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4.2 Medical Microbiology > Antimicrobials 2 > Flashcards

Antimicrobials 2 Flashcards

1
Q

Give two examples of how antibiotics target nucleic acid replication

A

Inhibit DNA replication e.g. Quinolones
Ihibit mRNA synthesis e.g. Rifampicin

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2
Q

How do inhibitors of DNA replication work?

A

They inhibit DNA replication by primarily targetting key enzymes required for bacterial DNA synthesis, therby preventing cell division and leading to bacterial cell death

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3
Q

What is the mechanism of action for fluoroquinolones?

A

Inhibit DNA gyrase and topoisomerase IV
These enzymes are crucial for the uninding and supercoiling of DNA during replication and transcription
Blocking these enzymes leads to breaks in bacterial DNA and prevents replication

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4
Q

Give some examples of fluoroquinolones

A

Ciprofloxacin (gen 2)
Levofloxacin (gen 3)
Moxifloxacin (gen 4)
Zabofloxacin

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5
Q

What is the spectrum of activity for fluoroquinolones

A

Broad-spectrum antibiotics which are affective against both gram positive and gram negative bacteria

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6
Q

Give some examples of where fluoroquinolones are commonly used as treatment

A

Bacterial conjunctivitis
Bacterial pneumonia
Tuberculosis
GI infections particularly shigellosis and gastroenteritis
UTIs
Genital infections - used to be main treatment for gonorrhea but we now have high level resistance against this

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7
Q

Give a more indept description of the mechanism of action of the fluoroquinolones

A

DNA gyrase normally relieves tension during DNA unwind, introducing negative supercoils to keep DNA untangles and properly coiled for efficient replication

by inhibiting DNA gyrase and topoisomerase DNA becomes damages and ROS accumulate

Eventually resulting in bacterial death

*should chat gpt this for exact mechanism of action etc

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8
Q

What is the normal role of DNA gyrase

A

DNA gyrase normally relieves tension during DNA unwind, introducing negative supercoils to keep DNA untangles and properly coiled for efficient replication

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9
Q

What are some examples other than fluoroquinolones of inhibitors of DNA replication?

A

Nitroimidazoles

Nitrofurans

Novobiocin

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10
Q

Give an example of a nitroimidazole and what is the mechanism of action of Nitroimidazoles

A

Example: Metronidazole

MOA: drug undergoes reduction in anaerobic conditions to form reactive oxygen species that cause direct DNA damage, leading to the inhibition of DNA synthesis

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11
Q

What is the spectru of activity for metronidazole, a nitroimidazole?

A

Effective mainly against anaerobic bacteria and certain protozoa

It is commonly used to treat infections such as bacterial vaginosis (anaerobes), clostridium difficile and protozoal infections likae amoebiasis

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12
Q

Give an example of a nitrofuran and give its mechanism of action

A

Example: Nitrofurantoin

MOA: the drug is reduced in bacterial cells to reactive intermediates that damage DNA and inhibit DNA replication

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13
Q

What is the spectrum of activity for a Nitrofuran such as Nitrofurantoin

A

Primarily used for urinary tract infections caused by E. Coli or other common uropathogens (nitro disc was used for E.Coli and ents)

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14
Q

What is the mechanism of action of novobiocin?

A

Novobiocin targets DNA gyrase (specifically the GyrB subunit)

It prevents the supercoiling necessary for replication

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15
Q

How is novobiocin used?

A

Less commonly used now in clinical settings

Was used to treat S. aureus infections and as a research tool in laborator studies

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16
Q

How do inhibitors of mRNA synthesis work?

A

These antibiotics work by inhibiting bacterial mNA synthesis (through binging to DNA polymerase?)

Essentially blocking the process by which DNA instructions are transcribed into messenger RNA (mRNA)

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17
Q

Give some examples of inhibitiors of mRNA synthesis

A

Rifampicin
Rifaximin
Rifapentine

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18
Q

What is the mechanism of action of rifampicin?

A

Binds to bacterial RNA polymerase enzyme
Preventing enzyme from initiating the transcription of DNA into mRNA
This stops the production of essential proteins, ultimately leading to bacterial cell death

It is highly specific for bacterial polymerase making it a highly selective bactericidal agent hence its use in long term treatment e.g. TB or leprosy

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19
Q

What infections is rifampicin used for?

A

Tuberculosis and leprosy (long term treatment of about 6 months etc)

MRSA infections

Prophylaxis for close contacts of meningococcal and Haemophilus meningitis

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20
Q

What spectrum of activity does rifampicin have?

A

Effective against gram-positive bacteria, mycobacterium tuberculosis, and some gram-negative bacteria

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21
Q

How do antibiotics Targeting Protein Synthesis work, when are they used?

A

They inhibit (or knock out) the bacterial ribosome which is the cellular machinery responsible for translating mRNa into proteins

Some of these agents have restricted use due to toxicity concerns

One of the few classes of antimiccorbials where new drugs have been developed - new ribosome - targeting antibiotics have shown practical succss in clinical use

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22
Q

List some common examples of antibiotics taregting protein synthesis

A

Aminoglycosides
Tetracyclines
Macrolides
Lincosamides
Chloramphenicol
Oxazolidinones
Streptogramins

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23
Q

In general what is the mode of action of antibiotics targeting protein synthesis

A

They bind to bacterial ribosome at either 30S or 50S

This stops the ribosome from binding to mRNA to form amino acid chains (30S) or elongate the chains to form proteins (50S)

Disruptive effect on many essential bacterial functions leading to cell death

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24
Q

How do aminoglycosides work and give an example of one?

A

Bind to 30S and cause the misreading of mRNA
e.g. Gentamicin

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25
Q

How do tetracyclines work and give an example of one?

A

Bind to 30S and block tRNA attachment

e.g. Doxycycline

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26
Q

How do macrolides work and give an example of one?

A

They bind to the 50S subunit and prevent translocation

e,g, azithromycin

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27
Q

How do lincosamides work and give an example of one?

A

They bind to the 50S subunit and inhibit elongation

e.g. Clindamycin

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28
Q

How does Chloramphenicol work?

A

Inhibits peptidyl transferase at 50S subunit

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29
Q

How does oxazolidinones work and give an example of one?

A

Prevent initiation complex at 50S e.g. linezolid

One of our newer classes

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30
Q

How do streptogramins work

A

Bind to 50S and disrupt elongation and release peptides

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31
Q

List the antibiotics that act on the 30S

A

Aminoglycosides
Tetracyclines

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32
Q

List the antibiotics that act on the 50S

A

Macrolides
Lincosamides
Chloramphenicol
Oxazolidinones
Streptogramins

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33
Q

In your own words how does 30S binding differ from 50S binding

A

30S binding (to mRNA) prevents amino acid chains being produced and from coming together

50S binding prevents elongation of chains

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34
Q

Talk about aminoglycosides, what are they used for

A

Antibiotics that work by targeting protein synthesis at the 30S ribosomal subunit, which is different from how most other antibiotics work -> this makes them especially effective for certain multi-drug resistant infections

They are known for their effectiveness in treating severe bacterial infections, primarily gram-negative bacteria

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35
Q

List some of the aminoglycosides and give the infection they are mostly used for

A

Gentamicin - widely used for various systemic infections

Amikacin - bacteria resistant to other aminoglycosides such as gentamicin

Tobramycin - pseudomonas aeruginosa infections

Streptomycin - originally for TB but now used for TB in combination therapy only due to resistance

Neomycin - topical and sometimes oral for gut decontamination

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36
Q

What is the mechanism of action of aminoglycosides

A

Binds to 30S ribosomal subunit of bacterial ribosomes

This binding disrupts protein synthesis by causing the misreading of mRNA

Incorrect or defective proteins are produced, leading to cell dysfunction and ultimately cell death

Causes misreading of messenger RNA resulting in defective or incorrect amion acids and therefore proteins that can no longer function

Bactericidial effect

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37
Q

Talk about aminoglycosides foor gram-negative bacteria

A

Aminoglycosides are used to treat serious infections usch as sepsis, hospital-acquired pneumonia and urinary tract infections

i.e. pathogens such as E. coli, Klebsiela species and Pseudomonas aeruginosa

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38
Q

Talk about aminoglycosides for gram positive infections

A

Often used in combination with a beta-lactam antibiotic or vancomycin,

When used in this way aminoglycosides can be effective against gram-positive bacteria including staph aureus

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39
Q

Talk about aminoglycosides for tuberculosis

A

Streptomycin was originally made for TB but resistance emerged so its now only used as part of combination therapy

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40
Q

What kind of side effects do aminoglycosides have?

A

Ototoxicity (hearing loss, vestibular damage)
Nephrotoxicity

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41
Q

Talk about the ototoxicity affects of aminoglycosides

A

Hearing loss:
- they can accumulate in the inner ear, leading to hearing loss, which may be irreversible

Vestibular damage:
- balance issue due to damage to vestibular apparatus

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42
Q

Talk about the nephrotoxic effects of aminoglycosides

A

Known for their potential to cause acute kidney injury due to accumulation of antibiotic in the renal cortex

Risks are higher in patiemts with pre-existing renal issues or those who are dehydrated

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43
Q

How do we monitor for toxicity of aminoglycosides

A

Monitor for early hearing loss symptoms is essential to mimise long-term damage

Regular monitoring of renal function e.g. serum creatinine levels is crucial to detect early signs of nephrotoxicity

Therapeutic drug monitoring is generally performed in clinical chemistry
- careful monitoring of drug levels in the blood (both peak and trough) is needed to avoid toxicity while ensuring efficacy

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44
Q

Talk about tetracyclines, how are they used

A

A class of broad-spectrum antibiotics antibiotics

Effective against a variety of gram-positive and gram-negative bacteria, as well as some atypical organism

They were first discovered in the 1940s but they quickly became popular due to their versatility

Commonly used for respiratory infections, acne and atypical bacteria

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45
Q

Give some examples of tetracyclines and what they are used for

A

Tetracycline: the original drug in this class

Doxycline: known for fewer side effects and good bioavailability

Minocycline: sometimes used for acne due to its anti-inflammatory properties

Tigecycline: a glycylcycline -> derived from tetracycline -> a new antibiotic -> used for resistant bacteria

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46
Q

What is the mechanism of action of tetracyclines?

A

Target protein synthesis

Bind to 30S ribosomal subunit of the bacterial ribosome

This prevents binding of tRNA which is necessary for adding amino acids to the growing protein chain

As a result protein synthesis is inhibited and thus bacterial growth is prevented

Bacteriostatic and not bacteriocidal

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47
Q

List the clinical uses of tetracyclines

A

Broad-spectrum activity

Atypical pathogens

Specific infections

48
Q

Talk about the broad-spectrum activity of tetracyclines

A

Effective against a range of Gram-positive and gram-negative bacteria, including staphylococcus, streptococcus, E. coli and Klebsiella

49
Q

Talk about tetracyclines for atypical pathogens

A

Useful for atypical infections caused by organisms like:
- Chlamydia
- Mycoplasma (dad had this)
- Rickettsia (dad had this)
- Borrelia burgdorferi (Lyme)

50
Q

Give some examples of where tetracyclines can be used for specific infections

A

Respiratory tract infections such as pneumonia caused by Mycoplasma pneumoniae

Tick-borne diseases e.g. Doxycycline for Lyme disease (drug of choice)

Doxycycline prophylaxis for malaria

Tetracyclines frequently used in dermatology for acne vulgaris due to its anti-inflammatory properties

51
Q

What are some of the side effects of tetracyclines?

A

Gastrointestinal disturbances as with all antibiotics

Photosensitivity can cause increased sensitivity to sunlight, leading to sunburns -> think of dad in sun -> patients advised to use sunscreen or avoid prolonged sun exposure

Tooth discolorisation - can bind to calcium leading to yellow or brown discoloration of teeth in children under 8 years or pregnant women -> used to treat whooping cough hence why some adults have these now

Hepatotoxicity -> at high doses can cause liver toxicity especially in pregnant women or patients with pre-existing liver conditions

52
Q

Why do we tend to limit the use of tetracyclines

A

Due to toxicity especially in pregnant women or young children

Increasing bacterial resistance limit use -> hence new drugs like tigecycline important in combating resistance

53
Q

Talk about glycyclines

A

A new generation of antibiotics derived from tetracyclines

Developed in response to increasing resistance to older tetracyclines

Designed to combat MDROs such as MRSA and VRE

Broad spectrum effective against gram +/ves, -/ves and atypicals

54
Q

What was the first glycyclcyclines?

A

Tigecycline
Approveed by FDA in 2005

55
Q

How do glycylcyclines differ from tetracyclines

A

Chemical modification

Structurally similar but with modifications that provide better binding to bacterial ribosomes and enhanced resistance to bacterial defense mechanisms

56
Q

What is the mechanism of action of glycylcyclines

A

Target protein synthesis

Bind to 30S ribosomal subunit

Prevent tRNA from binding to the ribosome, blocking the addition of amino acids to the growing protein chain

Result in inhibition of bacterial protein synthesis thus bacteriostatic like tetracyclines

57
Q

What is the spectrum of activity of glycylcylines

A

Gram positive bacteria
Gram negative bacteria
Anaerobic and atypical pathogens

58
Q

Talk about glycylcyclines for gram positives

A

Effective against resistant strains like MRSA and VRE

59
Q

Talk about glycylcyclines for gram negatives

A

Broad activity
ESBL producing Enterobacteriaceae and A. baumannii (baumannii tends to be very resistant but these are effetive against it)
Limited use against PA

60
Q

Talk about glycylcyclines for anaerobes and atypicals

A

Activity against clostridium species, mycoplasma pneumoniae, legionella and chlamydia

61
Q

What are the three main advantages of glycylcyclines

A

Address common tetracycline resistance mechanisms such as efflux pumps and ribosomal protection

Broad spectrum activity including MDR GPs and GNs

Effective for mixed infections involving multiple pathogens

62
Q

How do glycylcyclines overcome efflux pumps?

A

Structural modifications make tigecycline resistant to bacterial efflux pumps, which often render tetracyclines ineffective

63
Q

How do glycylcyclines overcome ribosomal protection?

A

Structural changes allow for stronger binding to ribosomes even in resistance strains

64
Q

Talk about oxazolidinones

A

These are the first in a new class of bacterial protein synthesis inhibitors

They have broad activity against gram-positive cocci, including MRSA and VRE

Resistance is rare

65
Q

Give two examples of oxazolidinones

A

Linezolid
Tedizolid

66
Q

How does linezolid work

A

Targets 23S rRNA within the 50S ribosomal subunit

It prevents the formation of a functional 70S initiation complex, thereby inhibiting protein synthesis

67
Q

Talk about Tedizolid and its uses

A

A newer oxazolidinone - an improved version of linezolid

Has extended activity compared to linezolid

It has improved pharmacokinetcs and fewer gastrointestinal side effects then linezolid

68
Q

Why is resistance rare against oxazolidinones?

A

Due to its unique mechanism of binding to 70S

This makes oxazolidinones highly effective even against resistant gram positives

69
Q

Antibiotics that are active against cell wall membranes work in what three different ways?

A

Those that disrupt the membrane structure

Those that alter membrane permeability

Those that affect membrane enzyme systems

70
Q

What antibiotics disrupt the cell wall membrane structure?

A

Pomyxins such as colistin
Polyenes such as amphotericin B or Nystatin
Newer agents such as lipopetides like Daptomycin

71
Q

Give an example of a polymyxin

A

Colistin

72
Q

Give two examples of polyenes

A

Amphotericin B
Nyastatin

73
Q

What kind of antibiotic is daptomycin

A

A lipopeptide

74
Q

Give an example of an antibiotic which alters membrane permeability

A

Gramicidins

75
Q

How do gramicidins work?

A

They disrupt the bacerial cell wall integrity, increasing permeability

76
Q

Give an example of an antibiotic that affects membrane enzyme systems

A

Antimycin

77
Q

How does antimycin work?

A

It interferes with membrane-associated enzymatic processes

78
Q

What is the spectrum of activity for colistin or polymyxin E

A

Theyre effective primarily against multi-drug resistant gram negative bacteria including Pseudomonas aeruginosa, Acinetobacter baumanii and K. pneumoniae

They were initially used wiely but use has declined due to toxicity however usage resurgence as a last-resort antibiotic due to increasing resistance

79
Q

What is the mechanism of action for colistin or polymyxin E?

A

They act on the bacterial cell membrane - bactericidal

They bind to LPS on the outer membrane of gram negative bacteria

They displace calcium and magnesium ions, leading to membrane destabilisation

This causes permeabilisation of the membrane, leading to leakage of intracellula contents and cell death

80
Q

What are some of the clinical indications for the use of colistin?

A

Pneumonia - hospital acquired or ventilator-associated
BSIs caused by MDR gram-negatives
UTIs especailly those caused by resistant strains
Nebulized formulation used in combination with other drugs to treat P. aeruginosa biofilm infection in CF

81
Q

What are the two main toxic effects of colistin?

A

Nephrotoxicity
Neurotoxicity

82
Q

Talk about the nephrotoicity of colistin

A

Can cause acute kidney injury especially with prolonged use
Requires close monitoring of renal function during therapy

83
Q

Talk about the neurotoxicity of colistin

A

May cause symptoms like dizziness, muscle weakness and neuromuscular blockade

In rare cases it may lead to respiratory paralysis

84
Q

When is colistin consiered a last-resort antibiotic?

A

Its often a last-resort ‘emergency antibiotic for MDR/CRE K. pneumo, P. aeruginosa and Acinetobacter

85
Q

What are polyenes?

A

A class of antifungal agents including amphotericin B (Fungizone and Nyastatin)

86
Q

What is the mechanism of action of polyenes?

A

Highly lipophilic -> they combine with membrane sterols, particularly ergosterol found in fungal cell membranes

Membrane disruption -> binding disrupts membrane structure and creates pores which leads to leakage of K+ ions and other essential cell components

87
Q

What is the spectrum of activity of polyenes?

A

Active against fungal, algal and protozan cells
Commonly used for the treatment of systemic fungal infections

88
Q

What is daptomycin, what is its spectrum of activity?

A

Dapto is a cyclic lipopeptide
It is used for gram-positive bacterial infections, partiularly effective against MRSA

89
Q

Why is daptomycin particularly useful in MRSA

A

Daptomycin reduces the expression of mecA in MRSa which is a key gene conferring methicillin resistance

NB no affect on mecC

90
Q

What is the mechanism of action of daptomycin?

A

Lipophilic Tail: binds to the cytoplasmic membrane of bacteria

Membrane permeabilisation: targets liposomes containing phosphatidylglycerol

This combination causes potassium efflux leading to membrane disruption and cell death

91
Q

How is daptomcin selective

A

It only targets liposomes containing phosphatidylglycerol which is abundant in bacterm CM but not human CM

92
Q

What spectrum of activity does daptomycin have?

A

Effective against gram-positive bacteria

Especially MRSA and VRE

93
Q

Daptomycin is only approved for specific uses, what are these?

A

Complicated Skin and Skin Structure Infections (CSSSI) -> MRSA, MSSA, Streptococus sp and enterococcus spp

Bacteremia and Endocarditis -> S. aureus BSI or Right-sided endocarditis (staph endocarditis)

Alternative to Vancomycin -> for those who are allergic or non responsive to vanc

Renal dysfunction where other therapies would be ess favourable like polymyxins

94
Q

What are competitive inhibitors also called?

A

Anti-metabolites

95
Q

What are competitive inhibitors? How do they work?

A

Antibiotics that inhibit bacterial metabolic pathways

Several antimicrobials inhibit bacteria metabolic processes

These agents act as structual analogues competing for active enzyme sites and thus blocking production

96
Q

Give two examples of classes of competitive inhibitors

A

Sulfonamides
Trimethoprim

97
Q

Talk about sulfonamides

A

They inhibit folate synthesis
They comete with PABA a precursor in folate synthesis, blocking dihydrofolic acid formation

98
Q

Talk about trimethoprim

A

They inhibit folate metabolism

By inhibiting dihydrofolate reductase, blocking tetrahydrofolate formation, which is crucial for DNA synthesis

99
Q

What does PABA stand for?

A

Para-aminobenoic acid

100
Q

What are the four main challenges in antibiotic development

A

Drying pipeline: theres currently o production pipeline - were going to face a ‘post-antibiotic era’

Theres only 5-20 novel drugs in clinical development but progress is very slow and expensive taking abou 15 years and over 800 million

Economics are broken -> leading to few new classes reaching phase III trials -> focus on making other drugs where resistance isnt an issue

Focus on gram positives -> new drugs like linezolid mainly target gram positives -> no drugs to keep up with gram negative resistance

101
Q

Talk about advancements in extending existing antibiotics

A

Fifth generation cephalosporins in development

New inhibitors such as avibactam and varobactam with extended activity of existing agents

102
Q

List some fifth-generation cephalosporins

A

Dalavancin
Ceftobiprole
Plazomicin
Solithromycin

103
Q

Give two examples of new inhibitors

A

Avibactam
Varobactam

104
Q

What are our novel antibiotics

A

Glycylcylines such as Eravacylcine
Oxazolidinones such as Tedizolid
Cyclic lipoptides such as daptomycin

105
Q

What are the three new methods of treating bacteria being looked at

A

Target specific pathogenesis e.g. inhibiting critical steps in the pathogen lifecycle

Disrupt pathogen maintenance e.g. lowers risk of inducin resistance

Resident microorganisms safe -> less likely to impact beneficial microbes (think C. diff)

106
Q

Give two examples of precision antimicrobials

A

Targetting biofilm

Taregtting UPEC binding

107
Q

Talk about targetting biofilms

A

Prevent biofilm formation through signalling pathway inhibition or biofilm breakdown using enzymes

108
Q

Talk about UPEC binding

A

Use of mannosides to block FimH adhesion in UTIs without affecting gut flora

109
Q

What are the 6 new antimicrobial strategies

A

Cellular pathways

Efflux pump inhibitors

Metallic nanoparticles

Immune-based therapies

Faecal microbiota transplant

110
Q

Talk about looking at cellular pathways as a new antimicrobial strategy, give an example

A

Looking for new metabolic targets

Targets central to metabolic pathways e.g. bedaquilline targets ATP synthase in TB

111
Q

Talk about eflux pump inhibitors as a new antimicrobial strategy, give an example

A

Reverse MDR phenotypes -> make resistant bacteria more resistant

Phophorbide A inhibits NorA in S. aureus and MexAB-OprM in P. aeruginosa

112
Q

Talk about metallic nanoparticles as a new antimicrobial strategy

A

Interact with negatively charged surfaces causing membrane disruption

Reactive oxygen species are then generation and metal ions are released

However toxicity is an issue and they tend to impact microbiomes thus limiting their clinical applications

113
Q

Give an example of an immune based therapy as a new antimicrobial strategy

A

MAB directed against P. aeruginosa LPS

114
Q

Talk about Faecal micorbiota transplant as a new antimicrobial strategy

A

Used to restore gut resistance to MDR enteric pathogens

-> C. diff

115
Q

Talk about Faecal micorbiota transplant as a new antimicrobial strategy

A

Used to restore gut resistance to MDR enteric pathogens

-> C. diff

116
Q

Talk about Faecal micorbiota transplant as a new antimicrobial strategy

A

Used to restore gut resistance to MDR enteric pathogens

-> C. diff

4.2 Medical Microbiology (20 decks)

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