It is therefore possible that other resistance mechanisms, such as ParE polymorphisms, other horizontally acquired resistance genes (such as oqxAB and aac(6 ‘ )-Ib for example), over-active efflux, or even novel mechanisms are present in some of the isolates. Resistance patterns in pathogens often mirror those in commensals. This is borne out by our recent documentation of quinolone resistance in Vibrio cholerae isolates recovered in the same time frame as the E. coli strains presented in this report

[21]. Fifteen of the 40 QREC isolates identified in this study belonged to ST10, Wortmannin or were single- or double-locus variants of this ST, pointing to the possibility of clonal expansion.

ST10-selleck inhibitor complex strains were isolated in all three years and therefore over-representation of these STs in our sample cannot be explained PD-1/PD-L1 Inhibitor 3 research buy by short-term, localized clustering. There are four major E. coli phylogenetic clades: ECOR A, B1, B2 and D. Few studies have looked at the geographical variance in the distribution of these groups but overall, QREC from Ghana were predominantly drawn from ECOR group A. Of the STs identified in this study that are classified into ECOR clades at the E. coli MLST database, ST10 complex (14 isolates) belong to ECOR group A, ST131 (1 isolate) to ECOR B2, STs101 and 410 (3 isolates) to ECOR B1 and STs 156, 206 and 210 (4 isolates) are hybrids of ECOR A and B1, that is AxB1. Available Methane monooxygenase data appear to suggest that ECOR A strains are highly prevalent in Africa, compared to some other world regions [22]. However, when we compared the sequence types of quinolone-resistant and -susceptible strains from Ghana only, we still found that resistant strains were over-represented in the ST10 complex. Pandemic clonal expansion of some QREC lineages has been reported in the literature [23–28]. For example, ST131 is a globally disseminated multi-resistant clone and was detected once among the QREC in this study. Recent reports suggest

that isolates from Europe and North America that belong to ST10- or ST131- clonal complexes may be less likely to carry virulence factors for invasive disease, but more likely to be fluoroquinolone resistant [24–28]. However it is equally likely that mutations to fluoroquinolone resistance are more likely to be stably inherited in a specific genetic background. Our own data also appear to suggest that, although horizontally acquired, qnrS1 is associated with ST10 complex. A recent paper by Davidson et al suggests that the antimalarial chloroquine may select for fluoroquinolone-resistant fecal bacteria in malaria endemic areas and proposes that chloroquine-mediated selection accounts for high levels of QREC in fecal flora in villages in South America [29].