WEEK 11: 11.2 Bacterial Pathogenicity, Growth & Antibiotics Flashcards

(43 cards)

1
Q

What are commensal bacteria?

A

Bacteria that colonise all surfaces of a host i.e. skin, mucosal epithelium of gut, lungs

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2
Q

What benefits do commensals provide to the host?

A

metabolic benefits
protection against pathogens
protection via competition for colonization sites

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3
Q

Can pathogens be commensal? how so?

A

Yes, for eg, S. pneumonia
they can become an opportunistic pathogen in response to immunological insult. for eg. influenza can cause secondary bacterial infection. trauma/tissue damage allows gut commensals to become opportunistic pathogens.

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4
Q

What are primary pathogens?

A

they do not provide any advantage to the host & not part of the normal microbiome. they also damage the host if they evade normal immune responses.

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5
Q

What is a pathogen?

A

an organism whose growth inflicts damage upon the host

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6
Q

describe indirect damage a pathogen can cause

A

the bacteria disturbs metabolic balance/nutrient acquisition

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7
Q

Describe direct damage a pathogen can cause

A

bacteria secretes toxins

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8
Q

What is pathogenesis

A

the mechanism of disease

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9
Q

What is virulence

A

capacity to cause disease/severity of symptoms

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10
Q

Describe the pathogenic cycle

A
  1. transmission from host/reservoir (this is where humans can have the greatest impact by prevention factors like hand-washing)
  2. colonisation (motility, adherence, invasion)
  3. proliferation within host (host provides nutrients for growth, may result in damage via toxins)
  4. evasion of host immune response
  5. can spread further to other hosts
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11
Q

Name some common transmission routes

A
  • Direct contact via bites/wounds/sex
  • Indirect contact via contaminated objects
  • Airborne
  • Facecal
  • Food-borne
  • Zoonotic
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12
Q

What is infectious dose (ID50)

A

the number of bacteria needed to affect 50% of individuals

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13
Q

What is inoculum size?

A

the amount of pathogen an individual is actually exposed to

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14
Q

What are virulence factors?

A

they determine the ID50 of a strain
presence/absence of flagella, fimbriae, toxins influence this

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15
Q

What extraceullaar enzymes are secreted to play a role in pathogenesis?

A

Beta haemolysin, a phospholipase

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16
Q

What is an exotoxin

A

a bacterial toxin in which proteins are made/secreted during bacterial growth

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17
Q

What are the two groupings of exotoxins, describe their function briefly

A

cytolysins - disrupt membrane homeostasis
A-B toxins - disrupt cellular processes

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18
Q

What is an endotoxin?

A

bacterial structural components that have toxic activity
lipid A component causes endotoxic shock
released on death of bacteria

19
Q

What are 3 outcomes of infection?

A
  1. clearance (without apparent disease)
  2. asymptomatic carriage - host is a reservoir and can spread disease
  3. symptomatic disease - high severity and can be followed by clearance, carriage or death
20
Q

What factors can affect the outcome of infection

A

age, immune status, prior exposure, diet, microbiome

21
Q

Describe disease patterns based on timing

A

acute- develops & resolves rapidly
chronic- develops slowly
latent- initially asymptomatic, becomes asymptomatic

22
Q

Describe disease patterns in terms of location

A

local
systemic

23
Q

How do bacterial populations grow?

A

Via binary fission

24
Q

How can optimal binary fission occur?

A

with access to nutrients and appropriate environmental conditions eg. temperature, pH

25
What are the 4 distinct phases of growth , describe them
Lag phase: cells adapt to new conditions, enzymes and new metabolites accumulate- minutes/hours Exponential phase: Maximum constant growth rate. Doubling time may be as short as 10 min Stationary phase: Population reaches very high. Oxygen/nutrient demands cannot be met, growth slows. Slow death of cells is balanced by slow multiplication Death phase: no of viable cells drops sharply. rate of cell death > cell division
26
What are the factors that affect growth
temperature, osmolarity pH
27
How can oxygen requirements differ between bacterial cultures
Some like obligate aerobes require O2 to meet energy demands Some like aerotolerant anaerobe do not use O2 and are unaffected by its presence
28
What are chemotherapeutic agents?
chemical agents used to treat disease, includes killing or inhibiting growth of pathogenic microbes within host.
29
What is the primary mechanisms of action of antimicrobial drugs
they are inhibitors of cell wall synthesis they are protein synthesis inhibitors they are metabolic antagonists they inhibit nucleic acid synthesis, which is essential for bacterial survival
30
Give an example of antibiotics that target cell wall synthesis
cycloserine, penicilin
31
What is the mode of action of penicillin
they bind to proteins involved in peptidoglycan assembly inhibit the last step in bacterial wall synthesis prevent cross linkage of peptidoglycan strands hence synthesis of complete cell walls leading to lysis of cell act only on growing bacteria that are synthesizing new peptidoglycan
32
What do protein synthesis inhbitors do?
they either bind specifically to prokaryotic ribosome & interfere with function, or inhibit a stage of protein synthesis
33
What are metabolic antagonists
sulfonamides, trimethoprim they interfere with enzymes involved in folic acid synthesis
34
How does nucleic acid synthesis inhibition work?
It either blocks DNA replication via inhibition of DNA polymerase/gyrase or blocks transcription via inhibition of RNA polymerase
35
Where can resistance genes be found on
bacterial chromosomes plasmids transposons integrons
36
Resistance genes can be freely exchanged between bacteria on mobile genetic elements via
transformation of chromosomal/plasmid DNA conjugation
37
Explain transformation
transfer of plasmid DNA or a fragment of free DNA from a lysed to a living cell
38
Explain conjugation
transfer of chromosomal/plasmid DNA by direct cell to cell contact
39
Explain transduction
transfer of genes between bacteria by bacterial viruses (bacteriophages)
40
What do resistance plasmids do
they can carry multiple antibiotic resistance genes, are usually transferred to other cells by conjugation & transformation often carry transposons that encode antibiotic resistance genes
41
What do composite transposons do
they contain genes for antibiotic resistance within a cell, they move rapidly between the chromosome & plasmids between cells, they move through a bacterial population
42
What are gene cassettes
sets of resistance genes that can exist as seperate genetic elements and can be part of transposons, integrons or located on bacterial chromosome
43