The current study was undertaken to screen the ESBL and fluoroquinolone resistance genes among E. coli and Salmonella isolated in diarrheal children in two rural communities of Burkina Faso. Consistent with global reports, an alarming increase in resistance to beta-lactam antibiotics (even to the extended-spectrum subclass) among clinical E. coli isolates is highlighted by the results of this study. Indeed, the proportion of resistant strains was 60% for E. coli and 50% for Salmonella. These findings were consistent with previous studies in developing countries which showed a resistant rate greater than 50% [31]. This high resistance is likely due to the extensive and excessive clinical use of antibiotics.
Our study showed that all the E. coli isolates (5/5) were ESBL producers in agreement with 95.60% reported in Togo [32]. The presence of ESBL-producing bacteria in hospitals is a major challenge that affects both developed and developing countries [22]. It is known that β-Lactams (mainly extended- past spectrum cephalosporins and carbapenems) and fluoroquinolones constitute the main therapeutic choices to treat infections caused by Enterobacteriaceae. Our findings revealed a strong resistance to beta-lactams and moderate rates of resistance to quinolones in E. coli and Salmonella isolated. Indeed, Cross-resistance phenotypes to quinolones (CRQ), Cross-resistance phenotypes to fluoroquinolones (CRFQ) and carbapenemase phenotypes were associated with different rates to our Salmonella and E. coli strains. In agreement with our results, resistance to these compounds has been reported increasingly in several countries [33–35]. According to the existing data, this study is the first of kind on rural samples of Burkina Faso. However, it has been shown that fecal carriage of ESBL-PE isolates is one of the main drivers for their dissemination in hospital and community settings worldwide [36]. Because of this mode of diffusion, the ESBLs constitute a significant threat for the countries of West Africa where `the weak socio-economic conditions result in poor hygienic conditions, promoting the spread of resistance.
The present study showed that the blaOXA genes were the most common ß-lactamase-producing genes (57.14%), followed by blaCTX−M (7.14%). These findings contrast with those previously reported in Burkina Faso [4, 22]. Otherwise, a spread of blaCTX−M, particularly CTX-M-15 in community and hospital settings has been reported [23, 36, 37]. This difference could be explained by the weakness of the number of multiresistant strains of enterobacteria tested in our study. On the other hand, we noted the simultaneous presence of the blaCTX−M and blaOXA genes in the same strain of E. coli. Our finding confirms the frequent association between blaCTX−M−15 and blaOXA−1 genes in ESBL-PE isolates which has been reported [36, 38–40]. This coexistence could reduces the therapeutic options for treatment with β-lactam antibiotics. Thus, combined production of CTX-M and OXA enzymes by E. coli and K. pneumoniae improved resistance to b-lactamase inhibitors, presumably explaining their non-susceptibility to amoxicillin/clavulanate [36, 40, 41]. The genes blaTEM and blaSHV were not identified in the present study. In contrast, these genes have been previously reported in three major hospitals of Ouagadougou [22]. A future study based on more multiresistant strains producing ESBL would shed more light on the existence and prevalence of these genes among rural dwellings.
We also reported the prevalence of plasmid-mediated quinolone resistance in Salmonella and E. coli. Only a single isolate of E. coli (20%) was positive for the qnrB gene which is lower than 67.21% reported in Togo [32] and higher than 3.17% reported in Niger [42]. No Salmonella strain was positive for the qnr genes in the present study. In France, a study revealed 0.2% of qnrA in single isolate of Salmonella [43]. These results may indicate a low dissemination rate of qnr genes among human Salmonella and E. coli isolates. Morever, the E. coli strain that harbored qnrB gene was also positive to ESBL and carbapenemase phenotypes. Indeed, qnr are genes that confer resistance to nalidixic acid and reduced susceptibility to fluoroquinolones [44] and there is frequent association of genes coding for expanded-spectrum b-lactamases (ESBLs) and these genes [43].
Further studies consisting of larger sample size than the number of multidrug-resistant isolates considered in the present study would be necessary. Despite this, the results of this study alert us to i) the emergence and spread of antibiotic resistance in young children, ii) the existence of bla and qnr genes in rural areas of Burkina Faso. In addition, the absence of these genes in certain investigated strains maybe due to other mechanisms of resistance to beta-lactams and quinolones.