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Medical Microbiology > Antimicrobial Chemotherapy > Flashcards

Antimicrobial Chemotherapy Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

Use of drugs to combat infectious agents

A

Use of drugs to combat infectious agents
❑ Antibacterial
❑ Antifungal
❑ Antiparasitic
❑ Antiviral
Differential toxicity: based on the concept that the drug is more toxic to the infecting organism than
to the hosT

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2
Q

What are antibiotics?

A

Antibiotics: Substances produced by a microorganism that in small
amounts inhibit the growth of or kill bacteria.
❖ Majority of antibiotics are based on naturally occurring compounds
❖ May be natural or synthetic
❖ Used in the body to treat infections

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3
Q

Discovery of antibiotics

A

➢ Discovered in 1928
➢ First antibiotic was named Penicillin, from
Penicillium fungus which produced it.
➢ Underfunded research until 1942 (WW2), when it
was then produced in bigger quantities…Helped
save millions of lives
➢ Before this, primitive treatments were used such
as Silver nitrate, Arsenic - Extremely cytotoxic

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4
Q

Antibiotic Producing Microorganisms

A

Gram-positive rods:
➢ Bacillus subtilis: Bacitracin
➢ Bacillus polymyxa: Polymyxin
Fungi:
➢ Penicillium notatum: Penicillin
➢ Cephalosporium spp: Cephalothin

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5
Q

Antibiotic Producing Microorganisms
7
Actinomycetes:

A

➢ Streptomyces venezuelae: Chloramphenicol
➢ Streptomyces griseus: Streptomycin
➢ Streptomyces nodosus: Amphotericin B
➢ Micromonospora purpurea: Gentamicin

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6
Q

What makes an ideal antibiotic?

A

Have the appropriate spectrum of activity for the clinical setting
➢ No toxicity to the host, be well tolerated
➢ Low propensity for development of resistance
➢ Does not include hypersensitivities in the host
➢ Have rapid and extensive tissue distribution
➢ Have a relatively long half-life
➢ Be free of interactions with other drugs
➢ Be convenient for administration
➢ Be relatively inexpensive

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7
Q

Spectrum of activity

A

Narrow
Broad

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8
Q

Narrow spectrum
effective how?

A

Effective against a limited number of species (either G +ve or G –ve
species). Main example: penicillin, G +ve bacteria

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9
Q

Broad spectrum

Effective how?

A

Effective against a wide variety of species (e.g. both G +ve and –ve).
Main examples is TetracyclineW

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10
Q

What is
Minimum Inhibitory Concentration (MIC):

A

Minimum concentration of antibiotic required to inhibit the growth of the test
organism

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11
Q

What does mean?

  1. Minimum Bactericidal Concentration (MBC)
A

Minimum concentration of antibiotic required to kill the test organism

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12
Q

What does mean

  1. Prophylaxis:
A

Antimicrobial agents are administered to prevent infection

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13
Q

General structural features of
bacterial cells

A

Cell shape
Cell wall
Cell membrane(s)
Capsules
Pili and/or Fimbriae
Cytoplasmic inclusions
Bacterial DNA and nucleic acids
Ribosomes
Flagella
Spores

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14
Q

Why is the cell wall important?

A

It is the most appealing target for antibiotics, found
in both Gram-positive and Gram-negative bacteria
❖ Contain peptidoglycan molecules NAM (n-acetyl
muramicacid) and NAG (n-acetyl glucosamine).
❖ They are cross-linked through activity of
transglycosylase and transpeptidase enzymes (PBP)
❖ Many antibiotics inhibit the activity of these two
enzymes

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15
Q

Gram negative
meaning

A

Gram negative : two cell
membranes: inner and
outer membrane. Cell wall
is in between these two

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16
Q

Gram positive meaning

A

Gram positive: one plasma
membrane, one thick cell
wall of peptidoglycan.

17
Q

Mechanisms of activity /
Mode of action

Step One

A
  1. Inhibition of cell wall synthesis:
    Cell wall active agents:
    Bactericidal, time
    -dependent killing
    -
    β
    -lactams:
    Penicillins, cephalosporins,
    cephamycin, carbapenems
18
Q

Role of the INNER cell membrane?

A

Thin structure lying inside the cell wall and enclosing the cytoplasm of the cell.
Role:
1) Selective barrier through which materials exit and enter the cell = selective
permeability
2) Large molecules e.g. proteins cannot pass through the membrane
3) Allows entry of smaller molecules: e.g. H2O, CO2 and some other sugars

19
Q

Role of the OUTER cell membrane?

A

Thin structure lying beyond the cell wall. Only Gram negative bacteria.
Role:
1) Selective barrier
2) Contains proteins for transport
3) Lipopolysaccharide – bacterial defence
4) Allows selective uptake and efflux

20
Q

Mechanisms of activity /
Mode of action

Step Two

A
  1. Disruption of cell membrane:
    ❑ Bactericidal, time dependent killing
    ❑ Antimicrobial peptides / Polypeptide antibiotics
    ➢ Polymyxin B, colistin (antibacterial) or miconazole
    (antifungal)
    ▪ Cationic (+ive charge)
    ▪ Affinity to Lipopolysaccharide (LPS) on cell surface (-ve
    charge)
    ▪ Interacts and disrupts membrane
    ▪ Pore formation
    ▪ Results in loss of metabolites and/or cell lysis
21
Q

What is the role of DNA/Chromosome?

A

Most have smaller rings of independently replicating DNA named
plasmids
Role:
▪ DNA replication, transcription.
➢ Differences between prokaryotic and eukaryotic DNA replication,
transcription and translation allows use of antibiotics to inhibit
bacterial growth without harming the host

22
Q

Mechanisms of activity / Mode of action

Step Three

A
  1. Inhibition of nucleic acid synthesis
    ❑ Binding to DNA gyrase and topoisomerase 5, two
    essential enzymes for DNA replication
    ❖ Class: Quinolones/ Fluoroquinolones
    (ciprofloxacin, norfloxacin, levofloxacin,
    moxifloxacin)
    ❖ Bactericidal, concentration dependent
    ❑ Inhibition of DNA-dependent RNA synthesis
    ❖ Class: Rifamycin (rifampicin, rifabutin
23
Q

Role of ribosomes

A

Cytoplasm of a bacterial cell contains numerous 70S ribosomes
(consisting of 50S and 30S subunits). Consists of rRNA and protein.
Role:
▪ Protein synthesis
▪ Antibiotic target site: e.g. streptomycin can attach to the small
subunit and inhibit protein synthesis

24
Q

Mechanisms of activity / Mode of action

Step Four

A
  1. Inhibition of protein synthesis (ribosomes are the site of protein synthesis)
    ❑ Many classes of antibiotics inhibit protein synthesis by binding to the
    ribosome.
    Classes:
    Macrolides, ketolides, Tetracyclines, Aminoglycosides, Streptogramins,
    Lincosamides
25
Q

Mechanisms of activity / Mode of action

Step Five

A
  1. Action on antimetabolites
    Block folic acid synthesis
    Class: Trimethoprim (trimethoprim, sulfamethoxazole)
    Bactericidal, concentration dependent
26
Q

Safety issues with use of antibiotics

A

➢ Toxicity
➢ Interactions with other medications
➢ Hypersensitivity reactions
➢ Fetal damage/risk to pregnant women
➢ Antibiotic Resistance

27
Q

Antimicrobial Resistance

A

Ability of an organism to resist the effects of a chemotherapeutic agent
to which it is normally susceptible.
➢ Natural (inherent) or genetically encoded at chromosomal or plasmid
level

28
Q

Consequences

A

➢ Treatment failure
➢ Increase in morbidity
➢ Surgical implications
➢ Lack of effective alternatives
➢ Increased costs
➢ Increased demand on the healthcare system

29
Q

Types of resistance?

A

Inherent (natural) resistance

Acquired resistance

30
Q

Inherent (natural) resistance

What is it?

A

▪ Lacks a transport system for an antibiotic
▪ Lacks the target of the antibiotic molecule
▪ Example: G –ve bacteria (e.g. Pseudomonas aeruginosa)

31
Q

Acquired resistance

What is it?

A

Acquired resistance:
▪ Modification of existing genetic material
▪ Acquisition of new genetic material. E.g. MRSA

32
Q

Emergence of resistance?

Why?

A

➢ Overuse:
▪ Viral infections (cold, flu often treated with antibiotics!)
▪ Overuse common in children (0-6 years)
➢ Veterinary Use:
▪ Overuse in animals – transmission to human

33
Q

How to prevent resistance?

A

▪ Promote responsible prescribing
▪ Improve infection prevention controls in human and animal systems
▪ Raise awareness of the problem
▪ Improve research to inform understanding
▪ Development of new drugs, vaccines…
▪ Improve strengthening of surveillance…
▪ Strengthen Uk & international collaborations

Medical Microbiology (10 decks)

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