The immune system is able to confer immunity by two steps: the 1st step is the innate (unspecific) immune response and the 2nd step is the adaptive (specific) immune response (Dougan et al, 2011).

The 1st innate and unspecific response is based upon several conditioning factors such as: the genetic predisposition and the defence mechanisms (physical, microbiological, chemical and cellular defence) which are based upon:

  • Genetic predisposition: some species of birds may lack the receptors required by certain infecting serovars.
  • Physical defence: skin, mucous membranes, cilia, bile salts, other secretions and peristalsis (coughing, vomiting, diarrhea).
  • Microbiological defence: dense and stable gut microflora population prevents invading disease organisms. Improper use of antibiotics or poor sanitation can disrupt the balance of the microflora.
  • Chemical defence: Low pH, cell destroying enzymes, complement system (cell communication).
  • Cellular defence: intraepithelial Phagocytes (macrophages, dendritic cells, granulocytes) and leucocytes involved in inflammatory response.

The 2nd adaptive and specific response consists of humoral immunity (based upon the action of the B-cells) and cell-mediated immunity (based upon the action of cytotoxic T-cells, also known as T-lymphocytes and other leucocytes such as CD4; CD8, NK cell-digesting). 

Considering the above, the innate immune response and recognition of the agent are crucial to activate the adaptive immune response, through induction of antigen presentation and the activation of all the co-stimulatory mechanisms (Dougan et al, 2011).

After field infection, the immune response against Salmonella depends on the host and serovar involved. The pathogenesis of Salmonella infection starts with the uptake of the bacteria, followed by intestinal colonization (ileum, caeca) and the invasion of the mucosa:

  • Within the gut, Salmonella attaches itself to the cells of the epithelium. It is known that the fimbriae and the “Salmonella pathogenicity islands” SPI-1 and SPI-2 play essential roles.
  • Salmonella enters the organism either via M-cells of the Peyer`s plaques, by invading the enterocytes or by para-cellular transportation. It has been found that the enterocytes could also behave as antigen-presenting cells.
  • Studies have shown that Salmonella Enteritidis can be detected in the Lamina Propria as early as 12 hours after infection (Methner et al 2007).
  • Those infective Salmonella that are able to survive within the macrophages after endocytosis, multiply within the macrophages (Salmonella Pathogenicity Island 2 is essential for this intracellular survival). Surviving Salmonella can be transported by wandering macrophages to any place within the body of the chicken and can reach deeper layers of the tissue after being released from the macrophages. In this manner, infected birds can become life-long carriers that transiently shed Salmonella.

After vaccination with live, attenuated vaccines the immune system develops two types of response: the cellular immunity and the local immune response (sIgA) against Salmonella infections. Live Salmonella vaccines are not injected into the birds, but applied via the drinking water. The application is easy and safe, and parallels the natural path of infection. Following oral uptake, the live vaccine enters the body through the intestinal wall for a short period.Those infective Salmonella that are able to survive within the macrophages after endocytosis, multiply within the macrophages (Salmonella Pathogenicity Island 2 is essential for this intracellular survival). Surviving Salmonella can be transported by wandering macrophages to any place within the body of the chicken and can reach deeper layers of the tissue after being released from the macrophages. In this manner, infected birds can become life-long carriers that transiently shed Salmonella (Korver, 2006).

After vaccination with an inactivated vaccine by subcutaneous or intramuscular injection, there is a primary humoral immune response of IgM (7 to 14 days post vaccination) followed by production of IgG, better known as IgY in poultry. There is a gradual rise in antibody production taking days to weeks (IgY). Once the plateau has been reached, antibody level declines. Without continued antigenic challenge, antibody levels drop below protective levels. There must be a second exposure to the same antigen to obtain a booster effect. The immunological “memory” cells then produce high and homogeneous long-lasting IgY serological titres that are transmitted to egg and progeny. The second administration of an inactivated vaccine, at least 4 weeks post initial vaccination, results in immediate production of protective antibodies, mainly IgY, but there may also be some IgM. IgM is the first immunoglobulin to be produced and IgY is the most abundant antibody found intravascularly and extravascularly. IgY is stored in egg yolks and yolk sacs and provides certain levels of humoral immunity to chicks during the first weeks of life (Jantsch et al, 2011).

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