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Micro: Antimicrobials Flashcards

1
Q

3 main selective targets for antibiotics

A
  • Inhibition of cell wall synthesis (peptidoglycan layer of cell wall)
  • Inhibition of bacterial protein synthesis
  • Inhibition of DNA gyrase and other prokaryote specific enzymes
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2
Q

How does the cell wall of gram pos and gram neg bacteria differ?

A

Gram pos: thick peptidoglycan layer, no outer membrane

Gram neg: thin peptidoglycan layer, has an outer membrane (some antibiotics can’t get through this)

*Gram pos stain purple, gram neg stain pink*

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3
Q

What is the broad mechanism of action of beta lactams?

A

Inhibition of cell wall synthesis

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4
Q

What 3 groups of antibiotics are classified as beta lactams?

A

Penicillins

Cephalosporins

Carbapenems

(used in sequence depending on resistance)

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5
Q

Describe the mechanism of action of beta lactams

A

Inhibits transpeptidase, which is an enzyme that forms cross links during the formation of the cell wall.

The resulting cell wall is therefore weak, and so the bacteria lyse because of osmotic pressure. (Bacterialcidal)

They are effective against rapidly dividing bacteria, which are constantly using transpeptidase to form their cell wall - NOT useful in bacteria that is not dividing as the cell wall has already been formed

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6
Q

Which bacteria are beta-lactams ineffective against

A

Ineffective against bacteria that lack a peptidoglycan cell wall (hence not gram pos or gram negative as both have a peptidoglycan cell wall).

Examples of such bacteria are: Chlamydia and Mycoplasma

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7
Q

Common examples of penicillins

A

Penicillin
Amoxicillin
Flucloxacillin
Piperacillin

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8
Q

What bacteria is penicillin mainly active against?

A

Gram +ve (specifically Strep and Clostridia - behind gastroenteritis )

Not effective against organisms with no peptidoglycan cell wall e.g. mycoplasma and chlamydia

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9
Q

What bacteria is amoxicillin active against?

A

Broad spectrum: gram +ve and many gram -ve

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10
Q

What is the main indication for Flucloxacillin

A

Skin infections (Staph A)

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11
Q

Main indication for Piperacillin

A

Commonly used in Hospital neutropaenic sepsis as covers pseudomonas (used as Tazocin)

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12
Q

Mechanism of resistance bacteria gain aganist penicillin

A

Beta lactamase (drug inactivation)

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13
Q

Examples of cephalosporins (3)

A

Cefuroxime (2nd generation)

Ceftriaxone (3rd generation)

Ceftazidime (3rd generation)

As cephalosporins progressed from 1st to 3rd generation, they became more effective against gram negative and less effective against gram positive - newer generation does not act against Staph A.

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14
Q

Important features of Cefuroxime

A
  • Stable to many beta lactamases by gram +ve
  • less active against anaerobes - hence used in combination with metronidazole in GI cases
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15
Q

Important features of Ceftriaxone

A
  • Broad spectrum
  • good cover against community acquired meningitis as has good penetration of CNS
  • associated with C. Diff
  • increasingly decreased utility due to ESBL
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16
Q

Important features of Ceftazidime

A
  • Activity against pseudomonas (useful for HAP)
  • Note it is less active against Staph A compared to other 1st and 2nd gen cephalosporins
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17
Q

Mechanism of resistance bacteria gain aganist cephalosporins

A

Extended Spectrum Beta Lactamase (ESBL) - these bacteria are resistant to both penicillins and cephalosporins

drug inactivation

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18
Q

Which beta lactam antibiotics are stable to ESBL organisms?

A

Carbapenems

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19
Q

Examples of Carbapenems (beta lactam)

A

Meropenem
Ertapenem

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20
Q

Main indication of Carbapenem

A

Used for ESBL producing bacteria

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21
Q

Mechanism of resistance bacteria gain aganist carbapenems- list specific bacteria this has been seen on

A

Carbapenamase (especially in Acinetobacter and Klebsiella) - drug inactivation

this has lead to an returned use of Monobactam antibiotics to treat carbapenamase bacteria

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22
Q

How can beta lactam resistance be overcome?

A

Include a beta lactamase inhibitor

Eg. Clavulanic acid + amoxicllin (in co-amoxiclav aka augmentin)

Eg. Tazobactam + piperacillin (in tazocin)

Note that clavulanic acid and Tazobactam are only effective at inhibiting group A beta lactamase

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23
Q

Recall the key features of beta lactams

A

Relatively non-toxic

Renally excreted so decrease dose if renal impairment

Short T1/2 (many are type 2/time-dependent drugs so aim to maximise the time where concentration > MIC)

Will not cross intact BBB (but can cross in meningitis)

Cross allergenic – penicillin has 10% cross reactivity with cephalosporins and carbapenems (becoming less common)

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24
Q

What is the mechanism of action of glycopeptide antibiotics?

A

Inhibition of cell wall synthesis by preventing peptide cross links in cell wall

They bind to the amino acid chains at the end of peptidoglycan precursors, to prevent glycosidic bond formation. They prevent transpeptidase activity without directly binding to the enzyme

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25
Name 2 glycopeptide antibiotics
Vancomycin Teicoplanin
26
What type of bacteria are glycopeptides effective against?
Gram pos only - they are large molecules so can't penetrate gram -ve cell wall Good for MRSA (IV) and C.Diff (Oral)
27
What are glycopeptides particularly useful for?
MRSA infection (especially in bacteriaemia and endocarditis). *This is because MRSA is resistant to all beta lactam antibiotics* Vancomycin specififcally useful for C-Diff
28
What is a caution of glycopeptide antibiotics?
They are nephrotoxic Hence important to monitor drug level (mainly the trough level - lowest level maintained after initial peak of intake lowers).
29
List antibiotic classes which inhibit protein synthesis (TAMCO)
Tetracyclines Aminoglycosides Macrolides Chloramphenicol Oxazolidinones
30
Recall the broad mechanism of action of aminoglycosides
Bind to 30s ribosomal subunit, preventing elongation of polypeptide chain and cause misreading of codons along mRNA However this does not fully explain their antimicrobial effect
31
Recall 2 examples of aminoglycoside antibiotics
Gentamicin Amikacin Tobramycin
32
What type of bacteria are aminoglycoside antibiotics effective against?
Gram -ve - sepsis - good cover for pseudomonas Aerobes - no activity against anaerobes as oxygen is required for the uptake of the antibiotic into the bacteria *Have synergetic effect with beta lactams and used to treat G+ve endocarditis*
33
What pharmokinetic pattern of activity do aminoglycosides
Rapid concentration dependent effect - meaning the high initial peak dose is crucial for its antimicrobial action, and following it they have a post-antibiotic effect where the antimicrobial action is maintained. This is why many aminoglycosides are given as a one-off high dose.
34
Recall 2 toxicities of aminoglycosides
Ototoxicity Nephrotoxicity
35
Mechanism of actions of Macrolides
Act on 50s ribosome Inhibit translocation Bacteriostatic action (doesn't kill bacteria it prevents it from dividing)
36
Examples of 2 macrolide antibiotics
Azithromycin Clarithromycin
37
What type of bacteria are macrolides effective against?
Gram +ve *cannot cross polar gram -ve outer membrane*
38
Recall 2 specific gram -ve bacteria that macrolides are effective against
Campylobacter sp Legionella pneumophila (macrolides = erythromycin/ azithromycin/ clarithromycin)
39
What are macrolides particularly useful for?
Used if patients have penicillin allergy - especially for mild staph or strep infections
40
Recall the broad mechanism of action of tetracyclines
Bind to 30s subunit of ribosomes *Bacteriostatic - not useful for sepsis but still useful in certain situations, especially with MRSA*
41
Example of a Tetracycline
Doxycyline
42
What type of bacteria are tetracylines effective against?
Broad spectrum (good cover for MRSA) + some intracellular bacteria (e.g. Chlamydia) Used for lyme disease
43
Who is contra-indicated to recieve tetracycline
Children under 12 or pregnant women
44
Recall one side effect of tetracycline antibiotics
Light-sensitive rash
45
Mechanism of action of Chloramphenicol
Acts on 50s ribosome inhibiting formation of peptide bonds in translocation Bacteriostatic
46
What type of bacteria is chloramphenicol effective against?
Broad spectrum HOWEVER is only used if beta lactams cannot be utilised (e.g. meningitis in pts with severe allergy to beta lactams
47
Why is chloramphenicol rarely used?
Due to severe side effects: - Aplastic anaemia - Grey baby syndrome in neonates due to inability to metabolise drug
48
What is the sole indication to use chloramphenicol
Bacterial conjunctivitis
49
Recall the broad mechanism of action of oxazolidinones
Binds to the 23s portion of the 50s ribosome subunit to prevent 70s subunit formation
50
Recall an example of oxazolidinones
Linezolid
51
Recall two types of bacteria that oxazolidinones are particularly active against
Highly active against gram positive organisms - especially MRSA and VRE
52
Recall one potential side effect of oxazolidinones
Bone marrow suppression (commonyl resulting in thrombocytopaenia) Irreversible optic neuritis if used longer than 4 weeks
53
Antibiotic class that inhibits DNA synthesis
Fluoroquinolones Nitroimidazole
54
Recall the broad mechanism of action of fluoroquinolones
Act on alpha subunit of DNA gyrase *Bacterialcidal*
55
Recall 2 examples of fluoroquinolone antibiotics
Ciprofolaxin Levofloxacin
56
Recall 4 uses of fluoroquinolones
*Broad antibacterial activity especially against gram negatives* * UTI * Atypical pneumonia (particularly pseudomonas) * Bacterial gastroenteritis
57
Side effects of Fluoroquinolones
- Lower seizure threshold (not to be used in epileptic patients) - Tendinitis
58
How do nitroimidazoles work?
Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage *Bacterialcidal*
59
Give examples of nitromidazole antibiotics
Metronidazole Tinidazole *Nitrofurantoin is a related component of nitromidazole antibiotics*
60
Recall types of organisms that metronidazole is effective against
Anaerobes Protozoa (giardia, amoeba)
61
Commonly in which cases do we use Nitroimidazole (specifically Metronidazole)
Commmonly used in combination with Cephalosporin for GI tract cases to allow cover for anaerobic bacteria (which is not achieved with cephalosporin alone)
62
Indication for nitrofurantoin and when should it be taken?
Simple UTIs Right after visiting the toilet as it sits in bladder
63
Recall the broad mechanism of action of Rifamycin (rifampicin)
Binds to DNA-dependent RNA polymerase to inhibit RNA synthesis
64
Recall the main use of rifampicin
TB treatment - always used in combination as resistance develops quickly as it requires solely one amino acid change
65
Recall one side effect of rifampicin
Turns secretions orange (red urine)
66
Give 2 examples of cell membrane toxins
Daptomycin (lipopeptide with limited activity to gram positives - potential alternative to linezolid and synercid for MRSA and VRE infections) Colistin (old antibiotic which is very nephrotoxic but it is active against gram negative organisms like pseudomonas)
67
Colistin is very toxic. Why is it coming back into use?
It is active against certain multi-drug resistant bacteria
68
What is daptomycin (type of colistin) licensed for the treatment of?
MRSA VRE
69
Recall the 2 classes of antibiotic that inhibit folate synthesis
Sulphonamides Diaminopyrimidines (e.g. trimethoprim)
70
Give an example of a sulphonamide
Sulfamethoxazole \*Sulfonamides aren't used on their own due to common resistance - should be in combination with trimethoprim (co-trimoxazole)
71
What is the main use of trimethoprim
Uncomplicated UTI
72
Common indication of Sulphamethoxazole
pneumocystis jirovecii (PCP) *As co-trimoxazole*
73
What are the 4 main mechanisms of resistance
1. Inactivation of the antibiotic (eg beta lactamases) 2. Modification of drug's target target - so antibiotic no longer binds (e.g. MRSA, Strep pneumoniae) 3. Reduced accumulation of drug by either impaired uptake or enhanced efflux (e.g. common in gram -ves) 4. Bypass antibiotic-sensitive step in pathway *Note that often resistance occurs from more than 1 mechanism happening*
74
How is MRSA resistant to all beta lactams?
It is resistant by modifying the drug's target in the microbe. MRSA has mecA gene which encodes novel penicillin binding protein (2A) / novel PBP 2a. This has low affinity for binding beta lactams Substitutes for essential functions of high affinity PBPs at otherwise lethal concentrations of antibiotics
75
How does Strep pneumoniae develop beta lactam resistance?
Penicillin resistance is the result of acquisition of stepwise mutations in PBP genes *As it is a stepwise acquisiton resistance, depending on level of mutations, resistance can range from lower level to high level. In the UK lower level resistance is commonest. This can be overcome by increasing dose of penicillin used - hence why for CAP abx regimes we begin with a high dose of amoxicillin. This is not the case in meningitis - because of the already existing difficulty in abx to cross the BBB, the concentration of abx is never enough to overcome lower level resistance. In cases of strep. p. meningitis you'd add vancomycin if any concern about resistance - note that here co-amoxiclav would not help as there beta lactamase is NOT the source of resistance*
76
Which bacteria typically forms "gram pos cocci in clusters"?
Staphylococcus
77
Which bacteria typically forms "gram pos cocci in chains"?
Streptococcus Strep sounds like 'stripe' = chain
78
What gram stain status are enterococci?
Positive ("Enter-o-coccus" = like letting someone in, positive thing to do)
79
Is streptococci gram pos or neg?
Gram pos
80
Is pseudomonas gram pos or gram neg?
Gram neg (Pseudo"moan"as - 'moan' = negative)
81
Is neisseria meningitis gram pos or gram neg?
Gram neg (Neisseria starts with N = negative)
82
Is haemophilus gram pos or neg?
Gram neg Ha"emo"philus - emo = negative
83
Is listeria gram pos or neg?
Positive Lister = good man = positive
84
Define the MIC
The minimum amount of abx required to inhibit bacterial growth (calculated in lab). It shows how susceptible an organism is to an antibiotic. Can compare to the breakpoint to see if clinically indicated. if breakpoint is lower than MIC then yes, if not then minimum concentration is too high and should not be given.
85
Outline the different pattern of activity antibiotics may exhibit
**Type 1 = Concentration-dependent killing and prolonged persistent effects** - You are trying to maximise the peak concentration of antibiotic above the MIC value. - Goal of therapy = maximising initial concentration of abx given - In these antibiotics they are often given as one-off high doses - Examples = Aminoglycosides, Fluoroquinolones, Daptomycin **Type 2 = Time-Dependent killing and minimal persistent effects** - You are trying to maximise the amount of time in which abx concentration is above the MIC - Goal of therapy = maximise duration of exposure to concentration > MIC - These antibiotics are often given as infusions or dose regimens require being taken more than once a day - Examples = Beta lactams, Erythromycin **Type 3 = Time-dependent killing and moderate/prolonged persistent effects** - You are trying to maximise the concentration of the drug, and also keep it as long as possible in maximised concentration above the MIC - A junction per say of the two above - Examples = Azithromycin, Tetracycline, Oxalidinones
86
Specific antibiotic recommendation for: N. Meningitidis Acute Osteomyelitis (adults) Bacterial endocarditis Group A Strep Simple Cystitis
N. Meningitidis --> 7 days Acute Osteomyelitis (adults) --> 6 weeks Bacterial endocarditis --> 4-6 weeks Group A Strep --> 10 days (7d in new NICE guide) Simple Cystitis --> 3 days (if pregnant, men, catheter = 7 days)
87
Common antibiotic regiment used for CAP
Beta Lactam + Macrolide (beta lactam covers against the common pathogens while macrolides covers against the atypicals which lack a cell wall and therefore bypass beta lactam action)
88
1st line abx for pseudomonas
aminoglycosides (gentamicin)
89
Outline the resistance mechanism seen in each circumstance below: 1. ESBL E. coli resistance to ceftriaxone 1. Resistance to macrolides 1. Resistance to trimethoprim and sulphonamides 1. MRSA resistance to flucloxacillin 1. Resistance to Rifampicin
1. ESBL E. coli resistance to ceftriaxone - Enzymatic inactivation of the antibiotic 1. Resistance to macrolides - Alteration of the target 1. Resistance to trimethoprim and sulphonamides - Bypass of antibiotic-sensitive step 1. MRSA resistance to flucloxacillin - Alteration of the target 1. Resistance to Rifampicin - Alteration of the target

PATH FINAL (36 decks)

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