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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
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 !!!
Decision to use
Optimal Selection
Optimal Dose
Optimal Duration
Optimal Antibiotic Use
Inappropriate antibiotic use
Viral Fevers
Throat swabs
+ve urine cultures in patients with Foleys
Skin cultures in bed sores
Prophylaxis
Fever without infection
Drug fever
Central Fever
DVT and PE
Atelectasis
Myocardial infarction
Pericarditis
Hypothermia Hypotension
Tachypnoea Oliguria
Feed intolerance Altered mentation
Oedema
Neutropaenia or philia Thrombocytopenia
Fluctuating sugars
Infection without fever
Community v/s Hospital Acquired
Presumed site
Knowledge of local susceptibility
Attempt to culture
De escalation Therapy
Optimal Selection
“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
Mechanism Example
Reduce intracellular conc. Imipenem
Drug inactivation Beta lactams
Target Modification Quinolones, PRP
Target Bypass Glycopeptides
Mechanisms of Resistance
Specific Pathogens (Community)
Penicillin Resistant Pneumococci
Salmonella Typhi
H influenza
Staph Aureus
ESBL producing Organisms
Gram -ve Rods Producing Amp C
Enterococci
Specific Pathogens (Hospital)
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
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
Newer Cephalosporins
Oral Cephalosporins - probably limited
role
Sinusitis, AECB, Otitis, UTI,
Gonorrhoea,Osteomyelitis, ? Enteric fever
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
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)
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
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)
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

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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 !!!
  • 3. Decision to use Optimal Selection Optimal Dose Optimal Duration Optimal Antibiotic Use
  • 4. Inappropriate antibiotic use Viral Fevers Throat swabs +ve urine cultures in patients with Foleys Skin cultures in bed sores Prophylaxis
  • 5. Fever without infection Drug fever Central Fever DVT and PE Atelectasis Myocardial infarction Pericarditis
  • 6. Hypothermia Hypotension Tachypnoea Oliguria Feed intolerance Altered mentation Oedema Neutropaenia or philia Thrombocytopenia Fluctuating sugars Infection without fever
  • 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
  • 10. Specific Pathogens (Community) Penicillin Resistant Pneumococci Salmonella Typhi H influenza
  • 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
  • 14. Newer Cephalosporins Oral Cephalosporins - probably limited role Sinusitis, AECB, Otitis, UTI, Gonorrhoea,Osteomyelitis, ? Enteric fever
  • 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