Dampened virulence and limited proliferation of Batrachochytrium salamandrivorans during subclinical infection of the troglobiont olm (Proteus anguinus)

Abstract Emerging infections add to existing threats to the survival of amphibians worldwide. The olm (Proteus anguinus) is a vulnerable, troglobiont urodele species with a small European range and restricted to underground karstic systems. Population declines to emerging threats like the chytrid fungus Batrachochytrium salamandrivorans, are likely to go unnoticed due to inaccessibility of the species’ habitat. We here studied the interaction between olms and B. salamandrivorans. Experimental inoculation of olms resulted in low-level, asymptomatic but persistent infections, with limbs as predilection sites. The lack of exponential fungal growth in the olms’ epidermis correlated with limited fungal proliferation and dampened virulence gene expression after exposure to olm skin compounds. The olm is one of few western Palearctic urodeles that is tolerant to B. salamandrivorans infection and may act as a subterranean disease reservoir, yet costs of subclinical infection may compromise olm fitness on the long term.

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Vibrio harveyi virulence gene expression in vitro and in vivo during infection in black tiger shrimp Penaeus monodon

Diseases of Aquatic Organisms ◽

10.3354/dao03475 ◽

2020 ◽

Vol 139 ◽

pp. 153-160

Author(s):

S Peeralil ◽

TC Joseph ◽

V Murugadas ◽

PG Akhilnath ◽

VN Sreejith ◽

...

Keyword(s):

Gene Expression ◽

Virulence Genes ◽

Vibrio Harveyi ◽

Penaeus Monodon ◽

Challenge Test ◽

Virulence Gene ◽

Economic Losses ◽

Virulence Gene Expression

Luminescent Vibrio harveyi is common in sea and estuarine waters. It produces several virulence factors and negatively affects larval penaeid shrimp in hatcheries, resulting in severe economic losses to shrimp aquaculture. Although V. harveyi is an important pathogen of shrimp, its pathogenicity mechanisms have yet to be completely elucidated. In the present study, isolates of V. harveyi were isolated and characterized from diseased Penaeus monodon postlarvae from hatcheries in Kerala, India, from September to December 2016. All 23 tested isolates were positive for lipase, phospholipase, caseinase, gelatinase and chitinase activity, and 3 of the isolates (MFB32, MFB71 and MFB68) showed potential for significant biofilm formation. Based on the presence of virulence genes, the isolates of V. harveyi were grouped into 6 genotypes, predominated by vhpA+ flaB+ ser+ vhh1- luxR+ vopD- vcrD+ vscN-. One isolate from each genotype was randomly selected for in vivo virulence experiments, and the LD50 ranged from 1.7 ± 0.5 × 103 to 4.1 ± 0.1 × 105 CFU ml-1. The expression of genes during the infection in postlarvae was high in 2 of the isolates (MFB12 and MFB32), consistent with the result of the challenge test. However, in MFB19, even though all genes tested were present, their expression level was very low and likely contributed to its lack of virulence. Because of the significant variation in gene expression, the presence of virulence genes alone cannot be used as a marker for pathogenicity of V. harveyi.

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Faculty Opinions recommendation of Inducible control of virulence gene expression in Listeria monocytogenes: temporal requirement of listeriolysin O during intracellular infection.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1009891.138457 ◽

2002 ◽

Author(s):

Colin Hill

Keyword(s):

Gene Expression ◽

Listeria Monocytogenes ◽

Virulence Gene ◽

Listeriolysin O ◽

Virulence Gene Expression ◽

Intracellular Infection

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Faculty Opinions recommendation of The integration host factor (IHF) integrates stationary-phase and virulence gene expression in Salmonella enterica serovar Typhimurium.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1030734.367872 ◽

2006 ◽

Author(s):

Stephen Busby

Keyword(s):

Gene Expression ◽

Stationary Phase ◽

Salmonella Enterica ◽

Salmonella Enterica Serovar Typhimurium ◽

Virulence Gene ◽

Integration Host Factor ◽

Host Factor ◽

Virulence Gene Expression ◽

Serovar Typhimurium

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Faculty Opinions recommendation of Small molecule control of virulence gene expression in Francisella tularensis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1168406.630587 ◽

2009 ◽

Author(s):

Vincenzo Scarlato

Keyword(s):

Gene Expression ◽

Francisella Tularensis ◽

Small Molecule ◽

Virulence Gene ◽

Virulence Gene Expression

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Plant nitrate supply regulates Erwinia amylovora virulence gene expression in Arabidopsis

Molecular Plant Pathology ◽

10.1111/mpp.13114 ◽

2021 ◽

Author(s):

Mahsa Farjad ◽

Gilles Clément ◽

Alban Launay ◽

Roua Jeridi ◽

Sylvie Jolivet ◽

...

Keyword(s):

Gene Expression ◽

Erwinia Amylovora ◽

Virulence Gene ◽

Virulence Gene Expression ◽

Nitrate Supply

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Carbapenem-Resistant Pseudomonas aeruginosa Strains-Distribution of the Essential Enzymatic Virulence Factors Genes

Antibiotics ◽

10.3390/antibiotics10010008 ◽

2020 ◽

Vol 10 (1) ◽

pp. 8

Author(s):

Tomasz Bogiel ◽

Małgorzata Prażyńska ◽

Joanna Kwiecińska-Piróg ◽

Agnieszka Mikucka ◽

Eugenia Gospodarek-Komkowska

Keyword(s):

Pseudomonas Aeruginosa ◽

Alkaline Protease ◽

Virulence Genes ◽

Virulence Gene ◽

Hospital Environment ◽

Gene Encoding ◽

Virulence Gene Expression ◽

Carbapenem Resistant ◽

Antimicrobial Resistance Genes ◽

The Difference

Pseudomonas aeruginosa is one of the most commonly isolated bacteria from clinical specimens, with increasing isolation frequency in nosocomial infections. Herein, we investigated whether antimicrobial-resistant P. aeruginosa strains, e.g., metallo-beta-lactamase (MBL)-producing isolates, may possess a reduced number of virulence genes, resulting from appropriate genome management to adapt to a changing hospital environment. Hospital conditions, such as selective pressure, may lead to the replacement of virulence genes by antimicrobial resistance genes that are crucial to survive under current conditions. The study aimed to compare, using PCR, the frequency of the chosen enzymatic virulence factor genes (alkaline protease-aprA, elastase B-lasB, neuraminidases-nan1 and nan2, and both variants of phospholipase C-plcH and plcN) to MBL distribution among 107 non-duplicated carbapenem-resistant P. aeruginosa isolates. The gene encoding alkaline protease was noted with the highest frequency (100%), while the neuraminidase-1 gene was observed in 37.4% of the examined strains. The difference in lasB and nan1 prevalence amongst the MBL-positive and MBL-negative strains, was statistically significant. Although P. aeruginosa virulence is generally more likely determined by the complex regulation of the virulence gene expression, herein, we found differences in the prevalence of various virulence genes in MBL-producers.

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Nutritional Regulation of the Sae Two-Component System by CodY inStaphylococcus aureus

Journal of Bacteriology ◽

10.1128/jb.00012-18 ◽

2018 ◽

Vol 200 (8) ◽

Cited By ~ 14

Author(s):

Kevin D. Mlynek ◽

William E. Sause ◽

Derek E. Moormeier ◽

Marat R. Sadykov ◽

Kurt R. Hill ◽

...

Keyword(s):

Gene Expression ◽

Virulence Factors ◽

Virulence Gene ◽

Nutrient Depletion ◽

Global Regulator ◽

Two Component System ◽

Component System ◽

Content Type ◽

Virulence Gene Expression ◽

Two Component

ABSTRACTStaphylococcus aureussubverts innate defenses during infection in part by killing host immune cells to exacerbate disease. This human pathogen intercepts host cues and activates a transcriptional response via theS. aureusexoprotein expression (SaeR/SaeS [SaeR/S]) two-component system to secrete virulence factors critical for pathogenesis. We recently showed that the transcriptional repressor CodY adjusts nuclease (nuc) gene expression via SaeR/S, but the mechanism remained unknown. Here, we identified two CodY binding motifs upstream of thesaeP1 promoter, which suggested direct regulation by this global regulator. We show that CodY shares a binding site with the positive activator SaeR and that alleviating direct CodY repression at this site is sufficient to abrogate stochastic expression, suggesting that CodY repressessaeexpression by blocking SaeR binding. Epistasis experiments support a model that CodY also controlssaeindirectly through Agr and Rot-mediated repression of thesaeP1 promoter. We also demonstrate that CodY repression ofsaerestrains production of secreted cytotoxins that kill human neutrophils. We conclude that CodY plays a previously unrecognized role in controlling virulence gene expression via SaeR/S and suggest a mechanism by which CodY acts as a master regulator of pathogenesis by tying nutrient availability to virulence gene expression.IMPORTANCEBacterial mechanisms that mediate the switch from a commensal to pathogenic lifestyle are among the biggest unanswered questions in infectious disease research. Since the expression of most virulence genes is often correlated with nutrient depletion, this implies that virulence is a response to the lack of nourishment in host tissues and that pathogens likeS. aureusproduce virulence factors in order to gain access to nutrients in the host. Here, we show that specific nutrient depletion signals appear to be funneled to the SaeR/S system through the global regulator CodY. Our findings reveal a strategy by whichS. aureusdelays the production of immune evasion and immune-cell-killing proteins until key nutrients are depleted.

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Cyclo(valine–valine) inhibits Vibrio cholerae virulence gene expression

Microbiology ◽

10.1099/mic.0.077297-0 ◽

2014 ◽

Vol 160 (6) ◽

pp. 1054-1062 ◽

Cited By ~ 4

Author(s):

Amit Vikram ◽

Vanessa M. Ante ◽

X. Renee Bina ◽

Qin Zhu ◽

Xinyu Liu ◽

...

Keyword(s):

Vibrio Cholerae ◽

Virulence Factor ◽

Inhibitory Activity ◽

Virulence Gene ◽

Side Chains ◽

Cyclic Dipeptides ◽

Virulence Gene Expression ◽

Factor Production ◽

Virulence Regulator ◽

Virulence Factor Production

Vibrio cholerae has been shown to produce a cyclic dipeptide, cyclo(phenylalanine–proline) (cFP), that functions to repress virulence factor production. The objective of this study was to determine if heterologous cyclic dipeptides could repress V. cholerae virulence factor production. To that end, three synthetic cyclic dipeptides that differed in their side chains from cFP were assayed for virulence inhibitory activity in V. cholerae. The results revealed that cyclo(valine–valine) (cVV) inhibited virulence factor production by a ToxR-dependent process that resulted in the repression of the virulence regulator aphA. cVV-dependent repression of aphA was found to be independent of known aphA regulatory genes. The results demonstrated that V. cholerae was able to respond to exogenous cyclic dipeptides and implicated the hydrophobic amino acid side chains on both arms of the cyclo dipeptide scaffold as structural requirements for inhibitory activity. The results further suggest that cyclic dipeptides have potential as therapeutics for cholera treatment.

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RegA, an AraC-Like Protein, Is a Global Transcriptional Regulator That Controls Virulence Gene Expression in Citrobacter rodentium

Infection and Immunity ◽

10.1128/iai.00770-08 ◽

2008 ◽

Vol 76 (11) ◽

pp. 5247-5256 ◽

Cited By ~ 44

Author(s):

Emily Hart ◽

Ji Yang ◽

Marija Tauschek ◽

Michelle Kelly ◽

Matthew J. Wakefield ◽

...

Keyword(s):

Mammalian Cells ◽

Virulence Gene ◽

Virulence Determinants ◽

Intestinal Colonization ◽

Citrobacter Rodentium ◽

Promoter Regions ◽

Reading Frame ◽

Virulence Gene Expression ◽

Genes Encoding ◽

Colonization Factors

ABSTRACT Citrobacter rodentium is an attaching and effacing pathogen which causes transmissible colonic hyperplasia in mice. Infection with C. rodentium serves as a model for infection of humans with enteropathogenic and enterohemorrhagic Escherichia coli. To identify novel colonization factors of C. rodentium, we screened a signature-tagged mutant library of C. rodentium in mice. One noncolonizing mutant had a single transposon insertion in an open reading frame (ORF) which we designated regA because of its homology to genes encoding members of the AraC family of transcriptional regulators. Deletion of regA in C. rodentium resulted in markedly reduced colonization of the mouse intestine. Examination of lacZ transcriptional fusions using promoter regions of known and putative virulence-associated genes of C. rodentium revealed that RegA strongly stimulated transcription of two newly identified genes located close to regA, which we designated adcA and kfcC. The cloned adcA gene conferred autoaggregation and adherence to mammalian cells to E. coli strain DH5α, and a kfc mutation led to a reduction in the duration of intestinal colonization, but the kfc mutant was far less attenuated than the regA mutant. These results indicated that other genes of C. rodentium whose expression required activation by RegA were required for colonization. Microarray analysis revealed a number of RegA-regulated ORFs encoding proteins homologous to known colonization factors. Transcription of these putative virulence determinants was activated by RegA only in the presence of sodium bicarbonate. Taken together, these results show that RegA is a global regulator of virulence in C. rodentium which activates factors that are required for intestinal colonization.

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