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Definição e significado de Chloramphenicol

Definição

chloramphenicol (n.)

1.an oral antibiotic (trade name Chloromycetin) used to treat serious infections (especially typhoid fever)

2.(MeSH)An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.

Chloramphenicol Acetyltransferase (n.)

1.(MeSH)An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.

Chloramphenicol (n.)

1.(MeSH)An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106)

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Chloramphenicol (n.) [MeSH]


chloramphenicol (n.)


chloramphenicol (n.) [MeSH]


Wikipedia

Chloramphenicol

                   
Chloramphenicol
Systematic (IUPAC) name
2,2-dichloro-N-[1,3-dihydroxy-1-(4-nitrophenyl)propan-2-yl]acetamide
Clinical data
AHFS/Drugs.com monograph
MedlinePlus a608008
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 56-75-7 YesY
ATC code D06AX02 D10AF03 G01AA05 J01BA01 S01AA01 S02AA01 S03AA08 QJ51BA01
PubChem CID 298
DrugBank DB00446
ChemSpider 5744 YesY
UNII 66974FR9Q1 YesY
KEGG D00104 YesY
ChEBI CHEBI:17698 YesY
ChEMBL CHEMBL130 YesY
Chemical data
Formula C11H12Cl2N2O5 
Mol. mass 323.1320 g/mol
 YesY (what is this?)  (verify)

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 an antibiotic of choice in the Third World.

Chloramphenicol, also known as chlornitromycin, 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 infection 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.[1] 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.[2]

Contents

  History

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.

  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.[3] 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.

  Therapeutic uses

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.

Chloramphenicol is also effective against Enterococcus faecium, which has led to its being considered for treatment of vancomycin-resistant enterococcus.

Although unpublished, recent research suggests chloramphenicol could also be applied to frogs to prevent their widespread destruction from fungal infections.[4] Chloramphenicol has recently been discovered to be a life-saving cure for chytridiomycosis in amphibians.[5] Chytridiomycosis is a fungal disease, blamed for the extinction of one-third of the 120 frog species lost since 1980.

  Adverse effects

  Aplastic anemia

The most serious side effect of chloramphenicol treatment is aplastic anaemia.[2] 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.[6] 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.[citation needed] The highest risk is with oral chloramphenicol[7] (affecting 1 in 24,000–40,000)[8] and the lowest risk occurs with eye drops (affecting less than 1 in 224,716 prescriptions).[9]

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[citation needed]. 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[citation needed]. 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.

  Leukemia

There is an increased risk of childhood leukemia, as demonstrated in a Chinese case-controlled study,[10] and the risk increases with length of treatment.

  Gray baby syndrome

Intravenous chloramphenicol use has been associated with the so-called gray baby syndrome.[11] 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.[12] 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.[13][14][15]

  Pharmacokinetics

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.

Chloramphenicol increases the absorption of iron.[16]

  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.[citation needed]

Chloramphenicol passes into breast milk, so should therefore be avoided during breast feeding, if possible.[17]

  Dose monitoring

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.[citation needed]

  Drug interactions

Administration of chloramphenicol concomitantly with bone marrow depressant drugs is contraindicated, although concerns over aplastic anaemia associated with ocular chloramphenicol have largely been discounted.[18]

Chloramphenicol is a potent inhibitor of the cytochrome P450 isoforms CYP2C19 and CYP3A4 in the liver.[19] 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.[20]

  Mechanism of action

Chloramphenicol is a bacteriostatic drug that stops bacterial growth by inhibiting protein synthesis. Chloramphenicol prevents protein chain elongation by inhibiting the peptidyl transferase activity of the bacterial ribosome. It specifically binds to A2451 and A2452 residues in the 23S rRNA of the 50S ribosomal subunit, preventing peptide bond formation.[21] While chloramphenicol and the macrolide class of antibiotics both interact with ribosomes, chloramphenicol is not a macrolide. It directly interferes with substrate binding, whereas macrolides sterically block the progression of the growing peptide. [22] [23] [24]

  Resistance

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).

Currently, some Enterococcus faecium and Pseudomonas aeruginosa strains are resistant to chloramphenicol. Some Veillonella app. and Staphylococcus capitis strains have also developed resistance to chloramphenicol to varying degrees. [25]

  Formulations

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.

  Intravenous

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.[26] 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.[27]

  Oily

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.[28]

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[29] and numerous studies since have demonstrated its efficacy.[30][31][32] 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.[33]

  Eye drops

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.[9] In Mexico, this is the treatment used prophylactically in newborns.

  Trade names

Chloramphenicol has a long history and therefore a multitude of trade names in many different countries:

  • Alficetyn
  • Amphicol
  • Biomicin
  • Chlornitromycin
  • Chloromycetin (U.S., intravenous preparation)
  • Chlorsig (U.S., Australia, eye drops)
  • Dispersadron C (Greece, eye drops)
  • Edrumycetin 250 mg (Bangladesh, capsule)
  • Fenicol
  • Kemicetine (UK, intravenous preparation)
  • Kloramfenikol (Denmark, eye drops)
  • Laevomycetin
  • UK as an eye treatment
    • Brochlor (Aventis Pharma Ltd)
    • Chloromycetin Redidrops (Goldshield Pharmaceuticals Ltd)
    • Golden Eye (Typharm Ltd)
    • Optrex Infected Eyes
  • Ocupol-D (eye ointment, India)
  • Oftan Chlora (eye ointment)
  • Optacloran (Bolivia, eye drops)
  • Paraxin
  • Phenicol
  • Posifenicol 1% (Germany, eye ointment)
  • Medicom
  • Nevimycin
  • 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)
  • Vernacetin
  • Veticol
  • Orchadexoline (Orchidia pharmaceutical ind., Egypt, eye drops)
  • Isoptophenicol (Egypt, eye drops)
  • Cedoctine (Egypt, intravenous preparation)
  • Chloramex (South Africa, eye ointment)
  • Cloranfenicol (Portugal)

  References

  1. ^ Falagas, M. E.; Grammatikos, A. P.; Michalopoulos, A. (October 2008). "Potential of old-generation antibiotics to address current need for new antibiotics". Expert Review of Anti Infective Therapy 6 (5): 593–600. DOI:10.1586/14787210.6.5.593. PMID 18847400. http://www.future-drugs.com/doi/abs/10.1586/14787210.6.5.593?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov. 
  2. ^ a b Rich, M.; Ritterhoff, R.; Hoffmann, R. (December 1950). "A fatal case of aplastic anemia following chloramphenicol (chloromycetin) therapy". Annals of Internal Medicine 33 (6): 1459–1467. PMID 14790529. 
  3. ^ Neu, H. C.; Gootz, T. D. (1996). "Antimicrobial Chemotherapy:Antimicrobial Inhibitors of Ribosome Function". In Baron, S. et al.. Baron's Medical Microbiology (4th ed.). University of Texas Medical Branch. ISBN 0-9631172-1-1. PMID 21413283. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.688. 
  4. ^ Griggs, K. (2007-10-30). "Frog killer fungus 'breakthrough'". BBC News. http://news.bbc.co.uk/2/hi/science/nature/7067613.stm. 
  5. ^ Poulter, R. T. M.; Busby, J. N.; Bishop, P. J.; Butler, M. I.; Speare, R.. "Chloramphenicol cures chytridiomycosis" (pdf). NZ Frogs. http://www.nzfrogs.org/site/nzfrog/files/poulter.pdf. 
  6. ^ Nagao, T.; Mauer, A. (July 1969). "Concordance for drug-induced aplastic anemia in identical twins". New England Journal of Medicine 281 (1): 7–11. DOI:10.1056/NEJM196907032810102. PMID 5785754. 
  7. ^ Holt, R. (1967). "The bacterial degradation of chloramphenicol". Lancet 289 (7502): 1259–1260. DOI:10.1016/S0140-6736(67)92720-1. PMID 4165044. 
  8. ^ Wallerstein, R.; Condit, P.; Kasper, C.; Brown, J.; Morrison, F. (June 1969). "Statewide study of chloramphenicol therapy and fatal aplastic anemia". JAMA 208 (11): 2045–2050. DOI:10.1001/jama.208.11.2045. PMID 5818983. 
  9. ^ a b Lancaster, T.; Stewart, A. M.; Jick, H. (1998). "Risk of serious haematological toxicity with use of chloramphenicol eye drops in a British general practice database". British Medical Journal 316 (7132): 667. DOI:10.1136/bmj.316.7132.667. PMC 28473. PMID 9522792. http://bmj.bmjjournals.com/cgi/content/full/316/7132/667. 
  10. ^ Shu, X.; Gao, Y.; Linet, M.; Brinton, L.; Gao, R.; Jin, F.; Fraumeni, J. (October 1987). "Chloramphenicol use and childhood leukaemia in Shanghai". Lancet 2 (8565): 934–937. DOI:10.1016/S0140-6736(87)91420-6. PMID 2889862. 
  11. ^ McIntyre, J.; Choonara, I. (2004). "Drug toxicity in the neonate". Biology of the Neonate 86 (4): 218–221. DOI:10.1159/000079656. PMID 15249753. 
  12. ^ Piñeiro-Carrero, V.; Piñeiro, E. (2004). "Liver" (pdf). Pediatrics 113 (4 Supplement): 1097–1106. PMID 15060205. http://pediatrics.aappublications.org/content/113/Supplement_3/1097.full.pdf. 
  13. ^ Feder, H. (1986). "Chloramphenicol: what we have learned in the last decade". Southern Medical Journal 79 (9): 1129–1134. DOI:10.1097/00007611-198609000-00022. PMID 3529436. 
  14. ^ Mulhall, A.; de Louvois J.; Hurley, R. (1983). "Chloramphenicol toxicity in neonates: its incidence and prevention". British Medical Journal (Clinical Research Edition) 287 (6403): 1424–1427. DOI:10.1136/bmj.287.6403.1424. PMC 1549666. PMID 6416440. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1549666. 
  15. ^ Forster, J.; Hufschmidt, C.; Niederhoff, H.; Künzer, W. (1985). "[Need for the determination of chloramphenicol levels in the treatment of bacterial-purulent meningitis with chloramphenicol succinate in infants and small children]" (in german). Monatsschrift Kinderheilkunde 133 (4): 209–213. PMID 4000136. 
  16. ^ Harold M. Silverman, Pharm.D. (editor-in-chief), ed. (2006). "Iron Supplements". Pill Book, The (12th revised ed.). New York: Bantam Dell. pp. 593–596. ISBN 978-0-553-58892-7. 
  17. ^ kidsgrowth.org --> Drugs and Other Substances in Breast Milk Retrieved on June 19, 2009
  18. ^ PRACTICE GUIDANCE: OTC CHLORAMPHENICOL EYE DROPS June 2005. Royal Pharmaceutical Society of Great Britain (RPSGB)
  19. ^ Park, J. Y.; Kim, K. A.; Kim, S. L. (November 2003). "Chloramphenicol Is a Potent Inhibitor of Cytochrome P450 Isoforms CYP2C19 and CYP3A4 in Human Liver Microsomes". Antimicrobial Agents and Chemotherapy 47 (11): 3464–3469. DOI:10.1128/AAC.47.11.3464-3469.2003. PMC 253795. PMID 14576103. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=253795. 
  20. ^ "Facts for prescribers (Fakta för förskrivare)" (in swedish). FASS - Swedish National Drug Formulary. http://www.fass.se/LIF/produktfakta/fakta_lakare_artikel.jsp?articleID=18352. 
  21. ^ "Chloramphenicol". The Merck Manual. Merck. http://merck.com/mmpe/sec14/ch170/ch170d.html. 
  22. ^ Jardetzky, O. (July 1963). "Studies on the Mechanism of Action of Chloramphenicol - The Conformation of Chloramphenicol in Solution" (pdf). The Journal of Biological Chemistry 238 (7): 2498–2508. PMID 14028808. http://www.jbc.org/content/238/7/2498.full.pdf. 
  23. ^ Wolfe, A. D.; Hahn, F. E. (1965). "Mode of Action of Chloramphenicol. IX. Effects of Chloramphenicol Upon a Ribosomal Amino Acid Polymerization System and Its Binding to Bacterial Ribosome". Biochimica et Biophysica Acta 95: 146–155. PMID 14289020.  edit
  24. ^ Hahn, F. E.; Wisseman, C. L. Jr.; Hopps, H. E. (1955). "Mode of Action of Chloramphenicol III. : Action of Chloramphenicol on Bacterial Energy Metabolism". Journal of Bacteriology 69 (2): 215–223. PMC 357505. PMID 14353832. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=357505.  edit
  25. ^ "Chloramphenicol spectrum of bacterial susceptibility and Resistance". http://www.toku-e.com/Upload/Products/PDS/20120507002160.pdf. Retrieved 15 May 2012. 
  26. ^ Glazko, A. J.; Dill, W. A.; Kinkel, A. W. (1977). "Absorption and excretion of parenteral doses of chloramphenicol sodium succinate in comparison with per oral doses of chloramphenicol (abstract)". Clinical Pharmacological Therapy 21: 104. 
  27. ^ Bhutta, Z.; Niazi, S.; Suria, A. (March–April 1992). "Chloramphenicol Clearance in Typhoid Fever: Implications for Therapy". Indian Journal of Pediatry 59 (2): 213–219. DOI:10.1007/BF02759987. PMID 1398851. 
  28. ^ Lewis, R. F.; Dorlencourt, F.; Pinel, J. (1998). "Long-acting oily Chloramphenicol for Meningococcal Meningitis". Lancet 352 (9130): 823. DOI:10.1016/S0140-6736(05)60723-4. PMID 9737323. 
  29. ^ Rey, M.; Ouedraogo, L.; Saliou, P.; Perino, L. (1976). "Traitement minute de la méningite cérébrospinale épidémique par injection intramusculaire unique de chloramphénicol (suspension huileuse)" (in french). Médecine et Maladies Infectieuses 6 (4): 120–124. DOI:10.1016/S0399-077X(76)80134-5. 
  30. ^ Wali, S.; Macfarlane, J.; Weir, W.; Cleland, P.; Ball, P.; Hassan-King, M.; Whittle, H.; Greenwood, B. (1979). "Single injection treatment of meningococcal meningitis. 2. Long-acting chloramphenicol". Transactions of the Royal Society for Tropical Medicine and Hygiene 73 (6): 698–702. DOI:10.1016/0035-9203(79)90024-5. PMID 538813. 
  31. ^ Puddicombe, J.; Wali, S.; Greenwood, B. (1984). "A field trial of a single intramuscular injection of long-acting chloramphenicol in the treatment of meningococcal meningitis". Transactions of the Royal Society for Tropical Medicine and Hygiene 78 (3): 399–403. DOI:10.1016/0035-9203(84)90132-9. PMID 6464136. 
  32. ^ Pécoulm B.; Varaine, F.; Keita, M.; Soga, G.; Djibo, A.; Soula, G.; Abdou, A.; Etienne, J.; Rey, M. (October 1991). "Long-acting chloramphenicol versus intravenous ampicillin for treatment of bacterial meningitis". Lancet 338 (8771): 862–866. DOI:10.1016/0140-6736(91)91511-R. PMID 1681224. 
  33. ^ Nathan, N.; Borel, T.; Djibo, A. (2005). "Ceftriaxone as effective as long-acting chloramphenicol in short-course treatment of meningococcal meningitis during epidemics: a randomised non-inferiority study". Lancet 366 (9482): 308–313. DOI:10.1016/S0140-6736(05)66792-X. PMID 16039333. 

  Additional reading

  • Jardetzky, O. (1963). "Studies on the Mechanism of Action of Chloramphenicol". Journal of Biological Chemistry 238 (7): 2498–2508. 

  External links

   
               

 

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