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The avian immune system

The avian immune system is
divided into non-specific and specific immune mechanisms.

Non-specific immune
mechanisms include the innate or inherent ways in which the chicken resists
disease. This protective system is often not considered when designing a
poultry health program. Many programs tend to rely primarily on vaccinations
and/or antibiotics to maintain flock health. The importance of non-specific
immune mechanisms should be realized. Examples include Genetic factors - birds
may not have complementary receptors to allow many disease organisms to infect
them. For example, some strains of chickens are genetically resistant to the
lymphoid leukosis virus.


Body temperature

: The high body temperature of the chicken precludes many diseases.
Blackleg disease of cattle is not a problem in poultry. If the body temperature
of the chicken is lowered, the disease may occur.


Anatomic features

: Many disease organisms cannot penetrate intact body coverings (skin
and mucous membranes) or are trapped in the mucus secretions. Some nutritional
deficiencies (biotin deficiency) or infectious diseases compromise the
integrity of the body coverings, allowing penetration of disease organisms.


Normal microflora

: The skin and gut normally maintain a dense stable microbial
population. This stable microflora prevents invading disease organisms from
gaining a foothold. Improper use of antibiotics or poor sanitation can disrupt
the balance of the microflora.


Respiratory tract cilia

: Parts of the respiratory system are lined with
cilia which remove disease organisms and debris. If the air in the poultry
house is of poor quality due to high levels of dust or ammonia, the ciliary
system may be overwhelmed and become ineffective.

Other factors involved in
innate resistance include nutrition, environment (avoid heat/cold stress), age
(young/old animals are more susceptible to disease), inflammatory processes,
metabolic factors, complement, and interferon.

The reason that good
management practices are important in maintaining poultry health is better understood
when the non-specific immune mechanisms are defined. For example: the overuse
of antibiotics or poor sanitation may lead to a disruption of the normal
microflora; poor nutrition may lead to deficiencies which allow disease
organisms to penetrate the protective body coverings; selection of disease
resistant strains of chickens may preclude or lessen the effects of certain
diseases; and others.

Specific immune mechanisms
(acquired system), on the other hand, are characterized by specificity,
heterogeneity, and memory. This system is divided into cellular and
non-cellular (humoral) components.

The non-celluar component
includes immunoglobulins (antibodies) and the cells which produce them.
Antibodies are specific (specificity) for the foreign material (antigen) to
which they attach. The antibody against Newcastle disease virus will attach
only to the Newcastle virus, not to the infectious bronchitis virus
(heterogeneity). There are three classes of antibodies that are produced in the
chicken after exposure to a disease organism: Ig M, Ig G, and Ig A. Ig M
appears after 4-5 days following exposure to a disease organism and then
disappears by 10-12 days. Ig G is detected after 5 days following exposure,
peaks at 3 to 3 1/2 weeks, and then slowly decreases. Ig G is the important
protective antibody in the chicken and is measured by most serological test
systems. Thus, if you are interested in determining antibody titer levels
following vaccination, you should collect sera after 3 to 3 1/2 weeks. If sera
is evaluated prior to this time, the antibody titer levels are still increasing
which makes interpretation of the vaccination program difficult. Ig A appears
after 5 days following exposure. This antibody is found primarily in the mucus
secretions of the eyes, gut, and respiratory tract and provides
"local" protection to these tissues.

The cells which produce
antibodies are called B-lymphocytes. These cells are produced in the embryonic
liver, yolk sac and bone marrow. The cells move to the bursa of Fabricius (BF)
after 15 days incubation through 10 weeks of age. The BF programs these cells
which then move to the blood, spleen, cecal tonsils, bone marrow, Harderian
gland, and thymus. Destruction of the BF at a young age by Gumboro disease or
Marek's disease prevents programming of B-cells. Thus, the chicken will not be
able to respond to diseases or vaccinations by producing antibodies.

When a disease organism
enters the body, it is engulfed by a phagocytic-type cell, the macrophage. The
macrophage transports the disease organism and exposes it to the B-lymphocytes.
The B-cells respond by producing antibodies after day 5 following exposure. The
lag period occurs because the B-cells must be programmed and undergo clonal
expansion to increase their numbers. If the chicken is exposed a second time to
the same disease, the response is quicker and a much higher level of antibody
production occurs (memory). This is the basis for vaccinating. Antibodies do
not have the capability to kill viruses or bacteria directly. Antibodies
perform their function by attaching to disease organisms and blocking their
receptors. The disease organisms are then prevented from attaching to their
target cell receptors in the chicken. For example, an infectious bronchitis
virus which has its receptors covered with antibodies will not be able to
attach to and penetrate its target cells, the cells lining the trachea. The
attached antibodies also immobilize the disease organism which facilitates
their destruction by macrophages.

The cellular component
includes all the cells that react with specificity to antigens, except those
associated with antibody production. The cells associated with this system, the
T-lymphocytes, begin as the same stem cells as the B-cells. However, the
T-lymphocytes are programmed in the thymus rather than the BF.

The T-lymphocytes include a
more heterogeneous population than the B-cells. Some T-cells act by producing
lymphokines (over 90 different ones have been identified); others directly
destroy disease organisms; some T-cells act to enhance the response of B-cells,
macrophages, or other T-cells (helpers); and others inhibit the activity of
these cells (suppressors). The cellular system was identified when it was shown
that chickens with damaged BF could still respond to and eliminate many disease
organisms.

A chicken may become immune
to a disease organism by producing antibodies itself or by obtaining antibodies
from another animal. When the chicken produces its own antibodies following
exposure to a foreign material, the process is called active immunity. This
occurs after the bird is exposed to a vaccine or a field disease challenge.
Active immunity is harmed by anything which damages the cellular or humoral
immune systems.

When the chick receives
pre-made antibodies from the hen through the egg, this is termed passive
immunity. These antibodies are not produced by the chick. Maternal antibodies
are present in the yolk, albumin, and fluids of the egg. If the hen has a high
antibody titer level to a disease, the chick should also be immune for several
weeks. However, since the immune system of the chick is not stimulated, there
will be no antibodies produced by the chick and no memory cells. The flock
manager must be aware of the maternal antibody levels in the chicks to schedule
vaccinations. If chickens are vaccinated when maternal antibody titer levels
are elevated, the vaccine may be buffered excessively resulting in a reduced
response. Conversely, if vaccinations are delayed and maternal titer levels are
low, a severe vaccine reaction may result.

In summary, the immune
system of the chicken is very helpful in preventing disease and helping to
insure maximum productive potential is realized. We must learn how to take
advantage of all parts of the system when designing health programs.

By Dr. Gary D. Butcher,
D.V.M., Ph.D. and Richard D. Miles, Ph.D., University of Florida IFAS Extension

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