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Abstract Multidrug-resistant (MDR) Acinetobacter baumannii (A. baumannii) is currently recognized not only as a significant nosocomial pathogen but also is an emerging bacterial infection in food-producing animals, posing a critical threat to global health. However, this is a hindrance to detailed bioinformatic studies of MDR A. baumannii of chicken origin due to the lack of its complete genome sequence. Here, we report whole-genome sequencing analysis of MDR A. baumannii Y03 isolated from chickens. The Y03 genome consists of 1 circular chromosome and 4 circular plasmids, The Y03 chromosome harbors 41 antimicrobial resistance genes conferring resistance to major classes of antibiotics, including β-lactams, phenicols, macrolides, lincosamides, aminoglycosides, and nitrofurans, as well as 135 virulence factors involved in effector delivery system, immune modulation, adherence, stress survival, biofilm, exotoxin, and nutritional/metabolic factor. The in vivo infection experiments certificated that Y03 was virulent to chickens. Meanwhile, we used PCR amplification method to detect 10 antimicrobial resistance genes including abeM, adeB, adeH, adeK, bla apmC , bla OXA−90 , catB9, macB, folP, and parE, as well as 14 virulence genes including lpxC, pilO, fimT, ompA, basA, bauA, gspL, csu, pgaC, plc2, tssA, tviB, bap, and vgrG. Whole-genome sequencing analysis revealed that Y03 contained 46 horizontal gene transfer elements, including 11 genomic islands, 30 transposons, and 5 prophages, as well as 518 mutations associated with reduced virulence and 44 mutations resulting in loss of pathogenicity. Furthermore, there were 22 antibiotic targets and 28 lethal mutations on the Y03 chromosome that could be used as potential targets to prevent, control, and treat infections caused by MDR A. baumannii Y03. Therefore, this study contributes to the development of strategies for the prevention, control, and treatment of A. baumannii infections and their spread in chickens.

Abstract Avian pathogenic Escherichia coli (APEC) is a significant pathogen infecting poultry that is responsible for high mortality, morbidity and severe economic losses to the poultry industry globally, posing a substantial risk to the health of poultry. APEC encounters reactive oxygen species (ROS) during the infection process and thus has evolved antioxidant defense mechanisms to protect against oxidative damage. The imbalance of ROS production and antioxidant defenses is known as oxidative stress, which results in oxidative damage to proteins, lipids and DNA, and even bacterial cell death. APEC uses transcription factors (TFs) to handle oxidative stress. While many TFs in E. coli have been well characterized, the mechanism of the YbdO TF on protecting against oxidative damage and regulating the virulence and pathogenicity of APEC has not been clarified. Here we focus on the regulatory mechanism of YbdO on the pathogenicity of APEC. The results from this study showed that YbdO attenuated the pathogenicity of APEC in chicks infection models by inhibiting the expression of virulence genes fepG and ycgV using quantitative real-time reverse transcription PCR (RT-qPCR) experiments. The electrophoretic mobility shift assays (EMSA) confirmed that YbdO specifically bound to the promoters of fepG and ycgV. Additionally, YbdO increases H2O2-induced oxidative damage to APEC via repressing the expression of oxidative stress response genes sodA, soxR, ahpC, ahpF, katG, and oxyR by binding to their promoter regions. The repression effect facilitates host immune response to eliminate APEC and to generate beneficial immune protection to the body, thereby indirectly attenuating the pathogenicity of APEC. These findings might provide further insights into the mechanism of oxidative damage to APEC and offer new perspectives for further studies on the prevention and control of APEC infections.