Abstract
Disseminated Mycobacterium avium complex (MAC) is treated with a macrolide and ethambutol. However, the kill rates are extremely slow so that therapy takes many months to years to achieve and even then more than 40% of patients are not completely cured. Recent studies have demonstrated that assays that detect extracellular MAC have a limited predictive value. Antibiotics kill at a much slower and more disappointing rate against bacilli within macrophages. Use of pharmacodynamic/pharmacokinetic models has resulted in design of new doses and dosing schedules for disseminated MAC, as well as new susceptibility breakpoints for ethambutol and moxifloxacin.
MeSH terms
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Anti-Bacterial Agents / pharmacokinetics
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Anti-Bacterial Agents / pharmacology
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Anti-Bacterial Agents / therapeutic use*
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Aza Compounds / pharmacokinetics
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Aza Compounds / pharmacology
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Aza Compounds / therapeutic use
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Ethambutol / pharmacokinetics
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Ethambutol / pharmacology
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Ethambutol / therapeutic use
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Fluoroquinolones
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Humans
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Macrolides / pharmacokinetics
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Macrolides / pharmacology
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Macrolides / therapeutic use
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Microbial Sensitivity Tests
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Moxifloxacin
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Mycobacterium avium Complex / drug effects*
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Mycobacterium avium-intracellulare Infection / drug therapy*
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Mycobacterium avium-intracellulare Infection / microbiology
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Quinolines / pharmacokinetics
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Quinolines / pharmacology
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Quinolines / therapeutic use
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Treatment Outcome
Substances
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Anti-Bacterial Agents
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Aza Compounds
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Fluoroquinolones
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Macrolides
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Quinolines
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Ethambutol
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Moxifloxacin