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Kat's Pathology > Antimicrobial Agents > Flashcards

Antimicrobial Agents Flashcards

1
Q

Inhibitors of cell wall synthesis (2)

A

Beta-lactam antibiotics (penicillins, cephalosporins and carbapenems)

Glycopeptides (vancomycin and teicoplanin)

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2
Q

Difference between gram +ve and gram -ve cell wall

A

Gram +ve = single thick layer of peptidoglycan

Gram -ve = peptidoglycan between an inner and outer membrane

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3
Q

Features of bata-lactams

A

Inactivate the enzymes that are involved in the terminal stages of cell wall synthesis (transpeptidases also known as penicillin binding proteins) – β-lactam is a structural analogue of the enzyme substrate
Bactericidal
Active against rapidly-dividing bacteria
Ineffective against bacteria that lack peptidoglycan cell walls (e.g. Mycoplasma or Chlamydia)

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4
Q

Beta lactam target

A

Transpeptidases (PBPs)

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5
Q

How do beta lactams cause cell death

A

Weakened cell wall results in osmotic lysis of the bacterial cell

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6
Q

Beta-lactam antibiotics

A

Penicillin
Amoxicillin
Flucloxacillin
Piperacillin

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7
Q

Indications for penicillin

A

Gram positive organisms, Streptococci, Clostridia; broken down by an enzyme (β-lactamase) produced by S. aureus

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8
Q

Indications for amoxicillin

A

Broad spectrum penicillin, extends coverage to Enterococci and Gram negative organisms ; broken down by β-lactamase produced by S. aureus and many Gram negative organisms

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9
Q

Indications for flucloxacillin

A

Similar to penicillin although less active. Stable to β-lactamase produced by S. aureus.

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10
Q

Indications for piperacillin

A

Similar to amoxicillin, extends coverage to Pseudomonas and other non-enteric Gram negatives; broken down by β-lactamase produced by S. aureus and many Gram negative organisms

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11
Q

What are some beta-lactamase inhibitors

A

Protect penicillins from enzymatic breakdown and increase coverage to include S. aureus, Gram negatives and anaerobes
Clauvanic acid and tazobactam

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12
Q

First generation cephalosporin

A

Cephaliexin

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13
Q

Second generation cephalosporin

A

Cefuroxime

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14
Q

Third generation cephalosporins

A

Cefotaxime
Ceftriaxone
Ceftazidime

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15
Q

What changes over the generations of cephalosporins

A

Increasing activity against gram negative bacilli

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16
Q

cefuroxime

A

Stable to many β-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes

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17
Q

Ceftriaxone

A

3rd generation cephalosporin

Associated with C.difficile

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18
Q

Ceftazidime

A

Anti-pseudomonas

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19
Q

Extended spectrum beta-lactamase (ESBL)

A

Organisms producing these are resistant to all cephalosporins

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20
Q

Indications for carbapenems

A

Stable to ESBL enzymes

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21
Q

Examples of carbapenems

A

Meropenem
Imipenem
Ertapenem

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22
Q

Difficulties with carbapenems

A

Carbapenemase enzymes becoming more widespread. Multi drug resistant Acinetobacter and Klebsiella species.

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23
Q

Key features of beta-lactams

A

Relatively non-toxic
Renally excreted (so low dose if renal impairment)
Short half life
Will not cross intact blood-brain barrier
Cross-allergenic (penicillins approx 10% cross-reactivity with cephalosporins or carbapenems)

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24
Q

MOA glycopeptides

A

Inhibit cell wall synthesis

Bactericidal

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25
Q

Indications for glycopeptides

A

IV treatment of serious MRSA

Oral vancomycin for c.difficile

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26
Q

Why must you be cautious with glycopeptides

A

Nephrotoxic - important to monitor drug levels to prevent accumulation

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27
Q

Inhibitors of protein synthesis

A

Aminoglycosides (e.g. gentamicin, amikacin,tobramycin)

Tetracyclines

Macrolides (e.g. erythromycin) / Lincosamides (clindamycin) / Streptogramins (Synercid) – The MSL group

Chloramphenicol

Oxazolidinones (e.g. Linezolid)

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28
Q

Aminoglcoside MOA

A

Bind to amino-acyl site of the 30S ribosomal subunit
Rapid, concentration-dependent bactericidal action
Require specific transport mechanisms to enter cells

Prevent elongation of the polypeptide chain
Cause misreading of the codons along the mRNA

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29
Q

Toxicity of glycopeptides

A

Nephrotoxic

30
Q

Toxicity of aminoglocosides

A

Ototoxic and nephrotoxic

31
Q

Aminoglycosides and beta-lactams

A

Synergistic effect

32
Q

Aminoglocosides have no activity against

A

Anaerobes

33
Q

Treatment of ps.aeruginosa

A

Gentamicin and tobramycin

34
Q

Tetracyclines active against

A

Intracellular pathogens (chlamydiae, rickettsiae, mycoplasmas)

35
Q

Tetracycline toxicity

A

Do not give to children or pregnant women

Light sensitive rash

36
Q

Tetracycline MOA

A

Reversibly bind to the ribosomal 30S subunit
Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis.

Bacteriostatic

37
Q

Macrolides

A

Minimal activity against Gram –ve bacteria

Useful agent for treating mild Staphylococcal or Streptococcal infections in penicillin-allergic patients

Also active against Campylobacter sp and Legionella. Pneumophila

38
Q

Macrolide examples

A

Erythromycin
Clarithromycin
Azithromycin

39
Q

Macrolides MOA

A

Bind to 50S subunit of the ribosome

Interfere with translocation
Stimulate dissociation of peptidyl-tRNA

40
Q

Chloramphenicol indication s

A

Rarely used, apart from eye preparations and special indications

41
Q

Chloramphenicol toxicity

A

Aplastic anaemia

Grey baby syndrome in neonates because of an inability to metabolise the drug

42
Q

Chloramphenicol MOA

A

Chloramphenicol binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation

43
Q

Oxazolinones (linezolid) MOA

A

Binds to the 23S component of the 50S subunit to prevent the formation of a functional 70S initiation complex (required for the translation process to occur).

44
Q

Oxazolidinones indications

A

Highly active against Gram positive organisms, including MRSA and VRE.
Not active against most Gram negatives.

45
Q

Oxazolidinones toxicity

A

Thrombocytopoenia

46
Q

Inhibitors of DNA synthesis

A

Quinolines (ciprofloxacin, levofloxacin, mocifloxacin)

Nitromidazoles (metronidazole and tinidazole)

47
Q

MOA floroquinolones

A

Act on -subunit of DNA gyrase predominantly, but, together with other antibacterial actions, are essentially bactericidal

48
Q

Indications for fluoroquinolones

A

Broad antibacterial activity, especially vs Gram –ve organisms, including Pseudomonas aeruginosa

Newer agents (e.g. levofloxacin, moxifloxacin) increased activity vs G +ves and intracellular bacteria, e.g. Chlamydia spp

Well absorbed following oral administration

Use for UTIs, pneumonia, atypical pneumonia & bacterial gastroenteritis

49
Q

Name a nitroimidazole

A

Metronidazole

50
Q

MOA nitromidazoles

A

Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage

Rapidly bactericidal

51
Q

Indications for nitromidazoles

A

Anaerobic bacteria and protozoa (e.g. giardia)

52
Q

What are nitrofurans

A

Related to nitoimidazoles.

Nitrofurantoin is useful for treating simple UTIs

53
Q

Rifamycins

A

Inhibitor of RNA synthasis

54
Q

Example of rifamycin

A

Rifampicin

55
Q

MOA rifampicin

A

Inhibits protein synthesis by binding to DNA-dependent RNA polymerase thereby inhibiting initiation

Bactericidal

56
Q

Indications for rifampicin

A

Mycobacteria

Chlamydiae

57
Q

What must be monitored with rifampicin

A

LFTs

Beware of interactions with other drugs that are metabolised in the liver (e.g oral contraceptives)

58
Q

What effect does rifampicin have on urine

A

May turn urine and contact lenses orange

59
Q

Why can you not use rifampicin as a single agent

A

Except for short-term prophylaxis (vs. meningococcol infection) you should NEVER use as single agent because resistance develops rapidly

Resistance is due to chromosomal mutation.

This causes a single amino acid change in the ß subunit of RNA polymerase which then fails to bind Rifampicin.

60
Q

Cell membrane toxins

A

Cyclic lipopeptides

Polymyxin

61
Q

Daptomycin

A

a cyclic lipopeptide with activity limited to G+ve pathogens. It is a recently-licenced antibiotic likely to be used for treating MRSA and VRE infections as an alternative to linezolid and Synercid

62
Q

Colistin

A

a polymyxin antibiotic that is active against Gram negative organisms, including Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella. pneumoniae. It is not absorbed by mouth. It is nephrotoxic and should be reserved for use against multi-resistant organisms

63
Q

Folate metabolism inhibitors

A

Sulfanamides

Diaminopyrimidines

64
Q

Example of a diaminopyrimidine

A

Trimethoprim

65
Q

MOA folate metabolism inhibitors

A

Includes sulfanamides and diaminopyrimidines

Act indirectly on DNA through interference with folic acid metabolism

Synergistic action between the two drug classes because they act on sequential stages in the same pathway

Sulphonamide resistance is common, but the combination of sulphamethoxazole+trimethoprim (Co-trimoxazole) is a valuable antimicrobial in certain situations (e.g. Treating Pneumocystis. jiroveci pneumonia)

66
Q

Trimethoprim

A

Community acquired UTIs

67
Q

Mechanisms of resistance

A

Chemical modifications or inactivation of the antibiotic
Modification or replacement of target
Reduced antibiotic accumulation (impaired uptake, enhanced efflux)
Bypass antibiotic sensitive step

68
Q

Beta lactamases

A

Beta Lactamases are a major mechanism of resistance to ß Lactam antibiotics in Staphylococcus aureus and Gram Negative Bacilli (Coliforms).

NOT the mechanism of resistance in penicillin resistant Pneumococci and MRSA.

Penicillin resistance not reported in Group A (S. pyogenes), B, C, or G ß haemolytic Streptococci.

69
Q

MRSA beta-lactam resistance

A

ecA gene encodes a novel PBP (2a).
Low affinity for binding beta Lactams.
Substitutes for the essential functions of high affinity PBPs at otherwise lethal concentrations of antibiotic.

70
Q

Streptococcus pneumoniae beta lactam resistane

A

Penicillin resistance is the result of the acquisition of a series of stepwise mutations in PBP genes.

Lower level resistance can be overcome by increasing the dose of penicillin used

71
Q

What are extended spectrum beta lactamases

A

Able to break down cephalosporins (cefotaxime, ceftazidime, cefuroxime)
Becoming more common in E. coli and Klebsiella species.
Treatment failures reported with ß Lactam/ ß Lactamase inhibitor combinations (eg. Augmentin/Tazocin).

72
Q

Macroline altered target resistance mechanism

A

Adenine-N6 methyltransferase modifies 23S rRNA
Modification reduces the binding of MLS antibiotics and results in resistance
Encoded by erm (erythromycin ribosome methylation) genes.

Kat's Pathology (105 decks)

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