance genes usually occur?
Acquisition of resistance genes from mobile genetic elements such as plasmids and transposons
27
Describe the mechanism of complex transposons
- Can contain antibiotic resistance genes - Move rapidly between chromosome and plasmids in cell - Move through a bacterial population (incl. across species)
28
Describe the mechanism of gene cassettes
- Can exist as separate genetic elements - Can be integrated into transposons, integrons, or bacterial chromosome
29
Describe an integron
- Sequence of DNA which can contain resistance to antibiotics (as well as other things). . - Integrase enzyme selectively adds genes to integron, thus adding genetic information to a bacterial cell
30
Describe the four phases of bacterial growth in an isolated system
1. Lag (Cells adapt to new conditions, enzymes accumulate) 2. Exponential phase (maximum constant growth rate) 3. Stationary phase: Population reaches 10^7-10^9, and oxygen/nutrient demands can no longer be met. Slow death balanced by slow proliferation 4. Death phase: number of viable cells drop as waste accumulates, death > proliferation
31
List factors that affect bacterial growth
- pH - Temperature - Osmolarity - Nutrient availability - Oxygen concentration
32
What are the five kinds of bacteria in terms of oxygen requirements?
- Strict anaerobe - Facultative anaerobe - Aerotolerant anaerobe - Microaerophile - Obligate aerobe
33
Which enzyme protects aerotolernat bacteria from oxygen free-radicals?
Superoxide dismutase
34
Which are the four mechanisms of inhibition by which antiobiotics achieve their effect:
Inhibit: - Cell wall synthesis - Protein synthesis - Nucleic acid synthesis - Certain metabolic pathways
35
Bacteriostatic vs Bacteriocidal antibiotics
Bacteriostatic: Inhibits growth Bacteriocidal: Kills the bacteria
36
Give an example of a class of antibiotic that inhibit nucleic acid synthesis
Fluoroquinolones
37
Give an example of a class of antibiotics that inhibit cell wall synthesis
- Penicillins
38
Describe the mechanism of action of penicillins
- Bind to proteins involved in peptidoglycan assembly (so-called penicillin binding proteins: PBPs) - Inhibits last step of cell wall synthesis - Prevents cross-linking of peptidoglycan strands -> leads to lysis of cell - Only acts on growing bacteria that are synthesising new peptidoglycan
39
Give two examples of antibiotics that bind to the 30S subunit of prokaryotic ribosomes
- Streptomycin - Gentamicin
40
Give an example of antibiotics that bind to the 50S subunit of prokaryotic ribosomes
- Erythromycin
41
Give two example of antibiotics that are metabolic antagonists
- Sulfonamides - Trimethoprim (interfere with enzymes involved in protein synthesis)
42
Which molecules do sulfonamides compete with to reduce folic acid synthesis in pathogens?
p-aminobenzoic acid (PABA)
43
What are some examples of points in protein synthesis which antibiotics can inhibit
- Inhibit polymerase (these can be highly toxic) - Inhibit DNA gyrase (quinolones) - Block transcription
44
Which class of antibiotics are less selective than the rest with their toxicity?
- Nucleic acid synthesis inhibitors - Not as selectively toxic since nucleic acid synthesis is similar between eukaryotes and prokaryotes

Foundations Of Medicine (98 decks)

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