ibeA, a virulence factor of avian pathogenic Escherichia coli

Abstract

The presence of ibeA, a gene encoding a known virulence factor of Escherichia coli strains responsible for neonatal meningitis in humans, was investigated in the genome of 213 avian pathogenic E. coli (APEC) strains and 55 non-pathogenic E. coli strains of avian origin. Fifty-three strains were found to be ibeA + , all of which belonged to the APEC group. The ibeA gene is therefore positively linked to the pathogenicity of strains (P<0?0001). Analysis of the serogroup of strains revealed a positive association of ibeA with serogroups O18, O88 and O2. On the contrary, only 1/59 O78 strains are ibeA + , indicating a negative association of ibeA with this serogroup (P<0?0001). The role of ibeA in the virulence of the APEC strain BEN 2908 was investigated by constructing an ibeA mutant. Challenge assays on 3-week-old chickens showed a reduced virulence for the ibeA mutant. Furthermore, the APEC strain BEN 2908 was able to invade brain microvascular epithelial cells, this invasion being significantly reduced upon inactivation of ibeA. Altogether, these results suggest a role of ibeA in the pathogenicity of some APEC strains and confirm the close relationship between APEC and other human extraintestinal pathogenic E. coli isolates.

Distribution of serotypes and virulence-associated genes in pathogenicEscherichia coliisolated from ducks

“…Sixteen O-serogroups, including O79, O117, O20, O51, O18, O61, O88, O154, O22, O78, O21, O137, O9, O142, O93 and O92, were found to be ibeA ' in this study. Germon et al (2005) reported a negative association of ibeA with O78 serotype (1/59); however, our result revealed that 5/28 O78 strains were ibeA ' . The difference in distribution frequency suggested that more APEC isolates from different geographical regions and hosts were needed to deduce the relationship between ibeA ' and certain serogroups.…”

“…In the present investigation, 10.6% of 254 APEC isolates were detected ibeA gene-positive (ibeA ' ), but none were found in isolates from healthy ducks (P B0.0001). The prevalence of ibeA in APEC isolates in this study was lower than that in APEC strains isolated from chickens with septicaemia (Germon et al, 2005), and greater frequencies of 33 to 40% were found in E. coli isolates associated with neonatal meningitis-causing E. coli (Johnson et al, 2001;Ewers et al, 2007). Our result indicated that the ibeA gene distributed in APEC strains from ducks linked to the pathogenic group.…”

“…A variety of virulence factors has been investigated to understand these extraintestinal diseases in avian species, including adhesins (F1-fimbriae, P-fimbriae, and F17-fimbriae, curli fibres, and afimbrial adhesins), haemolysins (haemolysin A/E and a temperature-sensitive haemagglutinin), iron-acquisition systems (aerobactin and yersiniabactin), antibactericidal factors (invasion of brain endothelium protein A, outer membrane protein A, protein for increased serum survival), and toxins (Shiga toxin 1 and 2, heat stable toxin, and flagella toxin) (Hacker et al, 1983;Louie et al, 1994;Kaper et al, 1997;Ludwig et al, 1999;Nagy et al, 2002;Parreira & Gyles, 2002;Ewers et al, 2004;Schubert et al, 2004;Germon et al, 2005;Beloin et al, 2006;Capitani et al, 2006;Belogurov et al, 2009). According to recent studies, many virulence genes associated with APEC are located on large plasmids, the importance of those large plasmids has been demonstrated by the plasmid-encoded genes shared among APEC strains (Dozois et al, 2003;Johnson et al, 2008;Tivendale et al, 2009).…”

“…Knowledge about epidemiology of APEC was obtained primarily from chickens (Parreira & Gyles, 2002;Ewers et al, 2004;Germon et al, 2005;McPeake et al, 2005). Little is known on the distribution of virulenceassociated genes and the O-serotypes of APEC isolates from ducks.…”

Sequencing and Functional Annotation of Avian Pathogenic Escherichia coli Serogroup O78 Strains Reveal the Evolution of E. coli Lineages Pathogenic for Poultry via Distinct Mechanisms

“…A number of other virulence factors have been identified by using defined mutants in poultry models, including the autotransported proteins AatA (22), Tsh (23,24), and Vat (25), fimbrial gene clusters pap (26), fim (27,28), stg (29), and csg (28), a degenerate inv/mxi-spa-like type III secretion locus termed ETT2 (30), and factors mediating iron uptake (31)(32)(33) and phosphate transport (34). Flagellin contributes to persistence and invasion after oral dosing of chicks with APEC O78 (28), and ExPEC invasins (Ibe proteins) also facilitate APEC invasion (35,36). Indirect effects on the expression of virulence-associated fimbriae have been reported for mutants with a constitutively activated pho regulon (37) and those lacking the pst system (38), ibeA, ibeB, and ibeT (36,39), the barA-uvrY-encoded two-component sensory system (40), and a type VI protein secretion system (41).…”