Immunity against Coccidiosis

The basic principles

Mobile sporozoites and merozoites have many and complex antigenic structures and try to attach to and subsequently invade the host cell (mucosal/epithelial lining). Sporozoites and merozoites, interacting with the host cell (attachment, invasion, development) are the critical immunogenic stages of the coccidiosis cycle. Coccidiosis immunity is present as soon as sporozoites or merozoites are unable to initiate their intracellular development.

The immune response in the avian species against any infectious agent consists of a complex interaction of thymus(T)-derived cell-mediated immunity (CMI) and bursa(B)-derived humoral immunity (immunoglobulins, antibody responses). The ability of chickens and turkeys to resist a coccidiosis re-infection (=immunity) is governed amost exclusively by CMI. Antibodies, as a protective component, play a very minor role (only some local immunoglobulin A [IgA] in the intestine)!

Important functional tissue that deals with coccidiosis immunity is located in the intestine and is called GALT (gut-associated lymphoid tissue). GALT are scattered aggregates of immune competent cells along the mucosal lining and in the lamina propria. The major cell types involved in the immune response and the coccidiosis associated CMI are (a) macrophages, (b) natural killer (NK) cell lymphocytes and (c) two types of T-derived lymphocyte populations, i.e., CD4+ (=T4) T cells and CD8+ (=T8) T cells. (CD = “cluster determinant”.)

Macrophages and CD4+ lymphocytes dominate the CMI reaction upon primary contact/infection. Also, NK cell activity is high during the early stages of a coccidiosis infection. CD8+ cells multiply particulary upon second contact (re-infection), i.e., at the time immunity becomes effective!

CD4+ and CD8+ cells are cytotoxic and cytolytic (e.g., interleukines, interferon g), this means they can kill and lyse parasitic stages during the coccidiosis cycle. CD4+ and CD8+ cells are the critical immune T cell populations involved in the coccidiosis CMI immune response.

There exists no cross-protection between the different Eimeria species. Different Eimeria species also differ by “immunogenicity” (= number of oocysts required to induce rapid and solid protection). E. maxima is the most immunogenic species (few oocysts required for a good immune response) and E. tenella and E. necatrix are the poorer ones. Other Eimeria species lie between both extremes.

Under practice conditions several coccidiosis cycles are necessary before full protective immunity to coccidiosis is acquired: a process that takes time, i.e., for a “natural” infection 4 weeks (partial protection) to 7 weeks (complete protection). For broilers this is almost an entire life cycle! Several factors (e.g., type of in-feed coccidiostat [mode of action], bird density, litter conditions, ...etc) affect the strength and the onset of the coccidiosis immune response. All those factors pertain to “coccidiosis infection pressure”, i.e., the magnitude (many or few oocysts ingested), timing (early or delayed infection) and intensity/frequency (slow or rapid re-cycling) of exposure to the parasite.

The immunity and the damage/disease provoked by a coccidiosis infection are proportionally related:

“severest infection pressure“

=

“severest infection”

=

 “severest damage and disease”

=

 “strongest immunity”