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Antimicrobials (1) Flashcards

1
Q

Name 3 selective targets of antibiotics

A

• Peptidoglycan layer of cell wall • Inhibition of bacterial protein synthesis • DNA gyrase and other prokaryote specific enzymes

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2
Q

Name 2 Inhibitors of Cell Wall Synthesis

A

beta-lactam antibiotics and glycopeptides

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3
Q

Name examples of beta-lactam antibiotics and what targets they have

A

penicillin, cephalosporins, carbapenems o Broad spectrum

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4
Q

Name examples of glycopeptides antibiotics and what targets they have

A

– vancomycin, teicoplanin o Gram-positive

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5
Q

What is the difference between gram positive and negative cell walls?

A

• Gram-positive cell wall – thick peptidoglycan cell wall (made of NAG - N-acetylglucosamine and NAM - N-acetylmuramic acid components) • Gram-negative cell wall – thinner peptidoglycan cell wall, outer membrane conferring resistance to some antibiotics o Can be more resistant and harder to treat due to outer membrane

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6
Q

What do Beta-lactams do?

A

• Inactivate enzymes involved in terminal stages of cell wall synthesis = transpeptidases / penicillin binding proteins o Beta lactam is a structural analogue of the enzyme substrate

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7
Q

Beta-lactams are bactericidal what does this mean and what are the consequences?

A

• Bactericidal (active against rapidly dividing bacteria) – if cell wall has already been formed, they have no effect o Ineffective against bacteria lacking peptidoglycan cell walls (mycoplasma, chlamydia) o Cause cell lysis

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8
Q

Name the penicillins

A

o Penicillin o Amoxicillin o Flucloxacillin o Piperacillin

o Clavulanic acid (Co-amoxiclav) and tazobacterm (Tazocin/Piptazobactam)

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9
Q

What bacteria does penicillin work on?

A

Gram positive organisms, Streptococci, Clostridia

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10
Q

What is penicillin broken down by?

A

Beta lactamases produced by S.aureus

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11
Q

What bacteria does amoxicillin act on?

A

Broad spectrum penicillin, extends coverage to Enterococci and Gram negative organisms

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12
Q

What is amoxicillin broken by?

A

broken down by β-lactamase produced by S.aureus and many Gram negative organisms

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13
Q

Which penicillin is stable to ß-lactamase by S.Aureus (gram -ve and e.coli)?

A

Flucloxacillin (and co-amoxiclav)

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14
Q

What bacteria does piperacillin act on?

A

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

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15
Q

What breaks down piperacillin?

A

broken down by β-lactamase produced by S. aureus and many Gram negative organisms

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16
Q

Name the cephalosporins.

A

First Generation: Cephalexin Second Generation: Cefuroxime Third Generation: Cefotaxime, Ceftriaxone and Ceftazidime

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17
Q

Which cephalosporin is resistant to beta lactamases produced by gram -ve bacteria?

A

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

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18
Q

What is Ceftriaxone associated with? What does it treat?

A

C. difficile

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19
Q

What is Ceftazidime used for?

A

Activity against pseudomonas (HAIs often)

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20
Q

What are Extended Spectrum β-lactamase producing organisms always resistant to?

A

all cephalosporins regardless of in vitro results

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21
Q

Name the carbapenems

A

Meropenem, Imipenem, Ertapenem

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22
Q

What are carbapenem used for?

A

Stable to ESBL enzymes – used against the ESBL organisms

However, carbapenemase enzymes becoming more widespread  MDR organisms

Danger from MDR – Acinetobacter and klebsiella species

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23
Q

How toxic is beta lactams?

A

Relatively not

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24
Q

How is beta lactams excreted

A

Renally so decrease dose if renal impairment

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25
What is the short life of beta lactams?
Short
26
How cross-allergenic are beta lactams?
penicillin has 10% cross reactivity with cephalosporins and carbapenems
27
What type of bacteria are glycopeptides effective against?
gram +ve (inhibit cell wall synthesis) o Large molecules so unable to penetrate gram -ve
28
What are glycopeptides uses?
o MRSA infections (IV) o C. difficile infection (oral – Vancomycin, teicoplanin)
29
How toxic are glycopeptides?
Nephrotoxic – must monitor for accumulation
30
How bactericidal are glycopeptides?
Slowly
31
Name the inhibitors of protein synthesis
- Aminoglycosides -Tetracyclines - Macrolides -Cloramphenicol - Oxazolidinones
32
Name the aminoglycosides
gentamicin, amikacin, tobramycin
33
Describe the MOA of aminoglycosides
* Bind to amino-acyl site of 30s ribosome subunit * Rapid, concentration-dependent bactericidal * Require specific transport mechanisms to enter * Accounts for some intrinsic resistance
34
Why must be monitor levels of aminoglycosides?
• Ototoxic & nephrotoxic, therefore must monitor levels
35
What aminoglycosides are effective against pseudomonas aeruginosa? What are aminglycosides ineffective against?
Gentamicin and tobramycin but not against anaerobes No activity vs anaerobes
36
What do aminoglycosides work synergistically with?
Beta lactams
37
What bacteria do tetracyclines act on?
• Broad-spectrum agents with activity against intracellular pathogens (e.g. chlamydiae, rickettsiae & mycoplasmas) as well as most conventional bacteria
38
Describe the MOA of tetracyclines
* Bacteriostatic * Reversibly bind to the ribosomal 30s subunit * Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis *
39
Tetracyclines are bacteriostatic, what does this mean?
A bacteriostatic agent or bacteriostat, abbreviated Bstatic, is a biological or chemical agent that stops bacteria from reproducing, while not necessarily killing them otherwise.
40
What are the problems with tetracyclines?
Widespread resistance limits usefulness to certain defined situations • Do not give to children or pregnant women • Light-sensitive rash
41
What bacteria are macrolides effective/not effective against?
• 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 • Newer agents include clarithromycin & azithromycin with improved pharmacological properties
42
What is the MOA of macrolides?
* Bacteriostatic - Binds to the 50s subunit of the ribosome
43
What is the MOA of chloramphenicol?
1. Binds to the peptidyl transferase of the 50S ribosomal subunit 2. Inihibits the formation of peptide bonds during translation 3. **Bacteriostatic**
44
When would you use cholramphenicol?
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
45
What are oxazolidinones used against?
Highly active against Gram positive organisms, including MRSA and VRE. Not active against most Gram negatives.
46
What is the MOA of Oxazolidinones?
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).
47
What is the issue with Oxazolidinones?
Expensive, may cause thrombocytopenia & optic neuritis; should only be used with micro/ID approval
48
Name the inhibitors of DNA synthesis
• Quinolones • Nitroimidazoles
49
Name the quinolones
ciprofloxacin (old), levofloxacin (new), moxifloxacin (new)
50
What bacteria do quinolones act on? Whats the MOA?
.Act on alpha unit of DNA gyrase, bactericidal
51
What illnesses are quinolones used for?
* Broad antibacterial activity, especially vs Gram –ve organisms, including Pseudomonas aeruginosa * Newer agents (e.g. levofloxacin, moxifloxacin) → activity vs G +ves and intracellular bacteria, e.g. Chlamydia spp
52
Name the Nitroimidazoles
metronidazole, tinidazole
53
What is the MOA of nitroimidazoles?
Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage • Rapidly bactericidal
54
What microorganisms are nitroimidazoles effectuve against?
Active against anaerobic bacteria and protozoa (e.g. Giardia) Nitrofurans are related compounds: nitrofurantoin is useful for treating simple UTIs
55
Name an inhibitor of RNA synthesis
• Rifamycins
56
Name the Rifamycins
rifampicin and rifabutin
57
What is the MOA of rifampicin?
Inhibits protein synthesis by binding to DNA-dependent RNA polymerase, inhibiting initiation Bactericidal
58
What bacteria is rifampicin active against?
•Active against certain bacteria, including Mycobacteria & Chlamydiae
59
What must be taken into account when giving rifampicin?
* Monitor LFTs * Beware of interactions with other drugs that are metabolised in the liver (e.g oral contraceptives) * May turn urine (& contact lenses) orange
60
Describe resistance to rifampicin.
* Except for short-term prophylaxis (vs. meningococcal 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.
61
Name the cell membrane toxins
• Daptomycin • Colistin
62
Which bacteria does daptomycin act on?
– 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
63
What bacteria is colistin effective against?
a polymyxin antibiotic that is active against Gram negative organisms, including Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella. pneumoniae
64
What is the problem with colistin?
It is not absorbed by mouth. It is nephrotoxic and should be reserved for use against multi-resistant organism
65
Name the 4 mechanisms of resistance and the bacteria that use them or the antibiotic that they evade
1. B Bypass antibiotic-sensitive step 2. E Enzyme chemical modification / inactivation of antibiotic --\> ESBLs 3. A Accumulation reduced of antibiotic i. Impaired uptake--\> Doxycycline ii. Enhanced efflux --\> Flucytosine 4. T Target modification or replacement--\> MRSA, S. pneumoniae, flucloxacillin, macrolides
66
Name the inhibitors of Folate Metabolism
• Sulphonamides • Diaminopyrimidines
67
How do inhibitors of Folate Metabolism work
• These act indirectly on DNA through interference with folic acid metabolism
68
Describe the inactivation mechanism of Beta lactams
• Beta lactamases are a major mechanism of resistance to beta lactam ABx in SA and gram -ve bacilli (coliforms) This is NOT the mechanism of resistance in penicillin resistant Penumococci and MRSA • Penicillin resistance not reported in group A (strep pyogenes), B, C, or G beta haemolytic streptococci
69
Name a Diaminopyrimidines
Trimethoprim - used to treat UTIs
70
Describe the altered target mechanism from Beta lactams
- Used by streptococcus pneumoniae - penicillin resistance is the result of the acquisition of a series of stepwise mutations in PBP genes
71
What type of antibiotics do ESBL act against? Which organisms is it becoming more common in?
• ESBLs can enzymatically break down cephalosporins (cefotaxime, ceftazidime, cefuroxime) as well as penicillins o But, not carbapenems Becoming more common in E.coli and Klebsiella species.
72
Describe the altered target mechanism in macrolides?
- Adenine-N6 methyltransferase modifies 23S rRNA - Modification reduces the binding of (MLS) Macrolide, lincosamide and streptogramin antibiotics and results in resistance - Encoded by erm (erythromycin ribosome methylation) gene
73
What are sulphonamides used to treat? Whats the problem with them?
* 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) * Trimethoprim is used for Rx community-acquired UTIs
74
What are ESBLs? Where can they be found?
Extended Spectrum ß Lactamases (ESBL) * 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)
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Microbiology (19 decks)

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