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Module 7: Multisystem > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What makes an antibiotic bacteriostatic?

A

They inhibit growth reversibly (prevents further replication)

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2
Q

How do bacteria become resistant to tetracyclines?

A
  1. Decreased uptake (often due to mutations in the OmpF porin)
  2. Efflux from the bacterial cell; actively pump drug out of cell before it’s able to bind to 30S ribosomal subunit
  3. Elongation factor-like proteins that protect 30S subunit
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2
Q

What are characteristics of Ketolides?

A

Inhibitors of Translocation

First ketolide approved by FDA: Telithromycin

New family of antimicrobials structurally related to macrolides

Mechanism:
binding within exit tunnel of 50S subunit, thus blocking exit of nascent polypeptides
Strongly binds simultaneously to two domains of subunit (macrolides only bind to one)

Bactericidal or bacteriostatic depending on bacterium

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3
Q

What are the aminopenicillins?

Which is has greater oral availability?

A

Ampicillin

AmOxicillin (greater Oral availability)

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4
Q

Clinical use of Metronidazole

A

GET GAP on the Metro

Giardia
Entamoeba
Trichomonas
Gardnerella
Anaerobes (Bacteriodes, C. diff)
H. Pylori

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4
Q

Side effect of linezolid?

A

Bone Marrow suppression

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5
Q

What are the carbapenems?

A

Imipenem/cilastatin
Meropenem

beta-lactamase resistant

Cilastatin inhibits renal dehydropeptidase I and decreases inactivation of the drug in renal tubules

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5
Q

What’s the toxicity of vancomycin?

A

Well tollerated in general

does NOT have many problems

Nephrotoxicity
Ototoxicity
Thrombophlebitis

Redman syndrome preventable with slow infusion rate and antihistamines

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5
Q

Clinical use of tetracyclines?

A

Borrelia burdorferi
M. pneumonia
Rickettsia
Chlamydia

Demeclocycline- ADH agoinst acts as a Diuretic in SIADH

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6
Q

Penicillin is bactericidal for:

A

Gm+ cocci

Gm+ rods

Gm- cocci

Spirochetes

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6
Q

What is the clinical use of Fluoroquinolones?

A

Gm- rods of urinary and GI tracts

Pseudomonas
Neisseria

some Gm+ organisms

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7
Q

What are characteristics of Lincomycin and Clindamycin?

A

Inhibitors of Peptidyl Transferase:
Narrow Spectrum

Bacteriostatic

Mechanism:
Similar to chloramphenicol

Selective Toxicity:
Very effective for treatment of G+ bacterial infections
Clindamycin: Very effective for staphylococcal and anaerobic G- infections

Resistance:
Methylation of 23S ribosomal RNA which prevents drug binding to 50S subunit

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7
Q

What’s the clinical use of trimethoprim?

A

SMX-TMP used for treating UTIs

Shigella
Salmonella
PCP

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8
Q

What are some beta-lactam antibiotics?

A

Penicillin (G, V)
Methicillin, nafcillin, dicloxacillin (penicillinase-resistant)
Ampicillin, amoxicillin (aminopenicillins)
Ticarcillin, carbenicillin, piperacillin (antipseudomonals)
Cephalosporins
Aztreonam
Carbapenem

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8
Q

What antibiotics cause photosensitivity?

A

Sun Too Quick

Sulfonamides
Tetracyclines
Quinolones

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9
Q

How do bacteria become resistant to beta-lactam antibiotics?

A
  • Inactivation through beta-lactamases
  • Altered PBP (mecA-PBP2a)
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10
Q

What antibiotics target Formation of initiation complexes in bacteria?

A
  1. Linezolid
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11
Q

What are characteristics of Tetracyclines?

A

Inhibitors of recognition:

Broad Spectrum

Bacteriostatic

Hydrophobic

Used to Treat:
Chlamydia, Mycoplasma, Rickettsia (intracellular pathogens)
and certain G+ and G- bacterial infections

Selective Toxicity: high affinity uptake of drugs by acterial cells and increased targeting of 70S

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12
Q

What are the characteristics of Aminoglycosides?

A

Inhibitors of activated tRNA recognition:

Broad Spectrum (G+/-)
Bactericidal
Target specific proteins in the 30S ribosomal subunit

Selective Toxicity: 1. 30S vs 40S subunit
2. actively transported into bacteria, not euks.

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12
Q

What are Positive and Negative aspects of aminoglycoside therapy?

A

Positive: Rapid bactericidal effect
Broad spectrum
effective against Pseudomonas (notoriously antibiotic resistance)

Negative: Resistance
Ototoxicity and nephrotoxicity
Antagonized by anaerobiasis
low pH
ineffective against intracellular bacteria
induce biofilm production

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12
Q

What causes grey baby syndrome?

A

Chloramphenicol

Premature neonates because they lack UDP-glucuronyl transferase, the drug builds up in the fetus, displacing bilirubin.

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12
Q
A
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13
Q

What are the characteristics of aztreonam?

A

monobactam resistant to B-lactamases

Synergistic with Aminoglycosides

No cross allerginicity with penicillins

Can use in patients with renal insufficiency

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14
Q

When do bactericidal drugs have a higher efficacy than bacteriostatic?

A

When the body’s defenses are insufficient to clear the invading agents.

i.e. bacterial endocarditis, bacterial meningitis, and infections in patients with low circulating neutrophils (agranulocytopenia)

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15
Q

What are the clinical uses for 3rd Gen cephalosporins?

A

CefTriaxone, cefotaxime, ceftazidime

Serious Gm- infections resistant to other B-lactams

Ceftriaxone-meningitis and gonorrhea

Ceftazidime- Pseudomonas

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15
Q

Clinical use of chloramphenicol?

A

Meningitis

H. influenzae
N. meningitidis
S. pneumoniae

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16
Q

What are the 3 mechanisms of action of Streptomycin?

A
  1. Misreading: at low concentrations, or in case of ribosomes engaged in elongation, we see insertion of incorrect AA
  2. Cyclic Polysomal Blockade: 70S complex forms but is unstable and falls apart; results in cell death due to inability to make proteins
  3. Faulty outer Membrane Proteins: Translational misreading results in mutant membrane proteins that cause bacterial membrane to be leaky, thus more drug is taken into cell and acts at 30S subunit
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17
Q

What organisms are not covered by Cephalosporins?

A

LAME

Listeria
Atypicals (Chlamydia, Mycoplasma)
MRSA
Enterococci

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19
Q

What are the antipseudomonals?

A

Ticarcillin
Carbenicillin
Piperacillin

TCP: Takes Care of Pseudomonas

20
Q

What is the clinical use of carbapenems?

A

Broad Spectrum

Gm+ cocci
Gm- rods
Anaerobes

GI distress, skin rash, and CNS toxicity (seizures) at high levels limit use of Imipenem to 2nd tier or life threatening infections

Meropenem has reduced risk of seizures at high plasma levels and is dihydropeptidase I resistant

21
Q

What’s the clinical use of Clindamycin?

A

Anaerobic infections above the diaphram

Bacteroides fragilis
Clostridium perfrigens

aspiration pneumonia

S. aureus osteomyelitis

22
Q

Clinical use of sulfonamindes

A

Gm+
Gm-

Nocardia
Chlamydia

Triple sulfas or SMX for simple UTI

22
Q

What’s the mechanism of Metronidazole?

A

Forms free radical toxic metabolites in the bacterial cell that damages DNA

Bactericidal, antiprotozoal

24
Q

What bacteria are treated with Streptogramins?

A

Staphylococci

Streptococci

Enterococcus faecium
(Restricted for treating vancomycin-resistant forms)

25
Q

What are the clinical uses for 2nd Gen cephalosporins?

A

cefoxitin, cefaclor, cefuroxime

Gm+ cocci

HEN PEcKS

H. influenzae
Enterobacter aerogenes
Neisseria spp.
Proteus mirabilis
E. coli
Klebsiella pneumonia
Serratia marcescens

26
Q

What’s the MOA mechanism of beta-lactam antibiotics?

A
  1. Bind penicillin-binding proteins
  2. Block transpeptidase cross-linking of peptidoglycan
  3. Activate autolytic enzymes
26
Q

What’s the mechanism of Trimethoprim?

A

inhibits bacterial dihydrofolate reductase

Causes megaloblastic anemia, leukopenia, granulocytopenia
(may be fixed with folic acid supplementation)

27
Q

What are characteristics of Chloramphenicol?

A

An inhibitor of Peptidyl transfer:

Broad Spectrum

Bacteriostatic

Mechanism:
Binds reversibly to 50S ribosomal subunit and alters the tRNA structure blocking peptidyl transfer

Selective Toxicity:
Cannot enter mitochondria
Does not bind to host 60S subunit

Resistance:
plasmid-encoded acetyltransferase that catalyze the acetylation of -OH groups; preventing 50S binding

28
Q

What are the characteristics of Linezolid?

A
  • Only clinically significant drug taht inhibits formation of 70S complex
  • First of new class of antibiotics called oxazolidinones
  • prevents formation of N-formylmethionyl-tRNA-mRNA-70S ribosomal ternary complex

Activity: Bacteriostatic for Staphylococci and enterococci
Bactocidal for Streptococci

NOT approved for catheter-related blood stream, catheter-site, or gram(-) infections

30
Q

What are the 4 steps of peptide chain synthesisn and which antibiotics target each step?

A
  1. Recognition:
    - Aminoglycosides
    - Spectinomycin
    - Tetracyclines
  2. Peptidyl Transfer:
    - Chloramphenicol
    - Lincomycin
    - Clindamycin
  3. Translocation:
    - Macrolides
    - Ketolides
    - Streptogramins
  4. Release:
    - None
32
Q

Clinical use of Aminoglycosides?

A

Gm- rods

Neomycin for bowel surgury

34
Q

What are the penicillinase-resistant penicillins used for clinically?

A

S. aureus

(not MRSA)

“Use naf(cillin) for staph”

35
Q

What antibiotics are included in the family of Aminoglycosides?

A

Streptomycin

Kanamycin

Tobramycin

Gentamycin

Neomycin

Amikacin

Paramomycin

37
Q

Clinical use of Penicillin

A

Gm+ (Staph pneumoniae, pyogenes; Actinomyces)

Treponema pallidum

37
Q

What’s the clinical use of vancomycin?

A

Gm+ only

Serious multidrug resistant organisms

S. aureus

Enterococci

C. difficile

38
Q

What are the B-lactamase inhibitors?

A

CAST

Claulanic Acid
Sulbactam
Tazobectam

Added to penicillins to prevent beta-lactamase destruction

39
Q

What is the mechanism of Macrolides?

A

Not entirely clear, but likely to:

  1. Prevent elongation
  2. prevent release of empty tRNA
  3. blockage of transpeptidation
41
Q

What are the clinical uses for 1st Gen cephalosporins?

A

Cefazolin, cephalexin

Gm+ Cocci

PEcK

Proteus mirabilis
E. coli
Klebsiella pneumoniae

42
Q

What antibiotics target the amino acid activation of bacteria?

A

None

  • there are NO clinically significant inhibitors of AA activation

(possibly due to the fact that prokaryotic and eukaryotic processes are so similar)

44
Q

How do many antibiotics specifically target bacteria, and not humans?

A

They target bacterial ribosomes and inhibit protein synthesis

45
Q

What makes an antibiotic bactericidal?

A

They kill microorganisms rapidly

46
Q

What are the sulfonamides?

A

Sulfamethoxazole (SMX)

sulfisoxazole

sulfadiazine

PABA antimetabolites inhibit dihydropteroate synthetase

47
Q

How do bacteria become resistant to Aminoglycosides?

A
  1. Altered target in 30s ribosomal subunit
  2. Decreased cellular uptake
  3. Enzymatic modifications of the aminoglycoside (typically by enzymes coded on transposons or plasmids)

Gentamicin specifically has:
Potential sites for acetylation
Potential sites of adenylylation or phosphorylation
- both of which alter the antibiotic activity, rendering it useless

48
Q

What is the mechanism of action of Vancomycin?

A

Binds D-ala, D-ala portion of cell wall precursors inhibiting mucopeptide formation

Bacteriocidal

50
Q

What are penicillinase resistant penicillins?

A

Methicillin

Nafcillin

Dicloxacillin

52
Q

What are characteristics of Macrolides?

A

Inhibitors of Translocation:

Characterized by macrocyclic lactone structure

Medium Spectrum

Bacteriostatic

Treatment:
infections caused by Mycoplasma, Legionella, Chlamydia, and Campylobacter
and G+ bacteria in patients allergic to penicillins

Azithromycin and Clarithromyin: certain Mycobacteria

53
Q

Clinical use of Macrolides

A

Atypical Pneumonias (mycoplasma, chlamydia, legionella)
URIs
STDs
Gm+ cocci
Neisseria

54
Q

What are some broad-spectrum antibiotics?

A

Amoxicillin
Carbapenems
Piperacillin/tazobactam
Fluoroquinolones
Streptomycin
Tetracycline
Chloramphenicol

56
Q

What’s the clinical use of Ticarcillin, carbenicillin, and piperacillin?

A

Pseudomonas spp.
Gm- rods

Use with beta-lactamase inhibitors

58
Q

What’s the clinical use of aminopenicillins?

A

Ampicillin, Amoxicillin
HELPSS kill enterococci
Extended spectrum penicillin

Haemophilus influenzae
E. Coli
Listeria monocytogenes
Proteus mirabilis
Salmonella
Shigella
enterococci

59
Q

What are characteristics of Streptogramins?

A

Inhibitors of Translocation:
Class of natural cyclic peptide antibiotics produced by certain subspecies of Streptomyces

Mechanisms:

Dalfopristin: binds to 50S subunit; prevents elongation and facilitates binding of quinupristin to 50S

Quinupristin: premature release of peptide chains from ribosome

Synercid (quinupristin+dalfopristin)
Alone = bacteriostatic
Together = bactericidal

61
Q

What are the protein systhesis inhibitors?

A

Target bacterial ribosome (70S)

buy AT 30, CCEL (sell) at 50

Aminoglycosides
Tetracyclines

Chloramphenicol, Clindamycin
Erythromycin
Linezolid

62
Q

What are characteristics of Spectinomycin?

A

Inhibitor of Recognition:

Bacteriostatic

Causes formation of unstable 70S initiation complexes (does not cause misreading or inhibit polysomal ribosomes)

Exclusively for treatment of gonorrhea caused by beta-lactamase-producing gonococci or to treat gonorrhea in patients allergic to penicillins

63
Q

What are two common antibiotics in the Macrolide family?

A

Azithromycin and Clarithromycin

(modified forms of erythromycin)

64
Q

Antibiotics to avoid in pregnancy:

A

Clarithromycin-embryotoxic
Sulfonamides-kernicterus
Aminoglycosides-ototoxic
Fluoroquinolones-cartilage damage
Metronidazole-mutagenesis
Tetracyclines-discolored teeth, bone growth problems
Ribavinin-teratogen
Griseofulvin-teratogen
Chloramphenicol- “gray baby”

Countless SAFe Moms Take Really Good Care

65
Q

Toxicity of Sulfa drugs?

A

hypersensensitivity
hemolysis if G6PD
nephrotoxicity
photosensitivity
kernicterus in infants
displace drugs from albumin

66
Q

Explain the tenants of selective toxicity

A

Characteristics of antibiotics that reduce side-effects:

  • Absence of target from host
  • permeability differences (effective [antibiotic] is too low to cause side effects in humans)
  • structural differences in target
67
Q

What bugs is Aztreonam used against?

A

Gm- rods only

no activity against Gm+ or anaerobes

69
Q

What is the mechanism of action for tetracyclines?

A

Tetrcyclines bind to 30S ribosomal subunit and inhibit bindign of aa-tRNA to the A site

70
Q

What contributes to Macrolide resistance?

A
  1. Methylation of 23S RNA of teh 50S subunit; which prevents binding of drug
  2. Hydrolysis of lactone ring by and esterase
  3. Efflux of drug
71
Q

That’s the mechanism of quinolones?

A

-floxacins

inhibit DNA gyrase (topoisomerase II)

Bactericidal

Module 7: Multisystem (15 decks)

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