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Year 5 Microbiology > 2: Antimicrobials 1 > Flashcards

2: Antimicrobials 1 Flashcards

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1
Q

3 targets of antimicrobials

A

Peptigolycan layer of cell wall

Inhibition of bacterial protein synthesis

DNA gyros and other prokaryote specific enzymes

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2
Q

what are the 2 types of inhibitors of cell wall synthesis and examples of them, differences

A

B-lactam abx = penicillins, cephalosporins, carbapenems

  • Broad spectrum

Glycopeptides = vancomycine, teicoplanin

  • Gram +ve
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3
Q

Gram +ve vs Gram -ve

A

Gram-positive cell wall – thick peptidoglycan cell wall (made of NAG and NAM components)

Gram-negative cell wall – thinner peptidoglycan cell wall, outer membrane conferring resistance to some antibiotics

  • Can be more resistant and harder to treat due to outer membrane
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4
Q

How do B-lactams work?

A

Inactivate enzymes involved in terminal stages of cell wall synthesis = transpeptidases / penicillin binding proteins

  • Beta lactam is a structural analogue of the enzyme substrate

Bactericidal (active against rapidly dividing bacteria) – if cell wall has already been formed, they haveno effect**

  • Ineffective against bacteria lacking peptidoglycan cell walls (mycoplasma, chlamydia)
  • Cause cell lysis
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5
Q

Give examples of penicillins (5)

A

Penicillin

Amoxicillin

Flucloxacillin

Piperacillin

Clavulanic acid + amoxicillin (co-amoxiclav) and tazobactam (tazocin/piptazobactam)

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6
Q

Penicillin

A

gram +ve, streptococci, clostridia

  • Broken down by beta lactamase (produced by SA and many other gram -ve organisms)
  • Allergy – need to get a clear history
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7
Q

Amoxicillin

A

broad-spectrum (enterococci to gram -ve)

  • Broken down by beta lactamase (produced by SA and many other gram -ve organisms)
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8
Q

Flucloxacillin

A

SA

  • Not broken down by beta-lactamase produced by SA
  • Similar to penicillin, less reactive
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9
Q

Piperacillin

A

broad-spectrum (pseudomonas, non-enteric gram -ve)

  • Broken down by beta lactamase (produced by SA and many other gram -ve organisms)
  • Similar to amoxicillin
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10
Q

Co-amoxiclav and tazobactam

A
  • Clavulanic acid = beta lactamase inhibitors → protect penicillin from enzymatic breakdown
  • Increase coverage to include SA, gram -ve (i.e. E. coli), anaerobes
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11
Q

What bacteria (G+ve) produced b-lactamase?

A

Staph aureus

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12
Q

Give examples of cephalosporins (4)

A

Cefuroxime

Ceftriaxone

Ceftazidime

Cefotaxime

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13
Q

Cefuroxime

A
  • Stable to many beta lactamases made by gram -ve
  • Similar cover to co-amox (less active against anaerobes)
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14
Q

Ceftriaxone

A
  • Associated with C. difficile
  • Treat meningitis (IM ceftriaxone)
  • NO COVER against Pseudomonas
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15
Q

Ceftazidime

A
  • Activity against pseudomonas (HAIs often)
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16
Q

Cefotaxime

A

The paediatric ceftriaxone

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17
Q

Give examples of Carbapenems

A

Meorpenem, imipenem, ertapenem (STABLE TO ESBL enzymes)

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18
Q

Give an example of monobactams

A

carumonam

19
Q

Key features of beta lactase

A
  • Relatively non-toxic
  • Renally excreted so decrease dose if renal impairment
  • Short T1/2 (many are type 2 drugs so aim to maximise the time > MIC)
  • Will not cross BBB
  • Cross allergenic – penicillin has 10% cross reactivity with cephalosporins and carbapenems
20
Q

Glycopeptides

A

Active against gram +ve (inhibit cell wall synthesis)

  • Large molecules so unable to penetrate gram -ve

Important uses:

  • MRSA infections (IV)
  • C. difficile infection (oral – Vancomycin, teicoplanin)

Slowly bactericidal

Nephrotoxic – must monitor for accumulation

21
Q

Gove 5 examples of inhibitors of protein synthesis

A

Aminoglycosides

Tetracyclines

Macrolides

Chloramphenicol

Oxazolidinones

22
Q

Give 3 examples of aminoglycosides

A

Gnetamicin, amikacin, tobramycin

G-ve action

23
Q

Aminoglycoside MoA

A
  • Bind to amino-acyl site of 30s ribosome subunit
  • Rapid, concentration-dependent bactericidal
  • Require specific transport mechanisms to enter
    • Accounts for some intrinsic resistance
    • Ototoxic and nephrotoxic – monitor levels
    • Gentamicin and tobramycin are particularly active against pseudomonas aeruginosa
    • Synergistic combination with beta lactams
      • Endocarditis treatment, pneumonia
    • No activity against anaerobes
24
Q

tetracylines MoA

A

Broad spectrum, activity against intracellular pathogens – chlamydia, rickettsia, mycoplasma

Bacteriostatic (stops bacteria from reproducing)

Widespread resistance now

Deposited in growing bone

  • Don’t give to children, pregnant women
  • SE: photosensitivity rash (summer effect)

TETRACYLINE, DOXYCYCLINE

25
Q

Give examples of Macrolides and their MoA

A

Erythromycin**, **lincosamides** – **clindamycin**, **streptogramins** – **synercid** – **MLS group

  • Bacteriostatic
  • Useful agent for treating mild staphylococcal or streptococcal infections in pen-allergic patients
  • Active against campylobacter species, legionella, pneumophilia
  • Newer agents include clarithromycin and azithromycin due to a better half-life
  • Little activity against gram -ve bacteria (membrane)

Useful to inhibit toxins produced by bacteria

26
Q

Chloramphenicol use and MoA

A

(if pen-allergic, used for meningitis)

  • Bacteriostatic
  • Broad antibacterial activity
  • Rarely used apart from eye preparations
    • Risk of aplastic anaemia
    • Risk of grey-baby syndrome in neonates because of inability to metabolise the drug
27
Q

Oxazolidinones (Linezolid) use and MoA

A
  • Highly active against gram +ve (MRSA & VRE)
  • Not active against most gram -ve
  • Expensive, may cause thrombocytopenia & optic neuritis; should only be used with micro/ID approval
  • Binds to 23S component of 50s subunit → prevents formation of a functional 70s initiation complex
28
Q

Give 2 examples of inhibitors of DNA synthesis

A

Quinolones/Fluoroquinolones

Nitroimidazoles

29
Q

Quinolones/fluoroquinolones

A

Ciprofloxacin, levofloxacin, moxifloxacin

  • Act on alpha unit of DNA gyrase, bactericidal
  • Broad antibacterial activity versus gram -ve (pseudomonas aeruginosa)
  • Newer agents (levofloxacin, moxifloxin) better against gram +ve and intracellular bacteria (Chlamydia spp.)
  • Well absorbed after PO administration (good bioavailability)
  • Use for UTI*, *pneumonia*, *atypical pneumonia*, *bacterial gastroenteritis
30
Q

Nitroimidazoles

A

Metronidazole, tinidazole

  • Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage
  • Rapidly bactericidal
  • Active against anaerobic bacteria and protozoa (Giardia)
  • Nitrofurans are related compounds (nitrofurantoin is good for cystitis and lower UTIs)
31
Q

What is an inhibitor of RNA synthesis?

A

Rifamycins – rifampicin and rifabutin

32
Q

How do Rifamycins work?

A
  • Inhibits protein synthesis by binding to DNA-dependent RNA polymerase, inhibiting initiation
  • Bactericidal
  • Active against mycobacteria and chlamydia
  • Interactions with other drugs metabolised in the liver (OCP) and so need to monitor LFTs
  • Turns secretions orange (urine and contacts) – can check compliance

Rifampicin resistance (never used as a single):

  • Resistance due to chromosomal mutation
  • Causes single amino acid change in beta subunit of RNA polymerase which fails to bind rifampicin
33
Q

Give 2 examples of cell membrane toxins

A

Daptomycin and colistin

34
Q

Daptomycin

A
  • Cyclic lipopeptide with activity limited to gram +ve
  • MRSA and VRE infections as an alternative to linezolid and synercid
35
Q

Colistin

A
  • Polymyxin antibiotic; not absorbed PO though
  • Active against gram -ve including pseudomonas aeruginosa, Acinetobacter baumannii, klebsiella pneumoniae
  • Nephrotoxic and reserved for use against multi-resistant organisms
36
Q

Give 2 examples of inhibitors of folate metabolism

A

Solphonamdes and diaminopyrimidines

37
Q

4 mechanisms of abx resistance

A
  1. Bypass antibiotic-sensitive step
  2. Enzyme chemical modification/inactivation of abx
  3. Accumulation reduced of abx (impaired uptake, enhanced efflux)
  4. Target modification or replacement
38
Q

what are the three ways beta lactams are inactivated?

A
  1. Beta-lactamases (SA and gram-ve bacteria aka coliforms)
  2. MRSA resistance (altered target)
  • mecA gene encodes novel PBP2A
  • low affinity for binding beta lactase
  • substitutes for essential functions of high affinity PBPs at otherwise lethal concentrations of antibiotics

3. Streptococcus pneumonia

  • penicillin resistance is the result of stepwise mutations in PBP genes
  • lower level resistance can be overcome by increasing dose of penicillin used
39
Q

What is the mechanism of macrolide resistance?

A
  • Adenine-N6 methyltransferase modifies 23S rRNA → reduces binding of MLS antibiotics and results in resistance
  • Encoded by erm (erythromycin ribosome methylation) genes.
40
Q

ESBL-based resistance (extended spectrum beta lactamases)

A
  • ESBLs can enzymatically break down cephalosporins (cefotaxime, ceftazidime, cefuroxime) as well as penicillins
    • But, not carbapenems
  • More common in E. coli and Klebsiella
  • Treatment failures reported with beta lactam and beta lactamase inhibitor combinations – augmentin/tazocin
  • Aminoglycoside used in combinations
  • New beta-lactamases are spreading MDR instead of just the ESBL-component of resistance (big problem)
    • If something is erythromycin-resistant, be careful about giving clindamycin (may make the bacteria MDR)
    • HPA guidance:
41
Q

By which mechanism is an ESBL E. coli resistance to ceftriaxone?

A

Enzymatic inactivation of the antibiotics

42
Q

Which mechanism mediates flucloxacillin resistance in S. aureus?

A

alteration of the target (flucloxacillin is stable to b-lactamases and its PBP2A alteration of target instead)

43
Q

Oxazolidinones (Linezolid) use and MoA

A
  • Highly active against gram +ve (MRSA & VRE)
  • Not active against most gram -ve
  • Expensive, may cause thrombocytopenia & optic neuritis; should only be used with micro/ID approval
  • Binds to 23S component of 50s subunit → prevents formation of a functional 70s initiation complex

Year 5 Microbiology (8 decks)

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