AUTHOR=Mancilla-Rojano Jetsi , Ochoa Sara A. , Reyes-Grajeda Juan Pablo , Flores Víctor , Medina-Contreras Oscar , Espinosa-Mazariego Karina , Parra-Ortega Israel , Rosa-Zamboni Daniela De La , Castellanos-Cruz María del Carmen , Arellano-Galindo José , Cevallos Miguel A. , Hernández-Castro Rigoberto , Xicohtencatl-Cortes Juan , Cruz-Córdova Ariadnna 

TITLE=Molecular Epidemiology of Acinetobacter calcoaceticus-Acinetobacter baumannii Complex Isolated From Children at the Hospital Infantil de México Federico Gómez

JOURNAL=Frontiers in Microbiology

VOLUME=Volume 11 - 2020

YEAR=2020

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2020.576673

DOI=10.3389/fmicb.2020.576673

ISSN=1664-302X

ABSTRACT=The Acinetobacter calcoaceticus - baumannii complex is regarded as a group of phenotypically indistinguishable opportunistic pathogens responsible for mainly causing hospital-acquired pneumonia and bacteremia. The aim of this study was to determine the frequency of isolation of the species that constitute the Acinetobacter calcoaceticus - baumannii complex, as well as the susceptibility to antibiotics, and their distribution at the Hospital Infantil de Mexico Federico Gomez. A total of 88 strains previously identified by Vitek 2®, 40 as A. baumannii and 48 as Acinetobacter calcoaceticus - baumannii complex which was isolated from 52 children from January 07, 2015 – September 28, 2017. A. baumannii accounted for 89.77% (79/88) of the strains; A. pittii, 6.82% (6/88); and A. nosocomialis, 3.40% (3/88). Most strains were recovered mainly from patients in the intensive care unit and emergency wards. Blood cultures provided 44.32% (39/88) of strains. The 13.63% (12/88) of strains were associated with primary bacteremia, 3.4% (3/88) with secondary bacteremia, and 2.3% (2/88) with pneumonia.  In addition, 44.32% (39/88) were multidrug-resistant strains and, 11.36% (10/88) were extensively drug-resistant. All strains amplified the blaOXA-51 gene; 51.13% (45/88), the blaOXA-23 gene; 4.54% (4/88), the blaOXA-24 gene; and 2.27% (2/88), the blaOXA-58 gene. Plasmid profiles showed that the strains had 1-6 plasmids. The strains were distributed in 52 pulsotypes, and 24 showed identical restriction patterns, with a correlation coefficient of 1.0. Notably, some strains with the same pulsotype were isolated from different patients, wards or years, suggesting the persistence of more than one clone. Twenty-seven sequence types were determined for the strains based on an multilocus sequence typing protocol Pasteur using massive sequencing; the most prevalent was ST 156 (27.27%, 24/88). The CRISPR-Cas IFb system provided amplification in A. baumannii and A. pittii strains (22.73% [20/88]). This study identified an increased number of multidrug-resistant strains and the relationship among strains through molecular typing. The data suggests that more than one strain could be causing an infection in some patient. The implementation of molecular epidemiology allowed the characterization of a set of strains and identification of different attributes associated with its distribution in a specific environment.