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835 > Antibiotic Resistance > Flashcards

Antibiotic Resistance Flashcards

1
Q

Bacterial Resistance

A
  • Mutation: small % resistance evoluation
  • Acquisition of bacterial resistance is most common
  • Transfer of genetic material coding for resistance is plasmid (P) or transposon (T) medicated
  • P/T are extrachromosomal pieces of DNA
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2
Q

P

A

Replicate within bacterial cell but limited in transfer between classes

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3
Q

T

A

Not limited but generally must be attached to chromosome, bacteriophage, or plasmid replication

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4
Q

Mechanisms of Resistance

A

Bacteria employ one or more of the basic mechanisms:

  • Enzymatic degradation of the antibiotic agents
  • Alterations of the targets of antibiotic agents
  • Changes in cell wall permeability
  • Production of efflux pumps
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5
Q

Alterations of Antibiotic Targets

A
  • Alteration in PBPs
  • Modified cell wall precursors
  • Alteration of ribosomal targets
  • Alterations in target enzymes
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6
Q

S. aureus - Penicillin Resistance

A
  • B-lactamase mediated
  • Hydrolysis of -cillins
  • Inhibited by B-lactamase inhibitors
  • Referred to as MSSA: prevalence >95%
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7
Q

S. aureus - Oxacillin Resistance

A
  • MecA gene encoding PBP 2a - alteration of PBPs (low affinity)
  • Affects activity of all B-lactams except Ceftaroline (5th generation cephalosporin)
  • Known as MRSA: prevalence 30-50%
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8
Q

VISA

A
  • Vanco-intermediate S. aureus

- Vanco MIC: 4-8 ug/mL

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9
Q

VRSA

A
  • Vanco-resistant S. aureus
  • Vanco MIC >= 16 ug/mL
  • vanA gene noted
  • All VRSA have arisen from MRSA
  • Usually hospital acquired
  • Co-colonization with vanco-resistant E. faecalis has been reported in several cases
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10
Q

E. faecalis/faecium First Line Therapy

A
  • Ampicillin + Gentamicin or Streptomycin
  • Vancomycin + Gentamicin or Streptomycin
  • Linezolid or Daptomycin
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11
Q

Enterococcal Resistance

A
  • Capable of exchanging genetic information with other enterococci and staph.
  • Many resistant genes are plasma-mediated with staph origin: B-lactamases, aminoglycoside modifying enzymes
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12
Q

Enterococcal Resistance + Drugs

A
  • Ampicillin/Penicillin: alteration in PBPs, B-lactamase production
  • Aminoglycosides: high-level of aminoglycoside-modifying enzymes
  • Vanco: Modified cell wall precursors and vanA gene
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13
Q

S. Pneumoniae Resistance + Drugs

A
  • Penicillins: decreased affinity for PBPs
  • Macrolides: methylation of 23S rRNA and efflux pumps (lower level of resistance)
  • Clindamycin: methylation of 23S rRNA
  • Fluoroquinolones: reduced binding affinity for topoisomerase and gyrase
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14
Q

S. pneumoniae - Overcoming Resistance

A
  • High dose PCNs
  • Increased doses of Macrolides (efflux pump)
  • Else, alternative agents
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15
Q

MLS Resistance

A
  • Macrolide-Lincosamide-Streptogramin resistance
  • Methylating enzymes that modify adenine residues on 23S ribosomal RNA
  • Methylated RNA can’t be binded
  • Can be Constitutive or inducible
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16
Q

Constitutive

A

rRNA methylase is always produced

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17
Q

Inducible

A
  • Methylase is produced in the presence of an inducing agent

- Erythromycin is an effective inducer but clindamycin is weaker

18
Q

Ribosomal Alterations

A
  • Aminoglycosides: mutation in 30s ribosomal subunit (streptomycin)
  • Linezolid: G257 6T mutation in domain V of 23S rRNA gene (can possibly revert back after antimicrobial pressure is removed)
19
Q

Enzymatic Degradation

A
  • B-lactamases: classical enzymes, ESBLs, AmpC, carbapenemases, metallo-enzymes
  • Aminoglycosides: acetylase
20
Q

B-lactamase

A
  • Over 340 different types
  • Based on biochemical and genetic properties
  • Plasmid vs chromosomally mediated
  • Constitutive or inducible production based on B-lactam exposure
21
Q

TEM/SHV B-lactamases

A
  • TEM-1, TEM-2, and SHV-1 (Classical)
  • Resistant to ampicillin, amoxicillin, early gen. cephalosporins
  • Later generation cephs resist hydrolysis
  • Inhibitors protect parent B-lactam compound
  • Produced by most enterobacteriaceae
22
Q

ESBLs

A
  • TEM or SHV-type (mutants of classicals)
  • Minor amino acid substitutions
  • Hydrolyze 3rd, 4th gen. cephalosporins and aztreonam
  • Inhibited by B-lactamase inhibitors
  • Carbapenems and cephamycins are spared
23
Q

CTX-M, OXA-Type

A
  • Type of ESBLs
  • CTX-M hydrolyze cefotaxime more efficiently than ceftazidime
  • OXA-type ESBLs mainly in P. aeruginosa
24
Q

AmpC B-lactamases

A
  • Normally produced in low levels by many organisms
  • High-level production can cause resistance to cephamycins, 1st/3rd gen. cephalosporins, monobactams, B-lactamase inhibitors
  • DON’T hydrolyze cefepime or carbapenems
  • Plasmid mediated or chromosomal
25
Q

Cephamycins

A
  • Cefotetan

- Cefoxitin

26
Q

Bacteria w/ Inducible AmpC Resistance (Chromosomal)

A 
S - Serratia marcescens
P  - Pseudomonas aeruginosa, Proteus
A - Acinetobacter baumannii
C - Citrobacter
E - Enterobacter
27
Q

Good AmpC Inducers

A
  • Cefoxitin
  • Imipenem
  • Ampicillin
  • Clavulanate
28
Q

ESBL Characteristics

A
  • Class A
  • BLI inhibited
  • Plasmid based
  • Not chromosomal
  • Not inducible
  • Present in all enterobacteriaceae
29
Q

AmpC Characteristics

A
  • Class C
  • Not BLI inhibited
  • Plasmid or chromosomal based
  • Inducible (when chromosomal)
  • SPACE = > chromosomal and enterobacteriaceae in plasmid involvement
30
Q

Treatment of ESBL/AmpC Producers

A
  • Carbapenems: frequently associated with treatment success
  • Avoid cephalosporins against ESBL
  • Can use cefepime for AmpC
  • ESBL carried on plasmid is also resistant to Bactrim, aminoglycosides, and fluoroquinolones
31
Q

Carbapenemase

A
  • CRE
  • Organisms of the enterobacteriaceae family with a number of transmissible genetic elements with multiple resistant genes
  • EX: KPC, NDH-1, VIM, and IMP
  • Resistant to all 3rd gen. cephalosporins and not susceptible to carbapenems
32
Q

CRE Significance

A
  • CRE associated with 40-50% mortality rates
  • Usually carry other genes that resistance to commonly used antimicrobials
  • Can spread resistance horizontally to common commensal organisms
  • Treatment options: Colistin and Tigecycline
33
Q

P. Aeruginosa

A
  • Resistant to carbapenems

- Related to overproduction of AmpC, less OprD porin channel production, and activation of efflux systems

34
Q

Cell Wall Permeability

A
  • Alterations in porins or channels
  • Associated with Gram-negative bacteria
  • Resistant to macrolides, B-lactams, aminoglycosides, TMP, tetracyclines, and quinolones
35
Q

Production of Efflux Pumps

A
  • Method of resistance

- Resistant to tetracyclines, macrolides, B-lactams, quinolones

36
Q

Altered Permeability + Chromosomal Mutations

A
  • Decrease size of OM porin
  • Increase in amount of smaller narrow OM porins
  • Decrease in specific type of OM porin
  • Alteration in proteins of OM porin producing lower permeability
  • Loss of specific entry channels
37
Q

Quinolone Resistance

A
  • Two mechanisms: alteration in target enzymes or impaired access to target enzymes (pumps/porins)
  • Chromosomal mutations
  • Recent plasmid-mediated resistances have emerged to stop quinolone binding with DNA gyrase
38
Q

AMG Resistance

A
  • Reduced uptake/cell permeability - P.aeruginosa and gram “-“ bacteria
  • Altered ribosome binding sites
  • Enzymatic modification - most common with highest level of resistance
39
Q

AMG + Enzymatic Modifications

A
  • Genes causing modifications usually found on plasmids and transposons
  • Usually found in gram “-“ bacilli with multiple genes
  • Three types of modifying enzymes: AAC, ANT, and APH
40
Q

AAC

A
  • N-acetyltransferases
  • AMG modifying enzyme
  • catalyzes acetyl-CoA-dependent acetylation of an amino group
41
Q

ANT

A
  • O-Adenyltransferases
  • AMG modifying enzyme
  • catalyzes ATP-dependent adenylation of hydroxyl group
42
Q

APH

A
  • O-phosphotransferases
  • AMG modifying enzyme
  • Catalyzes ATP-dependent phosphorylation of a hydroxyl group

835 (27 decks)

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