Urocanic acid, deaminated histidine and the first intermediate in the histidine utilization (Hut) pathway in bacteria, has recently been suggested to have adverse health effects by inducing scombrotoxicosis and immunosuppression after trans – cis isomerization. This work aimed to shed some light on the microbiology of its formation in scombroid fish, given that such information is very scarce. The isolation of urocanic acid producers from chub mackerel was basically based on enrichment of bacteria possessing the Hut pathway with histidine as the sole source of carbon, energy, and nitrogen. Morphological and molecular identification revealed that the isolates ( n = 12), taken from the skin, gills, and intestine, were comprised entirely of Acinetobacter from at least five species. This implies that the Hut pathway in the microbes can be particularly active and as such conferred a growth advantage. Dynamic monitoring of bacterial growth and urocanic acid production in fish juice broth indicated that urocanic acid is a primary metabolite and its production is a closely growth-associated process. This in turn implies that its production can be controlled directly by suppressing the bacterial growth. Several potential methods are proposed through a study of the growth characteristics and preservative susceptibility of representative isolates. In conclusion, this work suggests that Acinetobacter can constitute a potentially important group of urocanic acid producers in chub mackerel.
Hu Ruixue,Du Na,Chen Nan,Lin Li,Zhai Yanhua,Gu Zemao
The mechanisms of resistance to levofloxacin for Aeromonas hydrophila isolated from diseased fish and selected in vitro were examined in this study. Levofloxacin-resistant mutants were obtained by selection of A. hydrophila in vitro. The quinolone resistance-determining regions (QRDRs) of the gyrA and parC genes were sequenced in Lev R strains and reverse mutation strains. All Lev R strains carried a point mutation at codon 83 (Ser → Ile), and one strain (25 %) harbored a mutation at position 92 (Leu → Met) in the GyrA-QRDR. After being transferred in a levofloxacin-free medium, one strain of the mutants was successfully reversed and the reversion was related with mutations o f GyrA-QRDR at positions 81 (Gly → Asp) and 83 (Ile → Ser). No amino acid alteration was found in the ParC-QRDR. In addition, the minimum inhibitory concentration (MIC) of levofloxacin for the mutants was lower in the presence of reserpine, and all mutants were also resistant to some of the other quinolones. It was found that the mechanism of levofloxacin resistance of A. hydrophila selected in vitro was related to gyrA of type II topoisomerase, and an efflux mechanism was involved in the resistance as well.
危险品化学品经营许可证（带存储）