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Spontaneous quinolone resistance in the zoonotic serovar of Vibrio vulnificus.

ABSTRACT: This work demonstrates that Vibrio vulnificus biotype 2, serovar E, an eel pathogen able to infect humans, can become resistant to quinolone by specific mutations in gyrA (substitution of isoleucine for serine at position 83) and to some fluoroquinolones by additional mutations in parC (substitution of lysine for serine at position 85). Thus, to avoid the selection of resistant strains that are potentially pathogenic for humans, antibiotics other than quinolones must be used to treat vibriosis on farms.

SUBMITTER: Roig FJ

PROVIDER: S-EPMC2675197 | biostudies-literature | 2009 Apr

REPOSITORIES: biostudies-literature

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Spontaneous quinolone resistance in the zoonotic serovar of Vibrio vulnificus.

Roig Francisco J FJ Llorens A A Fouz B B Amaro C C

Applied and environmental microbiology 20090213 8

This work demonstrates that Vibrio vulnificus biotype 2, serovar E, an eel pathogen able to infect humans, can become resistant to quinolone by specific mutations in gyrA (substitution of isoleucine for serine at position 83) and to some fluoroquinolones by additional mutations in parC (substitution of lysine for serine at position 85). Thus, to avoid the selection of resistant strains that are potentially pathogenic for humans, antibiotics other than quinolones must be used to treat vibriosis o ...[more]

PMID: 19218407

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Host-nonspecific iron acquisition systems and virulence in the zoonotic serovar of Vibrio vulnificus.

Project description:The zoonotic serovar of Vibrio vulnificus (known as biotype 2 serovar E) is the etiological agent of human and fish vibriosis. The aim of the present work was to discover the role of the vulnibactin- and hemin-dependent iron acquisition systems in the pathogenicity of this zoonotic serovar under the hypothesis that both are host-nonspecific virulence factors. To this end, we selected three genes for three outer membrane receptors (vuuA, a receptor for ferric vulnibactin, and hupA and hutR, two hemin receptors), obtained single and multiple mutants as well as complemented strains, and tested them in a series of in vitro and in vivo assays, using eels and mice as animal models. The overall results confirm that hupA and vuuA, but not hutR, are host-nonspecific virulence genes and suggest that a third undescribed host-specific plasmid-encoded system could also be used by the zoonotic serovar in fish. hupA and vuuA were expressed in the internal organs of the animals in the first 24 h of infection, suggesting that they may be needed to achieve the population size required to trigger fatal septicemia. vuuA and hupA were sequenced in strains representative of the genetic diversity of this species, and their phylogenies were reconstructed by multilocus sequence analysis of selected housekeeping and virulence genes as a reference. Given the overall results, we suggest that both genes might form part of the core genes essential not only for disease development but also for the survival of this species in its natural reservoir, the aquatic environment.

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Analyzing Possible Native Functions of the Quinolone Resistance Gene qnr in Vibrio vulnificus.

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Project description:Ciprofloxacin was introduced for treatment of patients with cholera in Bangladesh because of resistance to other agents, but its utility has been compromised by the decreasing ciprofloxacin susceptibility of Vibrio cholerae over time. We correlated levels of susceptibility and temporal patterns with the occurrence of mutation in gyrA, which encodes a subunit of DNA gyrase, followed by mutation in parC, which encodes a subunit of DNA topoisomerase IV. We found that ciprofloxacin activity was more recently further compromised in strains containing qnrVC3, which encodes a pentapeptide repeat protein of the Qnr subfamily, members of which protect topoisomerases from quinolone action. We show that qnrVC3 confers transferable low-level quinolone resistance and is present within a member of the SXT integrating conjugative element family found commonly on the chromosomes of multidrug-resistant strains of V. cholerae and on the chromosomes of Escherichia coli transconjugants constructed in the laboratory. Thus, progressive increases in quinolone resistance in V. cholerae are linked to cumulative mutations in quinolone targets and most recently to a qnr gene on a mobile multidrug resistance element, resulting in further challenges for the antimicrobial therapy of cholera.

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Method for Specific Identification of the Emerging Zoonotic Pathogen Vibrio vulnificus Lineage 3 (Formerly Biotype 3).

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A transcriptomic study reveals that fish vibriosis due to the zoonotic pathogen Vibrio vulnificus is an acute inflammatory disease.

Project description:Vibrio vulnificus is a marine zoonotic pathogen associated with fish farms that is considered a biomarker of climate change. Zoonotic strains trigger a rapid death of their susceptible hosts (fish or humans) by septicemia that has been linked to a cytokine storm in mice. A toxin called RtxA1 produced by the bacteria might play an important role in bacterial invasion and subsequent death by septic shock since animals infected with a mutant deficient in rtxA1 suffer from septicemia but do not die. The aim of this study was to globally analyze the early eel immune response in blood against V. vulnificus, as well as the role of the RtxA1 toxin on this interaction.

2022-02-18 | GSE196944 | GEO

The Effect of the Environmental Temperature on the Adaptation to Host in the Zoonotic Pathogen Vibrio vulnificus.

Project description:Vibrio vulnificus is a zoonotic pathogen that lives in temperate, tropical and subtropical aquatic ecosystems whose geographical distribution is expanding due to global warming. The species is genetically variable and only the strains that belong to the zoonotic clonal-complex can cause vibriosis in both humans and fish (being its main host the eel). Interestingly, the severity of the vibriosis in the eel and the human depends largely on the water temperature (highly virulent at 28°C, avirulent at 20°C or below) and on the iron content in the blood, respectively. The objective of this work was to unravel the role of temperature in the adaptation to the host through a transcriptomic and phenotypic approach. To this end, we obtained the transcriptome of a zoonotic strain grown in a minimum medium (CM9) at 20, 25, 28, and 37°C, and confirmed the transcriptomic results by RT-qPCR and phenotypic tests. In addition, we compared the temperature stimulon with those previously obtained for iron and serum (from eel and human, respectively). Our results suggest that warm temperatures activate adaptive traits that would prepare the bacteria for host colonization (metabolism, motility, chemotaxis, and the protease activity) and fish septicemia (iron-uptake from transferrin and production of O-antigen of high molecular weight) in a generalized manner, while environmental iron controls the expression of a host-adapted virulent phenotype (toxins and the production of a protective envelope). Finally, our results confirm that beyond the effect of temperature on the V. vulnificus distribution in the environment, it also has an effect on the infectious capability of this pathogen that must be taken into account to predict the real risk of V. vulnificus infection caused by global warming.

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Isolation of Vibrio vulnificus from Seawater and Emerging Vibrio vulnificus Septicemia on Jeju Island.

Project description:Vibrio vulnificus is an opportunistic human pathogen, transmitted from seawater, raw oyster, and shellfish and responsible for severe septicemia. We studied V. vulnificus from surface seawater around Jeju Island between 2010 and 2011. In 2010, V. vulnificus was isolated and V. vulnificus septicemia was reported. Surface seawater temperature is an important factor for growth of V. vulnificus, and here we showed that high surface seawater temperature may influence growth of V. vulnificus and occurrence of emerging V. vulnificus septicemia on Jeju Island. This is the first report of isolation of V. vulnificus and emerging V. vulnificus septicemia on Jeju Island.

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Iron regulation in Vibrio vulnificus CMCP6

Project description:Vibrio vulnificus multiply rapidly in host tissues under iron overloaded conditions. To understand the effects of iron in the physiology of this pathogen we performed a genome-wide transcriptional analysis of this bacterium growing under three different iron concentrations. V.vulnificus CMCP6 cells were grown under three different iron concentrations (TSBS + EDDA 50uM, TSBS and TSBS + FAC 250 ug/ml) and samples taken at log phase. Keywords: Response to the iron concentration of the media

2008-08-07 | GSE10633 | GEO

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