Abstract
Avian pathogenic Escherichia coli (APEC) infections are a serious impediment to sustainable poultry production worldwide. Licensed vaccines are available, but the immunological basis of protection is ill-defined and a need exists to extend cross-serotype efficacy. Here, we analysed innate and adaptive responses induced by commercial vaccines in turkeys. Both a live-attenuated APEC O78 ΔaroA vaccine (Poulvac® E. coli) and a formalin-inactivated APEC O78 bacterin conferred significant protection against homologous intra-airsac challenge in a model of acute colibacillosis. Analysis of expression levels of signature cytokine mRNAs indicated that both vaccines induced a predominantly Th2 response in the spleen. Both vaccines resulted in increased levels of serum O78-specific IgY detected by ELISA and significant splenocyte recall responses to soluble APEC antigens at post-vaccination and post-challenge periods. Supplementing a non-adjuvanted inactivated vaccine with Th2-biasing (Titermax® Gold or aluminium hydroxide) or Th1-biasing (CASAC or CpG motifs) adjuvants, suggested that Th2-biasing adjuvants may give more protection. However, all adjuvants tested augmented humoral responses and protection relative to controls. Our data highlight the importance of both cell-mediated and antibody responses in APEC vaccine-mediated protection toward the control of a key avian endemic disease.
Highlights
Avian pathogenic Escherichia coli (APEC) cause colibacillosis, a complex of respiratory and systemic diseases that exert substantial welfare and economic costs on poultry producers worldwide
Licensed live-attenuated and formalin-inactivated vaccines based on APEC O78 are protective against homologous challenge in turkeys To evaluate the protective efficacy of existing vaccines and establish models in which the basis of protection can be dissected, turkeys were vaccinated using Poulvac® E. coli or an inactivated vaccine based on the parent strain of Poulvac® E. coli and compared to mock-vaccinated turkeys
We recently analysed innate and adaptive responses induced by primary APEC O78 infection and demonstrated an association of these with protection against homologous re-challenge [26]
Summary
Avian pathogenic Escherichia coli (APEC) cause colibacillosis, a complex of respiratory and systemic diseases that exert substantial welfare and economic costs on poultry producers worldwide. Losses are incurred through premature deaths, condemnation of carcasses at slaughter, reduced productivity and recurring costs associated with antibiotic prophylaxis and therapy. A major impediment to the design of effective vaccines is the remarkable diversity of E. coli associated with avian disease. Though serogroups O1, O2 and O78 and sequence types ST23 and ST95 are commonly observed, it is clear that E. coli has evolved to cause avian disease from diverse lineages via the acquisition of distinct virulence genes [3,4].
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