Section I. General Concepts
Page 4

A. Disease versus Health
B. Recognition of Disease Etiology
C. Recognition of Affected Systems
D. Evaluation of Body Condition
E. Bacterial vs. Viral vs. Fungal
Pathogens
F. Incubation Period
G. Serotype vs. Pathotype
Section II. A Brief Introduction to
Immunology Page 9

A. History
B. Non-Immunological Barriers
C. The Immune Response
D. Humoral Immunity
E. Primary vs. Secondary Response
F. Passive Immunity
G. Antibody Binding
H. Functions of Antibodies
I. Cell Mediated Immunity
J. Cells of the Immune System
K. Lymphoid Organs
Section III. Principles of Disease
Prevention Page 14

A. Infectious Dose
B. Sanitation and Bio-security
C. Protection by Vaccination
D. Importance of Vaccine (serotype)
Selection
E. Relationship of Vaccination to
Infectious Dose
F. Value of Multiple Vaccinations
G. Pathogen Attenuation
H. Hazard of Genetic
Recombination
I. Vaccination Strategy
J. Chemotherapy
Section IV. Diseases Affecting the
Nervous System Page 19

A. Marek's Disease
B. Botulism
C. Epidemic Tremor
D. Vitamin E, Selenium and
Thiamin deficiency
E. Aspergillosis
F. Fowl Cholera
Section V. Diseases Causing Tumors
Page 19

A. Marek's Disease
B. Avian Leukosis Viruses
C. Reticuloendotheliosis (turkeys)
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Poultry Diseases (POSC 3223)

Section VI. Diseases affecting the
Musculoskeletal System Page 20

A.
Nutritional
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
Section VII. Diseases Causing
Immunosuppression and General
Conditions Page 21

A.
Marek's Disease
B.
Infectious Bursal Disease
C.
Chick Anemia Virus
D. Mycotoxicosis
Section VIII. Diseases Primarily
Affecting the Respiratory Tract
Page 22

•
Conditions involving the Eyes and
Face
A.
Fowl Pox
B.
Infectious Coryza
C.
Fowl Cholera
D. Infectious Bronchitis
E.
Bordetellosis
F. Mycoplasmosis
•
Limited to the Upper Respiratory
Tract
A.
Fowl Pox
B.
Infectious Coryza
C.
Fowl Cholera
D. Infectious Bronchitis
E.
Bordetellosis
F.
Mycoplasmosis
G. Laryngotracheitis
•
Generalized Respiratory Conditions
A.
Avian Influenza
B.
Newcastle Disease
C.
Avian Pneumovirus
D.
Mycoplasmosis
E.
Fowl Cholera
F.
Chlamydiosis
G.
Avian Tuberculosis
H.
Aspergillosis
Section IX. Diseases Primarily Affecting
the Gastrointestinal Tract Page 26

•
Esophagus-Gizzard
A.
Fowl Pox
B.
Crop Mycosis
C.
Capillariasis
D. Gizzard/Proventricular
Erosions/Dialation
•
Small Intestine
A.
Coccidiosis
B.
Necrotic Enteritis
C.
Colibacillosis
D.
Roundworms
E.
Tapeworms
•
Ceca and Large Intestine
A.
Salmonellosis
B.
Histomoniasis
C.
Coccidiosis
Section X. Diseases Affecting both the
Respiratory and Gastrointestinal Tract
Page 30

A. Newcastle Disease
B.
Avian Influenza
C.
Fowl Cholera
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Section XI. Diseases Affecting the Renal
System Page 30

A. Ochratoxin
B. Infectious Bronchitis
Section XII. Diseases Causing Systemic
Generalized Disease Page 31

A. Fowl Cholera
B. Salmonellosis
C. Coccidiosis
D. Mycotoxicosis
E. Ascites Syndrome
Section XIII. Diseases Affecting the Skin
and Feathers Page 32

A. Molt
B. External Parasites
C. Wear on Feathers
D. Gangrenous Dermatitis
E. Cannibalism, Scratches and
Scabs
F. Tumor Causing Diseases
Section XIV. Glosary Page 34

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Poultry Diseases (POSC 3223)

I. General Concepts
Disease vs. Health

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.

Recognition of Infectious Disease Etiology Type:

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.

Recognition of Affected Physiological Systems:

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
4

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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.

Recognition of Body Condition:

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.

Bacterial vs. Viral vs. Fungal Pathogens

•
Bacterial Pathogens
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
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

5

Poultry Diseases (POSC 3223)

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

6

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discussed more thoroughly in related sections of this
text (please see related sections on Sanitation and
Bio-security, Immunology, and Vaccination
Strategies).

•
Fungal Pathogens
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 mycotoxinfungi
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).

Incubation Period:

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.

Serotype vs Pathotype:

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

7

Poultry Diseases (POSC 3223)

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.

8

Poultry Diseases (POSC 3223)

History: 1) Physical Barriers
II. A Brief Introduction to Immunology
1) Physical Barriers
II. A Brief Introduction to Immunology
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.

Non-Immunological Barriers To Infection

•
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 Immune Response

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)
2. Cell-mediated
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)
Humoral Immunity (Antibody-Mediated)

Pasture also found that blood serum obtained from a
horse that had previously received attenuated tetanus
toxin protected an unvaccinated horse for several

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Poultry Diseases (POSC 3223)

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.

Primary vs. Secondary Immune Response

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.

Passive Immunity

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.

Antibody Binding

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.
Antibodies do:

•
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,
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•
Neutralize and agglutinate compounds Monocytes are another type of phagocytic cell of the
(compounds are no longer able to bind to immune system. When monocytes are activated
receptors). against an infectious agent they move into the tissues

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).

Cells of the Immune System

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)

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.

Steps of Phagocytosis

1) Chemotaxis - bacterial invasion and tissue
destruction cause the release of chemical attractants
which, in turn, cause phagocytic cells to ‘crawl’ to
the site of infection or injury.
2) Adherence - trapping and binding of the
phagocytic cell to the foreign cell, antigen, or
antibody-coated antigen.
3) Ingestion - enclosure of the foreign substance into
a phagosome (a vacuole). This occurs when the
phagocytic cell wraps around the foreign substance
and engulfs it.
4) Destruction - killing and digestion of the foreign
substance with potent oxidizing agents and digestive
enzymes found with in the cell granules (or
lysosomes).
5) Processing and presenting of antibody by
macrophage - the antigen is processed by the
macrophage and presented to helper T-cells which
signal for other cells of the immune system to mount
an immune response against the antigen

Lymphocytes

There are three distinct types of lymphocytes:

1. B- Lymphocytes
2. T- Lymphocytes
3. NK- Lymphocytes
Lymphocytes are the key components of the immune
system. Although antigen is trapped and processed
by macrophages, it is the primary function of the

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lymphocytes to mount an immune response.
Lymphocytes are responsible for the production of
antibody and specific effector cells (e.g. cytotoxic T-
cells or killer T-cells), which respond to processed
antigen. It is also the responsibility of lymphocytes to
function as memory cells (to remember an antigen)
and therefore, to initiate the secondary immune
response when the antigen is presented to the host
later in life (through a subsequent infection or
vaccination with the same agent). In addition,
Lymphocytes work to regulate the immune response,
to make sure the number of cells for a particular
immune reaction are appropriate, and to be sure that
self-antigens are not destroyed.

1) T-Lymphocytes

T-cells are lymphocytes that are derived from the
thymus. That is, the immature lymphocytes migrate
from the bone marrow to the thymus where they
mature and are released into the circulation. There
are two categories of T-cells, effector T-cells and
regulator T-cells.
Effector T-cells or cytotoxic T-cells are responsible
for destroying virus-infected cells, cancerous cells
and foreign (non-self) cells.
There are two types of regulatory T-cells, Helper T-
cells and Suppressor T-cells. Helper T-cells respond
to antigen presented to them by macrophages and B-
cells by directing other cells of the immune system in
the immune response. When they are presented a
processed antigen, they secrete chemical messengers,
called Lymphokines. These Lymphokines activate
other cells of the immune system. T-helper cells can
also present the antigens they receive to B-cells
which stimulates them to produce antibodies. In a
primary immune response, it is necessary for the
antigen to be presented to the immune cells by the T-
helper cells. Presentation of this processed antigen by
the T-helper cells makes the lymphocyte differentiate
and become active for that antigen (each lymphocyte
is specific for only one antigen).
The other type of regulatory T-cell is the suppressor
T-cell. Suppressor T-cells work to keep the immune
system under control by blocking the effects of the
helper T-cells.

2) B-Lymphocytes

B-cells are lymphocytes that are derived from the
Bursa of Fabricius. In fact, the bursa of Fabricius
(also called the cloacal bursa) first allowed Dr. Bruce
Glick to determine that there were 2 general arms to
the immune system, the humoral and cell-mediated
arms. Immature lymphocytes migrate from the bone
marrow to the Bursa of Fabricius where they mature
and are released into the circulation. It is the
responsibility of the B-cells to produce antibodies

against foreign antigen. This antigen can be
processed antigen presented by other immune cells or
it can be free antigen circulating in the blood.
Following stimulation by antigen, the B-cells
proliferate and the new B-cells differentiate into
either plasma cells (which produce antibody) or
memory B-cells.

3) Natural Killer Cells

NK cells are lymphocytes that are responsible for
destroying cancerous cell.

Major Histocompatability Complex

Antigens and receptors used by the cells of
the immune system to Identify cells
MHC class I are used by the cells of the
immune system to distinguish from self and
non-self. MHC I molecules are present on
every nucleated cell in the body. They
present proteins produced by the cell for
identification by T-cells. This helps in the
identification and destruction of virus
infected cells.
MHC class II are present on
monocytes/macrophages, T-cells and B-
cells. MHC II molecules act as surface
regulator for the presentation of antigen to
T-helper cells.

Lymphoid Organs

Primary Lymphoid Organs
1) Thymus

The thymus is an organ in the neck of birds and
mammals. The thymus grows continuously until
puberty when it begins to shrink in size. In the adult
it is very small, but remains to have a small amount
of activity throughout the life of the animal. It is the
responsibility of the thymus to mature T-
Lymphocytes and release them into the circulation. It
is also the responsibility of the thymus to destroy (via
apoptosis - "programmed cell death") any T-
lymphocytes that may respond to self-antigen.

2) Bursa of Fabricius

The bursa of Fabricius is an organ that is unique to
birds. However there is believed to be a "bursal
equivalent" in other animals (perhaps the bone
marrow and Peyer’s Patches). The bursa of Fabricius
is located on the dorsal aspect of the cloaca just
cranial to the vent. Like the thymus, the bursa of
Fabricius grows continuously until puberty at which
time it begins to shrink in size. In the adult it is very
small, but remains to have a small amount of activity
through out the life of the bird. It is the responsibility
of the Bursa of Fabricius to mature B-Lymphocytes
and release them into the circulation. It is also the
responsibility of the Bursa of Fabricius to destroy

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Poultry Diseases (POSC 3223)

(via apoptosis - "programmed cell death") any B-
lymphocytes that may produce antibodies to self-
antigen.

Secondary Lymphoid Organs
1) Lymph nodes

-Structures that are placed in the
lymphatic channels to trap antigen.
- Lymph nodes contain lymphocytes
and macrophages.
- Most birds do not have true lymph nodes,
but they do have accumulations of lymphoid
tissue that function similar to lymph nodes.
2) Harderian Gland

- large accumulation of lymphoid tissue
located near the nose and eyes.
3) Cecal Tonsils

- These have large accumulations of
lymphoid tissue in the ceca near the junction
with the ileum.
4) Peyer’s Patches

- accumulation of lymphoid tissue in the
ileum of the intestine.
5) Meckel’s Diverticulum

- Have a large number of lymphoid cells by
two weeks of age, and functions until about
20 weeks of age.
6) Bone Marrow

- Large accumulations of lymphoid
and erythroid tissue.
7) Other

- The skin and lungs also have a large
number of lymphoid cells.
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Infectious Dose (Dilution is the Solution to
Pollution):
is essential. Second, every effort should be made to
reduce exposure to disease causing agents (as
discussed above). Third, specific appropriate
Section III. Principles of Disease Prevention
Pollution):
is essential. Second, every effort should be made to
reduce exposure to disease causing agents (as
discussed above). Third, specific appropriate
Section III. Principles of Disease Prevention
For most diseases caused by infectious disease-
causing agents (pathogens), the bird must be exposed
to a relatively large number of organisms (pathogens)
for infection to occur. This number of pathogens is
often referred to as the "minimal infectious dose".
Obviously, the minimal infectious dose changes with
age of the bird, general health and condition of the
bird, the amount of environmental stress, nutritional
quality, and many other factors that are sometimes
difficult to measure. The main point to be gained is
that a large number of most disease causing
organisms (pathogens) are required to cause
infection. Furthermore, for a given pathogen, the
severity of disease in an individual animal may be
related to the number of pathogens to which the
animal was initially exposed. Thus, sanitation, the
process of reducing the number of pathogens, has a
critically important role for poultry production in
spite of the fact that sterility (the total absence of
organisms) can almost never be achieved under real
world conditions. This gives credence to the
statement, that with regard to infectious diseases,
"dilution is the solution to pollution". If we can dilute
the pathogen below the infectious dose, infection
simply will not occur. Other times, perhaps a
reduction in the number (concentration) of pathogens
can be achieved but it is still above the infectious
dose. In this case, even though the birds become
infected, the severity of the disease may be reduced
by exposure to a lower infectious dose. Maintaining a
clean environment, rotating areas where birds are
held (movable cages), and frequently replacing or
changing bedding material, are frequently simple
techniques that will reduce the chances of significant
infections.
In some cases, protecting birds from an infectious
level of a specific disease causing agent is not
possible. As an example, Marek’s disease (discussed
below) virus is shed in the feather follicle dander of
infected birds and is readily transmitted to
susceptible chickens at doses which are infectious. In
this instance, cleanliness of the environment is not
likely to prevent infection and disease. In these cases,
it is necessary to increase the resistance of the bird by
increasing specific immunity through the use of an
appropriate vaccine. In effect, vaccines (discussed
below) increase the number of a specific disease-
causing agent which are required to infect and cause
disease. It is therefore important to remember that
there are three important considerations for
prevention of infectious disease in poultry. First,
proper nutrition and management to minimize stress

vaccines can increase the resistance to challenge by a
specific disease-causing agent. In healthy poultry,
infectious disease can be prevented by maintaining
resistance above the level of challenge, or by
reducing challenge below the level of resistance
(immunity).

Sanitation and Bio-security - Isolation of Poultry
from Infectious Disease Causing Agents:

There are two distinct sanitary principles that allow
for maintaining large numbers of poultry for food
production. While there are many individual
practices that can contribute to overall sanitation and
bio-security, these two principles should be observed
whenever possible.
1) Strict Isolation: If new pathogens are not
introduced, the number of infectious disease
problems will be limited to those pathogens present
in the environment or carried by the birds. The
original concept of all-in, all-out poultry production
is the basis for modern practices which allows
intensive poultry agriculture. By limiting the flock
origin to a single source obtained at a single time (all
the same age), pathogen exposure is greatly reduced.
Because many specific pathogens require a host for
long-term propagation and even survival, eliminating
multiple species, ages, and flock sources of birds
simultaneously present on a premise has greatly
reduced the introduction and persistence of
pathogens. A common breach of isolation and all-in,
all-out practices occurs when growers allow a few
birds to remain in the production facilities during
"down times" between flocks. This allows for
maintenance of a reservoir of pathogens in the
remaining birds. It is absolutely essential to make use
of any opportunity to depopulate the flock and begin
anew with healthy chicks from a single source. In
this way, old problems need not necessarily remain
problems indefinitely.
While there are a number of biological vectors or
carriers of diseases including poultry, wild birds,
rodents, some insects, and even other farm animals
(not common), the most important controllable
source of disease is other poultry and people that
travel between flocks. Additionally, animals
(including humans), equipment, and machinery can
serve to mechanically transmit disease causing
agents. For example, people visiting multiple flocks
may unintentionally transmit disease causing
organisms on clothing, boots, and tools carried onto a
premise. Similarly, neighbors, dogs, cats, wild
animals, and other sources may serve to

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unintentionally transmit disease causing organisms.
Since every contact contains risk, reducing the
number of contacts will reduce risk. Furthermore,
appropriate sanitation practices (please see below)
will also serve to reduce the risk of fomite
introduction.
2) Reduction of Pathogen Numbers: In most cases,
exposure to a relatively large number of infectious
organisms is required to infect a susceptible host as
described above. This number of infectious
pathogens of a single specific type is known as the
minimal infectious dose. This number will vary
widely depending on a variety of factors such as the
general health and age of the host and the specific
virulence of the pathogen. For poultry production, we
can exploit this knowledge to use sanitation
procedures whenever possible. Even though we
know that the environment can rarely be sterilized
(all organisms killed), we can often take steps to
reduce the number of infectious or potentially-
infectious agents in the environment. This process is
known as sanitation. Pathogen numbers in the
environment can be reduced by physical removal
(such as clean-out, replacement of used litter, and
physically washing) or by killing pathogens in place
(disinfection). Usually these procedures work best
when used together, physically cleaning the
environment prior to the application of chemical
disinfectants. When one realizes that physical
cleaning and disinfection can sometimes reduce the
number of pathogens below the minimal infectious
dose, one realizes that "dilution can truly be the
solution to pollution" when it comes to infectious
disease problems. There are many debates as to the
best disinfectant for a specific purpose. However,
there is no debate as to the benefits of physically
cleaning away infectious material. As a final step,
any disinfectant (including a dilute household bleach
solution) is usually quite effective.
In addition to physically cleaning and disinfecting the
environment, time also tends to work toward
reducing pathogen numbers in the environment. Most
of the important pathogens of poultry are obligate
pathogens, meaning that these organisms cannot
replicate in the absence of the poultry species which
they infect. Thus, as we remove all poultry from the
facility, these organisms tend to decline over time.
The survival of different pathogens, of course, is
highly variable, with some (e.g. Fowl Pox) persisting
for many years while others (e.g. Mycoplasma spp.)
are very fragile in the environment and disappear in a
matter of hours after poultry are removed.
Environmental conditions can also influence
pathogen half life, with higher temperatures, high
ammonia levels, drying, sunlight, and chemical

disinfectants tending to greatly reduce the survival
time, thereby accelerating death of pathogens. This
phenomenon is exploited in commercial poultry
operations using the all-in, all-out production concept
described above. The time between flocks is
important for reducing pathogen levels within the
environment. In commercial poultry operations,
veterinarians and field servicepersons will sometimes
elect to extend the "down time" between flocks to
more fully exploit this phenomenon, particularly
when faced with disease causing agents that decline
rapidly over time. In general, it is recommended that
the premise contains no poultry for at least 2 weeks
(after cleaning and disinfection) before arrival of new
birds.

Protection by Vaccination:

Vaccination is the process by which specific
immunity can be induced by exposing the host to a
weakened or killed organism that has the same
external "appearance" as the field pathogen to the
immune system. All specific disease-causing agents
have structures on the organism’s surface that appear
quite unique to the bird’s immune system. These
structures which can be recognized by the immune
system (epitopes) are generally unique for a specific
disease-causing agent. By exposing the bird’s
immune system to this vaccine prior to infection, the
chances of infection and/or disease can be greatly
diminished. The key to successful vaccination is to
administer the vaccine before the animal is infected.
After infection, vaccinations for that disease will not
help the birds recover and, in some cases, may hurt
the birds. Vaccine selection is based on the history of
infectious disease problems in a given premise and
the prevalence of a certain disease in a given area. It
should be noted that there are some diseases which
have worldwide prevalence and which vaccination
programs are always recommended (e.g. Marek’s
disease).

Importance of Vaccine (Serotype) Selection:

In some cases, a single disease agent can have
alternative "appearances" to the bird’s immune
system (multiple serotypes). In this case, it is
essential that the vaccine chosen appears the same to
the immune system as the actual disease-causing
agent to which the birds are likely to be exposed in
order to induce protective immunity. Because of this
problem, not all vaccines for a specific disease
problem are capable of protecting against all
organisms of the same disease name. In these cases,
the specific disease-causing agent must be isolated in
a diagnostic laboratory, and the serotype determined,
in order to choose an effective vaccine for present or
future flocks. The fact that some disease causing

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agents can present as one of a large variety of
serotypes (appearance to the immune system) is the
reason that vaccination is not usually useful for those
diseases (e.g. there are a large number of possible
serotypes for Avian Influenza and vaccination for
this disease is only done under very unusual
circumstances). However, for small flocks in
primitive areas it is recommended that chicks are
vaccinated against Marek’s Disease, Newcastle
Disease, and Infectious Bronchitis at the source
hatchery if possible. Only under specific
circumstances, beyond the scope of this book, are
other specific vaccines likely to be useful.

Relationship of Vaccination to Infectious Dose:

It is very important to remember that protection by
vaccination is also related to the concept of infectious
dose, discussed above. With exposure to higher
infectious doses, immunity can often be overcome.
Thus, the degree of immunity or protection is
relative. Vaccination usually provides protection
against a higher challenge lev