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Microbiology and Immunology - SGUL (Sem 4) > Antibiotics > Flashcards

Antibiotics Flashcards

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1
Q

What are antimicrobials

A

Antimicrobials are substances that kill or inhibit the growth of microorganisms

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2
Q

What are antibiotics

A
  • Substances produced by living organisms with activity against bacteria
  • Many of our current drugs are not true antibiotics but are either synthetic or semi-synthetic
  • Chemically modified to improve pharmacological and antimicrobial properties
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3
Q

Briefly describe how the first antibiotic was discovered

A
  • Alexander Flemming was growing a culture of staphylococcus aureus which was contaminated with penicillium notatum
  • The penicillium produced a substance that created a zone of inhibition on the culture
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4
Q

What does selective toxicity mean

A
  • Only targets specific cells due to the differences between the pathogen and the host
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5
Q

What does therapeutic margin mean

A
  • The difference between the therapeutic dose and the toxic dose
  • The greater the margin the safer the drug
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6
Q

What is the effect on normal microbiota when using antibiotics

A
  • The use of broad-spectrum antibiotics can lead to dybiosis
  • Loss of flora can lead to bacterial or pathogen overgrowth
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7
Q

How does antibiotics work along side immunity

A
  • Antibiotics work alongside natural immunity to clear bacteria.
  • When patients are immunosuppressed it affects the types of antibiotics used
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8
Q

How are antibiotics classified

A
  • Type of activity
  • Structure
  • Target site for activity
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9
Q

What types of activities can antibiotics be

A
  • Bactericidal
  • Bacteriostatic
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10
Q

What is the function of bactericidal antibiotics

A
  • Kill bacteria
  • Used when the host defence mechanisms are impaired
  • Required in endocarditis, kidney infection diseases
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11
Q

What is the function of bacteriostatic antibiotics

A
  • Inhibit bacteria
  • Used when the host defences mechanisms are intact
  • Used in many infectious diseases
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12
Q

How are antibiotics classified on their spectrum of activity

A
  • Broad spectrum antibiotics
  • Narrow spectrum antibiotics
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13
Q

Describe beta-lactams as antibiotics

A
  • Basic penicillins
  • Active against streptococci, pneumococci, meningococci, treopnemes
  • Most strains of Staphylococcus aureus are resistant.
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14
Q

Describe Anti-staphylococcal penicillins
e.g. flucloxacillin

A
  • narrow spectrum, Gram-positive, beta-lactamase resistant, less potent than PenG
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15
Q

Describe broader spectrum penicillins e.g. ampicillin

A

Spectrum of activity is similar to basic penicillins but also includes some Gram-negative organisms and also enterococci

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16
Q

Describe Anti-pseudomonal penicillins e.g. piperacillin

A

extended spectrum beta-lactam antibiotic also gram positive and negative anaerobes

17
Q

Describe Beta-lactam/beta-lactamase inhibitor combinations
e.g. co-amoxiclav (Augmentin)

A

Spectrum like amoxicillin plus activity against some Gram-negatives and Staph aureus

18
Q

List some targets of activity for antibiotics

A
  • Cell wall synthesis
  • DNA Gyrase
  • RNA elongation
  • DNA-directed RNA polymerase
  • Protein synthesis inhibitors 50S, 30S and tRNA
  • Cytoplasmic membrane structure
  • Folic acid metabolism
19
Q

Briefly describe how cell wall inhibitors work

A
  • Peptidoglycan synthesis involves enzymes called penicillin-binding proteins (PBPs)(Transpeptidases)
  • When new peptidoglycan units are added to a growing cell wall, the peptide side chain on one subunit must be linked to peptide side chain on another (Transpeptidation)
  • Structure of penicillins resembles the two amino acids at the end of the side chain – terminal D alanyl-D-alanine
  • The transpeptidation enzyme binds penicillin instead of its true substrate due to this structural similarity, thereby blocking the transpeptidation reaction that forms the peptidoglycan cross-links
20
Q

How does beta-lactams work on gram negative bacteria

A
  • Beta-lactams travel through porins present on outer membrane and bind transpeptidases
  • This stops production of the peptidoglycan layer
  • Activates autolytic enzyme mechanisms
21
Q

How does folic acid synthesis inhibitors work

A
  • Sulphonamides acts as competitive inhibitors for dihydropteroate synthetase in the production of folic acid
  • Trimethoprim inhibits dihydrofolate reductase
  • Conditions are synergistic and bactericidal
22
Q

Describe how protein synthesis inhibitors work

A
  • Either bind to the 30S or 50S subunit and blocks formation of peptide chain
23
Q

When do we use antibiotics

A
  • Treatment for bacterial infections
  • Prophylaxis - Prevent infections
  • Inappropriate use - viral sore throats
24
Q

What route of administrations are used

A
  • Oral
  • IV
  • Injection
  • Topical
25
Q

Why are antibiotic combinations used

A
  • Before an organism is identified in life-threatening infections
  • Polymicrobial infections
  • Less toxic doses of an individual drug possible
  • Synergy between more than one antibiotic
  • reduce antibiotic resistance
26
Q

What is meant by MIC dose

A
  • The minimum does required to cause inhibition
  • A therapeutic dose will be higher than the MIC
27
Q

What is antibiotic susceptibility testing

A
  • Test which antibiotics work against an infection and at what concentration

Microbiology and Immunology - SGUL (Sem 4) (30 decks)

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