Low level resistance to oleandomycin as a marker of ermA in staphylococci

Modugno, V. Di; Guerrini, Massimo; Shah, Saroj; Hamilton‐Miller, J. M. T.

doi:10.1093/jac/49.2.425

Cited by 5 publications

(8 citation statements)

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“…Phenotypic resistance patterns of ermA - or ermC -carrying staphylococci from hospital samples have already been described (Daurel et al , 2008; Di Modugno et al , 2002). The heterologously expressed erythromycin resistance of our ermA -positive environmental staphylococci was also observed by Di Modugno et al (2002) during MIC determinations. Di Modugno et al (2002) distinguished between the two end points, ‘changing from confluent to light growth’ and ‘changing from light growth to no growth’.…”

Section: Discussionmentioning

confidence: 99%

“…Although the percentage of macrolide-resistant staphylococci in the aquatic environment is lower (20 vs 70–80 % in clinical samples) (Faria et al , 2009; Heß & Gallert, 2014), 31.1 % of them were revealed to be inducible or have constitutive resistance to clindamycin (Heß & Gallert, 2014). Whereas clinical isolates with inducible MLS B resistance, which are genetically almost exclusively encoded by ermA or ermC , are phenotypically well characterized (Daurel et al , 2008; Di Modugno et al , 2002; Hamilton-Miller & Shah, 2000), little is known about ‘environmental’ iMLS B staphylococci. For successful medication after infection, identification and information about their phenotypic behaviour are necessary.…”

Section: Introductionmentioning

confidence: 99%

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Resistance behaviour of inducible clindamycin-resistant staphylococci from clinical samples and aquatic environments

Heß

Gallert

2014

Journal of Medical Microbiology

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In this study, the species diversity of staphylococci with inducible resistance to macrolides, lincosamides and streptogramin B (MLS B ) isolated from clinical samples, sewage and river water was investigated. Inducible clindamycin resistance was tested using a D-test and macrodilution assays. Inducible cross-resistance (iMLS B phenotype) was examined by PCR of erm gene classes A, B, C, F, G, Q, T and 43. Although ermC was the most frequently detected resistance gene in iMLS B phenotypes of environmental staphylococci (61.2 %), resistance genes encoding iMLS B were more diverse than in staphylococci from hospital samples. In 22.4 % of iMLS B staphylococci from aquatic environments, none of the eight tested erm genes was found. Those isolates and erm43-expressing Staphylococcus lentus displayed low erythromycin MICs (3-16 mg ml "1 ) compared with ermC-positive environmental staphylococci (¢256 mg ml "1 ). In contrast to clinical isolates with clearly defined resistance behaviour, resistance patterns against MLS B and MICs for clindamycin of environmental isolates were more diverse. Although the abundance of iMLS B staphylococci in the aquatic environment was lower than in staphylococci from hospital samples, the diversity of resistance genes encoding this phenotype seemed to be higher. Oleandomycin is the best marker to correlate iMLS B phenotype and the respective erm gene. The phenotypical behaviour of environmental isolates may differ from the resistance pattern of clinical iMLS B staphylococci expressing ermA or ermC, and this should be considered for successful treatment of infections.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Resistance behaviour of inducible clindamycin-resistant staphylococci from clinical samples and aquatic environments

Heß

Gallert

2014

Journal of Medical Microbiology

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“…Di Modugno and colleagues described this phenomenon for staphylococcal isolates with ermA; they described two end points obtained by broth microdilution, with a transition first from confluent to light growth and then from light growth to no growth (2). Single methylation of the ribosomal target by the ErmA methylase versus dimethylation by the ErmC methylase may be related to this phenomenon, or other factors may be involved.…”

Section: Discussionmentioning

confidence: 99%

“…However, the incidence of constitutive and inducible MLS B resistance varies by geographic region and even from hospital to hospital, with some studies showing high local incidence of either constitutive or inducible MLS B resistance in staphylococcal isolates (2,5,6,13,15). In addition, other mechanisms conferring resistance to macrolides and not lincosamides, such as efflux mechanisms encoded by msrA, are not uncommon (4) and may be increasing in frequency (15,18).…”

Section: Discussionmentioning

confidence: 99%

Practical Disk Diffusion Method for Detection of Inducible Clindamycin Resistance in Staphylococcus aureus and Coagulase-Negative Staphylococci

et al. 2003

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Bacterial resistance to antimicrobial agents generally involves drug inactivation, target site modification, impermeability, or efflux mechanisms. Macrolide antibiotic resistance in Staphylococcus aureus and coagulase-negative staphylococci (CNS) may be due to an active efflux mechanism encoded by msrA (conferring resistance to macrolides and type B streptogramins only) (16, 17) or may be due to ribosomal target modification, affecting macrolides, lincosamides, and type B streptogramins (MLS B resistance). erm genes encode enzymes that confer inducible or constitutive resistance to MLS agents via methylation of the 23S rRNA, reducing binding by MLS agents to the ribosome (15). Resistance is induced by the binding of a macrolide to upstream translational attenuator sequences, leading to changes in mRNA secondary structure, exposure of the ribosomal binding site, and translation of the erm methylase. Alterations in these 5Ј upstream sequences, including deletions, duplications, and other mutations, lead to constitutive expression of the methylase gene and constitutive MLS B resistance (1,15,24). Strains with inducible MLS B resistance (MLS B i) strains demonstrate in vitro resistance to 14-and 15-member macrolides (e.g., erythromycin), while appearing susceptible to 16-member macrolides, lincosamides, and type B streptogramins; strains with constitutive MLS B resistance (MLS B c strains) show in vitro resistance to all of these agents (15).MLS antibiotics are commonly used in treatment of staphylococcal infections. Clindamycin is a frequent choice for some staphylococcal infections, particularly skin and soft-tissue infections, and as an alternative in the penicillin-allergic patient. Inducible MLS B resistance is not recognized by using standard susceptibility test methods, including standard broth-based or agar dilution susceptibility tests. Failure to identify inducible MLS B resistance may lead to clinical failure of clindamycin therapy (3). Conversely, labeling all erythromycin-resistant staphylococci as clindamycin resistant prevents the use of clindamycin in infections caused by truly clindamycin-susceptible staphylococcal isolates.Low levels of erythromycin are the most effective inducer of inducible MLS B resistance (23). To detect MLS B i strains, there are special disk approximation tests that incorporate erythromycin induction of clindamycin resistance (23). These tests involve the placement of an erythromycin disk in close proximity to a disk containing clindamycin or lincomycin. As the erythromycin diffuses through the agar, resistance to the lincosamide is induced, resulting in a flattening or blunting of the lincosamide zone of inhibition adjacent to the erythromycin disk, giving a D shape to the zone (D-zone effect). Jenssen and colleagues suggested that closer spacing than in a standard disk dispenser was necessary to discern inducible resistance, with optimal spacing of 10 to 15 mm (6); 20-mm spacing of disks and a higher concentration of erythromycin (30 g) have also been suggested (18).

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“…The incidence and mechanisms of MLS resistance vary widely by geographic region and even from hospital to hospital, with some studies showing high local incidence of either constitutive or inducible MLS B resistance in staphylococcal isolates (16,17,18,19). The D-zone test is recommended by both CLSI and EUCAST for the detection of MLS resistance.…”

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confidence: 99%

Evaluation of the Automated Vitek 2 System for Detection of Various Mechanisms of Macrolide and Lincosamide Resistance in Staphylococcus aureus

et al. 2014

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We evaluated the performance of the automated Vitek 2 system against disk diffusion for susceptibility testing of Staphylococcus aureus strains showing various resistance mechanisms to macrolides and lincosamides (ML). The Vitek 2 system showed 100% concordance with the D-zone test in detection of the most common resistance mechanisms to ML, including methylase and efflux systems.A lthough structurally unrelated, macrolides, lincosamides, and streptogramins (MLS) have similar modes of action by binding to the peptidyl-transferase region of the 50S ribosomal subunit, which leads to inhibition of protein synthesis. Resistance to MLS in Staphylococcus aureus is mainly due to (i) active efflux by an efflux pump encoded by the msr(A) gene and conferring resistance to macrolides and type B streptogramins (MS B ) or (ii) ribosomal target site modification due to methylases encoded by erm genes and conferring resistance to MLS B (1, 2, 3). MLS B phenotypes are either constitutive (cMLS B ), showing in vitro resistance to all MLS B agents, or inducible (iMLS B ) following exposure to a macrolide (4). iMLS B strains demonstrate in vitro resistance to 14-and 15-member macrolides but appear susceptible to 16-member macrolides, lincosamides, and type B streptogramins (5, 6, 7).Among MLS, clindamycin (CLI) is most frequently used for therapy of staphylococcal infections, including osteomyelitis and skin and soft tissue infections (8). Its good oral bioavailability, tolerability, and excellent tissue penetration make it an important option for outpatient therapy and changeover after intravenous antibiotics (9). However, clindamycin treatment of infections caused by S. aureus strains with the iMLS B phenotype may result in clinical failure due to the selection of constitutive mutants (10).Clinical and Laboratory Standards Institute (CLSI) and EU-CAST recommend the use of the double disk diffusion method (D-zone test) to reveal the presence of the iMLS B phenotype in staphylococci (11,12). Therefore, several automated systems provide a test for detection of inducible clindamycin resistance (ICR) in staphylococci. For instance, Vitek 2 added an Advanced Expert System (AES), which is able to interpret the ICR test and clindamycin susceptibility for S. aureus strains. The aim of the present study was to evaluate the performance of the Vitek 2 system against the disk diffusion method for the detection of various mechanisms of MLS resistance in a set of genotypically well characterized S. aureus isolates.S. aureus strains were selected from a national reference collection composed of systematic national survey samples and isolates sent to the reference lab for outbreak investigations, exotoxin detection, or diagnostic problems (13). All strains were previously confirmed by a 16S rRNA-nuc-mecA triplex PCR and stored at Ϫ80°C for further analysis (14).Susceptibility to MLS was phenotypically tested by MIC determination and genotypically confirmed by PCR. The MICs for erythromycin and clindamycin were determined by the agar dilution met...

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Low level resistance to oleandomycin as a marker of ermA in staphylococci

Cited by 5 publications

References 4 publications

Resistance behaviour of inducible clindamycin-resistant staphylococci from clinical samples and aquatic environments

Resistance behaviour of inducible clindamycin-resistant staphylococci from clinical samples and aquatic environments

Practical Disk Diffusion Method for Detection of Inducible Clindamycin Resistance in Staphylococcus aureus and Coagulase-Negative Staphylococci

Evaluation of the Automated Vitek 2 System for Detection of Various Mechanisms of Macrolide and Lincosamide Resistance in Staphylococcus aureus

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