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Antibiotics Flashcards

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1
Q

Semi-synthetic antimicrobial agents are

A

based on naturally occurring molecules (e.g. penicillin), modified to alter pharmacological properties (kinetics, toxicity, modify its spectrum)

(…and make $$$ off patents)

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2
Q

bacteriostatic antimicrobial agents

A

halt growth of bacteria such that they are stuck in a premature stationary phase

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3
Q

Bactericidal antimicrobial agents

A

Kill bacteria (a 3-log reduction or 99.9% reduction in population)

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4
Q

Tetracycline

A
  • four-ringed antibiotic
  • 1940s
  • typhis fever tx
  • short half life
    • rapidly excreted in kidney and bile
    • tf take 4x day
  • lead to better derivatives (doxycycline, minocycline)
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5
Q

Beta-lactam antibiotics

A
  • square is beta-lactam ring
  • ‘house’ contains variable atom (S, O, or C) and variable bond (single, double)
  • not initially used as antibiotics; used to stop undesireable bacterial growth in cultures
  • 1940s soldiers getting infections –> explored use as antibiotics
  • carbapenam was the last to be discovered (1976)
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6
Q

penicillin G

A
  • naturally occurring (true antibiotic)
  • effective mainly against G+ cocci and bacilli, and G- cocci
  • acid labile (destroyed in stomach) –> intramuscular admin
  • dosage has increased due to resistance
  • led to development of penV (acid stabile)
  • Common targets (G&V): G+ rods, T. pallidum
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7
Q

Ampicillin

A
  • 1960s
  • widened spectrum: active against G+ c & b, G- c and G- b
  • orally
  • amoxycillin is essentially the same (made when patent ran out)
  • more soluble in the outer membrane tf can act on more G-ve bacteria
  • susceptible to b-lactamases
  • Common targets: G- rods, enterococci, Listeria
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8
Q

Amoxycillin

A
  • new patent of ampicillin
  • microbiologically the same
  • G+ and G - rods and bacilli (broad spectrum)
  • susceptible to b-lactamases
  • Common targets: G- rods, enterococci, Listeria
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9
Q

Methicillin

A
  • acts on resisitant Staph aureus
  • injection
  • nephrotoxic
  • not used anymore
  • replaced by flucoxacillin and dicloxacilin
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10
Q

Flucloxacillin

A
  • used in place of methicillin in kids
  • anti-staphylococcal (narrow spectrum)
  • Common targets: staphylococci except MRSA
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11
Q

Dicloxicillin

A
  • used in place of methicillin in adults
  • anti-staphylococcal (narrow spectrum)
  • Common targets: staphylococci (except MRSA)
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12
Q

MRSA

A
  • methicillin-resistant staphlococcus aureus
  • resistant to all B-lactams
  • has an altered penicillin binding protein (PBP)
    • produces mecA
      • it doesn’t destroy penicillin; produces something it won’t bind to and then it can still make functional cell walls
      • no beta-lactam can bind to it
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13
Q

carbenicillin

A
  • used against pseudomonas aeuriginosa (esp. in leukemia pt)
    • opportunistic antigen
    • resistant to many antiobiotics
    • infecting leukemia pt post-bone marrow transplants
  • no longer used bc needed large doses & to be injected IV
  • use ticarcillin and piperacillin derivatives
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14
Q
A

* = targets specific bacteria

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15
Q

beta-lactams and glycopeptides target

A

the cell wall & peptidoglycan synthesis

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16
Q

the cell wall/peptidoglycan synthesis is the target of

A

beta lactams and glycopeptides

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17
Q

polymyxins and polynes target the

A

cytoplasmic membrane

very toxic due to similarity to our membranes

polyenes are naturally occuring antifungal antibiotics

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18
Q

polyenes

A

act on the cytoplasmic membrane of fungi

naturally occurring

best antifungals

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19
Q

the cytoplasmic membrane is targeted by

A

polymyxins and polyenes (fungi)

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20
Q

ribosomes are targeted by

A

aminoglycosides, chloramphenicol

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21
Q

aminoglycosides and cholramphenicol target the

A

ribosomes

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22
Q

nucleic acids are targeted by

A

rifamycins, quinolones

particularly target transcription

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23
Q

rifamycins and quinolones target

A

nucleic acid metabolism (e.g. transcription)

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24
Q

folic acid is the target of

A

sulphonamides, trimethoprim

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25
Q

sulphonamides and trimethoprim target

A

folic acid

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26
Q

What comprises the backbone of peptidoglycan?

A

N-acetyl clucosamine and N-acetyl muramic acid

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27
Q

What joins the backbones of peptidoglycan?

A

Peptide chains (4AAs) attached to N-acetyl myramic acid

join to

pentapeptide bridges attached to N-acetyl glucosamine

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28
Q

What is the mechanism of synthesis of peptidoglycan?

A
  • precursors synthesized from intermediates in cyroplasm
  • immobilised on inner plasma membrane
  • synthesis of building block - has 2 terminal D-ala
  • transported to exterior membrane
  • linked to growing PTG chain (see card on cross-linking)
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29
Q

What is the mechanism of cross-linking PTG?

A
  • Last step of PTG synthesis
  • Pentaglycine att. to L-Lys (before terminal di-D-ala) knocks off another terminal D-ala and attaches to sub-terminal D-ala
    • enzymes: carboxypeptidase, glycopeptidase, endopeptidase, etc.
    • collectively: penicillin binding proteins
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30
Q

Vancomycin

A
  • 1950s
  • glycopeptide family (targets cell wall)
  • binds to the terminal D-alanine in PTG synthesis
    • blocks all transpeptidase enzymes/PBPs from recognizing their target D-ala
  • large number of charged groups tf insoluble in lipid
    • cannot get through outer membrane
    • tf only active on G+ bacteria
  • expensive, toxic, initally not widely used relative to penicillin
  • used more now as G+ develop resisitance to penicillin, methicillin (e.g. MRSA)
  • drug of choice for MRSA
  • suicide inhibitor, bactericidal
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31
Q

Enterococci

A
  • G+ cocci
  • normal flora in gut
  • opportunistic pathogens
  • resistant to vancomycin
    • ​D-lac (sugar) replaces terminal D-ala
    • tf vancomycin cannot bind
    • huge impact if this resistance is transferred to MRSA
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32
Q

VSSA

A

Vancomycin-susceptible staph aureus (normal s. aureus bacteria)

smooth surface on SEM

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33
Q

VISA

A

vancomycin intermediate (partially resistant) staph aureus

‘furry’ on SEM

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34
Q

How do VISA become resistant to vancomycin?

A
  • Create more PTG to soak up vancomycin
  • Enough left over to form normal cell wall
  • Boxes up vancomycin
  • Increasing vancomycin dosage has nasty side effects
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35
Q

By what mechanisms to beta-lactams/Penicillin G interfere with PTG synthesis?

A
  • b-lactam ring (e.g. Penicillin G) is similar to the D-ala–D-ala peptide bond
    • b-lactams then bind the PBPs that catalyze PTG synthesis here
    • can’t hydrolyze the bond
    • suicide inhibitor: renders itself & the enzyme useless
      • bactericidal
      • as is vancomycin
    • leads to self-destruction by overproduction of autolytic enzymes to destroy the cell wall
    • cell becomes hypertonic, swells, and bursts
  • counteracted by b-lactamase which hydrolyze the similar b-lactam bond
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36
Q

Beta-lactamases

A
  • Produced by bacteria
  • Hydrolyzes the bond that looks like D-ala–D-ala on b-lactam –> falls apart
  • chromosomally encoded in Pseudomonas aueriginosa, giving them Penicillin G, ampicillin - everything but carbenicillin
  • staph aureus had rare b-lactamase producing strains prior to penicillin usage
    • enriched through penicillin use
    • MRSA resistant to beta-lactamase
  • can bind with clavulanic acid, a suicide inhibitor of b-lactamases
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37
Q

Pseudomonas aureginosa

A
  • G- rod
  • produces chromosomally-encoded B-lactamase
    • destroys both ampicillin and penicillin G
    • carbecillin, ticarcillin is resistant to it
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38
Q

Clavulanic acid

A
  • beta-lactam antibiotic
  • weak antibacterial, can’t be used alone
  • when b-lactamase (from E. coli or S. aureus) binds to it, it becomes a suicide inhibitor of those b-lactamases because they cannot break it down
  • inhibits plasma-encoded beta-lactamases (e.g. E. coli, S. aureus)
  • does not inhibit chromosomally-encoded beta-lactamases (e.g. P. aureginosa)
  • can be mixed with amoxycillin (metabolised in the same way bc both b-lactams), called co-amoxyclav/Augmentin
    • clavulanic acid destroys the bacterial b-lactamase
    • allows amoxycillin to work
  • can be mixed with ticarcillin (P. aureginosa) = Ticarcillin
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39
Q

What are the two types of beta-lactamases?

A
  • plasmid-encoded like in S. aureus, responsible for acquired resisitance
    • ​INHIBITED by clavulanic acid
  • chromosomally-encoded like P. aureginosa
    • NOT INHIBITED by clavulanic acid
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40
Q

Co-amoxyclav

A
  • aka Augmentin
  • Amoxycillin + Clavulanic acid
    • CA destroys the bacterial-produced b-lactamase
    • allows amoxycillin to work on amoxycillin-resisitant bacteria
  • spectrum includes flucoxacillin-sensitive staph but not MRSA
41
Q

Ticaracillin

A
  • Tx: Pseudomonas aureginosa
  • not susceptible to the chromosomal b-lactamase of P. aureginosa
    • unless P. aureginosa picks up a plasmid w/b-lactamase that can break down ticarcillin
  • tf susceptible to plasmid-encoded b-lactamases
    • administer w/clavulanic acid = Timentin to overcome b-lactamase
  • Piperacillin is also anti-pseudomonal
42
Q

Timentin

A
  • Ticarcillin + Clavulanic acid
  • Tx: P. aureginosa
    • CA breaks down any plasmid-encoded b-lactamase
    • Ticarcillin can break down chromosomally-encoded b-lactamases
43
Q

Why can’t we use Augmentin to treat P. auerginosa infections?

What can we use?

A
  • chromosomally-encoded b-lactamase on P. aureginosa is what creates the resistance
  • chromosomally-encoded b-lactamase is not inhibited by clavulanic acid
  • tf the b-lactamase will break down the amoxycillin
  • ticarcillin is resistant to the chromosomally-encoded b-lactamases
    • tf effective against P. aureginosa if used in conjunction with clavulanic acid (for any plasmid-encoded b-lactamases) = Timentin
44
Q

Clavulanic acid does not inhibit

A

Chromosomal-encoded b-lactamases

45
Q

Clavulanic acid inhbits

A

Plasmid-encoded b-lactamases

46
Q

Where do aminoglycosides and tetracycline antibiotics act on protein synthesis?

A

Recognition

(they bind to 30s components of the ribosomes; all other drugs that act on protein synthesis bind to 50s subunit)

47
Q

Which antibiotics act on recognition in protein synthesis?

A

Aminoglycosides, tetracyclines

bind to the 30s ribosomal subunit (all others = 50s subunit)

48
Q

What antibiotics target peptidyl transfer in protein synthesis?

A

Chloramphenicol

49
Q

What does chloramphenicol target in protein synthesis?

A

Peptidyl transfer

50
Q

What antibiotics target translocation in protein synthesis?

A

Macrolides

51
Q

What do macrolides target in protein synthesis?

A

Translocation

52
Q

What does mupirocin target in protein synthesis?

A

Isoleucyl-tRNA synthesis

53
Q

What antibiotics target isoleucyl-tRNA synthesis?

A

Mupirocin

54
Q

What antibiotics target the formation of the initiation complex in protein synthesis?

A

Oxazolidones

55
Q

What do oxazolidones target in protein synthesis?

A

Formation of the initiation complex

56
Q

Aminoglycosides

A
  • 2nd to be discovered after penicillin
  • e.g.
    • gentamicin: naturally occurring, used against G-
    • tobramycin: naturally occurring, active against P. aureginosa
    • amikacin: semi-synthetic, complex
    • streptomycin (not used anymore)
57
Q

Penicillins

A
  • can be taken orally (penV)
  • IV for serious infecitions (e.g. severe streptococcal infections, pneumococcal pneumonia, and streptococcal cellulitis) and syphilis
58
Q

Cephalosporins

A
  • 1st generation: effective against G+
  • G+ spectrum then decreases as G- spectrum and b-lactamase resistance increase through 2nd+ generations
  • MRSA, enterococci, and Bacteroides fragilis are resistant to cephalosporins
  • 3rd gen can penetrate CSF - tf Tx: bacterial meningitis
59
Q

What is the mechanism of aminoglycoside action at ribosomes in protein synthesis?

A
  • Act during recognition phase
  • Bind to 30s component close to reading frame, distorting it
    • like a mutation
    • wrong AA incorporated
      • early termination (STOP)
      • abnormal protein chain formation
  • ^at low concentrations
    • only a few can get through G- CW
    • eventually messes up the CW proteins –> +concentration –> stop protein synthesis
60
Q

How can bacteria respond to aminoglycosides?

A

Enzymatic modification by:

  • acetylation
  • adenylation
  • phosphorylation
  • e.g. by gentamycin acetyl transferase (P. aureginosa)
  • just one modification can inactivate the aminoglycoside
  • usually by enzymes in periplasm
    • tf drug cannot get through to cytoplasm
61
Q

How can G- bacteria fend of aminoglycosides?

A
  • modification of the outer membrane (ok)
  • modifying enzymes in the periplasmic space (better)
62
Q

What are bacterial mechanisms of resistance to aminoglycosides?

A
  • G- outer membrane modification: reduced entry
  • modifying enzymes (G- in periplasm): reduced entry
  • efflux: pumping it out to prevent concentration
  • ribosomal mutation: reduced binding
    • bacteria mutates rRNA or protein
    • protein synthesis continues
    • drug has no target to bind to
63
Q

What are drug-inactivating mechanisms of resistance to antimicrobials?

A
  • drug inactivation: hydrolysis of b-lactams by b-lactamase
  • covalent modification: aminoglycosides by gentamycin acetyl transferase
64
Q

What are drug target-altering mechanisms of antimicrobial resistance?

A
  • modification to a less-sensitive form
    • targets that b-lactam can’t bind to (MRSA)
    • modify PBPs sp vancomycin can’t bind (VRE)
  • overproduction of target
    • VISA makes excess PTG to box up the vancomycin
65
Q

What mechanisms of antimicrobial resistance reduce access of the drug to targets?

A
  • reduced entry: modification of aminoglycosides or G- OM
  • increased efflux: aminoglycosides, tetracylines (prevent concentration building up in the bacteria)
66
Q

What is the mechanism of antimicrobial resistance to prodrugs?

A
  • inactive drug forms that must be activated by microbial agents
  • resistance mechansims fail to activate it
  • e.g. metronidazole, isoniazid
    • metronidazole: NO2 group reduced to N=O via nitro-reductase (e.g. reducing/anaerobic environments)
    • isoniazid: Tx for TB
      • ​must be activated by KAT enzyme/catalase
      • missing from some TB strains, tf these strains are resisistant to isoniazid
67
Q

Metronidazole

A
  • prodrug, must be activated
  • reduction of NO2 –> N=P by nitro-reductase
  • in anaerobic environemtns
  • acts on anaerobic bacteria (Bacteroides, Clostridium), protozoa (amoebe like Entamoeba histolytica, causes amoebiasis; Giardia, Trachoma), and animals
  • bacteria and protozoa can become resistant by failing to activate it
68
Q

Carbapenem-resistant Enterobacteriaceae (CRE)

A
  • enterobactiaciae e.g. E. coli klebisella, G- rods
  • Carbapenems (1976) were best b-lactams (nothing resisitant) until carbapenemase developed
    • plasmid-encoded b-lactamase that is not inhibited by clavulanic acid (even though it should be)
    • we have no drugs to treat CREs
69
Q

What are examples of antibiotic-resistant bacteria?

A
  • MRSA
  • PRP (pen-res pneumococci)
  • VRE
  • VISA
  • CRE
  • multi-drug resistant G- rods
  • hypervirulent Clostridium difficile
  • multi-drug resistant Mycobacterium tuberculosis (MDR-TB)
    • resistant to 2/4 TB first-line Tx drugs
  • extensively drug-resistant M. tuberculosis (XDR-TB)
    • resistant to 4/4 TB first-line Tx drugs
70
Q

Mycoplasma

A
  • true bacterium, lacks PTG in CW
  • tf intrinsically resistant to:
    • penicillin (beta lactams)
    • vancomycin
    • (both act on PTG synthesis)
71
Q

What is the transformation mechanism of bactarial gene transfer?

A
  • donor bacterium dies, releases DNA
  • DNA taken up by competent cell (not all bacteria can pick up DNA, some are naturally competent e.g. pneumococci)
  • homologous recombination incorporates DNA fragment into chromosome

Requirements:

  • closely related donor and recipient
    • restriction enzymes will chop up DNA that is not similarly methylated (i.e. foreign)
    • must be certain amount of homology for homologous recombination to occur
72
Q

Shigatoxin

A
  • encoded by a bacterial virus
  • can pass between E. coli –> food poisoning outbreak (Germany, 2011)
  • have a temperate bacterophage non-homologously incorporated into genome (lysogenic cycle)
73
Q

What is the temperate phage/lysogenic bacteriophage cyle?

A
  • bacterial virus (most are DNA) infects bacteria
  • replicates happily with the incorporated DNA
  • e.g. E. coli w/DNA-encoded Shigatoxin
74
Q

What is the virulent phage/lytic bacteriophage cycle?

A
  • viral DNA replicates like crazy, making 100s of coppies
  • burst out of cell
  • cell dies
  • e.g. enteroviris
75
Q

What is the transduction mechanism of bacterial gene transfer?

A
  • bacteriophage infects donor bacterium
  • some host/donor chromosome is packaged = rare abnormal phage
  • can infect other cells and recombine DNA (homologously or non-homologously) to become part of that bacteria
  • e.g. phages that infect different species of staphylococci
    • staph epidermis (skin, mucous membranes, conjunctivae) - normal flora (100% of you!)
    • every time you take antibiotics, it becomes resistant
    • bros with S. aureus which can be infected by the same virus
    • tf resistance can be transmitted to S. aureus
      • bad news bears
      • likely where mecA gene in MRSA came from that makes it resistant to all penicillin (the altered PBP that beta-lactams can’t bind to)
76
Q

What is the plasmid-mediated conjugation mechanism of bacterial gene transfer?

A
  • the worst
  • requires cell-to-cell contact
  • plasmid is in DNA solely bc it cannot replicate on its own
  • don’t need to be closely related
    • e.g. from G+ enterococci to G- bacteria
  • sex pillus forms (cytoplasmic bridge)
  • one strand of the dsDNA plasmid via pillus into recipient bacteria
    • donor keeps the identical plasmid
77
Q

Salmonella typhi

A

causes Typhoid fever

78
Q

Streptomycin

A
  • aminoglycoside
  • active against salmonella typhi but doesn’t treat typhoid fever
79
Q

Enteric fever

A

Caused by Salmonella paratyphi A and B

80
Q

What is the use of antimicrobial susceptibility testing?

A

Determines the susceptibility of bacteria that may have acquired resistance.

81
Q

What are the two types of antimicrobial susceptibility testing?

A
  • dilution methods
  • diffusion methods
82
Q

What is the MIC?

A

minimum inhibitory concentration

the minimum concentration of antibiotic needed to inhibit bacterial growth

83
Q

What is the alternative AST to MIC?

A

Disc susceptibility test

Epsilometer test

84
Q

What does a low MIC reflect?

A

More susceptible/less resistant

85
Q

What does a high MIC reflect?

A

More resistant/less susceptible

86
Q

What needs to be considered in the choice of an antimicrobial agent?

A
  • spectrum
  • efficacy
  • route of administration and excretion
  • pharmacokinetics/pharmacodynamics
  • availability
  • cost
87
Q

What are the considerations in empirical/best-guess antimicrobial chemotherapy?

A
88
Q

What is the rationale for using antibiotics in combination?

A
  • temporary measures in ill patients
  • delaying emergence of resistance (e.g. mycoTB)
  • to treat mixed infections
  • to reduce toxicity
  • to achieve synergistic effects
89
Q

What is an indifferent or additive effect?

A

The added benefit of using A + B together could also be achieved by using more of A or B on its own

In a checkerboard dilution, the tubes with growth would be along the line between the wells just below the MICs

90
Q

What is an antagoinstic effect?

A

Using A + B together is worse than using A or B alone

or

A + B is the same as A, tf B is not doing anything (but may be adding toxicity)

In checkerboard dilution, there would be wells with growth above the line between the wells just below the MICs

91
Q

What is a synergistic effect?

A

Using A + B together is more potent than expected

In a checkerboard dilution, there would be a few empty wells below the line between the wells just below the MICs

e.g endocarditis injection in animals testing stretomycin, penG, and the two together was most effective (cured all animals in that group)

92
Q

co-trimoxazole

A
  • think trimethoprim (it’s doing all the work, most bacteria are resistant to sulphonamides)
  • mixture of trimethoprim (aminoglycoside) and salphamethoxazole (sulphonamide)
  • interfere with folic acid, blocking sequential steps in a metabolic pathway
93
Q

pneumocystis

A
  • used to be protozoa (carinii), now a yeast/fungus (jirovecii)
    • responds to folic acid antagonists like protozoa (e.g. malaria) do
  • pneumocystis pneumonia is an AIDS-defining illness
  • treated with co-trimoxazole (trimethoprim + sulphamethoxazole), a folic acid antagonist
  • can infect us normally without problem
  • causes problems in immunocompromised (esp. -T-cells)
94
Q

What is an AIDS-defining illness?

A
  • marker of progression from HIV+ to AIDS
  • indicate depressed T-cell mediated immunity
  • e.g.
    • pneumocystis
    • non-mycobacterium TB
    • streptococcus meningitis
95
Q

What are the mechanisms of synergy?

A
  • block steps in a metabolic pathway (e.g. co-trimoxazole, folic acid antagonist)
  • inhibit enzymatic degradation (e.g. co-amoxyclav, clavulanic acid inhibits the B-lactamase)
  • enhanced antimicrobial uptake by bacterial cells (aminoglycosides that inhibit protein synthesis, increased entry by penicillin interference with cell wall synthesis & PTG barrier)
96
Q

What are the mechanisms of antagonism?

A
  • inhibition of bactericidal activity by a bacteriostatic agent
    • penicillin requires bacteria to be growing
    • won’t work if growth is inhibited (e.g. tetracyclines which are bacteriostatic)
  • induction of enzymatic degradation
    • ampicillin is susceptible to B-lactamase and also an inducer of its oroduction
    • can make susceptible non-inducers like piperacillin less effective
  • competition for binding to the same target
  • inhibition of target
97
Q

What are Jawetz’s Laws?

A

bacteriostatic + bacteriostatic = additive or indifferent

bacteriostatic + bactericidal = antagonistic

bactericidal + bactericidal = synergistic

*must be confirmed by lab tests*

98
Q

What is a checkerboard dilution?

A
  • above the line: antagonistic
  • below the line: synergistic
  • on the line: additive

Microbiology and Immunology (9 decks)

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