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Flashcards in Antibiotics JB stylie Deck (24)
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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



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



-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



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.



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



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



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



30 s ribosome binding → inhibits protein synthesis reversible inhibitor
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



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.


erythromycin, tylosin

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


lincomysin, clindamycin

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



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


1 generation cephalosporins

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.


2nd generation cephaolsporins

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.


3rd generation cephalosporins

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


Antipseudomonas penicillins

(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.



(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.


Antistaphylococcal penicillins

(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.


Prostate penetrators

TMS, Baytril, chloramphenicol, tetracycline, erythromycin


Not for abscesses

Aminoglycosides, Macrolides, Sulfas



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



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


ABs affective against G-

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),


Ab's affective against G+

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