Chloramphenicol is a substance produced originally from cultures of Streptomyces venezuelae but is now manufactured synthetically.

Crystalline chloramphenicol is a stable compound that is rapidly absorbed from the gastrointestinal tract and widely distributed into tissues and body fluids, including the CNS and CSF; it penetrates cells well. Most of the drug is inactivated in the liver by conjugation with glucuronic acid or by reduction to inactive arylamines. Excretion is mainly in the urine, 90% in an inactive form. Although chloramphenicol is usually administered orally, the succinate can be injected intravenously in similar dosage..

Chloramphenicol is a potent inhibitor of protein synthesis in microorganisms. It blocks the attachment of amino acids to the nascent peptide chain on the 50S unit of ribosomes by interfering with the action of peptidyl transferase. Chloramphenicol is principally bacteriostatic, and its spectrum, dos- age, and blood levels are similar to those of the tetracyclines. Chloramphenicol has been used to treat many types of infection (eg, from salmonellae, meningococci, H influenzae), but it is no longer the drug of choice for any infection.

Chloramphenicol resistance is caused by destruction of the drug by an enzyme (chloramphenicol acetyltransferase) that is under plasmid control.

Chloramphenicol infrequently causes gastrointestinal upsets. However, administration of more than 3 g/day regularly  induces disturbances in red blood cell maturation, elevation  of serum iron, and anemia. These changes are reversible upon discontinuance of the drug. Very rarely, individuals exhibit an apparent idiosyncrasy to chloramphenicol and develop severe or fatal aplastic anemia that is distinct from the dose-related reversible effect described earlier. For these reasons, the use of chloramphenicol is generally restricted  to infections in which it is clearly the most effective drug by laboratory test or experience.

In premature and newborn infants, chloramphenicol can induce collapse ("gray syndrome") because the normal mechanism of detoxification (glucuronide conjugation in the liver) is not yet developed.

مواضيع ذات صلة

التجميع الإنزيمي للبتيد السباعي للفانكوميسين وكلوروإرموميسين (chloroermomycin)

تعديلات السلسلة الجانبية في مضادّات الكيفالوسبورين: أجيال متعددة

Drug targets and mechanisms of action

تعديلات السلسلة الجانبية( side chain modifications) في أنواع البنسيلين

ANTIBIOTIC CLASSES AND THEIR SOURCES

كيف تتطور مقاومة المضادات الحيوية ؟

PRINCIPLES OF ANTIBIOTIC RESISTANCE

Tyrocidins

التتراسايكلينات Tetracyclines

المضادات الحيوية الصناعية Synthetic Antibiotics

Streptose

مضادات ببتيدية مستقيمة السلسلة Straight Peptide Antibiotics