Although it is generally accepted that phages drive bacterial evolution, how these dynamics play out in the wild remains poorly understood. We found that susceptibility to viral killing in marine Vibrio is mediated by large and highly diverse mobile genetic elements. These phage defense elements display exceedingly fast evolutionary turnover, resulting in differential phage susceptibility among clonal bacterial strains while phage receptors remain invariant. Protection is cumulative, and a single bacterial genome can harbor 6 to 12 defense elements, accounting for more than 90% of the flexible genome among close relatives. The rapid turnover of these elements decouples phage resistance from other genomic features. Thus, resistance to phages in the wild follows evolutionary trajectories alternative to those predicted from laboratory-based evolutionary experiments.
Hatcheries constitute nowadays the only viable solution to support the husbandry of bivalve molluscs due to the depletion and/or overexploitation of their natural beds. Hatchery activities include the broodstock conditioning and spawning, rearing larvae and spat, and the production of microalgae to feed all stages of the production cycle. However, outbreaks of disease continue to be the main bottleneck for successful larval and spat production, most of them caused by different representatives of the genus Vibrio. Therefore, attention must be paid on preventive and management measures that allow the control of such undesirable bacterial populations. The present review provides an updated picture of the recently characterized Vibrio species associated with disease of bivalve molluscs during early stages of development, including the controversial taxonomic affiliation of some of them and relevant advances in the knowledge of their virulence determinants. The problematic use of antibiotics, as well as its eco-friendly alternatives are also critically discussed.
Coevolution between bacteriophages (phages) and their bacterial hosts occurs through changes in resistance and counter-resistance mechanisms. To assess phage-host evolution in wild populations, we isolated 195 Vibrio crassostreae strains and 243 vibriophages during a five month time-series from an oyster farm and combined these isolates with existing V. crassostreae and phage isolates. Cross-infection studies of 81,926 host-phage pairs delineated a modular network where phages are best at infecting cooccurring hosts, indicating local adaptation. Successful propagation of phage is restricted by the ability to adsorb to closely related bacteria and further constrained by strain-specific defence systems. These defences are highly diverse and predominantly located on mobile genetic elements, and multiple defences are active within a single genome. We further show that epigenetic and genomic modifications enable phage to adapt to bacterial defences and alter host range. Our findings reveal that the evolution of bacterial defences and phage counter-defences are underpinned by frequent genetic exchanges with, and between, mobile genetic elements.
Thalassotalic acids A–C and thalassotalamides A and B are new N-acyl dehydrotyrosine derivatives produced by Thalassotalea sp. PP2–459, a Gram-negative bacterium isolated from a marine bivalve aquaculture facility. The structures were elucidated via a combination of spectroscopic analyses emphasizing two-dimensional NMR and high-resolution mass spectral data. Thalassotalic acid A (1) displays in vitro inhibition of the enzyme tyrosinase with an IC50 value (130 μM) that compares favorably to the commercially-used control compounds kojic acid (46 μM) and arbutin (100 μM). These are the first natural products reported from a bacterium belonging to the genus Thalassotalea.
Vibriosis represents the main bottleneck for the larval production process in shellfish aquaculture. While the signs of this disease in bivalve larvae are well known, the infection process by pathogenic Vibrio spp. during episodes of vibriosis has not been elucidated. To investigate the infection process in bivalves, the pathogens of larvae as V. tubiashii subsp. europaensis, V. neptunius and V. bivalvicida were tagged with green fluorescent protein (GFP). Larvae of Manila clam (Ruditapes philippinarum) were inoculated with the GFP-labeled pathogens in different infection assays and monitored by microscopy. Manila clam larvae infected by distinct GFP-tagged Vibrio spp. in different challenges showed the same progression in the infection process, defining three infection stages. GFP-tagged Vibrio spp. were filtered by the larvae through the vellum and entered in the digestive system through the esophagus and stomach and colonized the digestive gland and particularly the intestine, where they proliferated during the first 2h of contact (Stage I), suggesting a chemotactic response. Then, GFP-tagged Vibrio spp. expanded rapidly to the surrounding organs in the body cavity from the dorsal to ventral region (Stage II; 6-8h), colonizing the larvae completely at the peak of infection (Stage III) (14-24h). Results demonstrated for the first time that the vibriosis is asymptomatic in Manila clam larvae during the early infection stages. Thus, the early colonization and the rapid proliferation of Vibrio pathogens within the body cavity supported the sudden and fatal effect of the vibriosis, since the larvae exhibited the first signs of disease when the infection process is advanced. As a first step in the elucidation of the potential mechanisms of bacterial pathogenesis in bivalve larvae the enzymatic activities of the extracellular products released from the wild type V. neptunius, V. tubiashii subsp. europaensis and V. bivalvicida were determined and their cytotoxicity was demonstrated in fish and homeothermic cell lines for the first time. That activity was lost after heat treatment.
The health of marine bivalve larvae is greatly affected by bacteria in the environment particularly when reared in marine hatcheries. This is generally because high stocking densities resulting in high organic loads of both food and faeces, can support increased bacterial growth and biomass levels. Increased bacterial load can lead to larval disease referred to as bacillary necrosis (BN) leading in turn to rapid larval mortality and loss of production. Despite more than 50 years since the first detailed description of BN, we still do not fully understand its causes and mechanisms. Through the manipulation of a model larval culture of the Australian blue mussels (Mytilus galloprovincialis), we determined that BN is linked with rapid and systematic changes in the bacterial community. Early investigation of larval mortality in bivalve larval cultures in the 1950s reported mortality associated with infection by gram negative bacilli that necrotised larval tissues, leading to the descriptive term bacillary necrosis (BN) 1. The disease is capable of causing total collapse of larval cultures (larval crash) in a period of 24-48 hours and is today, the most prevalent hatchery disease worldwide, affecting more than 20 bivalve species. Whilst it is difficult to quantify the impact of BN in shellfish hatcheries, frequent recurrence can severely impact hatchery production with repercussions often felt throughout the supply chains. The prevailing view that BN is an opportunistic disease leads to the emphasis on sound husbandry practices primarily to reduce excess build-up of organic matter. However, whether and how enriched organic conditions are linked with development of BN is unclear. Efforts to study BN have also been complicated by the unpredictable nature of the outbreaks. To address this problem, we deliberately overfed a series of identical small-scale larval cultures with microalgae to create an environment that would increase the incidence of the disease. In cultures that developed mass mortal-ities, automated ribosomal intergenic spaces analysis (ARISA) demonstrated that BN involves rapid and systematic changes in the bacterial community, firstly in the seawater, then rapidly proceeding to the larvae as the disease progresses and necrosis occurs (Figure 1). This study shows that, at least within the system analysed here, BN is a condition of abnormal changes in seawater-associated communities that are capable of affecting the larvae, suggestive of seawater-to-larvae infectivity. The similarity of bacterial communities in seawater and larvae at the onset of mortality suggest swamping by outgrowth of particular bacteria. Bacterial diversity examination using Illumina MiSeq sequencing of 16S rRNA ampli-cons showed that mortality in the model systems was linked with a bacterial community increasingly dominated by Psychroserpens, Polaribacter, Marinomonas, and members of the Candidatus phylum Gracilibacteria. The observation that BN did not occur in all overfed cultures suggests variability in causation made it difficul...
The VPAP30 strain was isolated as the highly predominant bacteria from an episode of massive larval mortality occurring in a commercial culture of the Chilean scallop Argopecten purpuratus . The main aims of this study were, to characterize and identify the pathogenic strain using biochemical and molecular methods, to demonstrate its pathogenic activity on scallop larvae, to characterize its pathogenic properties and to describe the chronology of the pathology. The pathogenic strain was identified as Vibrio bivalvicida based on its phenotypic properties, the multilocus sequence analysis (MLSA) of eight housekeeping genes ( fts Z, gap A, gyr B, mre B, pyr H, rec A, rpo A, and top A) and different in silico genome-to-genome comparisons. When triplicate cultures of healthy 10 days old scallop larvae were challenged with 1 × 10 5 colony forming units (CFU) mL -1 of the VPAP30 strain, percentages of larval survival of 78.9 ± 3.3%, 34.3 ± 4.9%, and 0% were observed at 12, 2,4 and 36 h, respectively, whereas uninfected larval cultures showed survival rates of 97.4 ± 1.2% after of 48 h. Clinical symptoms exhibited by the scallop larvae infected with the VPAP30 strain include the accumulation of bacteria around the scallop larvae, velum disruption and necrosis of digestive gland. The 50% lethal dose (LD 50 ) of VPAP30 strain at 24 and 48 h was 1.3 × 10 4 and 1.2 × 10 3 CFU mL -1 , respectively. The invasive pathogenic activity of the VPAP30 strain was investigated with staining of the bacterial pathogen with 5-DTAF and analyzing bacterial invasion using epifluorescence, and a complete bacterial dissemination inside the larvae at 24 h post-infection was observed. When scallop larvae were inoculated with cell-free extracellular products (ECPs) of VPAP30, the larval survival rate was 59.5 ± 1.7%, significantly ( P < 0.001) lower than the control group (97.4 ± 1.2%) whereas larvae treated with heat-treated ECPs exhibited a survival rate of 61.6 ± 1.8% after 48 h of exposure. V. bivalvicida VPAP30 exhibits high pathogenic activity on scallop larvae, mediated both by bacterial invasion and the production of toxigenic heat-stable compounds. This report constitutes the first isolation of V. bivalvicida out of Europe and extends the host range of this species, having demonstrated its pathogenic activity on the Chilean scallop larvae ( A. purpuratus ). These results supporting the pathogenic potential of V. bivalvicida to kill the larvae of a broad range of bivalve species reared in hatcheries located in the Atlantic and the Paci...
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