In recent years, reports of anaerobes resistance features showed an increasing tendency, but few were from China. In this study, 115 Bacteroides spp. clinical strains were isolated from a 3000-bed tertiary teaching hospital in China and showed a higher resistance rates to multiple commonly used antibiotics, including several β-lactams, metronidazole, et al. Especially, the resistance rates of Bacteroides spp. isolates to carbapenem and metronidazole was at a higher level, and the isolates were mainly B. fragilis. It is well known that the mechanism of carbapenem resistance within B. fragilis is mianly mediated by cfiA gene and the upstream IS element is required. In this study, the positive rate of cifA gene of carbapenem resistant B. fragilis reached up to 38.9%, which is obviously higher than other reports published recently [7, 17]. It is noteworthy that B. fragilis strains with cfiA gene can easily converted to be resistant ones by the effects of its upstream IS element , which implies that a larger group of patients maybe a potential reservoir of carbapenem resistant B. fragilis producers, who are colonized or infected by B. fragilis with silent cfiA gene. Since the B. fragilis isolates tested in this study were mainly from intra-abdominal samples, intestinal screening of cfiA positive B. fragilis within a specific group of people seems to be beneficial for better understanding the actual distribution of cfiA gene. So far, few reports showed that IS-less activation mechanism were found to be existed at B. fragilis isolates with elevated imipenem MICs or imipenem reisistant strains . In this study, two B. fragilis isolates and 1 non-B. fragilis isolate resistant to carbapenem were found to be cfiA positive and IS element was deficient. The potential non-IS resistance mechanism needs to be further investigated. Also, a longer IS element (3290 bp) was detected in a carbapenem resistant B. fragilis isolate, which was significantly different with other IS elements observed in this study. For this isolate , the MIC value of imipenem and meropenem were both higher than 32 μg/mL, which may possess a special regulating mechanism in mediating carbapenem resistance.
Besides carbapenem antibiotics, the resistance rates of B. fragilis isolates to several other β-lactam antibiotics were all higher than those of non-B.fragilis isolates, including ampicillin/sulbactam, amoxicillin/clavulanic acid, peperacillin and peperacillin/tazobactam. Consistent with resistance phenotype, the prevalence of cepA and cfxA genes among B. fragilis isolates were significantly higher than those of non-B. fragilis isolates. Veloo ACM et al  reported that cfiA and cepA genes together were responsible for amoxicillin resistance, but none of the B. fragilis isolates harboured the both genes in this study. However, resistance of amoxicillin was not detected and a total of 20 B. fragilis isolates harboured both cfiA and cepA in this study. It is noteworthy that 9 non-B. fragilis isolates harboured cepA, which was obviously different with those reported in some previous reports [5, 19, 20]. Kierzkowska M et al  reported that in B. fragilis, cefoxitin phenotypic resistance was strongly correlated with cfxA gene expression. However, only 2 B. fragilis isolates and 2 non-B. fragilis isolates were resistant to cefoxitin and none of the isolates harboured cfxA gene in this study. Owing to the limitation of the number of isolates, the correlation between cefoxitin resistance and expression of cfxA gene can’t be confirmed.
The resistance rate of B. fragilis to metronidazole in this study was 7.5%, which is obviously higher than previous reports [5, 6, 7, 9, 21, 22], and no metronidazole resistant non-B. fragilis isolate was detected. To date, the mechanism of metronidazole resistance is still not well-known, and it is reported that nim genes are closely correlated with metronidazole resistance . The positive rate of nim gene in this study was 38.9% and 11.4% for B. fragilis and non-B. fragilis isolates, respectively, but the correlation between metronidazole resistance and expression of nim gene was not observed. For 6 metronidazole resistant B. fragilis isolates, only 3 isolates were positive with nim gene.
In this study, total resistance rate of B. fragilis isolates to clindamycin reached up to 87.5%, significantly higher than that reported by Fernández-Canigia L et al  and Justesen US et al . It is well known that erm(A-F) are widely distributed in Bacteroides spp. strains and are responsible for macrolide-lincosamide-streptogramin B resistance in B. fragilis . In the present study, the positive rate of ermF gene (94.7%) was comparable with the phenotypic resistance rate (87.5%), which suggests that ermF gene may be mainly responsible for B. fragilis resistance in this study.
The resistance rate to moxifloxacin was 16.5% and is significantly lower than that observed in another recent study from China , but there is no obvious difference between B. fragilis isolates and non-B. fragilis isolates. It is reported that fluoroquinolone resistance may be correlated with multiple mechanism, including mutation of quinolone resistance determining region of the genes of gyrase and/or topoisomerase IV, as well as increased efflux [10, 26]. However, the related resistance genes were not detected and exploration of the resistance mechanism didn’t fall the scope of this study.
For tigecycline, the MIC50 and MIC90 for both B. fragilis and non-B. fragilis isolates in this study were all higher than those reported in a previous study . Since there is no available breakpoint for tigecycline, it is not feasible to assess its clinical significance until now. Also, the antibiotics susceptibility testing method used in this study was broth microdilution method, the results need to be further verified with agar dilution method in subsequent investigation.