Vibrio mimicus

Therapeutic Uses of Phycocolloids

Published in Leonel Pereira, Therapeutic and Nutritional Uses of Algae, 2018

Leonel Pereira

The anti-microbial activities of numerous algal species have been tested and reported, presenting an extended spectrum of action against bacteria and fungi (Pereira et al. 2017). Carrageenans have proved to have effects against some bacterial strains such as Salmonella enteritidis, S. typhimurium, Vibrio mimicus, Aeromonas hydrophila, Escherichia coli, Listeria monocytogenes, and Staphylococcus aureus. The growth of all the bacterial strains except L. monocytogenes was significantly inhibited by them, particularly by the ι-carrageenan. A growth inhibition experiment using S. enteritidis showed that the inhibitory effect of the carrageenans was not bactericidal but bacteriostatic. Removal of the sulfate residues eliminated the bacteriostatic effect of ι-carrageenan, suggesting that the sulfate residues in carrageenan play an essential role in this effect (Venugopal 2008). In 2014, Sebaaly et al. reported that carrageenans isolated from the red alga Corallina sp. exhibited anti-bacterial activity against Staphylococcus epidermis. Infra-red spectroscopy (IR) showed that the isolated carrageenan was of λ-type.

Published in Ronald M. Atlas, James W. Snyder, Handbook Of Media for Clinical Microbiology, 2006

Ronald M. Atlas, James W. Snyder

Use: For the isolation of pathogenic vibrios, especially Vibrio cholerae. This medium is suitable for the growth of Vibrio cholerae, Vibrio parahaemolyticus, and most other Vibrios. Most of the Enterobacteriaceae encountered in faeces are totally suppressed for at least 24 hours. Slight growth of Proteus species and Enterococcus faecalis may occur but the colonies are easily distinguished from vibrio colonies. Whilst inhibiting non-vibrios, it promotes rapid growth of pathogenic vibrios after overnight incubation at 35°C. Vibrio cholerae El Tor biotype forms yellow colonies, Vibrio parahaemolyticus forms blue-green colonies, Vibrio alginolyticus forms yellow colonies, Vibrio metschnikovii forms yellow colonies, Vibrio fluvialis forms yellow colonies, Vibrio vulnificus forms blue-green colonies, Vibrio mimicus forms blue-green colonies, Enterococcus species form yellow colonies, Proteus species form yellow-green colonies, Pseudomonas species form blue-green colonies and some strains of Aeromonas hydro-phila produce yellow colonies, but Plesimonas shigelloides does not usually grow well on this medium.

Aeromonas

Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018

Chi-Jung Wu, Maria José Figueras, Po-Lin Chen, Wen-Chien Ko

First described by Stainer in 1943, the genus Aeromonas (that is, gas-forming units) belongs to the class Gammaproteobacteria, order Aeromonadales, and family Aeromonadaceae.1,3,4 Members of the Aeromonas genus are oxidase- and catalase-positive gram-negative bacilli, with the ability to produce acid with gas from many carbohydrates including D-glucose, reduce nitrate to nitrite, and resist a vibriostatic agent (2,4 diamino-6,7-diisopropylpteridine; O/129, 150 μg/disk). However, sensitivity to O/129 has been described for Aeromonas cavernicola and Aeromonas australiensis, and a new species Aeromonas aquatilis.3,5–7 Almost all species, except Aeromonas trota, are resistant to ampicillin.1,8 The optimum growth temperature varies between 22°C and 37°C, but ranges from 0°C to 45°C.4 Most Aeromonas species are mesophilic (optimal growth at 35°C–37°C), motile, and nonpigmented, although Aeromonas salmonicida, mainly implicated in fish diseases, also includes nonmotile pigmented psychrophilic strains (optimum growth at 22°C–25°C). Motility is due to the presence of a single polar flagellum, but lateral flagella may be present in some species.3,4 The dual flagella system is noted in 60% of mesophilic Aeromonas spp., enabling the polar flagellar motility in liquid environments or lateral flagellar movement across solid surfaces or viscous environments.3 A comprehensive study on phenotypic characterization of Aeromonas spp. has been reported by Abbott et al.8 However, conventional and automatic phenotypic identification methods can produce misidentification of the species, and often erroneously identify most strains as Aeromonas hydrophila.9–14Aeromonas species may be confounded by the closely related genus Vibrio, which can grow in 6%, but not 0%, NaCl, except Vibrio cholerae and Vibrio mimicus.1 To clarify this confusion, a genus probe targeting the lipase glycerophospholipid-cholesterol acyltransferase gene (gcat), recently has been adapted for direct detection of Aeromonas in water.15

Pyrrole-2-carboxylic acid inhibits biofilm formation and suppresses the virulence of Listeria monocytogenes

Published in Biofouling, 2023

Yuxi Yue, Kai Zhong, Yanping Wu, Hong Gao

Furthermore, a flow-cytometric assay with PI staining revealed that PCA induced membrane damage in L. monocytogenes biofilm cells and thus decreased their vitality. As a viability-fluorescent marker, PI only penetrates impaired cells and intercalates with nucleic acid (Handorf et al. 2021). As depicted in Figure 2B, PCA treatment caused a shift in fluorescence spectrum with intensity increments in a dose-dependent manner, indicating that PCA caused membrane damage and prevented biofilm formation. In particular, PCA at concentrations of 0.188–0.750 mg ml−1 led to cell membrane damage in a range of 17.1–28.4%. However, in the absence of PCA, only 7.61% of the untreated control group showed a PI fluorescence signal. Similar findings were reported for EGCG that specifically triggered PI influx and disturbed the Vibrio mimicus biofilm (Li, Lu, et al. 2020). Taken together, these observations suggest that PCA may impact the membrane function of L. monocytogenes biofilm cells.

Type VI secretion system-associated FHA domain protein TagH regulates the hemolytic activity and virulence of Vibrio cholerae

Published in Gut Microbes, 2022

Guangli Wang, Chan Fan, Hui Wang, Chengyi Jia, Xiaoting Li, Jianru Yang, Tao Zhang, Song Gao, Xun Min, Jian Huang

A review of previously published data showed that HlyA is strictly controlled by multiple regulatory factors at the transcriptional and post-translational levels.40,42,43 At the transcriptional level, our results showed that the deletion of tagH significantly upregulated the transcription and promoter activity of hlyA and hlyU and downregulated fur transcription (Figure 3). The binding site of HlyU in the promoter region of hlyA is located at −563···−627, while the binding site of Fur in the promoter region of hlyA is located at −545··· −59642, indicating that two binding sites partially overlap. Therefore, we speculate that the transcriptional regulation of hlyA by TagH may depend on the subtle coordination of HlyU and Fur, which is consistent with a previous report.42 Furthermore, a previous study found that HlyA was highly expressed in the early stages of logarithmic growth,42 and our research mainly focused on this stage. At the post-translational level, several proteases have been shown to be involved in the activation and degradation of HlyA in V. cholerae.40Vibrio mimicus has also been shown to display a very similar phenomenon, in which endogenous metalloproteases cleave and activate hemolysin at an early stage but inactivate hemolysin after further incubation.53 PrtV of V. cholerae is a Zn2+-binding extracellular protease belonging to the M6 metalloprotease family.54,55 HlyA is a substrate of the PrtV protease, and PrtV is the main contributing factor to HlyA inactivation.56 Our data showed that the tagH knockout significantly inhibited the transcription of the prtV gene (Figure 4a), and the ΔtagHΔprtV mutant only slightly increased HlyA expression when compared to the ΔtagH mutant (Figure 4d). We speculate that the tagH knockout inhibits prtV transcription at a very low level (approximately 16% of the wild level), resulting in no further impact on HlyA expression when prtV is knocked out in the context of the ΔtagH mutants.