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PHRM 865 > Resistance (Kays) > Flashcards

Resistance (Kays) Flashcards

1
Q

What are PBPs?

A

penicillin-binding proteins; the enzymes vital for cell wall synthesis, cell shape, and structural integrity

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2
Q

What is the most important PBP and why?

A

transpeptidase
it catalyzes final cross link between sugar and peptide in peptidoglycan molecule

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3
Q

What are the 3 types of genetic exchange that lead to resistance?

A
  1. conjugation
  2. transduction
  3. transformation
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4
Q

What is conjugation?

A

direct contact or mating via sex pilli (most common)

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5
Q

What is transduction?

A

genes transferred via bacteriophages (viruses) between bacteria

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6
Q

What is transformation?

A

uptake of “free floating” DNA from the environment then gets integrated into the hosts DNA

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7
Q

Plasmids or transposons:

  • transferred from organism to organism
  • self-replicating
  • extrachromosomal DNA
A

plasmid

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8
Q

What are the 3 main mechanisms of bacterial resistance?

A
  1. enzymatic inactivation
  2. alteration of target site
  3. altered permeability of bacterial cell
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9
Q

Give examples of antibiotic resistance via enzymatic inactivation.

A
  • beta-lactamases
  • aminoglycoside-modifying enzyme
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10
Q

Give examples of antibiotic resistance via alteration of the target site.

A
  • PBPs
  • cell wall precursors
  • ribosomes
  • DNA gyrase/topoisomerase
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11
Q

Give examples of antibiotic resistance via altered permeability of the bacterial cell.

A
  • efflux pumps
  • porin changes
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12
Q

What are beta-lactamases and how do they work?

A

they inactivate beta-lactam antibiotics by hydrolyzing/splitting the amide bond

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13
Q

What gene in beta lactamases are we expected to know?

A

AmpC

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14
Q

Which bacteria typically contain AmpC?

A

SPICE

(serratia, pseudomonas, indole-positive proteus, citrobacter, enterobacter)

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15
Q

What drugs are beta-lactamase inhibitors?

A
  • tazobactam
  • clavulanic acid
  • sulbactam (resistance to the SPICE organisms has happened)
  • avibactam (lactamase inhibited in SPICE by this drug does happen)
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16
Q

How is AmpC induced?

A

the gene is normally repressed; when a beta-lactam is present, the gene gets DEREPRESSED which causes beta-lactamase production

when inducer is removed, the gene gets repressed again

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17
Q

What antibiotics are strong inducers of AmpC?

A
  • Penicillin G
  • Ampicillin
  • 1st gen cephalosporins
  • Cefoxitin
  • Clavulanic acid = potent inducer of AmpC beta-lactamases
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18
Q

SPICE are typically constitutively making beta-lactamases… what antibiotics should we avoid using because of developed resistance?

A

avoid 3rd generation cephalosporins

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19
Q

ESBLs are seen most frequently in what bacteria?

A
  • K. pneumoniae
  • E.Coli
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20
Q

ESBLs are _____ mediated and tend to hydrolyze _______ and ______.

A

plasmid mediated;
hydrolyze PCNs and cephalosporins

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21
Q

What drug may be useful for the CTX-M enzyme of ESBLs?

A

tazobactam

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22
Q

What is normally the treatment of choice for ESBLs?

A

carbapenems

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23
Q

What are the 3 most important carbapenemases?

A
  • KPC (klebsiella pneumoniae carbapenemase)
  • OXA-type (seen in acinetobacter)
  • NDM (New Dehli metallo-beta-lactamases)
24
Q

True or false: CRE can last in the body for a maximum of 6 months.

A

False; carbapenemase-resistant enzymes can last in the body for 12 months (bacteria can get spread allllll over)

25
Q

NDM-1 is resistant to all antibiotics except what?

A

Colistin

26
Q

What is the best way to treat CRE bugs?

A

serine carbapenemase = ceftazidime + avibactam

NDM-1/metallo-beta-lactamase = aztreonam

27
Q

What are the aminoglycoside modifying enzyme mechanisms? (3 total)

A
  • acetylation
  • nucleotidylation
  • phosphorylation
28
Q

Aminoglycoside-modifying enzyme:
they modify the structure by transferring an indicated chemical group to a ___________;
this will impair ______ and/or _______

A

to a specific side chain
impair cellular uptake/binding to ribosome

29
Q

Bifunctional enzyme that modifies aminoglycosides:
mainly seen in what bacteria?
the enzyme leads to high level resistance to ______ but not _______

A

mainly seen in ENTEROCOCCI
resistance to gentamicin
not resistant to streptomycin

30
Q

Resistance mechanisms:
What are examples of altered target sites - PBPs?

A
  • S. Pneumoniae resistant to PCN and cephalosporins
  • Staphylococci is resistant to methicillin via mecA gene
31
Q

Methicillin resistance is seen in which antibiotics because of what gene?

A

staphylococci; mecA gene

32
Q

The mecA gene encodes for production of a new PBP that is called ______.

A

PBP2A or PBP2’

33
Q

How does vancomycin normally work as an antibiotic?

A

inhibits cell wall synthesis by binding to D-alanine-D-alanine terminus of pentapeptide (a peptidoglycan precursor)

34
Q

What bacteria is known to have vancomycin resistance through the VanA gene?

A

S. Aureus = VRSA

35
Q

How does the VanA gene cause resistance?

A

D-Ala-D-Ala part becomes D-Ala-D-Lac and vancomycin can’t bind

36
Q

Altered ribosomal targets lead to resistance in what antibiotics?

A
  • macrolides
  • azolides
  • aminoglycosides
  • tetracyclines
  • clindamycin
37
Q

Altered DNA gyrase/topoisomerases lead to resistance in which drug class?
This resistance is seen in what organisms most?

A

fluoroquinolones
seen in S. Pneumoniae and gram-negative

38
Q

What are some drugs that have had reported chromosomal/plasmid mediated resistance with efflux pumps?

A
  • Macrolides/Azolides
  • Carbapenems
39
Q

What bug has had reported efflux pump resistance to macrolides/azolides?

A

S. Pneumoniae

40
Q

What bug has had reported efflux pump resistance to carbapenems?

A

P. Aeruginosa

41
Q

For P. Aerugonisa that’s resistant to carbapenems, which carbapenem is best to use? (because it does not get effluxed out)

A

imipenem

42
Q

Porins will typically allow a drug to go through it when the drug is…

  • small or large?
  • more or less negative?
  • hydrophobic or hydrophillic?
A
  • small
  • less negative charges (prefers zwitterionic charge)
  • hydrophillic
43
Q

Mutations in porins are seen most commonly in what organisms?

A

Enterobacteriaceae and P. Aeruginosa

44
Q

What resistance mechanisms are most common for beta-lactam drugs?

A
  • hydrolysis (aka beta lactamase)
  • altered target site
  • efflux
45
Q

What resistance mechanisms are common for aminoglycosides?

A
  • aminoglycoside modifying enzymes
  • altered target site
  • efflux
46
Q

What resistance mechanisms are most common for glycopeptides (aka vancomycin)?

A

altered cell wall precursors (D-Ala-D-Lac)

47
Q

What organism has intrinsic resistance to beta-lactams?

A

Mycoplasma

48
Q

What organisms have intrinsic resistance to vancomycin?

A

gram-negative (no peptidoglycan)

49
Q

What organism has intrinsic resistance to cephalosporins?

A

enterococci

50
Q

What organisms have intrinsic resistance to aminoglycosides?

A

anaerobes

51
Q

P. Aeruginosa: common resistance mechanisms?

A
  • ESBLs
  • Efflux Pump
  • Reduced outer membrane permeability
52
Q

K. Pneumoniae: common resistance mechanisms?

A

carbapenemases

53
Q

E. Coli: common resistance mechanisms?

A

ESBL

54
Q

S. Aureus: common resistance mechanisms?

A
  • Methicillin resistance (mecA)
  • Vancomycin resistance
55
Q

Enterococci: common resistance mechanisms?

A

vancomycin resistance via altered cell wall precursors

PHRM 865 (59 decks)

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