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Medical Microbiology > Antibiotic Resistance > Flashcards

Antibiotic Resistance Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q
  1. Should antibiotic resistance be a very big concern for us? If so, why?
A

Yes it should be!!
There are many consequences of antibiotic resistance , such as:
->Increases mortality
->challenges control of infectious diseases
->threatens a return to the pre-antibiotic era
->increases the costs of health care
->jeopardizes health-care gains to society

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2
Q
  1. Is bacteria that are resistant to antibiotics a superbug?
A

nope!
Because a bacteria is resistant to antibiotics it means that its more difficult to treat DOES NOT mean that it is more virulent or the presentation of the disease is worse

Dont use this superbug term

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3
Q
  1. Explain briefly the history of methicillin resistant Staphylococcus aureus?
A

pre-antibiotics = poor prognosis
(1947) Penicillin worked so well for about 5 years but then because it was used so much , 70% of Staphylococcus aureus was resistance to Penicillin, years later had multiple resistance to pen, strep, Cap, tet
1960- Methicillin ( used to treat Staphylococcus aureus ) worked well for around 15 yrs.’ and then we got MRSA – methicillin resistant Staphylococcus Aureus by acquiring a NEW penicillin binding protein , no longer competitively inhibited by methicillin

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4
Q
  1. Explain how we get MRSA that is also Vancomycin resistant?
A

Enerococci live in our gut (they are G+ve) , they are naturally Vancomycin resistant . Not causing infection though

Acinetobacters G-ve, in our gut too and have multiple resistance

MRSA G-ve also live in our gut

So these bacteria all exchange genes so co-infection and genetic exchange = Vancomycin Resistant MRSA – Enterococci swapped genes with MRSA.

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5
Q
  1. What are the 6 main mechanisms in which bacteria can become resistant to antibiotics?
A
  1. Drug Inactivation
  2. Metabolic by-pass
  3. Altered or new target
  4. Efflux Pump
  5. Overproduction of target
  6. Intrinsic Impermeability
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6
Q
  1. How does drug inactivation result in antibiotic resistance?
A

Bacteria have acquired enzymes called Beta Lactamase that will destroy the beta lactam ring in antibiotics (eg penicillin’s and cephalosporins) , so they will be resistant to a lot of beta lactams

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7
Q
  1. How will an altered/mutated target or the acquisition of a new target result in antibiotic resistance?
A

Many antibiotics have one target for e.g. Rifampicin targets RNA polymerase, so if there is a slight mutation in that RNA polymerase then the antibiotic wont be able to target that target . A lot of rifampicin resistant TB because of these mutations. Or mutations in Ribosomes ,Porins ,DNA Gyrase.
Also can get a new target – MRSA has acquired a new penicillin binding protein ( PBP 2a) . Or an acquired new porin completely

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8
Q
  1. What kind of changes to the efflux pump in bacteria can result in antibiotic resistance?
A
  • > Bacteria can have up-regulation of efflux pumps or acquire completely new efflux pumps
  • > These are pumps that sit in the bacterial cell membrane that pump out antibiotics
  • > So more activity so antibiotics cant really accumulate in the cell
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9
Q
  1. How does an impermeability membrane give resistance to antibiotics?
A

->Some bacteria we can intrinsically resistant- membranes are so impermeable , don’t allow antibiotics through. Very resistant . Naturally impermeable (didn’t mutate or acquire genes)

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10
Q
  1. How does overproducing the target of the antibiotic, create resistance?
A

The bacteria can overproduce enzymes (for eg in folic acid , overproduce enzymes needed to produce folic acid or the precursor PABA) so that there is more enzyme than the competitive inhibitor of the antibiotic .

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11
Q

11 . What kind of metabolic by pass would allow for antibiotic resistance?

A

Vancomycin works by breaking down peptidylglycans by targeting the terminal D-Ala, D-Ala, so some bacteria have developed a metabolic by pass where they code for a terminal D-Ala, D-Lac now so that Vancomycin cant bind and interrupt the process

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12
Q
  1. What are the three main types of antibiotic resistance?
A

Natural resistance

Genetic Mechanisms - acquired

Non-Genetic Mechanisms (growth phases)

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13
Q
  1. What are some ways a bacteria can be naturally resistant to an antibiotic?
A
  • > So obviously the drug must reach the target to have an effect, so the bacterium can have natural barriers, porins and export pumps to prevent the drug getting to the drug
  • > G+ve bacteria have the peptidoglycan layer which is highly porous (antibiotics can pass through)
  • > G-ve have an outer membrane which acts as a barrier and gives a resistance adavantage
  • > Mutation in porins (antibiotic target) then multiple resistance
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14
Q
  1. What are the two types of genetic mechanisms of antibiotic resistance?
A
  1. Chromosome Mediated

2. Plasmid-Mediated

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15
Q
  1. What is chromosome mediated antibiotic resistance?
A

Because bacteria replicate so often they have lots of spontaneous mutations – out of these a few will contain a gene that will make it resistant to antibiotics. If there is a continued use of antibiotics, these spontaneous mutations will be selected for (not induced by the bacteria) and so they will grow and survive and reproduce. Very important to grasp that the bacteria doesn’t intentionally make these resistant forms, they happen by chance and because of continued antibiotic use these resistant bacteria get selected for.

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16
Q
  1. What is plasmid mediated antibiotic resistance?
A

Common in Gram-negative rods
Transferred via conjugation
Multidrug resistance

17
Q
  1. What are the three ways that bacteria can transfer genes ?
A
  1. Transformation (Uptake of DNA from another bacteria that has been lysed )
  2. Transduction ( Fragment of DNA from another bacterial cell - phage’s previous host transferred to next host)
  3. Sex (conjugation. DNA and plasmid DNA passed through sex pili, not all bacteria can conjugate)
18
Q
  1. How can G+ve bacteria be resistance to beta lactam antibiotics (eg penicillins and cephalosporins)
A
  • > Have an enzyme beta-lactamase which breaks down beta lactam ring
  • > Alteration of the transpeptide enzyme PBP so that cant be targeted by eg vancomycin
19
Q
  1. How can G-ve bacteria be resistance to beta lactams?
A
  • > Has beta lactamase enzyme which degrades beta-lactam ring
  • > ALTERED porins
20
Q
  1. What is special about the drug Augmentin - why is it like ths?
A

We can combine drugs for eg Augmentin contains both Clavulanic acid (a beta lactamase inhibitor) and Amoxicillin ( a beta lactam – a broader spectrum penicillin)
Clavulanic acid contains no anti-bacterial activity of its own , it just inactivates the beta lactamases so that amoxicillin can do its job

21
Q
  1. The usual mechanisms by which antibiotics can act on G-ve bacteria is
  2. Entry through porins
  3. Binds to penicillin binding protein (PBP) which prevents peptidlycan formation
  4. Autolytic enzymes introduced
  5. Bacteria dies

PLEASE list the different ways in which a resistance bacteria can counteract the above steps?

A
  1. Porin mutates or new porin type
    Multi-resistant
  2. PBP - mutates or bacteria
    acquires a new PBP eg PBP2a

.3. bacteria acquires a
beta-lactamase enzyme= no longer a structural mimic

22
Q
  1. List 4 mechanisms by which bacteria can become resistant to penicillin?
A

Produce penicillinases / beta lactamases that cleave the beta lactam ring
- penicillin is inactivated

Acquire alternative forms of / or mutations in penicillin binding proteins (PBPs) - penicillin can’t bind

Acquire alternative forms of / mutations in porins,
- penicillin cannot get into cell

Acquire alternative forms of / mutations in efflux pumps
- penicillins are pumped out faster

23
Q
  1. What is the only effective treatment of MRSA ( methicillin resistant Staph aureus) ?
A

Only effective treatment is vancomycin,

a 1.5 kDa glycopeptide

24
Q
  1. How can bacteria become vancomycin resistant?
A

Bacteria can acquire a van operon by transposition
This makes the usual D-ala, D-ala —–> into D-ala,D-lactate . This prevents vancomycin binding and so it cant prevent peptidoglycan formation

25
Q
  1. What are the two main types of non-genetic mechanisms to cause resistance?
A
  1. inaccessibility to drugs ( Certain situations are very difficult to get the drug to the correct site for eg Deep wound abscess’s or Lesions in TB)
  2. Stationary Phase/Vegetations and Biofilms (non-susceptible to inhibitors of cell wall synthesis)
26
Q
  1. What are some ways we can prevent antibiotic resistance?
A
  1. Complete Course
  2. New or modified drugs
  3. Combination therapy
  4. Infection Control
27
Q
  1. Explain the history of resistance of Neisseria Gonorrhoea?
A

First we use to treat it with a single shot of penicillin
Soon we got penicillin resistant
Then we used Ciprofloxacin
Then it gained resistance to that
Then used Cefixime
Now we use Ceftriaxone and Azithromycin
Had to increase dose to deal with increasing MIC

28
Q
  1. What are Carbapenems?
A

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

New strains destroy antibiotics  resistant

  • acquired a new gene, ndm1
  • extended spectrum beta lactamase - ESBLs

Medical Microbiology (15 decks)

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