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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
Indications for glycopeptides
IV treatment of serious MRSA | Oral vancomycin for c.difficile
26
Why must you be cautious with glycopeptides
Nephrotoxic - important to monitor drug levels to prevent accumulation
27
Inhibitors of protein synthesis
Aminoglycosides (e.g. gentamicin, amikacin,tobramycin) Tetracyclines Macrolides (e.g. erythromycin) / Lincosamides (clindamycin) / Streptogramins (Synercid) – The MSL group Chloramphenicol Oxazolidinones (e.g. Linezolid)
28
Aminoglcoside MOA
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
29
Toxicity of glycopeptides
Nephrotoxic
30
Toxicity of aminoglocosides
Ototoxic and nephrotoxic
31
Aminoglycosides and beta-lactams
Synergistic effect
32
Aminoglocosides have no activity against
Anaerobes
33
Treatment of ps.aeruginosa
Gentamicin and tobramycin
34
Tetracyclines active against
Intracellular pathogens (chlamydiae, rickettsiae, mycoplasmas)
35
Tetracycline toxicity
Do not give to children or pregnant women | Light sensitive rash
36
Tetracycline MOA
Reversibly bind to the ribosomal 30S subunit Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis. Bacteriostatic
37
Macrolides
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
Macrolide examples
Erythromycin Clarithromycin Azithromycin
39
Macrolides MOA
Bind to 50S subunit of the ribosome Interfere with translocation Stimulate dissociation of peptidyl-tRNA
40
Chloramphenicol indication s
Rarely used, apart from eye preparations and special indications
41
Chloramphenicol toxicity
Aplastic anaemia Grey baby syndrome in neonates because of an inability to metabolise the drug
42
Chloramphenicol MOA
Chloramphenicol binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation
43
Oxazolinones (linezolid) MOA
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
Oxazolidinones indications
Highly active against Gram positive organisms, including MRSA and VRE. Not active against most Gram negatives.
45
Oxazolidinones toxicity
Thrombocytopoenia
46
Inhibitors of DNA synthesis
Quinolines (ciprofloxacin, levofloxacin, mocifloxacin) | Nitromidazoles (metronidazole and tinidazole)
47
MOA floroquinolones
Act on -subunit of DNA gyrase predominantly, but, together with other antibacterial actions, are essentially bactericidal
48
Indications for fluoroquinolones
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
Name a nitroimidazole
Metronidazole
50
MOA nitromidazoles
Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage Rapidly bactericidal
51
Indications for nitromidazoles
Anaerobic bacteria and protozoa (e.g. giardia)
52
What are nitrofurans
Related to nitoimidazoles. | Nitrofurantoin is useful for treating simple UTIs
53
Rifamycins
Inhibitor of RNA synthasis
54
Example of rifamycin
Rifampicin
55
MOA rifampicin
Inhibits protein synthesis by binding to DNA-dependent RNA polymerase thereby inhibiting initiation Bactericidal
56
Indications for rifampicin
Mycobacteria | Chlamydiae
57
What must be monitored with rifampicin
LFTs Beware of interactions with other drugs that are metabolised in the liver (e.g oral contraceptives)
58
What effect does rifampicin have on urine
May turn urine and contact lenses orange
59
Why can you not use rifampicin as a single agent
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
Cell membrane toxins
Cyclic lipopeptides | Polymyxin
61
Daptomycin
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
Colistin
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
Folate metabolism inhibitors
Sulfanamides | Diaminopyrimidines
64
Example of a diaminopyrimidine
Trimethoprim
65
MOA folate metabolism inhibitors
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
Trimethoprim
Community acquired UTIs
67
Mechanisms of resistance
Chemical modifications or inactivation of the antibiotic Modification or replacement of target Reduced antibiotic accumulation (impaired uptake, enhanced efflux) Bypass antibiotic sensitive step
68
Beta lactamases
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
MRSA beta-lactam resistance
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
Streptococcus pneumoniae beta lactam resistane
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
What are extended spectrum beta lactamases
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
Macroline altered target resistance mechanism
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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