Mechanism of enrofloxacin-induced multidrug resistance in the pathogenic Vibrio harveyi from diseased abalones

Vibrio harveyi infection had caused severe economic losses in aquaculture. A pathogenic V. harveyi strain had been successfully induced to be a multiple-resistant strain by enrofloxacin (EFX), then the mechanism of multidrug resistance was analyzed. It suggested that the minimum inhibitory concentration of EFX increased by 32-folds. Results of the Kirby-Bauer test showed that the inhibitory zone diameter was 25.3 mm for the sensitive strain (labeled as HL-S) and 8.5 mm for the resistant strain (labeled as HL-R). After 20 serial passages, even when the stress of EFX was removed, the resistance persisted. After induction of EFX, HL-R resisted to other fluoroquinolones, it even resisted to furazolidone and streptomycin, although it was sensitive to these antibiotics initially. Its sensitivity to rifampicin and doxycycline also decreased obviously. Results showed that 3522 differentially expressed genes were identified. Expression of the multidrugs efflux resistance-nodulation-cell division was significantly upregulated (164.61-folds) in HL-R. Other key genes connected with drug efflux were also upregulated significantly (p<0.05). Notably, recA encoded for recombination protein was upregulated significantly, lexA was downregulated significantly in HL-R. Research results showed that the efflux system and the save our souls system have played crucial roles during the development of multidrug resistance of V. harveyi.