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Microbio > Ex 1: Principles 1-4 Biological basis for antibacterial action > Flashcards

Ex 1: Principles 1-4 Biological basis for antibacterial action Flashcards

1
Q

What is a chemotheraputic agent?

A

chemical compounds used to treat disease

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2
Q

What is an antimicrobial?

A

destroy pathogenic microbes or
inhibit their growth within host

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3
Q

What is an antibiotic?

A
  • destroy or inhibit bacteria
  • a class of chemotherapeutic agents
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4
Q

What are most antibiotics made of?

A

made of microbial products or their derivatives

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5
Q

What is selective toxicity?

A

ability of drug to kill or inhibit pathogen while damaging host as little as possible

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6
Q

What is the therapeutic dose?

A

drug level required for clinical treatment

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7
Q

What is the toxic dose?

A

drug level at which drug becomes too toxic for patient

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8
Q

What is the therapeutic index?

A

ratio of toxic dose to therapeutic dose

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9
Q

What do bacteriocidal antibiotics do?

A

kill bacteria

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10
Q

What do bacteriostatic antibiotics do?

A

inhibit growth of bacteria

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11
Q

What do broad-spectrum antibiotics do?

A

attack many different bacteria (Gram + and Gram -)

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12
Q

What do narrow-spectrum antibiotics do?

A

attack only a few different bacteria

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13
Q

What is the minimal inhibitory concentration (MIC)?

A

lowest concentration of drug that inhibits growth of pathogen

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14
Q

What is the minimal bacteriocidal concentration (MBC)?

A

lowest concentration of drug that kills pathogen

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15
Q

What are the two ways to determine the level of antimicrobial activity?

A

– minimal inhibitory concentration (MIC)
– minimal bacteriocidal concentration (MBC)

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16
Q

What are the two techniques routinely used to determine MIC and MBC?

A
  • dilution susceptibility tests
  • disk diffusion test
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17
Q

What is the dilution susceptibility test?

A

inoculating media containing different concentrations of drug

– broth or agar with lowest concentration showing no
growth is MIC
* broth from which microbe cannot be recovered is MBC

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18
Q

What is the disk diffusion test?

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

What is the 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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20
Q

What are the zone diameters based on for disk diffusion tests?

A

based on studies to establish the levels a drug can safely reach in the human body

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21
Q

concentration of drug at infection site must be _______ MIC to be effective

A

> greater than

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22
Q

What are factors that influence the effectivenss of antimicrobial drugs?

A
  • ability of drug to reach site of infection
  • ability of drug to reach concentrations in body that exceed MIC of pathogen
  • susceptibility of pathogen to drug
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23
Q

What factors affect the ability of drug to reach site of infection?

A
  • mode of administration
    – oral
    – topical
    – parenteral routes
  • drug can be excluded by blood clots or necrotic tissue
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24
Q

What factors influence the ability of the drug to reach concentrations above MIC?

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

What are the main mechanisms of action of antimicrobial agents?

A

can impact pathogen by targeting some function necessary for its reproduction or survival

  • disrupt bacterial cell wall
  • inhibit protein synthesis
  • inhibit nucleic acid synthesis
  • target folic acid pathways
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26
Q

What are the cateogories of antimicrobial agents that disrupt bacterial cell walls?

A

B-lactams
Glycopeptides
Polypeptides
Other (cycloserine, isoniazid & ethionamide, ethambutol)

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27
Q

What are the antimicrobial agents in the B-lactams group?

A

penicillins
cephalosporins
carbapenems & monobactams
(+ b-lactamase inhibitors)

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28
Q

What are the antimicrobial agents in the glycoprotein group?

A

vancomycin & teichoplanin

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29
Q

What are the antimicrobial agents in the polyprotein group?

A

bacitracin & polymixins

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30
Q

What are the steps to peptidoglycan synthesis?

A

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

31
Q

What process creates the crosslinks in peptidoglycan?

A

Transpeptidation
- the exchange of one peptide bond for another

32
Q

What is the crosslink in gram negative bacteria?

A

between D-ala and DAP

33
Q

What is the crosslink in gram positive bacteria?

A

peptide interbridge of gly

34
Q

What do B-lactam antibiotics inhibit?

A

transpeptidation (formation of crosslinking)

35
Q

What type of bacteria does ampicillin target?

A

gram-positive and gram-negative

36
Q

What type of bacteria does methicillin target?

A

penicillinase-resistant bacteria

37
Q

What is the function of B-lactamase inhibitors?

A

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
38
Q

What are examples of B-lactamase inhibitors?

A

clavulanic acid
sulbactam
tazobactam

39
Q

How do you use B-lactamase inhibitors?

A

use in combination with B-lactam antibiotics

ex: amoxicillin + clavulanic acid

40
Q

How does vancomycin work?

A
  • binds terminal D-Ala-D-Ala and sterically inhibits addition of peptidoglycan subunits to the cell wall
  • inhibits the transpeptidation reaction that crosslinks the chains
41
Q

Why are vancomycin and teicoplanin important antimicrobial agents?

A

important for treatment of antibiotic resistant staphylococcal and enterococcal infections

42
Q

What do polypeptide antimicrobial agents do?

A
  • Prevent recycling of lipid carrier
  • Binds phospholipids and disrupts outer and inner membranes of gram negative bacteria
43
Q

How are polypeptide antimicrobial agents given?

A

topically because of more general mode of action = more toxic to humans

44
Q

What is cycloserine used for?

A

Second line treatment for
Mycobacterium tuberculosis

45
Q

Why is cycloserine used only as a second line of treatment?

A

crosses blood brain barrier and is an NMDA receptor agonist (with uses and side effects)

46
Q

What do isoniazid and ethionamide do?

A

Inhibits Mycobacteria by affecting synthesis of mycolic acid

47
Q

What does ethambutol do?

A

Inhibits Mycobacteria by affecting attachment of mycolic acid in the cell wall

48
Q

What groups of drugs inhibit protein synthesis?

A
  • Oxazolidinones (linezolid)
  • Tetracyclines
  • Aminoglycosides (streptomycin, amikacin, gentamycin, tobramycin)
  • Chloramphenicol
  • Lincosamides
  • Macrolides (Erythromycin, azithromycin, clarithromycin)
49
Q

What is the cycle of protein synthesis?

A
  1. 30S ribosomal subunit and mRNA
  2. forms 30S initiation complex
  3. 50S ribosomal subunit becomes the 70S initiation complex
  4. peptidyltransferase reaction
  5. translocation reaction
  6. restart
50
Q

How do oxazolidinones (linezolid) work?

A

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

51
Q

How do tetracyclines work?

A

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

52
Q

How do aminoglycosides (streptomycin, amikacin, gentamycin, tobramycin) work?

A

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

53
Q

How do chloramphenicols work?

A

Bind to 50S subunit and inhibit
peptidyltransferase activity

54
Q

How do lincosamides work?

A

blocks the peptidyltransferase
reaction

55
Q

How do macrolides (Erythromycin, azithromycin, clarithromycin) work?

A
  • Bind 23S rRNA in the 50S subunit and block the translocation reaction
  • also prevent formation of the 50S subunit
56
Q

What are the drugs that inhibit nucleic acid synthesis?

A
  • quinolones (ciprofloxacin)
  • rifampin and rifabutin
  • metronidazole
57
Q

How do quinolones (ciprofloxacin) work?

A

Interfere with type II topoisomerases and stabilizes DNA double strand breaks

58
Q

How do rifampin and rifabutin work?

A

Bind to RNA polymerase and prevent the initiation of transcription

59
Q

How do metronidazoles work?

A
  • a prodrug with no inherent antimicrobial activity
  • produces DNA-damaging radicals under anaerobic conditions via enzymes functioning in anaerobes and microaerophiles
60
Q

What do antimetabolites (Sulfonamides, trimethoprim, dapsone, p-aminosalicylic acid) do?

A

disrupt the bacterial folic acid synthesis pathways

61
Q

What are the four main ways of drug resistance?

A
  • modified cell wall protein
  • modified drug target
  • drug-inactivating enzyme
  • efflux pump
62
Q

What mechanism are bacteria resistant to penicillins and cephalosporins?

A

hydrolysis of b-lactam ring by b-lactamase

63
Q

What mechanism are bacteria resistant to methicillin?

A

change in penicillin-binding protein

64
Q

What mechanism are bacteria resistant to tetracyclines?

A

efflux pump pushes drug out of cell

65
Q

What mechanism are bacteria resistant to oxazolidinones?

A

mutations in 23S rRNA

66
Q

What mechanism are bacteria resistant to quinolones?

A

mutations in genes encoding DNA gyrase and topoisomerase IV

67
Q

What are the two ways bacteria become drug resistant

A
  • New mutations of bacterial genes that encode the targets of antibiotics
  • Pre-existing resistance genes that are transmitted from one bacterium to another
68
Q

What are the five genetic elements involved in drug resistance?

A
  • Plasmids: conjugation
  • Transducing bacteriophage: transduction
  • Bacterial chromosomal genes: mutations/transformation
  • Transposons
  • Integrons
69
Q

What is a superinfection?

A

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

70
Q

How do superinfections occur?

A

Killing of normal flora removes the inhibitory effect of the normal flora. This allows for uninhibited growth of potentially pathogenic bacteria & fungi

71
Q

What are the common organisms in superinfections?

A
  • Clostridium difficile
  • MDR (multi-drug-resistant) gram-negative rods
  • MRSA (methicillin-resistant Staphylococcus aureus)
  • Candida or other fungi
72
Q

What are the ways to prevent emergence of drug resistance?

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
73
Q

What are the upcoming major antibiotic resistant threats?

A
  • clostridium difficile
  • carbapenem-resistant enterobacteriaceae
  • neisseria gonorrhoeae
  • fluconazole-resistant candida
74
Q
A
75
Q
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75
Q
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Microbio (11 decks)

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