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Vol. 14. Issue 6.
Pages 564-568 (November - December 2010)
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Vol. 14. Issue 6.
Pages 564-568 (November - December 2010)
Open Access
Distribution of erm genes and low prevalence of inducible resistance to clindamycin among staphylococci isolates
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Vivian de Lima Spode Coutinho
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viviandels@bol.com.br

Correspondence to:Rua Ramiro Barcelos, 2350, Porto Alegre - RS CEP: 90035-903 Phone: +55 51 33598860; Fax: +55 51 33598310.
, Rodrigo Minuto Paiva, Keli Cristine Reiter, Fernanda de-Paris, Afonso Luis Barth, Alice Beatriz Mombach Pinheiro Machado
Department of Microbiology and Molecular Biology, Universidade Federal do Rio Grande do Sul
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Abstract
Introduction

Resistance to macrolides, lincosamides and streptogramins B (MLSB antibiotics) in staphylococci may be due to modification in ribosomal target methylase encoded by erm genes. The expression of MLSB resistance lead to three phenotypes, namely constitutive resistance (cMLSB), inducible resistance (iMLSB), and resistance only to macrolides and streptogramins B (MSB). The iMLSB resistance is the most difficult to detect in the clinical laboratory.

Objective

This study investigated the expression of MLSB resistance and the prevalence of the erm genes among 152 clinical isolates of Staphylococcus aureus and coagulase-negative Staphylococcus (CNS) from Hospital de Clínicas de Porto Alegre.

Methods

Primary MLSB resistance was detected by the disk diffusion method. Isolates with iMLSB phenotype were tested by double-disk induction method. All isolates were tested by a genotypic assay, PCR with specific primers.

Results

A total of 46.7% of staphylococci were positive for cMLSB; 3.3% for iMLSB and 3.3% for MSB. One or more erm genes were present in 50.1% of isolates. The gene ermA was detected in 49 isolates, ermC in 29 and ermB in 3.

Conclusion

The prevalence of the ermA, ermB and ermC genes were 29.6%, 17.1% and 0.66% respectively, and constitutive resistance was the most frequent as compared to the other two phenotypes.

Keywords:
Staphylococcus
resistance
erm genes
macrolides
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References
[1.]
W.E. Kloos, T.L. Bannerman.
Update on clinical significance of coagulase-negative staphylococci.
Clin Microbiol Rev, 7 (1994), pp. 117-140
[2.]
M.A. Pfaller, L.A. Herwaldt.
Laboratory clinical and epidemiological aspects of coagulase-negative staphylococci.
Clin Microbiol Rev, 1 (1988), pp. 281-299
[3.]
M.E. Rupp, G.L. Archer.
Coagulase-negative staphylococci pathogens associated with medical progress.
Clin Infect Dis, 19 (1994), pp. 231-245
[4.]
R. Leclercq.
Mechanisms of resistance to macrolides and lincosamides: Nature of the resistance elements and their clinical implications.
Clin Infect Dis, 34 (2002), pp. 482-492
[5.]
M.C. Roberts, J. Sutcliffe, P. Courvalin, L.B. Jensen, J. Rood, H. Seppala.
Nomenclature for macrolide-lincosamide-streptogramin B resistance determinants.
Antimicrob. Agents Chemother, 43 (1999), pp. 2823-2830
[6.]
E.A. Eady, J.I. Roos, J.L. Tipper, C.E. Walters, J.H. Cove, W.C. Noble.
Distribution of genes encoding erythromycin ribosomal methylases and an erythromycin efflux pump in epidemiologically distinct groups of staphylococci.
Antimicrob Agents Chemother, 31 (1993), pp. 211-217
[7.]
S.A. Khan, R.P. Novick.
Terminal nucleotide sequences of Tn 551 a transposon specifying erythromycin resistance in Staphylococcus aureus: homology with Tn3.
Plasmid, 4 (1980), pp. 148-154
[8.]
F. Rossi, D.B. Andreazzi.
Interpretando o Antibiograma.
Atheneu 1° Ed, São Paulo, (2005), pp. 41-43
[9.]
B. Weisblum.
Erythromycin resistance by ribosome modification.
Antimicrob Agents Chemother, 39 (1995), pp. 577-585
[10.]
K.R. Fiebelkorn, S.A. Crawford, M.L. McElmeel, J.H. Jorensen.
Practical Disk Diffusion Method for Detection of Inducible Clindamycin Resistance in Staphylococcus aureus and Coagulase Negative Staphylococci.
J Clin Microbiol, 41 (2003), pp. 4740-4744
[11.]
Clinical and Laboratory Standards Institute.
Performance standards for antimicrobial susceptibility testing: seventeenth informational supplement. M100-S16.
Clinical and Laboratory Standards Institute, (2007),
[12.]
J. Sutcliffe, T. Grebe, A. Tait-Kamradt, L. Wondrack.
Detection of Erythromycin-Resistance Determinants by PCR.
Antimicrob Agents and Chemother, 40 (1996), pp. 2562-2566
[13.]
M.K. York, L. Gibbs, F. Chehab, G.F. Brooks.
Comparison of PCR Detection of mecA with Standard Susceptibility Testing Methods To Determine Methicilin Resistance in Coagulase-Negative Staphylococci.
J Clin Microbiol, 34 (1996), pp. 249-253
[14.]
L. Gerard, A. Quaglia, M.E. Reverdy, R. Lequerq, F. Vandenesch, J. Etienne.
Distribution of Genes Encoding Resistance to Macrolides, Lincosamides, and Streptogramins among Staphylococci.
Antimicrob Agents Chemother, 43 (1999), pp. 1062-1066
[15.]
Z. Aktas, A. Aridogan, C.B. Kayacan, D. Aydin.
Resistance to Macrolide, Lincosamide and Streptogramin Antibiotics in Staphylococcus Isolated in Istanbul, Turkey.
J Microbiol, 45 (2007), pp. 286-290
[16.]
L. Merino-Díaz, A. Cantos de la Casa, M.J. Torres-Sanchez, J. Aznar-Mantin.
Detección de resistencia inducible a clindamicina em aislados cutáneos de Staphylococcus ssp. por métodos fenotípicos y genotípicos.
Enferm Infecc Microbiol Clin, 25 (2006), pp. 77-81
[17.]
J.M.T. Hamilton-Miller, S. Shah.
Patterns of phenotypic resistance to the macrolide-lincosamide-ketolide-streptogramin group of antibiotics in staphylococci.
J Antimicrob Chemother, 46 (2000), pp. 941-949
[18.]
N. Delialioglu, G. Aslan, C. Ozturk, V. Baki, S. Sen, G. Emekdas.
Inducible Clindamycin Resistance in Staphylococci Isolate from Clinical Samples.
Jnp J Infect Dis, 58 (2005), pp. 104-106
[19.]
Z. Saribas, F. Tunckanat, A. Pinar.
Prevalence of erm genes encoding macrolide-lincosamide-streptogramin (MLS) resistance among in a Turkish university hospital.
Clin Microbiol Infect, 12 (2006), pp. 797-799
[20.]
G. Yialmz, K. Aydin, S. Iskender, R. Caylan, I. Koksal.
Detection and prevalence of inducible clindamycin resistance in staphylococci.
J Med Microbiol, 56 (2007), pp. 342-345
[21.]
L.R. Perez, J. Caierão, A.L. Antunes, P.A. d’Azevedo.
Use of the D Test Method to Detect Inducible Clindamycin Resistance in Coagulase Negative Staphylococci (CoNS).
Braz J Infect Dis, 11 (2007), pp. 186-188
[22.]
F. Martineau, F. Picard, N. Lansac, C. Ménard, P.H. Roy, M. Ouellette, M.G. Bergeron.
Correlation between the Resistance Genotype Determined by Multiplex PCR Assays and the Antibiotic Susceptibility Patterns of Staphylococcus aureus an Staphylococcus epidermidis.
Antimicrob Agents and Chemother, 44 (2000), pp. 231-238
[23.]
F.J. Schmitz, R. Sadurski, A. Kray, M. Boos, M. Geisel, K. Köhrer, J. Verhoef, C. Fluit.
Prevalence of macrolide-resistance genes in Staphylococcus aureus and Enterococcus faecium isolates from 24 European university hospitals.
J Antimicrob Chemother, 45 (2000), pp. 891-894
[24.]
H. Westh, D.M. Hougaard, J. Vuust, T. Rosdahl.
Prevalence of erm gene classes in erythromycin-resistance Staphylococcus aureus strains isolated between 1959 and 1988.
Antimicrob Agents Chemother, 39 (1995), pp. 369-373
[25.]
W.O. Chung, C. Werckenthin, S. Schwarz, M.C. Roberts.
Host range of the ermF methylase gene in bacteria of human and animal origin.
J Antimicrob Chemother, 43 (1999), pp. 5-14
[26.]
A. Brisson-Noël, P. Delrieu, D. Samain, P. Courvalin.
Inactivation of lincosamide antibiotics in Staphylococcus. Identification of lincosamide o-nucleotidyltransferases and comparison of the corresponding resistance genes.
J Biol Chem, 263 (1988), pp. 15880-15887
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