Abstract
Carbapenem-resistant determinants and their surrounding genetic structure were studied in Acinetobacter spp. from neonatal sepsis cases collected over 7 years at a tertiary care hospital. Acinetobacter spp. (n = 68) were identified by ARDRA followed by susceptibility tests. Oxacillinases, metallo-β-lactamases (MBLs), extended-spectrum β-lactamases and AmpCs, were detected phenotypically and/or by PCR followed by DNA sequencing. Transconjugants possessing the blaNDM−1(New Delhi metallo-β-lactamase) underwent further analysis for plasmids, integrons and associated genes. Genetic environment of the carbapenemases were studied by PCR mapping and DNA sequencing. Multivariate logistic regression was used to identify risk factors for sepsis caused by NDM-1-harboring organisms. A. baumannii (72%) was the predominant species followed by A. calcoaceticus (10%), A. lwoffii (6%), A. nosocomialis (3%), A. junni (3%), A. variabilis (3%), A. haemolyticus (2%), and 14TU (2%). Fifty six percent of the isolates were meropenem-resistant. Oxacillinases present were OXA-23-like, OXA-58-like and OXA-51-like, predominately in A. baumannii. NDM-1 was the dominant MBL (22%) across different Acinetobacter spp. Isolates harboring NDM-1 also possessed bla(VIM−2, PER−1, VEB−2, CTX−M−15), armA, aac(6′)Ib, aac(6′)Ib-cr genes. blaNDM−1was organized in a composite transposon between two copies of ISAba125 in the isolates irrespective of the species. Further, OXA-23-like gene and OXA-58-like genes were linked with ISAba1 and ISAba3 respectively. Isolates were clonally diverse. Integrons were variable in sequence but not associated with carbapenem resistance. Most commonly found genes in the 5′ and 3′conserved segment were aminoglycoside resistance genes (aadB, aadA2, aac4′), non-enzymatic chloramphenicol resistance gene (cmlA1g) and ADP-ribosylation genes (arr2, arr3). Outborn neonates had a significantly higher incidence of sepsis due to NDM-1 harboring isolates than their inborn counterparts. This study demonstrates the significance of both A. baumannii and other species of Acinetobacter in cases of neonatal sepsis over an extended period. Oxacillinases and blaNDM−1 are the major contributors to carbapenem resistance. The dissemination of the blaNDM−1 is likely linked to Tn125 in diverse clones of the isolates.
Highlights
Acinetobacter, a non-fermenting Gram-negative coccobacilli, has been noted as a pathogen in neonatal units in several parts of the globe and outbreaks caused by this organism have been reported (Huang et al, 2002; Chan et al, 2007; Hammerum et al, 2015)
Though most studies report the presence of this enzyme in A. baumannii, NDM-1 has been detected in other species such as A. lwoffii and A. pittii (Hu et al, 2012; Pasteran et al, 2014)
More than 75% isolates were resistant to extended spectrum cephalosporins (79% isolates were resistant to ceftazidime, 75% isolates were resistant to cefepime), 85% isolates were resistant to aztreonam, 50% were resistant to doripenem, 51% were resistant to both imipenem and meropenem
Summary
Acinetobacter, a non-fermenting Gram-negative coccobacilli, has been noted as a pathogen in neonatal units in several parts of the globe and outbreaks caused by this organism have been reported (Huang et al, 2002; Chan et al, 2007; Hammerum et al, 2015). Though A. baumannii has been predominantly implicated in neonatal infections or sepsis, “other species” within the genus have been reported to have caused sepsis in neonates (Beaufort et al, 1999; Kilic et al, 2008).The ability of the species to acquire antibiotic resistance has resulted in the acquisition of the potent carbapenem resistant gene, blaNDM−1 (Bonnin et al, 2012; Boulanger et al, 2012; Chuanfu et al, 2013) This enzyme, New Delhi Metallo-β–lactamase-1 (NDM1), is an addition to the wide array of antimicrobial resistance mechanisms that have been described for Acinetobacter spp. The use of molecular methods in this study to discriminate the different species of Acinetobacter gives an insight about the different species of Acinetobacter as a causative agent of neonatal sepsis
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