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id & micro - bacteriology - pharmacology

id & micro - bacteriology - pharmacology

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Published by jmosser

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Published by: jmosser on Jan 19, 2010
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02/21/2015

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Pharmacology: ID & Micro

Introduction to Antibiotics................................ ................................ ................................................................ ...................... 2 Cell Wall Active Antibiotics (I & II).......................................................................................................................................... 5 Sulfonamides and Antimicrobial Antifolates................................................................................................ ........................ 11 Ribosomal Inhibitors................................ ................................................................................................ ............................. 14 Drugs for Mycobacterial Infections................................ ................................ ................................ ....................................... 21 Quinolones................................................................ ................................................................................................ ............ 25 Antibiotic Resistance................................ ................................................................ ................................ ............................. 27

2
Introduction to Antibiotics
AntibioticDefinitio n:
\ue000
Classic: substances produced by one microorganismto inhibit growtho r destroy another
\ue000
Functional: Drugs that kill \u201cbugs\u201d (mostly bacteria but also others)
Example: for a given clinical syndrome, figure out what the most common organism is,
then choose an appropriateclass &dr ug and individualize therapy (all depends on who
& where pt is). Afterempi ri c therapy, get lab results (if applicable) & givedefinitive tx.
Empiric therapy: begin broad
\ue000
\u201cWhat\u2019s likely?\u201d - depends on probability of organism in given clinical syndrome (pt.,geography, hospital vs
community, etc.)
\ue000
Worst-case scenario \u2013 what\u2019s the worst that could happen even if less probable
\ue000
Local antibiotic sensitivity patterns (community, esp. hospital)
Definitive therapy: go narrow
\ue000
Getc ul tur e & knows ensi tiv i ty
\ue000
Side effects, co-morbidities, other patient characteristics inform choice
\ue000
Notpro bability -dependent
Narrowest spectrum good: \u2193 resistance, adverse effects, cost; \u2191 adherence, simplicity
Obstacles: tons of organisms, tons of abx with different characteristics; agents can cause many syndromes & vice versa,
many causes still unknown, causes for a syndrome can vary with population, geography, age
RIGHT DRUG
Selective toxicity: less sensitivity to toxicity inhumans thanbacter ia
\ue000
Therapeutic window=host efficacy
host toxicity
Selective toxicity=bac te ri al to xi c i ty
host toxicity
\ue000
Relies on the distant genetic relationship between humans & bacteria (as opposed to fungi, parasites, viruses)
\ue000
Various mechanisms (see table)
Adverse effects
\ue000
Oftenu nrelated to antimicrobial effects
\ue000
Large therapeutic index usually (can give
a high molar quantity)
Coverage: individualize for organism, local
epidemiology / resistance, patient
\ue000
E.g. antibiotic guidelines / susceptibility grids for each hospital.
Bactericidal vs. Bacteriostatic
\ue000
Microbiologic definition = MBC:MIC > 4 for \u2018cidal
o
Minimum bactericidal concentration : minimum bacteriostatic concentration > 4
\ue000
Clinical definition:
o
\u2018Cidal
=
Deadbugs
o
\u2018Static + good immune system & good penetration
=
Deadbugs
o
\u2018Static drug alone (immune dysfunction or sanctuary)=
Sleepingbugs
Therapeutic objectives:

1. Rightdr ug
2. Rightpl ac e
3. Righttime

3
\ue000
Table has good summary but not hard & fast rules.
\ue000
Bacteriostatic are mainly ribosome inhibitors.
\ue000
Can bev ar i abl e even for a given drug (\u2018static against
some, \u2018cidal against others)
\ue000
Clinical relevance: sometimes \u2018static drugs penetrate
better, or \u2018cidal drugs are needed (see table)
o
Endocarditis: poor penetration, slow growth
o
Meningitis: poor penetration, immune
sanctuary
o
Osteomyelitis: poor penetration
o
Neutropenia: immunosuppresion
Combinations of antibiotics: save for special situations
\ue000
Mixed infection: at least 2 microorganismsgr owi ng and
causing disease, e.g. intra-abdominal infection
\ue000
Resistance prevention: e.g. anti-TB therapy
\ue000
Initial empiric therapywi th seriousinfect io n
\ue000
Synergy: a few situations where 1+1 > 2 in the clinic
RIGHT PLACE
Antibiotic Tissue Penetration
\ue000

Recall first unit: []blood, size, protein binding in plasma, lipid
solubility, ionic charge, tissue binding, active transport,
excretion pathways

\ue000
Inflammation: some drugs can penetrate better in places of
inflammation (e.g. get into sanctuary like past BBB if
inflammation present).
o
Example: penicillin <1% CSF penetration without
inflammation, 5% with inflamed meninges
o
Penicillins usually pumped out across BBB;
inflammation reduces this efflux
Extravascular penetration of drugs
\ue000
Interstitial fluid: rapid equilibrium with vascular space
\ue000
Large reservoir (e.g. pleural fluid): equilibrium occurs slowly, smaller fluctuations (akin to oral dosing)
\ue000
Specialized site with barrier (e.g. CSF): much lower concentrationsov erall
\ue000
Loading dose can rapidly achieve target concentration
o
Especially relevant if reservoir situation
o
How fast you can get it up to 95% still depends on half-life!
Bacterial penetration:
\ue000
Outer membrane of Gram (-) bacteria, periplasmic\u03b2-lactamases around cell wall,
\ue000
Need to get past cytoplasmicmembrane & cytoplasmicpumps
\ue000
Think: how does drug work? Where? How does it get there? How could resistance block its arrival?
RIGHT TIME
Pharmacokinetics / pharmacodynamics:
\ue000
time course of drugc onc entr ati on oftendoes n\u2019t parallel time course of drugeffec t
Time vs. Concentration-dependent killing

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