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Cleocin Clindamycin treatment of invasive infections caused by community-acquired, methicillin-resistant and methicillin-susceptible Staphylococcus aureus in children.
Martinez-Aguilar G, Hammerman WA, Mason EO Jr, Kaplan SL.
Baylor International Pediatrics Aids Initiative, Baylor College of Medicine, Texas Children's Hospital, Houston, USA.
BACKGROUND: Community-acquired, methicillin-resistant Staphylococcus aureus (CA-MRSA) is an established pathogen in several areas of the United States, but experience with clindamycin for the treatment of invasive MRSA infections is limited. We compared the outcome of therapy for MRSA with that of methicillin-susceptible (MSSA) invasive infections in children treated with clindamycin, vancomycin or beta-lactam antibiotics. METHODS: The demographics, hospital course and outcome of children at Texas Children's Hospital between February and November 2000 and between August 2001 and August 2002 with invasive S. aureus infections were reviewed from medical records in this retrospective study. RESULTS: CA-MRSA and community-acquired methicillin-susceptible S. aureus (MSSA) caused invasive infections in 46 and 53 children, respectively. The median ages (range) of the children were: MRSA, 3.5 years (2 months to 18.6 years); MSSA, 4.8 years (3 months to 19.8 years). The sites of infection for MRSA vs. MSSA isolates, respectively, were: bacteremia, 3 vs. 6; osteomyelitis, 14 vs. 14; septic arthritis, 5 vs. 7; pneumonia, 11 vs. 3; lymphadenitis, 7 vs. 14; other, 5 vs. 8. Among MRSA patients 39 (20 received clindamycin only, 18 had vancomycin initially and 8 were treated with a beta-lactam initially) received clindamycin and 6 received vancomycin as primary therapy. Among MSSA patients, clindamycin, nafcillin or other beta-lactam antibiotics were used in 24, 18 and 9, respectively. The median number of febrile days was 3 (0 to 14) and 2 (0 to 6) for MRSA and MSSA patients, respectively (P = 0.07). The median number of days with positive blood cultures was 2 for the MRSA (n = 16) and 1 for the MSSA (n = 18) patients (P = 0.04). CONCLUSION: Clindamycin was effective in treating children with invasive infections caused by susceptible CA-MRSA isolates.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12867833&dopt=Abstract clindamycin antibiotic Cleocin-T
Cleocin Potential clindamycin resistance in clindamycin-susceptible, erythromycin-resistant Staphylococcus aureus: report of a clinical failure.
Levin TP, Suh B, Axelrod P, Truant AL, Fekete T.
Temple University Hospital, Section of Infectious Diseases, 3401 North Broad St., Philadelphia, PA 19140, USA. TLevin9696 yahoo.com
The erm gene product confers clindamycin resistance on Staphylococcus aureus. We report a clindamycin clinical failure where resistance developed on therapy in a D-test-positive strain. D tests of 91 clindamycin-susceptible, erythromycin-resistant S. aureus isolates showed that 68% of methicillin-susceptible and 12.3% of methicillin-resistant S. aureus strains were D-test positive.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15728934&dopt=Abstract clindamycin antibiotic Cleocin-T
Cleocin The Relationship Between the Anticoccidial Effects of Clindamycin and the Development of Immunity in the Eimeria pragensis/Mouse Model of Large Intestinal Coccidiosis.
Yunus M, Horii Y, Makimura S, Smith AL.
Laboratory of Veterinary Internal Medicine, Department of Veterinary Science, Faculty of Agriculture, Miyazaki University.
The therapeutic effect of clindamycin on Eimeria pragensis (E. pragensis) infection in C57BL/6 mice was demonstrated by suppression of oocyst production and the appearance of degenerated endogenous stages of parasite in the intestine. Short-term clindamycin treatment, from 1 to 4 days or 4 to 8 days post infection (pi) at a dose of 800 mg/kg/day was effective to reduce clinical symptoms, oocyst production and schizogonic development. Interestingly, the short-term treatment schedules allowed the development of a measurable degree of protective immunity to challenge infection in the treated mice. In contrast, clindamycin treatment for the full 12 days period, which almost completely inhibited clinical symptoms and oocyst output, prevented the full development of protective immunity in the treated mice. All these data indicate that clindamycin is efficacious as an anti-eimerian agent and that both early and late endogenous developmental stages of E. pragensis exert a deep influence on the development of effective immunity to challenge infection.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15750312&dopt=Abstract clindamycin antibiotic Cleocin-T
Cleocin Erythromycin-induced resistance to clindamycin in Staphylococcus aureus.
Marr JK, Lim AT, Yamamoto LG.
Emergency Department, Kapiolani Medical For Women And Children, USA.
PURPOSE: To describe the incidence of erythromycin-induced resistance to clindamycin in a sample of Staphylococcus aureus isolates. METHODS: 100 erythromycin-resistant and clindamycin-sensitive S. aureus were collected as a convenience sample from February to August 2003. Inducible clindamycin resistance was identified using the D-zone disc method. RESULTS: Of the 100 Staphylococcus aureus isolates, 64 were methicillin sensitive (MSSA) and 36 were methicillin resistant (MRSA). Of the 64 MSSA isolates, 22 (34%) had inducible resistance. Of the 36 MRSA isolates, 4 (11%) had inducible resistance. Overall, 26% of these clindamycin sensitive S. aureus isolates, exhibited inducible resistance to clindamycin. CONCLUSIONS: In this sample, MSSA isolates were almost three times more likely to have inducible MLS resistance compared to MRSA isolates. Inducible resistance may compromise the efficacy of clindamycin. The frequency of inducible resistance in this series of "clindamycin sensitive" S. aureus isolates is 26%. It is likely that the true percentage of clindamycin resistance is being underestimated since testing for inducible resistance is not routinely performed.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15751751&dopt=Abstract clindamycin antibiotic Cleocin-T
Cleocin In vitro selection of resistance to clindamycin related to alterations in the attenuator of the erm(TR) gene of Streptococcus pyogenes UCN1 inducibly resistant to erythromycin.
Fines M, Gueudin M, Ramon A, Leclercq R.
Service de Microbiologie, CHU Cote de Nacre, Avenue Cote de Nacre, 14033 Caen cedex, France. fines-m chu-caen.fr
A clinical isolate of Streptococcus pyogenes UCN1 intermediate to erythromycin (MIC 1 mg/L) and susceptible to clindamycin (MIC 0.03 mg/L) harboured an inducible erm(TR) gene encoding a ribosomal methylase. We have selected in vitro, in the presence of concentrations of clindamycin ranging from 0.12 to 1 mg/L, one-step mutants that are highly resistant to this antibiotic (MIC 64 mg/L) at a frequency of 10(-7). By contrast, in an erythromycin-susceptible strain of S. pyogenes UCN5, mutants could be selected only by a low concentration of clindamycin (0.12 mg/L) at a frequency of 10(-9). Clindamycin resistance in four of six S. pyogenes UCN1 mutants was associated with deletions of 163 and 6 bp, as well as a tandem duplication of 101 bp in the regulatory sequence of the erm(TR) gene. The role of these structural alterations in clindamycin resistance was demonstrated by cloning the erm(TR) gene from the wild-type and mutant strains in Escherichia coli DB10, a mutant susceptible to macrolides. Clindamycin resistance was expressed only when the erm(TR) gene was preceded by an altered attenuator. Mutations could lead to the formation of mRNA secondary structures accounting for the accessibility of the ribosome-binding site and the initiation codon of the ErmTR methylase to the ribosomes, and subsequently for the translation of the erm(TR) transcripts. The easy selection in one step of mutants resistant to high levels of clindamycin by concentrations of this antibiotic ranging from four to 40 times the MIC leads us to recommend caution in the use of clindamycin therapy in group A Streptococcus infections.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11533008&dopt=Abstract clindamycin antibiotic Cleocin-T
Cleocin The use of intradiscal antibiotics for discography: an in vitro study of gentamicin, cefazolin, and clindamycin.
Klessig HT, Showsh SA, Sekorski A.
Pain Clinic of Northwestern Wisconsin, Eau Claire, Wisconsin 54702, USA. painclwi2 aol.com
STUDY DESIGN: In vitro determination of minimum inhibitory concentrations (MICs) of gentamicin, cefazolin, and clindamycin, alone and in combination with iohexol against laboratory strains of Eschericia coli B, Staphylococcus aureus, and Staphylococcus epidermidis. OBJECTIVE: To study the effects of iohexol on the efficacy of gentamicin, cefazolin, and clindamycin. SUMMARY OF BACKGROUND DATA: Prophylactic antibiotics have been advocated to prevent discitis following discography. Intravenous cefazolin administered before discography has been shown to penetrate the intervertebral disc. However, the use of systemic antibiotics for prophylaxis may lead to bacterial resistance. Intradiscal antibiotic administration is an attractive alternative to systemic antibiotic prophylaxis before discography, but there is no data documenting the efficacy of commonly used antibiotics in the presence of iohexol. METHODS: MICs were determined by adding standard concentrations of bacteria to serial dilutions of antibiotic with and without the addition of iohexol in Todd-Hewitt Broth medium. MICs were determined as the lowest concentration well that demonstrated inhibition of cell growth. RESULTS: Gentamicin, cefazolin, and clindamycin remain efficacious in the presence of iohexol. MICs were lower for cefazolin and gentamycin than for clindamycin. Iohexol alone also demonstrated some inhibition of cell growth. CONCLUSION: This study supports the use of intradiscal antibiotics for prophylaxis of disc space infection during discography. lntradiscal placement of antibiotic should obviate the need for systemic antibiotic prophylaxis and its attendant risk of generating antimicrobial resistance.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12897501&dopt=Abstract clindamycin antibiotic Cleocin-T
Cleocin-T (clindamycin antibiotic) References
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