scholarly journals Virulence as a Side Effect of Interspecies Interaction in Vibrio Coral Pathogens

mBio ◽  
2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Esther Rubio-Portillo ◽  
Ana B. Martin-Cuadrado ◽  
Andrés M. Caraballo-Rodríguez ◽  
Forest Rohwer ◽  
Pieter C. Dorrestein ◽  
...  
Keyword(s):  
Interspecific Competition ◽  
Physiological Response ◽  
Coral Disease ◽  
Platelet Activating Factor ◽  
Coral Tissue ◽  
Type Vi Secretion System ◽  
Pathogenic Potential ◽  
Content Type ◽  
Coral Microbiome ◽  
Vibrio Coralliilyticus

ABSTRACT The increase in prevalence and severity of coral disease outbreaks produced by Vibrio pathogens, and related to global warming, has seriously impacted reef-building corals throughout the oceans. The coral Oculina patagonica has been used as a model system to study coral bleaching produced by Vibrio infection. Previous data demonstrated that when two coral pathogens (Vibrio coralliilyticus and Vibrio mediterranei) simultaneously infected the coral O. patagonica, their pathogenicity was greater than when each bacterium was infected separately. Here, to understand the mechanisms underlying this synergistic effect, transcriptomic analyses of monocultures and cocultures as well as experimental infection experiments were performed. Our results revealed that the interaction between the two vibrios under culture conditions overexpressed virulence factor genes (e.g., those encoding siderophores, the type VI secretion system, and toxins, among others). Moreover, under these conditions, vibrios were also more likely to form biofilms or become motile through induction of lateral flagella. All these changes that occur as a physiological response to the presence of a competing species could favor the colonization of the host when they are present in a mixed population. Additionally, during coral experimental infections, we showed that exposure of corals to molecules released during V. coralliilyticus and V. mediterranei coculture induced changes in the coral microbiome that favored damage to coral tissue and increased the production of lyso-platelet activating factor. Therefore, we propose that competition sensing, defined as the physiological response to detection of harm or to the presence of a competing Vibrio species, enhances the ability of Vibrio coral pathogens to invade their host and cause tissue necrosis. IMPORTANCE Vibrio coralliilyticus and Vibrio mediterranei are important coral pathogens capable of inducing serious coral damage, which increases severely when they infect the host simultaneously. This has consequences related to the dispersion of these pathogens among different locations that could enhance deleterious effects on coral reefs. However, the mechanisms underlying this synergistic interaction are unknown. The work described here provides a new perspective on the complex interactions among these two Vibrio coral pathogens, suggesting that coral infection could be a collateral effect of interspecific competition. Major implications of this work are that (i) Vibrio virulence mechanisms are activated in the absence of the host as a response to interspecific competition and (ii) release of molecules by Vibrio coral pathogens produces changes in the coral microbiome that favor the pathogenic potential of the entire Vibrio community. Thus, our results highlight that social cues and competition sensing are crucial determinants of development of coral diseases.

scholarly journals Alien vs. Predator: Pathogens open niche space for opportunists, unless controlled by predators

2015 ◽  
Author(s):  
Rory M Welsh ◽  
Stephanie M Rosales ◽  
Jesse R.R. Zaneveld ◽  
Jérôme P Payet ◽  
Ryan McMinds ◽  
...  
Keyword(s):  
Coral Tissue ◽  
Structure Stability ◽  
Niche Space ◽  
Gram Negative ◽  
Pathogen Invasion ◽  
Coral Microbiome ◽  
Opportunistic Bacteria ◽  
Pathogen Challenge ◽  
Vibrio Coralliilyticus ◽  
Coral Pathogen

Coral microbiomes are known to play important roles in organismal health, response to environmental stress, and resistance to disease. Pathogens invading the coral microbiome encounter diverse assemblages of resident bacteria, ranging from defensive and metabolic symbionts to opportunistic bacteria that may turn harmful in compromised hosts. However, little is known about how these bacterial interactions influence the overall structure, stability, and function of the microbiome during the course of pathogen challenge. We sought to test how coral microbiome dynamics were affected by interactions between two of its members: Vibrio coralliilyticus, a known temperature-dependent coral pathogen, and Halobacteriovorax, a unique bacterial predator of Vibrio and other gram-negative bacteria. We challenged specimens of the important reef-building coral Montastraea cavernosa with Vibrio coralliilyticus pathogens in the presence or absence of Halobacteriovorax predators, and monitored microbial community dynamics with 16S rRNA gene time-series. In addition to its direct effects on corals, pathogen challenge reshaped coral microbiomes in ways that allowed for secondary blooms of opportunistic bacteria. As expected, Vibrio coralliilyticus addition increased the infiltration of Vibrio into coral tissues. This increase of Vibrios in coral tissue was accompanied by increased richness, and reduced stability (increased beta-diversity) of the rest of the microbiome, suggesting strong secondary effects of pathogen invasion on commensal and mutualistic coral bacteria. Moreover, after an initial increase in Vibrios, two opportunistic lineages (Rhodobacterales and Cytophagales) increased in coral tissues, suggesting that this pathogen opens niche space for opportunists. Based on the keystone role of predators in many ecosystems, we hypothesized that Halobacteriovorax predators might help protect corals by consuming gram-negative pathogens. In keeping with a protective role, Halobacteriovorax addition alone had only minor effects on the microbiome, and no infiltration of Halobacteriovorax into coral tissues was detected in amplicon libraries. Simultaneous challenge with both pathogen and predator eliminated detectable V. corallyticus infiltration into coral tissue samples, ameliorated changes to the rest of the coral microbiome, and prevented secondary blooms of opportunistic Rhodobacterales and Cytophagales. Thus, we show that primary infection by a coral pathogen is sufficient to cause increases in opportunists, as seen in correlational studies. These data further provide a proof-of-principle demonstration that, under certain circumstances, host-associated bacterial predators can mitigate the ability of pathogens to infiltrate host tissue, and stabilize the microbiome against complex secondary changes that favor growth of opportunistic lineages.

scholarly journals Detection and Quantification of the Coral Pathogen Vibrio coralliilyticus by Real-Time PCR with TaqMan Fluorescent Probes

2010 ◽  
Vol 76 (15) ◽  
pp. 5282-5286 ◽  
Author(s):  
F. Joseph Pollock ◽  
Pamela J. Morris ◽  
Bette L. Willis ◽  
David G. Bourne
Keyword(s):  
Real Time ◽  
Coral Disease ◽  
Disease Diagnosis ◽  
Coral Tissue ◽  
Gene Encoding ◽  
Real Time Quantitative Pcr ◽  
Novel Approach ◽  
Detection Assay ◽  
Vibrio Coralliilyticus ◽  
Coral Pathogen

ABSTRACT A real-time quantitative PCR-based detection assay targeting the dnaJ gene (encoding heat shock protein 40) of the coral pathogen Vibrio coralliilyticus was developed. The assay is sensitive, detecting as little as 1 CFU per ml in seawater and 104 CFU per cm2 of coral tissue. Moreover, inhibition by DNA and cells derived from bacteria other than V. coralliilyticus was minimal. This assay represents a novel approach to coral disease diagnosis that will advance the field of coral disease research.

scholarly journals Compositional homogeneity in the pathobiome of a new, slow-spreading coral disease

Microbiome ◽  
2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Michael Sweet ◽  
Alfred Burian ◽  
James Fifer ◽  
Mark Bulling ◽  
David Elliott ◽  
...  
Keyword(s):  
Coral Disease ◽  
Disease Outbreaks ◽  
Coral Tissue ◽  
Anna Karenina ◽  
Coral Microbiome ◽  
Β Diversity ◽  
Compositional Homogeneity ◽  
The One ◽  
Patch Disease ◽  
Apparently Healthy

Abstract Background Coral reefs face unprecedented declines in diversity and cover, a development largely attributed to climate change-induced bleaching and subsequent disease outbreaks. Coral-associated microbiomes may strongly influence the fitness of their hosts and alter heat tolerance and disease susceptibility of coral colonies. Here, we describe a new coral disease found in Micronesia and present a detailed assessment of infection-driven changes in the coral microbiome. Results Combining field monitoring and histological, microscopic and next-generation barcoding assessments, we demonstrate that the outbreak of the disease, named ‘grey-patch disease’, is associated with the establishment of cyanobacterial biofilm overgrowing coral tissue. The disease is characterised by slow progression rates, with coral tissue sometimes growing back over the GPD biofilm. Network analysis of the corals’ microbiome highlighted the clustering of specific microbes which appeared to benefit from the onset of disease, resulting in the formation of ‘infection clusters’ in the microbiomes of apparently healthy corals. Conclusions Our results appear to be in contrast to the recently proposed Anna-Karenina principle, which states that disturbances (such as disease) trigger chaotic dynamics in microbial communities and increase β-diversity. Here, we show significantly higher community similarity (compositional homogeneity) in the pathobiome of diseased corals, compared to the microbiome associated with apparently healthy tissue. A possible explanation for this pattern is strong competition between the pathogenic community and those associated with the ‘healthy’ coral holobiont, homogenising the composition of the pathobiome. Further, one of our key findings is that multiple agents appear to be involved in degrading the corals’ defences causing the onset of this disease. This supports recent findings indicating a need for a shift from the one-pathogen-one-disease paradigm to exploring the importance of multiple pathogenic players in any given disease.

scholarly journals Alien vs. Predator: Pathogens open niche space for opportunists, unless controlled by predators

2015 ◽  
Author(s):  
Rory M Welsh ◽  
Stephanie M Rosales ◽  
Jesse R.R. Zaneveld ◽  
Jérôme P Payet ◽  
Ryan McMinds ◽  
...  
Keyword(s):  
Coral Tissue ◽  
Structure Stability ◽  
Niche Space ◽  
Gram Negative ◽  
Pathogen Invasion ◽  
Coral Microbiome ◽  
Opportunistic Bacteria ◽  
Pathogen Challenge ◽  
Vibrio Coralliilyticus ◽  
Coral Pathogen

Coral microbiomes are known to play important roles in organismal health, response to environmental stress, and resistance to disease. Pathogens invading the coral microbiome encounter diverse assemblages of resident bacteria, ranging from defensive and metabolic symbionts to opportunistic bacteria that may turn harmful in compromised hosts. However, little is known about how these bacterial interactions influence the overall structure, stability, and function of the microbiome during the course of pathogen challenge. We sought to test how coral microbiome dynamics were affected by interactions between two of its members: Vibrio coralliilyticus, a known temperature-dependent coral pathogen, and Halobacteriovorax, a unique bacterial predator of Vibrio and other gram-negative bacteria. We challenged specimens of the important reef-building coral Montastraea cavernosa with Vibrio coralliilyticus pathogens in the presence or absence of Halobacteriovorax predators, and monitored microbial community dynamics with 16S rRNA gene time-series. In addition to its direct effects on corals, pathogen challenge reshaped coral microbiomes in ways that allowed for secondary blooms of opportunistic bacteria. As expected, Vibrio coralliilyticus addition increased the infiltration of Vibrio into coral tissues. This increase of Vibrios in coral tissue was accompanied by increased richness, and reduced stability (increased beta-diversity) of the rest of the microbiome, suggesting strong secondary effects of pathogen invasion on commensal and mutualistic coral bacteria. Moreover, after an initial increase in Vibrios, two opportunistic lineages (Rhodobacterales and Cytophagales) increased in coral tissues, suggesting that this pathogen opens niche space for opportunists. Based on the keystone role of predators in many ecosystems, we hypothesized that Halobacteriovorax predators might help protect corals by consuming gram-negative pathogens. In keeping with a protective role, Halobacteriovorax addition alone had only minor effects on the microbiome, and no infiltration of Halobacteriovorax into coral tissues was detected in amplicon libraries. Simultaneous challenge with both pathogen and predator eliminated detectable V. corallyticus infiltration into coral tissue samples, ameliorated changes to the rest of the coral microbiome, and prevented secondary blooms of opportunistic Rhodobacterales and Cytophagales. Thus, we show that primary infection by a coral pathogen is sufficient to cause increases in opportunists, as seen in correlational studies. These data further provide a proof-of-principle demonstration that, under certain circumstances, host-associated bacterial predators can mitigate the ability of pathogens to infiltrate host tissue, and stabilize the microbiome against complex secondary changes that favor growth of opportunistic lineages.

scholarly journals Helicobacter saguini, a Novel Helicobacter Isolated from Cotton-Top Tamarins with Ulcerative Colitis, Has Proinflammatory Properties and Induces Typhlocolitis and Dysplasia in Gnotobiotic IL-10−/−Mice

2016 ◽  
Vol 84 (8) ◽  
pp. 2307-2316 ◽  
Author(s):  
Z. Shen ◽  
A. Mannion ◽  
M. T. Whary ◽  
S. Muthupalani ◽  
A. Sheh ◽  
...  
Keyword(s):  
Draft Genome ◽  
Illumina Miseq ◽  
Type Vi Secretion System ◽  
Necrosis Factor Alpha ◽  
Pathogenic Potential ◽  
Content Type ◽  
Novel Bacterium ◽  
Tnf Α ◽  
H Pylori ◽  
Ht 29

A urease-negative, fusiform, novel bacterium namedHelicobacter saguiniwas isolated from the intestines and feces of cotton-top tamarins (CTTs) with chronic colitis.Helicobactersp. was detected in 69% of feces or intestinal samples from 116 CTTs. The draft genome sequence, obtained by Illumina MiSeq sequencing, forH. saguiniisolate MIT 97-6194-5, consisting of ∼2.9 Mb with a G+C content of 35% and 2,704 genes, was annotated using the NCBI Prokaryotic Genomes Automatic Annotation Pipeline.H. saguinicontains homologous genes of known virulence factors found in other enterohepatic helicobacter species (EHS) andH. pylori. These include flagellin, γ-glutamyl transpeptidase (ggt), collagenase, the secreted serine proteasehtrA, and components of a type VI secretion system, but the genome does not harbor genes for cytolethal distending toxin (cdt).H. saguiniMIT 97-6194-5 induced significant levels of interleukin-8 (IL-8) in HT-29 cell culture supernatants by 4 h, which increased through 24 h. mRNAs for the proinflammatory cytokines IL-1β, tumor necrosis factor alpha (TNF-α), IL-10, and IL-6 and the chemokine CXCL1 were upregulated in cocultured HT-29 cells at 4 h compared to levels in control cells. At 3 months postinfection, allH. saguini-monoassociated gnotobiotic C57BL/129 IL-10−/−mice were colonized and had seroconverted toH. saguiniantigen with a significant Th1-associated increase in IgG2c (P< 0.0001).H. saguiniinduced a significant typhlocolitis, associated epithelial defects, mucosa-associated lymphoid tissue (MALT) hyperplasia, and dysplasia. Inflammatory cytokines IL-22, IL-17a, IL-1β, gamma interferon (IFN-γ), and TNF-α, as well as inducible nitric oxide synthase (iNOS) were significantly upregulated in the cecal tissues of infected mice. The expression of the DNA damage response molecule γ-H2AX was significantly higher in the ceca ofH. saguini-infected gnotobiotic mice than in the controls. This model using a nonhuman primateHelicobactersp. can be used to study the pathogenic potential of EHS isolated from primates with naturally occurring inflammatory bowel disease (IBD) and colon cancer.

scholarly journals MetR-Regulated Vibrio cholerae Metabolism Is Required for Virulence

mBio ◽  
2012 ◽  
Vol 3 (5) ◽  
Author(s):  
Ryan W. Bogard ◽  
Bryan W. Davies ◽  
John J. Mekalanos
Keyword(s):  
Amino Acid ◽  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Current Knowledge ◽  
Intestinal Colonization ◽  
Wild Type ◽  
Pathogenic Potential ◽  
Content Type ◽  
Mouse Intestine

ABSTRACTLysR-type transcriptional regulators (LTTRs) are the largest, most diverse family of prokaryotic transcription factors, with regulatory roles spanning metabolism, cell growth and division, and pathogenesis. Using a sequence-defined transposon mutant library, we screened a panel ofV. choleraeEl Tor mutants to identify LTTRs required for host intestinal colonization. Surprisingly, out of 38 LTTRs, only one severely affected intestinal colonization in the suckling mouse model of cholera: the methionine metabolism regulator, MetR. Genetic analysis of genes influenced by MetR revealed thatglyA1andmetJwere also required for intestinal colonization. Chromatin immunoprecipitation of MetR and quantitative reverse transcription-PCR (qRT-PCR) confirmed interaction with and regulation ofglyA1, indicating that misregulation ofglyA1is likely responsible for the colonization defect observed in themetRmutant. TheglyA1mutant was auxotrophic for glycine but exhibited wild-type trimethoprim sensitivity, making folate deficiency an unlikely cause of its colonization defect. MetJ regulatory mutants are not auxotrophic but are likely altered in the regulation of amino acid-biosynthetic pathways, including those for methionine, glycine, and serine, and this misregulation likely explains its colonization defect. However, mutants defective in methionine, serine, and cysteine biosynthesis exhibited wild-type virulence, suggesting that these amino acids can be scavenged in vivo. Taken together, our results suggest that glycine biosynthesis may be required to alleviate an in vivo nutritional restriction in the mouse intestine; however, additional roles for glycine may exist. Irrespective of the precise nature of this requirement, this study illustrates the importance of pathogen metabolism, and the regulation thereof, as a virulence factor.IMPORTANCEVibrio choleraecontinues to be a severe cause of morbidity and mortality in developing countries. Identification ofV. choleraefactors critical to disease progression offers the potential to develop or improve upon therapeutics and prevention strategies. To increase the efficiency of virulence factor discovery, we employed a regulator-centric approach to multiplex our in vivo screening capabilities and allow whole regulons inV. choleraeto be interrogated for pathogenic potential. We identified MetR as a new virulence regulator and serine hydroxymethyltransferase GlyA1 as a new MetR-regulated virulence factor, both required byV. choleraeto colonize the infant mouse intestine. Bacterial metabolism is a prerequisite to virulence, and current knowledge of in vivo metabolism of pathogens is limited. Here, we expand the known role of amino acid metabolism and regulation in virulence and offer new insights into the in vivo metabolic requirements ofV. choleraewithin the mouse intestine.

scholarly journals White Syndrome-Affected Corals Have a Distinct Microbiome at Disease Lesion Fronts

2016 ◽  
Vol 83 (2) ◽  
Author(s):  
F. Joseph Pollock ◽  
Naohisa Wada ◽  
Gergely Torda ◽  
Bette L. Willis ◽  
David G. Bourne
Keyword(s):  
Disease Ecology ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Health States ◽  
Host Coral ◽  
Tissue Samples ◽  
Content Type ◽  
White Syndrome ◽  
Community Profiling

ABSTRACT Coral tissue loss diseases, collectively known as white syndromes (WSs), induce significant mortality on reefs throughout the Indo-Pacific, yet definitive confirmation of WS etiologies remains elusive. In this study, we integrated ecological disease monitoring, bacterial community profiling, in situ visualization of microbe-host interactions, and cellular responses of the host coral through an 18-month repeated-sampling regime. We assert that the observed pathogenesis of WS lesions on acroporid corals at Lizard Island (Great Barrier Reef) is not the result of apoptosis or infection by Vibrio bacteria, ciliates, fungi, cyanobacteria, or helminths. Histological analyses detected helminths, ciliates, fungi, and cyanobacteria in fewer than 25% of WS samples, and helminths and fungi were also observed in 12% of visually healthy samples. The abundances of Vibrio-affiliated sequences (assessed using 16S rRNA amplicon sequencing) did not differ significantly between health states and never exceeded 3.3% of reads in any individual sample. In situ visualization detected Vibrio bacteria only in summer WS lesion samples and revealed no signs of these bacteria in winter disease samples (or any healthy tissue samples), despite continued disease progression year round. However, a 4-fold increase in Rhodobacteraceae-affiliated bacterial sequences at WS lesion fronts suggests that this group of bacteria could play a role in WS pathogenesis and/or serve as a diagnostic criterion for disease differentiation. While the causative agent(s) underlying WSs remains elusive, the microbial and cellular processes identified in this study will help to identify and differentiate visually similar but potentially distinct WS etiologies. IMPORTANCE Over the past decade, a virulent group of coral diseases known as white syndromes have impacted coral reefs throughout the Indian and Pacific Oceans. This article provides a detailed case study of white syndromes to combine disease ecology, high-throughput microbial community profiling, and cellular-scale host-microbe visualization over seasonal time scales. We provide novel insights into the etiology of this devastating disease and reveal new diagnostic criteria that could be used to differentiate visually similar but etiologically distinct forms of white syndrome.

scholarly journals Helicobacter pullorum Isolated from Fresh Chicken Meat: Antibiotic Resistance and Genomic Traits of an Emerging Foodborne Pathogen

2015 ◽  
Vol 81 (23) ◽  
pp. 8155-8163 ◽  
Author(s):  
Vítor Borges ◽  
Andrea Santos ◽  
Cristina Belo Correia ◽  
Margarida Saraiva ◽  
Armelle Ménard ◽  
...  
Keyword(s):  
Membrane Filter ◽  
Acquired Resistance ◽  
Foodborne Pathogen ◽  
Meat Products ◽  
Chicken Meat ◽  
Filter Method ◽  
Type Vi Secretion System ◽  
Genetic Traits ◽  
Content Type ◽  
Meat Samples

ABSTRACTMeat and meat products are important sources of human intestinal infections. We report the isolation ofHelicobacter pullorumstrains from chicken meat. Bacteria were isolated from 4 of the 17 analyzed fresh chicken meat samples, using a membrane filter method. MIC determination revealed that the four strains showed acquired resistance to ciprofloxacin; one was also resistant to erythromycin, and another one was resistant to tetracycline. Whole-genome sequencing of the four strains and comparative genomics revealed important genetic traits within theH. pullorumspecies, such as 18 highly polymorphic genes (including a putative new cytotoxin gene), plasmids, prophages, and a complete type VI secretion system (T6SS). The T6SS was found in three out of the four isolates, suggesting that it may play a role inH. pullorumpathogenicity and diversity. This study suggests that the emerging pathogenH. pullorumcan be transmitted to humans by chicken meat consumption/contact and constitutes an important contribution toward a better knowledge of the genetic diversity within theH. pullorumspecies. In addition, some genetic traits found in the four strains provide relevant clues to how this species may promote adaptation and virulence.

scholarly journals Development of oriC-Based Plasmids for Mesoplasma florum

2017 ◽  
Vol 83 (7) ◽  
Author(s):  
Dominick Matteau ◽  
Marie-Eve Pepin ◽  
Vincent Baby ◽  
Samuel Gauthier ◽  
Mélissa Arango Giraldo ◽  
...  
Keyword(s):  
Systems Biology ◽  
Synthetic Biology ◽  
Genetic Engineering ◽  
Genome Engineering ◽  
Antibiotic Resistance Genes ◽  
Viable Cell ◽  
Pathogenic Potential ◽  
Strong Basis ◽  
Content Type ◽  
Basic Biology

ABSTRACT The near-minimal bacterium Mesoplasma florum constitutes an attractive model for systems biology and for the development of a simplified cell chassis in synthetic biology. However, the lack of genetic engineering tools for this microorganism has limited our capacity to understand its basic biology and modify its genome. To address this issue, we have evaluated the susceptibility of M. florum to common antibiotics and developed the first generation of artificial plasmids able to replicate in this bacterium. Selected regions of the predicted M. florum chromosomal origin of replication (oriC) were used to create different plasmid versions that were tested for their transformation frequency and stability. Using polyethylene glycol-mediated transformation, we observed that plasmids harboring both rpmH-dnaA and dnaA-dnaN intergenic regions, interspaced or not with a copy of the dnaA gene, resulted in a frequency of ∼4.1 × 10−6 transformants per viable cell and were stably maintained throughout multiple generations. In contrast, plasmids containing only one M. florum oriC intergenic region or the heterologous oriC region of Mycoplasma capricolum, Mycoplasma mycoides, or Spiroplasma citri failed to produce any detectable transformants. We also developed alternative transformation procedures based on electroporation and conjugation from Escherichia coli, reaching frequencies up to 7.87 × 10−6 and 8.44 × 10−7 transformants per viable cell, respectively. Finally, we demonstrated the functionality of antibiotic resistance genes active against tetracycline, puromycin, and spectinomycin/streptomycin in M. florum. Taken together, these valuable genetic tools will facilitate efforts toward building an M. florum-based near-minimal cellular chassis for synthetic biology. IMPORTANCE Mesoplasma florum constitutes an attractive model for systems biology and for the development of a simplified cell chassis in synthetic biology. M. florum is closely related to the mycoides cluster of mycoplasmas, which has become a model for whole-genome cloning, genome transplantation, and genome minimization. However, M. florum shows higher growth rates than other Mollicutes, has no known pathogenic potential, and possesses a significantly smaller genome that positions this species among some of the simplest free-living organisms. So far, the lack of genetic engineering tools has limited our capacity to understand the basic biology of M. florum in order to modify its genome. To address this issue, we have evaluated the susceptibility of M. florum to common antibiotics and developed the first artificial plasmids and transformation methods for this bacterium. This represents a strong basis for ongoing genome engineering efforts using this near-minimal microorganism.

scholarly journals Influence of Chemotaxis and Swimming Patterns on the Virulence of the Coral PathogenVibrio coralliilyticus

2018 ◽  
Vol 200 (15) ◽  
Author(s):  
Blake Ushijima ◽  
Claudia C. Häse
Keyword(s):  
Type Strain ◽  
Wild Type Strain ◽  
Bacterial Colonization ◽  
Valuable Insight ◽  
Wild Type ◽  
Coral Mucus ◽  
Content Type ◽  
Swimming Pattern ◽  
Vibrio Coralliilyticus ◽  
Insight Into

ABSTRACTChemotaxis, the directed movement toward or away from a chemical signal, can be essential to bacterial pathogens for locating hosts or avoiding hostile environments. The coral pathogenVibrio coralliilyticuschemotaxes toward coral mucus; however, chemotaxis has not been experimentally demonstrated to be important for virulence. To further examine this, in-frame mutations were constructed in genes predicted to be important forV. coralliilyticuschemotaxis. MostVibriogenomes contain multiple homologs of various chemotaxis-related genes, and two paralogs of each forcheB,cheR, andcheAwere identified. Based on single mutant analyses, the paralogscheB2,cheR2, andcheA1were essential for chemotaxis in laboratory assays. As predicted, the ΔcheA1and ΔcheR2strains had a smooth-swimming pattern, while the ΔcheB2strain displayed a zigzag pattern when observed under light microscopy. However, these mutants, unlike the parent strain, were unable to chemotax toward the known attractants coral mucus, dimethylsulfoniopropionate, andN-acetyl-d-glucosamine. The ΔcheB2strain and an aflagellate ΔfliG1strain were avirulent to coral, while the ΔcheA1and ΔcheR2strains were hypervirulent (90 to 100% infection within 14 h on average) compared to the wild-type strain (66% infection within 36 h on average). Additionally, the ΔcheA1and ΔcheR2strains appeared to better colonize coral fragments than the wild-type strain. These results suggest that although chemotaxis may be involved with infection (the ΔcheB2strain was avirulent), a smooth-swimming phenotype is important for bacterial colonization and infection. This study provides valuable insight into understandingV. coralliilyticuspathogenesis and how this pathogen may be transmitted between hosts.IMPORTANCECorals are responsible for creating the immense structures that are essential to reef ecosystems; unfortunately, pathogens like the bacteriumVibrio coralliilyticuscan cause fatal infections of reef-building coral species. However, compared to related human pathogens, the mechanisms by whichV. coralliilyticusinitiates infections and locates new coral hosts are poorly understood. This study investigated the effects of chemotaxis, the directional swimming in response to chemical signals, and bacterial swimming patterns on infection of the coralMontipora capitata. Infection experiments with different mutant strains suggested that a smooth-swimming pattern resulted in hypervirulence. These results demonstrate that the role of chemotaxis in coral infection may not be as straightforward as previously hypothesized and provide valuable insight intoV. coralliilyticuspathogenesis.

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