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microbiology > antibiotics and resistance > Flashcards

antibiotics and resistance Flashcards

1
Q

Antibiotics

A 
a class of chemotherapeuticagents
• Chemotherapeutic agents are chemical compounds used to treat disease
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2
Q

• Antimicrobials

A

• Antimicrobials destroy pathogenic microbes or

inhibit their growth within host

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3
Q

• Antibiotics

A

• Antibiotics destroy or inhibit bacteria
• Most antibiotics are microbial products or their
derivatives

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4
Q

where do many antibiotics come from

A

many are derived from microbes as compounds produced to compete with other microbes

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5
Q

• selective toxicity

A

– ability of drug to kill or inhibit pathogen while

damaging host as little as possible

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6
Q

• therapeutic dose

A

– drug level required for clinical treatment

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7
Q

• toxic dose

A

– drug level at which drug becomes too toxic for patient

i.e., produces side effects

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8
Q

• therapeutic index

A

– ratio of toxic dose to therapeutic dose

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9
Q

• Bacteriocidal antibiotics

A

• Bacteriocidal antibiotics

– kill bacteria

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10
Q

• Bacteriostatic antibiotics

A

– inhibit growth of bacteria

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11
Q

Broad-spectrum antibiotics

A

– attack many different bacteria (Gram + and Gram -)

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12
Q

Narrow-spectrum antibiotics

A

– attack only a few different bacteria

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13
Q

Determining the Level of Antimicrobial Activity

A

effectiveness expressed in two ways: MIC and MBC

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14
Q

MIC

A

– minimal inhibitory concentration (MIC)

• lowest concentration of drug that inhibits growth of pathogen

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15
Q

MBC

A

minimal bacteriocidal concentration (MBC)

• lowest concentration of drug that kills pathogen

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16
Q

tests used to detemrine MIC/MBC

A

dilution susceptibility and disk diffusion

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17
Q

dilution susceptability

A

• involves inoculating media containing different concentrations of drug
– broth or agar with lowest concentration showing no growth is MIC
– if broth used, tubes showing no growth can be subcultured into drug-free medium
• broth from which microbe cannot be recovered is MBC

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18
Q

Disk Diffusion Tests

A
  • disks impregnated with specific drugs are placed on agar plates inoculated with test microbe
  • drug diffuses from disk into agar, establishing concentration gradient
  • observe clear zones (no growth) around disks
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19
Q

table for disk diffusion tests

A

radius of inhibiton zone: larger= able to inhibit at lower concentrations= lower MIC
may be resistant with smaller inhibition zone

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20
Q

Kirby-Bauer method

A
  • standardized method for carrying out disk diffusion test
  • sensitivity and resistance determined using tables that relate zone diameter to degree of microbial resistance
  • table values plotted and used to determine if concentration of drug reached in body will be effective
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21
Q

Measurement of Drug
Concentrations in the Blood
when effective?
tests?

A

concentration of drug at infection site must be > MIC to be effective
• microbiological, chemical, immunological, enzymatic, or chromatographic assays can be used to determine concentration of drug in blood

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22
Q

Factors Influencing the Effectiveness of Antimicrobial Drugs

A
  • ability to reach site of infection
  • ability to exceed MIC of pathogen
  • susceptibility of pathogen
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23
Q

Ability of drug to reach site of infection factors

A

• depends in part on mode of administration
– oral: some drugs destroyed by stomach acid
– topical
– parenteral routes: nonoral routes of administration

• drug can be excluded by blood clots or necrotic tissue

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24
Q

Factors influencing ability of drug to reach concentrations exceeding MIC

A
  • amount administered
  • route of administration
  • speed of uptake
  • rate of clearance (elimination) from body
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25
Q

Susceptibility of pathogen to drug factors

A
  • Does a drug require bacterial cell growth to be effective? (can spores be targeted)
  • Speed of action of a drug
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26
Q

concepts for Mechanism of Action of Antimicrobial Agents, how we target/ideally?

A
  • can impact pathogen by targeting some function necessary for its reproduction or survival
  • Ideally, targeted function is very specific to pathogen= high therapeutic index– Not always possible
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27
Q

Mechanisms of Action of Antimicrobial Agents

A

target bacterial cell wall
inhibition of protein synthesis
inhibition of NA synthesis
antimetabolites

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28
Q

Disruption of bacterial cell wall drug classes

A

b-lactams
Glycopeptides
Polypeptides
Others

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29
Q

how can we target the cell wall?

A

peptidoglycan unique to both +/- bacteria, most pathgens contain this

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30
Q

Peptidoglycan Synthesis basic steps and diagrammed

A

– peptidoglycan repeat unit forms incytoplasm
• involves use of uridine diphosphate (UDP) as a carrier
– repeat unit then transported across membrane by bactoprenol (“lipid”)
– repeat unit attached to growing peptidoglycan chain
– cross-links formed by transpeptidation

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31
Q

transpeptidation

A

how cross links form in peptidoglycan

exchange of one peptide bond for another

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32
Q

b-lactam function

A

b-lactam antibiotics inhibit transpeptidation

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33
Q

types of B lactams (names)

A

penicillins
cephalosporins
carbapenems
monobactams

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34
Q

different penicillins

A

many with different side chains modifications for variable properties

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35
Q

b-lactamase inhibitors

A

Not antibiotics, but help b-lactam antibiotics by preventing their degradation by b-lactamases
b-lactamases are enzymes produced by some bacteria that are resistant to b-lactam antibiotics

36
Q

Examples of b-lactamase inhibitors, 1st combo?

A

Examples of b-lactamase inhibitors: clavulanic acid, sulbactam, and tazobactam

Augmentin was 1st combination = amoxicillin + clavulanic acid

37
Q

Vancomycin action, counter to this?

A

Vancomycin binds terminal D-Ala-D-Ala and sterically inhibits addition of peptidoglycan subunits to the cell wall.
Vancomycin binding to existing peptidoglycan chains inhibits the transpeptidation reaction that crosslinks the chains.
mutated d-ala-d-lac can counter this and prevent binding

38
Q

vancomycin has been important for treatment of?

A

vancomycin has been important for treatment of antibiotic resistant staphylococcal and enterococcal infections

39
Q

Vancomycin and teichoplanin are?

A

Vancomycin and teichoplanin are glycopeptides

40
Q

Polypeptide names

A

bacitracins and polymixins

41
Q

bacitracins action

A

Prevent recycling of lipid carrier, bactoprenol

42
Q

polymixins action, usual mode of delivery and why?

A

Binds phospholipids and disrupts outer and inner membranes of gram negative bacteria (topical because of more general mode of action = toxicity possible)

43
Q

Cycloserine an along of? How it functions?
second line treatment for?
possible side effect?

A

Cycloserine is a cyclic analog of alanine, blocks formation of the d-ala/d-ala
Second line treatment for Mycobacterium tuberculosis
- Also crosses blood brain barrier and is an NMDA receptor agonist (with
uses and side effects)

44
Q

Isoniazid, Ethionamide actions

A

affecting synthesis of mycolic acid (abundant wax in the cell wall)

45
Q

glycopeptide antibiotics names

A

vancomycin & teichoplanin

46
Q

other antibiotics

A

cycloserine
isoniazid & ethionamide
ethambutol

47
Q

Ethambutol action

A

affecting attachment of mycolic acid in the cell wall

48
Q

bacterial protein synthesis summarized

A
  1. small RNA subunit attatches to mRNA
  2. charged met tRNA recruited
  3. forms 30S initiation complex
  4. large subunit recruited
  5. forms 70S initiation complex
  6. elonagtion, charged tRNA brought into A site>peptidyltransferase
    reaction> translocation reaction
  7. termination
49
Q

how can we target bac pro syn

A

different ribosomes from our own, although toxicity still possible

50
Q

Oxazolidinones name

A

linezolid

51
Q

Oxazolidinones actions

A

Binds 23S rRNA and prevents formation of 70S initiation complex

52
Q

Tetracyclines action

A

Bind 16S rRNA of 30S subunit and prevent binding of aa-tRNA to
A site

53
Q

Aminoglycosides names

A

streptomycin
amikacin
gentamycin
tobramycin

54
Q

Aminoglycosides action

A

Bind to 30S subunit and distort A site, causing translation misreading, which inhibits protein synthesis

55
Q

Chloramphenicol/ Lincosamides actions

A

Bind to 50S subunit and inhibit peptidyltransferase activity= inhibits the peptidyltransferase reaction

56
Q

Macrolides names

A

Erythromycin, azithromycin, clarithromycin

57
Q

Macrolides function

A
  • Bind 23S rRNA in the 50S subunit and block the translocation reaction
  • also prevent formation of the 50S subunit
58
Q

Quinolones names

A

ciprofloxacin and other -floxacins

59
Q

Quinolones function

A

Interfere with type II topoisomerase (DNA gyrase or topoisomerase IV) and
stabilize DNA double strand breaks, prevents DNA from getting untangled/reattached in replication

60
Q

Rifampin & Rifabutin action

A

bind to RNA polymerase and prevent

the initiation of transcription

61
Q

Metronidazole function

A
  • a prodrug with no inherent antimicrobial activity

* produces DNA-damaging radicals under anaerobic conditions via enzymes functioning in anaerobes and microaerophiles

62
Q

Antimetabolites names

A

Sulfonamides, trimethoprim, dapsone, and p-aminosalicylic

acid

63
Q

antimetabolites function

A

target folic acid synthesis, we do not have this process only bacteria/pathogens

64
Q

Drug Resistance

A

Big problem for clinical treatment of infections

Resistance can often be transmitted to other bacteria

65
Q

possible ways of resistance

A

impermeable barrier
target modification
antibiotic modification
efflux pump

66
Q

impermeable barrier

A

cell wall become imperm to Ab

67
Q

target mod

A

target of the Ab is modded (mutation, plasmid, etc), Ab can no longer target effectively

68
Q

Ab mod

A

bacteria produces compound to counter the Ab/destroy it

69
Q

efflux pump

A

ab actively pumped out of cell before it can act

70
Q

penicillins, cephalosporins resistance mech

A

hydrolysis of b-lactam ring by b-lactamase

71
Q

methicillin resistance mech

A

change in penicillin-binding protein

72
Q

tetracyclines resistance mech

A

efflux pump

73
Q

oxazolidinones resistance mech

A

mutations in 23S rRNA

74
Q

quinolones resistance mech

A

mutations in genes encoding DNA gyrase and

topoisomerase IV

75
Q

The Origin of Drug Resistance

A

• New mutations of bacterial genes that encode the targets of antibiotics
OR
• Pre-existing resistance genes that are transmitted from one bacterium to another

76
Q

Genetic elements involved in resistance gene dissemination

A 
Plasmids
Transducing bacteriophage
Bacterial chromosomal genes
Transposons
Integrons
77
Q

plasmids and resistance

A

some can promote their own transfer by conjugation to other cells via sex pili

78
Q

Transducing bacteriophage

A
  • can package non-phage DNA (= transfer by transduction) allowing resistance transfer
79
Q

Bacterial chromosomal genes and resistance

A
  • mutations

- transfer by transformation (uptake of DNA)

80
Q

Transposons and reisistance

A
  • hop into other genetic elements
81
Q

Integrons and resistance, found?

A

Integrons

  • segments of DNA containing complete sets of genes
  • found on plasmids, transposons, and bacterial chromosomes
82
Q

R plasmids and transposons

A

transposon for resistance genes may be found on plasmids= R plasmids

83
Q

Superinfection

A

development and spread of drug-resistant pathogens
caused by drug treatment, which destroys drug sensitive strains

Killing of normal flora removes the inhibitory effect of the normal flora (which produce antibacterial substances & compete for essential nutrients).
This allows for uninhibited growth of potentially pathogenic bacteria & fungi

84
Q

Common organisms in Superinfections include:

A

Clostridium difficile (spore-forming agent of pseudomembranous colitis)
MDR (multi-drug-resistant) gram-negative rods
MRSA (methicillin-resistant Staphylococcus aureus)
Candida or other fungi

85
Q

Preventing emergence of drug resistance

future solutions?

A
  • give drug in high concentrations
  • give two or more drugs at same time
  • use drugs only when necessary

• possible future solutions
– continued development of new drugs
– use of bacteriophages to treat bacterial disease

microbiology (42 decks)

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