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Microbiology And Immunology > Antibiotics Resistance > Flashcards

Antibiotics Resistance Flashcards

1
Q

What are the potential effects of antibiotic resistance (5)?

A
  1. Increases mortality
  2. Challenges the control of infectious diseases
  3. Threatens a return to the pre-antibiotic era
  4. Increases the costs of health care
  5. Jeopardizes health-care gains to society
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2
Q

Why should drug resistant bacteria not be considered as superbugs?

A

They aren’t more pathogenic -> fewer antibiotic options for treatment

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3
Q

Give an example of antibiotic resistant infection that threatens global
healthcare and how it can further evolve?

A
  • Methicillin resistant Staphylococcus aureus (MRSA)
  • Can further evolve by co-existing with other organisms - co-infection and genetic exchange -> e.g. vancomycin R+ MRSA
  • Another e.g. Enteroccoci: G+ve, Affects gut, Vancomycin, origin - chickens
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4
Q

Describe 6 key paths or targets for antibiotic resistance stating examples? (PART 1)

A
  1. Directed at antibiotic itself (drug inactivation): Degrading the drug, Modifying the drug, e.g. beta-lactamase
  2. New or Altered target (mutation of…): antibiotic no longer binds e.g. PBPs - PBP2a in MRSA
    - e.g. Ribosome • Porin • PBPs - Folic acid peptidoglycan synthesis • DNA gyrase Intrinsic • RNA polymerase impermeability, Mcr1 & colisti
  3. Altered transport: Actively pumping drug out -> efflux pump porins no longer influx drug
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5
Q

Describe 6 key paths or targets for antibiotic resistance stating examples? (PART 2)

A
  1. Metabolic by-pass: metabolic change D-ala-D-lac and vancomycin
  2. Intrinsic impermeability
  3. Overproduction of target e.g. trimethoprim
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6
Q

State the 3 mechanisms of resistance?

A
  • Natural resistance
  • Genetic Mechanisms - acquired
  • Non-Genetic Mechanisms (growth phases): tolerance (can handle a certain amount of AB)
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7
Q

Describe how natural resistance occurs within both G + ve and G-ve bacteria?

A
  • Drug must reach target - natural barriers, porins, export pump
  • G+ve peptidoglycan - highly porus - no barrier to diffusion
  • G-ves outer membrane - barrier - resistance advantage
  • Porins - single mutation - multiple resistance
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8
Q

Describe the two type of acquired genetic mechanisms of Antibiotic resistance? (PART 1)

A
  • Chromosome-mediated
  • A. Due to spontaneous mutation:
  • i. in the target molecule
  • ii. in the drug uptake system
  • Mutants are SELECTED (random); they are NOT induced
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9
Q

Describe the two type of acquired genetic mechanisms of Antibiotic resistance? (PART 2)

A
  • Plasmid-mediated gene exchange
  • Common in Gram-negative bacteria
  • Transferred (a resistant gene) via conjugation
  • Multidrug resistance
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10
Q

Describe the concept behind how bacteria become resistant when using Antibiotics

A
  • As bacteria grows, random mutations can occur which grows itself
  • Targeting the strain of mutations using AB
  • Ends up killing all sensitive organisms except from mutated strain as its resistant to AB
  • Clonal expansion of resistant strains + selection of random mutations
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11
Q

Describe some general features of gene transfer

A
  • Mechanism for genetic heterogeneity and evolution
  • Rapid, cross-species
  • Used for Virulence (toxins), drug resistance, antigens (immune evasion)
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12
Q

Describe the 3 mechanisms of gene transfer

A
  1. Transformation: Bacterial transformation is a process where bacteria take up a fragment of DNA from the environment or another bacterial cell
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13
Q

Describe the 3 mechanisms of gene transfer

A
  • Transduction: The process by which a virus transfers DNA from one bacterium to another.
  • Viruses called bacteriophages (phage) are able to infect bacterial cells and use them as hosts to make more viruses.
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14
Q

Describe the 3 mechanisms of gene transfer

A
  • Conjugation: The process by which one bacterium transfers genetic material to another through direct contact.
  • During conjugation, one bacterium serves as the donor of the genetic material, and the other serves as the recipient, where it transfer via the conjugal tube
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15
Q

State what genes/enzyme can be altered or acquired to cause resistance to beta-lactams in G + ve and G - ve?

A
  • Gram Positive: B-lactamase (Penicillinase), Alteration of the transpeptidase enzyme (PBP)
  • Gram Negative: B-Lactamase (Penicillinase), Alteration of porins
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16
Q

How does penicillinase cause resistance to beta lactams?

A

Destroys the active part of penicillin molecule (beta-lactam ring)

17
Q

What are the drugs of augmentin/co-amoxiclav and state its mechanism of action to cause resistance?

A
  • Augmentin/co-amoxiclav are types of penicillin
  • A combination of Clavulanic acid + Amoxicillin -> inhibits protein synthesis
  • Binds to and inactivates beta-lactamases
  • No anti-bacterial activity of its own
18
Q

State the 4 mechanisms by which beta-lactam resistance arises in G-ve bacteria?

A
  1. Porin mutates or new porin type - Multi-resistant: Pencillin can’t get into cell
  2. PBP - mutates or bacteria acquires a new PBP: Can’t bind
  3. Acquire alternative forms of / mutations in efflux pumps: penicillins are pumped out faster
  4. Bacteria acquires a beta-lactamase enzyme: Cleaves beta-lactam ring - inactivates BL
19
Q

What is the only effective treatment of MRSA and describe its mechanism?

A

Only effective treatment is vancomycin, a 1.5 kDa glycopeptide
- Binds to terminal D-ala D-ala residues, prevents incorporation of subunit into growing peptide glycan, kills cells as it can’t make peptide

20
Q

Describe how vancomycin resistance occurs?

A
  1. Acquisition of van operon (enzymes) by transposition
  2. Drives new metabolic pathway
  3. Makes D-ala-D-lactate (altered target for Vancomycin)
  4. Prevents Vancomycin binding and inhibition
21
Q

State the 2 non-genetic mechanisms of AB resistance? (PART 1)

A
  1. Inaccessibility to drugs (e.g., abscess, TB lesion)
    - Drugs are unable to reach site of infection•
22
Q

State the 2 non-genetic mechanisms of AB resistance? (PART 2)

A
    1. Stationary phase vegetations and biofilms (non-susceptible to inhibitors of cell wall synthesis)
  • a. Overall is in a state of drug tolerance as relevant enzymes that AB target are not being used
  • b. During the stationary phase, cells switch to a survival mode of metabolism. As growth slows, so too does the synthesis of peptidoglycans, proteins, and nucleic-acids; thus, stationary cultures are less susceptible to antibiotics that disrupt these processes.
  • c. By forming a biofilm, bacteria protect themselves from host defense, disinfectants, and antibiotics. Bacteria inside biofilm are much more resistant to antimicrobial agents
  • i. Biofilm is a complex structure of microbiome having different bacterial colonies or single type of cells in a group; adhere to the surface
23
Q

How to prevent/overcome AB resistance?

A
  • Control use: not in animal feeds complete course [DOTS for TB] appropriate prescribing
  • New or modified drugs: few in past 25 years
  • Combination therapy: Allows for different targets, overcome mutation rates
  • Infection control: individual - ward - society
24
Q

How is gonorrhoea treated?

A
  • Switched to single oral dose - cefixime
  • Then i/m ceftriaxone + 1g Azithromycin
  • 125mg -> 250mg -> 500mg increasing MIC
  • 2019 now 1g and no azithro (due to resistance)
  • Can also use Ciproflocaxin (inhibits DNA gyrase), but can cause drug resistance
  • Must monitor short term, patient and public health aspects
25
Q

State the antibiotic used to treat E.coli or klebsiella

A

Carbapenems - broad spectrum antibiotics of last resort for Gram negative bacteria e.g. E.coli or Klebsiella (CREs)

26
Q

How resistance has arised for this?

A
  • New strains destroy antibiotics resistant
  • Acquired a new gene, ndm1
  • Extended spectrum beta lactamase - ESBLS

Microbiology And Immunology (32 decks)

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