Clonal spread and accumulation of β-lactam resistance determinants in Enterobacter aerogenes and Enterobacter cloacae complex isolates from infection and colonization in patients at a public hospital in Recife, Pernambuco, Brazil

Abstract

Enterobacter aerogenes and Enterobacter cloacae complex are the two species of this genus most involved in healthcare-associated infections that are ESBL and carbapenemase producers. This study characterized, phenotypically and genotypically, 51 isolates of E. aerogenes and E. cloacae complex originating from infection or colonization in patients admitted to a public hospital in Recife, Pernambuco, Brazil, by antimicrobial susceptibility profile, analysis of β-lactamase genes (blaTEM, blaSHV, blaCTX-M, blaKPC, blaVIM, blaIMP and blaSPM), PCR and DNA sequencing, plasmid profile and ERIC-PCR. In both species, the genes blaTEM, blaCTX-M and blaKPC were detected. The DNA sequencing confirmed the variants blaTEM-1, blaCTX-M-15 and blaKPC-2 in isolates. More than one gene conferring resistance in the isolates, including the detection of the three previously cited genes in strains isolated from infection sites, was observed. The detection of blaCTX-M was more frequent in isolates from infection sites than from colonization. The gene blaKPC predominated in E. cloacae complex isolates obtained from infections; however, in E. aerogenes isolates, it predominated in samples obtained from colonization. A clonal relationship among all of E. aerogenes isolates was detected by ERIC-PCR. The majority of E. cloacae complex isolates presented the same ERIC-PCR pattern. Despite the clonal relation presented by the isolates using ERIC-PCR, different plasmid and resistance profiles and several resistance genes were observed. The clonal dissemination and the accumulation of β-lactam resistance determinants presented by the isolates demonstrated the ability of E. aerogenes and E. cloacae complex, obtained from colonization and infection, to acquire and maintain different resistance genes.

Detection of virulence and β-lactamase encoding genes in Enterobacter aerogenes and Enterobacter cloacae clinical isolates from Brazil

“…The resistance profile found in the studied isolates corroborate with a study conducted by Cabral et al, 4 which analyzed a Brazilian collection of E. aerogenes and E. cloacae complex isolates, and found the lowest resistance rates in amikacin, gentamicin and tobramycin. However, they found low levels of resistance to trimethoprim–sulfamethoxazole while we found 71.4% resistance for this antibiotic.…”

“… 2 , 3 Among the species, E. aerogenes and E. cloacae stand out as opportunistic pathogens, especially in patients on mechanical ventilation. 4 …”

Emergence of aph(3’)-VI and accumulation of aminoglycoside modifying enzyme genes in KPC-2-possessing Enterobacter aerogenes isolates from infections and colonization in patients from Recife-PE, Brazil

“…The isolates were identified biochemically using the Bactec 9120 or Phoenix™ automated systems (BD). The presence of bla KPC-2 in these isolates was previously reported 6 . The minimum inhibitory concentration for antimicrobials was determined using the Phoenix™ system, according to CLSI criteria 11 .…”

“…One of the major causes of carbapenem-resistance in Enterobacteriaceae is the production of Klebsiella pneumoniae carbapenemase (KPC). This enzyme has been frequently reported in E. aerogenes 5,6 . KPC-producing bacteria are often resistant to other antimicrobials, such as aminoglycosides, which may be due to the presence of the bla KPC gene, genes encoding aminoglycoside modifying enzymes (AMEs), and 16S rRNA methyltransferase genes in the same plasmid 7,8 .…”

Emergence of bla NDM-1 associated with the aac(6’)-Ib-cr, acrB, cps, and mrkD genes in a clinical isolate of multi-drug resistant Klebsiella pneumoniae from Recife-PE, Brazil

“…Scavuzzi AML et al -blaNDM-1 in Klebsiella pneumoniae from Recife bla IMP and bla NDM ), those encoding resistance to aminoglycoside (aac(3')-Ia; aac(3')IIa, and aac(6')-Ib), the efflux pump gene (acrB), and the virulence genes (cps, mrkD and irp2) were investigated using the (polymerase chain reaction (PCR) technique. A description of the primers and amplification conditions utilized are presented in Table 1 [6][7][8][9][10][11][12] . Negative and positive controls were included in each PCR.…”