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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
NDM-1 is resistant to all antibiotics except what?
Colistin
26
What is the best way to treat CRE bugs?
serine carbapenemase = ceftazidime + avibactam NDM-1/metallo-beta-lactamase = aztreonam
27
What are the aminoglycoside modifying enzyme mechanisms? (3 total)
* acetylation * nucleotidylation * phosphorylation
28
Aminoglycoside-modifying enzyme: they modify the structure by transferring an indicated chemical group to a \_\_\_\_\_\_\_\_\_\_\_; this will impair ______ and/or \_\_\_\_\_\_\_
to a specific side chain impair cellular uptake/binding to ribosome
29
Bifunctional enzyme that modifies aminoglycosides: mainly seen in what bacteria? the enzyme leads to high level resistance to ______ but not \_\_\_\_\_\_\_
mainly seen in ENTEROCOCCI resistance to gentamicin not resistant to streptomycin
30
Resistance mechanisms: What are examples of altered target sites - PBPs?
* *S. Pneumoniae* resistant to PCN and cephalosporins * *Staphylococci* is resistant to methicillin via mecA gene
31
Methicillin resistance is seen in which antibiotics because of what gene?
staphylococci; mecA gene
32
The mecA gene encodes for production of a new PBP that is called \_\_\_\_\_\_.
PBP2A or PBP2'
33
How does vancomycin normally work as an antibiotic?
inhibits cell wall synthesis by binding to D-alanine-D-alanine terminus of pentapeptide (a peptidoglycan precursor)
34
What bacteria is known to have vancomycin resistance through the VanA gene?
*S. Aureus* = VRSA
35
How does the VanA gene cause resistance?
D-Ala-D-**Ala** part becomes D-Ala-D-**Lac** and vancomycin can't bind
36
Altered ribosomal targets lead to resistance in what antibiotics?
* macrolides * azolides * aminoglycosides * tetracyclines * clindamycin
37
Altered DNA gyrase/topoisomerases lead to resistance in which drug class? This resistance is seen in what organisms most?
fluoroquinolones seen in *S. Pneumoniae* and gram-negative
38
What are some drugs that have had reported chromosomal/plasmid mediated resistance with efflux pumps?
* Macrolides/Azolides * Carbapenems
39
What bug has had reported efflux pump resistance to macrolides/azolides?
*S. Pneumoniae*
40
What bug has had reported efflux pump resistance to carbapenems?
*P. Aeruginosa*
41
For *P. Aerugonisa* that's resistant to carbapenems, which carbapenem is best to use? (because it does not get effluxed out)
imipenem
42
Porins will typically allow a drug to go through it when the drug is… * small or large? * more or less negative? * hydrophobic or hydrophillic?
* small * less negative charges (prefers zwitterionic charge) * hydrophillic
43
Mutations in porins are seen most commonly in what organisms?
*Enterobacteriaceae* and *P. Aeruginosa*
44
What resistance mechanisms are most common for beta-lactam drugs?
* hydrolysis (aka beta lactamase) * altered target site * efflux
45
What resistance mechanisms are common for aminoglycosides?
* aminoglycoside modifying enzymes * altered target site * efflux
46
What resistance mechanisms are most common for glycopeptides (aka vancomycin)?
altered cell wall precursors (D-Ala-D-Lac)
47
What organism has intrinsic resistance to beta-lactams?
*Mycoplasma*
48
What organisms have intrinsic resistance to vancomycin?
gram-negative (no peptidoglycan)
49
What organism has intrinsic resistance to cephalosporins?
enterococci
50
What organisms have intrinsic resistance to aminoglycosides?
anaerobes
51
*P. Aeruginosa*: common resistance mechanisms?
* ESBLs * Efflux Pump * Reduced outer membrane permeability
52
*K. Pneumoniae*: common resistance mechanisms?
carbapenemases
53
*E. Coli*: common resistance mechanisms?
ESBL
54
*S. Aureus*: common resistance mechanisms?
* Methicillin resistance (mecA) * Vancomycin resistance
55
Enterococci: common resistance mechanisms?
vancomycin resistance via altered cell wall precursors

PHRM 865 (59 decks)

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