| Urinary tract infections (UTIs) are among the most common human diseases, causing significant morbidity and seldom mortality. Most community-acquired UTIs are due to uropathogenic Escherichia coli (UPEC) infections. Colibacillosis refers to any localized or systemic infection caused entirely or partly by avian pathogenic Escherichia coli (APEC), including septicaemia, granuloma (Hjarre's disease), air sac disease, chronic respiratory disease (CRD), avian cellulitis, swollen head syndrome, peritonitis, salpingitis, osteomyelitis/synovitis, panophthalmitis, and omphalitis/yolk sac infection.With a wide range of pathogenic potential, APEC and UPEC can both cause extra-intestinal infection. Based on this wide range of pathogenic potential, UPEC and APEC are classified with a new pathogenic Escherichia coli——extraintestinal pathogenic Escherichia coli (ExPEC). The extra-intestinal infection of APEC and UPEC may be concerned with virulence characteristics, such as adhesins, iron-related, protectins, toxins and so on. Many studies have shown that APEC and UPEC share a similar content of virulence genes.Since APEC and UPEC may encounter similar challenges when establishing infection in extra-intestinal locations, they may share a similar content of virulence genes and capacity to cause disease. It is becoming more and more apparent that the common presence of a set of virulence associated genes among APEC and UPEC strains as well as similar disease patterns and phylogenetic background indicate a genetic relationship between APEC and UPEC isolates. The potential whether APEC might serve as a reservoir of virulence genes for UPEC should be considered. One APEC isolate E516 and one UPEC isolate U56 both belonging to 01 serotype were compared by their phylogenetic type, content of virulence genes and pathogenicity in chicks. Enterohemorrhagic Escherichia coli (EHEC) 933 and K-12 were used as controls. The competitive growth between E516 and U56 in vivo and in vitro was also compared. The results showed that these two strains both belonged to B2 phylogenetic type and shared a similar content of virulence genes. Study of the pathogenicity of UPEC U56 in chicks showed the similar symptoms and lesions compared to those caused by APEC E516. The results of competitive growth in vivo and in vitro showed that the competitiveness of UPEC U56 was lower than that of APEC E516, which may be related to the potential virulence genes of unknown existed in APEC E516. Based on these results, the potential that APEC might serve as a reservoir of virulence genes for UPEC should be considered.To relatively quantify the expression of ompT and feoB genes of APEC strain E516 and UPEC strain U56, two-step real time quantitative RT-PCRs (qRT-PCR) were developed based on SYBR GreenⅠ, respectively. EHEC 933 and K-12 were used as controls. ompT and feoB were as target genes and gapA as internal reference, respectively. Three standard curves were established using a series dilution of cDNA synthesized from the RNA of APEC E516 grown to exponential phase in rich medium. In chicken and mouse challenge model, the expression of ompT in APEC E516 were up-regulated at a 3.73- and 1.45-fold compared to that of APEC E516 grown to exponential phase in rich medium, respectively. The expression of feoB in APEC E516 were up-regulated at a 1.30-fold in chicken model but down-regulated at a 0.84-fold in mouse challenge model. The expression of ompT in UPEC U56 were up-regulated at a 1.52- and 2.57-fold in chicken and mouse challenge model and the expression of feoB in UPEC U56 were up-regulated at a 2.15-and 1.37-fold. As control, the expression of ompT and feoB in EHEC933 and K-12 was both down-regulated in chicken and mouse challenge model. The results showed that the expression of ompT and feoB in APEC E516 and UPEC U56 were similar, which suggested that ompT and feoB may be the important virulence genes of APEC and UPEC. |
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