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1.
Microbiol Spectr ; 12(7): e0007924, 2024 Jul 02.
Artículo en Inglés | MEDLINE | ID: mdl-38860819

RESUMEN

The incidence of Vibrio vulnificus infections, with high mortality rates in humans and aquatic animals, has escalated, highlighting a significant public health challenge. Currently, reliable markers to identify strains with high virulence potential are lacking, and the understanding of evolutionary drivers behind the emergence of pathogenic strains is limited. In this study, we analyzed the distribution of virulent genotypes and phenotypes to discern the infectious potential of V. vulnificus strains isolated from three distinct sources. Most isolates, traditionally classified as biotype 1, possessed the virulence-correlated gene-C type. Environmental isolates predominantly exhibited YJ-like alleles, while clinical and diseased fish isolates were significantly associated with the nanA gene and pathogenicity region XII. Hemolytic activity was primarily observed in the culture supernatants of clinical and diseased fish isolates. Genetic relationships, as determined by multiple-locus variable-number tandem repeat analysis, suggested that strains originating from the same source tended to cluster together. However, multilocus sequence typing revealed considerable genetic diversity across clusters and sources. A phylogenetic analysis using single nucleotide polymorphisms of diseased fish strains alongside publicly available genomes demonstrated a high degree of evolutionary relatedness within and across different isolation sources. Notably, our findings reveal no direct correlation between phylogenetic patterns, isolation sources, and virulence capabilities. This underscores the necessity for proactive risk management strategies to address pathogenic V. vulnificus strains emerging from environmental reservoirs.IMPORTANCEAs the global incidence of Vibrio vulnificus infections rises, impacting human health and marine aquacultures, understanding the pathogenicity of environmental strains remains critical yet underexplored. This study addresses this gap by evaluating the virulence potential and genetic relatedness of V. vulnificus strains, focusing on environmental origins. We conduct an extensive genotypic analysis and phenotypic assessment, including virulence testing in a wax moth model. Our findings aim to uncover genetic and evolutionary factors that drive pathogenic strain emergence in the environment. This research advances our ability to identify reliable virulence markers and understand the distribution of pathogenic strains, offering significant insights for public health and environmental risk management.


Asunto(s)
Enfermedades de los Peces , Variación Genética , Filogenia , Vibriosis , Vibrio vulnificus , Vibrio vulnificus/genética , Vibrio vulnificus/patogenicidad , Vibrio vulnificus/aislamiento & purificación , Vibrio vulnificus/clasificación , Animales , Vibriosis/microbiología , Vibriosis/veterinaria , Humanos , Virulencia/genética , Enfermedades de los Peces/microbiología , Peces/microbiología , Tipificación de Secuencias Multilocus , Factores de Virulencia/genética , Genotipo , Genoma Bacteriano/genética
2.
Virulence ; 9(1): 1640-1657, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30270715

RESUMEN

Colibacillosis caused by avian pathogenic E. coli (APEC), is an economically important bacterial disease of poultry. APEC are a subgroup of extra intestinal pathogenic E. coli (ExPEC) and poultry are considered potential sources of foodborne ExPEC to humans. Currently, APEC infections in poultry are controlled by antibiotics and/or vaccination; however, their effect is limited due to emergence of antibiotic resistant strains and infections with heterologous serotypes. Therefore, novel approaches are needed. Here, using the bioluminescent quorum sensing (QS) autoinducer 2 (AI-2) indicator Vibrio harveyi BB170, we screened the cell free culture supernatant of APEC O78 prepared from cultures grown in the presence of 4,182 small molecules (SMs; 100 µM). A total of 69 SMs inhibited > 75% of APEC O78 AI-2 activity in the indicator bacteria. Ten SMs that showed highest AI-2 inhibition were selected for further studies. Most of these SMs inhibited the AI-2 activity of other APEC serotypes and significantly reduced APEC O78 biofilm formation and motility. Most compounds showed minimal toxicity on human intestinal cells (Caco-2), chicken macrophage (HD-11), and chicken and sheep red blood cells, and reduced APEC survival in HD-11 and THP-1 macrophages. The SMs induced no or minimal toxicity and conferred protection against APEC in wax moth larval model. SMs affected the expression of APEC O78 QS, virulence, biofilm and motility associated genes providing insight on their potential mode(s) of action. Further testing in chickens will facilitate development of these SMs as novel therapeutics to control APEC in poultry and thereby also reduce zoonotic transmission.


Asunto(s)
Infecciones por Escherichia coli/veterinaria , Escherichia coli/efectos de los fármacos , Homoserina/análogos & derivados , Lactonas/antagonistas & inhibidores , Percepción de Quorum/efectos de los fármacos , Bibliotecas de Moléculas Pequeñas/farmacología , Animales , Biopelículas/efectos de los fármacos , Biopelículas/crecimiento & desarrollo , Células CACO-2 , Pollos , Medios de Cultivo , Expresión Génica , Homoserina/antagonistas & inhibidores , Homoserina/metabolismo , Humanos , Lactonas/metabolismo , Mariposas Nocturnas , Enfermedades de las Aves de Corral/microbiología , Células THP-1 , Virulencia , Factores de Virulencia/genética
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