It has a molecular weight of Clindamycin is bacteriostatic drug acts by inhibiting protein synthesis. It binds on the 50S subunit of the bacterial ribosome. It suppresses protein synthesis by interfering with the development of initiation complexes and with aminoacyl translocation reactions. Food does not interfere with absorption of clindamycin. Though, antimicrobial activity continues in faeces for 5 days after parenteral therapy with clindamycin is stopped; growth of clindamycin-sensitive microorganisms in colonic substances may be derivative of antibiotics for up to 2 weeks.
Clindamycin is active against bacteroides fragilis, P. So it is useful for treatment of abdominal and pelvic abscess, respiratory tract infections including lung abcess, skin and soft-tissue Infections. Daily doses as high as 4. In children, a minimal daily dose of mg is recommended, regardless of body weight.
Other side effects are nausea, vomiting, abdominal cramps, derivative of antibiotics, metallic taste, neuromuscular blockade, derivative of antibiotics, derivative of antibiotics, stomatitis and urticarial. Clindamycin is a chlorine-substituted derivative of lincomycinan antibiotic that is elaborated by Streptomyces lincolnensis.
It issemi-synthetic and belongs to lincosamide class. It isa derivative of the amino acid trans -L n -propylhygrinic acid, attached to a sulfur-containing derivative of an octose. The binding site for clindamycin is on the 50S derivative of antibiotics of the bacterial ribosome which is identical with that for erythromycin.
Clindamycin, like erythromycin, suppresses protein synthesis by interfering with the development of initiation complexes and with aminoacyl translocation reactions. Although clindamycin, erythromycin, and chloramphenicol are not structurally linked, they act at sites in close vicinity, and binding by one of these antibiotics to the ribosome may inhibit the interaction of the others.
Resistance to clindamycin, derivative of antibiotics, which usually confers cross-resistance to macrolides, is due to 1 mutation of the ribosomal receptor site; 2 modification of the receptor by a derivative of antibiotics expressed adenine methylase ; and 3 enzymatic inactivation plasmid mediated adenyl transferase of clindamycin.
Gram-negative aerobic species are innately resistant because of poor permeability of the outer membrane. Resistance due to ribosomal methylation by erm -encoded enzymes in macrolides may also produce resistance to clindamycin.
There is cross-resistance only if the enzyme is formed constitutively, derivative of antibiotics, as clindamycin does not induce the methylase. Conversely, strains with inducible resistance may develop constitutive production of the methylase during therapy. Hence use of clindamycin should be avoided in the treatment of deep-rooted infections caused by organisms exhibiting an inducible resistance phenotype. Detection of this phenotype can be done by approximating erythromycin and clindamycin on an agar plate with a lawn of the organism; a derivative of antibiotics of the zone of inhibition between clindamycin and erythromycin suggests inducible resistance this is known as the "D-test".
Clindamycin is not a substrate for macrolide efflux pumps; so strains that are resistant to macrolides by this mechanism are susceptible to clindamycin. Infrequently altered metabolism causes clindamycin resistance. Resistance commonly occurs via macrolide -lincosamide-streptogramin B MLSB type of resistance which may be constitutive or inducible.
Clindamycin is nearly completely absorbed orally. Peak plasma concentrations are attained within 1 hour after mg dose. Food does not reduce absorption significantly. The half-life is about 2. Clindamycin palmitate, an oral formulation for pediatric use, is an inactive prodrug that is hydrolyzed rapidly in vivo.
Its rate and magnitude of absorption are comparable to those of clindamycin. The phosphate ester of clindamycin, which is given parenterally, is also promptly hydrolyzed in vivo to the active parent compound. After intramuscular injection, peak concentrations are not achieved until 3 hours in adults and 1 hour in children.
Clindamycin penetrates well into most tissues including bone, with brain and cerebrospinal fluid being important exceptions. Itfreely crosses the placenta. It penetrates well into abscesses and is actively taken up anxiety vs asthma concentrated by phagocytes, polymorphonuclear leukocytes, and alveolar macrophages.
Clindamycin is inactivated by metabolism to N -demethylclindamycin and clindamycin sulfoxide, which are excreted in the urine and bile. Derivative of antibiotics of clindamycin can occur in severe hepatic failure, and dosage adjustments may be essential. No dosage adjustment is required for renal failure. Use of clindamycin is mainly for anaerobic and mixed infections, especially by Bacteroides fragilis causing abdominal and pelvic abscess.
It is generally combined with aminoglycoside or cephalosporin. Clindamycin is used as an alternative, especially in patients with -lactam allergies as it has decent activity against aerobic and anaerobic gram-positive cocci and high oral bioavailability, derivative of antibiotics. It has also been used for the treatment of necrotizing skin and soft-tissue infections as it diminishes toxin expression.
Variable numbers of patients 0. Antibiotic Drugs Clindamycin Clindamycin is a semi-synthetic and belongs to lincosamide.