RESUMEN
Bacteriophage-encoded genetic elements control bacterial biological functions. Enterohemorrhagic Escherichia coli (EHEC) strains harbor lambda-phages encoding the Shiga-toxin (Stx), which is expressed during the phage lytic cycle and associated with exacerbated disease. Phages also reside dormant within bacterial chromosomes through their lysogenic cycle, but how this impacts EHEC virulence remains unknown. We find that during lysogeny the phage transcription factor Cro activates the EHEC type III secretion system (T3SS). EHEC lambdoid phages are lysogenic under anaerobic conditions when Cro binds to and activates the promoters of T3SS genes. Interestingly, the Cro sequence varies among phages carried by different EHEC outbreak strains, and these changes affect Cro-dependent T3SS regulation. Additionally, infecting mice with the related pathogen C. rodentium harboring the bacteriophage cro from EHEC results in greater T3SS gene expression and enhanced virulence. Collectively, these findings reveal the role of phages in impacting EHEC virulence and their potential to affect outbreak strains.
Asunto(s)
Colifagos/metabolismo , Escherichia coli Enterohemorrágica/efectos de los fármacos , Escherichia coli Enterohemorrágica/genética , Regulación Bacteriana de la Expresión Génica/efectos de los fármacos , Proteínas Represoras/farmacología , Proteínas Reguladoras y Accesorias Virales/farmacología , Factores de Virulencia/genética , Animales , Cromosomas Bacterianos/efectos de los fármacos , Citrobacter rodentium/patogenicidad , Colifagos/genética , Modelos Animales de Enfermedad , Infecciones por Enterobacteriaceae/metabolismo , Infecciones por Enterobacteriaceae/patología , Escherichia coli Enterohemorrágica/patogenicidad , Escherichia coli Enterohemorrágica/virología , Escherichia coli/genética , Infecciones por Escherichia coli/microbiología , Proteínas de Escherichia coli/genética , Genes Bacterianos/efectos de los fármacos , Células HeLa , Humanos , Lípidos , Lisogenia , Ratones , Ratones Endogámicos C3H , Proteínas Represoras/genética , Toxina Shiga/genética , Factores de Transcripción , Sistemas de Secreción Tipo III/efectos de los fármacos , Sistemas de Secreción Tipo III/genética , Sistemas de Secreción Tipo III/metabolismo , Ensayo de Placa Viral , Proteínas Reguladoras y Accesorias Virales/genética , Virulencia/efectos de los fármacos , Virulencia/genéticaRESUMEN
Pathogenic gut bacteria, such as those comprising the Enterobacteriaceae family, have evolved sophisticated virulence mechanisms, including nutrient and chemical sensing, to escape host defense strategies and produce disease. In this review we describe the mechanisms utilized by the enteric pathogen enterohemorrhagic Escherichia coli (EHEC) O157:H7 to achieve successful colonization of its mammalian host.
Asunto(s)
Infecciones por Escherichia coli/inmunología , Infecciones por Escherichia coli/microbiología , Escherichia coli O157/fisiología , Interacciones Huésped-Patógeno , Compuestos Orgánicos/metabolismo , Transducción de Señal , Factores de Virulencia/biosíntesis , Adhesión Bacteriana , Escherichia coli O157/metabolismo , HumanosRESUMEN
The present study determined the effect of Clostridium perfringens isolates taken from necrotic enteritis (NE) outbreaks on organic farms in a NE virulence testing model. Thirteen strains were isolated in the course of the study. Six C. perfringens field isolates were taken from a naturally occurring NE outbreak on an organic farm. Polymerase chain reaction toxinotyping was used to establish C. perfringens strains, as well as to create a toxin profile. All field isolates were found to be type A and positive for alpha, beta-2 and netB toxin genes. During the NE virulence model, digesta samples were collected before oral inoculation to define the C. perfringens found as part of the natural flora. Three of the five natural flora isolates were found to be C. perfringens type E while the other two isolates were type A; only four of five isolates were positive for either netB or beta-2 toxin genes. Two isolates collected after inoculation were C. perfringens type A positive for cpb2 and netB. All isolates were tested positive for the quorum-sensing-related gene luxS, regardless of the strain source. The presence of luxS, alpha, netB and beta-2 toxin genes seems not to be a determinant of the disease as they were present in isolates from both outbreak birds as well as healthy and pre-inoculated birds. The C. perfringens field isolates induced mild NE lesions in one-half of the birds during the challenge study. Other mechanisms must play a role in the development of the disease beyond toxinotype, potentially including intestinal ecology and health, which would account for acute disease as seen in the field outbreak.