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AB Flashcards

1
Q

What is an example of an antibiotic with a high chemotherapeutic index value? Low value?

A

Penicillin – high

Aminoglycosides – lower

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2
Q

MIC and MBC related to which type of agents?

A

MIC: minimum inhibitory concentration
MBC: minimum bactericidal concentration

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3
Q

Name 3 bacteriostatic drugs:

A

Chloramphenicol, clindamycin, macrolides

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4
Q

Name 3 bactericidal drugs:

A

Penicillin & cephalosporin, vancomycin, rifampin

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5
Q

Direct toxic damage caused by the following drugs:

A

Aminoglycosides – kidney, nerves
Chloramphenicol – bone marrow
Vancomycin – kidneys
Antifungal drugs – liver
Tetracycline – teeth (avoid in children under 8)
Quinolones – bones and cartilage (especially Achilles tendon)
Cephalosporin – may cause gall stones

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6
Q

Which are the beta-lactam antibiotics?

A

Penicillin, cephalosporin, carbapenem, monobactam

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7
Q

What is the penicillin mechanism of action?

A

Penicillin molecules bind penicillin binding protein & transpeptidation is inhibited, cell wall synthesis is blocked so autolytic enzymes are activated

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8
Q

Which penicillin generation is acid sensitive? What is the consequence?

A

Ist, only injectable

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9
Q

Which bacteria lacks a cell wall and therefore is resistant to penicillin?

A

Mycoplasm tb

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10
Q

Which bacteria are resistant to penicillin due to beta-lactamase production?

A

Staphylococcus, Neisseria, enteric bacteria (ESBL)

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11
Q

Which bacteria are resistant to penicillin due to lack or alteration of binding protein

A

Streptococcus pneumoniae, MRSA

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12
Q

Which penicillin derivative is a narrow spectrum antibiotic, primarily to gram + cocci and bacilli? How is it administered?

A

Penicillin G, paraenterally

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13
Q

Which penicillin is used to treat oral infections?

A

Penicillin V (has higher serum concentration)

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14
Q

What are penicillin derivatives (G, V) effective against?

A

Streptococcus, Neisseria, Treponema, Bacillus anthracis

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15
Q

What are the penicillin with extended spectrum and what are they effective against?

A

Aminopenicillins: wide spectrum, G+/-
Carboxypenicillin: Proteus, Pseudomonas (ineffective against S. aureus, enterococcus)
Ureidopenicillin: Pseudomonas
ALL are sensitive to beta-lactamase

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16
Q

Give examples of beta lactamase inhibitors:

A

Clavulanic acid, sulbactam, tazobactam (Unasyn, Augmentin)

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17
Q

Which penicillin derivatives are penicillinase (=beta-lactamase) resistant? What is their downside?

A

Methicillin, oxacillin, cloxacillin, nafcillin

Less effective

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18
Q

What are mechanisms of cephalosporin resistance?

A

Difficult penetration, lack of penicillin binding protein, broken down by beta-lactamase enzyme

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19
Q

What is the cephalosporin spectrum?

A

Broad, bactericidal

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20
Q

What are the synthetic derivatives of cephalosporins?

A 
1st gen – Gram + cocci
2nd gen – Gram -
3rd gen – Gram - 
4th gen – Gram + and gram - 
5th gen  - MRSA (ceftarolin), pseudomonas (ceftobiprole)
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21
Q

What are monobactams (aztreonam) used for?

A

Gram-negative aerobic bacteria: neisseria, pseudomonas

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22
Q

What are carbapenems (impenem, meropenem) used for?

A

Gram + and Gram - (mostly for MDR bacteria, but ineffective against MRSA)

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23
Q

Which are the glycopeptide antibiotics?

A

Vancomycin, teicoplanin

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24
Q

glycopeptide antibiotics

What is a side effect? Why are they important?

A

Oto- and nephrotoxicity

Used against MRSA, VRE

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25
Q

glycopeptide antibiotics

What is their spectrum? Mode of action?

A
  • Narrow – only against gram + b/c CANNOT cross outer membrane and penetrate inside because too big, bacteria, bactericidal
  • Bind terminal D-ala-D-ala (D-ala-D-lactate) and block crosslink with pentagylcin bridge to inhibit cell wall synth
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26
Q

What is fosfomycin spectrum, what is it used for? What is its mechanism?

A

Broad, UTI (single dose)

Inhibits early stage synthesis of peptidoglycan

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27
Q

What is bacitracin and what is it used for?

A

Polypeptide, inhibits peptidoglycan synthesis (translocation of precursor across membrane), effect against gram - and gram + (especially MRSA!)

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28
Q

Which are protein synthesis inhibitors? Which ribosomal subunit do they act on?

A

30S: Aminoglycosides, tetracyclines
50S: chloramphenicol, macrolides (streptogramins, linezolid)

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29
Q

Some examples of aminoglycosides?

A

Streptomycin (used against TB), gentamicin (used parenterally or in eye drops), neomycin (eye drops)

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30
Q

How do aminoglycosides work?

A

Bind 30S subunit, don’t allow tRNA to bind ribosome which is bactericidal

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31
Q

What is the resistance mechanism of aminoglycosides?

A

Changing receptor on ribosome – mutation
Breaking down by enzymes – encoded on plasmids
Efflux pump
Side molecule can’t penetrate into cell (aerobic)

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32
Q

What are side effects of aminoglycosides?

A

Oto and nephrotoxic, neurotoxic at high doses

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33
Q

Which was the first broad spectrum antibiotic (against gram - and +)

A

Cloramphenicol

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34
Q

What is the mechanism of chloramphenicol?

A

Binds 50S subunit of ribosome, so peptidyl transferase is inhibited

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35
Q

What is the side effect of chloramphenicol?

A

Defective bone marrow function, gray-syndrome, aplastic anaemia

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36
Q

What is the resistance mechanism of chloramphenicol?

A

Acetyl-transferase

37
Q

Which antibiotics disrupt the cell membrane?

A

Polymixins, lipopeptides

38
Q

Which is the mode of action of the macrolide antibiotics?

A

Binds 50S subunit of ribosome, bacteriostatic

Bind peptidyl transferase center

39
Q

What is the spectrum of macrolides?

A

Gram + cocci, legionella, mycoplasma, chlamydia trachomatis

40
Q

What is the resistance mechanism of macrolides?

A

Target modification

Efflux pump

41
Q

What is the side effect of tetracyclines? What is their resistance mechanism?

A

Forms complex with Ca2+ which colorizes enamel, shouldn’t be used in children!
Mutations

42
Q

Which antibiotic is good to use against intracellular bacteria? Which bacteria?

A

Tetracycline, chlamydia, mycoplasma, rickettsia

43
Q

What is the action of clindamycin? What is it an antagonist of?

A

50 S subunit

Macrolides

44
Q

Which bacteria is linezolid NOT effective against?

A

Gram negative

45
Q

What are streptogramins effective against?

A

VRE and VRSA

46
Q

Which antibiotics inhibit nucleic acid synthesis?

A

Quinolons
Inhibitors of folate synthesis
Metronidazol
RNA synthesis inhibitor (Rifampin

47
Q

Inhibitors of folic acid synthesis include:

A

P-amino-benzol-sulfonamides – p-Amino benzoic acid (PABA) antagonist
Trimethoprim – dihydrofolate reductase inhibitor

48
Q

Which antibiotic inhibits DNA gyrase enzyme?

A

Nalidix acid and fluoroquinolons (inhibit DNA gyrase enzyme)

49
Q

What is the original compound in quinolons?

A

Nalidixic acid

50
Q

Rifamycin B (rifampin) mechanism and spectrum?

A

mRNA synthesis inhibition, Gram + cocci, mycobacterium (URT infections)

51
Q

Mechanism of action of nitroimidazole – metronidazole? Limitations?

A

Damages DNA – no DNA synth

Bactericidal, effective only in anaerobic conditions

52
Q

Spectrum of polymyxin and mode of action?

A

Narrow, gram -, bactericidal

Binds membrane phospholipids and inhibits membrane transport

53
Q

Which antibiotic that alters membrane functions is antifungal and toxic (therefore has to be administered locally)?

A

Nystatin (steroid of membrane binding disintegrates PM)

54
Q

When do we use daptomycin? Why is it limited?

A

Used against vancomycin resistant enterococci and staphylococcal infections
ONLY active against gram + (b/c cannot cross outer membrane of gram negatives)

55
Q

Mechanisms of daptomycin:

A

Mutations in genes that involve synthesis of phosphatidylglycerol
Some phenotypes of staphylococcus aureus with VISA phenotype are less susceptible b/c of thicker wall less access

56
Q

Which antibiotics should be completely avoided in pregnancy and young children?

A

Quinolon

57
Q

Which are some important “synergies” or combinations of antibiotics that can be used?

A

Sumetrelim: TMX (tetramethoprim) + SMX (sulfamethoxazole)
Synercid: quinopristin + dalfopristin
Penicillin + gentamycin

58
Q

Which antibiotics are contraindicated to be used together?

A

Beta-lactams and macrolides

Ciprofloxacin+ tetracycline

59
Q

Which antibiotics can be used to treat MRSA?

A

Vancomycin, teicoplanin
Bacitracin
5th generation cephalosporin (cephtarolin)

60
Q

Which are the problem bacteria/problems associated with the following straings:
Staph. Aureus
Enterococcus faecalis, faecium
Mycobacterium TB

A

Staph. Aureus – MRSA, VRSA
Enterococcus faecalis, faecium – VRE
Mycobacterium TB – MDR, XDR

61
Q

Which are the carbapenem resistant gram-negative bacteria?

A

Acinobacter baumanni, pseudomonas aeruginosa, Klebsiella spp, stenotrophomonas maltophila Enterobacteriaceae

62
Q

What do extended spectrum beta lactamases (ESBL) do? Which type of bacteria are they?

A

Hydrolyze penicilins, cephalosporins
Do not hydrolyze carbapenems, monobactams
Gram negative

63
Q

What does metallo beta-lactamase do? Which type of bacteria are they?

A

Hydrolyze carbapenems

Gram negative bacteria

64
Q

What are other antibiotics that work through enzyme inactivation?

A

Aminoglycoside (N-acetyltransferase, O-phosphotransferase, O-adenylotransferase)
Chloramphenicol (acetyltransferase)

65
Q

Which are antibiotic resistance problems seen in gram + bacteria?

A

MRSA – methicillin resistant staphylococcus aureus
PRP – penicillin resistant pneumococcus
VRE – vancomycin resistant enterococcus

66
Q

Why is MRSA resistant to all beta-lactams?

A

PBP2a has low affinity to all beta-lactams

67
Q

What does vancomycin bind in its process of inhibiting cell wall synthesis?

A

D-alanine D-alanine

68
Q

Which kinds of bacteria are resistant to vancomycin?

A

All gram-negative bacteria!

69
Q

Why can’t vancomycin be given per os? When should it be given per os?

A

No absorption in GI

To kill gram + bacteria in GI that overgrow after other antibiotics were taken

70
Q

What is the mechanism of vancomycin resistance? (VRE)

A

Vancomycin can’t bind to the D-ala-D-lactate structure

71
Q

What are the most important MDR bacteria?

A 
ESKAPE: 
Enterococcus, 
S. aureus, 
Klebsiella, 
Acinetobacter, 
p. aeruginosa, 
Enterobacter spp.
72
Q

What are the fundamental mechanisms of extrinsic (acquired) resistance?

A
  1. Receptor is absent
  2. Resistance against the antibiotic which was produced by themselves
  3. Cell wall barrier (gram negatives) or lack of a cell wall (mycoplasma)
  4. Lack of a transport system
  5. Antibiotic concentration is low at the receptor
73
Q

How is resistance described clinically?

A

MIC is higher than maximal dose tolerable by the host

74
Q

Which type of resistance results from the following:
Absence of sterols in cell membrane of bacteria
Mycoplasms have no cell wall
Isoniazid inhibits synthesis of mycolic acid
Gram-negative bacteria have complex cell wall
Some bacteria need energy from the membrane potential to be absorbed

A
  1. Absence of sterols in cell membrane of bacteria resistance to antifungal polyenes (amphotericin B, nystatin)
  2. Mycoplasms have no cell wall beta-lactams are ineffective
  3. Isoniazid inhibits synthesis of mycolic acid only works on mycobacteria, nothing else has mycolic acid in cell walls
  4. Gram-negative bacteria have complex cell wall penicillin G can’t reach penicillin-binding-protein
  5. Some bacteria need energy from the membrane potential to be absorbed inhibition of transport results in resistance to aminogylcosides
75
Q

What is virulence?

A

The degree of pathogenicity of a microbe, depends on presence/absence of certain structures, exotoxins and endotoxins

76
Q

Which bacteria are toxin producing?

A

Clostridium tetani, Corynebacterium diphtheriae

77
Q

Which bacteria produce the following toxins?

Neurotoxins, Cyotoxins

A

Neurotoxins – clostridium botulinum, tetani

Cyotoxins – staphylococci, streptococci, clostridia toxins (cause non-specific necrosis)

78
Q

What is a superantigen?

A

Binds MHC class II molecules at a location outside the groove normally bound by antigenic peptides, then binds part of the beta-chain of the T-cell which can trigger T—cell activation

79
Q

What is the function of non-toxic virulence factors:

A

Capsule: macrophages and neutrophils can’t phagocytose
Flagella: motility, chemotaxis
Pili (fimbrae): adherence
Biofilm: binding of prosthetic devices
Invasin: provides most direct and efficient manner of host cell invasion
Extracellular enzymes: antiphagocytic effect (coagulase, haemolysins, proteases), fascilitate invasion (streptokinase, collagenase, hyaluronidase)

80
Q

Why are there only vaccines for viruses and bacteria?

A

Immune responses against them are antibody mediated

81
Q

What are the types/components of vaccines?

A

Inactivated, attenuated, toxoid, subunit, conjugate

82
Q

Which vaccine contains pathogens grown in culture and destroyed by chemical, heat, radioactivity or antibiotics? Examples?

A

Inactivated vaccines

Cholera, bubonic plague, pertussis

83
Q

Which vaccine contains live pathogens? Examples?

A

Attenuated

Typhoid, TB (BCG - modified strain), typhus

84
Q

What Is a toxoid vaccine? Examples?

A

Contains bacterial toxin components that have been inactivated (chemically or by heat)
Botulism, tetanus, diphtheria

85
Q

What is a subunit vaccine? How can they be made more immunogenic and T-dependent?

A

Contains a subcomponent of the pathogenic organism (proteins or polysaccharides)
Conjugation with proteins

86
Q

Which vaccines contain capsular polysaccharide?

A
  • HiB, haemophilus influenzae type B
  • Prevenar 13/Pneumovax 23
  • Meningococcus vaccines (against ACWY – not B)
87
Q

Which infections require passive immunity?

A

Diphtheria, tetanus, measles, rabies, botulism

88
Q

What are examples of anti-phagocytotic substances on the bacterial surface?

A 
Polysaccharide capsules
M protein and fimbrae 
Surface slime (polysaccharides)
O antigen associated with LPS
K antigen of E coli
Cell bound or soluble protein A

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