Cleocin
Prevalence and mechanisms of erythromycin resistance in group A and group B Streptococcus: implications for reporting susceptibility results.

Desjardins M, Delgaty KL, Ramotar K, Seetaram C, Toye B.

Division of Microbiology, Department of Medicine, The Ottawa Hospital, 501 Smyth Rd., Ottawa, ON, Canada. madesjardins ottawahospital.on.ca

Increased rates of erythromycin resistance among group B Streptococcus (GBS) and group A Streptococcus (GAS) have been reported. Cross-resistance to clindamycin may be present, depending on the mechanism of resistance. We determined the prevalence of macrolide-resistant determinants in GBS and GAS isolates to guide the laboratory reporting of erythromycin and clindamycin susceptibility. Susceptibilities were determined by the disk diffusion and broth microdilution methods. Inducible and constitutive resistance to clindamycin was determined by the double-disk diffusion method. The presence of the ermTR, ermB, and mefA genes was confirmed by PCR. Of the 338 GBS isolates, 55 (17%) were resistant to erythromycin, whereas 26 (8%) were resistant to clindamycin. The erm methylase gene was identified in 48 isolates, 22 of which had inducible resistance to clindamycin and 26 of which had constitutive resistance to clindamycin. The remaining seven resistant isolates had mefA. Of the 593 GAS isolates, 49 (8%) and 6 (1%) isolates were resistant to erythromycin and clindamycin, respectively. Erythromycin resistance was due to mefA in 33 isolates, whereas 14 isolates had erm-mediated resistance (9 isolates had inducible resistance and 5 isolates had constitutive resistance). In our population, erythromycin resistance in GAS was predominantly mediated by mefA and erythromycin resistance in GBS was predominantly mediated by erm. Regional differences in mechanisms of resistance need to be taken into consideration when deciding whether to report clindamycin susceptibility results on the basis of in vitro test results. Testing by the double-disk diffusion method would be an approach that could be used to address this issue, especially for GAS.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15583291&dopt=Abstract clindamycin antibiotic Cleocin-T



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Different antimicrobial agents in treatment and prophylaxis of experimentally induced intraabdominal sepsis.

Lahnborg G, Nord CE.

A reproducible experimental model of intraabdominal infection in rats has been worked out in order to simulate intraabdominal sepsis seen in humans and to test different antimicrobial agents in treatment and prophylaxis of intraabdominal infections. This experimental model was used to evaluate the efficacy of benzylpenicillin, benzylpenicillin plus sulbactam, cefoxitin, thienamycin, clindamycin, tinidazole, netilmicin, clindamycin plus netilmicin, and tinidazole plus netilmicin in the treatment of intraabdominal sepsis. Sixty-five per cent of the untreated animals died within two days. Within four days, 43% of the animals receiving clindamycin alone, 22% receiving tinidazole alone and 46% receiving netilmicin alone died. Animals treated with piperacillin, clindamycin plus netilmicin or tinidazole plus netilmicin showed a significantly decreased mortality and increased cure rates during the experimental period. Sixty-five per cent of the untreated animals and the animals given sulbactam alone died within 48 h. Over 90% of the animals given benzylpenicillin died within five days. Animals treated with benzylpenicillin plus sulbactam, cefoxitin or thienamycin had a significantly decreased mortality. Within four days 22% of the animals receiving tinidazole alone, 43% receiving clindamycin alone and 46% receiving netilmicin alone died. Animals treated with tinidazole plus netilmicin or clindamycin plus netilmicin had a significantly decreased mortality and increased cure rates during the experimental period. Only 5% of these animals died. In the prophylaxis experiment the following agents were tested: cefoxitin, doxycycline, tinidazole plus netilmicin, clindamycin plus netilmicin, and trimethoprim-sulfa plus tinidazole. One dosage of the antimicrobial(s) reduced the mortality rate significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6592741&dopt=Abstract clindamycin antibiotic Cleocin-T



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Clindamycin resistance in anaerobic bacteria.

Tally FP, Cuchural GJ Jr, Bieluch VM, Jacobus NV, Malamy MH.

Knowledge of the mechanisms of antimicrobial resistance and resistance transfer in anaerobic bacteria has been gained over the past several years. There is widespread resistance to the beta-lactam antibiotics in the B. fragilis group of organisms and there is emerging penicillin resistance in other Bacteroides species. These resistances are usually mediated by chromosomal beta-lactamases. There have been two new beta-lactamases described in Bacteroides; a penicillinase which inactivates ureidopenicillins and another that inactivates cefoxitin. The transfer of the common beta-lactamase, penicillinase, and cefoxitin resistance has been documented in B. fragilis. The mechanism of tetracycline resistance in B. fragilis is the lack of accumulation of intracellular drug; the resistance is widespread in anaerobic bacteria and is seen in two-thirds of the B. fragilis strains. The transfer of tetracycline resistance is common, however, no transfer factor has yet been isolated. Clindamycin-erythromycin resistance in Bacteroides was first recognized in the mid-1970s and transferable resistance was described in 1979. The mechanism of resistance is probably similar to macrolide-lincosamide-streptinogramin-resistance seen in aerobic bacteria. Two clindamycin resistance transfer factors, pBFTM10 and pIP410 (pBF4) have been described. A common resistance determinant found both on plasmids and chromosomes is widely distributed in nature and it probably resides on a transposon. DNA homology studies indicate that there is more than one type of clindamycin resistance in Bacteroides; a newly recognized clindamycin resistance determinant is transferable. Local outbreaks of clindamycin resistance have been noted in the United States and in Europe. The susceptibility of Bacteroides in the United States in 1983 from a multi-center study reveals a 5% incidence of resistance in B. fragilis and 1% in Bacteroides species. The rate of clindamycin resistance has remained steady over the past three years in the Bacteroides fragilis group.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6598519&dopt=Abstract clindamycin antibiotic Cleocin-T



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Clindamycin as an anti-staphylococcal agent--indications and limitations.

Hedstrom SA.

In a general survey it is stated that for single Staphylococcus aureus infections, clindamycin is not considered to be a first-line drug. Its chief indication is penicillin allergy. Penetration and accumulation of clindamycin within leukocytes demonstrated in vitro may be of value in the treatment of S. aureus diseases resulting in large abscesses. An insidious risk of the development of Clostridium difficile diarrhoea limits the use of clindamycin in ambulatory long-term treatment of diabetic osteitis and chronic osteomyelitis. Such patients must therefore be carefully checked during clindamycin therapy. In staphylococcal endocarditis treated with clindamycin, relapses and development of resistance have been reported. Mixed staphylococcal and anaerobic infections in skin, subcutaneous tissue, the diabetic foot, bone and joints are primary indications for clindamycin. S. epidermidis infections, especially septicemia and endocarditis, are not suitable for clindamycin therapy due to a high rate of resistance.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6598522&dopt=Abstract clindamycin antibiotic Cleocin-T



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Clindamycin enhances opsonization of Staphylococcus aureus.

Milatovic D, Braveny I, Verhoef J.

Staphylococcus aureus 502A was grown in the presence of one-third of the minimal inhibitory concentration of clindamycin. Phagocytosis of the antibiotic-treated bacteria by human polymorphonuclear leukocytes was significantly enhanced, compared with that of the untreated control (P less than 0.001). Study of opsonization kinetics by a chemiluminescence assay demonstrated that clindamycin-treated staphylococci were opsonized more rapidly than control bacteria and that the serum concentration required for sufficient opsonization was lower. Complement was consumed much faster, and the opsonic fragment C3b was fixed more rapidly to the bacterial surface when the staphylococci were preincubated with clindamycin. Electron micrographs showed an alteration of the staphylococcal cell wall after clindamycin treatment.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6638997&dopt=Abstract clindamycin antibiotic Cleocin-T



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In-vivo effects of clindamycin on neutrophil function--a preliminary report.

Faden H, Hong JJ, Ogra PL.

Neutrophil functions were evaluated in six normal subjects who had received 300 mg of clindamycin orally four times each day for two days. The mean serum concentration was 1.0 mg/l at the time of neutrophil collection. Clindamycin increased phagocytosis of a clindamycin-resistant staphylococcus from 0.8 to 1.0 organism per polymorphonuclear leukocyte (P less than 0.05). The proportion of killed intracellular bacteria increased from 23.8% to 29.8%. Zymosan-induced chemiluminescence was reduced from 130 X 10(3) to 86 X 10(3) counts per 0.2 min (P less than 0.05). Chemotaxis was unaffected. These preliminary results demonstrate measurable effects of clindamycin on neutrophil functions in the host; however, further studies are needed in order to confirm the observed changes.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6643340&dopt=Abstract clindamycin antibiotic Cleocin-T