Clindamycin chemical structure
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Clindamycin

Clindamycin is a lincosamide antibiotic. Clindamycin is a semisynthetic antibiotic and derived from lincomycin by the addition of chloride. Clindamycin is sold under brand names such as Dalacin and Cleocin. It is most effective against infections involving the following types of organisms: more...

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  • Aerobic gram-positive cocci, including some members of the Staphylococcus and Streptococcus (eg. pneumococcus) genera.
  • Anaerobic gram-negative bacilli, including some members of the Bacteroides and Fusobacterium genera.

It is used primarily to treat infections caused by susceptible anaerobic bacteria. Such infections might include respiratory infections, septicemia and peritonitis. In penicillin allergic patients clindamycin may be used to treat susceptible aerobic infections as well. It is also used to treat bone-infections caused by Staphylococcus aureus. Topical application of clindamycin phosphate can be used to treat severe acne.

Available forms

Clindamycin is commonly administered in penal caps as hydrochloride or in oral suspension as palmitate hydrochloride. It is also available for intravenous injection as phosphate. In topical preparations clindamycin is as hydrochloride or phosphate (Evoclin®).

Mechanism of action

Clindamycin has a bacteriostatic effect. Clindamycin interferes with bacterial protein synthesis, in a similar way as erythromycin and chloramphenicol, by binding to the 50S subunit of the bacterial ribosome. This causes antagonism if administered simultaneously and possible cross-resistance.

Pharmacokinetics

Almost all of orally administered clindamycin is absorbed from the gastro-intestinal tract, and it is widely distributed throughout the body, excluding the central nervous system. Clindamycin phosphate, as injection, is inactive, but it is rapidly hydrolysed in the blood to active clindamycin. High concentrations of clindamycin can be found in the bile (up 100 times higher than in the plasma). Adequate concentrations can also be found in the bone, and there is also active uptake into leucocytes.

Metabolism

Most of clindamycin is metabolised in the liver, and some of its metabolites are active, such as N-demethyl and sulphoxide-metabolites, and some are inactive. Clindamycin's half-life is 21 hours. Both active clindamycin and its metabolites are excreted primarily in the urine and some in the bile.

Side effects

Common side effects are mainly gastrointestinal disturbances. Clindamycin can cause a potentially lethal condition, pseudomembranous colitis, which is caused by Clostridium difficile, a clindamycin resistant bacteria (all the other bacteria have been killed by clindamycin, allowing C. difficile to over-proliferate and cause inflammation of the colon). Rare instances of polyarthritis (inflamation of several joints) have also been reported. In some cases this polyarthritis side effect feels like extreme flu-like aching througout the body.

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Comparison of national, regional, and state susceptibilities of streptococcus pneumoniae isolates to clindamycin and erythromycin: results of the antimicrobial
From CHEST, 10/1/05 by John G. Gums

PURPOSE: The ARM Program, an ongoing project of the University of Florida, documents trends in antimicrobial susceptibility patterns in inpatient/outpatient isolates to track antibiotic resistance. To date, 358 institutions from 6 US geographic regions have been enrolled at no cost. Each provides a minimum of 3 years of antibiogram/sensitivity report data in a HIPAA-compliant non-identifying format. These data comprise a national aggregate database containing 28.3 million isolates, 250,423 of which are S pneumoniae.

METHODS: The database was interrogated to determine resistance patterns for S pneumoniae isolates against Clindamycin and erythromycin as surrogate markers for macrolide resistance at the national, regional, and state level for data collected from 1997-2004. States were stratified in terms of resistance rates; only states with 5 or more institutions in the database were included.

RESULTS: Nationally, pneumococcal isolate susceptibility to clindamycin was 89% (range, 86.9% in Southwest to 91.4% in North Central). The 5 states with isolates most susceptible to clindamycin were Illinois (97.6%), Maryland (94.9%), Tennessee (93%), Arkansas (92.4%) and West Virginia (92%); the 5 states with isolates least susceptible to clindamycin were Virginia (87.9%), Georgia (86.5%), Alabama (83.9%), Florida (83.8%), and Nevada (76.9%). For erythromycin, national susceptibility was 67.8% (range, 62.1% in Southeast to 76.2% in Southwest). The 5 states with isolates most susceptible to erythromycin were Arizona (79.8%), Indiana (78.8%), Massachusetts (78.8%), Kansas (76.4%), and Pennsylvania (76.1%); the 5 states with isolates least susceptible to erythromycin were Virginia (62.7%), South Carolina (62.5%), Georgia (62.2%), Florida (60.5%), and West Virginia (57.9%). Virginia, Georgia, South Carolina, and Florida had low susceptibility to both erythromycin and clindamycin; West Virginia, Tennessee, Arkansas, South Carolina, and Virginia had the largest difference between clindamycin and erythromytin.

CONCLUSION: Susceptibility patterns for S pneumoniae isolates against clindamycin and erythromycin suggest the highest level of methylation-induced resistance (MLS-b) is in Nevada, while the highest level of efflux-mediated resistance (M-type) is in West Virginia.

CLINICAL IMPLICATIONS: Surveillance programs such as ARM provide the ability to track both frequency and severity of macrolide resistance.

DISCLOSURE: John Gums, None.

John G. Gums PharmD * University of Florida, Gainesville, FL

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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