MI: Antimicrobials 1 Pt.3 Flashcards

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1
Q

Recall one side effect of rifampicin

A

Turns secretions orange

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2
Q

Recall one condition of rifampicin prescription

A

Should never be prescribed alone as resistance develops very quickly

*Resistance is caused by a single amino acid change*

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3
Q

Colistin is very toxic. Why is it coming back into use?

A

It is active against certain multi-drug resistant bacteria

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4
Q

What is daptomycin licensed for the treatment of?

A

MRSA

VRE

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5
Q

Recall the 2 classes of antibiotic that inhibit folate synthesis

A

Sulphonamides

Diaminopyrimidines (e.g. trimethoprim)

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6
Q

Give an example of a sulphonamide

A

Sulfamethazole

*Sulfonamides aren’t used on their own - should be in combination with trimethoprim (co-trimoxazole)

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7
Q

What is the main use of trimethoprim

A

Uncomplicated UTI

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8
Q

Which antibiotic is best for treating pneumocystis jirovecii?

A

Co-trimoxazole

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9
Q

Give 2 examples of cell membrane toxins

A

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)

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10
Q

What are the 4 main mechanisms of resistance

A
  1. Inactivation of the antibiotic (eg beta lactamases)
  2. Altered target - so antibiotic no longer binds
  • E.g. penicillin resistant pneumococci or MRSA where bacteria change the penicillin-binding protein
  • E.g. protein-synthesis inhibitors where the binding of the ribosome subunit is prevented
  1. Reduced accumulation (most important in gram negs - either due to enhanced efflux or to reduced uptake)
  2. Bacteria bypasses antibiotic sensitive step (particularly important for folate inhibitors - bacteria can change the enzyme they use)
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11
Q

How is MRSA resistant to all beta lactams?

A

mecA gene encodes novel penicillin binding protein (2A) / novel PBP 2a

Low affinity for binding beta lactams

Substitutes for essential functions of high affinity PBPs at otherwise lethal concentrations of antibiotics

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12
Q

How does Strep pneumoniae develop beta lactam resistance?

A

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

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

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13
Q

How do bacteria become resistant to macrolides?

A

Adenine-N6 methyltransferase modifies 23S rRNA -> reduces binding of MLS antibiotics and results in resistance

Encoded by erm gene (erythromycin ribosome methylation)

*If bacteria is resistant to erythromycin in this manner but still sensitive to clindamycin, only use clindamycin with caution - sometimes the in-vitro tests aren’t reliable*

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14
Q

Which bacteria typically forms “gram pos cocci in clusters”?

A

Staphylococcus

“Staff” work together in groups/clusters

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15
Q

Which bacteria typically forms “gram pos cocci in chains”?

A

Streptococcus

Strep sounds like ‘stripe’ = chain

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16
Q

What gram stain status are enterococci?

A

Positive

(“Enter-o-coccus” = like letting someone in, positive thing to do)

17
Q

Is streptococci gram pos or neg?

A

Gram pos

18
Q

Is pseudomonas gram pos or gram neg?

A

Gram neg

(Pseudo”moan”as - ‘moan’ = negative)

19
Q

Is neisseria meningitis gram pos or gram neg?

A

Gram neg

(Neisseria starts with N = negative)

20
Q

Is haemophilus gram pos or neg?

A

Gram neg

Ha”emo”philus - emo = negative

21
Q

Is listeria gram pos or neg?

A

Positive

Lister = good man = positive