Tables of poultry viral diseases Dr Fares El khayat

Tables of Poultry Diseases
‫اد‬ ‫ا‬
‫ا‬‫ر‬ ‫آ‬/‫ط‬ ‫ا‬ ‫رس‬
‫ي‬ ‫ا‬ ‫ا‬ ‫وا‬ ‫ا‬ ‫اض‬ ‫أ‬
‫ا‬ ‫آ‬

Viral Diseases of Poultry
Dr Fares El-Khayat
1-Newcastle disease = Ranikhet disease = Pneumoencephalyetis = Pseudo fowl pest ‫ض‬‫آ‬ ‫ا‬ : Infectious, contagious,
septicemic and zoonotic disease. The causative agent is a Hemagglutinating Paramyxovirus type-1 "PMV-1" ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫ا‬
which have five pathotypes (velogenic viscerotropic, velogenic neurotropic, mesogenic, lentogenic & asymptomatic enteric
strains).
It is an enveloped, RNA, 100-150 nm in diameter. It is propagated in 9-11 days old ECE via allantoic sac causing death of embryo
in 2-6 days PI. Infection occurs by ingestion, inhalation of polluted air or feed. Transmitted by direct and indirect contact. There
is minor antigenic variation.
Host Signs & Lesions P & T
P-Prophylactic
Vaccination.
Chicken, turkey,
quails, ostrich &
pheasant.
‫و‬٢٩٦
‫ودا‬‫أ‬
‫آ‬
‫ض‬ ‫ا‬ ‫ا‬
‫ا‬ ‫أ‬ ‫دة‬ ‫ا‬
‫ا‬ ‫ا‬.
I.P is 5-7 days.
General signs: Rapid spread of morbidity & mortality.
Enteric signs: Thrist, distended crop + bad-odered content, light bright greenish
diarrhea.
Resp. Signs: Nasocular discharge, wheezing sound, gasping, coughing & rales.
Nervous signs: follow or associate the respiratory signs and include ataxia, tremors,
circling, convulsions, torticallus, paresis & paralysis.
In adults → moderate resp. signs + partial or complete drop in egg production that
may reach zero with egg abnormalities. Flock signs last 2-3 wks.
Hemorrhage on the tips of the gastric glands. Hemorrhagic ulcers in the duodenum,
cecal tonsil. Hemorrhagic tracheitis, air sacculitis & pneumonia.
Ureter is distended with urates.
In adults, ovarian congestion with rupture of some ovules in the abdominal cavity.
T- Emergency
vaccination +
supportive
therapy.
Prevention: Biosecurity measures + vaccination of chicks by live vaccines as Hitchner B1, LaSota, avenew, clone 30, clone 79,
Komarov as well as Killed vaccines either single or combined. The method of applications of ND vaccines includes drinking water,

eye drop, spraying and injection. The choise of the suitable method is dependent on the size of the flock, the concurrent infection
and the epidemiology of the disese.
The most protective type of immunity is the mucosal or local type follwed by the cell mediated type "CMI", followed by the
humoral type and the passive or maternal type protect the chicks for about 3 weeks.
Intra-cerebral pathogenicity indexes or indices "ICPI" of the different vaccinal strains of NDV:
Vaccinal NDV strains Pathotyping Standerd ICPI of pathotypes ICPI of the strain Tropism
Ulcer strain Asypmtopatic enteric 0.04 -0.20 Enteric
Phy LMV 42 Asypmtopatic enteric
0.0 -0.2
0.16 Enteric
F1 strain Lentogenic 0.25 Respiratory
Hitchner B1 Lentogenic 0.20 Respiratory
Lasota strain Lentogenic 0.25 - 0.44 Respiratory
Clone 30 Lentogenic 0.3 Respiratory
Clone 79 Lentogenic
0.2 – 0.7
0.3 Respiratory
Komarov Mesogenic 1.41 Respiratory
Roakin Mesogenic
1.0 – 1.5
1.45 Respiratory
Lasota strain is the best vaccine giving very potent and protective immune response against ND, but its disadvantage is the
induction of severe post-vaccination reaction. This post-vaccination reaction is induced mostly due to the presence of a concurrent
infection with avian mycoplasmosis.
M.gallisepticum secret trypsin enzyme which makes artificial cleavage of the F epitope of the Lasota virus vaccine rendering it into a
virus having a degree of virulence. To overcome this effect, we should use antimycoplamal drugs during the first 3 days of life and
recyle this drug 20 days later.
Control: Non specific treatment is present for the disease, but carrying out the sanitary measures regarding to the isolation of
clinically diseased birds and the proper disposal of dead birds is helpful. Emergency vaccination in the face of an outbreak using
LaSota, avenew strains are also used very useful in controlling the disease. Emergency vaccination is dependent on the induction
of interference phenomena under the effect of the interferone production from the immune cells. Supportive therapy as spraying of
minthol preparations and immunostimulant may give a good effect. The adminstration of broad spectrum antibiotics may give a
good effect in controlling the secondary bacterial bacteria.

2-Viscerotropic velogenic ND = Exotic ND: Hemagglutinating PMV-1
Chicken
I.P is 3-7 days.
Sudden onset and rapid spread of high morbidity without any signs followed by facial
swelling with sticky ocular and nasal exudates. They appear to have “black eyes”.
Severe thrist, distended crop with bad-odered content, light bright greenish diarrhea
and high mortality. Adults show partial or complete drop in egg production that may
reach zero with egg abnormalities.
Hemorrhage on tips of gastric glands. Hemorrhagic ulcers in the duodenum & cecal
tonsil.
In adults, ovarian congestion with rupture of some ovules in the abdominal cavity.
As ND
3-Pigeon PMV1 infection = Paramyxovirosis: Pigeon PMV-1 is a sub-group of NDV which cross-reacts with the classic NDV. The
pathotype of pigeon PMV-1 falls between the lentogenic and mesogenic NDV. All other biologic properties are the same as NDV.
Pigeon
I.P is 2-7 days.
There are thin broken solid droppings in a pool of liquid as light bright greenish
diarrhea, fine tremor of eyes or head, staggering in gait, somersaulting in flight, crash
landing, difficulty picking up seed, pecking and missing, tossing seed backwards,
twisting neck, head upside down (torticollis, star gazing), paralysis of legs or wings,
spiraling in flight, flying backwards, turning in circles and having fits.
There are not respiratory symptoms in Paramyxovirosis.
Petecheal hemorrhages on the heart, stomach and intestinal serosa.
Cyanosis of skin and muscles.
The course is 10-14 days.
As ND, biosecurity
measures and
vaccination of
pigeons against
Pigeon PMV.

4-PMV-2 infection “Yucaipa”: Hemagglutinating PMV-2. Infection occurs by ingestion, inhalation of polluted air or feed.
Transmission is by wild birds and fomites. Wild birds are believed to be especially important. Vertical transmission does not usually
occur.
P. Biosecurity and
all-in/all-out
production.
Chicken &
turkey and wide
range of feral
birds.
Variable mortality, depending on the affected species and whether infection is
complicated by other factors and diseases. In chickens it is mild, but turkeys are more
severely affected.
In uncomplicated cases, → mild respiratory signs + reduced egg production. Depression,
inappetance, coughing.
In the complicated cases due to any secondary bacterial pathogens as E.coli or any
environmental stress as ammonia → severe respiratory disease + cesation of egg
production + high mortality.
No specific gross lesions are present in PMV-2 infection.
T.None but
supportive therapy
give a good effect.
Antibiotics to
control secondary
bacteria.
5-PMV-3 infection: Paramyxovirus PMV-3 infects turkeys, occasionally chickens and psittacine birds. The infection is transmitted
by birds including wild bird and contact with fomites. Vertical transmission does not occur. Mortality is low. Hemagglutinating
PMV-3 is serologically related with NDV. Infection occurs by ingestion, inhalation of polluted air or feed.
Turkey,
psittacines &
cage birds.
In turkey, there are mild respiratory signs, depression, inappetance, coughing with drop
in egg production and egg quality with loss of egg pigmentation. The effect on egg
production depending on the presence or absence of the secondary bacterial agents
and/or any environmental stressors.
In psittacines, cage & feral birds, there are nervous symptoms with high mortality.
As PMV-2
6-PMV-6 infection: it occurs in turkeys and inapparent in ducks & geese.. Infection is transmitted by direct contact with wild bird
and indirect contact with fomites.
Turkey and
exotic pet birds.
Reduction in egg production with mild respiratory signs. Mortality is 0–5%.
No specific lesions.
As PMV-2

7-Turkey Rhinotrachitis = TRT: A disease of turkeys caused by the viruses of Pneumovirus genus ‫ا‬ ‫ت‬ ‫و‬ ‫,ا‬ Paramyxoviridae.
Two subgroups have been identified on the basis of the G-protein sequence(cross protection between them occur): A (original UK
isolates) and B (original southern Europe isolates).
There is rapid lateral transmission with infection by aerosol through the respiratory route; vertical transmission is uncertain. As for
many infections, fomites can be important in moving infection between farms. Maternal antibody may protect. Pneumovirus is
enveloped RNA, 80-100 nm in diameter. Isolated in tracheal organ culture from turkey embryo causing ciliostasis 4-5 days PI.
Host Signs & Lesions (P) & (T)
P.Biosecurity and
chlorination of
drinking water.
L. vaccines.
Turkey < 10 wks
and turkey
breeders
Morbidity is 10-100% and mortality 1-30%.
Decreased appetite, weight gain and feed efficiency, loss of voice, oculonasal discharge,
conjunctivitis, snicking sound, dyspnoea and sinusitis with sudden drop in production
that lasts 2-3 weeks and eggs depigmented and thin-shelled.
Serous rhinitis and tracheitis, sometimes pus like material present in bronchi. If there is
secondary E.coli infection then pneumonia, airsacculitis and perihepatitis.
T.None but the
supportive therapy
give a good effect.
8-Swollen head syndrome = SHS = Dekkop ‫ض‬‫أس‬ ‫ا‬ ‫رم‬ : A viral disease of chickens, guinea fowl and possibly pheasants. It is
caused by a Pneumovirus of the Paramyxoviridae family as TRT.
Chicken < 10
wks.
The incubation period is 5-7 days, morbidity is 10-100% and mortality can be 1-10%.
Reduced appetite, weight gain & feed efficiency, facial & head swelling, loss of voice,
ocular & nasal discharge, snick, dyspnoea, conjunctivitis, sinusitis.
Serous rhinitis and tracheitis. If secondary invasion as E.coli occur, pneumonia,
airsacculitis & perihepatitis, congestion, edema & pus in the airspace of the skull occur in
a proportion of affected birds.
As TRT
9-Avian Influenza ‫ر‬ ‫ا‬ ‫ا‬ ‫:أ‬ A highly infectious and contagious avian disease caused by a Hemagglutinating Orthomyxovirus-
Influenza A ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It has 16 H epitopes and 9 N epitopes with possible 144 serotypes. The virulent serotypes are
those containing H5 and H7 epitopes. They cause a particularly severe course of AI, known as classical fowl plague (highly
pathogenic AI, HPAI). HPAI is an acute disease of fowl-like birds with a mortality of up to 100%. Serotypes containing H9 epitopes

are immunosuppressive. It is characterized by antigenic drift "minor antigenic variation" and antigenic shift "major antigenic
variation". It is enveloped with segmented RNA (8 segments), 80-100 nm in diameter.
There are two pathotypes; low and high pathogenic AIV. It is propagated in 9-11 day old ECE via allantoic sac causing death of
embryo in 1-2 days. Infection occurs by ingestion, inhalation, cloacal, conjunctival, wound and blood sucking insects. Transmission
occurs via the miagratory birds, contaminated shoes, equipments, clothing, direct and indirect contact with infected birds.
All birds. The
aquatic birds
are clinically
diseased and
carriers).
I.P is 1-3 days.
According to the pathotypes; there 2 forms of the disease:
Mild Form = Low pathogenic AIV: mild signs or no observable signs in chickens. In
turkey, moderate mortality due to the higher chance of co-infection with mycoplasmosis
that aggreviate the infection.
Highly virulent Form = Highly pathogeniv AIV (fowl plague): severe disease take one
of 2 coarses as follows:
-Peracute form: Sudden high mortality without any symptoms or lesions.
-Acute form: Sudden onset & rapid spread of high morbidity, sudden death, fever,
marked inappetance, cessation of normal flock vocalization, depression, coughing,
sneezing, nasal & ocular discharge, Sharp drop in egg production, swollen face due to
edema in head region, severe cyanosis of comb & wattles, watery greenish diarrhea,
nervous signs as paralysis, patchy hemorrhage in the shaft of long bone with very high
mortality (up to 80-100% in 2-5 days in chicken & turkeys).
Mortality increases in an exponential fashion i.e. 5-10 times as the preceeding day and
peaks at the 6th -7th day of illness.
Rapid rigor mortis, dehydration, S/C yellowish-red edema in the head region. Skin
necrosis in the comb & wattles. Sinusitis, trachitis, conjunctivitis & air sacculitis.
Hemorrhage on and in the pectoral muscle, inner surface of keel bone, coronary fat,
proventriculus mucosa, under the cuticle of the gizzard & lymphoid tissue of intestinal
tract. Hemorrhagic enteritis in the duodenum with blotchy hemorrhage in pancreas.
Ovarian regression or hemorrhage. Turkey lesions is less marked than those of chickens,
while ducks may be symptomless, lesionless (asymptomatic carriers).
P-Proper cleaning
& disinfection of
pens with
vaccination by
inactivated
vaccines.
T- None but
notification of the
authorities is a
must. Rapid
culling of the
stocks.

Differentiation between ND and HPAI:
Criteria ND HPAI
Incubation period 5-7 days 1-3 days
HA of rabbit RBC -ve +ve
Elution of HA Very fast. Very slow.
Disease in pigeon +ve -ve
Course of disease Few hours or more. 3 days or more.
Histopathology No perivascular cuffing. Perivascular cuffing in brain.
10-Infectious Bronchitis ‫ي‬ ‫ا‬ ‫ا‬ ‫ب‬ ‫:ا‬ Highly infectious and contagious disease caused by Coronavirus ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It is an
enveloped, ssRNA, 80-120 nm in diameter. It is originally non-hemagglutinating and can hemagglutinates RBC after chemical
(tanic and phosphoric acid) or enzymatic treatment (trypsin). It is propagated in 9-11 days old ECE via allantoic sac causing
dwarfing, curling and death of embryo after serial passages. The virus has classic and variant serotypes with or without cross
protection. Massachusset's strains induce cross protection for all serotypes by about 45%. Infection occurs by inhalation of polluted
air. It is transmitted via the polluted shoes, equipment, clothing as well as the direct & indirect contact with infected birds.
Intercurrent diseases as ND, ILT, coryza, E.coli, CRD & H9N2 predispose to more severe and prolonged disease.
IBV serotypes
Isolates of IBV are divided into different serotypes based on the virus neutralization test in embryonated eggs, tracheal organ
cultures or identified molecularly using RT-PCR and the RFLP test or nucleotide sequencing. In general, different serotypes of the
virus do not cross-protect. However, some strains of the virus are quite effective at inducing cross protection against other
serotypes or genotypes.
Variant serotypes
IBV has the ability to change rapidly resulting in new variant serotypes. The prevalence of variant IB serotypes must first be
determined before the use of a vaccine containing these viruses. Variant viruses may be present when “IB-like” problems are seen
in flocks properly vaccinated with Massachusetts type vaccines. On the other hand, existing vaccines may represent the
protectotype needed in order to get protection against the variant strain. When currently available products prove to give
insufficient protection against an emerging virus, the development of a homologous vaccine against the new variant is justified
(e.g. IBV 4/91).

IB variant D1466
IB variant D1466, a strain belonging to D212 serotype, is of particular importance because it behaves somewhat differently from
other important IBVs. Molecular analysis of the S1 spike of the virus genome has shown that D1466 is the least related genetically
of the known IB variants. This is confirmed by protection studies which show that little cross protection is provided by
heterologous vaccines. However, there was evidence of an increased incidence of disease problems associated with D1466 and
some indication that these new isolates may have increased in virulence. A live and inactivated D1466 vaccine was developed for
use in breeders and layers. The inactivated vaccine continues to be used, but currently no live attenuated D1466 vaccine is available
to help control the disease outbreaks caused by D1466.
Chickens
I.P is 18-36 hours.
In chicks under 5 wks: Rapid onset & spread,gasping, rales with some gasping,
sneezing,coughing, chirping, watery eyes & high mortality up to 25% especially if the
condition is complicated by any bacterial invasion. The coarse is 3-6 days.
In growing chickens (6-10 wks): Similar but milder than those in young chicks but with
marked retardation in the growth. Low mortality (5-10%) in 7-10 days.
In semi-mature & laying chickens: Very mild respiratory signs with drastic drop in egg
production up to 50%. Egg abnormalities (small-sized, deformed, rough-shelled or soft-
shelled & shell-less eggs & watery albumin). Return to full lay may take 4-6 wks but the
expected potential production is nerver attained. Flock signs may last 10-14 days.
False, blind or internal layers are commonly observed 8-10 wks after the onset of an
outbreaks of IB in pullets. They are apparentlly healthy, visit the nest frequently but lay
no eggs & easily detected by using the trap nests.
Lesions of IB: Catarrhal tracheitis, bronchitis & pneumonia. In classic cases, there is a
yellowish white caseous plug at the tracheal bifurcations which block the air passage and
may cause asphxyation . Air sacculitis may or may not occur.
In false layers, shortening & narrowing of oviducts with abdominal ovulation & egg
peritonitis.
P-Vaccination of
chicks in the first
week of life using
live H120 vaccine.
Vaccination of
breeders and
layers 4 weeks
before lay if an
important problem
in your flock.
T-None for
treatment but all
try supportive
therapy.

11-IB–793b Variant Sudden Death Syndrome in Broiler Parents:
Chickens
Sudden death in affected birds. Muscular shivering, otherwise as for standard IB. Edema
of the pectoral muscles and subcutaneously on abdomen.
Lesions progress to necrosis and scarring of deep pectorals in convalescence. In layers the
ovules are intensely congested. Other lesions of classic IB are encountered in this
condition.
As IB
12-Infectious nephritis nephrosis = INNS = Infectious uremia: Variant nephro-pathogenic strains of Cronavirus as T, Gray or
Holte strains. All properties are similar to that of IBV. Heavy breeds, males and brown egg types are more severely affected. High
protein% in feed espcially of meat meal is an exacerbating factor for the disease.
Chicken 3-9 wks
(average 6 wks)
are mostly
affected but
adults are also
affected.
I.P is 1-2 days.
Rapid onset and spread of the disease. Mild respiratory signs followed by marked
depression, loss of appetite, severe thrist, voiding urates in the droppings with high
mortality up to 30%. In adults, drop in egg production up to 50% with lowered
hatchability about 10-30%. Flock signs last 2-3 wks.
Dehydration of carcass with dark-red discoloration of muscles. Marked kidney
enlargement with urates accumulation and sometimes urolith in the ureters. In severe
cases, urates is present in pericardium, peritonium and air sacs.
P-Vaccination.
T-None but all try
supportive therapy
& low protein% of
feeds + ammonium
chloride in feed "2-
3 kg/tonn" + acetyl
salycilic acid in
drinking waters.
13-QX strain infection of IB = IBV variant D388 (QX):
Chicken 4
weeks of age
and layer birds
Respiratory signs in broilers older than 4 weeks of age + low egg production rate with
peak levels reaching only between 30-55% in apparently healthy flocks. The affected bird
gas a penguin like position.
Cystic oviducts with watery contents that could exceed one liter or partially atrophic
oviducts with large cystic dilatations. Thin oviduct walls and transparent in the cystic
areas. The ovaries in the birds are functional and look normal.
P-Vaccination with
H120 at one day
old and 4/91 at 14
days.
T-None but all try
supportive
therapy.

Protectotypes
New serotypes may emerge as a result of small changes in amino acid sequence of the S1 gene of the virus spike. Although it
appears to be a new serotype, most of the viral genome remains unchanged. This may be the reason why IB vaccines of a specific
serotype can protect against strains of IB not belonging to the same serotype. From a practical point of view is more relevant to
think in terms of protectotypes than serotypes.
Studies have shown that vaccination with two different types of IBV vaccine can provide broad protection against different IBV
types. The best combination of vaccines was reported to be MA5 at 1-day of age followed by 4/91 at 14 –days of age.
14

-Infectious Laryngeotrachitis = ILT ‫ا‬ ‫ا‬ ‫وا‬ ‫ة‬ ‫ا‬ ‫ب‬ ‫:أ‬ It is highly infectious and contagious respiratory disease caused by
Herpesvirus ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It is an enveloped DNA virus. It is propagated in 9-11 days old ECE via CAM causing death of embryo
within 2-12 days with the formation of plaques on CAM (2 days PI) and intranuclear inclusion bodies (36 hrs PI). Infection occurs
by inhalation and ocular route. It is transmitted via direct and indirect contact with infected birds, carrier and vaccinated birds,
contaminated shoes & equipments. Some recovered birds remain carriers for about 2 years.
Chickens,
pheasants &
their crosses.
I.P is 4-12 days.
The disease has two forms:
1-Epizootic = acute Form = Hot bird disease: Rapid spread of high morbidity (90-100%)
and high mortality (10-25%). There is pump-handle respiration due to dysnea. Coughing,
sneezing, nasal and ocular discharge with shaking of head to get rid of the mucous
exudates present in the trachea. Gurgling sound with expecturation of blood-tinged mucus
which is observed on the wall of the farm at the level of the head of affected birds. There is
sharp drop in egg production up to 40%. The course may last 10-14 days.
ILT recycling is reported in caged layers in which the disease affect most but not all of birds
then in about 10-12 days a second wave of the disease sweeps through the flock. The
recycling may occur in chickens vaccinated via drinking water.
In early stage, catarrhal laryngitis and tracheitis with intranuclear inclusion bodies that is
detected in this stage in 1-3 days postinfection. In later stage, hemorrhagic tracheitis with
degeneration of tracheal mucosa with the presence of blood tinged mucus in the tracheal
lumen.
2-Enzootic or mild Form: unthriftness of birds, drop in egg production up to 20%, watery
eyes, conjuctivitis (may be hemorrhagic), pesistent nasal discharge and swelling of the
infraorbital sinuses. Low morbidity (up to 5%) and very low mortality. Course may last 3-4
wks.
Edema, conjuctival congestion and enlarged infraorbital sinuses are the only lesions of this
form.
P-Vaccinate, but
only if a problem
in your area and
do not vaccinate
unnecessarily.
T-Emergency
vaccination with
supportive
therapy may give
good
interferance.

15-Avian encephalomyelitis = Epidemic tremors =AE ‫ا‬ ‫ش‬ ‫ر‬ ‫:ا‬ caused by Enterovirus ‫ا‬ ‫ت‬ ‫و‬ ‫ا‬ which is belonging to
Picornaviridae ‫ا‬ ‫ا‬ ‫ه‬ ‫ر‬ ‫وآ‬ ‫ا‬ ‫ه‬ ‫ت‬ ‫و‬ ‫.ا‬ Non-enveloped, RNA, 16-25 nm. It is propagated in 5-6
days old ECE via yolk sac causing paralysis of legs & muscular dystrophy of the embryo after adaptation by 5-12 blind passages. It
is also propagated by intra-cerebral inoculation in 1-day old chicks. The infection occurs by vertical transmission and horizontal
route via direct contact with infected birds & indirect contact through ingestion of the contaminated feed or water. There is no
antigenic difference between strains of the Enterovirus.
Chicken,
turkey,
pheasant &
Japanese quail.
All ages are
affected but the
nervous signs
are only seen in
1-6 wks old
(mainly 12-21
days of age).
I.P is dependent on the route of infection. It is 1-7 days (vertical transmission) but it is 10-17
days (horizontal transmission).
In young chicks (1-6 wks), there are nervous signs including ataxia, incoordination of gait,
paresis or paralysis of the two legs with intermittent rapid tremors of the head & neck that
particularly evident if the birds is held in palm of the hand, prostration (due to starvation)
& death (due to trampling).
Morbidity may reach 50% and mortality ranges from 5-20% (may reach 60%). Some
recovered birds may develop blindness due to unilateral or bilateral opacity of pupil
(catarct).
In semi-mature and adult, no nervous signs but in adults, there is transient drop in egg
production (10-15%) which lasts for 10-14 days. Low hatchability due to late embryonic
mortality & hatched chicks have ataxia & paralysis of legs. In turkey & other species, the
disease is similar but milder than that in chicken.
No gross PM lesions belonging to AE.
Microscopical involvement of brain "perivascular cuffing" and in the proventriculus,
gizzard and pancreas "massive lymphocytic infiltration" with no involvement of peripheral
nerves.
P-Vaccination of
layer & breeders
at 12 wks old by
live vaccine via
drinking water or
wing web
sticking.
Beta-
propiolactone
Killed vaccine
also used at 8-16
wks old.
T-None.

16-Infectious bursal diseases = Infectious bursitis ‫ي‬ ‫ا‬ ‫آ‬ ‫ب‬ ‫أ‬=‫ج‬ ‫ا‬ ‫ز‬ ‫أ‬=‫رو‬ ‫ا‬ ‫ض‬ : A highly infectious and
contagious disease caused by Birnavirus ‫زي‬ ‫ا‬ ‫وي‬ ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It is non-enveloped, RNA, 60 nm in diameter. It has 2
serotypes; serotype-1 which is pathogenic to chicken and serotype-2 is apathogenic for chicken and isolated from turkeys.
Serotype-1 has different subtypes "virulent = classic, very virulent and variant subtypes". It is propagated in 9-11 days old ECE via
CAM causing death of embryo within 8 days PI that appear edematous, stunted in growth and show liver necrosis. It is also
propagated in tissue cultures. Infection by ingestion and inhalation of the polluted air, feed and water. Transmission via direct and
indirect contact with infected birds. The lesser meal worm (Alphitobius diapernus) harbors the virus for weeks.
Chickens
(3-6 wks old) but
it may occur up
to 11 wks.
-Subclinical Form: It occurs if the infection occurs in chicks under 3 wks of age either
with classic or variant strains. It causes rapid profund bursal atrophy leading to severe
persistent immuosuppression with no clinical signs.
-Clinical Form: I.P is 2-3 days. It occurs due to infection of chicks older than 3 wks of age
and has two phases:
-Inflammatory stage: It is about 5 days. Sudden loss of appetite, tremors of the whole
body, self-vent picking, incoordination with hunched up appearance of the affected
birds that squate with their neck extended. Profuse watery yellowish-white diarrhea
with oily texture soiling the vent region with straining during defecation. The course
last 5-9 days.
High morbidity (10-30%) with low mortality (1-20% - average 7%) in commercial
broilers but in commercial layers & native breeds, the mortality may reach to 60%.
Mortality occurs in a charactersitic spiking curve with peak mortality is reached in the
4th day of the disease and then gradually decline to zero during the next five days.
Dehydrated mucles, ecchymotic hemorrhage on the thigh muscles. Patchy hemorrhage
on the junction between the proventriclus and gizzard. Hepatomegaly with peripheral
yellow infarct. Moderate splenomegaly. Marked enlargement of bursa of Fibricius to
twice the normal size. The exterior of bursa is covered by gelatenous exudate. The
interior of bursa is edematus, reddened or hemorrhagic with prominent plicae.
-Resolution phase: it starts from theend of the 5th day of infection. In it, no mortality
occur and the size of the BF reduced to one third iof its normal size.
P-Biosecurity &
vaccination.
T-None but
metaphylaxis or ring
vaccination may be
helpful using D-78
vaccine.

Gumboro-related diseases:
These are diseases in which the incidence of it increases with the occurrence of Gumboro disease or with the vaccination with hot
Gumboro vaccine. They include gangrenous dermatitis, inclusion-body hepatitis anemia syndrome and may include E.coli
infections.
Prevention:
Biosecurity + getting rid of the lesser meal worm + trice vaccination of chicks with live vaccine via drinking water or eye drop "at 7,
13 and 20 days old in commercial broilers – 7, 14, 21 and 28 in chicks commercial layers and breeders + vaccination of layer and
breeders at 18 wks old by Killed vaccine". The vaccination program depends on multiple factors, the most important of them are
the degree and homogenicity of the MDA, the breed of birds, the type of vaccines and the half life time of the MDA.
Control: No sepcific treatment is present for the disease but metaphylaxis or ring vaccination in multi-house system may be helpful
using D-78 vaccine. The previous measures are tried in addition to the adminstration of potent diuretics and using a low protein %
of feed to reduce the urate production.

17-Chicken infectious anemia = CIA = blue wing disease ‫ج‬ ‫ا‬ ‫ا‬ ‫:ا‬ A disease caused by Circovirus. It is non-enveloped,
ssDNA, 25 nm in diameter. It is propagated by IM inoculation in 1-day old chick and also in MDCC-MSB1 tissue culture cells (these
are cell line derived from MD lymphoma). Vertical & horizontal infection occurs via the contact exposure shortly post-hatch via
ingestion and inhalation of the polluted air, feed and water.
Chickens (2-3
wks old).
I.P is 12-17 days.
Diseased birds are anorexic, lethargic, depressed and markedly pallor due to the reduced
erythrocytic number. Packed cell volume "PCV "is less than 25%, the blood smears reveal
severe anemia and leucopenia. Blood is watery and clot slowly i.e. prolonged clotting
time. The mortality is around 10% but may reach to 50% depending on the presence of the
concurrent infections.
CIA is a highly and deeply immunosuppressive disease due to its severe effect on the
thymic tissue leading to very deep effect on the T-lymphocytes i.e. immunosuppressive
on the CMI.
Age resistance to disease begin at 1 wk old and is completed at 2 wks post-hatching but it
can be overcome by CIA co-infection with other immunosuppressive agents as IBDV,
MD, REV and mycotoxicosis.
Pale organs, thymic and bursal atrophy, pale or yellowish discolord bone marrow.
Hemorrhage may be present in or under the skin (especially at the tip of the wing hence
its name Blue wing disease), skeletal muscles and other organs. Enlarged liver and
gangrenous dermatitis may also be present.
P- Vaccination of
breeders at 11 wks
old by live
vaccine.
T-None.
18-Pox: An infectious, slow spreading avian disease caused by Avipox virus. It is DNA virus, 300 nm in diameter. It has four
strains; fowl pox virus, turkey pox virus, pigeon pox virus & canary pox virus. It is propagated in 9-12 days old ECE via CAM
causing formation of greyish plaques of cell prolifiration on CAM and the formation of intracytoplasmic inclusion bodies
(Bollinger’s body inside of which there very minute bodies known as Borrel's bodies).

The infection occurs by direct contact with infected birds, wound infection and mosquitoes bites. The disease has a seasonal
incidence mostly in spring and summer due to the high mosquitos' populations.
Turkeys,
Chicken
Pigeons
Canaries
Pheasants
Quails
I.P is 4-10 days.
Skin = cutaneous = dry Form: The presence of small yellow warts-like nodules on
wattles, comb, face, legs around vent and under the wings. They increase in size and
become dark brown scabs then drop off.
Diphtheritic = Mucous membrane = Wet Form: The presence of yellow, cheesy
necrotic lesions (Diphtheritic or pseudomembrane) on the Mucous membrane of
mouth, nares, pharynx, larynex & trachea. It is diffecult to remove and leave
hemorrhagic or eroded surface when forcely removed. It interferes with swallowing
and respiration leading to starvation and suffocation.
Mixed Form: both symptoms of the two forms are present.
Naso-ocular Form → coryza-like signs.
Mortality ranges from 3-10% up to 50% in case of complications. The course is 3-4 wks
and may be 6-8 wks in case of complications.
P-Vaccination in areas
of high mosquito
populations.
Succsseful vaccination
is detected by the
presence of “takes”.
T-Swab lesion with
Tr. of iodine 5% after
rubbing it against a
hard object in
addition to antibiotic
oxytetracycline.
Takes: It is a wart like lesion occurs as a post-vaccination reaction at the site of vaccination. It is formed 7-10 days post-vaccination.
By mean of takes, the successful vaccination can be estimated. The presence of takes in the majority of taken sample means a
successful vaccination.
19-Marek's disease = MD: It is a highly infectious, contagious and oncogenic poultry disease caused by Herpes B virus. It is highly
cell associated virus due to which it escapes the effect of the antibodies after it once gains entry into the body.
There are three serotypes: Serotype-1 is pathogenic for chicken, the serotype-2 is apathogenic for chicken and the serotype-3 is
apathogenic for turkey. All these serotypes have the MD tumor associated surface antigen (MATSA) and so all of them can be used
as a vaccinal virus. Infection occurs by inhalation of feather dander that contain fully infective enveloped virus.

Chickens, very
rare in turkey,
pheasant, quail
& pigeon.
I.P is as short as 3-4 wks & as long as months.
I-Classic form: occur in 3-5 months old although most cases occur around 3 months with
affections in peripheral nerves or nerve plexuses & eyes.
-Peripheral nerves involvements:
-If sciatic neve involved, progressive lameness of legs with one stretched foreward & one
is stretched backward as ballerna-like.
-If brachial n. Involved; droopiness of wings.
-If vagus & intercostal n. involved; dysnea + gasping.
-If crop & gastric neve involved, there are crop impaction & digestive troubles & diarrhea.
-If cervical neve involved→torticollis.
In peripheral nerve affections, birds cann’t reach feed & water →loss of weight, pale
comb & wattles & die from starvation.
-Ocular form = Gray eye: Unilateral or bilateral concentric annular or spotty depigmentation or
diffuse grayish fading of iris + irregular pupil (serrated, slit or pin-head like) leading to
blindness.
II-Acute form: → young birds raised intensively at 1.5-2.5 months with rapid coarse &
high morbidity & mortality up to 50%. Affected birds are depressed, some birds show
skin. tumors at the feather follicle & others may die suddenly without preceeding
symptoms but, only small percent of birds show paralysis.
The PM lesions are as follows:
I-In classic Form, affected nerves show localized or diffuse swelling due to edema &
mononuclear infiltration + loss of cross striations.
II-In acute Form, lymphoid tumors in gonads (cauliflower), spleen, kidneys, lung, heart,
liver, digestive tract, mesentery, skeletal muscles & skin with or without nerve lesions.
P-Vaccination of 1
day-old chicks &
nowadays the
intraoval
vaccination is
used.
T-None.

20-Trnsient paralysis
Chickens
(5-18 wks)
It is uncommon encephalitic symptom of MDV infection in which birds suddenly develop
various degree of paresis of legs, wings & neck. Mortality is low and the disease is
characterized by spontaneous recovery. The signs usually disappear within 1-2 days.
---
21-Erythroleucosis = Erythroblastosis: It is one form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. The
leucosis-sarcoma viruses are divided into 6 different subgroups; A,B,C,D,E & J. Egg borne i.e. transmitted to very young chicks
from infected older birds.
Mature chicken
over 6 months of
age.
I.P is 2-5 months.
It is a sporadic cases characterized by neoplastic prolifiration of erythroid cells and their
intravascular accumulation causes splenomegaly. Progressive anemia (pale yellowish
discoloration of comb & wattles), weakness, emaciation, diarrhea and drop in egg
production.
Blood changes: Blood is pale, watery, slow to clot with reduced hemoglobin%
Critaria Plasma WBC RBC
Normal 55 1 44
Case 88 1 11
Diffuse splenomegaly, hepatomegaly, enlarged kidney, lung, heart with cherry red
dicoloration of these organs.
None

22-Myeloblastosis = Granuloblastosis: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses.
Mature chicken
over 6 months of
age.
I.P is 2-5 months.
It is a sporadic cases characterized by extravascular prolifiration of granulocytes which
spread to internal organs causing diffuse splenomegaly, hepatomegaly and enlarged
kidney with greyish mottling and granular appearance. The enlarged, granular, grayish
brown liver is described as Morroco leather appearance of liver. Bone marrow is pale or
pink. Anemia (pale comb & wattles),weakness, diarrhea, emaciation and drop in egg
production.
Blood changes: Blood is pale, watery, slow to clot with reduced hemoglobin%.
Critaria plasma WBC RBC
Normal 55 1 44
Case 16 69 15
None
23-Myelocytomatosis: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. Subgroup J. Egg borne.
Chicken
(3-11 wks).
I.P is 2-5 months.
It is a sporadic cases that is characterized by tumor formation as small yellowish white
solid friable like cheese along the inner surface of ribs, inside the keel bone, pelvis &
cranium and sometimes in spleen, liver and bone marrow.
Blood changes: absent
None

24-Osteopetrosis: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses.
Mature chicken
(2-3 months)
more in male
than in female.
I.P is 2-5 months.
Jerkey gait with bilateral, irregular thickening of the diaphysis long bones of legs then
marked thickening of legs with “boot-like appearance”.Affected legs are warm.
Blood changes: reduction of marrow tissues with relative or absolute lymphocytosis.
Lesions: Bilateral thickenings of the diaphysis of the long bones of legs, wings, pelvic
girdle & spines. The marrow cavity is narrowed or completely oblitrated.
None.
25-Other sarcoma tumors: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses.
Chicken
I.P is 2-5 months.
Nephroblastomas → tumor of epithelial tissue of kidney which occurs between 1.5-6
months of age.
Endotheliomas → tumor of vascular organs " spleen, liver or bone marrow".
Hemangiomas & teratomas are other types of tumors.
None.

26-Lymphoid leucosis = Visceral lymphomatosis = Big liver disease: Retrovirus. Oncogenic RNA viruses.
Chickens over 16
wks old
More in females
than in males.
I.P is 2-5 months.
Anemia manifested by pale comb & wattles with progressive emaciation of birds, green
diarrhea and easily palpated hepatomegaly. Sick birds usually die.
Blood changes: massive prolifiration of immature lymphoblastes.
Lesions: There are 3 forms of LL:
Focal = nodular Form: The formation of cicumscribed greyish tumors of various sizes in
the liver, kidneys, heart (tigeroid heart), seosal surfaces, ovary, spleen and the lungs.
Diffuse Form: The diffuse enlargement with greyish mottling of the same organs
especially the liver giving rise to the so called “Big liver disease” in which the liver size
may reach half of the whole body size.
Mixed Form: the symptoms of both forms are present.
None
27-Reticuloendotheliosis: Neoplastic disease caused by Retrovirus type C. Oncogenic RNA viruses that are serologically and
genetically distinct from avian leucosis-sarcoma group. Infection occurs horizontally.
Chickens,
turkeys, ducks,
geese (15-20
wks) and quail
(6-10 wks)
Chronic neoplasia, a runting disease syndrome has occurred in flocks and some birds
show a peculiar feathering abnormality “nakanuke” in which wing feathers have
adhesions of the barbule to part of the feather shaft. Some birds show paralysis.
REV is an immunosuppressive disease. It has 2 forms of neoplasia:
Acute reticulum cell neoplasia. In liver, spleen, gonads, heart, kidney & pancreas.
Chronic lymphoid neoplasia. In visceral organs plus peripheral nerves.
None

28-Lymphoproliferative diseases of turkey: Retrovirus type C. Oncogenic RNA viruses that distict serologically and genetically
from avian retrovirus. Infection is horizontally and the incidence of infection is higher than that of the disease.
Turkeys
(7-18 wks).
Affected bird die suddenly after a period of depression. About 20% of birds may be
affected.
Marked splenomegaly that is pale and marbled. Moderate hepatomegaly that have miliary
grayish white foci. Miliary or diffuse tumor infiltrations occur in gonads, intestinal wall,
pancreas, lungs, myocardium & thymus. Peripheral nerves may be enlarged.
Blood changes: Leucocytosis and leucopenia.
None
29-Other tumors:
Disease +
Cause + host
Signs & Lesions P & T
Connective
tissue tumors
Fibroma & fibrosarcoma, Myxoma & myxosarcoma, Histiocytic sarcoma, Chondroma,
Osteoma & osteogenic sarcoma
None
Epithelial
tumors
Nephroblastoma Embryonal nephroma, renal adenocarcinoma, adenosarcoma,
nephroblastoma, cystadenoma, Nephroma Papillary cystadenoma, carcinoma of the
kidney, Hepatocarcinoma, Adenocarcinoma of the pancreas, Thecoma, Granulosa cell
carcinoma, Seminoma Adenocarcinoma of the testis, Squamous cell carcinoma.
None
Endothelial
tumors
Hemangioma Hemangiomatosis, endothelioma, hemangioblastomas,
hemangioendotheliomas, Angiosarcoma, Endothelioma, Mesothelioma.
None

30-Avian adenoviruses ‫ا‬ ‫ت‬ ‫و‬ ‫:ا‬ It is icosahedral, non-enveloped DNA viruses. It is highly resistant viruses to the adverse
environmental and chemical condition. It is divided into 3 groups:
The first group or conventional adenoviruses: They are isolated from chicken, turkeys, geese, and other avian species. Its role
as a primary pathogens is not well defined but they appear to have a role as a secondary pathogens in association with CIV
and IBDV which the latters enhance the pathogenicity of the adenoviruses. Vertical transmission is very important but
horizontal spread is also important. It hemagglutinates rat RBC. Incubation period is short (1-2 days). The diseases and
disorders caused by or associated with viruses in this group are inclusion body hepatitis "IBHV in chickens - 70-90 nm), Mild
Respiratory Disease (MRDV -- 70-90 nm), hydro-pericardium-hepatitis syndrome "HHS" = Angara disease and quail bronchitis
"QBV - 69-75 nm).
The second group: It includes: Hemorrhagic enteritis "HEV of turkey -70-80 nm", Marble spleen disease "MSDV of pheasant -
70-90 nm) and avian adenovirus splenomegaly "AASV of chicken – 70-90 nm). The adenoviruses of this group are transmitted
mainly through oral and cloacal routes and unlike group I adenoviruses, there is no epidemiological evidence for egg
transmission.
The third group: It includes the viruses isolated from ducks and chickens with egg drop syndrome (75-80 nm). It
hemagglutinates the avian RBC of chickens, ducks, turkeys, geese, pigeons and parrots. There are three types of egg drop
syndrome:
1-Classic type: In which the route of transmission is mainly vertical route.
2-Endemic type: In which the route of infection is mainly the oral route and the infection is usually transmitted via the egg
trays.
3-Sporadic type: In which the route of infection is mainly the oral route and the infection is usually transmitted via the wild
ducks and geese.

Disease Host Cause Signs & Lesions P & T
IBH
Gumboro-
related disease
Commercial
broilers
(3-7 wks).
Group-I
Depression, inappetance, ruffled feathers, pale comb and wattles.
Swollen yellowish mottled liver with petechiae and subcapsular
hemorrhage.
Kidneys and bone marrow are pale discolord. Blood is thin.
Bursa and spleen are small sized.
Microscopically – basophilic intranuclear inclusions.
P.Biosecurety.
T.None.
MRD Chickens Group-I
Mild snick and cough without mortality.
Mild catarrhal tracheitis.
P.Biosecurety.
T.None.
HHS =
Angara
disease
Chickens Group-I
QB
Quail
(1-5 wks)
Group-I
Respiratory distress, coughing, sneezing, rales, watery eyes and
conjunctivitis with mortality may be 100% in birds < 2wks and up
to 25% in birds > 4 wks. The disease course is 3-6 days.
HE of turkey Turkeys Group-II
Sudden death and bloody droppings from vent. The usual
mortality is 0.5-3%. Immunosuppression with increased
susceptibility to colibacillosis. Severe hemorrhage mostly in the
upper part of intestine plus splenomegaly and mottling.
P-Vaccination.
T-None.
MSD Pheasant Group-II
It affects semi-mature and mature pheasants. Sudden death
without signs. Splenomegaly with mottling (marbling) and
massive lung edema.
None
AAS Chicken Group-II Splenomegaly with mottling (marbling). None.
EDS 76
Chickens +
Ducks
Group-III
Egg drop at peaking time or failure to peak (5-50%) and last for 3–
4 weeks. Rough, thin or soft-shelled eggs and shell-less eggs. Loss
of shell pigment. Poor internal egg quality. Lack of signs in the
birds themselves.
No specific lesion – only a slight atrophy of ovary and oviduct.
P.Vaccination
with killed
vaccine prior to
lay.
T.Supportive.

31-Viral arthritis: Reo virus ‫ا‬ ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫ا‬ infection. Reo means respiratory enteric orphan virus.
Commercial
broiler and
breeders
IP is I-13 days.
Lameness, low morbidity, poor growth. Hock arthritis, swelling of tendon sheath,
unthriftiness, rupture of gastrocnemius tendon. Swelling and arthritis of digital flexor
(footpads) and metatarsal extensor tendon sheaths (hock joints).
The tendon sheaths contain yellowish or pus like fluid. Articular surfaces of tibia and
metatarsal show erosions. Footpad is swollen. Articular cartilages is ulcerated. Tissues
hemorrhage and fibrosis is present in chronic cases.
32-Runting syndrome = Helicopter Syndrome = Pale bird disease = femoral head necrosis: Reo virus infection
Chicken
1-2 week old
birds
About 5-20% show the disease with deaths not exceed 2-4% due to concurrent
complications, due to immunodeficiency due to bursal atrophy.
Externally there is poor feathering and poor shank pigmentation.
Internally, intestinal tract is found distended with poorly digested food. Gall bladder
remains distended with bile. BF & thymus remain small & atrophic. Pancreas may be
atrophic or even fibrosed. Ceca filled with froth & gas. Proventriculus may also be
inflamed.
33-Pasty Vent Disease (Cloacal Pasting): Reo virus infection.
Chicks
3-4 days old.
White pasty excreta, which stick around the vent feathers, forming a lump. About 10-
15% chicks may be affected, causing 3-5% mortality. The disease subsides in about 2-3
weeks.
Catarrhal enteritis and cloacal distension with white, pasty excreta. Small necrotic foci
may be seen in the liver. The abdomenal distension due to the closure of the vent by
the lump of the excreta.

34-Respiratory disease due to reovirus: Reo virus infection
Chicks
3-4 days old.
Some authors isolated a reovirus from cases of chronic respiratory disease (CRD) but their
significance was overshadowed by the recognition of M. gallisepticum being mainly
responsible for CRD.
Others produced respiratory disease experimentally with reovirus. The real significance of
this virus and the disease produced by it in nature has yet to be fully understood.
35-Rota virus infection: Rota virus
Chick in first
week of life.
Inappetance, diarrhea & increased mortality. Only diarrhea is observed in adult birds.
Dehydration, intestines & ceca abnormally show fluid & gaseous contents.
Cacking of feet and digits with dried faecal crusts is commonly seen. Mortality is around
5%. Viruses replicate mainly in mature villous epithelial cells.
38-Duck virus hepatitis:
All duck
species except
Muscovy
ducks. It affects
ages < 5 wks.
I.P is 2-5 days.
Sudden death of the affected birds, death in good condition, depression, fall on
side, paddling of legs, arching of back, rapid deterioration and death occurs
within an hour often in an opisthotonus position.
Liver swollen with punctate/diffuse hemorrhages. Kidneys and spleen are
swollen with diffuse hemorrhages.
P.Vaccination of breeder to
give MDA.
T.Injection of antiserum of
recovered birds (0.5 ml IM)
or injection of hyper-
immune yolk from eggs of
vaccinated dam + effective
antibiotics.
Prevention: Vaccination of breeder by live vaccine at 70 day "primer dose" and 130 day "booster dode" to give high level of
maternally derived immunity which protect the newlly hatched birds for about 1 month.

Control: Injection of hyper-immune antiserum of recovered birds (0.5 ml IM) or injection of hyper-immune yolk from eggs of
vaccinated dam + effective antibiotics.
38-Duck virus Enteritis:
Duck & geese.
I.P is 3-7 days.
Sudden death of affected ducks with rapidly spreading disease. Drop egg
production. Photophobia. Ataxia and tremor. The affected ducks hold its body in
their wings. Closed eyes. Severe thirst and diarrhea, sometimes with dysentery.
Dehydration. Paresis. Paraphemosis "penile prolapse in drakes".
Cyanosis of the bill in the young. Severe enteritis, crusty plaques from esophagus to
bursa (covered by yellowish plaques in later stages). Hemorrhage in intestine, body
cavities, heart, pericardium, liver & spleen. Young ducks show thymic and bursal
lesions.
P.Vaccination.
T.None, but Emergency
vaccination is of value.
39-Goose Viral Hepatitis (Dorsey's Disease): Parvovirus ‫ا‬ ‫ا‬ ‫ه‬ ‫ر‬ ‫وآ‬ ‫ا‬ ‫ه‬ ‫ت‬ ‫و‬ ‫.ا‬ Vertical
transmission resulting in congenital infection
Geese < 5 wks
& Muscovy
ducks up to 12
wks.
I.P is age dependant; in very young it is 3-5 days but in older it is 5-10days.
For goslings < 1 wk of age the signs are anorexia, reduced feed intake, excessive
water intake, swollen eyelids, ocular & nasal discharge, profuse white diarrhea &
prostration. Mortality with deaths occurring in 2-5 days.
Older birds depending on the level of MDA exhibit anorexia, polydipsia,
weakness with reluctance to move, nasal & ocular discharge, swollen & red
uropygial gland, eyelids & profuse white diarrhea. Membrane covering tongue,
loss of down, reddened skin especially at the cloacal region.
Pericardial effusion "about 5-10 ml of faint yellow discolord fluid" with fibrinous
pericarditis, pale myocardium, swelling & congestion of liver, spleen & pancreas.
Ascites, & perihepatitis.
P.Vaccination of breeder to
give MDA.
T.Injection of antiserum of
recovered birds (0.5 ml IM)
or injection of hyper-
immune yolk from eggs of
vaccinated dam + effective
antibiotics.

40-Muscovy ducks Parvovirus: Muscovy ducks Parvovirus is distinct from GVH virus. It is transmitted by horizontal and vertical
routes.
Muscovy ducks.
I.P is 4-7 days.
Inappetance, thrist, crowding, conjuctivitis & nasal discharge. The feed & water are refused
completely before death. The recovered birds are stunted.
P.Vaccination of
breeder to give
MDA.
T-None.

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