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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
Q

Other than antibiotic resistance, what other genetic information might be carried on an R plasmid?

A
  • Sugar metabolism
  • Heavy metal resistance
  • Resistance to osmotic stress
26
Q

How does the spread of resistance genes usually occur?

A

Acquisition of resistance genes from mobile genetic elements such as plasmids and transposons

27
Q

Describe the mechanism of complex transposons

A
  • Can contain antibiotic resistance genes
  • Move rapidly between chromosome and plasmids in cell
  • Move through a bacterial population (incl. across species)
28
Q

Describe the mechanism of gene cassettes

A
  • Can exist as separate genetic elements
  • Can be integrated into transposons, integrons, or bacterial chromosome
29
Q

Describe an integron

A
  • 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
Q

Describe the four phases of bacterial growth in an isolated system

A
  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
Q

List factors that affect bacterial growth

A
  • pH
  • Temperature
  • Osmolarity
  • Nutrient availability
  • Oxygen concentration
32
Q

What are the five kinds of bacteria in terms of oxygen requirements?

A
  • Strict anaerobe
  • Facultative anaerobe
  • Aerotolerant anaerobe
  • Microaerophile
  • Obligate aerobe
33
Q

Which enzyme protects aerotolernat bacteria from oxygen free-radicals?

A

Superoxide dismutase

34
Q

Which are the four mechanisms of inhibition by which antiobiotics achieve their effect:

A

Inhibit:
- Cell wall synthesis
- Protein synthesis
- Nucleic acid synthesis
- Certain metabolic pathways

35
Q

Bacteriostatic vs Bacteriocidal antibiotics

A

Bacteriostatic: Inhibits growth
Bacteriocidal: Kills the bacteria

36
Q

Give an example of a class of antibiotic that inhibit nucleic acid synthesis

A

Fluoroquinolones

37
Q

Give an example of a class of antibiotics that inhibit cell wall synthesis

A
  • Penicillins
38
Q

Describe the mechanism of action of penicillins

A
  • 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
Q

Give two examples of antibiotics that bind to the 30S subunit of prokaryotic ribosomes

A
  • Streptomycin
  • Gentamicin
40
Q

Give an example of antibiotics that bind to the 50S subunit of prokaryotic ribosomes

A
  • Erythromycin
41
Q

Give two example of antibiotics that are metabolic antagonists

A
  • Sulfonamides
  • Trimethoprim
    (interfere with enzymes involved in protein synthesis)
42
Q

Which molecules do sulfonamides compete with to reduce folic acid synthesis in pathogens?

A

p-aminobenzoic acid (PABA)

43
Q

What are some examples of points in protein synthesis which antibiotics can inhibit

A
  • Inhibit polymerase (these can be highly toxic)
  • Inhibit DNA gyrase (quinolones)
  • Block transcription
44
Q

Which class of antibiotics are less selective than the rest with their toxicity?

A
  • 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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