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Mechanisms of Resistance Flashcards

1
Q

what are the ways of bacteria getting resistant to antibiotics?

A
  • -Sensitive organisms may become resistant by mutation
  • -Some bacteria inherently resistant – may be selected by antimicrobial therapy
  • -Resistant bacteria can transfer resistance remember genetic exchange mechanisms
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2
Q

what are the problems caused by Antimicrobial resistance?

A
  • Some infections untreatable
  • Time lost with inappropriate treatment
  • Increased hospital stay
  • Increased antibiotic use
  • More toxic, less effective, more expensive drugs may be required
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3
Q

what are the factors contributing to resistance

A
  • Antimicrobial use
  • Availability of antimicrobials over the counter
  • Inadequate infection control procedures
  • Overcrowding in healthcare and children facilities
  • Increased travel
  • Increasingly elderly population
  • Unnecessary use of antimicrobials
  • Patient non-compliance e.g. TB
  • A too-short length of therapy
  • Sub-therapeutic dosing
  • Low penetration to body sites
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4
Q

what are the ways of genetic material transfer?

A
  1. Transformation
  2. Transduction
  3. Conjugation
  4. Transposition
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5
Q

what is the bacterial transformation?

A

Uptake of free segments of naked bacterial DNA from the surroundings through the cell membrane (only competent bacteria) → combination of new DNA material with bacterial pre-existing DNA → degradation of unused DNA → expression of the new genes → transformation process
This process can be performed by the following bacteria:
–Neisseria
–Haemophilus influenzae (type b)
–Streptococcus pneumonia

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6
Q

what bacteria are commonly used transformation

A
  • -Neisseria
  • -Haemophilus influenzae (type b)
  • -Streptococcus pneumonia
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7
Q

what is the transduction?

A

Distribution of genetic information by infection of a bacterium with a bacteriophage. Bacteriophages are viruses that only infect bacteria. The infection leads to either the production of a new virus with the destruction of the bacterium (lytic phage) or the integration of phage DNA in the bacterial genome (prophage). The integration of phage DNA can result in uptake of pathogenicity factors.
Transduction happens through either the lytic cycle or the lysogenic cycle. If the lysogenic cycle is adopted, the phage chromosome is integrated (by covalent bonds) into the bacterial chromosome, where it can stay dormant for thousands of generations. If the lysogen is induced (by UV light for example), the phage genome is excised from the bacterial chromosome and initiates the lytic cycle, which culminates in lysis of the cell and the release of phage particles. The lytic cycle leads to the production of new phage particles that are released by lysis of the host.

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8
Q

what is the generalized transduction?

A

Bacteriophage infects bacterium → cleavage of bacterial DNA (this DNA does not incorporate into DNA of infected bacterium) → viral DNA is packaged into phage capsid (bacterial DNA may also be incorporated) → lysis of infected bacteria → new bacteriophage infects other bacteria

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9
Q

what is the specialized transduction?

A

Bacteriophage infects bacteria → viral DNA from the bacteriophage incorporates into the bacterial DNA → bacterial DNA is excised with regions of both viral and bacterial genetic material → combined DNA is packed into phage capsid → lysis of infected bacteria → new bacteriophages infect other bacteria
The genes for the following toxins are transferred from one bacterium to another by specialized transduction:
–Erythrogenic toxin (Streptococcus pyogenes)
–Cholera toxin (Vibrio cholera)
–Diphtheria toxin (Corynebacterium diphtheriae)
–Shiga toxin (Shigella spp.)

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10
Q

what toxin genes are transferred by specialized transduction?

A
  • -Erythrogenic toxin (Streptococcus pyogenes)
  • -Cholera toxin (Vibrio cholera)
  • -Diphtheria toxin (Corynebacterium diphtheriae)
  • -Shiga toxin (Shigella spp.)
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11
Q

what is the bacterial conjugation?

A
  • -Transfer of plasmids (genetic material) by a bridge-like connection between two bacteria
  • -F= fertility factor: bacterial plasmid that enables the transfer of genetic material between bacteria
    1) F+: bacteria with a plasmid that contain genes for sex pilus (to attach to recipient cell) and the F factor; act as donors
    2) F-: bacteria without F factor and sex pilus; act as recipients
    3) F+ bacteria connect with F- bacteria via the sex pilus → a single strand of plasmid DNA (no chromosomal DNA) is transferred from the F+ bacteria to the F- bacteria (mating bridge)
    4) Result: 2 F+ bacteria
  • -Conjugation mediated by Hfr cells (= high-frequency recombination cells)
    1) Hfr cells: bacteria with a conjugative plasmid (e.g., F factor) integrated into their chromosomal DNA
    2) HFr bacteria connect with F- bacteria via the sex pilus → transfer and replication of DNA material on recipient F- bacteria (only the leading part of the plasmid and some adjacent genes are transferred) → F- bacteria have new genes
    3) Result: HFr bacteria and F- cell with new genetic material
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12
Q

what is the bacterial transposition?

A

1) Exchange of genetic information via transposons (jumping genes) within the genome or between genomes of various bacteria
2) Transposons (segments of DNA) within bacteria can copy, insert, reinsert, and excise from different locations along the genetic material of plasmid and chromosomal DNA.
3) Development of antibiotic resistance by creating plasmids with different genetic sequences for resistance
- -Enterococcus (VRE) and Staphylococcus aureus (VRSA) carry the vanA gene that grants vancomycin resistance.

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13
Q

what are the mechanisms of resistance?

A
  1. Inactivation of the agent before it reaches its target e.g. inactivating enzymes
  2. The bacterial cell becomes impermeable to the agent
  3. Bacterial cell able to pump antimicrobial back out
  4. Target altered so it no longer recognizes the antimicrobial (Binding site modification)
  5. Bacteria acquire an alternative metabolic pathway by-passing the site of action
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14
Q

how bacteria acquire resistance to antimicrobials?

A
  1. Mutations on the chromosome

2. Plasmid acquired resistance

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15
Q

what is the pleiotropic mechanism of resistance?

A

The same mechanism encodes resistance to a number of antibiotic classes.
Eg Aminoglycosides + Quinolones + fluoroquinolones

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16
Q

what are the steps to prevent resistance in hospitalized patients?

A

1) prevent transmission
- -contain the contagion
- -isolate the pathogen
2) use antimicrobials wisely
- -stop treatment when cured
- -know when to say no to Vanco
- -treat infection, not colonization/contamination
- -use local data of resistance
- -practice antimicrobial control
3) diagnose and treat effectively
- -access the experts
- -target the pathogen
4) prevent infection
- -get the catheters out
- -vaccination

17
Q

what are the modes of resistance to the β-lactam Antimicrobial Agents

A 
Drug Exclusion (Don’t Let It In)
Drug Evasion (Change the Goal Posts)
Drug Elimination (Inactivating Enzymes)
18
Q

what are the enzymes that are used by bacteria to inactivate antibiotics

A
  1. beta-lactamases produced by Gram-positive and -negative organisms (plasmid or chromosomal)
  2. Aminoglycoside-modifying enzymes-add chemical groups to the antibiotic altering its structure and interferes with its transport.
19
Q

how does beta-lactamase work?

A
  1. beta-lactamases produced by Gram-positive and -negative organisms (plasmid or chromosomal)
  2. aminoglycoside-modifying enzymes-add chemical groups to the antibiotic altering its structure and interferes with its transport.
20
Q

what is the ESBL

A

ESBLs are extended-spectrum b-lactamases, produces by some Gram-negatives (eg E. coli, P. aeruginosa) that can destroy many b-lactam antibiotics (eg penicillin,1st, 2nd, 3rd generation cephalosporins)—antibiotic preparation that includes a b-lactamase inhibitor (eg Co-amoxiclav).

21
Q

what is carbapenemase?

A
  • -Carbapenems are b-lactams that can’t be destroyed by ESBLs (eg meropenem)
  • -However, some Gram-negatives (eg some E. coli, some K, pneumoniae) produce carbapenemases that destroy carbapenems—Carbapenemase Producing Enterobacteriaceae (CPE)
22
Q

how impaired permeability confers antibiotic resistance?

A
  • If permeability is impaired, the agent cannot penetrate as well
  • changes in OM porins (Gram-negs) or CM transport proteins
  • can make it harder for some antibiotics to gain entry
23
Q

give an example of bacteria with impaired permeability to antibiotics

A

e.g. gentamicin resistance and P. aeruginosa

24
Q

do bacteria require ATP to pump out antibiotics

A

energy-dependent

  • -It can pump it back out so that it does not accumulate or reach its target.
  • -new proteins synthesized to facilitate removal – drug pumped out of cell e.g. tetracycline-resistance or quinolone-resistance in Gram-negative bacteria.
  • -This is an energy-dependent process powered by ATP.
25
Q

how bacteria modify antibiotic targets to avoid its action?

A

The antimicrobial agent does not bind as well due to modification at the binding site of the target
• Altered penicillin-binding protein PBP2’ and MRSA, PBP2’ has lower affinity for penicillin

26
Q

give an example of bacteria that modifies their targets

A

Resistance to macrolides which target the 50S ribosomal subunit
• Streptomycin binds to the 30S ribosomal subunit, amino acid change can prevent binding.

27
Q

how bacteria bypass some metabolic pathways to be resistant to antibiotics

A
  • Described for sulphonamides and trimethoprim
  • These antibiotics inhibit enzymes involved in tetrahydrofolate synthesis
  • Bacteria can activate new metabolic pathways for the production of tetrahydrofolate (purines) even in the presence of agents
28
Q

what are the modes of resistance to aminoglycosides

A
  • Aminoglycoside-modifying enzymes – agent inactivated

- High-level aminoglycoside resistance mediated by methylation of 16S ribosomal RNA – target of agent modified

29
Q

what are the modes of resistance to quinolones?

A

1)Mutations in DNA gyrase/topoisomerase – target modification
2)by agent
3)Plasmid-mediated mechanisms
–Qnr genes- target protected by adding chemical groups
–Efflux pumps
–Aac(6’)-lb-cr

30
Q

what are the PBPs

A

A group of bacterial proteins that are essential for cell wall synthesis. They function as transpeptidases, permitting crosslinking of peptidoglycan within the cell wall. Virtually all beta-lactam antibiotics function by inhibiting penicillin-binding proteins.

31
Q

what are the beta-lactamase inhibitors?

A

Beta-lactamases, which are usually produced by gram-negative and anaerobic organisms, can split the beta-lactam ring and render certain beta-lactam antibiotics ineffective.
Beta-lactamase inhibitors increase the spectrum of antibiotic activity.
Drugs
–Clavulanic acid (combined with amoxicillin = co-amoxiclav)
–Sulbactam (combined with ampicillin)
–Tazobactam (combined with piperacillin)

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