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Medsci 202 > Lecture 4: Antibiotics > Flashcards

Lecture 4: Antibiotics Flashcards

1
Q

define the term antibiotic

A

sustance produces by a microorgansim that is effective in killing or inhibiting growth of other microorganisms

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2
Q

define the term antimicrobial agent

A

any synthetic drug used to treat and infectious disease
- antibacterial
- antifungal
- antiprotozoal
- antiviral

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3
Q

what is an organic antibiotic

A

isolated from bacteria or fungi (penicillin, erythromycin)

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4
Q

whats a semi-synthetic antibiotic?

A

derived from an organic compound for greater efficacy eg. amoxicillin, methicillin, oxacillin etc. derived from penicillin

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5
Q

what are synthetic antibitoics/antimicrobial drugs

A

generated in the lab (eg. sulfonamides, quinolones)

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6
Q

List the ideal qualities of an antibiotic

A

*kill or inhibit growth of pathogens
*cause no damage to the host
*cause no allergic reaction to the host
*be stable for storage as solid or liquid
*remain in specific tissue long enough to be effective
*kill the pathogens before they mutate and become
resistant

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7
Q

why is inhibiton sometimes enough instead of killing? explain what happens

A

Could be enough to inhibit – infection, organism colanises and proliferateis, immmune system overwhelmed

Substance that stops bacteria from proliferating, immune system can handle those

Bacteriostatic antibitic is good enough

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8
Q

What is the antibacterial spectrum and what are the two features?

A

range of activity against bacteria eg. broad or narrow

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9
Q

explain the term narrow-spectrum AB

A

works only against a limited variety of bacteria
e.g. vancomycin (only against Gram-positives)

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10
Q

explain the term broad-spectrum AB

A

works against a variety of Gram+/- bacteria
e.g. amoxicillin, tetracyclin

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11
Q

define bacteriostatic activity and explain why its useful

A

level of antimicrobial activity that inhibits growth of organism.
Static useful bc own immune system has upper hand to deal with the bacteria

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12
Q

define bactericidal activity

A

level of antimicrobial activity that kills organism

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13
Q

what is the purpose of antibiotic combination

A

combining different antibiotics for:
- broaden the antimicrobial spectrum
- treatment of polymicrobial infections
- prevent emergence of resistant organism
- achieve a synergistic killing effect

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14
Q

define the term anitibiotic antagonism

A

activity of one antibiotic interferes with activity of other, e.g.
the sum of activity is less then the most active individual drug
(penicillin-chloramphenicol). Like 1+1= <1

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15
Q

define the term antibiotic synergism

A

antimicrobial activity is higher than the sum of combined drugs
(e.g. penicillin-streptomycin). Like 1+1= >2

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16
Q

what is an antibiogram

A

result of lab testing for sensitivity of an isolated strain to different antibiotics

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17
Q

What are the three antibiogram methods

A
  1. Semi-quantitative based on diffusion (Kirby-Bauer method)
  2. Quantitative based on dilution series
  3. Determining the Minimum Bacteriocidal Concentration (MBC)
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18
Q

What is caluclated in the kirby bauer method?

A

In Kirby-Bauer testing, bacteria are placed on a plate of solid growth medium and wafers of antibiotics (white disks, shown) are added to the plate. After allowing the bacteria to grow overnight, areas of clear media surrounding the disks indicate that the antibiotic inhibits bacterial growth.

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19
Q

What is MIC and what does it tell us?

A

MIC - minimum inhibitory concentration, calculated for the diamter of AB disk - antibiotic concentration highest at centre of disc and lowest at edges

tells us in vitro levels of susceptibility or resistance of specific bacterial strains to applied antibiotic.

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20
Q

how can MIC be established i.e what methodology

A
  • using agar plates
  • using viles
21
Q

how is MIC established using vials

A

quantitative based on dilution series
last vial in which no bacteria grow contains antibiotic at Minimum Inhibiotry Concentration

22
Q

what is it and how is the Minimum Bacteriocidal Concentration determined?

A
  • the lowest concentration of an antibacterial agent required to kill a bacterium over a fixed period under a specific set of conditions
  • determined by using different test tubes with different concentrations of antibiotic concentrations and subculturing the clear broth (with no bacterial growth) onto antibiotic free solid media to see wether the AB is bacteriostatic or bacteriocidal (i.e if bacteria will grow on agar or not)
  • if it doesnt grow then the tube with the least concentration of AB that killed bacteria is the MBC
23
Q

what are the different classifications of antibiotics?

A
  1. drugs that bloc bacterial cell wall synthesis
  2. inhibitors of RNA transcription
  3. inhibitors of nucleic acid synthesis
  4. antimetabolites
  5. inhibition of protein synthesis
24
Q

give some examples of drugs that block bacterial cell wall synthesis

A

a. ß-lactam antibiotics
b. glycopeptides

25
Q

explain how ß-lactam antibiotics work and give examples

A
  • inhibit peptidoglycan synthesis by irreversible inhibition of transpeptidase (=penicillin binding protein, PBP)
  • prevents cross-linking of peptide chains
  • weak cell wall and osmotic lysis
  • bactericidal
  • penicillins, cephalosporins, carbapenems
26
Q

why are gram-negative bacteria resistant to penicillin

A

penicillin does not pass through outer membrane porins
- thats why we have extended spectrum penicillins (amoxicillin, ampicillin)
- semi-synthetic

27
Q

Explain how glycopeptides work and give and example

A
  • inhibits PG synthesis by binding to the peptides of the peptidoglycan monomers
  • weak cell wall and osmotic lysis
  • mainly against gram postives
  • last resort drugs eg. for MRSA use vancomycin
28
Q

Explain how inhibitors of RNA transcription work

A

Rifamycins
- inhibits bacterial RNA polymerase which is needed for protein synthesis
- AB binds to enzyme and induces a change in structure, nucleotides no longer fit so we cannot make mRNA
- typically used against mycobacteria

29
Q

What are examples of Rifamycins

A

Rifampin, tuberculosis, leproys, MRSA

30
Q

Explain how inhibitors of nucleic acid synthesis works

A

quinolones and fluoroquinolones (synthetic)
- bind DNA topoisomerases (enzymes needed for supercoiling, replication and
separation of circular bacterial DNA), e.g. gyrase, topoisomerase IV, helicase
- prevent DNA supercoiling, broad spectrum, bactericidal
- commonly used against urinary tract infections.

31
Q

Explain how antimetabolites work and the subdivisions

A

a. Sulfonamides (synthetic)
- analogues of PABA, competitively inhibits pteridine synthase
b. Trimethoprim (synthetic)
- inhibits bacterial dihydrofolate reductase (DHFR)

both antibiotics block pathway required for the synthesis of tetraydrofolic acid, a cofactor needed to make nucleic acids

32
Q

antimetabolites are used for what types of infections?

A

urinary tract infections
they are bacteriostatic

33
Q

Explain how inhibition of protein synthesis work and the different methods used

A
  1. by binding to the 30s subunit
    - aminoglycosides
    - tetracyclines
  2. by binding to the 50s subunit
    - macrolides
    - chloramphenicol

of ribosome

34
Q

explain how aminoglycosides work

A

-freeze the 30S initiation complex (30S-mRNA-tRNA)
-misreading of DNA due to frame-shifts
-mostly effective against aerobic, Gram-negative bacteria, bactericidal
-synergistic with penicillins

35
Q

explain how tetracyclines work

A

-inhibit binding of aminoacyl-t-RNA to the acceptor site on the ribosome. = no more translation
-broad-spectrum, bacteriostatic, used against many bacterial infections

36
Q

explain how macrolides work

A

-inhibit translocation of the peptidyl tRNA from the A to the P site
-against Gram-positives, Mycoplasma, bacteriostatic

37
Q

explain how chloramphenicol works

A

-broad-spectrum, bacteriostatic
-toxic, used mostly in topical applications (e.g. eye drops)

38
Q

what are the types of antibiotic resistance

A
  1. non genetic (intrinsic) drug resistance
  2. genetic resistance
39
Q

what are the non-genetic (intrinsic) drug resistance mechanisms

A

a. Metabolic inactivity
most drugs only effect metabolically active cells, not dormant cells
b. Lack of target structure
Mycoplasmas lack cell wall (resistance to penicillins, cephalosporin, vancomycin)
c. Exclusion
antibiotic can’t enter cell (e.g. penicillin/Gram-negative bacteria)

40
Q

what are the genetic resistance mechanisms of antibiotic resistance

A

a. Chromosomal resistance
- spontaneous mutation in a gene encoding a target receptor: mutation of RNA-
polymerase gene results in rifamycin resistance.

b. acquired resistance
- transformation, conjugation, transduction

41
Q

explain the three terms of acquired antibiotic resistance

A

transformation - a bacterium takes up a piece of DNA floating in its environment
transduction - DNA is moved from one bacterium to another by a virus.
conjugation - DNA as plasmid is transferred between bacteria through a tube between cells.

42
Q

explain the process of selection for antibiotic resistant strains

A
  • selective pressure
  • natural selection - survival of the fittest
  • mutations in bacteria can become useful and allow them to survive = resistance
43
Q

what are the six antibiotic resistnace mechanisms

A
  1. exclusion of antibiotic from site of action - porins wg. penicillin from gram negative
  2. efflux pump for the removal of AB from site of action
  3. enzymatic modification - modify AB in cell and make it inactive
  4. destruction - ßlactamase destroys penicillin
  5. modify antibiotic insensitive target - penicllin binding protein or transpetidase to make cell wall cross links, modified so ab cant recognise it anymore. or substiuted by another one with similar function
  6. new insensitive target – alternative PBP, penicillin wont recognise but it still cross links cell wall
44
Q

explain how ß-lactamases work

A
  • enzymatic destruction of the ß-lactam ring (bottom of garage cleaved)
  • they are plasmid encoded enzymes that can be
    transferred between bacterial strains and species.
45
Q

What are some ß-lactamase resistant penicillins

A

-methicillin, oxacillin, flucloxacillin
these are unaffected by b-lactamase
Clavulanic acid: b-lactamase inhibitor (used with amoxicillin so that b-lactamse doesnt cleave amoxicillin)
Augmentin= amoxicillin + clavulanic acid

46
Q

explain how resistnce to ß-lactamase-resistant penicillins works

A

production of an altered PBP with a lower affinity for most β-lactam antibiotics mainly in gram-positives

eg. MRSA: Methicillin-resistant S. aureus - carry Staphylococcal Cassette Chromosome mec (SCCmec)

47
Q

what is Staphylococcal Cassette
Chromosome mec (SCCmec)

A

SCCmec is a large mobile genetic element that includes the mecA gene and confers resistance to β-lactam antibiotics in methicillin-resistant Staphylococcus aureus (MRSA)

  • integrated in bacterial genome
  • SCCmecII: mainly in hospital MRSA strains, also encodes resistance to macrolide–lincosomide–streptogramin B antibiotics and spectinomycin
  • SCCmecIV: mainly in community-acquired MRSA

this can grow, hence longer chains found in hosptials etc, pick up more parts

48
Q

what are the two classes of drug resistance

A

Multidrug-resistant strains: resistant to more than one class of drugs
Pandrug-resistant strains: resistant to all clinically safe drugs

Medsci 202 (28 decks)

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