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| __NOTOC__
| | {{Details0|Chloramphenicol succinate (injection)}} |
| {{Chloramphenicol}} | | {{Details0|chloramphenicol (ophthalmic)}} |
| {{CMG}};{{AE}}{{AK}} | |
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| ==Overview==
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| '''Chloramphenicol''' is a [[bacteriostatic]] [[antimicrobial]] originally derived from the [[bacterium]] ''[[Streptomyces venezuelae]]'', isolated by [[David Gottlieb]], and introduced into clinical practice in 1949.
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| It was the first antibiotic to be manufactured synthetically on a large scale. Chloramphenicol is effective against a wide variety of microorganisms; it is still very widely used in low income countries because it is exceedingly cheap, but has fallen out of favour in the West due to a very rare but very serious side effect: [[aplastic anemia]].
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| In the West, the main use of chloramphenicol is in [[eye drop]]s or [[ointment]] for bacterial [[conjunctivitis]].
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| [[Thiamphenicol]] is a related compound with a similar spectrum of activity that is available in Italy and China for human use, and has never been associated with aplastic anaemia. Thiamphenicol is available in the U.S. and Europe as a [[veterinary]] antibiotic, and is not approved for use in humans.
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| ==Mechanism and resistance==
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| Chloramphenicol is [[Bacteriostatic agent|bacteriostatic]] (that is, it stops bacterial growth). It functions by inhibiting [[peptidyl transferase]], preventing peptide bond formation. While chloramphenicol and the macrolide class of antibiotics both interact with the 50S ribosomal subunit, chloramphenicol is not a macrolide. Furthermore, their mechanisms are slightly different. While chloramphenicol directly interferes with substrate binding, macrolides sterically block the progression of the growing peptide.
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| There are three mechanisms of [[Antibiotic resistance|resistance]] to chloramphenicol: reduced membrane permeability, mutation of the 50S ribosomal subunit and elaboration of chloramphenicol acetyltransferase. It is easy to select for reduced membrane permability to chloramphenicol ''in vitro'' by serial passage of bacteria, and this is the most common mechanism of low-level chloramphenicol resistance. High level resistance is conferred by the ''cat''-gene; this [[gene]] codes for an [[enzyme]] called [[chloramphenicol acetyltransferase]] which inactivates chloramphenicol by covalently linking one or two [[acetyl]] groups, derived from acetyl-S-coenzyme A, to the [[hydroxyl]] groups on the chloramphenicol molecule. The acetylation prevents chloramphenicol from binding to the ribosome. Resistance-conferring mutations of the 50S ribosomal subunit are rare.
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| Chloramphenicol resistance may be carried on a plasmid that also codes for resistance to other drugs. One example is the [[ACCoT]] plasmid (A=[[ampicillin]], C=chloramphenicol, Co=[[co-trimoxazole]], T=[[tetracycline]]) which mediates multi-drug resistance in typhoid (also called [[R factors]]).
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| ==US Brand Names==
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| CHLORAMPHENICOL® '''(DISCONTINUED)'''
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| ==FDA Package Insert==
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| ''' [[Ceftriaxone description|Description]]'''
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| '''| [[Ceftriaxone clinical pharmacology|Clinical Pharmacology]]'''
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| '''| [[Ceftriaxone microbiology|Microbiology]]'''
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| '''| [[Ceftriaxone indications and usage|Indications and Usage]]'''
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| '''| [[Ceftriaxone contraindications|Contraindications]]'''
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| '''| [[Ceftriaxone warnings and precautions|Warnings and Precautions]]'''
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| '''| [[Ceftriaxone adverse reactions|Adverse Reactions]]'''
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| '''| [[Ceftriaxone overdosage|Overdosage]]'''
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| '''| [[Ceftriaxone clinical studies|Clinical Studies]]'''
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| '''| [[Ceftriaxone dosage and administration|Dosage and Administration]]'''
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| '''| [[Ceftriaxone Compatibility and Stability|Compatibility and Stability]]'''
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| '''| [[Ceftriaxone how supplied|How Supplied]]'''
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| '''| [[Ceftriaxone labels and packages|Labels and Packages]]'''
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| ==References==
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| {{Reflist|2}}
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| http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=aed29594-211d-49ef-813f-131975a8d0e3
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| [[Category:Antibiotics]]
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| [[Category:Wikinfect]]
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