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The underlying factors that lead to specific strains within a species to emerge as human pathogens remain mostly enigmatic. The diarrheal disease cholera is caused by strains from a phylogenetically confined group within theVibrio choleraespecies, the pandemic cholera group (PCG), making it an ideal model system to tackle this puzzling phenomenon. Comprehensive analyses of over 1,840V. choleraegenomes, including environmental isolates from this study, reveal that the species consists of eleven groups, with the PCG belonging to the largest and located within a lineage shared with environmental strains. This hierarchical classification provided us with a framework to unravel the ecoevolutionary dynamics of the genetic determinants associated with the emergence of toxigenicV. cholerae. Our analyses indicate that this phenomenon is largely dependent on the acquisition of unique modular gene clusters and allelic variations that confer a competitive advantage during intestinal colonization. We determined that certain PCG-associated alleles are essential for successful colonization whereas others provide a nonlinear competitive advantage, acting as a critical bottleneck that clarifies the isolated emergence of PCG. For instance, toxigenic strains encoding non-PCG alleles of a)tcpFor b) a sextuple allelic exchange mutant for genestcpA,toxT,VC0176,VC1791,rfbT,andompU, lose their ability to colonize the intestine. Interestingly, these alleles do not play a role in the colonization of newly established model environmental reservoirs. Our study uncovers the evolutionary roots of toxigenicV. choleraeoffering a tractable approach for investigating the emergence of pathogenic clones within an environmental population. 

Climate change is having increasingly profound effects on human health, notably those associated with the occurrence, distribution, and transmission of infectious diseases. The number of disparate ecological parameters and pathogens affected by climate change are vast and expansive. Disentangling the complex relationship between these variables is critical for the development of effective countermeasures against its effects. The pathogenVibrio vulnificus, a naturally occurring aquatic bacterium that causes fulminant septicemia, represents a quintessential climate-sensitive organism. In this review, we useV.vulnificusas a model organism to elucidate the intricate network of interactions between climatic factors and pathogens, with the objective of identifying common patterns by which climate change is affecting their disease burden. Recent findings indicate that in regions native toV.vulnificusor related pathogens, climate-driven natural disasters are the chief contributors to their disease outbreaks. Concurrently, climate change is increasing the environmental suitability of areas non-endemic to their diseases, promoting a surge in their natural populations and transmission dynamics, thus elevating the risk of new outbreaks. We highlight potential risk factors and climatic drivers aggravating the threat ofV.vulnificustransmission under both scenarios and propose potential measures for mitigating its impact. By defining the mechanisms by which climate change influencesV.vulnificusdisease burden, we aim to shed light on the transmission dynamics of related disease-causing agents, thereby laying the groundwork for early warning systems and broadly applicable control measures. 

A Gram-stain-negative, rod-shaped bacterial strain, designatedVibrio floridensisIRLE0018 (=NRRL B-65642=NCTC 14661), was isolated from a cyanobacterial bloom along the Indian River Lagoon (IRL), a large and highly biodiverse estuary in eastern Florida (USA). The results of phylogenetic, biochemical, and phenotypic analyses indicate that this isolate is distinct from species of the genusVibriowith validly published names and is the closest relative to the emergent human pathogen,Vibrio vulnificus. Here, we present the complete genome sequence ofV. floridensisstrain IRLE0018 (4 535 135 bp). On the basis of the established average nucleotide identity (ANI) values for the determination of different species (ANI <95 %), strain IRLE0018, with an ANI of approximately 92 % compared with its closest relative,V. vulnificus, represents a novel species within the genusVibrio. To our knowledge, this represents the first time this species has been described. The results of genomic analyses ofV. floridensisIRLE0018 indicate the presence of antibiotic resistance genes and several known virulence factors, however, its pathogenicity profile (e.g. survival in serum, phagocytosis avoidance) reveals limited virulence potential of this species in contrast toV. vulnificus. 

Abstract Printing functional devices on flexible substrates requires printing of high conductivity metallic patterns. To prevent deformation and damage of the polymeric substrate, the processing (printing) and post-processing (annealing) temperature of the metal patterns must be lower than the glass transition temperature of the substrate. Here, a hybrid process including deposition of a sacrificial blanket thin film, followed by room environment nozzle-based electrodeposition, and subsequent etching of the blanket film is demonstrated to print pure and nanocrystalline metallic (Ni and Cu) patterns on flexible substrates (PI and PET). Microscopy and spectroscopy showed that the printed metal is nanocrystalline, solid with no porosity and with low impurities. Electrical resistivity close to the bulk (~2-time) was obtained without any thermal annealing. Mechanical characterization confirmed excellent cyclic strength of the deposited metal, with limited degradation under high cyclic flexure. Several devices including radio frequency identification (RFID) tag, heater, strain gauge, and temperature sensor are demonstrated.