Antibiotic Resistance Flashcards

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1
Q

Antibiotic resistance bacteria

A
  • Not more pathogenic than normal bacteria but there is less antibiotics to treat them
  • We have some in our body that do not cause disease:
    • > Enterococci which is G +ve, lives in the gut is resistant to vancomyocin.
    • > Acinetobacter which is G -ve, lives in the gut is resistant to multiple drugs
    • > MRSA which is G +ve, lives in the gut and wound but isn’t resistant.
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2
Q

How is the superbug formed?

A

Combination of antibiotic resistant bacteria that although individually do not cause disease, because they all live together they are able exchange genetic material which leads to co-infection leading to vancomyocin resistant MRSA.

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3
Q

6 mechanisms of antibiotic resistance

A
  • Drug inactivation
  • Mutated/altered target or acquisition of a new target
  • Mutated or new porins
  • Intrinsic impermeability - NATURAL
  • Overproduction of target
  • Metabolic by pass - D-ala
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4
Q

Drug inactivation - beta lactam enzymes

A
  • The bacteria acquires an enzyme which breaks down the drug or the active component of the drug.
  • For example; acquires an enzyme which breaks down the beta lactam ring in the beta lactams and therefore the drug can no longer inhibit cell wall formation
  • A lot of bacteria has this resistance
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5
Q

Mutated/altered target or acquisition of a new target

A
  • RNA pol can get mutated which means the drug can no longer bind to it. this happens in romaficin resistant TB
  • Can get acquisition of a new target protein/enzyme such as in MRSA when it gets a new PBPIIA meaning the beta lactam can no longer bind and inhibit cell wall formation.
  • Can get mutation in the DNA gyrase enzyme, meaning again the drug such as Quindilones isn’t able to bind and inhibit coiling and uncoiling.
  • Mutation in ribosomal RNA means the drug won’t be able to block the protein synthesis.
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6
Q

Mutated or new porins

A
  • The antibiotics needs porins in order to enter Gram -ve bacteria and the bacteria is able to exchange genes and acquire genes for a completely new porin.
  • This means the drug will no longer be able to enter or if it does the bacteria can pump it out via the porin.
  • They can also acquire efflux pump which pump out all the intracellular components the bacteria doesn’t want including antibiotics and therefore the MIC will never be reached.
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7
Q

Intrinsic impermeability

A
  • This is a natural mechanism some bacteria such as G -ve bacteria have, they DO NOT ACQUIRE MUTATION
  • They have impermeable outer membranes which means they are resistant to a lot of bacteria such as celosia which causes UTI and pseudomonas which causes cystic fibrosis.
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8
Q

Overproduction of target

A
  • The bacteria can upregulate the genes for the enzymes and their natural substrate so despite the antibiotic acting as a competitive inhibitor the natural substrate is able to bind and the bacteria is able to continue making folic acid
  • They can also upregulate the metabolic pathway that increases the synthesis of the natural synthesis for example for folic acid
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9
Q

Metabolic by pass - D-ala

A
  • Bacteria can acquire a whole set of new genes that encode a whole different biosynthetic pathway which is different to D-ala on peptidoglycan so the beta lactam is no longer able to work.
  • They can generate D-lac which is different and therefore leads to vancomyocin resistance
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10
Q

How do you get acquired mutations?

A
  • Via chromosomes acquisition of genes

- Via plasmid acquisition of genes

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11
Q

Explain how mutations are acquired via chromosomes acquisition of genes

A
  • Bacteria replicate at a high rate and therefore they are likely to acquire a large number of mutants.
  • If by chance one of these mutations is antibiotic resistance, under the pressure of antibiotic usage, this mutation will be selected for.
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12
Q

Explain how mutations are acquired via plasmid acquisition of genes

A

Common in G -ve, transferred via conjugation and multi-drug resistance

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13
Q

How does gene transfer in bacteria occur?

A

Through heterogenicity and evolution. The rapid cross species exchange leads to formation of new toxins, drug resistance and immune evasion.

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14
Q

3 ways the gene transfer in bacteria can occur

A
  1. Transformation: uptake naked DNA from a bacterium that has lysed into another healthy bacteria for example in Streptoccoi
  2. Transduction: Bacteria gets infected with a phage (virus) and the virus would’ve contained the DNA from a lysed bacterium
  3. Conjugation: This is when 2 bacteria come together to form a bridge called pili and exchange chromosomal and plasmid DNA.
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15
Q

G+ ve in beta lactam resistance

A
  • Acquire beta lactamase enzymes such as Penicilinase which means they are destroying the beta lactam ring and the 3D structure of the drug.
  • Acquire alteration in the transpeptidase enzyme such as PBP
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16
Q

G -ve in beta lactam resistance

A
  • Acquire beta lactamase enzymes such as Penicilinase which means they are destroying the beta lactam ring and the 3D structure of the drug.
  • Acquire alteration in the transpeptidase enzyme such as PBP
  • Acquire alteration in porins
17
Q

How is beta lactam resistant bacteria overcome?

A

Combination of Augmentin/Co-amoxiclav is able to overcome the bacteria which contain beta lactamase and hence are resistant to beta lactams

  • Amoxicillin is a broad spectrum beta lactam and Clavulanic acid is an inhibitor of the beta lactamase enzyme
  • Therefore, together they are a very potent antibiotic
18
Q

How do bacteria which do not acquire mutation have resistance?

A
  • Inaccessibility to drug - the drug isn’t able to access the infected areas such as in TB
  • Stationary phase - bacteria grow on the organ such as in endocarditis, they form a polysaccharide so the antibiotic cannot enter
19
Q

How to prevent antibiotic resistance?

A
  • Control use
  • Come up with new drugs
  • Come up with combination therapy
  • Have infection control