Antivirulence Therapy for Animal Production: Filling an Arsenal with Novel Weapons for Sustainable Disease Control

Defoirdt, Tom

doi:10.1371/journal.ppat.1003603

Cited by 31 publications

(21 citation statements)

References 35 publications

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“…Inhibiting the production of these virulence factors, a strategy that has been termed 'antivirulence therapy' is an interesting alternative to antibiotics for controlling bacterial infections (Defoirdt, 2013). Inhibiting the production of these virulence factors, a strategy that has been termed 'antivirulence therapy' is an interesting alternative to antibiotics for controlling bacterial infections (Defoirdt, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…Pathogenic bacteria produce several virulence factors, that is, gene products that enable them to enter and damage the host. Inhibiting the production of these virulence factors, a strategy that has been termed 'antivirulence therapy' is an interesting alternative to antibiotics for controlling bacterial infections (Defoirdt, 2013). In this respect, it is important to obtain a better understanding of mechanisms involved in bacterial infection as this knowledge can lead to the development of novel control agents.…”

Section: Introductionmentioning

confidence: 99%

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The catecholamine stress hormones norepinephrine and dopamine increase the virulence of pathogenic Vibrio anguillarum and Vibrio campbellii

Julyantoro

Suong

Bossier

et al. 2014

FEMS Microbiology Ecology

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Obtaining a better understanding of mechanisms involved in bacterial infections is of paramount importance for the development of novel agents to control disease caused by (antibiotic resistant) pathogens in aquaculture. In this study, we investigated the impact of catecholamine stress hormones on growth and virulence factor production of pathogenic vibrios (i.e. two Vibrio campbellii strains and two Vibrio anguillarum strains). Both norepinephrine and dopamine (at 100 μM) significantly induced growth in media containing serum. The compounds also increased swimming motility of the tested strains, whereas they had no effect on caseinase, chitinase, and hemolysin activities. Further, antagonists for eukaryotic catecholamine receptors were able to neutralize some of the effects of the catecholamines. Indeed, the dopaminergic receptor antagonist chlorpromazine neutralized the effect of dopamine, and the α-adrenergic receptor antagonists phentolamine and phenoxybenzamine neutralized the effect of norepinephrine, whereas the β-adrenergic receptor antagonist propranolol had limited to no effect. Finally, pretreatment of pathogenic V. campbellii with catecholamines significantly increased its virulence toward giant freshwater prawn larvae. However, the impact of catecholamine receptor antagonists on in vivo virulence was less clear-cut when compared to the in vitro experiments. In summary, our results show that—similar to enteric pathogens—catecholamines also increase the virulence of vibrios that are pathogenic to aquatic organisms by increasing motility and growth in media containing serum.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The catecholamine stress hormones norepinephrine and dopamine increase the virulence of pathogenic Vibrio anguillarum and Vibrio campbellii

Julyantoro

Suong

Bossier

et al. 2014

FEMS Microbiology Ecology

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“…Hence, it is important to distinguish those QQ compounds that must enter the cell to be effective (e.g., brominated furanones) from QQ compounds that work extracellularly (e.g., lactonases), since there may be less pressure to evolve resistance to extracellular compounds because greater efflux should not affect the use of these compounds (54). Although, to our knowledge, no experimental efforts have been devoted to explore this possibility, it can be anticipated that ways in which bacteria develop resistance to these agents may be to (i) increase autoinducer production, (ii) synthesize modified autoinducers (which are less susceptible to the attack of the degrading enzymes), or (iii) evolve mutations in the LuxR-like receptors that increase their affinity to the autoinducers (so that the necessary threshold of autoinducer concentration will decrease).…”

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confidence: 99%

Resistance to Quorum-Quenching Compounds

García‐Contreras

Maeda

Wood

2013

Appl Environ Microbiol

104

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c Bacteria have the remarkable ability to communicate as a group in what has become known as quorum sensing (QS), and this trait has been associated with important bacterial phenotypes, such as virulence and biofilm formation. Bacteria also have an incredible ability to evolve resistance to all known antimicrobials. Hence, although inhibition of QS has been hailed as a means to reduce virulence in a manner that is impervious to bacterial resistance mechanisms, this approach is unlikely to be a panacea. Here we review the evidence that bacteria can evolve resistance to quorum-quenching compounds. Infectious diseases are the leading cause of death (1), and all antibiotics fail (2); therefore, it is imperative to develop novel ways to fight microbial infections. Here we review the use of chemicals that interfere with cell communication and investigate the likelihood that bacteria will evolve resistance to these compounds.QS and QQ. Bacteria use secreted chemicals as signals for a variety purposes, including virulence and biofilm formation. When the compounds build to a threshold concentration and trigger gene expression, the signals are known as quorum-sensing (QS) signals. Examples of well-studied QS signals include acylhomoserine lactones, autoinducer 2, and peptide signals, but many other signals, such as indole, exist (3). In addition to signals, signal synthases, signal receptors, signal response regulators, and regulated genes (QS regulon) are key components of any QS system (4). For example, LuxI-type enzymes are signal synthases which synthesize acylhomoserine lactones. In addition, LuxR-type regulators are receptor proteins for the autoinducer signals, and signalreceptor binding is responsible for the expression of QS regulons. Since numerous compounds that inhibit QS have been identified, since QS is linked to virulence, and since inhibition of QS does not usually affect growth (in rich medium), it has been reasoned that inhibition of QS may be an effective means of reducing pathogenicity that is not subject to the usual resistance mechanisms of bacteria (1,(5)(6)(7)(8). Inhibition of QS is also known as quorum quenching (QQ) and is a form of antivirulence.The well-known examples (9) of QQ compounds include lactonases/acylases that degrade the N-(3-oxoctanoyl)-homoserine lactone (HSL) autoinducers, synthase inhibitors, like analogues of anthranilic acid that block synthesis of quinolone signals (10), and receptor inhibitors, such as brominated furanones (11). In addition, low concentrations of azithromycin, ceftazidime, and ciprofloxacin (antibiotics) inhibit QS in Pseudomonas aeruginosa (12). Also, among the thousands of drugs approved for clinical use, the anthelmintic drug niclosamide is a QQ compound (13); this drug reduces surface motility, biofilm formation, and production of the secreted virulence factors elastase, pyocyanin, and rhamnolipids. The rhizosphere bacterium Stenotrophomonas maltophilia produces cis-9-octadecenoic acid, which is a QQ compound that reduces violacein production by Chromoba...

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“…Most studies performed so far have used axenic Artemia fransciscana as a test organism. This system has allowed for the investigation of several aspects of crustacean-Vibrio interactions, such as colonization (of pathogenic or probiotic isolates), biofilm formation, toxicity of exoenzymes, and infection route (26)(27)(28)(29). However as a heterologous system, this model may exclude species-specific pathogens and specific virulence mechanisms.…”

Section: Experimental Challenge Still Remains the Only Way To Determimentioning

confidence: 99%

Diagnosis of vibriosis in the era of genomics: lessons from invertebrates

Roux¹

2016

Rev. Sci. Tech. OIE

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Global changes linked to increases in temperature and ocean acidification, but also to more direct anthropogenic influences such as aquaculture, have caused a worldwide increase in the reports of Vibrio-associated illnesses affecting humans and also animals such as shrimp and molluscs. Investigation of the emergence of Vibrio pathogenesis events requires the analysis of microbial evolution at the gene, genome and population levels, in order to identify genomic modifications linked to increased virulence, resistance and/or prevalence, or to recent host shift. From a more applied point of view, the elucidation of virulence mechanisms is a prerequisite to devising prophylactic methods to fight infectious agents. In comparison with human pathogens, fairly little is known about the requirements for virulence in vibrios pathogenic to animals. However, the advent of genome sequencing, especially next-generation technologies, the possibility of genetically manipulating most of the Vibrio strains, and the recent availability of standardised animals for experimental infections have now compensated for the considerable delay in advancement of the knowledge of non-model pathogens such as Vibrio and have led to new scientific questions.

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Antivirulence Therapy for Animal Production: Filling an Arsenal with Novel Weapons for Sustainable Disease Control

Cited by 31 publications

References 35 publications

The catecholamine stress hormones norepinephrine and dopamine increase the virulence of pathogenic Vibrio anguillarum and Vibrio campbellii

The catecholamine stress hormones norepinephrine and dopamine increase the virulence of pathogenic Vibrio anguillarum and Vibrio campbellii

Resistance to Quorum-Quenching Compounds

Diagnosis of vibriosis in the era of genomics: lessons from invertebrates

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