Vaccination of breeder hens with a polyvalent killed vaccine for pathogenic Enterococcus cecorum does not protect offspring from enterococcal spondylitis. Issue 1 (2nd January 2019)

• Record Type: Journal Article
• Authors: Borst, Luke B.; Suyemoto, M. Mitsu; Chen, Laura R.; Barnes, H. John
• Is Part Of: Avian pathology. Volume 48:Issue 1(2019)
• Page Start: 17
• Page End: 24
• Publication Date: 2019-01-02
• Subjects: Enterococcus cecorum -- kinky-back -- vaccine -- broiler health -- lameness -- enterococcal spondylitis; Poultry -- Diseases -- Periodicals; Birds -- Diseases -- Periodicals; 571.918
• DOI: 10.1080/03079457.2018.1536819
• Languages: English
• ISSNs: 0307-9457

Abstract

ABSTRACT: Pathogenic strains of Enterococcus cecorum cause symmetrical paralysis in broilers due to infection of the free thoracic vertebra. The disease caused by pathogenic E. cecorum, known as enterococcal spondylitis or "kinky-back" continues to be responsible for significant losses to the broiler industry worldwide. In outbreaks of pathogenic E. cecorum, gut colonization and sepsis occur in the first three weeks-of-life. Since maternal antibodies are present during this period, we postulated that vaccination of breeders with a polyvalent killed vaccine would protect chicks from challenge. To test this hypothesis, representative isolates from seven genotype groups of pathogenic E. cecorum circulating in the US were chosen to produce adjuvanted killed vaccines (bacterins) and given to broiler-breeder hens. No single strain produced high titres of antibodies to all other strains; however, the combination of serologic reactivity of pathogenic isolates (designated SA3 and SA7) was sufficient to react with all genotypes. Vaccination of commercial broiler-breeder hens with a bacterin composed of SA3 and SA7 did not have any adverse effects. Vaccinated hens developed E. cecorum specific antibodies; however, no significant difference in survival was observed in infected embryos from hens in vaccine or adjuvant only groups. Chicks from vaccinated hens also failed to resist homologous or heterologous challenge during experimental infection. In a macrophage killing assay, pathogenic E. cecorum were found to evade opsinophagocytosis with elicited antibodies. These data suggest that pathogenic strains of E. cecorum possess virulence mechanisms that confound antibody-mediated opsinophagocytosis, complicating vaccine development for this pathogen of broilers.