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Medical Microbiology lectures > L.12 Antibiotics > Flashcards

L.12 Antibiotics Flashcards

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1
Q

What are antimicrobials?

A

Compounds naturally or synthetically used to control microbial growth including antibiotics, antifungals, and disinfectants

Antimicrobials encompass a broad range of substances that combat various types of microorganisms.

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2
Q

What is the primary use of antibiotics?

A

To control bacterial growth

Antibiotics specifically target bacteria and do not affect other types of microorganisms.

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3
Q

What are antifungals used for?

A

To control fungal growth

Antifungals are designed to treat infections caused by fungi.

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4
Q

What is the function of antivirals?

A

Used to control viral growth

Antivirals target viruses, inhibiting their ability to replicate.

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5
Q

What defines an antibiotic?

A

Originally natural compounds produced by living microorganisms that has inhibitory effect on microorganisms in human host

This definition highlights the natural origin of many antibiotics.

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6
Q

How are modern antibiotics characterized?

A

All antibacterial products including semi-synthetic and synthetic

Modern antibiotics may be derived from natural sources or created through chemical synthesis.

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7
Q

What is selective toxicity?

A

Ability to kill or inhibit growth of an organism without harming the cells of the host

Selective toxicity is crucial for effective antibiotic treatment.

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8
Q

What does bacteriostatic mean?

A

Inhibits bacteria from reproducing but doesn’t actively kill them

Bacteriostatic antibiotics stop the growth of bacteria rather than killing them outright.

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9
Q

What does bactericidal mean?

A

Actively kills bacteria

Bactericidal antibiotics lead to the death of bacteria.

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10
Q

What percentage of pathogens are typically destroyed in the first 4-8 hours of antibiotic treatment?

A

At least 99%

This highlights the effectiveness of antibiotics in the initial phase of treatment.

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11
Q

What factors influence the mode of action of antibiotics?

A

Drug composition and bacterial species

Different antibiotics have varying mechanisms based on their chemical structure and the type of bacteria.

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12
Q

How does linezolid act against different bacteria?

A

Bacteriostatic against Staph and Enterococcus but bactericidal against Strep

This illustrates that the same antibiotic can have different effects on different bacterial species.

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13
Q

What is one mechanism by which antibiotics inhibit bacterial growth?

A

Inhibits cell wall synthesis or function

Many antibiotics work by disrupting the structural integrity of bacterial cell walls.

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14
Q

Name a class of antibiotics that inhibit cell wall synthesis.

A

Beta Lactams, Penicillins, Cephalosporins, carbapenems, vancomycin

These antibiotics are commonly used to treat various bacterial infections.

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15
Q

Which antibiotics inhibit nucleic acid synthesis?

A

Quinolones (inhibit DNA Gyrase +/- Topoisomerase IV)

Quinolones are effective against a range of bacterial infections by targeting DNA processes.

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16
Q

What antibiotic inhibits folate synthesis?

A

Trimethoprim

Trimethoprim is often used in combination with other antibiotics for enhanced effect.

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17
Q

What creates free radicals as a mechanism of action?

A

Metronidazole, nitrofurantoin

These antibiotics disrupt bacterial function by generating reactive species.

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18
Q

Which antibiotics inhibit protein synthesis at the 50S subunit?

A

Macrolides, clindamycin, linezolid

These antibiotics target the bacterial ribosome to prevent protein production.

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19
Q

Which antibiotics inhibit protein synthesis at the 30S subunit?

A

Aminoglycosides, tetracyclines

Targeting the 30S ribosomal subunit is a common mechanism for several antibiotic classes.

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20
Q

What is the definition of broad spectrum antibiotics?

A

Act on both Gram-positive and Gram-negative bacteria

Useful for empirical treatment when the organism is unknown and can disrupt the microbiome.

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21
Q

What is the definition of narrow spectrum antibiotics?

A

Act against a limited number of bacteria

Typically used when known organisms are identified, with less effect on the microbiome.

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22
Q

What is a key consequence of using broad spectrum antimicrobials?

A

Higher likelihood of emergence of antimicrobial resistance

Resistance emergence is based on time and use, emphasizing the need for antimicrobial stewardship.

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23
Q

How does the emergence of resistance compare between broad and narrow spectrum antimicrobials?

A

Occurs more rapidly in broad spectrum antimicrobials than in narrow spectrum

This underlines the importance of selecting appropriate antibiotics.

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24
Q

What are the characteristics of an ideal antimicrobial?

A

Selective toxicity, bactericidal activity, narrow spectrum of activity if appropriate, slow emergence of resistance

These features are crucial for effective treatment.

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25
What factors influence the choice of antibiotic?
Pathogen, host, properties of antimicrobial ## Footnote Each factor plays a significant role in determining the most effective treatment.
26
What factors determine the duration of antimicrobial treatment?
Nature and site of infection, growth rate of pathogen ## Footnote These considerations are critical for effective management of infections.
27
What is the typical duration of treatment for an uncomplicated urinary tract infection?
5 day course ## Footnote This is a standard treatment duration for uncomplicated cases.
28
What is the typical duration of treatment for a bloodstream infection?
2-3 week course ## Footnote Treatment duration may vary based on the specific circumstances of the infection.
29
What is the typical duration of treatment for tuberculosis?
6 month course ## Footnote This extended duration is necessary due to the nature of the infection.
30
What are beta-lactams?
Most-commonly used antimicrobials worldwide.
31
Who discovered penicillin and when?
Alexander Fleming in 1928.
32
What is the structure feature of beta-lactams?
They have a Beta-lactam ring in their structure.
33
What is the mechanism of action (MOA) of beta-lactams?
Inhibition of cell wall synthesis in bacteria.
34
What are the three major classes of beta-lactams?
* Penicillins (e.g., penicillin, methicillin, augmentin) * Carbapenems (e.g., ertapenem) * Cephalosporins (e.g., cefotaxime)
35
How do beta-lactam antibiotics target bacteria?
They target penicillin-binding proteins (PBPs) in bacterial cell membranes.
36
What role do penicillin-binding proteins (PBPs) play in bacteria?
They catalyse the cross-linking of peptidoglycan strands, crucial for cell wall stability.
37
What happens when beta-lactams bind to PBPs?
They disable the cross-linking activity needed for cell wall stability.
38
What is the consequence of inadequate cross-linking in bacterial cell walls?
The cell wall weakens and collapses, especially during bacterial division—leading to cell death.
39
What do some bacteria do to resist beta-lactams?
They acquire or upregulate beta-lactamase genes.
40
What is the function of beta-lactamases?
They break the beta-lactam ring of antibiotics like penicillin, rendering them ineffective.
41
What is the effect of beta-lactamases on bacterial survival?
Bacteria survive and multiply as cell wall synthesis continues.
42
What are beta-lactamase inhibitors?
Molecules that bind and inhibit beta-lactamase enzymes, protecting beta-lactam antibiotics.
43
How do beta-lactamase inhibitors function?
They structurally resemble beta-lactams and bind to beta-lactamases, inactivating the enzyme.
44
Give an example of a beta-lactamase inhibitor.
Clavulanic acid.
45
What are modified beta-lactams?
Structurally altered beta-lactam antibiotics that resist beta-lactamase breakdown.
46
How are modified beta-lactams designed?
With larger side chains that hinder access to beta-lactamase active site.
47
Give an example of a modified beta-lactam.
Methicillin.
48
What is the primary effectiveness of narrow-spectrum antibiotics like penicillins?
Primarily effective against GPC ## Footnote Examples include Augmentin and methicillin, but they do not work well against many Gram-negative aerobes.
49
Which bacteria commonly show resistance to narrow-spectrum antibiotics?
Staphylococcus aureus (→ MRSA), Streptococcus pneumoniae, Neisseria gonorrhoeae ## Footnote Resistance is rising in these organisms.
50
What defines extended-spectrum antibiotics?
Effective against a wide range of Gram-positive and Gram-negative organisms ## Footnote An example is cephalosporins like Cefotaxime.
51
What are extended-spectrum beta-lactamases (ESBLs)?
Organisms that produce enzymes which can degrade antibiotics ## Footnote This is a significant resistance mechanism against extended-spectrum antibiotics.
52
What are reserve antibiotics, and give an example?
Antibiotics reserved for serious, multi-drug resistant infections; e.g., Carbapenems = Meropenem ## Footnote They inhibit PBPs like other beta-lactams but have increased stability.
53
What is the structural distinction of Carbapenems?
Carbon replaces sulfur in the ring ## Footnote This change increases stability and spectrum of activity.
54
What type of bacteria do reserve antibiotics like Carbapenems target?
GP, GN, and anaerobes ## Footnote They are reserved due to the risk of resistance development.
55
Where are Carbapenemases commonly emerging?
Worldwide, often in enterobacterales ## Footnote These enzymes contribute to antibiotic resistance.
56
What is the primary target organism for Monobactams like Aztreonam?
Strong activity against Gram-negative bacteria, including Pseudomonas aeruginosa ## Footnote They have no activity against GP bacteria or anaerobes.
57
How do Monobactams interfere with bacterial function?
Binds to PBP-3 → interferes with bacterial cell wall synthesis ## Footnote This mechanism is crucial for their antibacterial activity.
58
What is the structural uniqueness of Monobactams?
Single beta-lactam ring, no fused second ring ## Footnote This structure makes them resistant to many beta-lactamases.
59
What is Vancomycin known for?
Most well-known glycopeptide ## Footnote It is effective but nephrotoxicity limits its use.
60
What infections is Vancomycin primarily used to treat?
MRSA infections, endocarditis, Clostridium difficile infections ## Footnote It is especially effective in oral form for C. difficile.
61
How is Teicoplanin used in comparison to Vancomycin?
Used similarly, particularly in Europe for GP infections ## Footnote It has a similar spectrum but is often preferred for its longer half-life.
62
What are Dalbavancin and Oritavancin?
Newer glycopeptides with a long half-life ## Footnote They offer advantages in dosing frequency.
63
What is the mechanism of action of glycopeptides?
Inhibit cell wall synthesis by interfering with peptidoglycan synthesis pathway ## Footnote Glycopeptides bind specifically to the D-Ala-D-Ala terminus of the peptidoglycan precursor units
64
How do glycopeptides affect the peptidoglycan chain?
Binding blocks incorporation of new PG subunits into growing PG chain ## Footnote This prevents cross-linking by PBP enzyme, weakening cell wall and leading to cell lysis
65
What is the mechanism of action of fluoroquinolones?
Inhibition of DNA replication ## Footnote Most widely used fluoroquinolone is Ciprofloxacin
66
What bacterial enzymes do fluoroquinolones inhibit?
DNA Gyrase (topoisomerase II) in GN bacteria and Topoisomerase IV in GP bacteria ## Footnote Results in disruption of DNA replication, blocked cell division, and accumulation of DNA breaks causing cell death
67
What is the spectrum of activity for fluoroquinolones?
Excellent against Gram-negative rods, good against Gram-positive cocci, effective against Mycobacterium tuberculosis ## Footnote Includes Pseudomonas aeruginosa and Staphylococcus aureus (some MRSA activity)
68
What are the clinical uses of fluoroquinolones?
UTIs, STIs (chlamydia), GI infections
69
How do antibiotics targeting protein synthesis function?
Inhibit bacterial ribosomes and selectively block translation at various stages ## Footnote This can lead to bacteriostatic or bactericidal effects
70
What are examples of antibiotics that inhibit protein synthesis?
Tetracyclines, Macrolides (Erythromycin)
71
What is the mechanism of action of tetracyclines?
Binds to 30S ribosomal subunit – blocks initiation of mRNA polypeptides
72
What is the mechanism of action of macrolides?
Binds to 50S ribosomal subunit – inhibits peptide bond formation and mRNA elongation
73
What types of bacteria are tetracyclines effective against?
Broad: Gram-positive, Gram-negative, atypicals (e.g. Chlamydia, Rickettsia, Mycoplasma) ## Footnote Limited use for acne, malaria prophylaxis, Lyme disease
74
What are the limitations of tetracyclines?
Causes discoloring of teeth due to calcium depositing
75
What are the specific uses of macrolides?
Used to treat upper and lower respiratory tract infections, STIs, skin infections ## Footnote Particularly useful in penicillin allergy
76
Do macrolides have activity against Enterobacterales?
No activity against Enterobacterales ## Footnote Some activity against Gram-negative (H. influenzae)

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