high yield antibiotics stuff you need to memorize

Question 1

Antibiotic side effects

Answer 1

all antibiotics-> antibiotic associated diarrhea (C. difficile)
Tetracycline-> discoloration of teeth
Amino glycosides-> auditory damage
Chloramphenicol->aplastic anemia (bone marrow blood cell damage)
Penicillin-> anaphylactic shock

Question 2

Mechanisms of antibiotic resistance

Answer 2

1. horizontal gene transfer
2. Spontaneous mutation

Mechanisms:

1. Mod/inactivate the antibiotic itself
2. mod antibiotic target
3. reduce antibiotic concentration (pump out thru efflux pumps, mutations in porins to prevent access)

Question 3

Beta Lactams

Answer 3

Broad spectrum

Four main classes: Penecillin, Cephalosporins, Carbepenems, Monobactam (all work at different levels of PG synthesis)

Penecillin (all end in cillin)
Cephalosporins (all begin with ceph except cefazolin and cefadroxil)
Carbepenems (all end in penem)
Monobactam (only one- axtreonam)
MOA: bind to penecillin-binding-proteins (aka transpeptidase used to crosslink) inactivating them and disrupting crosslinking of peptidogylcan

Resistance mechanism:
1. B-lactamase- cleaves the enzyme inactivating it (overcome with b-lactamase inhibitors like clavulanic acid, tazobactam, and sulbactam. Slow releasing b-lactamase inhibitors to prevent b-lactamase)

2. Reducing Permeability: making it hard for B-lactam to access the PBP
3. PBP mutations- prevents B-lactam binding most common in MRSA mecA gene

Question 4

Vancomyocin

Answer 4

glycopeptide antibiotic not a B lactam
Mechanism of action: binds to D-ala-D-ala at the end of the peptide side chain on peptidoglycan precursors

Only effective in gram positive bugs bc its bulky af and cant get into gram neg om

mechanism of resistance bacteria acquire genes that produce an altered pg structure D-ala-D-lac the genes that encode resistance are on plasmids or transposons (VRSA)

Question 5

Cycloserine

Answer 5

mechanism: inhibits peptidoglycan crosslinking by acting as a competitive inhibitor of D-ala

Useful in second line anti-TB therapy

Question 6

Bacitracin

Answer 6

Mechanism: binds to pyrophosphate on the lipid carrier for peptidoglycan precursors and blocks recycling inhibiting pg layer

Group A streptococci are very sensative so useful for diagnostic tests

too toxic for systemic use

Question 7

Cell envelope antibiotics

Answer 7

Daptomycin:
Mechanism- binds and disrupts cytoplasmic membrane, causing rapid membrane depolarization
narrow spectrum (useful for gram + and MRSA)

Polymyxins:
Mechanism: bind to LPS in outer membrane of gram - leading to messed up outer and inner membranes

novility allows for use against abx resistant gram - bacteria

Question 8

Protein synthesis inhibitors

Answer 8

specifically target smaller bacterial ribosome 70 s (30 and 50 s subunit)

30 s inhibitors: aminoglycosides (bacteriacidal), and tetracyclines (bacteriostatic)
30 A T

50 s inhibitors: Chloramphenicol, clindamycin (bactericidal), erythromycin/macrolides (bacteriostatic), linezolid (variable)

50 CCEL

Buy AT 30 CCEL (sell) at 50

Question 9

Tetracycline

Answer 9

MoA: binds to 30s subunit interfering with the binding of aminoacyl tRNA to the ribosome

resistance: efflux pump and ribosomal mutations

tetra is mostly resistant but doxy and mino are still used

Side effects: teeth discoloration, photosensitivity for children

Tigecycline (new bacteriostatic form)

Question 10

Aminoglycosides

Answer 10

gentamicin, amikacin, tobramycin, kanamycin etc

MoA: binds to 30 s to cause misreading and release from mRNA

side effects: ototoxic and nephrotoxic

resistance: enzymatic modification of Abx

Question 11

Macrolides

Answer 11

erthryomycin, azithromycin, clarithromycin etc

MoA: Binds to 50 s to block elongation (macroslides)

often used for people allergic to B-lactams and against gram + bacteria

Resistance: Methylation of rRNA and efflux pumps

Question 12

Clindamycin

Answer 12

same MoA as macrolides
resistance: methylation of rRNA and and cross resistance with macrolides

useful for MRSA, anaerobes above the diaphragm

Question 13

Chloramphenicol

Answer 13

blocks elongation thru 50 s, aplastic anemia (gray bababy)

resistance: alters drug

Question 14

Linezolid

Answer 14

MoA: binds to a unique 50s location to prevent formation of the ribosome

resistance: mutations in ribosomal components

Question 15

DNA Replication inhibitors

Answer 15

1st generation quinolones- nalidix acid
2nd gen fluoroquinolones-norfloxacin, ciprofloxacin

MoA: bind to bacterial DNA gyrase to inhibit catalytic function- disrupting DNA replication and repair

Resistance: point mutations in bacterial DNA gyrase preventing antibiotic binding

Efflux pumps

Question 16

Metronidazole

Answer 16

MoA: free radical produced in anaerobic environments leading to toxic metabolites that damage DNA

only useful in ANAEROBIC infections (c diff and pseudomonas colitis)

Question 17

RNA synthesis inhibitors

Answer 17

Rifamins 4 Rs: RNA polymerase inhibitor, Ramps up microsomal cytochrome, Red/orange body fluids, Rapid resistance if used alone

MOA: binds to B subunit of RNAP to inhibit RNA synthesis,

Resistance: acquisitions of mutations in the B subunit of RNAP that prevent antibiotic from binding

Fidaxomicine: MOA: noncompetitive inhibitor of RNA synthesis by binding bacterial RNAP

uced agains c diff to preserve normal gut flora

Question 18

Antimetabolate

Answer 18

Trimethoprim+Sulfamethoxazole (TMP/SMX) Bactrim

Metabolic analogs are structurally similar to natural metabolic intermediates and block the normal pathways
FOLATE INHIBITORS
Bacteriostatic

resistance: acquisition o f another gene: dihydrofolate reductase

Question 19

Examples of transduction

Answer 19

Cholera toxin: core element and repetitive sequence
Has 5 bindning subunits and 1 enzymatic subunit, binding subunit attaches to ganglioside GM1, interacts with adenylate cyclase, converting ATP to cAMP enhancing secretion of water and electrolytes

Shiga Toxin phage: Temperate (has a lytic and lysogenic phase) 5B-1A subunits. B subunit binds to Gb3 glycolipid and modifies ribosome acceptor site blocking protein synthesis. Causes HUS (hemolytic-uremic syndrome)-severe diarrhea and hemorrhaging