Urinary Tract Infections in a South American Population: Dynamic Spread of Class 1 Integrons and Multidrug Resistance by Homologous and Site-Specific Recombination
Author(s) -
Carolina Márquez,
Maurizio Labbate,
Claudia Raymondo,
Jimena Fernández,
Alicia M. Gestal,
Marita Holley,
Graciela Borthagaray,
H. W. Stokes
Publication year - 2008
Publication title -
journal of clinical microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.349
H-Index - 255
eISSN - 1070-633X
pISSN - 0095-1137
DOI - 10.1128/jcm.00835-08
Subject(s) - integron , transposable element , biology , genetics , homologous recombination , microbiology and biotechnology , transposition (logic) , population , strain (injury) , antibiotic resistance , gene , antibiotics , genome , medicine , linguistics , philosophy , environmental health , anatomy
One hundred four bacterial strains mediating urinary tract infections in separate individuals from a Uruguayan community were isolated. Forty-six strains conferred a multidrug resistance phenotype. All 104 strains were examined for the presence of class 1, 2, and 3 integrons. Class 1 integrons were found in 21 isolates across four distinct bacterial genera. A large class 1 integron in a Klebsiella pneumoniae strain was fully sequenced and was 29,093 bp in length. This integron probably arose by homologous recombination since it was embedded in a hybrid Tn21-like transposon backbone which comprised a Tn5036-like tnp transposition module at the IRi integron end and a Tn21 mer module at the IRt integron end. The parent integron/transposon that contributed the Tn5036 module was not related to Tn1696 since the integron insertion points in the transposon backbones were 16 bases apart. Examination of the other 20 class 1 integron-containing strains revealed further evidence of genetic exchange. This included a strain that possessed a Tn5036 module at the IRt end but not at the IRi end and another that possessed a tnp module beyond IRi that was a hybrid of Tn21 and Tn5051 and that is presumed to have arisen by site-specific recombination. This study highlights the ability of different genetic elements to act cooperatively to spread and rearrange antibiotic resistance in a community.
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