The spread of antibiotic resistance in bacterial agents causing life-threatening sepsis is a serious immediate global threat.1 Timely antibiotic therapy is critical, with delays in effective therapy being directly associated with increased mortality,2 and preservation of antibiotic susceptibility by controlling inappropriate antibiotic use (“antibiotic stewardship”) has thus become a primary public health agenda.3 Different antibiotics are known to have different effects on the composition of the gut microbiome4, 5 and a better understanding of these effects is needed to guide stewardship decisions, due to possible implications for both the transmission of antibiotic resistance determinants and the establishment of resistant populations.
E. coli are a major cause of life-threatening sepsis, and transmissible antibiotic resistance in this species is increasing.6 In this study, we compared E. coli populations in 12 ICU patients before and after cefepime (FEP) therapy, by sequencing representative pools of perineal E. coli clones from each patient. Extracted DNA was sequenced using paired-end Illumina MiSeq technology. Assembled reads were run against the NCBI database using BLAST7 and we used our automated Attacca system8 to correctly annotate genetic features linked to transmissible antibiotic resistance (resistance, plasmid replicase (rep) and relaxase (mob) genes). In the 'after' FEP sample, the frequency of specific genes with strong links to multiple resistance clusters (e.g. strAB, sul2) was increased, and other genes (e.g. blaCMY-2) and markers of relevant transmission vehicles (e.g. IncI1rep) were detected exclusively in this sample. This increase in transmissible resistance genes is consistent with observed increases in resistance to selected antibiotics after cefepime treatment.9 An explanation for this might be provided by accelerated horizontal gene transfer in proteobacterial blooms,10,11 which are more common and persistent after exposure to drugs like cefepime.11,12