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Published on: September 5, 2013
The mef(E)-carrying genetic element (mega) of Streptococcus pneumoniae: insertion sites and association with other
Maria Del Grosso1, Romina Camilli, Francesco Iannelli
1Department of Infectious, Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.
Abstract:
The structure of the macrolide efflux genetic assembly (mega) element, its genomic locations, and its association with other resistance determinants and genetic elements were investigated in 16 Streptococcus pneumoniae isolates carrying mef(E), of which 1 isolate also carried tet(M) and 4 isolates also carried tet(M) and erm(B). All isolates carried a mega element of similar size and structure that included the operon mef(E)-msr(D) encoding the efflux transport system. Among tetracycline-susceptible isolates, six different integration sites were identified, five of which were recognized inside open reading frames present in the R6 genome. In the five isolates also carrying tet(M), mega was inserted in different genetic contexts. In one isolate, it was part of previously described Tn916-like element Tn2009. In another isolate, mega was inserted in a transposon similar to Tn2009 that also included an erm(B) element. This new composite transposon was designated Tn2010. Neither Tn2009 nor Tn2010 could be transferred by conjugation to pneumococcal or enterococcal recipients. In the three isolates in which mega was not physically linked with tet(M), this gene was associated with erm(B) in transposon Tn3872, a Tn916-like element. Homologies between the chromosomal insertions of these composite transposons and sequences of multidrug-resistant pneumococcal genomes in the databases indicate the presence of preferential sites for the integration of composite Tn916-like elements carrying multiple resistance determinants in S. pneumoniae.
Insights
The macrolide efflux genetic assembly (mega) element in Streptococcus pneumoniae frequently integrates into specific genomic sites. This element, encoding an efflux system, often co-localizes with other antibiotic resistance genes, contributing to multidrug resistance.
Area of Science:
- Microbiology
- Genetics
- Molecular Biology
Background:
- Antibiotic resistance in Streptococcus pneumoniae is a growing public health concern.
- The macrolide efflux genetic assembly (mega) element is a mobile genetic element associated with macrolide resistance.
- Understanding the genomic context and associations of the mega element is crucial for tracking resistance dissemination.
Purpose of the Study:
- To investigate the structure, genomic locations, and associations of the mega element in Streptococcus pneumoniae.
- To identify the genetic contexts in which the mega element integrates, particularly in relation to other antibiotic resistance genes.
Main Methods:
- Analysis of 16 Streptococcus pneumoniae isolates carrying the mef(E) gene.
- Characterization of the mega element's structure and size.
- Identification of integration sites within the bacterial genome.
- Investigation of co-localization with tetracycline (tet(M)) and erythromycin (erm(B)) resistance genes.
Main Results:
- All 16 isolates possessed a similar mega element containing the mef(E)-msr(D) operon.
- Six different integration sites for the mega element were identified in tetracycline-susceptible isolates, with five within open reading frames.
- In isolates with tet(M), the mega element was found in various genetic contexts, including within Tn2009 and a novel composite transposon Tn2010 (mega-erm(B)).
- The mega element was not physically linked to tet(M) in three isolates, where tet(M) was associated with erm(B) in Tn3872.
- Tn2009 and Tn2010 were not transferable by conjugation.
Conclusions:
- The mega element is a conserved genetic assembly in Streptococcus pneumoniae.
- Preferential integration sites exist for composite Tn916-like elements carrying multiple resistance determinants in S. pneumoniae.
- The co-localization of mega with tet(M) and erm(B) in novel composite transposons highlights mechanisms for the spread of multidrug resistance.
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