Antibiotics JB stylie

Question 1

Penicillin

Answer 1

Cell wall synthesis inhibitor (inhibits crosslinking of peptidoglycan by binding of penicillin binding proteins) results in cell lysis with continued organism growth; time dependent
gm+ bacteria, and gm+ and gm- obligate anaerobes that do not produce β-lactamase

Question 2

Cephalosporins

Answer 2

Skin, urinary tract, soft tissue, bone infections, and before and after surgery. Advantage over penicillins = activity against β-lactamase producing Staphylococci, and gm- bacteria like Enterobacteria.
Except for 3rd generations, they are ineffective against Pseudomonads. None are effective against Enterococci. They are not especially effective against anaerobes. Short shelf life when reconstituted. Oral 1st generations are well absorbed.
Pseudomonas resistance dt absorption problem
1st gen = G+. 2nd gen = Increased G-, 3rd gen even more G- but less G+.
They will also get betalactamase producing staph and G- bact like enterobacteria

Question 3

Aminoglycosides

Answer 3

-gentamycin, tobramycin, kanamycin
-Bind to 30 s ribosome irreversible inhibition of protein synthesis [] dependent. Rapidly bactericidal. G- aerobes
-No anaerobic spectrum (O2 and energy dependent uptake), activity reduced in necrotic tissue
G- synergy with betalactams
Nephrotoxic at the prox tubules

Question 4

Fluoroquinolone

Answer 4

DNA gyrase inhibitors → req for bacterial DNA replication, repair, and recombination. Rapidly cidal
G-, enterobacter, pseudomonas, staph, variable strep
Poor agains enterococci and anaerobic
Concentration in lungs, kidneys, liver, muscle, heart, and intestine equalled or exceeded the plasma drug concentrations during therapy. Concentrations in the bile and urine were many fold higher.

Question 5

Metronidazole

Answer 5

Structural changes d/t reduction of the nitro group once inside the → resulting in oxygen free rads → cell results in DNA damage
G- anaerobes (not facultative anaerobes)
Distributed into all tissues including eyes, CNS, bone and abscess cavities
Poor aerobic spectrum

Question 6

Trimethoprim-Sulfonamide

Answer 6

Act synergistically to inhibit the synthesis of folate → nec for microbial production of DNA. Sulfas block 1st step (compete with PABA) and trimethas the 2nd step in folic acid synthesis
Adverse effects. Anemia, leukopenia, Thrombocytopenia is rare. Allergic reactions (type III hypersensitivity. ) Also Keratoconjunctivitis sicca.
Inhibited by cellular debris (so not good for abscess)
Broad spect esp most G- and staphylococci in skin

Question 7

Vancomycin

Answer 7

A glocpeptide
Disrupts peptidoglycan synthesis (major cell wall polymer) → different mech than β lactams, inhibits cell wall synthesis also inhibits bacterial RNA synthesis and alters membrane permeability.
Gets G+ cocci, staph. aureus, most streptococcus, some anaerobes (clostridium)
VRE = Vanc resistant enterococci

Question 8

Tetracyclines

Answer 8

30 s ribosome binding → inhibits protein synthesis reversible inhibitor
Broadspectrum
Limited activity against staph and non against enterococci, pseudomonas, enterobacteria.
Doxycycline excreted in small intestine, all others in urin
Brown teeth and hindered bone growth ass w Ca chelation

Question 9

Chloramphenicol

Answer 9

50 s ribosomal binder → inhibits protein synthesis reversible inhibitor
Antagonism with other 50s inhibitors
Broad spectrum of activity against Strep, Staph, brucella, Pasteurella, Mycoplasma, and anaerobes. Poor activity against Pseudomonads. Bacteria, especially gm- easily develop resistance.
Adv Rxn - irreversible pancytopenia, impacts bone marrow most severely. Ribosome in mitochondria is bacterial type and can get hit.

Question 10

Macrolides

erythromycin, tylosin

Answer 10

Another 50s ribosomal binder
Bacteriostatic for most animals
Effective against Staph, Strep, Campylobacter, Clostridium, Mycoplasma, and Chlamydia and toxoplasmosis
Not effective agains G-, does not get into urine well
Adv effect - Bact overgrowth of clostridium

Question 11

Lincosamides

lincomysin, clindamycin

Answer 11

Another 50s ribosomal binder
Bacteriostatic for most animals
Effective against Staph, Strep, Campylobacter, Clostridium, Mycoplasma, and Chlamydia and toxoplasmosis
Not effective agains G-, does not get into urine well
Adv effect - Bact overgrowth of clostridium

Question 12

Rifampin

Answer 12

Forms a stable drug-enzyme complex w/ bacterial RNA polymerase → inhibits function and DNA transcription
Broad spectrum. Including G+ cocci

Question 13

1 generation cephalosporins

Answer 13

Almost all gm+ bacteria, including β-lactamase positive staph and strep. Some activity against E. coli, Proteus and Klebsiella, but resistance is common. β-lactamase resistance can be induced in bacteria with first exposure to 1st generations.

Question 14

2nd generation cephaolsporins

Answer 14

Greater activity against gm- that are resistant to 1st generations, but are no more active against gm+. In general, poor activity against anaerobes. Few can be administered orally.

Question 15

3rd generation cephalosporins

Answer 15

More activity against gm-. Defined as MIC<1.0 ug/ml against 90% of β-lactamase producing E. coli. They have less activity against Staph and Strep. Few have activity against Pseudomonads. Few are available for oral administration

Question 16

Antipseudomonas penicillins

Answer 16

(carbenicillin, ticarcillin, piperacillin, azlocillin) -penetrate the cell wall of Pseudomonads and gm- bacteria.

• Still susceptible to β-lactamases.
• synergistic activity with aminoglycosides.
• In general, not orally effective.

Question 17

Aminopenicillins

Answer 17

(ampicillin, amoxicillin, and hetacillin).
-Addition of amino group to penicillin molecule gives them the ability to penetration of gm- bacteria.
-more stable in stomach pH
-Still can be inactivated by β-lactamases.
Pharmacokinetics: bioavailability reduced when given with food.

Question 18

Antistaphylococcal penicillins

Answer 18

(oxacillin, cloxacillin, and dicloxacillin, methicillin and nafcillin).
-Resistance to β-lactamase of Staphylococcus.
Most common for skin and soft tissues. Preparations are absorbed orally.
β-lactamase inhibitors Always combined with β-lactam AB”S. Clavulanic acid, sulbactam.

Question 19

Prostate penetrators

Answer 19

TMS, Baytril, chloramphenicol, tetracycline, erythromycin

Question 20

Not for abscesses

Answer 20

Aminoglycosides, Macrolides, Sulfas

Question 21

Bactericidal

Answer 21

Penicillins, Cephalosporins, Aminoglycoside, Metronidazole, TMS, Vancomycin, Rifampin

Question 22

Bacteriostatic

Answer 22

Tetracycline, Chloramphenicol, Macrolides (Erythromycin, Tylosin), Lincosamides (Lincomycin, Clindamycin)

Question 23

ABs affective against G-

Answer 23

2nd and 3rd generation cephalosporins, Fluoroquinolones, Metronidazole (G- anaerobes), TMS, Aminopenicillins (amoxi, ampi), Antipseudomonal pens (eg ticarcillin etal), Carbapenims (imipenim), Aminoglycosides (gentamycin, amikacin), Tetracyclines, Chloramphenicol (but resistance is rapid),

Question 24

Ab’s affective against G+

Answer 24

Penicillins (and all the variations), Cephalosporins, tetracyclines, macrolided, chloramphenicol, fluoroquinolones (they lean more G-), TMS (also leans G-)