Abstract
The extraintestinal pathogen, avian pathogenic E. coli (APEC), known to cause systemic infections in chickens, is responsible for large economic losses in the poultry industry worldwide. In order to identify genes involved in the early essential stages of pathogenesis, namely adhesion and colonization, Signature-tagged mutagenesis (STM) was applied to a previously established lung colonization model of infection by generating and screening a total of 1,800 mutants of an APEC strain IMT5155 (O2:K1:H5; Sequence type complex 95). The study led to the identification of new genes of interest, including two adhesins, one of which coded for a novel APEC fimbrial adhesin (Yqi) not described for its role in APEC pathogenesis to date. Its gene product has been temporarily designated ExPEC Adhesin I (EA/I) until the adhesin-specific receptor is identified. Deletion of the ExPEC adhesin I gene resulted in reduced colonization ability by APEC strain IMT5155 both in vitro and in vivo. Furthermore, complementation of the adhesin gene restored its ability to colonize epithelial cells in vitro. The ExPEC adhesin I protein was successfully expressed in vitro. Electron microscopy of an afimbriate strain E. coli AAEC189 over-expressed with the putative EA/I gene cluster revealed short fimbrial-like appendages protruding out of the bacterial outer membrane. We observed that this adhesin coding gene yqi is prevalent among extraintestinal pathogenic E. coli (ExPEC) isolates, including APEC (54.4%), uropathogenic E. coli (UPEC) (65.9%) and newborn meningitic E. coli (NMEC) (60.0%), and absent in all of the 153 intestinal pathogenic E. coli strains tested, thereby validating the designation of the adhesin as ExPEC Adhesin I. In addition, prevalence of EA/I was most frequently associated with the B2 group of the EcoR classification and ST95 complex of the multi locus sequence typing (MLST) scheme, with evidence of a positive selection within this highly pathogenic complex. This is the first report of the newly identified and functionally characterized ExPEC adhesin I and its significant role during APEC infection in chickens.
Highlights
Research on avian pathogenic E. coli (APEC) has increased greatly over the years where the pathogen has been known to cause disease among chickens and other fowls which usually results in large economic losses for the poultry industry [1]
These pathogens have recently gained even more importance, being classified under the category of extraintestinal pathogenic E. coli (ExPEC), a group which includes both human pathogens like the uropathogenic E. coli (UPEC) and newborn meningitic E. coli (NMEC) and animal pathogens, which in turn suggest the possibility of APEC having zoonotic potential [3,4,5]
Colonization is crucial to pathogenesis of bacteria, being the earliest stage during onset of the disease and the ability to adhere to host surfaces is by far the most vital step in the successful colonization by microbial pathogens [7,8]
Summary
Research on avian pathogenic E. coli (APEC) has increased greatly over the years where the pathogen has been known to cause disease among chickens and other fowls which usually results in large economic losses for the poultry industry [1]. Some of the well known fimbriae present among ExPEC strains are Type I fimbriae (fim), P fimbriae or the pilus associated with pyelonephritis (pap), curli fibre (csg), S fimbriae or the sialic acid-specific fimbriae (sfa), F1C fimbriae (foc), afimbrial adhesin/ Dr antigen-specific adhesin (afa/dra), heat-resistant agglutinin (hra) and others [4]. Each of these adhesins recognizes a specific receptor as a group they share common genomic organization, assembly and even quaternary structural traits [10]
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