DEPARTMENT OF VETERINARY MEDICINE, SURGERY AND THERIOGENOLOGY,

USMANU DANFODIYO UNIVERSITY, SOKOTO

VMD 5102: AVIAN MEDICINE
LECTURE IV: VIRAL DISEASES

Laryngotracheitis (LT).
This is an acute respiratory disease with depression, gasping, expectoration of
bloody exudate, causing losses in egg production and occasionally, high
mortality, caused by herpes virus.

Epidemiology: Chickens are the only natural host, all ages are susceptible but
the characteristic signs appear mostly in adults. Incubation is about 6 - 12
days. Morbidity may be up to 90% - 100%, mortality varies from 5% to 70%.

Clinical Signs: In severe cases, there is nasal discharge, moist rales, coughing
and gasping, dyspnea, expectoration of bloody mucus. The blood mucus is a
rather unique sign. In milder cases, there is unthriftiness, reduction in egg
production, watery eyes, conjunctivitis, swelling of the infraorbital sinuses,
persistent nasal discharge and hemorrhagic conjunctivitis.

Pathogenesis. The virus enters through the upper respiratory tract and via the
conjunctiva, less frequently orally. Virus replication is limited to the
respiratory system, with little or no evidence of viremia. Egg transmission has
not been demonstrated.

Gross and Histopathologic Lesions. The overall picture is a mucoid

inflammation and degeneration, resulting in necrosis and possibly in
hemorrhages, with desquamated epithelial tissues and blood clots.
Inflammation may extend to the bronchi and alveoli. Histopathology is
consistent with gross lesions. Intranuclear inclusion bodies are found in
numerous cells in areas showing gross lesions.

Diagnosis. Clinically, the expulsion of bloody mucus is the only distinguishing

feature from many other respiratory diseases. An early clue is the intranuclear
inclusion bodies in upper respiratory tissues, otherwise FA of diseased
epithelial tissues, and/or Viral Isolation on chorioallantoic membrane of
embryonating chicken eggs or in chicken embryo kidney cell culture is used.
Prevention and Control. Management is via isolation of sick birds from the
healthy ones. This probably will have to be done in larger housing or
management units, rather than on an individual bird basis. Immunization with
attenuated live virus vaccines administered via infraorbital sinuses, intranasal
instIllation, was used efficiently. Administration via drinking water, although it
is very economical, is prone to be erroneous, leaving some birds unimmunized
or not having acquired sufficient immunizing dose.

Infectious Bronchitis (IB).

This is a worldwide distributed, economically important, acute, highly
contagious, respiratory disease of chickens, characterized clinically by tracheal
rales, coughing and sneezing. Laying flocks suffer decreased egg production
and laying of poor quality eggs.

The Virus. There are 6 serotypes of IBV, complicating immunization against IB.

Epidemiology. The chicken is the only natural host. All ages are susceptible,
but young chicks suffer a clinically more severe disease, with occasional
mortality. The clinical signs appear in 18 - 36 hours. Morbidity may be 100%,
but mortality is very low.

Clinical Signs. In young chickens these are gasping, coughing, tracheal rales,
wet eyes, occasional sinus swelling. The chickens are depressed and huddle
under or near the heat sources. In growing chickens the signs are tracheal
rales, gasping coughing which are less severe than in young chicks.

In adult laying flocks one observes tracheal rales, gasping and coughing. Very
importantly, egg production may drop by 50%, particularly in the latter part of
the laying year. Soft-shelled, rough-shelled, misshapen eggs are laid, which
may have thin and watery albumen. The drop in egg production is the
economically most important damage caused by IBV.

Pathogenesis. The chickens are infected with virus-carrying aerosol via the
respiratory epithelium. Initial replication occurs here, followed by replication
in the kidneys and bursa of Fabricius.

Gross and Histopathological Lesions. Serous, catarrhal, caseous exudate in

the trachea, the nasal passages and the sinus of the chickens is present. In

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laying hens, the oviduct length and weight are reduced, kidneys are swollen
and pale, with tubules and ureters distended with uric acid crystals.

Histologically, there is infiltration and edema of the mucosa, submucosa,

vascular congestion, hyperplasia and vacuolation of the epithelium in the
respiratory tract. The mucosa may be deciliated.

Diagnosis. Diagnosis is based mainly on VI or on demonstration of ascending

antibody titer. FA test or VI can demonstrate virus in embryonating chicken
eggs via allantoic sac inoculation resulting in dwarfing of the embryos.
Antibodies are demonstrated by VN or by agar gel precipitation
(immunodiffusion) tests. The disease must be differentiated from Newcastle
disease, laryngotracheitis and infectious coryza.

Prevention and Control. Isolation of sick birds is useful in lowering the losses,
but is not sufficient in completely preventing the spread of IB. Prevention is
based on immunization. Inactivated and modified live virus, monovalent or
multivalent vaccines are available. The monovalent vaccines protect 90-100%
against homologous, but only an average 38% against infection with
heterologous strains. This complicates the task of generating a reliable and
high degree of protection over a long period of time. IBV vaccines, combined
with NDV are also available. Experience with these vaccines suggests that
whenever possible and practical IBV vaccines should be administered alone.

Avian influenza (AI).

The disease caused by type A influenza viruses in domestic or confined birds,
once known as fowl plague (FP). It is worldwide distributed. Signs range from
mild upper respiratory disease to reproductive failure (loss of egg production)
and acute highly fatal generalized disease. In terms of the epidemiology of the
disease, it is important that a large number of AI strains are isolated from
free-flying water fowl.

The Virus. There are low- and high-pathogenicity strains. The RNA genome is
composed of 8 segments that freely reassort when a cell is infected with 2
different strains resulting in genetic recombinants that express characteristics
inherited from both parents. Antigenic variation occurs in two ways: shift and
drift. Antigenic shift, i.e. exchange of large sections of viral genome results in

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large antigenic divergence. Antigenic drift, i.e. point mutations in the genes
coding for the H and/or N antigens, results in more subtle changes. The
biologic properties of influenza virus strains are extremely variable, especially
with regard to host range and virulence. Thus, in working with influenza
viruses year after year it is very important to follow not only the changes that
may happen in the antigenicity of the strains, but also to analyze changes in
the biologic properties of newly isolated strains.

Epidemiology. Chickens have been relatively free from AI, as compared to

turkeys and ducks. Prior to the 1983 AI outbreak in Pennsylvania, only two
cases have been reported in chicken in the US. Although turkeys have been
and are the most frequently infected domestic species, they frequently do not
have clinical AI, but are still able to secret and pass on the virus to other
species. The virus may be transmitted by direct contact but direct contact is
not necessary. The respiratory tract is the main route for the acquisition of the
virus. Chickens may acquire the AIV from other species of domestic poultry, or
from exotic captive birds, or from other animal species. In terms of
heterologous transfer swine are particularly important. Because of the
prevalent social and cultural conditions in rural China resulting in very close
confinement of humans, chickens and pigs, China is the main source of new
AIV strains, particularly those that acquire the capacity of cross-species
infection.

Clinical Signs. The signs are extremely variable and depend on the species
affected, the age and sex of the infected chickens, concurrent infections with
other agents, bacterial or viral, environmental factors, etc. which also will
affect the extreme range of morbidity and mortality observed. There may be
fulminating cases where birds die without signs. The signs of a typical
influenza case are decreased activity, decreased feed consumption,
emaciation, increased broodines of hens, decreased egg production, mild to
severe respiratory signs, coughing, sneezing, rales, excessive lacrimation,
huddling, ruffled feathers, sinusitis, edema of the head and face, cyanosis of
unfeathered skin, nervous signs, such as torticollis, and diarrhea. The
complexity of the signs indicates a true multisystemic viral infection.

Gross Lesions. Highly varied. Congestive, hemorrhagic, and necrotic changes

in the skin, comb and wattles, and yellow-gray, necrotic foci in the liver,
spleen, kidneys and lungs are seen. Yellow exudates on the air sacs,

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peritoneum, oviducts and fibrinous pericarditis have also been observed.
Sinusitis has been described in several species including turkeys, ducks,
chickens, partridge, and pheasants.

Histopathologic Lesions. Edema, hyperemia, hemorrhages, perivascular

cuffing (particularly in the brain), parenchymal degeneration and necrosis in
spleen, liver, kidney are present. In the affected sinuses there is cell
degeneration, epithelial hyperplasia, infiltration with heterophils, and acute
inflammation of lamina propria were found.

Diagnosis. Differential diagnosis includes Newcastle disease, other

paramyxoviruses, chlamydia, mycoplasmas, and bacteria. Definitive diagnosis
is based on laboratory procedures. AI strains have been recovered from both
live and dead birds by swabbing the trachea and cloaca, and inoculating
chicken embryos by the allantoic sac route. The allantoic fluid is tested for
HAg activity. For serology 2 samples, harvested 2 weeks apart are analyzed for
HAg-inhibiting antibodies.

Prevention and Control. Prevention and control are very difficult tasks.
Prevention of influenza in humans is based on vaccination. This requires
constant vigilance and analysis of current influenza virus isolations to
determine and their sero- and bio-type. In animals, as for humans, free-flying
waterfowl represent a constant and major threat. For these reasons the only
effective means of controlling the spread of influenza from animal sources is
eradication (detection, slaughter and destruction). Such procedures have been
effectively employed against FP and as well as AI, such as in the 1983 AI
outbreak, or the more current influenza outbreaks in the Far East. Obviously,
eradication can only be used to either control animal-to-animal or animal- to-
human transfer. All these control measures should be based on biological
characteristics (biotypes) of the strain involved and not on antigenic
relatedness. It is entirely conceivable that a new serotype strain will have no
increased virulence. Vice versa, influenza strains of the same serotype main
represent new and increased threat. There are no federally licensed vaccines,
although experimental inactivated have been developed.

Public Health Significance. Strains of AIV are found in mammals (harbor

seals), and influenza viruses of mammalian characteristics (humans, swine) are
found in avian species. The relative ease and frequency with which influenza

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virus strains cross species barriers is the greatest threat to both animal and
human health by this virus.

NEWCASTLE DISEASE

Synonyms: Pseudo-fowl pest, pseudo-poultry plague, avian pest, avian

distemper, Ranikhet disease, avian pneumoencephalitis.

It is probably the most important viral disease of poultry. It is a worldwide

distributed, infectious, highly contagious, destructive disease of chickens,
turkeys, numerous species of wild and captive birds. The occasional human
infection results mostly in mild conjunctivitis.

Aetiology: NDV isolates are categorized into lentogenic, mesogenic and

velogenic strains, which refer to highly variable biotype. Lentogenic strains are
almost avirulent, even for very young, a few days old, chickens. Some
lentogenic NDV strains (B1, LaSota) have been used as vaccines without any
attenuation. The mesogenic strains are more virulent, but at least one strain
(Roakin) has also been used as a vaccine, but only in older birds. The velogenic
strains are the most virulent, pathogenic ones and are used as challenge virus
in vaccine efficacy trials.

Epidemiology: Five clinical forms or pathotypes of ND are caused by

morphologically and antigenically similar NDV strains.

1. Viscerotropic Velogenic ND (VVND). This has been originally named as

Doyle's form by the name of the researcher who characterized it, or as Asiatic
ND where it appeared most frequently. It is caused by viscerotropic, velogenic
NDV strains. It is an acute highly lethal infection of all ages of chickens.
Hemorrhagic lesions of the digestive tract are prominent, giving the name of
the form.

2. Pneumoencephalitic or Neurotropic ND (PNND). This has been originally

named as Beach's form. It is caused by pneumotropic, velogenic strains. It is
an acute and frequently lethal infection of chickens of all ages, characterized
by lesions in the respiratory and nervous system. There are no hemorrhages in
the digestive tract, a lesion very important in distinguishing VVND from PNND.

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3. Beaudette's form is known only by the investigator's name and is caused by
mesogenic strains. It is an acute respiratory and sometimes lethal nervous
infection of young chickens. In older birds mortality is rare. Some of these
strains used as viable vaccines.

4. Hitchner's form is known only the investigator's name. It is caused by

lentogenic strains and is a mild or inapparent respiratory infection of young
chickens. Mortality is rare in any age of chickens. Several strains are used as
viable vaccines. The B1 NDV vaccine is a lentogenic NDV strain, used as
originally isolated by Hitchner, in the largest number of doses of any and all
animal virus vaccines around the world.

5. Asymptomatic enteric form, is not manifested in a clinical disease, but is

still a form of NDV infection lentogenic strains. It results in no clinical signs or
pathology, but can confuse diagnostic situations. .

Transmission. The NDV spreads via aerosols, by drinking water or by fomites.

As the virus is quite labile the latter two means of transmission are not as
important as the aerosol transmission. There is no evidence for egg-
transmission.

Clinical Signs. Incubation varies from 2 to 15 days. Signs are as follows:

VVND. The disease appears suddenly, some birds die without any clinical
signs. Others are listless, hyperpneic, weak, prostrated and die in 4 - 8 days.
Edema around the eyes and throat, greenish, sometimes bloodstained
diarrhea may be seen. Clonic spasms, muscular tremors, torticollis,
opisthotonus, paralysis of the legs and wings show involvement of the CNS.
Mortality in susceptible populations is usually 90% or more, irrespective of the
age of the birds.

PNND. The disease appears suddenly, and spreads rapidly. Respiratory

distress, marked coughing, gasping, anorexia, drop in egg production are seen.
Diarrhea is rare as the GI tract is not affected in this form. Paralysis of legs and
wings, torticollis indicate CNS involvement. Mortality in susceptible flocks
varies from 10% to 90%, irrespective of the age of the birds.

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Beaudette. This is an acute respiratory disease of adult chicken with coughing
but rarely gasping. Anorexia and lowered egg production, and drop in egg
quality may be present.

Hitchner. It may be completely inapparent in adult birds. If the suspicion of

this form arises, close listening to the breathing of the birds will reveal
respiratory rales. Death is very rare, negligible although in adult birds. In one
case, in very young birds mortality of 30% did occur.

Gross Lesions. The gross lesions are not pathognomonic and are highly
variable. In VVND there are necrotic hemorrhages of variable size in the
posterior half of the duodenum, jejunum and ileum. Diphtheroid necrotic
buttons in the large intestine and cloaca are considered highly suggestive for
VVND.

In the other forms, the primary lesions are found in the respiratory tract.
Serous catarrhal exudate, hemorrhages are present in nasal passages, larynx,
trachea. Thickened membranes of one or more air sacs is common in young
birds.

Histological Lesions. Hyperemia, edema, hemorrhages, hydropic degeneration

of the media, hyalinization, necrosis of endothelial cells of the blood vessels
are seen. Hemorrhagic-necrotic lesions are in the lymphoid aggregates in the
intestinal walls. In the central nervous system (spinal cord, medulla, midbrain,
cerebellum) neuronal degeneration, perivascular cuffing, hypertrophy of
endothelial cells are found.

Diagnosis. Unequivocal diagnosis can be established only by laboratory tests.

The most decisive information is gained by isolation, identification of the virus
and subsequent production of the disease in susceptible chickens. This is
necessary because of the ubiquitous distribution of ND vaccine strains in the
poultry population. Cloacal and tracheal swabs, taken in the incubative and
early clinical stages of the disease, are the most useful samples. Virus isolation
is done preferably in embryonating chicken eggs or in cultured cells. Antigenic
subtyping is done by HAg and neuraminidase-inhibition tests. Specific
antibodies can be demonstrated by VN, plaque neutralization, complement
fixation, ELISA tests.

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Prevention and Control. Sanitary management and separation of sick from
healthy birds is important. The main thrust of prevention is by vaccination.
Newcastle disease vaccines are probably the most frequently used vaccines
among all animal virus vaccines. A number and variety of monovalent or
polyvalent, inactivated and live virus vaccines are available. Live virus vaccines
may be lentogenic or mesogenic strains, and are administered by several
methods, e.g. by wing-web stick, IM injection, intranasal, conjunctival sac
instillation, spraying or nebulizing or in the drinking water. Immunization is
supplemented by eradication particularly in case of the virulent forms (VVND,
PNND). Strains, causing these forms, particularly those causing VVND are so
virulent and pathogenic that even correctly performed immunizations cannot
be assumed to be fully or sufficiently protective.

AVIAN ENCEPHALOMYELITIS
Avian encephalomyelitis (AE) is a viral disease of young chickens caused by
Picorna virus from the Hepatoviridae family and characterised by central
nervous system signs (Epidemic Tremors). It can be the cause of significant
economic loss.
Susceptible species
• AE occurs naturally in chickens, turkeys, pheasants and Japanese quail.

Transmission
AE virus is transmitted both vertically and horizontally i.e. through the egg and
by contact. Eggs laid by hens with sub-clinical infection will carry the virus.
While hatchability drops, eggs will hatch and chicks will develop clinical
disease soon after. Affected chicks shed virus in faeces and will infect
susceptible in-contact chicks. To date wild birds have not been incriminated
as reservoirs.
Clinical signs
Chickens of all ages are susceptible, but clinical signs of encephalitis only
develop in those younger than four weeks. The disease is similar in turkeys
and chickens. Under field conditions disease is most common in the 1–2 week
age group. Following initial dull expression of the eyes, the following signs are
seen: - progressive ataxia with the chick losing control of legs, sitting on its
haunches and falling onto its side;
- tremor of the head and neck.

- Ataxia progresses to paralysis and death results from inability to feed

or drink, or through being trampled.

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 -
Some birds recover, and others may survive with persistent clinical
signs.

In susceptible adult birds, infection is usually sub-clinical, although there may

be a transient drop in egg production.
Post-mortem findings
• In chicks dying of AE there are no characteristic gross lesions.
Histological examination of brain and spinal cord reveals characteristic
encephalomyelitis with neuronal degeneration, perivascular cuffing and
gliosis.

Infectious bursal disease.

The disease, once called avian nephrosis, is worldwide distributed, causing
considerable losses by the clinical disease and even more by
immunosuppression resulting in gangrenous dermatitis, inclusion body
hepatitis-anemia syndrome and vaccination failures.

The Virus. It has double-stranded, double-segmented genome: "birna" virus. It

is highly resistant. Ether, chloroform, pH 2 will not affect the infectivity of the
virus, but exposure to 0.5% formalin for 6 hrs inactivates it.

Epidemiology. The disease occurs in all major poultry producing areas of the
world. The main host is chickens, though natural infection in turkeys and
ducks was reported. The clinical disease in chickens is usually subclinical to
mild before 3 weeks of age, and mild to severe between 3 - 6 weeks of age.
The disease is highly contagious, transmitted mainly by water, feed and
droppings. There is no evidence for egg transmission. In fully susceptible
flocks, sudden and high (100%) morbidity, spiking mortality, ranging from nil
to 20-30%, are seen.

Clinical Signs. Clinical signs appear in 2-3 days, starting with the infected birds
picking at their own vents. Soiled vent feathers, whitish or watery diarrhea,
anorexia, depression, ruffled feathers, trembling, severe prostration,
dehydration, subnormal temperature and death, complete the clinical picture.

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Pathogenesis. The bursa of Fabricius is the main target for the virus, where
antigen-antibody complexes may induce Arthus-type hypersensitivity reaction
leading to necrosis, hemorrhagen and appearance of large numbers of
polymorphs. Increased clotting time may lead to the observed hemorrhages.

Gross Lesions. Dehydration, darkened pectoral muscles, hemorrhage in the

thigh and pectoral muscles are found. The bursa of Fabricius undergoes a
typical sequence of weight changes: by day 3 it is enlarged somewhat, day 4
twice its normal size, day 6 it returns more or less to its normal size and
weight, then atrophies to about one third its normal size by day 8. This is all
associated with the initial Arthus-type hypersensitivity reaction, an
inflammation, followed by the necrosis of bursal tissues.

Histological Lesions. Edema, hyperemia, hyperplasia, degeneration, necrosis

are seen sequentially and in various combinations in the cloacal bursa, spleen,
thymus harderian gland and cecal tonsil.

Diagnosis. Clinical signs in acute cases are helpful. Gross pathology is helpful
in confirming the disease but final diagnosis requires laboratory work. Virus
isolation from the bursa and the spleen on chorioallantoic membrane of
embryonating chicken eggs is the most sensitive laboratory method. FA
demonstrates viral antigen in tissues. Immunodiffusion or ELISA is used to
demonstrate antibodies. The disease is to be differentiated from coccidiosis,
infectious bronchitis, and in some instances from Marek's disease.

Prevention and Control. The virus is quite resistant, difficult to eliminate,

management has limited value. Breeder flock immunization with live virus
vaccines to provide passive (maternal) immunity via the yolk is practiced.. The
vaccine virus replicates in the thymus, spleen and bursa. Oil-adjuvanted, killed
virus vaccines are used to boost immunity of breeder flocks. Providing passing
immunity via immune yolk of the embryonating egg is a particularly powerful
and economical means of distributing immunity to the very large number of
offsprings, characteristic for the poultry industry.

CHICKEN ANEMIA VIRUS

The chicken anemia virus (CAV) was first described in 1979 in commercially
produced chickens. Since that time, the virus has been detected by isolation
or serology in most countries in both laying and broiler chickens.

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The virus, when transmitted by the transovarian route, can result in severe
disease in progeny characterized by anemia, subcutaneous hemorrhage, and a
decreased resistance to secondary bacterial diseases such as gangrenous
dermatitis. Affected birds, if coinfected with infectious bursal disease virus,
may develop a profound immunosuppression with enhanced susceptibility to
a wide range of viral and bacterial pathogens
Infections with CAV are considered to be economically significant because of
the clinical disease associated with vertical transmission and because of its
potential for inducing immune dysfunction alone or in combination with other
pathogens reported that apparent subclinical infections of commercially
produced broilers may result in increased mortality and condemnations.

Aetiology :The CAV is a small nonenveloped virus resistant to thermal

inactivation and treatment with lipid solvents and many of the common
disinfectants. The viral genome is a single-stranded DNA

Clinical Signs: Disease usually occurs during the first 3 wk of life resulting from
vertical transmission or contact exposure close to hatch. Chickens at any age
are susceptible to infection by the oral or respiratory routes, but do not show
apparent signs of disease because of an age associated resistance that is
consistent with the maturation of the immune system. The period of
susceptibility to disease may be extended by early exposure to infectious
bursal disease virus, Marek’s disease virus, or selected avian reoviruses that
interfere with normal immune system development. Severely affected birds
generally die within 2 to 4 wk of age and survivors are often stunted. Because
of the immunosuppression, affected chickens frequently develop secondary
infections. There may also be an increased susceptibility to adenovirus-
associated inclusion body hepatitis and respiratory disease.

Gross Lesions: Lesions of uncomplicated CAV infection in young chickens

typically consist of bone marrow aplasia with reduction in hematocrit values.
Chickens are anorexic, depressed, and exhibit a marked pallor that may
extend to the internal organs. Hemorrhages can be observed in the
musculature and subcutaneously, with the wing tips frequently affected. The
bone marrow is pale or yellow in color and may have a fatty consistency.
Thymic atrophy and congestion is common and is considered diagnostic when
associated with other typical signs or lesions. Bursa atrophy is generally
modest and transitory, typically occurring at 10 to 14 d of age in chickens

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vertically infected. All of the aforementioned lesions are exacerbated and
more persistent in chickens coinfected with infectious bursal disease virus or
other lymphocidal agents.

Microscopically, the bone marrow of CAV-infected chickens is depleted of

erythrocytes, thrombocytes, and granulocytes and their precursor cells, which
are replaced by adipose tissue. Thymic atrophy is the result of lymphocyte
depletion in both the cortex and medulla. The bursa of Fabricius and spleen
may also be depleted of lymphoid cells, but the involvement and duration is
less extensive than seen with the thymus. Survivors of CAV infection usually
return to normal by approximately 4 wk of age, which coincides with the
onset of measurable antibody responses.

Prevention and Control

Chicken Anemia Virus is generally considered to be ubiquitous in both egg and
meat-type chickens worldwide. Because the virus is very resistant to
inactivation and easily transmitted, it is probably unrealistic to assume that
exposure can be limited with conventional housing and production
parameters.
Infections of breeder flocks naturally or by the introduction of CAV prior to the
onset of egg production will render them immune to subsequent exposure
and prevent transovarian transmission. Based on serological evaluations, most
flocks produced in the U.S. are infected prior to 12 wk of age. However, it is
not uncommon, particularly in new production facilities, to find pullet flocks,
that are serologically negative but that become infected with CAV during or
just prior to the onset of production and shed virus to progeny. When this
occurs, vertical transmission, on a flock basis, generally persists for 4 to 6 wk
and ends when a majority of the hens seroconvert. Acquired immunity
prevents vertical transmission for the life of the flock.

FOWL POX
Pox is a relatively slow spreading viral infection of chickens
characterized by scab-like lesions on the skin of the unfeathered body parts
and/or diphtheritic (wet) membranes lining the mouth or air passages. It has
been present in chickens since earliest times and is found throughout the
world. Infection with the fowl pox virus will cause the chickens to have poor
growth, poor feed conversion and a precipitous fall in egg production.

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Mortality will seldom be marked if the lesions are limited to the skin.
However, death may occur if the oral cavity or air passages become involved.
The disease may occur in any age bird. The virus is stable and can be
transmitted by direct contract with an infected chicken or by mosquitoes.
Pox is readily diagnosed based on flock history, presence of typical
lesions, and in some instances by microscopic examination of affected tissues
(characteristic intracytoplasmic, eosinophilic inclusion bodies – Borrel bodies)
and virus isolation studies.
There is no treatment for fowl pox. Control and prevention in chickens
is accomplished by vaccination by the wing web method with a commercially
available fowl pox or pigeon pox vaccine. Vaccinated birds should be
examined for takes about seven to ten days following inoculation. A take
consists of swelling of the skin or a scab at the site where the vaccine was
applied. A high percentage of chickens showing reaction (takes) indicates a
satisfactory vaccination. The absence of a take could be the result of vaccine
being administered improperly, use of a vaccine with inadequate potency
(improperly stored or used after expiration date), or vaccine being applied to
an immune bird.
Precautions should be taken when administering the pox vaccine as it is
a live type of virus vaccine. Because the pox vaccine produces a mild form of
the disease, only healthy birds should be vaccinated. It is strongly
recommended that all chickens in a house be vaccinated on the same day. The
vaccine must be applied only to the vaccination site, and precautions taken to
prevent contamination of other parts of the chicken, the premises and the
equipment. Mosquito control should also be part of the preventive program.

ADENOVIRUS INFECTIONS
Egg Drop Syndrome - 1976 (EDS 76): is an infectious disease in layer hens
manifested by a quick drop in egg production, failure to reach peak
production, irregularly shaped eggs, soft-shelled or shell-less eggs and
depigmentation. The aetiological agent is an adenovirus of group III. The
horizontal transmission occurs slowly in battery systems and rapidly in floor
housing systems. The first sign is the loss of egg pigmentation, rapidly
followed by the appearance of soft-shelled, shell-less of deformed-shell eggs.
If defective eggs are discarded, the remaining ones have no problem with
fertilization and hatching. The drop could be sudden or prolonged. Usually, it
lasts for 4-10 weeks and the egg production is reduced by about 40%. Apart
from the inactive ovaries and oviduct atrophy, there are no other lesions. The

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replication of the virus in epithelial cells of oviduct glands results in severe
inflammatory and dystrophic changes in the mucous coat. The appearance of
eggs with impaired quality and the dropped egg production are suggestive for
EDS 76. The diagnosis is supported by serological tests and is confirmed after
isolation and identification of the virus. In many instances, no antibodies are
detected in infected flocks until egg production approaches levels between
50% and peak production.

REOVIRUS INFECTIONS
Viral arthritis/tenosynovitis. The most frequent reovirus-associated disease in
poultry is viral arthritis. Clinically it is manifested by lameness and swellings
affecting primarily tarsometatarsal joints and the feet. Many infected birds are
in a good general condition, but some could be lethargic and exhausted. The
mortality is very low. The infections affect predominantly meat type poultry.
In some cases, joint cavities or tendon sheaths contain a small amount of
straw-yellow exudate whereas in other the exudate is haemorrhagic or
fibrinous.
The inflammation of the tendon progresses to a chronic type lesion
characterized by tissue fibrosis in the affected area. The aetiological agent is a
reovirus, member of the Orthoreovirus genus, Reoviridae family. Several
serotypes are identified. For their identification, the agar gel precipitation test
could be used. Reoviruses are highly resistant to a number of environmental
factors (temperature, pH etc.).
Stunting syndrome in broilers. The stunting syndrome in broilers is associated
with a reovirus infection but according to some studies, the role of the
reovirus is probably secondary. It is characterized by a considerably reduced
live weight in affected birds and a various degree of ununiformity in the flock
varying from 5-10% to 40-50%, usually seen after the age of 14 days.
The growing primary wing feathers are abnormally big for chickens with
retarded growth, they protrude at various angles, so the disease is termed
“helicopter disease". One-day old chickens are the most susceptible to the
infection.
Usually, a high-degree atrophy of the pancreas is observed. Reoviruses are
shed with faeces and could contaminate the egg shells. The transmission of
the infection to susceptible chickens is realized horizontally. The vertical route
of transmission is also proved. Reoviruses could persist in infected birds for
more than 40 weeks.

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 The small intestine is pale, dilated and contain undigested feed.
The tentative diagnosis of viral arthritis and stunting syndrome could be made
on the basis of symptoms and lesions. The detection of reovirus antibodies via
ELISA supports the diagnosis. Viral arthritis should be differentiated from M.
synov/ae-induced, staphylococcal arthrites and the spontaneous rupture of
the tendon of the gastrocnemius muscle. The vaccination of broiler breeder
flocks with live or inactivated vaccines protects one-day-old chicks. Infected
birds should be removed from the premises. The iodine disinfectants are
effective for inactivation of agents.

NEOPLASTIC DISEASES
INTRODUCTION
Two distinct lymphomatous diseases occur in the field in domestic fowl: Marek's disease,
which is caused by a herpesvirus and lymphoid leukosis, which is caused by an
oncornavirus. They are the most common neoplastic diseases of the chicken, and Marek's
disease, before the advent of vaccination in 1971, was one of the commonest causes of
mortality in commercial fowl.
MAREKS DISEASE
Marek's disease (MD) is one of the most common lymphoproliferative diseases of chickens
which cause mononuclear infiltration of one or more of the following organs: peripheral
nerves, gonad, iris, muscle, viscera, and skin. MD has been called by several names
including "range paralysis", "neural lymphoma" and "skin leucosis".
Causative Organism: MD is caused by herpesvirus, which can be differentiated from other
lymphoid neoplastic diseases.
Transmission: MDV can be transmitted by direct and indirect contact between birds.
Transmission is primarily by airborne route as the virus is shed in epithelial cells of the
feather follicle, dander, chicken house dust, feces and saliva. The virus has a long survival
time in dander. Virus has been isolated from houses that have been depopulated for many
months. Transmission by egg has no significance.
Clinical signs: MD commonly affects pullets between 12-24 weeks of age, but can infect
broilers as early as 6 weeks of age. The incubation period ranges from 3-4 weeks to several
months. Signs may vary according to the nerve or nerves affected. Asymmetric progressive
paralysis of one or more of the extremities can be seen. Wing involvement is characterized
by drooping of the wing. Torticollis if nerves controlling the neck are affected. Vagal
involvement will lead to dilatation of the crop and/or gasping. If the iris is involved, eyes
will lose their ability to accommodate light intensity and blindness may occur (once called
"grey eye"). Many birds die suddenly without symptoms. There are nonspecific signs such
as weight loss, paleness, anorexia, and diarrhea.
Pathology:

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Macroscopic lesions: Nerve lesions can be seen as grayish, edematous, two or three times
the normal thickness, and loss of the normal striated white glistening appearance. Nerves
commonly affected include the brachial and sciatic plexi, celiac plexus, abdominal vagus
and intercostals nerves. Nerve enlargement may not always be seen in affected birds at
necropsy, although characteristic lesions may be found histologically. Also, tumors such as
lymphoma occur in the ovary along with the nerve lesions. Macroscopic appearance in
affected viscera, with the exception of the bursa of Fabricius, are indistinguishable from
leukotic lesions induced by other agents (e.g. lymphoid leucosis virus). Organs are enlarged
with diffuse grayish discoloration.
Microscopic lesions: There are two main types of lesions in peripheral nerves. Type A is
interpreted as neoplastic in character, consisting of masses of proliferating lymphoblastic
cells. Sometimes, demyelination and proliferation of Schwann cells are seen with these
lesions. Type B is inflammatory in nature and is characterized by diffuse infiltration of
lymphocytes and plasma cells, edema, and sometimes demyelination and Schwann cell
proliferation.
Skin lesions are mostly inflammatory but can also be lymphomatous. Inflammatory cells
are localized around the infected feather follicle. With small lesions, the integrity of the
skin is maintained, but disruption of the epidermis leading to ulcer formation may occur
with massive proliferation.
Herpesviruses replicate in the bursa of Fabricius and the thymus which results in
degenerative changes in these organs. Atrophy of the thymus can be severe and involve
the cortex and medulla. In some cases, lymphoid proliferation in the thymus is seen.
Arterial lesions may occur in the aorta, coronary, celiac, gastric and mesenteric arteries
which may show fatty proliferative changes.
Diagnosis: Since there is no truly pathognomonic gross lesions of MD and because MD
lesions can closely resemble those of lymphoid leucosis (LL), the clinical diagnosis of MD has
been considered difficult in practice. Infection of MDV, not necessarily accompanied by the
clinical disease, can be detected by virus isolation or agar gel precipitation tests of viral
antigen in feather tips or antibody in serum. These are useful features to differentiate
Marek's disease from lymphoid leucosis.
Treatment: There is no effective practical treatment for MD.
Prevention: Vaccination: Vaccines are extremely effective (90%+) in the prevention of
Marek's disease.
Genetic selection: MD resistant chicks are obtained.
FAPP (filtered air positive pressure) ventilation: Biological filters to keep out airborne viruses
are used.
Lymphoid Leukosis Complex

The second lymphoid tumour of the chicken is lymphoid leukosis: a complex of viral
diseases with various manifestations such as lymphoid leukosis, myeloblastosis,

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erythroblastosis, osteopetrosis, myxosarcomas, fibrosarcomas.

Lymphoid leukosis,
formerly called ‘big liver’, is the most commonly naturally occurring tumour caused by ALV's

For many years the lymphomas of Marek's disease and lymphoid leukosis were confused
pathologically under the general term visceral lymphomatosis, and this added to the
problem of recognizing them as etiologically distinct diseases.

It affects chickens worldwide with susceptibility varying considerably among different

strains and types of stock - egg layers are generally more susceptible to lymphoid leukosis.

The causal virus is recognized as an RNA virus of the oncornavirus group.

Transmission and shedding of ALV infections

Two main transmission mechanisms:
 Congenital. Transmission is mediated by virus shedding to egg albumen and infection
of the embryo. Most of these chickens will become immunologically tolerant
viraemics (V+) without antibody (A-) and become shedders (S+) of antigen and virus.
Both can be detected in cloacal or vaginal swabs and egg albumens using ELISA tests.

 Horizontal. Infection occurs through close contact with hatchmates or penmates.

Horizontal spread of exogenous ALV from bird to bird by contact normally leads to an
immune response characterized by the development of virus-neutralizing antibodies.
Sources of virus from infected birds are feces, saliva, and skin. Some birds infected in this
way may become occasional shedders of ALV in their eggs and consequently transmitters of
ALV to their progeny. In contrast, birds that are congenitally infected become
immunologically tolerant to the virus, do not develop neutralizing antibodies, and have a
persistent viremia. Hens so infected are persistent shedders of ALV in their eggs and
transmitters of ALV to their progeny. Infected cocks are generally considered not to
transmit ALV to their progeny.

Morbidity is low but case fatality is high. Mortality tends to be chronically higher than
normal for a prolonged period. Egg production is somewhat reduced. There may be
increased susceptibility to other infectious diseases due to damage to the immune system.
Vertical transmission is most important by infection of the egg white in infected breeders
(who are long-term carriers), lateral transmission is poor but infection may occur by the
faecal-oral route, especially in young birds. In lymphoid leukosis the incubation period is
about 4-6 months; it may be as short as 6 weeks for some of the other manifestations. The
causative viruses are rapidly inactivated at ambient temperature and on exposure to most
disinfectants.

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Signs:

 Depression.
 Emaciation.
 Loss of weight.
 Persistent low mortality.
 Enlargement of abdomen.
 Many are asymptomatic.

Post-mortem lesions

Focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. Liver may
be very large.

Microscopic - cells lymphoplastic

Diagnosis

History, age, lesions, cytology.

Differentiate from Marek's disease, coligranuloma.

Treatment

None.

Prevention

Good hygiene, all-in/all-out production, control arthropods, eradication - checking of

antigen in the albumen is a basis for eradication

DDX: MAREKS DISEASE AND LYMPHOID LEUKOSIS

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 Feature Marek's disease Lymphoid
leucosis
Age 6 weeks or older 16 weeks or
older
Symptoms Frequently paralysis Non-specific
Incidence Frequently 5%+ in unvaccinated flocks Rarely above
5%

Macroscopic Lesions
-Neural enlargement -Frequent -Absent
-Bursa of Fabricius -Diffuse enlargement or atrophy -Nodular
tumors
-Tumors in skin, -May be present -Usually
muscle, absent
proventriculus

Microscopic lesions
-Neural involvement -Yes -No

-Liver tumors -Diffuse -Often focal

-Spleen -Either atrophy of follicles or interfollicular -
tumor Intrafollicular
tumors
-Bursa of Fabricius -Yes -No
CNS
-Lymphoid -Yes -No
proliferation of skin
and feather follicles

Cytology of tumors Pleomorphic lymphoid cells including Lymphoblasts

lymphoblasts, small, medium and large
lymphocytes and reticulum cells. Rarely may
only be lymphoblasts

Category of T cell B cell

neoplastic lymphoid
cell

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DISEASES OF WATER FOWLS (DUCKS AND GEESE)

DUCK VIRAL ENTERITIS

synonym “duck plague” DVE

Etiology herpes virus.

Occurrence and Economic Significance

Duck viral entertitis occurs in all areas where ducks and geese are raised. The
infection is responsible for severe losses in susceptible flocks.

Transmission
Duck viral enteritis is transmitted directly by contact of susceptible birds with
infected viremic ducks or recovered carriers. Concentration of ducks in
intensive production areas and common use of ponds by commercial flocks
and migratory and free-living resident waterfowl predisposes to infection.

Clinical Signs
Morbidity varies according to the strain of virus and the susceptibility of the
flock and may range from 10% to 100% with a corresponding mortality rate.
Ducks are usually infected from three weeks onwards with an incubation
period of 5 to 7 days.
Mature breeding flocks show a precipitous decline in egg production
immediately preceding a significant rise in mortality.
Affected ducks demonstrate extreme depression, ruffled plumage, diarrhea
and photophobia.
Clinical signs in mature ducks composed paresis, flaccidity of the neck and
terminally, tremors of the head and limbs. These signs should be
differentiated from botulism. Highly pathogenic strains of the virus may cause
hemorrhages from the nares and cloaca.

Pathology
Characteristic lesions of duck viral enteritis include:
• Free blood in the body cavity.
• Hemorrhages of the ovary in mature ducks.
• Free blood in the lumen of the intestine.
• Hemorrhages of the serosa of the intestine, pericardium and capsule of the
liver which are evident as petechiae and ecchymoses.

Hemorrhagic changes are observed in all lymphoid tissues including the

thymus, bursa of Fabricius in ducklings and the annular lymphoid bands (gut
associated lymphoid tissue) of the intestine. Degenerative changes in the
intestinal tract extending from the esophagus to the cecum include
hemorrhagic areas in the early stages of the disease, progressing to confluent

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maculae resembling a diphtheritic pseudomembrane reminiscent of clostridial
enteritis in chickens.

Diagnosis
Characteristic lesions are highly suggestive of the diagnosis. Hemorrhage from
nares and cloaca is characteristic of DVE. Histological examination discloses
the presence of intranuclear inclusion bodies in hepatocytes.
It is important to differentiate duck viral enteritis from highly pathogenic avian
influenza,
botulism, pasteurellosis and duck viral hepatitis.

Treatment: None.

Prevention
A live attenuated chicken-embryo derived vaccine has been used in Europe to
prevent outbreaks. Where possible, commercial ducks should be isolated from
free-living waterfowl which are reservoirs of infection.

DUCK VIRUS HEPATITIS

Etiology
A picornavirus is responsible for duck virus hepatitis. This agent is distinct
from hepadnavirus (duck hepatitis B)

Occurrence and Economic Significance

Duck virus hepatitis occurs in ducklings under 4 weeks of age in all intensive
duck-rearing areas of the world. Mortality results in extensive losses especially
with intercurrent bacterial infections including chlamydiosis, Riemerella and E.
coli infection, mycotoxicosis and environmental stress.

Transmission
Free-living waterfowl introduce the virus. Rodents serve as reservoir hosts on
affected farms. Direct contact between infected and susceptible flocks
especially in multiage operations predisposes to disease.

Clinical Signs
Morbidity in susceptible flocks may range from 50% to 100%. Mortality is
dependent on the age of the flock, with losses of up to 90% in batches under
one week of age, declining in severity to under 10% at 4 weeks of age.
Mortality is exacerbated by intercurrent bacterial infections.
Ducklings demonstrate per-acute mortality preceded by lateral recumbency
and occasionally, opisthotonos ( hyperextension of the neck, “stargazing”).

Pathology

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The significant lesion comprises enlargement of the liver with punctuate or
ecchymotic hemorrhages. In the presence of chlamydiosis or Riemerella spp
infection, airsacculitis and peritonitis may be observed.

Diagnosis
The picornaviruses responsible for duck virus hepatitis can be isolated from
livers using 9 day old embryonated SPF chickens inoculated by the allantoic
sac route. Serologic procedures include agar gel diffusion precipitin test, virus
neutralization in duck embryos and a plaque reduction test to quantify
neutralizing antibody.

Treatment
No specific treatment is available. Supportive therapy is recommended.

Prevention
Breeders can be immunized with a live attenuated chicken-embryo origin
vaccine. Some vaccines have shown reversion to virulence when applied to
large flocks. Where possible, single-age isolated placement programs should
be followed. Rodents should be eradicated.
High mortality in newlyplaced ducklings has a wide differential diagnosis
including DVH., salmonellosis, E. coli, and Riemerella infection, aspergillosis
and mycotoxicosis.

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