Involvement of N-acetylneuraminate cytidylyltransferase in Edwardsiella piscicida pathogenicity

Tran, Nhung Thi; Vo, Linh Khanh; Komatsu, Masaharu; Shiozaki, Kazuhiro

doi:10.1016/j.fsi.2022.04.033

Cited by 2 publications

(2 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Edwardsiella tarda is a severe bacterial pathogen that habitat in water and infects a wide range of hosts from humans to fish. − This bacterium is notorious in aquaculture that causes disease in economic fish including tilapia, salmon, grouper, turbot, and Japanese flounder, , resulting in significant economic losses in a global aquaculture . Diseased fish show symptoms of septicemia and necrosis in different tissues of fish, known as edwardsiellosis. , E.…”

Section: Introductionmentioning

confidence: 99%

“…1−3 This bacterium is notorious in aquaculture that causes disease in economic fish including tilapia, salmon, grouper, turbot, and Japanese flounder, 3,4 resulting in significant economic losses in a global aquaculture. 5 Diseased fish show symptoms of septicemia and necrosis in different tissues of fish, known as edwardsiellosis. 6,7 E. tarda also causes food-borne and water-borne diseases in human beings.…”

Section: ■ Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Functional Proteomics Analysis of Norfloxacin-Resistant Edwardsiella tarda

Wu,

Li,

Tan

et al. 2023

J. Proteome Res.

View full text Add to dashboard Cite

Multidrug-resistant Edwardsiella tarda threatens both sustainable aquaculture and human health, but the control measure is still lacking. In this study, we adopted functional proteomics to investigate the molecular mechanism underlying norfloxacin (NOR) resistance in E. tarda. We found that E. tarda had a global proteomic shift upon acquisition of NOR resistance, featured with increased expression of siderophore biosynthesis and Fe3+-hydroxamate transport. Thus, either inhibition of siderophore biosynthesis with salicyl-AMS or treatment with another antibiotic, kitasamycin (Kit), which was uptake through Fe3+-hydroxamate transport, enhanced NOR killing of NOR-resistant E. tarda both in vivo and in vitro. Moreover, the combination of NOR, salicyl-AMS, and Kit had the highest efficacy in promoting the killing effects of NOR than any drug alone. Such synergistic effect not only confirmed in vitro and in vivo bacterial killing assays but also applicable to other clinic E. tarda isolates. Thus, our data suggest a proteomic-based approach to identify potential targets to enhance antibiotic killing and propose an alternative way to control infection of multidrug-resistant E. tarda.

show abstract