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Bacteriology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are antibiotics

A

Molecules that kill bacteria or inhibit their growth-can be biological origin (produced by environmental microbes) or (semi) synthetic origin (produced by chemists)

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2
Q

What makes a useful antibiotic

A

inhibit specific cellular processess in bacterial cells exhibit toxic effects on bacteria, but not on humans-selective toxicity

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3
Q

What is selective toxicity

A

Selective toxicity – antibiotics exert their activity by inhibiting
gene products found in bacterial cells, but not in humans
Ideally, such targets are completely absent from human cells (enzymes that make peptidoglycan) or, if present in human cells, possess unique properties in bacteria that can be exploited to confer specificity (ribosomes)
-> Minimize side effects

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4
Q

Disinfectants

A

Toxic to humans and bacteria (e.g. bleach)
Nonspecific effects
Used to eliminate organisms on inanimate objects, surfaces

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5
Q

Antiseptics

A

Generally toxic to bacteria
Nonspecific effects (e.g. protein denaturation)
Too toxic for systemic use in humans (e.g. peroxides, alcohols)
OK for topical use

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6
Q

Antibiotics

A

Target specific cellular processes
Exhibit effects on bacteria but not on humans – selective toxicity
Can be administered systemically

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7
Q

Antibiotics can be classified as what two things

A

bacteriostatic

bacteriocidal

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8
Q

bacteriostatic

A

inhibit growth of bacteria (but do not kill
them) - rely on immune system to eradicate

-number of viable cells doesn’t decrease, but it doesn’t increase. it just stays constant

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9
Q

Bacteriocidal

A

: kill bacteria directly
important for immunocompromised patients, device-associated
infections, endocarditis
-graph would should number of bacteria decreasing

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10
Q

pharmacology/bioavailability

A

Not all antibiotics penetrate all tissues
equally. To be effective, an antibiotic needs to get to site of infection at
therapeutic levels

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11
Q

Spectrum of activity

A
  • the collection of bacterial species that is
    susceptible to a given antibiotic
    -narrow spectrum
    -broad spectrum
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12
Q

Narrow spectrum antibiotic

A

effective against a relatively small group of

bacteria (e.g. aerobic Gram-positive bacteria)

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13
Q

Broad spectrum antibiotic

A

effective against a wide range of bacteria (e.g.

Gram-positive and Gram-negative bacteria)

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14
Q

Are broad spectrum antibiotics desirable, list an advantage and a disadvantage

A

Advantage: Can be used when infectious agent is unknown or in emergency

Disadvantage:
Affects many members of natural microbiota, leading to
undesirable secondary effects
(diarrhea, antibiotic resistance)

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15
Q

What does susceptibility mean?

A

Bacteria are considered to be “susceptible” to an antibiotic if their growth
can be inhibited by concentrations of the antibiotic that can be readily
achieved in a patient at the site of infection
Susceptibility determinations are made with in vitro susceptibility tests – they
require pure cultures of infectious organism, obtained from the infected
patient
(i.e. need to isolate infectious agent away from normal microbiota)

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16
Q

Why do we need to measure susceptibility?

A

-Infectious bacteria must be susceptible for an antibiotic to be clinically effective

-But, all isolates of a given bacterial species are NOT susceptible to the
same antibiotics (e.g. some staphylococci are susceptible to methicillin;
some are resistant)

-So, simply identifying the bacterial cause of a disease is not enough – for
optimal therapy, must know the antibiotic susceptibility profile for that
specific isolate (antibiogram)

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17
Q

Relating to bacterial suseptibility, for optimal therapy what must you know

A

the antibiotic susceptibility profile for that specific isolate (antibiogram)

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18
Q

How do we measure susceptibility

A
  • bacterial growth in liquid medium: quantitative approaches
  • MIC
  • MBC
  • put in tubes with increasing amounts of antibiotic. the amount of antibiotic where growth stops is MIC, when bacteria die it is MBC
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19
Q

Minimum Inhibitory Concentration

A

Defines the lowest concentration of antibiotic that inhibits growth
-there should be no bacterial growth

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20
Q

Minimum bacterial concentration

A

defines the lowest concentration of antibiotic that kills a defined proportion of bacterial population after specified time (99.9% of bacteria killed after 24 hours)

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21
Q

To be therapeutically effective what must be true of an antibiotic

A

to therapeutically effective, antibiotic must achieve or exceed these concentrations at site of infection in host

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22
Q

Toxic side effects of drugs examples

  • tetracycline
  • streptomycin
  • chloramphenicol
A
  • tetracycline: discoloration
  • streptomycin: auditory damage
  • chloramphenicol :anemia
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23
Q

Hypersensitivity

A

Anaphylactic shock in resonse to peniciclin

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24
Q

Alteration of normal microflora

A
  • antibiotic-associated diarrhea/enterocolitis

- clostridium difficile is responsible for many of the severe complications (pseudomembraneous enterocolitis)

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25
Q

Selection for antibiotic resistance

A

Heritable change in bacterial genotype that confers enhanced growth in the presence of an antibiotic-renders antibiotic useless

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26
Q

List 4 Unintended consequences of antibiotics

A
  • toxic effects
  • hypersensitivity
  • alteration of normal microflora
  • selection for antibiotic resistance
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27
Q

How do bacteria become antibiotic resistant?

A
  • genotypic changes that enable growth in the presence of an antibiotic usually occur by one of these mechanisms
  • horizontal gene transfer
  • spontaneous mutations
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28
Q

Horizontal gene transfer

A
  • Acquisition of foreign DNA encoding resistance genes, (getting DNA from someone else that has the resistance genes)
  • can enable rapid emergence of multi-drug resistant strains
  • (plasmids and transposons)
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29
Q

Spontaneous mutations

A

-(strong selection for growth superimposed on large populations of bacteria can lead to emergence of rare resistant mutants)

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30
Q

Three mechanisms by which bacteria overcome inhibition by antibiotics

A
  1. Modification (inactivation) of antibiotic molecule itself
  2. Modification (reprogramming) of antibiotic target
  3. Reduction of antibiotic concentration/prevent access to target
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31
Q

Modification (inactivation) of antibiotic molecules itself

A
  • Cleavage of β-lactams by β-lactamases

- Enzymatic modification of aminoglycosides, chloramphenicol (cat)

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32
Q

Modification (reprogramming) of antibiotic target

A
  • Point mutations in gyrA, rpoB, ribosomes, PBPs

- Alternative peptidoglycan structure for vancomycin resistance

33
Q

Reduction of antibiotic concentration/prevent access to target

A
  • Efflux pumps (tetracycline [tetA, tetK], macrolides) eject antibiotics from cell
  • some efflux pumps exhibit broad substrate specificity (can pump out many antibiotics)
  • altered cell-envelope permeability prevents penetration of drug (mutations in porins)
34
Q

List antibiotics that target peptidoglycan synthesis

A 
B-lactams
Vancomycin
Bacitracin
Fosfomycin
D-cycloserine
35
Q

List antibiotics that target RNAP and RNA synthesis is the target of some antibiotics

A

Rifampin

Fidaxomicin

36
Q

List antibiotics that target key metabolic reactions

A

Trimethoprim/sulfamethoxazole

37
Q

List antibiotics that target cell membrane

A

Polymyxins

Daptomycin

38
Q

List antibiotics that target DNA replication and repair

A

Fluoroquinolones

Metronidazole

39
Q

List antibiotics that target Ribosomes and protein synthesis

A 
Tetracyclines 
Clindamycin
Aminoglycosides Chloramphenicol
Macrolides
 Tigecycline
Oxazolidinones
40
Q

peptidoglycan

A

polymer of alternating sugars (GlcNAc-MurNAc) crosslinked via peptide side chains

-thicker in gram positive, but gram negative have an outer membrane that has porins, and serves as a permeability barrier)

41
Q

List the four core concepts for antibiotics that target peptidoglycan synthesis

A

-peptidoglycan must be synthesized during growth

  • peptidoglycan provides critical structural integrity to bacterial cells that protects them from lysis due to osmotic pressure-therefore, growing cells will lyse if peptidoglycan synthesis is inhibited
  • peptidoglycan (and the enzymes that synthesize it) is unique to bacteria
  • Therefore, peptidoglycan biosynthesis is a good target for antimicrobial agents
  • high specificity and low toxicity for host
42
Q

Describe the specificity and toxicity for drugs that target peptidoglycan synthesis

A

high specificity and low toxicity

43
Q

Peptidoglycan biosynthesis occurs in 3 stages. List them

A

Stage 1: synthesis of MurNAc-pentapeptide precursors-cytoplasm

Stage 2: lipid linkage and transport of disaccharide precursors across membrane

Stage 3: polymerization & crosslinking of precursors into peptidoglycan - extracellular(via PBPs)

44
Q

PBPs Penicillin binding proteins

A

-key enzymes that catalyze polymerization and cross linking of peptidoglycan (D-Ala to L-Ala)

45
Q

What family of drugs target peptidoglycan

A

B-lactam

46
Q

List the dugs that target peptidoglycan intracellularly

A

fosfomycin

D-cycloserine

47
Q

List the drugs that target peptidoglycan synthesis extracellularly

A

glycopeptides
B-lactams
bacitracin

48
Q

What is the substrate for the enzyme that assists in peptidoglycan cross linking?

A

This enzyme is called PBP

its substrate is D-Ala

49
Q

How to B-lactam antibiotics work

A

they inactivate PBP in various ways so there is no peptidoglycan cross-linking and therefore no peptidoglycan synthesis and the cell lyses and dies…no bacterial growth

50
Q

What class of drugs block peptidoglycan crosslinking

A

B lactam

51
Q

What is the mechanism of action of B-lactams

A

there are four types but they all inhibit bacterial growth by the same mechanism
-B-lactams bind PBPs and inactivate them to prevent peptidoglycan cross-linking (bactericidal)

52
Q

B lactam drugs that have a B lactam ring

A 
penicillin
ampicillin
amoxicillin
methicillin
oxacillin
ticarcillin
piperacillin
53
Q

Carbapenem B-lactam drugs

A

imipenem
meropenem
ertapenem
doripenem

54
Q

Cephalosporin B-lactam drugs

A 
cefazolin
cephalexin
cefuroxime
cefoxitin
ceftriaxone
ceftazidime
cefepime
55
Q

Monobactam B-lactam drugs

A

aztreonam

56
Q

How do B-lactams inhibit PBPs to prevent peptidoglycan synthesis

A

they mimic the natural substrate of PBPs ( D-Ala-D-Ala)

57
Q

How do the four types of B-lactams differ

A

they have different R groups, which alters their properties, such as their spectrum of activity but does NOT alter their mechanism of action.

58
Q

Possible side effect of B-lactams

A

they can cause hypersensitivity (allergic reactions0 in some people, sometimes very severe

59
Q

Primary mechanisms of bacterial resistance to B-lactam antibiotics

A
  1. Production of an enzyme called a “β-lactamase” that catalyzes the enzymatic inactivation of β-lactam antibiotics (cleavage of β-lactam ring) (Gram-Negative Bacteria mostly)
  2. Reduced permeability that prevents β-lactam antibiotics from accessing PBPs (intrinsic resistance of some Gram-; mutations in porins that reduce access to periplasmic space)
  3. Altered PBPs that prevent binding of β-lactam antibiotics
    (modification of antibiotic target) (Gram positive)
60
Q

Describe how B-lactamases work

A

-B-lactamases are enzymes that bacteria have that cleave the B-lactam ring of the antibiotic, rendering it inactive, the PBPs are then free to cross-link peptidoglycan

-some bacteria (e.g. Pseudomonas
aeruginosa) encode B-lactamase in their
chromosome (usually inducible not always on)

-often encoded on plasmids that are easily transferred among bacteria

  • many different types of B-lactamases, each with specificity for a certain subset
    of B-lactams
-recent emergence of ESBLs (extended
spectrum -lactamases) with broad
substrate specificities that can cleave a
wide range of -lactams (found primarily
in Gram-negative bacteria)
61
Q

In which class of bacteria are B-lactamases usually found

A

*******usually gram negative

-they can occasionally be found in gram positive (penicillinases prevalent in staphylococcus aureus)

62
Q

Reduced permeability as a bacterial resistance mechanisms

A

prevents β-lactam antibiotics from accessing PBPs (intrinsic resistance of some Gram-; mutations in porins that reduce access to periplasmic space)

63
Q

Altered PBPs as a mechanism of bacterial resistance

A

prevent binding of β-lactam antibiotics (modification of antibiotic target)
• Most common mechanism of
B-lactam resistance found in penicillin resistant Streptococcus and methicillin-resistant Staphylococcus aureus (MRSA; acquisition of ‘low-affinity’ PBP2a, encoded by mecA on the “mec” cassette)

64
Q

What is the most common mechanism of B-lactam resistance found in penicillin resistant Streptococcus and methicillin-resistant Staphylococcus aureus

A

Altered PBPs ex: acquisition of a low affinity PBP2a that the antibiotics can’t interfere with

65
Q

how do scientist overcome B-lactamases

A

B-lactamase inhibitors

66
Q

B-lactamase inhibitors

A
  • (clavulanic acid, sulbactam, tazobactam) share structural features with B-lactam antibiotics – all contain a B-lactam ring
  • The inhibitors possess little intrinsic antibacterial activity
  • Inhibitors bind to b-lactamase & are released very slowly (forms inactive complex), which inhibits B-lactamase activity (only some types of B-lactamases can be inhibited)
  • Inhibitors are administered to patients in combination with a B-lactam antibiotic; the inhibitors prevent B-lactamase activity, allowing the B-lactam antibiotic to inactivate PBPs and prevent bacterial growth
67
Q

How do we inhibit growth of gram positive bacteria (Staphylococcus, Streptococcus)

A
  • B-lactams

- block PBP from binding to D-Ala substrate by having a B-lactam ring that looks like the substrate D-Ala

68
Q

How do gram positive bacteria (Staphylococcus, Streptococcus) Develop resistance to B-lactam drugs

A

Altered PBPs

-prevent binding of B-lactam antibiotics via modification of antibiotic target

69
Q

How do scientist overcome bacterial resistance to B-lactams in gram positive bacteria

A

you can’t….if it is B-lactam resistant try a different drug with a different mechanism

70
Q

How do we inhibit growth of gram negative bacteria (eg E coli, Psuedomonas)

A

B-lactam drug

-block PBP from binding to D-Ala substrate by having a B-lactam ring that looks like the substrate D-Ala

71
Q

How do gram negative bacteria develop resistance to antibiotics

A

B-lactamses that break the B-lactam ring of the antibiotic

72
Q

How do scientist overcome bacterial resistance to B lactams (via B lactamases) in gram negative bacteria

A

B-lactamase inhibitor

not super effective as an antibiotic as its own, bt is often given with a B-lactam drug.

SO you prescribe a B-lactam to inhibit peptidoglycan synthesis and kill bacteria, and then you prescribe a B-lactamase to overcome bacteria resistacne to the B-lactam

73
Q

Antibiotics

A

Small molecules that inhibit specific cellular processes in
bacterial cells and exhibit toxic effects on bacteria, but not on humans
– selective toxicity

74
Q

Antibiotic properties:

A

Bactericidal vs bacteriostatic; narrow vs broad spectrum

75
Q

Adverse effects

A

Antibiotic-associated diarrhea, antibiotic resistance
• Resistance is inevitable: Antibiotic use selects for emergence of
resistant bacteria; resistance traits can be passed between bacteria
on mobile genetic elements

76
Q

3 basic mechanisms of antibiotic resistance:

A 
-modification of the
antibiotic, 
-modification of the antibiotic target, or 
-reduction in antibiotic
concentration
77
Q

B-lactam antibiotics target

A

cell wall biosynthesis by preventing PBPs from crosslinking peptidoglycan

78
Q

Bacterial resistance to

B-lactams is mediated by

A 
enzymes that cleave
the antibiotic (B-lactamases) or by modifications in PBPs that prevent binding of antibiotic
79
Q

How do we use B-lactamase inhibitors

A

B-lactamase inhibitors can be used in combination with

B-lactams to prevent cleavage of the antibiotic by B-lactamases

Bacteriology (15 decks)

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