Virulence genotype and phenotype of two clinical isolates of Arcobacter butzleri obtained from patients with different pathologies

The surge in human arcobacteriosis has increased interest in determining the mechanisms involved in the pathogenesis of Arcobacter butzleri. Here, genomic analyses and in vitro Caco-2 infection, motility, urease and antimicrobial susceptibility testing (AST) assays were used to characterise the viru...

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Detalles Bibliográficos
Autores: Baztarrika Uria, Itsaso, Salazar Sánchez, Adrián, Hernaez Crespo, Silvia, López Mirones, José Israel, Canut Blasco, Andrés, Alonso Monsalve, Rodrigo, Martínez Ballesteros, Ilargi, Martínez Malax-Echevarría, Irati
Tipo de recurso: artículo
Fecha de publicación:2023
País:España
Institución:Universidad del País Vasco
Repositorio:Addi. Archivo Digital para la Docencia y la Investigación
OAI Identifier:oai:addi.ehu.eus:10810/67336
Acceso en línea:http://hdl.handle.net/10810/67336
Access Level:acceso abierto
Palabra clave:Arcobacter butzleri
caco-2 infection
comparative genomics
antimicrobial resistance
virulence
Descripción
Sumario:The surge in human arcobacteriosis has increased interest in determining the mechanisms involved in the pathogenesis of Arcobacter butzleri. Here, genomic analyses and in vitro Caco-2 infection, motility, urease and antimicrobial susceptibility testing (AST) assays were used to characterise the virulence and antimicrobial resistance (AMR) determinants of strains HC-1, isolated from a patient with travellers’ diarrhoea, and HC-2, isolated from another with pruritus. AMR determinants conferring resistance to tetracycline (tetO, present in both genomes) and to ampicillin and amoxicillin–clavulanic acid (bla3, present in HC-2) were identified. The same determinants associated with flagellum, chemotaxis, adhesion and invasion were detected in both, but HC-1 lacked eight flagellar genes. The urease cluster was only present in HC-1. Motility and urease tests confirmed the genetic differences between strains, but no genetic marker related to the inability of HC-2 to adhere and invade was identified. This inability could be conditioning the patient’s pathology.