Using T cell lymphokines of hyperimmunized chickens with Salmonella pullorum to protect layer hens against Salmonella pullorum infection

Abstract EN

Salmonella pullorum (SP) is well adapted to cause an acute systemic infection in hens with a high mortality rate.

This study aimed to assess the efficacy and safety of a salmonella-immune lymphokine (SILK) produced by hyperimmunized pullets with Salmonella pullorum during the layer hens' production stage to boost their immune response against Salmonella pullorum infection.

In this study, two groups of 25 pullets were used to produce lymphokines; the first group received three doses of the Salmonella pullorum vaccine at 12, 14, and 16 weeks, while the second group only received phosphate buffer saline (PBS), which served as the control.

At 18 weeks, non immune lymphokines (NILK) were isolated from the T cells of the second group, and salmonella-immune lymphokines (SILK) were isolated from the T cells of the first group.

Then, 100-layer hens (ISSA Brown), at 30 weeks old, which entered the production stage, were separated into four groups, each with 25 chickens.

Gl : infected with SP and treated with SILK.

G2 : infected with SP and treated with NILK.

G3 : untreated and SP-challenged G4 : no treatment or challenge.

The current study aimed to describe the host humoral immune responses to infection in serum samples and bacterial shedding in hens challenged with SP during 31-33 weeks by qPCR techniques.

Internal organ bacterial loads were estimated to evaluate the persistence of bacteria.

The results show that the spleen, liver, and caecal tonsils tested were positive for bacteria in both groups (G2, G3), proving that Salmonella was not eliminated from the birds and suggesting that internal organ colonization bacteria may act as a reservoir for ongoing bacterial shedding with low IgG titer in compared to Gl with extremely low persistence and high IgG titer in weeks 31, 32, and 33.

The current investigation shows that using SILK provides layer hens with better homogenous protection against SP and less internal organ persistence.