Immunity in birds: general concepts
The immune system of the birds consists of two primary lymphoid organs, the thymus and the bursa of Fabricius (BF), but also of many secondary lymphoid organs or structures, which include bone-marrow, spleen, Harderian gland, Peyer's patches, Meckel diverticulum, caecal tonsils and other lymphoid aggregates distributed in the body (birds lack the equivalent of mammalian lymph nodes).
In the primary organs , which develop during the embryo stage, a differentiation of the germinal immune cells into two types of lymphocytes takes place, T-cells in the thymus and B-cells in the BF. These cells produce a specific immune response against antigen which are extraneous to the organism. In the secondary structures, besides
lymphocyte storage areas, there are the differentiation sites for other immune cells, such as monocytes and macrophage s, granulocytes, killer (K) and natural killer (NK) cells, which are produced in the bone-marrow and generally play a non-specific role in immunity. B-lymphocytes, after transformation into plasmocytes, are responsible for immunoglobulin or antibody production, in response to antigen stimulation.
T-lymphocytes are responsible for cell-mediated immunity and for regulation of the immune system reactions, including the activation of B-cells.
M acropha ges (derived from circulating monocytes), granuloytes, NK and K cells are involved non-specifically in immune reactions by phagocytosis or by cytotoxicity. Macrophages are also important in antigen processing and presenting cell to T and B lymphocytes. lmmunoglobulins (lg) or antibodies are glycoprotein molecules, able to react specifically, both in vivo and in vitro, with the antigens which originally induced their production.
In birds, three main classes of lg have been reported:
lgM, which appear very soon, 2-4 days after the initial immune stimulation, reaching their peak concentration at the 9th day; they represent the first immune barrier to infection; lgG (or, better, lgY, showing some structural differences to mammalian lgG), which are the main lg in the serum (70-80%) and the main effectors of humoral immunity; they are the only antibodies able to transfer to the yolk-sac and provide systemic immunity to the newborn chick; lgAS, which are the lg present in mucosal secretions and in biological fluids, as bile and responsible for mucosal immunity; the existence of lgD and lgE, as in mammals, is very likely, but little is known on this matter.
Humoral immunity is subdivided into active and passive.
Active immunity is triggered by contact with the antigen, pathogen or vaccine and is characterized , after a variable latent period (3 to 10 days), by an initial rapid short increase in lgM, followed by a slower increase in lgG and lgA, which persists longer (primary response). Subsequent contact with the same pathogen or antigen induces a higher, more rapid and long-lasting production of specific lgG and lgA (secondary response). The rapidity of the secondary response is due to the presence of "memory lymphocytes", produced during the primary response; for this reason it is also named the "anamnestic" response. Repeated vaccinations (hyperimmunization or booster effect) enable the attainment of high specific antibody levels. Passive immunity is provided almost exclusively by lgG, transferred from the blood stream to the ovary and then transmitted to the chicks via the yolk-sac; the level of antibodies in the yolk sac generally
Correlates with the mother's antibody level.
Du ring passage of the egg through the oviduct, the albumen acquires rather low levels of lgM and lgA, which pass through the amniotic fluid to the gut, providing temporary protection to the mucosa. The level of maternal antibodies i n the progeny normally decreases in about 15-20 days; the rate of decrease is partly linked to the
degree of growth of the chick.
The protection provided by passive antibodies varies, depending on the disease: for example, it is strong against infectious anaemia , encephalomyelitis, infectious bursa! disease, fairly effective against Newcastle disease and poor against mucosa! diseases, such as infectious bronchitis and laryngotracheitis and against Marek's disease.
Cell-mediated immunity (CMI) is controlled by T-lymphocytes, which do not produce antibodies, but operate destroying the “target” directly or indirectly, inducing other accessory cells to destroy it by intermediation of soluble factors, the interleukines. T-lyphocytes are divided into three subpopulation: T-Helper , T-suppressor and
T-cytotoxic cells, beside memory cell-:
T-helper cells have regulatory activity, modulating the immune
response and intervening in the cooperation between cell-mediated and humoral immunity;
T-suppressor cells have regulatory activity, limiting the antibody
Response, when this tends to become excessive;
T-cytotoxic cells have effector activity, attacking and destroying infected or altered target cells. CMI is of primary importance in immune defences against microorganisms with intracellular parasitism (viruses, some bacteria, protozoans, etc.). In general, while humoral immunity can be measured quite easily by checking in vitro the level of antibodies in the serum, it is more difficult or complex, in a routine check, to evaluate the degree of mucosa! and CML Moreover, the degree of protection provided by a vaccine cannot be always strictly correlated to the level of antibodies in the serum.
Live attenuated vaccines are prepared with:
- naturally apathogenic microorgan isms ( turkey herpesvirus, N ewcastle disease virus strains N DV 6/ 10 or Hitchner B l);
- microorganisms, whose pathogenicity has been artificially reduced
or removed by serial passages through an appropriate substratum, such as embryonated egg or tissue-cultures (infectious bronchitis virus, infectious bursa! disease virus and many other vaccinal viruses);
- other techniques, for the moment mainly experimental (deletion, expression of antigen in live apathogenic vectors).
The artificial attenuation of microorganisms is sometimes unstable
and, after some back-passages in the natural host, it may be reduced (laryngotracheitis , infectious bursa! disease, infectious bronchitis viruses, etc.). Attenuated vaccines are normally administered to birds by the natural route, like the pathogenic microorganisms, but they induce very low or no symptoms of disease.
The common route of administration in the field is by drinking water or spray or, individually, by eye or nasal-drop administration or wing-web injection. Protection due to the vaccination is often provided quite quickly after administration (local immunity system),
Although antibodies appear in the serum only after 10-15 days. For some diseases, just one vaccination at a variable age, depending on the vaccine, is sufficient to protect birds for a long time ( Marek's disease, fowl pox, laryngotracheitis, encephalomyelitis, infectious anaemia) or for the period when they are susceptible (infectious bursal disease).
For other diseases, revaccinations or boosters are required to strengthen the protection (Newcastle disease, infectious bronchitis, etc.). For some pathogens, the birds are susceptible only up to 2-3 weeks of age and it is sufficient to vaccinate parent mens before going into lay (infectious anaemia, encephalomyelitis) to protect the young progeny. Live vaccines may present
some risk of contamination with foreign agents present in the substrate (leukosis, infectious anaemia, etc.), or accidentally introduced during their processing (or manufacturing). In any event, the use of eggs from well-controlled SPF flocks and the adoption of severe purity controls, firstly of master seeds, but also of each batch of vaccine, are essential. Some live vaccines are also prepared with attenuated bacteria or protozoa ns (for instance, salmonellas, mycoplasmas and coccidia). Inactivated vaccines are prepared with microorganisms, or part of them, which have lost their virulence and ability to replicate and spread through the organism. However, their immunogenicity remains intact. Such vaccines are administered by individual injection, intramuscularly or subcutaneously.
They are often associated with adjuvants, which strengthen the
Immune. Reaction. The adjuvants mainly used are mineral oil (emulsion) or aluminium hydroxide. The strengthening of antibody production and, partially, of cell-mediated reactivity, is due to a gradual release of antigen (depot effect) and local irritation, with specific activation of lymphocytes. The immunity provided by inactivated vaccines is completely established in 3-4 weeks and, for some diseases, lasts longer than that produced by live vaccines. Inactivated vaccines are often administered, with a better booster effect, after a priming with live vaccines