Avian colibacillosis is caused by a group of pathogens designated avian pathogenic Escherichia coli (APEe).
Despite being known for over a century, avian colibacillosis remains one of the majar endemic diseases
affiicting the poultry industry worldwide. Autologous bacterins provide limited serotype-specific protection,
yet multiple serogroups are associated with disease, especially 01, 02 and 078 among many others.
Experimental infection models have facilitated the identification of some key APEC virulence gene s and
have allowed testing ofvaccine candidates. Well-recognized virulence factors indude Type 1 (FI) and P (Pap/
Prs) fimbriae for colonization, IbeA for invasion, iron acquisition systems, TraT and Iss for serum survival,
K and O antigens for anti-phagocytic activity, and a temperature-sensitive haemagglutinin of imprecise
function. Intriguingly, these factors do not occur universally among APEC, suggesting the presence of
multiple alternative mechanisms mediating pathogenicity. The recent availability of the first complete APEC
genome sequence can be expected to accelerate the identification of bacterial genes expressed during
infection and required for virulence. High-throughput molecular approaches like signature-tagged
transposon mutagenesis have already proved invaluable in revealing portfolios of gene s expressed by
pathogenic bacteria during infection, and this has enabled identification of APEC 02 factors required for
septicaemia in the chicken model. Complimentary approaches, such as in vivo-induced antigen technology,
exist to define the activities of APEC in vivo. In recent years, reverse vaccinology and immuno-proteomic
approaches have also enabled identification of novel vaccine candidates in other bacterial pathogens.
Collectively, such information provides the basis for the development or improvement of strategies to control
APEC infections in the food-producing avian species.