María Teresa Reguero

Publications (3)2.58 Total impact

• Article: Antibiotic resistance patterns of Acinetobacter calcoaceticus-A. baumannii complex species from Colombian hospitals.

  María Teresa Reguero, Olga Esther Medina, María Andrea Hernández, Diana Vanessa Flórez, Emilia María Valenzuela, José Ramón Mantilla
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  ABSTRACT: INTRODUCTION: Only automated phenotypic methods are currently used in Colombian hospitals for identifying isolates of the Acinetobacter calcoaceticus-A. baumannii complex (ACB). The phenotypical similarities in these species mean that they cannot be differentiated by manual or automated methods, thereby leading to their identification as A. baumannii, or ACB complex in clinical settings. Our objective was to identify to the species level 60 isolates, from four hospitals, evaluate their antibiotic susceptibility, and detect resistance-related genes. METHODS: 16S-23S rRNA internal transcribed spacer (ITS) region and rpoB gene partial sequences were amplified. Resistance genes for cephalosporin, carbapenem and aminoglycoside were detected by PCR. Possible mutations in the quinolone resistance-determining region (QRDR) were evaluated. The association of ISAba-1 with bla(OXA) and bla(ADC) genes was determined by PCR. Amplification products of ITS region, rpoB gene and some resistance genes were sequenced and compared using the BLAST tool. RESULTS: 16S-23S rRNA ITS region and partial rpoB gene sequence analysis allowed 51isolates to be identified as A. baumannii, 8 as A. nosocomialis, and 1 isolate as A. pitti. A. baumannii isolates were highly resistant to all antibiotics tested, while the others were susceptible to ciprofloxacin and ampicillin/sulbactam. Quinolone resistance, found only in A. baumannii, was associated with mutations in the QRDR region of gyrA and parC genes. CONCLUSION: This is the first investigation in Colombia that has identified ACB complex species using molecular methods, and determined differences in antibiotic resistance and resistance genes among the species. It is of the highest importance to identify isolates to the species level for future resistance and epidemiology studies in our region.
  Enfermedades Infecciosas y Microbiología Clínica 09/2012; · 1.49 Impact Factor
• Article: [Distribution of extended spectrum β-lactamases-codifying genes in Klebsiella pneumoniae isolates from hospitals of Bogota, D.C., Colombia].

  Ingrid Yamile Pulido, José Ramón Mantilla, Emilia María Valenzuela, María Teresa Reguero, Elsa Beatriz Gonzalez
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  ABSTRACT: Extended spectrum β-lactamases (ESBL) are the most widely distributed enzymes in Enterobacteriaceae of Latin America and are key enzymes in resistance to antibiotics in common use. However, in Colombia, little information is available concerning the identity of genes coding for these enzymes in Klebsiella pneumoniae. The bla genes were identified in K. pneumoniae isolated from hospitals in Bogotá D.C., Colombia. Materials and methods. One hundred seventy-seven isolates of ESBL producers were collected from 10 hospitals in Bogota between 2003 and 2005. Antibiotic susceptibility was determined by disk diffusion, and the number of β-lactamases in each isolate was assessed by isoelectric focusing. blaCTX-M, blaSHV and blaTEM were identified by PCR and subsequent sequencing. Besides, the resitenance to third generation cephalosporins, 44.7 % and 49.7 % were resistant to amikacyn and thrimetoprim-sulaphametoxazole respectively. Lower resistance rates to other antibiotics were observed as well. An average of three β-lactamases were detected by isoelectric focusing, and the genes blaCTX-M-12 (56.0%) and blaSHV-12 (33.3%) were the most prevalent. blaSHV-5 (11.8%), blaCTX-M-1-1 (4.0%), blaSHV-27 (2.8%), blaSHV-2 (2.8%), blaCTX-M-1-2 (1.7%) and blaCTX-M-1-15 (0.6%) were present in smaller percentages. In addition, three genes were identified that coded for narrow spectrum β-lactamases. Eleven bla genes were identified, eight of which were ESBL-coding. The diversity of the bla genes suggested a continuing exposure of K. pneumoniae to strong antibiotic pressures in Bogota hospitals.
  Biomédica: revista del Instituto Nacional de Salud 03/2011; 31(1):15-20. · 0.55 Impact Factor
• Article: [Molecular characterization of an outbreak caused by CTX-M-12-producing Klebsiella pneumoniae in a Colombian hospital's neonatal intensive care unit].

  José Ramón Mantilla, María Teresa Reguero, Elsa Beatriz González, Ibonne Ayde García, Aura Lucía Leal, Paula Andrea Espinal, Celia Alpuche, Ismael Alberto Valderrama, Martha Isabel Garzón, Narda María Olarte
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  ABSTRACT: Molecular characterisation of Klebsiella pneumoniae strains is a tool that assits in the reduction of the disemination of drug resistance and the control of nosocomial infections that are caused by this pathogen. Objective. Molecular description of an outbreak of nosocomial infection caused by Klebsiella pneumoniae in a neonatal intensive care unit in a tertiary level hospital in Bogotá. Eleven Klebsiella pneumoniae isolates were analysed. Production of Extended Spectrum Beta-Lactamases was verified by agar diffusion tests. Isoelectric points of the enzymes were determined by isoelectric focusing. The bla(CTX-M-12) gene was detected by PCR and pulsed field gel electrophoresis genotyping was done. All the isolates were Extended Spectrum Beta-Lactamase producers. Pulsed field gel electrophoresis and BOX-PCR genotyping grouped two isolates from hospital objects and eight infection-causing isolates into a single epidemic clone. The isolate from a thermometer was not grouped into the epidemic clone and showed a different resistance pattern. Isoelectric focusing revealed simultaneous beta-lactamase production having different isoelectric points. PCR amplification revealed the presence of the bla(CTX-M-12) gene in the 11 isolates studied. This is the first report of a molecularly characterised outbreak of CTX-M-12-producing Klebsiella pneumoniae from Colombia. The results of this study provide additional evidence of the global dissemination of CTX-M ESBL and the need for epidemiological follow-up in our hospitals.
  Biomédica: revista del Instituto Nacional de Salud 10/2006; 26(3):408-14. · 0.55 Impact Factor