Chloramphenicol Systematic (IUPAC) name 2,2-dichloro-N-[1,3-dihydroxy-1-(4-nitrophenyl)propan-2-yl]acetamide Clinical data AHFS/Drugs.com MedlinePlus Pregnancy cat. C (systemic), A (topical) Legal status Ocular P, else POM (UK) Routes Topical (ocular), oral, IV, IM Pharmacokinetic data Bioavailability 75–90% Metabolism Hepatic Half-life 1.5–4.0 hours Excretion Renal Identifiers CAS number ATC code D06 D10 G01 J01 S01 S02 S03 QJ51 PubChem DrugBank ChemSpider UNII KEGG ChEBI ChEMBL Chemical data Formula C11H12Cl2N2O5 Mol. mass 323.1320 g/mol SMILES & (what is this?)
Chloramphenicol (INN) is a bacteriostatic antimicrobial that became available in 1949. It is considered a prototypical broad-spectrum antibiotic, alongside the tetracyclines, and as it is both cheap and easy to manufacture it is frequently found as a drug of choice in the third world.
Chloramphenicol is effective against a wide variety of Gram-positive and Gram-negative bacteria, including most anaerobic organisms. Due to resistance and safety concerns, it is no longer a first-line agent for any indication in developed nations, although it is sometimes used topically for eye infections. Nevertheless, the global problem of advancing bacterial resistance to newer drugs has led to renewed interest in its use. In low-income countries, chloramphenicol is still widely used because it is inexpensive and readily available.
The most serious adverse effect associated with chloramphenicol treatment is bone marrow toxicity, which may occur in two distinct forms: bone marrow suppression, which is a direct toxic effect of the drug and is usually reversible, and aplastic anemia, which is idiosyncratic (rare, unpredictable, and unrelated to dose) and in general fatal.
- 1 Spectrum of activity
- 2 Therapeutic uses
- 3 Adverse effects
- 4 Pharmacokinetics
- 5 Mechanism of action
- 6 Resistance
- 7 Formulations
- 8 History
- 9 In popular culture
- 10 References
- 11 External links
Spectrum of activity
Because it functions by inhibiting bacterial protein synthesis, chloramphenicol has a very broad spectrum of activity: it is active against Gram-positive bacteria (including most strains of MRSA), Gram-negative bacteria and anaerobes. It is not active against Pseudomonas aeruginosa, Chlamydiae, or Enterobacter species. It has some activity against Burkholderia pseudomallei, but is no longer routinely used to treat infections caused by this organism (it has been superseded by ceftazidime and meropenem). In the West, chloramphenicol is mostly restricted to topical uses because of the worries about the risk of aplastic anaemia.
The original indication of chloramphenicol was in the treatment of typhoid, but the now almost universal presence of multiple drug-resistant Salmonella typhi has meant it is seldom used for this indication except when the organism is known to be sensitive. Chloramphenicol may be used as a second-line agent in the treatment of tetracycline-resistant cholera.
Because of its excellent BBB penetration (far superior to any of the cephalosporins), chloramphenicol remains the first choice treatment for staphylococcal brain abscesses. It is also useful in the treatment of brain abscesses due to mixed organisms or when the causative organism is not known.
Chloramphenicol is active against the three main bacterial causes of meningitis: Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenzae. In the West, chloramphenicol remains the drug of choice in the treatment of meningitis in patients with severe penicillin or cephalosporin allergy and GPs are recommended to carry intravenous chloramphenicol in their bag. In low income countries, the WHO recommend that oily chloramphenicol be used first-line to treat meningitis.
Chloramphenicol has been used in the U.S. in the initial empirical treatment of children with fever and a petechial rash, when the differential diagnosis includes both Neisseria meningitidis septicaemia as well as Rocky Mountain spotted fever, pending the results of diagnostic investigations.
Although unpublished, recent research suggests chloramphenicol could also be applied to frogs to prevent their widespread destruction from fungal infections. Chloramphenicol has recently been discovered to be a life-saving cure for chytridiomycosis in amphibians. Chytridiomycosis is a fungal disease, blamed for the extinction of one-third of the 120 frog species lost since 1980.
The most serious side effect of chloramphenicol treatment is aplastic anaemia. This effect is rare and is generally fatal: there is no treatment and no way of predicting who may or may not get this side effect. The effect usually occurs weeks or months after chloramphenicol treatment has been stopped, and there may be a genetic predisposition. It is not known whether monitoring the blood counts of patients can prevent the development of aplastic anaemia, but patients are recommended to have a blood count check twice weekly while on treatment. The highest risk is with oral chloramphenicol (affecting 1 in 24,000–40,000) and the lowest risk occurs with eye drops (affecting less than 1 in 224,716 prescriptions).
Thiamphenicol, a related compound with a similar spectrum of activity, 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.
Bone marrow suppression
Chloramphenicol commomly causes bone marrow suppression during treatment; this is a direct toxic effect of the drug on human mitochondria. This effect manifests first as a fall in hemoglobin levels, which occurs quite predictably once a cumulative dose of 20 g has been given. The anaemia is fully reversible once the drug is stopped and does not predict future development of aplastic anaemia.
Possible Related Adverse Effects
Chloramphenicol is particularly toxic to people sensitive to benzene-based preservatives, such as preservatives 210 and 211. Chloramphenicol poisoning can cause sensitivity reactions to organic acids and salicylates. It is also known to cause tinnitus and balance problems through inner ear damage. It also causes folic acid depletion, resulting in adverse effects to the thyroid, pituitary and prostate through effects on PABA levels. There may also be links to chronic lymphocytic leukemia (CLL) through folic acid "depletion" and resultant high levels of folic acid in the mutant lymphocytes that characterize CLL. Chloramphenicol stops the body's production of vitamin D and pregnenolone. This results in major hormone depletion, including DHEA and testosterone, that can result in death and also lowers the body's resistance to viral infection. Chloramphenicol can cause testes pain, possibly through hormone effects. Chinese research showed chloramphenicol affects motor neurones. It also affects insulin Igf1 levels and glutamate levels. Both conditions are considered indicative of a type of motor neurone disease. The adverse genetic effects of chloramphenicol are considered heritable.
Gray baby syndrome
Intravenous chloramphenicol use has been associated with the so-called gray baby syndrome. This phenomenon occurs in newborn infants because they do not yet have fully functional liver enzymes (i.e. UDP-glucuronyl transferase), so chloramphenicol remains unmetabolized in the body. This causes several adverse effects, including hypotension and cyanosis. The condition can be prevented by using the drug at the recommended doses, and monitoring blood levels.
Chloramphenicol is extremely lipid soluble; it remains relatively unbound to protein and is a small molecule. It has a large apparent volume of distribution of 100 litres, and penetrates effectively into all tissues of the body, including the brain. The concentration achieved in brain and cerebrospinal fluid (CSF) is around 30 to 50%, even when the meninges are not inflamed; this increases to as high as 89% when the meninges are inflamed.
Use in special populations
Chloramphenicol is metabolized by the liver to chloramphenicol glucuronate (which is inactive). In liver impairment, the dose of chloramphenicol must therefore be reduced. There is no standard dose reduction for chloramphenicol in liver impairment, and the dose should be adjusted according to measured plasma concentrations.
The majority of the chloramphenicol dose is excreted by the kidneys as the inactive metabolite, chloramphenicol glucuronate. Only a tiny fraction of the chloramphenicol is excreted by the kidneys unchanged. Plasma levels should be monitored in patients with renal impairment, but this is not mandatory. Chloramphenicol succinate ester (the inactive intravenous form of the drug) is readily excreted unchanged by the kidneys, more so than chloramphenicol base, and this is the major reason why levels of chloramphenicol in the blood are much lower when given intravenously than orally.
Plasma levels of chloramphenicol must be monitored in neonates and in patients with abnormal liver function. Plasma levels should be monitored in all children under the age of four, the elderly and patients with renal failure. Peak levels (one hour after the dose is given) should be 15–25 mg/l; trough levels (taken immediately before a dose) should be less than 15 mg/l.
Administration of chloramphenicol concomitantly with bone marrow depressant drugs is contraindicated, although concerns over aplastic anaemia associated with ocular chloramphenicol have largely been discounted.
Chloramphenicol is a potent inhibitor of the cytochrome P450 isoforms CYP2C19 and CYP3A4 in the liver. Inhibition of CYP2C19 causes decreased metabolism and therefore increased levels of, for example, antidepressants, antiepileptics and proton pump inhibitors if they are given concomitantly. Inhibition of CYP3A4 causes increased levels of, for example, calcium channel blockers, immunosuppressants, chemotherapeutic drugs, benzodiazepines, azole antifungals, tricyclic antidepressants, macrolide antibiotics, SSRIs, statins and PDE5 inhibitors.
Mechanism of action
Chloramphenicol is bacteriostatic (that is, it stops bacterial growth). It is a protein synthesis inhibitor (more specifically inhibiting protein chain elongation), causing inhibition of peptidyl transferase activity of the bacterial ribosome, binding to A2451 and A2452 residues in the 23S rRNA of the 50S ribosomal subunit, preventing peptide bond formation. While chloramphenicol and the macrolide class of antibiotics both interact with ribosomes, chloramphenicol is not a macrolide. It directly interferes with substrate binding; macrolides sterically block the progression of the growing peptide.   
There are three mechanisms of 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 permeability 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.
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 multiple-drug resistance in typhoid (also called R factors).
Chloramphenicol is available as 250 mg capsules or as a liquid (125 mg/5 ml). In some countries, it is sold as chloramphenicol palmitate ester (CPE). CPE is inactive, and is hydrolysed to active chloramphenicol in the small intestine. There is no difference in bioavailability between chloramphenicol and CPE.
Manufacture of oral chloramphenicol in the U.S. stopped in 1991, because the vast majority of chloramphenicol-associated cases of aplastic anaemia are associated with the oral preparation. There is now no oral formulation of chloramphenicol available in the U.S.
In molecular biology, chloramphenicol is prepared as 25-50 mg/ml stock in ethanol.
The intravenous (IV) preparation of chloramphenicol is the succinate ester, because pure chloramphenicol does not dissolve in water. This creates a problem: Chloramphenicol succinate ester is an inactive prodrug and must first be hydrolysed to chloramphenicol; however, the hydrolysis process is often incomplete, and 30% of the dose is lost and removed in the urine. Serum concentrations of IV chloramphenicol are only 70% of those achieved when chloramphenicol is given orally. For this reason, the dose needs to be increased to 75 mg/kg/day when administered IV to achieve levels equivalent to the oral dose.
Oily chloramphenicol (or chloramphenicol oil suspension) is a long-acting preparation of chloramphenicol first introduced by Roussel in 1954; marketed as Tifomycine, it was originally used as a treatment for typhoid. Roussel stopped production of oily chloramphenicol in 1995; the International Dispensary Association has manufactured it since 1998, first in Malta and then in India from December 2004.
Oily chloramphenicol is recommended by the World Health Organization (WHO) as the first-line treatment of meningitis in low-income countries, and appears on the WHO essential drugs list. It was first used to treat meningitis in 1975 and numerous studies since have demonstrated its efficacy. It is the cheapest treatment available for meningitis (US$5 per treatment course, compared to US$30 for ampicillin and US$15 for five days of ceftriaxone). It has the great advantage of requiring only a single injection, whereas ceftriaxone is traditionally given daily for five days. This recommendation may yet change, now that a single dose of ceftriaxone (cost US$3) has been shown to be equivalent to one dose of oily chloramphenicol.
In the West, chloramphenicol is still widely used in topical preparations (ointments and eye drops) for the treatment of bacterial conjunctivitis. Isolated case reports of aplastic anaemia following use of chloramphenicol eyedrops exist, but the risk is estimated to be less than 1 in 224,716 prescriptions. In Mexico, this is the treatment used prophylactically in newborns.
Chloramphenicol has a long history and therefore a multitude of trade names in many different countries:
- Chloromycetin (U.S., intravenous preparation)
- Chlorsig (U.S., Australia, eye drops)
- Dispersadron C (Greece, eye drops)
- Edrumycetin 250 mg (Bangladesh, capsule)
- Kemicetine (UK, intravenous preparation)
- Kloramfenikol (Denmark, eye drops)
- UK as an eye treatment
- Brochlor (Aventis Pharma Ltd)
- Chloromycetin Redidrops (Goldshield Pharmaceuticals Ltd)
- Golden Eye (Typharm Ltd)
- Optrex Infected Eyes
- Oftan Chlora (eye ointment)
- Optacloran (Bolivia, eye drops)
- Posifenicol 1% (Germany, eye ointment)
- Renicol (India,eye drops)
- Silmycetin (Thailand, eye drops)
- Synthomycine (Israel, eye ointment and skin ointment)
- Tifomycine (France, oily chloramphenicol)
- Unison (Thailand, skin ointment)
- Vanmycetin (Hong Kong, eye drops)
- Orchadexoline (Orchidia pharmaceutical ind., Egypt, eye drops)
- Isoptophenicol (Egypt, eye drops)
- Cedoctine (Egypt, intravenous preparation)
- Chloramex (South Africa, eye ointment)
- Cloranfenicol (Portugal)
Chloramphenicol was originally derived from the bacterium Streptomyces venezuelae, isolated by David Gottlieb, and introduced into clinical practice in 1949, under the trade name Chloromycetin. It was the first antibiotic to be manufactured synthetically on a large scale.
In popular culture
Author/editor Eric Flint chose the drug in his 1632 series as one which could be produced by seventeenth century technology and prevent disease deaths during the alternate history's modified Thirty Years War.
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- ^ Flint, Eric, Grantville Gazette Vol-1, (November 2004), "Portraits", and other linked events and mentions in the series to date up to and including 1635: The Eastern Front (5 October 2010)—which has Gustavus Adolphus mention the affair to Stearns when making him General.
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Chloramphenicol — Strukturformel Allgemeines Freiname Chloramphenicol Andere Name … Deutsch Wikipedia
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