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π“œπ‘’π’Ήπ’Ύπ’Έπ’Άπ“ π“œπ’Ύπ’Έπ“‡π‘œπ’·π’Ύπ‘œπ“π‘œπ‘”π“Ž > Antibiotic Resistance > Flashcards

Antibiotic Resistance Flashcards

1
Q

What are the 4 main issues with antibiotic resistance?

A

➝ Increases mortality
➝ Challenges control of infectious diseases
➝ Threatens a return to pre-antibiotic era
➝ increases healthcare costs
➝ Jeopardizes health care gainst to society

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2
Q

What are β€˜superbugs’?

A

➝ Drug resistant bacteria that are not more pathogenic

➝ there are fewer options for treatment

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3
Q

How has S.aureus become resistant to penicillin?

A

➝ by acquiring a new PBP

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4
Q

What do gram +ve pyogenic cocci cause?

A

➝ Surgical sepsis

➝ endocarditis

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5
Q

What are enterococci naturally resistant to?

A

➝ Vancomycin resistant

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6
Q

Where do enterococci live?

A

➝ in the gut

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7
Q

Where do acinetobacter live?

A

➝ in the gut

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8
Q

How do vancomycin resistant MRSA arise?

A

➝ MRSA in the gut
➝ enterococci are vancoymycin resistant
➝ all the bacteria live together in the gut
➝ they exchange genes between each other and vancomycin resistant MRSA can arise

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9
Q

What are the 7 mechanisms of antibiotic resistance?

A 
➝  Mutated target
➝  New target
➝  Efflux pumps
➝  Intrinsic impermeability
➝  Overproduction of target
➝  Metabolic bypass
➝  Drug inactivation
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10
Q

Why is MRSA not inhibited by beta lactams?

A

➝ it has acquired a new penicillin binding protein PBP2A so it is not inhibited by the beta lactam

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11
Q

How do efflux pumps work?

A

➝ new efflux pumps or upregulation of genes that code for efflux pumps
➝ they pump out antibiotics

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12
Q

How does intrinsic impermeability work?

A

➝ Membranes are naturally impermeable that they are resistant to a range of antibiotics without mutations

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13
Q

How does overproduction of the target work?

A

➝ Bacteria can overcome sulfonamides and trimethoprim by overproducing the target
➝ they upregulate genes that code for the enzyme so there is more enzyme than competitive inhibitor

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14
Q

How does metabolic bypass work with vancomycin?

A

➝ Vancomycin binds to terminal D-ala, D-ala
➝ the resistant bacteria have acquired a new biosynthetic pathway
➝ instead of generating D-ala, D-ala it maked D-ala lactate that vancomycin can’t bind to

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15
Q

How does a mutated target work?

A

➝ If RNA polymerase acquires a new mutation then the drug can no longer bind to it so the bacteria is resistant to rifampicin (TB)
➝ mutations in ribosomes and porins
➝ bacteria can acquire a gene for a completely new porin

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16
Q

How does drug inactivation work?

A

➝ beta lactamase destroys beta lactam and inactivates it

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17
Q

What are the mechanisms of natural resistance for gram + and -?

A

➝ Gram +ve peptidoglycan is highly porous and has no barrier to diffusion
➝ Gram -ve outer membrane forms a barrier

18
Q

What is the Lamarck model for antibiotic resistance?

A

➝ Antibiotic is introduced and suddenly all the bacteria mutate

19
Q

What is the right model for antibiotic resistance?

A

➝ There is a random mutation that occurs spontaneously
➝ lots of other mutations occur
➝ as soon as an antibiotic is added
➝ all the bacteria that do not have the mutation die off
➝ the mutants are the ones that are left

20
Q

What are the chromosome mediated genetic mechanisms of antibiotic resistance?

A

➝ spontaneous mutation in the target molecule or the drug uptake system

21
Q

What are the plasmid mediated genetic mechanisms of antibiotic resistance?

A

➝ common in gram -ve rods
➝ transferred via conjugation
➝ multidrug resistance

22
Q

What are the three ways in which bacteria can take up genes?

A

➝ Transformation
➝ Transduction
➝ Conjugation

23
Q

What is transformation?

A

➝ bacteria can take up bacterial DNA that has been lysed

24
Q

What is transduction?

A

➝ bacteria can get infected by viruses (phage)

➝ the phage usually brings a piece of DNA from the previous bacterial host

25
Q

What is conjugation?

A

➝Forming pili through which DNA is exchanged

➝ chromosomal DNA and plasmid DNA can be exchanged

26
Q

How have gram +ve bacteria acquired resistance to beta lactams?

A

➝ Beta lactamase

➝ alteration of transpeptidase enzyme (PBP)

27
Q

How have gram -ve bacteria acquired resistance to beta lactams?

A

➝ alteration of porins

28
Q

What does augmentin/co-amoxiclav do?

A

➝ Binds to and inactivates beta lactamases

29
Q

What is penicillin given with and why?

A

➝ Clavulanic acid
➝ is an inhibitor of a beta lactamase enzyme
➝ allows broad spectrum penicillin to work

30
Q

What are the three ways in which a bacteria can become resistant to beta lactams?

A

➝ If the porin mutates or there is a new type of porin the beta lactam cannot enter
➝ the bacteria can encode a new PBP like MRSA and the beta lactam can’t bind to the new PBP
➝ bacteria can acquire a beta lactamase enzyme

31
Q

What are the 4 ways in which bacteria 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 PBPs so penicillin can’t bind
➝ acquire alternative forms of/or mutations in porins so penicillin can’t get into the cell
➝ acquire alternative forms of/mutations in efflux pumps so penicillins are pumped out faster

32
Q

What is the only effective treatment for MRSA?

A

➝ Vancomycin

33
Q

How is MRSA becoming resistant to vancomycin?

A

➝ Acquisition of the van operon by transposition
➝ makes D-ala D-lactate that prevents vancomycin binding
➝ because vancomycin recognises D-ala, D-ala

34
Q

What are 2 non-genetic reasons that an antibiotic may be resistant?

A

➝ Inaccessibility to drugs

➝ Stationary phase/vegetations and biofilms

35
Q

What kind of antibiotics don’t work on biofilms?

A

➝ inhibitors of cell wall synthesis

36
Q

What kind of diseases are inaccessible to drugs?

A

➝ Abscess

➝ TB

37
Q

What are 4 ways of preventing antibiotic resistance?

A

➝ Control use - not in animal feeds
➝ New or modified drugs
➝ combination therapy
➝ Infection control

38
Q

What was the old treatment for gonorrhoea and why is this not used anymore?

A

➝ single intramuscular injection of penicillin

➝ 15% increase in resistance rates

39
Q

What was the drug used after penicillin for gonorrhoea and why is this not used anymore?

A

➝ Ciprofloxacin (inhibits DNA gyrase)

➝ resistance rates increased

40
Q

What is the new treatment for gonorrhoea?

A

➝ intramuscular injection of ceftriaxone + 1g azithromycin

41
Q

What are carbapenems used for?

A

➝ broad spectrum antibiotics used as a last resort for gram -ve bacteria

42
Q

What are CREs?

A

➝ carbapenem resistant enterococci

π“œπ‘’π’Ήπ’Ύπ’Έπ’Άπ“ π“œπ’Ύπ’Έπ“‡π‘œπ’·π’Ύπ‘œπ“π‘œπ‘”π“Ž (17 decks)

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