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antibiotics.ppt
1. The emergence of pathogens with increased resistance
to available antibiotics has historically been followed
by development of “modern” antibiotics with
improved activity for these resistant isolates.
After a variable period resistance frequently emerges
to these new antibiotics, which then leads to
development of even more modern antibiotics and the
cycle repeats itself.
Optimal use of antibiotics is an important part of the
effort to contain resistance
ANTIBIOTIC THERAPY
2. ANTIBIOTIC THERAPY
Antibiotics are unique
For all other drugs administration to a single
patient has no direct effect on other patients
Use of an antibiotic can have an impact that
extends beyond that patient
When a physician prescribes an antibiotic ,he
could initiate a process that makes that
antibiotic ineffective globally !!!
7. Community v/s Hospital Acquired
Presumed site
Knowledge of local susceptibility
Attempt to culture
De escalation Therapy
Optimal Selection
8. “we know everything about antibiotics except how
much to give” Maxwell Finland
(The 500 mg 6hrly era)
Bacterial Killing is a function of drug
concentration and time of exposure
Concentration independent Killing
Concentration dependant Killing
Optimal Dose
9. Mechanism Example
Reduce intracellular conc. Imipenem
Drug inactivation Beta lactams
Target Modification Quinolones, PRP
Target Bypass Glycopeptides
Mechanisms of Resistance
11. Staph Aureus
ESBL producing Organisms
Gram -ve Rods Producing Amp C
Enterococci
Specific Pathogens (Hospital)
12. B lactamase -inhibitor combination
Ticarcillin + Clavulanic acid (Timentin)
Piperacillin + Tazobactam (Zosyn)
Cefoperazone + Sulbactum (Magnex)
Inhibitors Bind and inactivate B lactamases
Potentiate Action of partner antibiotic
Addition does not enhance activity against
susceptible bacteria
13. B lactamase -inhibitor combination
Many strains of Pseudomonas, Enterobacter
(Amp C producers) - resistant
MRSA completely resistant
Enterococci moderately resistant
PRP resistant (not Magnex)
Usually combined with Aminoglycosides
Clavulanic Acid may induce C lactamases
Tazobactam & clavulanic acid have greater inhibitory potency
15. Newer Cephalosporins (Cefpirome)
Has activity against gram +ve (not MRSA)
more effective against Enterobacter
May be effective against Enterobacter &
Pseudomonas producing Type I B
lactamase (Amp C)
Effective against some ESBL
16. Imipenem & Meropenem
Imipenem with cilastatin (inhibits metabolism in kidney)
Highly B lactamase stable & excellent penetration into GNB
Ineffective against MRSA, MRSE, Enterococci, C.diff,
Meropenem better against Gram -ve
Imipenem should not be combined with B lactams
Seizures seen with Imipenem (renal failure, CNS disorders)
Pseudomonas now becoming Resistant but meropenem could
be tried (use another porin channel)
17. Glycopeptides (Teicoplanin & Vancomycin)
Inhibit cell wall synthesis
No cross resistance with B lactams
Effective against almost all gram +ve
Combined with Aminoglycoside (endocarditis)
Inferior to Clox for MSSA
Vancomycin levels to be monitored in renal failure
Teicoplanin can be given IM
Red man Syndrome with Vancomycin
Nephro & Ototoxicity if combined with Aminoglycosides
18. Newer Fluoroquinolones
Act on two topoisomerases (resistance less)
Better against gram +ve (Pneumonia, AECB)
Levo also used for bone, skin &soft tissue
Gati has higher AUIC (? Significance)
19. Linezolid
Oral Bioavailibility very good
Reserved For MRSA skin & soft tissue
infections
VRE
Blood Counts to be monitored
Monitor BP if adrenergic drugs being used