Drs. Gullermo Tellez*, Akrum Hamdy** and Billy
A. Disease versus Health
<!--Recognition of Disease Etiology
<!--Recognition of Affected Systems
<!--Evaluation of Body Condition
<!--Bacterial vs. Viral vs. Fungal Pathogens
<!--Serotype vs. Pathotype
<!--The Immune Response
<!--Primary vs. Secondary Response
<!--Functions of Antibodies
<!--Cell Mediated Immunity
<!--Cells of the Immune System
<!--Sanitation and Bio-security
<!--Protection by Vaccination
<!--Importance of Vaccine (serotype) Selection
<!--Relationship of Vaccination to Infectious Dose
<!--Value of Multiple Vaccinations
<!--Hazard of Genetic Recombination
A. Marek's Disease
C. Epidemic Tremor
D. Vitamin E, Selenium and Thiamin deficiency
F. Fowl Cholera
A. Marek's Disease
B. Avian Leukosis Viruses
C. Reticuloendotheliosis (turkeys)
B. Infectious Causes of Malabsorption
C. Mycoplasma Infection
D. Tibial Dyschondroplasia
E. Viral Arthritis
F. Bacterial Arthritis and Turkey Osteomyelitis Complex
G. Chronic Fowl Cholera
A. Marek's Disease
B. Infectious Bursal Disease
C. Chick Anemia Virus
<!--Conditions involving the Eyes and Face
A. Fowl Pox
B. Infectious Coryza
C. Fowl Cholera
D. Infectious Bronchitis
<!--Limited to the Upper Respiratory Tract
A. Fowl Pox
B. Infectious Coryza
C. Fowl Cholera
D. Infectious Bronchitis
<!--Generalized Respiratory Conditions
A. Avian Influenza
B. Newcastle Disease
C. Avian Pneumovirus
E. Fowl Cholera
G. Avian Tuberculosis
A. Fowl Pox
B. Crop Mycosis
D. Gizzard/Proventricular Erosions/Dialation
B. Necrotic Enteritis
<!--Ceca and Large Intestine
A. Newcastle Disease
B. Avian Influenza
C. Fowl Cholera
A. Fowl Cholera
B. External Parasites
C. Wear on Feathers
D. Gangrenous Dermatitis
E. Cannibalism, Scratches and Scabs
F. Tumor Causing Diseases
For any discussion of disease, a solid knowledge of the physiologic homeostatic mechanisms which maintain health is required. Students using these notes are expected to have a general grasp of introductory biology, chemistry and avian physiology. Those lacking in these areas are encouraged to review old notes and course material for this course. For additional help, please contact the instructor(s).
Many people mistakenly equate the word "disease" with "infectious disease". Students in this course will quickly realize that this is far too narrow. Disease can be defined as an absence of health. Any factor or insult that removes the animal from the condition that we recognize as health, therefore, may cause disease. Many common diseases of poultry are caused by environmental problems, toxins, genetic factors, nutritional deficiencies and trauma, without the involvement, at least in the beginning, of infectious agents. As a sequela to diseases of toxic, nutritional, traumatic or other non-infectious causes, secondary infections may sometimes be observed. Thus, infectious pathogens are sometimes involved, secondarily, in diseases of non-infectious origin.
To begin to understand a particular disease problem, the first step is to ascertain the primary cause and nature of the disease. Obviously, merely treating the secondary infections is not the most appropriate means of dealing with non-infectious diseases. Nevertheless, this is sometimes where field servicepeople and diagnostic laboratories leave their recommendations for improving the health of poultry flocks. An improved understanding of the nutritional, toxic, environmental and traumatic causes of
disease, can lead to improved diagnosis and an improved level of performance by addressing the primary causes of certain diseases.
After determining that a disease problem is infectious in nature, the next step in the diagnostic process is to develop a preliminary diagnosis of the type of infectious agent involved. This is sometimes very difficult without laboratory support. Nevertheless, many times the astute field serviceperson or veterinarian will have a strong presumptive diagnosis in the field, later to be proven correct based on laboratory testing. The first step is to determine if the infectious agent involved is a virus, bacterium or fungus.
When we remember that many viruses cause disease by destroying cells during viral replication, it is easy to realize how viral diseases may look similar. Bacterial pathogens, on the other hand, have a more complex array of means to damage the host, often resulting in a larger variety of lesions produced. Bacteria can produce endotoxins (internal toxins released when primarily Gram negative bacteria lyse) or exotoxins (secreted by both Gram positive and negative bacteria). For common poultry diseases, these bacterial toxins are potent attractors of heterophils, the avian polymorphonuclear leukocyte serving as the first line of defense (phagocyte). Remembering that large numbers of heterophils are observed grossly as "pus", the presence of purulent exudates are often a strong clue that a bacterial pathogen is at work. Also, some of these toxins, primarily endotoxins, cause capillary fragility and rupture, leading to hemorrhage. These tiny hemorrhages, referred to as petechial hemorrhages, are often best observed against the relatively light background of fat tissue at necropsy. Most commonly, these hemorrhages will be observed in the abdominal fat pad or the pericardial fat.
Fortunately, there are only a few fungal pathogens of poultry, and the most common of these diseases (crop mycosis, aspergillosis) usually present with clinical signs and lesions that are peculiar to these diseases.
Viral-caused diseases often cause inflammation with an absence of large amounts of pus or systemic petechial hemorrhages. As virus replication causes cell death and tissue destruction, tissue erosions and ulcers are sometimes observed. Congestion of blood vessels without hemorrhage is often a lesion associated with viral pathogens. When combined with an absence of pus, viral-etiology is usually the best bet.
The student is advised to remember that these means of differentiation are guidelines and may be different for individual diseases and at different stages of disease.
Another way of reducing the number of potential etiologies one must consider for an observed disease problem is to determine the system(s) affected. As the classification (toxic, nutritional, infectious, etc.) of the disease problem has been established, the involved system(s) should be considered. Many diseases are relatively specific with regard to the system(s) primarily affected. For example, some nutritional diseases primarily affect bone strength (e.g. rickets, osteomalacia) and some affect skeletal muscle and brain function (e.g. hypovitaminosis E, selenium deficiency). Alternatively, some viral diseases primarily affect the respiratory tract (e.g. infectious bronchitis), others affect both the respiratory and gastrointestinal tract (e.g. avian influenza and Newcastle disease), while others cause most observable disease at the level of the intestinal tract alone (e.g. Hemorrhagic Enteritis of turkeys). Mental organization of diseases according to the system(s) affected is an excellent way to reduce the number of possible etiologies that must be considered (called differential diagnoses). Therefore, the following text on specific diseases are not only grouped by pathogen type, but also by system(s) affected.
Often the body condition of poultry is indicative of the chronicity (duration) of a particular disease problem and, obviously, this characteristic is of paramount importance when considering affects on production efficiency. Broilers and turkeys have "normal" breast muscles forming a pronounced convex curvature when evaluated from the keel to the ribs laterally. Leghorns (egg-type chickens) normally have a breast forming more of a straight line from the ventral aspect of the keel to the ribs. In broilers and turkeys, loss of this normal convexity of the breast in broilers and turkeys is suggestive that the animal has begun using muscle tissue for energy purposes and is thus starving (remember, starvation can occur even with the presence of feed). Similarly, the development of a concavity of the breast muscle (from the ventral aspect of the keel laterally to the ribs) is strongly suggestive of early starvation in egg-type chickens.
The amount of body fat is also a very useful indicator of the severity and duration of starvation. Usually, with recognizable changes in pectoral muscles there is a pronounced reduction of subcutaneous and abdominal fat. As starvation continues, the last area of fat to disappear is that associated with the heart (pericardial fat) in poultry. When an absence of fat tissue is noticed on the heart, the starvation condition is severe.
Bacteria are ubiquitous (found almost everywhere) in the world and there are literally thousands of bacterial species that have been characterized. Most bacteria in the world are not capable of causing disease in poultry; others only cause disease when an opportunity (e.g. immune suppression, concurrent disease, wounds) allows them to infect the bird. A third group of bacteria are primary pathogens and propagate mostly or solely in the host bird. These bacteria are known as obligate bacterial pathogens and generally constitute the most virulent pathogens of poultry.
Bacteria differ from viruses in that they usually contain all of the required machinery for self replication. Thus, these organisms are able to replicate outside living host cells given the proper environment. Nevertheless, for the obligate bacterial pathogens, the proper environmental conditions may not normally exist outside a living host or a diagnostic laboratory.
Many of the bacterial pathogens of poultry produce toxins, either endotoxins (e.g. numerous Gram negative bacteria such as Salmonella), exotoxins (such as Staphylococcus) or both. These toxins sometimes result in leakage from capillaries and other blood vessels resulting in hemorrhage. Very small points of hemorrhage, known as petechial hemorrhage, are often indicative of bacterial septicemia (or bacteremia). These organisms, partly through the release of these toxins, are particularly effective in attracting heterophil infiltration of infected areas. Large numbers of heterophils are visualized grossly by the presence of pus. Accumulation of pus (i.e. purulent lesions) are another gross lesion suggestive of bacterial infections.
Bacterial infections are identified (diagnosed) in the laboratory based on observation of the characteristics of the organism. The type of cell wall (Gram negative or Gram positive), the morphology (shape and size) of the organism sometimes give important clues as to the identity of the pathogen. The requirements for growth (medium type supporting growth), colony morphology and biochemical reactions produced by the isolated bacterium are all used in the laboratory to "fingerprint" the identity of the pathogen.
Recognition of bacterial disease in poultry production is important because bacterial pathogens are the only diseases that can potentially be treated with available drugs (antibiotics).
Viral pathogens differ from bacterial pathogens in a number of ways. Viruses are much more simple and do not contain the necessary cellular machinery to self replicate in the absence of a host cell, regardless of the complexity of the local environment. This is because the virus actually "borrows" the components of the host cell and "instructs" the host cell to begin manufacturing more virus. Because the virus is not able to replicate outside the host cell, some have argued that viruses are not actually living organisms. Regardless, these pathogens are clearly able to replicate as long as a suitable susceptable host is present and infected.
Animal viruses are generally classified by the type of nucleic acid (RNA or DNA), the presence and structure of the capsid, presence and absence of a protective envelope and the actual size and shape of the particle.
In poultry medicine, the identity of the virus is often determined by identifying the specific proteins that are present on the surface. Some of these specific proteins, known as antigens, are highly specific for a given virus pathogen. Since antibodies (produced by vertebrate B-cells) are capable of recognizing highly specific proteins that are foreign to the host, antibodies can be used to determine the presence or absence of specific antigens. For example, a specific antibody preparation, obtained from an animal that has become immune to a single virus, can be labeled with a marker molecule such as fluorescein. When the labeled antibody is incubated with cells from a bird infected with that particular virus, the antibody binds to those antigens, resulting in fluorescent spots on the cell when observed under a special microscope using ultraviolet light (this technique is known as fluorescent antibody-, or FA- testing). Other techniques use specific antibodies to neutralize the virus, disableing the virus from infecting new cells in the laboratory (known as virus neutralization testing). Thus, known antibodies, created in the host animal for the purpose of creating immunity, can be used in the laboratory as a powerful diagnostic tool.
The virus type can be further sub-typed based on the specific serotype of the pathogen. Each distinct protein (usually a 5-8 amino acid sequence) that is recognizable by a specific antibody molecule is known as an epitope. The specific epitopes present can be determined as described above using highly specific antibodies (produced by immunizing an animal with just that chemically purified epitope). In this way, the specific epitopes present can be determined which accounts for the serotype of the virus.
Please note that serotyping, performed in a similar manner, is also used for bacterial pathogens. The serotype is important for appropriate vaccine selection and for tracking the spread of a virus in a given geographical region (called epidemiology).
While it is important to know the serotype for vaccine selection and for epidemiological investigations, the serotype does not necessarily infer the virulence of the specific pathogen. The degree of virulence, known as the pathotype, must be infered from clinical findings or determination of ability to cause disease in experimental animals or embryos.
It is important to remember that, at the present time, there are no approved, effective or affordable chemotherapeutic drugs available for commercial poultry for viral infections. Treatment of viral infections with antibiotics may sometimes be done with the intent of controling or preventing secondary bacterial infections in flocks suffering from viral disease. However, this is not a generally recommended practice and, frequently, this practice is known to actually harm the flock. The concept of antimicrobial therapy is really one of "selective toxicity". The idea is to poison the pathogen without poisoning the host. Since the viral infection is not directly affected by the antibiotic, treatment often means adding an ineffective mild poision to an existing infectious disease. Furthermore, the ineffective antibiotic treatment may kill normal flora (normal helpful bacteria) in the host which reduces competetion for space and nutrients with specific bacterial pathogens. Paradoxically, the host can therefore actually become more susceptable to bacterial pathogens to which it is exposed. Lastly, indiscriminate use of antibiotics increases the level of resistance of bacteria within the environment. This increases the chance that pathogenic bacteria that are introduced in the future will rapidly acquire resistance by plasmid transfer (please see section on Chemotherapy). Thus, antibiotic therapy of viral infections should usually initiated only upon expert advice in specific situations.
Viral pathogens generally replicate and cause disease in a similar fashion, although the specific tissues attacked (tissue tropism), species and ages affected, and severity of lesions varies with specific viruses. The first stage in viral reproduction is adherence to specific attachment sites on the host cell known as "receptors". The virus must then penetrate the host cell membrane to enter the cytoplasm of the cell. Following entrance into the cell, the virus must undergo several steps to initiate replication of the virus parts by the machinery of the host cell. Once the virus parts are made, the virus must initiate assimilation of the complete virus replicates, again using the host machinery. After a predetermined number of copies of virus are available within the host cell (usually many thousands of copies), the virus must induce release of the replicated copies, usually through host cell lysis. The cumulative cell death and associated tissue damage that occurs following a number of virus replication cycles results in disease for the host. The degree of tissue damage and location (tissue specificity) are generally related to the specific clinical signs and lesions that are observed during a viral infection.
Prevention of viral infections of poultry is the only real mechanism for avoiding the related disease and production losses. Prevention is based on one of 2 mechanisms: avoiding exposure of the flock to a specific pathogen (sanitation and bio-security) or through immunization. Each of these mechanisms are discussed more thoroughly in related sections of this text (please see related sections on Sanitation and Bio-security, Immunology, and Vaccination Strategies).
Yeasts, molds and mushrooms are in the family that are called fungi. These are very simple eukaryotes but share a number of common characteristics with eukaryotic vertebrates. Thus, it has proven difficult to develop cost-effective antifungal chemotherapeutic agents for use in commercial poultry. Since the game of antimicrobial therapy is one of selective toxicity, the shared structures and characteristics make this a very difficult pursuit. Several effective antifungal medications are available for use in human and other areas of veterinary medicine, but to date, these have proven too toxic or expensive for use in commercial poultry.
Because fungal pathogens are usually not affected by common antibiotics used in commercial poultry, these antibiotics may actually allow the opportunity for pathogenic fungal infections by eliminating bacterial flora (normal non-pathogenic bacteria) that usually compete with the fungi for nutrients and space (e.g. Crop Mycosis). Indeed, most fungal infections of poultry are opportunistic. For example, the severe respiratory disease called pneumomycosis (brooder pneumonia) is caused by the inhalation of tremendously high numbers of fungal spores (often Aspergillus fumagatus) due to moldy conditions in the environment.
As there are no really effective treatments for fungal infections of poultry, the only cost-effective strategy for avoiding these disease problems is avoidance of the conditions that predispose to fungal infection.
It is important to note that mycotoxins (myco = fungal) are preformed toxins generally produced by fungal species that are non-pathogenic for poultry. These species may infect grain-bearing plants such as corn and produce toxins even prior to harvest. Mycotoxins are generally highest in years of high stress (e.g. drought) for the plants, supporting the concept that many of these toxins are produced even before harvest. However, the greatest problem with mycotoxin generation probably occurs after harvest during grain storage and shipment. Warm moist conditions are particularly suitable for mycotoxin-fungi to grow and contaminate grain sources. Generally grain moisture contents less than 14% do not support mycotoxin-producing fungal growth.
In some warm areas with high humidity, particularly with sub-optimal grain storage facilities, mold inhibitors are added to grains and finished poultry feeds to retard the growth of fungi and production of mycotoxins. It is important to note that mold inhibitors do nothing to remove existing mycotoxins, they only prevent continued growth and production of toxins by the fungi. There is growing interest in a family of clay-like compounds known as aluminosilicates for remediation (treatment) of feed contaminated with certain mycotoxins. These compounds bind some mycotoxins very tightly in the gastrointestinal tract, thereby preventing absorption by the animal. Presently, commercial products are available only for a select few mycotoxins and these products are not completely effective. Nevertheless, treatment of contaminated feed is sometimes recommended. While over 200 mycotoxins have been described, routine assays are only available for a select few (please see section on Mycotoxins).
Throughout these notes, you will notice that incubation periods are listed for many diseases. Knowledge of the incubation period for some diseases is very helpful because it helps to determine the possible sources of the disease problem, leading to the ability to correct or prevent the problem for the subsequent flock. The incubation period usually represents the number and time required for sufficient pathogen replication cycles to occur to produce a critical level of tissue damage for expression of clinical signs and lesions. Obviously, an animal can loose a fairly large number of cells and tissue from most parts of the body without causing recognizable disease. This occurs during the incubation period. Once sufficient damage has occurred to cause loss of function or pain in a particular tissue, there are recognizable signs of disease and, often, grossly recognizable lesions at necropsy.
Sometimes the virulence of a pathogen is related to the pathogen replication time. If the pathogen can replicate to sufficient numbers to cause tissue damage (short incubation period) before being suppressed by the immune system, the pathogen likely is virulent.
Antigens are molecules that can be specifically recognized by the immune system as foreign to the host. Antigens, usually proteins, may be recognized specifically by antibodies from the humoral immune system and by other types of cells after initial exposure to the antigen. The specific portion of the foreign molecule recognized by the immune system is the epitope. Generally the epitope consists of 5 to 8 amino acids in sequence. Thus, if two pathogens share common epitopes, immunity against one will sometimes produce at least partial immunity against another, usually closely related pathogen. However, when there are no epitopes (highly specific binding sites) in common between two pathogens, immunity against one will produce absolutely no protection against the second, non-related, pathogen. Because human cold viruses are numerous and frequently non-related, humans can contract one cold after another. Because the first cold virus actually stresses and sometimes immunosuppresses the immune system of the host, the individual that has just experienced a cold may actually be more susceptible to a subsequent, non-related, infection. This helps explain why some years some of us never seem to contract a cold, and other years we face one cold virus infection after another. The same events commonly occur in poultry flocks. Pathogens with identical epitope combinations are, therefore, of a single serotype.
We all know that some pathogens are more virulent than others. The human ebola virus, for example, kills the vast majority of humans that become infected. This virus is highly virulent or, is sometimes referred to as highly pathogenic. Contrast this to a relatively low virulence common cold virus of humans. Occasionally, pathogens of a single serotype may have different virulences. In this case, the single serotype is said to have multiple pathotypes. It is essential to understand the difference between serotype and pathotype. Knowledge of the serotype is necessary for vaccine choice for example. Pathotype is important to predict the duration and severity of the diseases and, sometimes, for necessary regulatory decisions like implementation of eradication procedures.
In the twelfth century, smallpox epidemics were a frequent occurrence and were associated with high mortality and morbidity. However, it was known that recovered individuals remained healthy during subsequent epidemics. For that reason, Chinese royalty deliberately infected their infants with small pox by rubbing scabs from infected individuals into small cuts on the child. The surviving infants were protected for life. Exposure of the children soon after birth had one main advantage; the presence of maternal antibodies in newborn children would reduce the severity and duration of the disease induced.
It was also discovered that the least mortality was associated with inoculations when scabs were obtained from individuals with mild cases of smallpox. By utilizing this technique the mortality associated with smallpox dropped from 20% to 1%. The smallpox inoculations became very popular in China and by the 18th century were widely employed in Europe, too.
In 1798 Edward Jenner an English physician found that milk maids were often immune to smallpox. Investigation proved that cow pox virus from the teats of cows via skin lesions gave little or no illness but protected against smallpox. Jenner named this new procedure of inoculating people with cow pox, vaccination. (Vacca= Latin for cow)
However, the implications of this vaccination procedure were not realized until 1879, when Louis Pasture in France began to study a disease called fowl cholera caused by a bacterium (named Pasteurella multocidia after Pasture). Pasture was investigating the high mortality and severe disease associated with the bacteria, when his assistant went on vacation and left a sample of the bacteria on a lab bench. Upon returning the assistant inoculated a group of chickens with the bacterial sample. The chickens receiving this "aged" sample did not have any signs of disease. Being short of research funds, Pasture used these same group of birds and inoculated them with a fresh culture of bacteria. He found that these birds did not get sick. However, some previously uninoculated birds, which did not receive the "aged" culture, also received the fresh culture and did show signs of disease. Pasture then realized that attenuation (weakening) of bacterium prior to inoculation provided protection with little or no disease. Pasture later used this procedure in a widespread vaccination against anthrax. He also found that attenuation of viruses (rabies) worked much the same as attenuation of bacteria.
1) Physical Barriers
<!--Epithelium (skin, intestine, mucus membranes, etc.)
<!--Positive pressure flow (flow of milk, urine, mucus, etc.)
<!--The low pH of the proventriculus
2) Normal Bacterial Flora
<!--competition for nutrients
<!--competition for binding sites
<!--production of compounds toxic for other (including pathogenic) bacteria
3) Enzymes (lysosymes in tears and nasal mucus)
4) Iron Binding (all organisms need iron, which is bound very tightly within vertebrates)
The primary task of an immune response is to protect the body against an invasive organism. Therefore, there is a need for the immune system to be able to identify and destroy foreign cells and substances. However, there must be some method to identify self-antigens and not destroy them.
Three Types Of Immune Responses
1. Antibody-mediated (also called humoral Immunity)
3. Tolerance (the ability to recognize self-antigen from
non-self or foreign antigen)
Six Basic Steps in Gaining Immunity
1. A method of trapping and processing antigens
2. A mechanism for recognizing and reacting specifically with the antigens or foreign cells.
3. Cells to produce antibodies and cells to participate in the cell mediated immune response.
4. Cells to retain the memory of the event and to react specifically to the antigen in the future.
5. Cells to regulate and control the immune system (auto- or self-regulation)
6. The ability of immune cells to recognize "self" antigen (as compared to antigen which is foreign to the body), and not mount an immune response against self antigens (thereby avoiding autoimmune disease)
Pasture also found that blood serum obtained from a horse that had previously received attenuated tetanus toxin protected an unvaccinated horse for several weeks. These factors that allow protection are called antibodies. Foreign substances (in this case tetanus toxoid) which stimulate the production of antibodies are known as antigens.
If you were to measure the concentration of circulating antibody (titer) after a vaccination you would find that little or no antibody would be produced during the first week after inoculation. During the second week antibody titers would gradually increase, and peak levels would be achieved from 14- 21 days after inoculation. You would also find that the antibody titers would begin to fall rapidly, soon after they peak.
If you measure antibody titers after a second vaccination you would find that levels would climb very rapidly and would remain high for several months or years.
1) Primary Immune Response
The response following initial exposure to an antigen. This response is characterized by:
a) IgM is the immunoglobulin which is produced in the highest concentrations.
b) There is a long latency period before any antibody is produced.
c) Antibody is produced in high concentrations for a relatively short period of time (short duration of response).
d) The overall peak concentration of antibody (titer) is relatively low.
2) Secondary Immune Response
The response following secondary exposure to an antigen (referred to as the anamnestic response). This response is characterized by:
a) IgG is the immunoglobulin which is produced in the highest concentrations.
b) There is a short latency (lag) period before antibody is produced.
c) Antibody is produced in high concentrations for a long period of time (long duration of response = anamnestic, or memory response).
d) The overall peak concentration of antibody (titer) is much higher than in the primary immune response.
c) Primarily the highest affinity antibodies are stimulated to be produced with the secondary immune response.
A Young chick’s immune system is immature and not ready to fight off infections. Therefore, there must be a mechanism to protect them while their immune system matures. This protection is supplied by the mother. While the egg yolk is in the mother, she gives it a very high concentration of antibody which protects the chick during incubation and for several weeks after hatch. This process of passing antibodies may also occur in the uterus for some mammals (e.g. humans) or immediately after birth (through special milk) for others. Some mammals (e.g. ruminants) produce milk which is very high in antibody for the first 24 hours after birth. This milk is called colostrum. The ability of the young to absorb these antibodies from the milk is lost within 24- 48 hours after birth.
Active (or Acquired) Immunity
Once a chick's immune system has matured and the maternal antibody levels have fallen to a level where they are no longer sufficient to prevent infection, the chick’s immune system generates an immune response to any foreign antigen. This response is called active or acquired immunity. This immunity is long-lived and with the help of memory cells, it protects the chick from subsequent infections to that particular antigen. The term Active or acquired immunity can be used for both humoral and cell-mediated immune responses.
Antibodies are produced against foreign proteins (antigens). There are specific amino acid sequences that a particular antibody will bind. This specific sequence that an antibody will bind is called an epitope. Each epitope consists of approximately 5-8 amino acids of the protein.
Foreign proteins also must be a certain size before they will stimulate antibody production. In most situations, a protein must be 10,000 amino acids long before it will cause an inflammatory reaction. However, if small foreign proteins bind to larger proteins inside the body, this foreign protein-self protein combination can stimulate antibody production.
Examples of proteins that stimulate antibody production
Bacterial - cell walls, capsules, pili, flagella
Viral - capsids
Cell-Surface Antigens - blood types, auto-antigens
Function of Antibodies
Antibodies do not kill cells.
<!--Label antigen for identification by cells of the immune system or for destruction by macrophages and heterophils (labels foreign proteins, bacterial cells, or self-cells acting as host for pathogen),
<!--Activate complement and membrane attack complexes which rupture cells,
<!--Neutralize and agglutinate compounds (compounds are no longer able to bind to receptors).
Types of Antibody
IgM - Antibody found in primary immune response
IgG - Antibody found in secondary immune response*
IgA - Antibody found in body secretions
IgE - Antibody found with parasitic infections and allergies
IgD - Found on immature B-cells
*Some scientists refer to IgG of poultry as "IgY" because there is a subtile difference in the hinge region of the molecule as compared to the structure of mammalian IgG. For this text, we will continue to use the term "IgG".
Cell Mediated Immunity
If a area of skin is removed from one animal and surgically placed on another unrelated animal, the graft only survives for about 10 days before it is rejected by the recipient animal’s immune system and destroyed. If a second graft is then made from the same donor and placed on the same recipient, the graft only last 1-2 days before it is rejected. This reaction, much like humoral immune reactions, is specific for a particular donor animal. However, serum from a sensitized animal to a normal animal does not transfer sensitization. Therefore, this immune response is not caused by antibodies. It is caused by the cytotoxic actions of a specific type of T-lymphocyte (cytotoxic T-cells).
Heterophils (Polymorphonuclear or Granulocytes)
Heterophils function by migrating from the blood to the tissues to destroy infectious agents. This migration is stimulated by either bacterial invasion into the body, or damage to the cells of the body. When heterophils find an infectious agent they phagocytize (ingest) it. Once the infectious agent is phagocytized, it is destroyed by oxidases and lysosomal enzymes.
Heterophils can survive only a few days in the tissue. However, they can move into tissues very rapidly to attack infectious agents. Therefore, heterophils form the bird’s first line of defense against an infection.
Eosinophils- similar to heterophils but respond to a parasitic infection.
Basophils- also similar to heterophils but infiltrate the tissues under the influence of lymphocytes and provoke inflammation by releasing chemical agents such as histamine.
Macrophage or Monocytes (Mononuclear cells)
Monocytes are another type of phagocytic cell of the immune system. When monocytes are activated against an infectious agent they move into the tissues to attack it. When it moves into the tissue it is called a macrophage. Unlike heterophils, macrophages can survive for about 100 days in the tissues. However, macrophages are much slower than heterophils and take at least 3 days to enter the tissues. Therefore, they are known as the bird’s second line of defense. Macrophages are effective at removing debris from infectious agents, and dead or dying cells. Removal of these dying cells and cells that harbor the infectious agents speeds the healing process.
Additionally, macrophages perform several tasks that heterophils cannot. Macrophages release chemical mediators which act to activate the other cells of the immune system and thereby amplify the immune response. Macrophages also process and present antigen to lymphocytes (T- helper cells) which then stimulate the cytotoxic or humoral immune responses.
Dendritic cells- Monocytic cells adapted for antigen processing, highly concentrated in lymphoid organs and skin.