Abstract
BackgroundSurgical-site infection is the most frequent health care-associated infection in the developing world, with a strikingly higher prevalence than in developed countries We studied the prevalence of resistance to antibiotics in Enterobacteriaceae isolates from surgical-site infections collected in three major tertiary care centres in Bangui, Central African Republic. We also studied the genetic basis for antibiotic resistance and the genetic background of third-generation cephalosporin-resistant (3GC-R) Enterobacteriaceae.ResultsBetween April 2011 and April 2012, 195 patients with nosocomial surgical-site infections were consecutively recruited into the study at five surgical departments in three major tertiary care centres. Of the 165 bacterial isolates collected, most were Enterobacteriaceae (102/165, 61.8%). Of these, 65/102 (63.7%) were 3GC-R, which were characterized for resistance gene determinants and genetic background. The blaCTX-M-15 and aac(6′)-Ib-cr genes were detected in all strains, usually associated with qnr genes (98.5%). Escherichia coli, the most commonly recovered species (33/65, 50.8%), occurred in six different sequence types, including the pandemic B2-O25b-ST131 group (12/33, 36.4%). Resistance transfer was studied in one representative strain of the resistance gene content in each repetitive extragenic palindromic and enterobacterial repetitive intergenic consensus sequence-PCR banding pattern. Plasmids were characterized by PCR-based replicon typing and sub-typing schemes. In most isolates (18/27, 66.7%), blaCTX-M-15 genes were found in incompatibility groups F/F31:A4:B1 and F/F36:A4:B1 conjugative plasmids. Horizontal transfer of both plasmids is probably an important mechanism for the spread of blaCTX-M-15 among Enterobacteriaceae species and hospitals. The presence of sets of antibiotic resistance genes in these two plasmids indicates their capacity for gene rearrangement and their evolution into new variants.ConclusionsDiverse modes are involved in transmission of resistance, plasmid dissemination probably playing a major role.
Highlights
Surgical-site infection is the most frequent health care-associated infection in the developing world, with a strikingly higher prevalence than in developed countries We studied the prevalence of resistance to antibiotics in Enterobacteriaceae isolates from surgical-site infections collected in three major tertiary care centres in Bangui, Central African Republic
Rapid international spread of CTX-M-15 has been associated with global dissemination of Escherichia coli clones, such as sequence type 131 (ST131) harbouring blaCTX-M-15 on incompatibility group (Inc) FII conjugative plasmids [2]
We studied the prevalence of resistance to antibiotics in Enterobacteriaceae isolates from surgical-site infections collected in three major tertiary care centres in Bangui, Central African Republic; we studied the genetic basis for antibiotic resistance and the genetic background of Third-generation cephalosporin-resistant (3GC-R) Enterobacteriaceae
Summary
Surgical-site infection is the most frequent health care-associated infection in the developing world, with a strikingly higher prevalence than in developed countries We studied the prevalence of resistance to antibiotics in Enterobacteriaceae isolates from surgical-site infections collected in three major tertiary care centres in Bangui, Central African Republic. The resistance is mediated mainly by acquired extended-spectrum beta-lactamase (ESBL) genes carried by mobile genetic elements such as plasmids and transposons This situation is of great concern, as ESBL enzymes can hydrolyse almost all beta-lactams (except carbapenems and cephamycins) and are frequently associated with genes that confer resistance to several other classes of antibiotic. Plasmid-mediated quinolone resistance has emerged in Enterobacteriaceae, with three mechanisms described: Qnr, which mediates target protection; AAC(6′)-Ib-cr, which mediates drug modification; and OqxAB and QepA, which mediate drug efflux [3] These mechanisms increase the minimum inhibitory concentration (MIC) of fluoroquinolones, thereby facilitating the selection of mutants with greater resistance in the presence of quinolones through sequential chromosomal mutations in genes coding for the target enzymes, DNA gyrase and DNA topoisomerase IV [3]
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