Responses of microbial community and antibiotic resistance genes to co-existence of chloramphenicol and salinity

In recent years, the risk from environmental pollution caused by chloramphenicol (CAP) has emerged as a serious concern worldwide, especially for the co-selection of antibiotic resistance microorganisms simultaneously exposed to CAP and salts. In this study, the multistage contact oxidation reactor (MCOR) was employed for the first time to treat the CAP wastewater under the co-existence of CAP (10-80 mg/L) and salinity (0-30 g/L NaCl). The CAP removal efficiency reached 91.7% under the co-existence of 30 mg/L CAP and 10 g/L NaCl in the influent, but it fluctuated around 60% with the increase of CAP concentration and salinity. Trichococcus and Lactococcus were the major contributors to the CAP and salinity shock loads. Furthermore, the elevated CAP and salinity selection pressures inhibited the spread of CAP efflux pump genes, including cmlA, tetC, and floR, and significantly affected the composition and abundance of antibiotic resistance genes (ARGs). As the potential hosts of CAP resistance genes, Acinetobacter, Enterococcus, and unclassified_d_Bacteria developed resistance against high osmotic pressure and antibiotic environment using the efflux pump mechanism. The results also revealed that shifting of potential host bacteria significantly contributed to the change in ARGs. Overall, the co-existence of CAP and salinity promoted the enrichment of core genera Trichococcus and Lactococcus; however, they inhibited the proliferation of ARGs.

Automated summary

The risk from environmental pollution caused by chloramphenicol (CAP) has become a serious global concern, especially for antibiotic resistance microorganisms co-exposed to CAP and salts. This study used a multistage contact oxidation reactor (MCOR) to treat CAP wastewater under the co-existence of CAP and salinity. The results showed that the co-existence of CAP and salinity promoted the enrichment of core genera Trichococcus and Lactococcus, but also inhibited the proliferation of antibiotic resistance genes (ARGs).