Avian Viral Diseases (Exclusive of Respiratory Diseases)
AVIAN POX
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(Fowl pox, Canker, Avian diphtheria)
AVIAN LEUKOSIS
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Lymphoid Leukosis (L.L.)
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Differential Diagnosis of L.L. and M.D.
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Marek's Disease (M.D.)
EPIDEMIC TREMOR
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(Avian Encephalomyelitis)
INFECTIOUS BURSAL DISEASE
INCLUSION BODY HEPATITIS (I.B.H.)
TRANSMISSIBLE ENTERITIS OF TURKEYS
A number of viral diseases of poultry produce symptoms and lesions primarily
exclusive of the respiratory system. Among them are some of the most devastating
diseases of chickens and turkeys. Considered in this group are avian pox,
leukosis, avian encephalomyelitis (epidemic tremor) and bluecomb disease.
AVIAN POX
(Fowl pox, Canker, Avian diphtheria)
Avian pox is a relatively slow-spreading viral infection of birds, characterized
by wart-like nodules on the skin and diphtheritic necrotic membranes lining
the oral cavity and upper respiratory system. It has been present in birds
since the earliest history and is universal in distribution. It may cause
severe economic loss in chickens and turkeys due to poor growth, feed efficiency,
reduced production, increased cull rates and downgrading. Mortality usually
is not significant unless the respiratory involvement is marked. The disease
may occur in any age bird any time during the warm months, particularly when
mosquito populations are high.
Cause: Avian pox is caused by a viral agent. There are at least three
different strains or types of avian pox virus: fowl pox virus, pigeon pox
virus and canary pox virus. Although some workers include turkey pox virus
as another distinct strain, many feel that it is identical to fowl pox virus.
Each virus strain is infective for a number of species of birds in addition
to its primary host. For example, among others, fowl pox virus may infect
chickens, turkeys, pheasants, quail and ducks; pigeon pox virus may infect
pigeons, chickens and turkeys; and canary pox virus may infect canaries,
chickens, pigeons and sparrows.
Natural occurring pox in chickens, turkeys and other domestic fowl is considered
to be caused by fowl pox virus.
Transmission: Fowl pox can be transmitted by direct or indirect contact.
The virus is highly resistant in dried scabs, and under certain conditions
may survive for months on contaminated premises. The disease may be transmitted
by a number of species of mosquitoes, this being the usual manner by which
the infection is introduced to a premise. Mosquitoes may harbor infective
virus for a month or more after feeding on affected birds. After the infection
is introduced, it spreads within the flock by mosquitoes as well as by
direct
and indirect contact. Recovered birds do not remain carriers.
Symptoms and lesions: Since fowl pox usually spreads slowly a flock
may be affected for several months. The course of the disease in the individual
bird is 3 to 5 weeks. Affected young birds are retarded in growth. Laying
birds experience a drop in production. Birds of all ages which have oral
or respiratory system involvement have difficulty eating and breathing.
The disease manifests itself in one or two ways.
Cutaneous or dry pox: Lesions start as small whitish foci which develop
into wart-like nodules. The nodules eventually are sloughed and scab formation
precedes final healing. Lesions are seen most commonly around the featherless
facial parts (comb, wattles, ear lobes and eyes) but may be found on the
body.
Diptheritic or wet pox: Lesions are associated with the oral cavity
and the upper respiratory tract, particularly the larynx and trachea. The
lesions are diptheritic in character and involve the mucous membranes to
such a degree that when removed, an ulcerated or eroded area is left.
Diagnosis: Fowl pox readily is diagnosed on the basis of flock history
and presence of typical lesions. In some instances, laboratory diagnosis
by tissue or transmission studies is necessary.
Prevention and treatment: There is no treatment for fowl pox. Disease
control is accomplished best by preventive vaccination since ordinary management
and sanitation practices will not prevent it. Several kinds of vaccines are
available: pigeon pox, pigeon pox-like and fowl pox vaccine. The pigeon pox
vaccine is of questionable value and its use usually is not recommended.
The pigeon pox-like vaccines are newer and have wider acceptance. Fowl pox
vaccine is an efficient product and is in common use in Texas. Its use varies
according to the type of operation, but generally the following recommendations
apply:
Broilers: Vaccination usually is not required; but in some areas where
the mosquito population is high, as in parts of Texas, it may be necessary
to prevent the disease. In such instances, the vaccine is applied to chicks
(as young as 1 day) using the wing-web method but using only one applicator
needle.
Replacement birds: Vaccinate all replacement chickens against fowl
pox. One application of fowl pox vaccine results in permanent immunity. Birds
can be vaccinated at any convenient time during the growing period, usually
between 6 and 10 weeks of age.
Turkeys: Fowl pox vaccine does not produce lasting immunity in turkeys.
Vaccinate turkeys when they are between 4 and 10 weeks of age. Turkeys to
be retained as breeders should be revaccinated as adults. This usually is
done as the breeding flock is selected. Birds not selected and vaccinated
should be marketed within a day or two.
Examine vaccinated birds for "takes" about 7 to 10 days following vaccination.
A high percentage showing a reaction indicates a satisfactory vaccination.
AVIAN LEUKOSIS
The diseases which make up the avian leukosis complex are transmissible virus
diseases of birds characterized by tumor formations. The diseases are widespread
and have been the most devastating of those affecting mature laying chickens.
In recent years these diseases have become an increasingly significant cause
of losses in broilers and growing birds.
Of the separate and distinct diseases which form the complex, lymphoid
leukosis and Marek's disease produce the most losses.
Lymphoid Leukosis (L.L.)
Characteristically, lymphoid leukosis is a disease of adult chickens; however,
the disease appears to be of increasing importance in turkeys and other species
such as the pheasant. Although the virus of lymphoid leukosis may produce
various responses (for example: blood forms - erythroblastosis and
myeloblastosis; bone forms - osteopetrosis), the lymphoid tumor response
is the most common.
Cause and transmission: Lymphoid leukosis is caused by a group of
enveloped RNA viruses which closely resemble those of the myxovirus group.
The disease is transmitted in a number of ways. The agent is eliminated naturally
from the body of the infected bird via eggs and feces. The virus may be
transmitted mechanically from infected birds to susceptibles by blood-sucking
parasites or by man in such procedures as fowl pox vaccination.
Most infections are acquired during the first few weeks of life. This suggests
that most flocks acquire the disease by egg transmission or by direct or
indirect contact with older infected birds during the early brooding period.
Manifestations of disease: Lymphoid leukosis is characterized by the
formation of lymphoid tumors, particularly in the liver and spleen. Affected
birds may die without preliminary symptoms, but the disease usually is chronic
in nature with affected birds showing loss of appetite, progressive emaciation
and diarrhea. Clinically affected birds invariably die. Although losses due
to the disease may be most severe shortly after the onset of production,
losses in the affected flocks continue as long as it is retained and may
total 20 percent or more during the productive life of the flock.
Autopsies of affected birds reveal tumors. Although the liver and the spleen
are commonly involved, other visceral organs may be affected. The neoplastic
process may be diffuse involving 100 percent of the affected organ, or it
may be a nodular type. Affected structures, the liver in particular, may
be greatly enlarged.
Osteopetrosis is the bone form of the disease. Until recently it was thought
to be a disease primarily of older birds, particularly males; however, it
is now known to be quite common in young chickens and is one of the more
serious causes of broiler condemnations. The disease is characterized by
a thickening and deformation of bone, the long bones in particular. This
frequently results in lameness and faulty body conformation.
Blood forms of L.L. are diagnosed infrequently.
Diagnosis: The clinical diagnosis of L.L. is based upon flock history
and disease manifestations. The lymphoid disease cannot be readily distinguished
from the visceral response to Marek's disease (M.D.); however, there are
some features which aid in differential diagnosis. Some of these features
are outlined in the table at the top of the next column.
It should be kept in mind that the clinical differentiation of L.L. and M.D.
is often presumptive at best. Histopathological differentiation is more accurate,
but not completely so.
Treatment and prevention: There is no treatment for lymphoid leukosis.
Although the disease cannot be prevented completely, there are certain steps
which can be taken to help control the level of infection in a flock.
Some of these are listed below.
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Buy resistant strains of birds. Most reputable breeders have invested a great
deal of time and money breeding for L.L. resistance,
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Brood in isolation. Most L.L. is acquired early (under 6 weeks of age). If
replacement birds are brooded in strict isolation, contact transmission (direct
and indirect) from adult carriers will be minimal,
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Keep incubator sanitary,
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Control blood-sucking parasites, and
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Do not use gimmicks in disease control (e.g. explosive outbreaks of L.L.
have occurred following indiscriminate use of turkey blood in M.D. "control"
programs).
DIFFERENTIAL DIAGNOSIS OF L.L. AND M.D.
FEATURE |
LYMPHOID LEUKOSIS |
MAREK'S DISEASE |
Incubation period |
Prolonged |
Short |
Usual age incidence |
Over 6 months |
Under 6 months |
Visceral lesions |
Most commonly liver & spleen |
Generalized |
Skin lesions |
No |
Yes |
Ocular lesions |
No |
Yes |
Neural lesions |
No |
Yes |
Marek's Disease (M.D.)
Marek's disease characteristically is a disease of young chickens; however,
the disease commonly is seen in adult birds. In contrast to L.L., the tumor
response of M.D. is limited to the lymphoid type. However, the response may
be much more diverse in location than that usually seen in lymphoid leukosis.
Cause and transmission: Marek's disease is caused by a virus belonging
to the Herpesvirus group. Much is unknown about the transmission of the virus;
however, it appears that the virus is concentrated in the feather follicles
of affected birds and is shed in dander. The virus apparently has a long
survival time in dander, and viable virus may be demonstrated in depopulated
houses months after infected birds have been removed. The usual mode of
transmission is by aerosols containing infected dander and dust. As with
L.L., young birds are most susceptible to infection with M.D.; however,
since
the incubation period of M.D. is short, clinical disease can appear much
earlier than is the case with lymphoid leukosis.
Manifestations of disease: Marek's disease may produce a variety of
clinical responses, all lymphoid in character. These are acute visceral,
neural, ocular and skin; or commonly a combination of the responses may be
seen.
Marek's disease of the visceral type may be characterized by widespread
involvement. The lesions most commonly are associated with the gonads (testes
or ovaries), liver, spleen and kidney; however, other organs such as the
lungs, heart and musculature are commonly involved. The disease often is
acute, with apparently healthy birds dying very rapidly with massive internal
tumors. The disease may appear in broiler-age birds and be a significant
cause of death loss and condemnations. More commonly the disease produces
the most severe losses in replacement pullets near or at the onset of production.
At this time, the disorder is seen frequently in birds with acute coccidiosis,
leading some to suspect there is a relationship between the two diseases.
Presently the only relationship is considered to be that of a bird with
coccidiosis or M. D., whichever the case, being more susceptible to the other
disease.
Marek's disease of the neural type is the classical type, Neural
leukosis was the first disease known as M.D. before the etiologic
relationships of the various diseases in the leukosis complex were established.
Neural leukosis is characterized by a progressive paralysis of the wings,
legs and neck. Loss of body weight, anemia, labored respiration and diarrhea
are common symptoms. When affected birds are autopsied, lesions, if observed
in uncomplicated cases, are confined to the nerve trunks and plexuses innervating
the paralyzed extremities. Affected nerve tissue is swollen as a result of
an accumulation of lymphocytes and tissue fluids. Frequently no gross lesions
are observed.
Ocular leukosis (gray eye) is responsible for much of blindness in chickens.
This type of M.D. usually is seen in early maturity. Morbidity and subsequent
mortality usually are low, but in some instances approach 1 5 to 25 percent.
Ocular leukosis is characterized by spotty depigmentation or diffuse graying
of the iris caused by lymphocytic infiltrations. The pupil develops an irregular
shape and fails to accommodate to light. Emaciation, diarrhea and death usually
follow because of partial to complete blindness.
Skin leukosis is the form of M.D. that produces the most severe losses in
broilers. Losses more commonly are due to condemnation at processing time.
The disorder is characterized by enlargement of the feather follicles due
to accumulations of lymphocytes. As stated, most infective virus is produced
in the regions of the feather follicle and is shed with skin dander.
Course of disease: Acute M.D. can be extremely rapid in its course,
producing mortality in apparently healthy birds. However, it has been
demonstrated that the lesions of M.D. (particularly of skin leukosis) may
regress, and clinically affected birds may make complete recoveries.
Diagnosis: The clinical diagnosis of M.D. is based upon flock history
and disease manifestations (refer to table under the diagnosis of lymphoid
leukosis). Accurate diagnosis may depend on the employment of sophisticated
laboratory procedures.
Prevention and treatment: As is the case with L.L., there is no treatment
for Marek's disease, and until recently there have been no effective preventive
measures.
A vaccine is now available which appears to be extremely effective (90 percent)
in the prevention of M.D. The vaccine is made with a Herpesvirus of turkeys
(H.V.T.) that prevents the virus of M.D. from transforming cells to produce
tumors. It is applied to day-old chickens by injections in strict accordance
with the manufacturer's recommendations. Other approaches to control include
the genetic and management/sanitation.
EPIDEMIC TREMOR
(Avian Encephalomyelitis)
Avian encephalomyelitis is a viral infection which affects chickens of all
ages, but usually produces clinical manifestations only in young birds. In
recent years, the disease also has been observed in turkeys. Signs of infection
include incoordination, nervousness, a jerky or irregular gait, falling over
on the side with outstretched wing and muscular tremors especially noticeable
in the head and neck. The commonly used term epidemic tremor is misleading
because muscular tremors are not evident in many otherwise typical outbreaks.
This disease, reported first in New England in 1932, now exists in all
poultry-producing areas of the United States and has been reported in several
other countries.
The custom of hatcheries to adjust for losses due to epidemic tremor has
led other segments of the poultry industry to regard the disease as of minor
importance and significant primarily to hatcherymen. Such losses are costly,
troublesome and reduce efficiency in all operations, especially in breeder
and broiler flocks. Thus, epidemic tremor poses a major problem for the entire
poultry industry.
Cause: Epidemic tremor is caused by a relatively small virus which
produces microscopic lesions in the bird's nervous system.
Transmission: The virus is transmitted to the chick through eggs of
infected parent flocks. Such outbreaks in parent flocks often are unnoticed
and usually last 21 to 30 days. It appears that affected flocks do not remain
carriers and are not susceptible to the disease again for a reasonable time;
consequently such flocks are desirable as hatchery supply flocks.
Apparently, other modes of transmission are responsible for outbreaks in
production flocks. The disease can be transmitted by direct or indirect contact,
but this is not of major significance.
Symptoms and lesions: In a small percentage of outbreaks, the disease
may be suspected because of poor hatchability or morbidity in birds at hatching
time. The incubation period varies from 5 to 40 days with an average of 9
to 21 days. The typical outbreak becomes noticeable when birds are 17 to
21 days old. Some individuals in flocks exposed during hatching may develop
clinical evidence of infection up to 7 weeks later. Morbidity rates vary
from only a few individuals to 30 percent, but average 5 to 10 percent.
Outbreaks in young chicks are characterized by an inability to walk normally.
Affected birds may become paralyzed and lie propped on one wing. Visible
trembling of the head and neck may be present, but is not apparent in many
outbreaks. Affected birds usually do not recover, but they will survive for
long periods if food and water are provided. New cases developing after the
fifth or sixth week are rare. Mortality usually is negligible but visibly
affected individuals should be removed and destroyed.
No lesion is visible with the naked eye. Microscopic lesions are widespread
and are a diagnostic aid.
In adult flocks, there may be no evidence of infection other than a 5 to
10 percent drop in egg production, with a decrease in hatchability. Most
outbreaks in adult flocks are not suspected unless the caretaker is a keen
observer and keeps good records.
Diagnosis: The disease usually is diagnosed on the basis of case history
and typical signs. Atypical cases present diagnostic problems and every reliable
aid must be used to make an accurate diagnosis.
Treatment and prevention: The disease readily is prevented by vaccinating
breeder replacements prior to the onset of production. Vaccine is applied
in drinking water when the birds are approximately 10 to 14 weeks old. The
vaccination of breeder stock in this way prevents subsequent infection and
egg transmission of the virus.
There is no treatment. Remove and kill all birds showing clinical evidence
of the disease, since they do not develop into profitable birds.
INFECTIOUS BURSAL DISEASE
(Gumboro)
Infectious bursal disease (I.B.D.), commonly referred to as Gumboro disease,
is an acute, highly contagious viral disease of young chickens. It is found
most often in the highly concentrated poultry producing areas of the state.
It causes marked morbidity and mortality in affected flocks but usually
disappears after 1 to 2 weeks.
Cause: A virus or virus-like agent referred to as the infectious bursal
agent causes this disease.
Transmission: The transmission or spread of the disease can occur
by direct contact (bird to bird), contaminated litter and feces, caretaker,
contaminated air, equipment, feed, servicemen and possibly insects and wild
birds. It is extremely contagious.
Symptoms and lesions: Birds have ruffled feathers, a slight tremor
at onset of the disease, strained defecation, loss of appetite and are
dehydrated. Affected birds have a tendency to sit, and when made to move
have an unsteady gait. Vent picking is common. Early in the disease there
is a rise in body temperature, but it soon becomes subnormal. This often
is followed by prostration and death. The litter of contaminated houses becomes
sticky during the course of the disease.
Postmortem lesions include dehydration and changes in bursa, skeletal muscle,
liver and kidney. All affected birds have some bursal changes commonly
characterized by swelling change in shape (oblong), color (pink, yellow,
red, black) and the formation of gelatinous film around the bursa.
Diagnosis: The diagnosis of I.B.D. usually is based on flock history
and postmortem lesions. Laboratory procedures may be used to substantiate
the diagnosis.
Prevention and treatment: Management and sanitation practice alone
cannot be relied upon to prevent the occurrence of the disease.
Early exposure (before 14 days of age) to the agent of I.B.D. apparently
acts as an immunization procedure, and many flocks that are exposed and infected
do not develop noticeable disease symptoms.
Vaccines are available but must be given under the supervision of a poultry
pathologist or regulatory official. If given correctly, good control can
be obtained.
There is no specific treatment for I.B.D. In fact, indiscriminate medication
with certain drugs (e.g. the sulfonamides) may severely aggravate mortality.
Supportive measures, such as increasing heat, ventilation and water consumption,
are beneficial.
INCLUSION BODY HEPATITIS (I.B.H.)
Inclusion body hepatitis is an acute infectious disease of chickens characterized
by sudden onset, marked depression, jaundice of the unfeathered skin and
high mortality. The disease was first reported in 1963 as a rare condition
in chickens. However, at the present time the disease appears to be widespread
among commercial flocks.
Cause: The etiological agent of I.B.H. is an adeno virus.
Transmission: How the disease is introduced into a flock is not fully understood.
Some researchers believe the virus is egg transmitted. Horizontal transmission
may take place by direct or indirect contact with infected birds, litter
and equipment.
Signs and lesions: The disease has a sudden onset. A dramatic increase
in mortality in an apparently healthy flock of birds may be the only sign
observed. Mortality rate remains high during the first 3 to 5 days and then
declines. Total mortality may range between 2 and 10 percent. As the disease
progresses in a flock, affected chickens may be seen. Signs at this time
include anemia, jaundice of the unfeathered skin, marked depression, weakness
and prostration. Birds showing signs of the disease usually die within a
few hours. It is often observed that sick birds selected for diagnosis die
on their way to a diagnostic laboratory if more than a few hours of travel
is required.
Gross lesions of I.B.H. include discoloration (paleness) of liver, bone marrow
depletion, swelling and discoloration of kidneys, along with atrophy of spleen
and bursa of Fabricius. Hemorrhagic areas generally are evident in various
organs and muscles. The hematocrit value may be one half to one tenth of
the normal value.
Diagnosis: I.B.H. tentatively can be diagnosed on the basis of history,
clinical signs and lesions. Virus isolation and agar gel precipitin test
is performed to confirm the diagnosis.
Treatment and control: There is no treatment for I.B.H. At present no vaccine
is available for preventive immunization of susceptible birds.
TRANSMISSIBLE ENTERITIS OF
TURKEYS
(Bluecomb)
Transmissible enteritis is an acute to chronic disease of turkeys characterized
by sudden onset, marked depression and severe diarrhea. Death losses may
be high, particularly in young poults, but heaviest losses in adults are
due to loss of condition. The disease at one time was considered to be the
same as so-called "bluecomb" of chickens. Now it is recognized as a distinct
entity.
Cause: The etiologic agent of turkey bluecomb is now known to be a
corona virus. Substantial evidence exists; however, the disease as seen in
the field is the result of an interaction of several agents, among which
the virus is considered to be primary.
Transmission: The disease spreads by contact with infected birds or
premises. Droppings of infected birds are especially rich in virus. No specific
environmental factors appear to influence the occurrence; however, the stress
of adverse weather conditions may be a factor in the severity of the disease
in range birds.
Symptoms and lesions: When the disease strikes young poults under
3 to 4 weeks of age, onset is sudden. Affected poults appear cold and seek
heat. Feed and water consumption drops markedly, and poults lose weight rapidly.
Morbidity and mortality may approach 100 percent in uncontrolled outbreaks.
Young poults show few lesions other than those associated with the intestinal
tract. Intestines usually are distended and lack muscle tone. Intestinal
contents are fluid and gaseous (foamy).
Morbidity is variable in older flocks of turkeys. It may be extremely low
in some flocks but extremely high in others. Feed intake drops markedly and
birds may lose up to 5 pounds of body weight in just a few days. Birds usually
have profuse diarrhea. Cyanosis of the head parts is common.
When older birds are autopsied, the following lesions may be seen. The body
musculature is dehydrated. Minute hemorrhages may be seen on the viscera
and necrotic foci seen on the liver. Kidneys commonly are swollen and contain
an excess of urates. Severe catarrhal enteritis is seen often, and mucous
casts may be present. The pancreas usually presents multiple chalky white
areas. The crop frequently is distended and contains sour-smelling contents.
Diagnosis: Transmissible enteritis must be differentiated from common
bacterial infections such as paratyphoid, fowl cholera, fowl typhoid and
erysipelas. Diagnosis usually is based on history, symptoms, lesions and
negative bacteriological findings for the common bacterial infections.
Prevention and treatment: Until more is known about the spread of
bluecomb, no specific recommendations for prevention can be made. However,
consider recovered birds as potential carriers. Clean and disinfect houses
in which outbreaks have occurred. Leave vacant for at least 30 days. Apply
routine management and sanitation practices for disease prevention.
During outbreaks older turkeys can be flushed with molasses at the rate of
1 pint molasses to 5 gallons of drinking water for 1 day. Then give antibiotics
in feed or drinking water at the rate of at least 200 grams/ton of feed or
200 to 400 milligrams/gallon of water. Continue treatment for at least 5
to 7 days.
Do not flush young turkey poults. Give antibiotics at the rate of up to 400
grams/ton of feed or 1 gram/gallon of drinking water. Give this high level
for 2 or 3 days, after which time antibiotics may be reduced, depending on
flock response. Total treatment period should be at least 5 to 7 days.
