Viral diseases of aquatic birds. Dr Fares El-Khayat

1. Viral Diseases of Aquatic birds.

2. IntroductionIntroduction

3. Facts:
1-All RNA viruses are single stranded except for reovirus
& IBDV.
2-All DNA viruses are double stranded except for
Parvovirus.

4. Emergency V - + - -
Target organ Liver & Kidneys Heart Heart Heart
Age dependency +↑ +↓ +↑ +↑
R.O.I Allantoic sac "I",
amniotic sac "II",
CAM "III"
CAM Allantoic sac Allantoic sac
M.O.T Direct and indirect
contact.
Direct and
indirect
contact.
Direct and
indirect contact.
Direct and
indirect contact.
M.O.I Oral, respiratory, IM
No egg transmission
Oral, nasal,
parentral,cloaca
l routes. Blood-
suckers.
Vertical.
Vertical. Vertical.
Variation + - + +
IP 2-3 days 3-7 days 3-10 days 3-5 days
Diseases DVH DVE Derszy's DPV
Host Ducklings except
Muscovy
Ducks Duckling &
gosling
Muscovy
Type of NA Picornavirus,
Astrovirus, Picorna
unrelated , RNA
Herpesvirus
DNA
Parvovirus
ssDNA
Parvovirus
ssDNA
Criteria DVH DVE Derszy's DPV

5. Emergency V - -
Target organ S/C tissues in head "chickens"
Respiratory organs esp. sinus
"turkey"
GIT, Achilles tendon
Age
dependency
- -
R.O.I Yolk sac 5-7 days Yolk sac 5-7 days
M.O.T Direct and indirect contact. Lateral + vertical
M.O.I Respiratory + venereal (turkey) Respiratory + enteric
Variation - +
IP Short 1-14 days
Diseases "SHS" &"TRT" Helicopter S, SRS, Viral
arthritis
Host Chickens "SHS"
Turkeys "TRT"
Chickens
Type of NA Pneumovirus
RNA
dsRNA
Criteria APV Reovirus

6. Duck Virus Hepatitis
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7. Duck Virus HepatitisDuck Virus Hepatitis
DVHDVH
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DefinitionDefinition: Acute, infectious, highly fatal, contagious, viral disease
of young ducklings characterized by a short incubation period,
sudden onset and rapid spread, high mortality and characteristic
ecchymotic or patchy hemorrhagic liver lesions.
Historical information:Historical information: First reported in 1945 by Levine and
Hofstad.
The disease is present and very famous in Egypt.

8. EtiologyEtiology: DHV has 3 different forms caused by 3 different viruses:
-DHV type I “most severe & widely distributed” caused by
Picornavirus-1 that causes disease in ducklings under 5 wks old.
-RNA virus, 20-40 nm in size
-Propagated in CEE & DEE via allantoic sac “9-11 day” causing death
of embryo in 3-6 days which appear stunted and edematous and show
liver necrosis and greenish discoloration of embryonic fluid.
-Does not hemagglutinate avian or mammalian RBC.
-Egg transmission does not occur, transmitted experimentally by
parenteral or oral administration of infected tissues.
-Famous in Egypt, Northern America, Europe, Africa & Asia.

9. -DHV type II caused by an Astrovirus are spherical RNA virus,
which causes disease in ducklings between 6-10 wks old, difficult to
be propagated under laboratory conditions. Amniotic sac is the
route of inoculation which requiring several blind passages. It is
present in England.
-DHV type III caused by Picornavirus unrelated to DHV type I,
which causes milder disease. DHV-III is a member of the
Picornaviridae, antigenically distinct from type I virus, and can be
propagated via CAM “10-12 days” in DEE (but not CEE). It is
present in USA.

10. Characteristics of DVH virus:Characteristics of DVH virus:
1-Non hemagglutinating.
2-SS RNA virus.
3-Non-enveloped « ether & chloroform resistant”.
4-Relatively heat stable.
Distribution:Distribution: DHV-I is present in Northern America, Europe,
Africa & Asia, DHV-II is restricted to the United Kingdom,
DHV-III is restricted to the USA. DHV is not present in the
Pacific Region. DHV-I is present in Egypt.
Susceptible species:Susceptible species: Ducklings. In naturally occurring
outbreaks, DVH type 1 occurred only in duckling. Adult
breeders did not become clinically ill.

11. Epizootology:Epizootology:
Source of Infection:
-Infected ducklings.
-Recovered ducklings → virus in feces for up to 8 wks PI.
-Wild birds → mechanical carrier.
-Brown rats → a reservoir host up to 35 days and the virus
is excreted 18-22 days PI, serum antibodies is also present
for 12-24 days PI.
Transmission: direct contact with infected ducks and indirect
contact with contaminated environment.
Mode of Infection: oral, respiratory and IM routes. No egg
transmission from infected breeders.
Incubation period: 2-3 days.

12. Clinical Findings:Clinical Findings: All 3 types produce similar signs & lesions.
In DHV Type I: Rapid onset & spread. Affected ducklings are
lethargic, lose balance “fail to keep up with stop moving”, squat
down with partially closed eye, fall on one side “right mostly” or
back “rarely” with spasmodic paddling movement of both legs
and die in opisthotionus position within 1-2 hrs and in a good
condition.
Morbidity may reach 100% and mortality is age dependent. All
deaths occur within 3-4 days after onset of signs.
Duckling less than 1 wk → mortality → 85-95%.
Duckling 1-3 wk age → mortality reaches 50% or less.
Duckling 4-5 wk age → morbidity & mortality are low.
Clinical signs are not seen in ducks > 6 wk old.

13. •The clinical course of DHV Type II is similar to that of Type I
and occur in ducklings immune to Type I infection.
•The clinical course of DHV Type III is less severe, and
mortality is rarely > 30%. DHV Type III infections occur in
ducklings despite immunity to Type I virus.

17. Lesions:Lesions:
The lesions caused by all three types of DHV are similar.
Hepatomegaly with ecchymotic or patchy hemorrhage “ranged
from pin headed to 1 cm in diameter. Sometimes the liver has a
reddish mottling.
Enlarged & mottled spleen.
Swollen kidneys with congested renal blood vessels.

21. Diagnosis:Diagnosis:
Suggestive diagnosis is based on history, signs and lesions.
Sudden onset, rapid spread, and short course, together with
characteristic liver lesions, are highly suggestive of DVH.
Type I virus is isolated in DEE, day-old ducklings, and duck-
embryo liver cell cultures, or less easily in chicken embryos.
The virus can be identified by neutralization with specific
anti-sera or by inoculation into both susceptible and immune
ducklings.
Type II and III viruses are not neutralized by classic Type I
antiserum.

22. Differential diagnosis:Differential diagnosis:
Sudden onset, rapid spread, acute course, hemorrhagic liver
lesions of duckling up to 3 wks of age are pathognomonic for
DVH type 1.
DVE, coccidiosis, mycotoxicosis, IS, paratyphoid, aflatoxicosis
(ataxia, convulsions, opisthonous).
Specimens required for diagnosis. Liver specimen can be
collected at PM for virus identification.
Serological test is possible using serum neutralization,
however due to the short course of the disease serological test
is not used for diagnosis on live ducklings.

23. PreventionPrevention:: S/C or I/M vaccination with live vaccine.
Breeders: “Live egg adapted strain vaccine = Asplin strain”.
-Primary vaccination: at 7 wks of age S/C.
-Booster in 2 wks prior to each laying season S/C.
Duckling: “Live egg adapted strain vaccine = Asplin strain”. Duckling
are vaccinated via foot pad stipping.
-Duckling “from vaccinated ducks” → vaccinated at 7-10 days of age.
-Duckling “from non-vaccinated ducks” → hatchery vaccination.
Vaccination of duckling is not applied in the field.

24. Control:Control:
Passive immunization at time of first death in an outbreak is an
effective method for control.
IM or S/C injection of 0.5-1.0 ml DVH type-1 hyper-immune
serum:
-first dose at the onset of the disease.
-second dose at 14 days apart.
IM or S/C injection of 0.5-1.0 ml DVH type-1 hyper-immune yolk
taken from eggs produced from hyper-immune breeder ducks.
-first, second and third doses at the onset of the disease.

25. Duck Virus Enteritis = Duck PlagueDuck Virus Enteritis = Duck Plague
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26. DefinitionDefinition: DVE is an acute, infectious, highly contagious viral
disease of ducks, geese, swans and migratory waterfowl
characterized by short course, high mortality, drop in egg
production, vascular damage, tissue hemorrhages, digestive
mucosal eruption, lesions of lymphoid organs, degenerative
changes in the paranchymatous organs.
DVE is characterized as an acute disease; however, chronic or latent
infections may occur rarely. Higher incidence is mostly occur in
spring.
Susceptibility to DVE vary with age, management practices and the
presence of concurrent disease agents. DVE is referred to as duck
plague, anatid herpes and peste de canard. The infection is not
reported in other avian species, mammals or humans.
Historical Information:Historical Information: The disease was first reported in
Netherlands in 1923 and in Egypt in 1986.

27. Etiology:Etiology: Herpesvirus. DNA enveloped virus that replicate in
nucleus “INIB”. Non-hemagglutinating, non-hemadsorbing virus.
All isolates appear immunologically identical. Propagated on CAM
of 10-12 day old duck embryo.
Susceptibility:Susceptibility: Domestic ducks, geese, swans and migratory
waterfowl.
White Peking, Khaki Campbell, Muscovy ducks are more
susceptible than other species.
Indian Runner, hybrids & native ducks are less susceptible.
All ages are susceptible but susceptibility increases with the
advancement of age.
Surviving birds may intermittently shed virus for a long time
“years” following infection.

28. Mode of infection:Mode of infection: Oral, intranasal, parentral and cloacal routes.
Blood-sucking arthropods may be possible during viremia. Vertical
transmission via eggs are possible.
Mode of transmission:Mode of transmission: Direct contact between infected and
susceptible birds. Indirect contact of susceptible ducks with
contaminated feed, water and carrier birds or recovered shedder of
the virus (Recovered birds may be carriers and shed the virus in
feces or on the surface of eggs over a period of years).
Detection of carrier birds is nearly impossible because of the
intermittent nature of virus shedding and the fact that both
antibody-positive and antibody-negative birds may shed virus.
Incubation period:Incubation period: 3-7 days.

29. Clinical Signs:Clinical Signs: varies with species, age, sex and virulence of virus.
In domestic breeder ducks:In domestic breeder ducks: Sudden, high, persistent mortality is
the first sign. Mature ducks die in good flesh. Prolapsed penis (male).
Marked drop in egg production “period of highest mortality (25-40%)”.
With disease progresses, a more signs are observed as photophobia with
half closed eyes, pasted eyelids, extreme thirst (polydipsia), soiled vents,
ataxia, unable to stand " Sick birds may maintain an upright stance by
using their wings for support", ruffled feathers, nasal discharge, watery
diarrhea, drooping outstretched wings and head down. On forced to
move → tremors of head, neck and body.
In young commercial duckling (2In young commercial duckling (2--7 wks age):7 wks age): Losses are lower
than in older birds. Signs include dehydration, weight loss, diarrhea,
blue beaks and bloodstained vent. Death occurs within 1-5
days. Recently, a low-virulent isolate causing immunosuppression was
isolated from White Peking ducklings.
Morbidity and MortalityMorbidity and Mortality are usually high and ranges from 5-50%.
Adult breeder ducks show greater mortality than young ducks.

30. Gross Lesions:Gross Lesions:
Gross PM lesions varies with species, age and sex and the
virulence of the virus.
Generally, vascular damage, eruptions at specific mucosal
surface of GIT, lesions in lymphoid organs with degeneration
of paranchymatous organs.
The suggestive and diagnostic lesions of DVE include:

31. Heart:Heart:
Myocardial petechial, echymotic hemorrhage.
Epicardial petechial hemorrhage esp. within coronary groove
give the surface a red paintbrush appearance esp. in mature
ducks.
Endocardial mural and valvular hemorrhages.

34. GIT:GIT: Raised hemorrhagic spots which later be covered with crusty
yellowish-white plaques.
--Oral erosions:Oral erosions: → in birds with persistent infection → opening of
sublingual salivary glands.
--EsophagealEsophageal––proventricularproventricular sphincter:sphincter: hemorrhagic ring resembling to
diphtheritic membranes. Size of lesions range from 1-10 mm in length.
Esophageal lesions occur parallel to longitudinal folds (a patchy diphtheritic
membrane).
--Gizzard & intestinal lumen:Gizzard & intestinal lumen: filled with blood with petechial, echymotic
hemorrhage or larger extravasation of blood on visceral organs and
supporting structures (mesentery & serous membranes).
--Liver:Liver: pale copper colored, enlarged with pinpoint hemorrhages that later
change to whitish areas of focal necrosis and dark bronze or bile stained
with these necrotic foci.
--CloacaCloaca has crusty necrotic plaques whose size ranges from 1-10 mm.

37. ORGAN : Small intestine
LESIONS : Necrosis & sloughing of intestinal mucosa.
SUSP.DIS. : DVE

39. --Ovary:Ovary: deformed, discolored ovarian follicles with massive
ovarian hemorrhage filling the abdominal cavity.
--Lymphoid organsLymphoid organs
11--Spleen:Spleen: Normal to small in size, dark, mottled.
22--Thymus:Thymus: Multiple petechiae with focal yellow surface.
33--Bursa ofBursa of fabriciusfabricius:: Reduced in size at early infection,
surrounded by clear yellow fluid.
44--Intestinal annular bands:Intestinal annular bands: hemorrhagic dark red with
yellow pinpoint areas on mucosal surface. Michael’s
diverticulum hemorrhagic with fibrinous core.

40. ORGAN : Intestine of duck
LESIONS : Congestion of annular fold
SUSP. DIS. : DVE

43. Histopathologic lesions:Histopathologic lesions: Eosinophilic intranuclear inclusion
bodies occur in the hepatocytes. Hemorrhagic and necrotic lesions
are observed in other organs.

44. Diagnosis:Diagnosis:
-Tentative diagnosis → signs, gross and histopathologic lesions.
-Isolation & identification → necessary for confirmation. Primary
isolation occurs in 10-12-day-old embryonated duck eggs via CAM.
-Confirmed by inoculation of one-day-old susceptible ducklings.
-Virus can be isolated on White Peking or Muscovy duck embryo
fibroblast, liver or kidney cells. Cytopathic effect (CPE) is
characterized by the appearance of rounded clumped cells that
enlarge and become necrotic 2–4 days later.
Immunofluorescent test is used to detect viral antigens in tissue
sections or cell cultures.
PCR is a fast and sensitive method for diagnosis.
ELISA is used to detect serum antibodies.

45. Differential diagnosis:Differential diagnosis:
Disease producing hemorrhage and necrosis as DVH, FC, NE,
mycotoxycosis, R.anatipestifera infection and coccidiosis.
Prevention:Prevention:
Immunity:Immunity: Recovered birds are immune to reinfection. CMI and
Humoral are involved in protection. Active immunity followed live
vaccine.
•Progeny of breeder ducks vaccinated with live vaccine are fully
susceptible.
•Immunization with a chicken embryo-adapted live avirulent
vaccine is used for prevention.
•Breeder ducks are routinely immunized by yearly vaccination. In
case of an outbreak, the vaccine is also used in younger ducklings.

46. •Use of attenuated live vaccine. Diluted in specific diluent given by
IM or SC route 0.5 ml dose/bird (500 dose/vial).
• Don’t vaccinate breeder during molting.
•In healthy environment, for future breeder give it at 7-11 wk of
age.
•In hot areas given at 1-7 days old and repeated every 11 wks.
Injection prior to each laying cycle.
•Market duckling: inject at 1-14 days.
•An inactivated virus vaccine provides significant protection
against experimental infection.

47. ••Control:Control:
Control through emergency vaccination with freeze-dried
modified live vaccine or chicken embryo-adapted live avirulent
vaccine .

48. Goose Parvovirus Infection
Derzsy’s disease - - Goose influenza
Goose plague - - Goose hepatitis
Goose enteritis
Infectious myocarditis
Ascetic-hepato-nephritis

49. Definition:Definition: Highly contagious disease affecting young gosling and
Muscovy ducks (only). It may be acute, sub-acute and chronic. All
breeds of domestic geese and Muscovy ducks are susceptible. In
acute form 100% mortality in gosling under 10 days of age.
Historical information:Historical information: First reported in China 1956.
Distribution:Distribution: World wide distributed.
Etiology:Etiology: Parvovirus, un-enveloped virus. Recently, antigenic
difference between goose isolate and Muscovy isolate (Muscovy
Parvovirus).
Age Susceptibility:Age Susceptibility: The disease is strictly age dependent. 100%
mortality occur in gosling and Muscovy duckling under 1 wk of
age. Negligible losses occurring in 4-5 wk old birds. Older birds
don’t show clinical signs, but respond immunologically.

50. Transmission:Transmission: Direct and indirect contact.
Infected birds excrete large amount of virus in feces resulting in a
rapid spread of infection by direct or indirect contact. Carrier status
exists and transmission of virus to susceptible birds occurs in the
hatchery. No biological vectors have been identified.
Mode of InfectionsMode of Infections:: Vertical Transmission.
Incubation Period:Incubation Period: Age dependant.
•In duckling under one week = 3-5 days.
•In duckling over one week = 5-10 days

51. Clinical Signs:Clinical Signs:
••In birds under 1 wk of age:In birds under 1 wk of age: Very rapid course, death within 2-5
days, anorexia, prostration.
••In more older birds or with variable maternal antibodies:In more older birds or with variable maternal antibodies: More
longer course with characteristic signs including anorexia, severe
thirst, weakness, reluctant to move, nasal and ocular discharge, head
shacking, uropygial glands and red swollen eyelids, profuse white
diarrhea, fibrinous pseudomembrane cover tongue and oral cavity.
••In survived chronic casesIn survived chronic cases → profound growth retardation, loss of
downs around the back and neck reddening of the exposed skin.
Accumulation of ascetic fluid in the abdomen "Penguin likes
posture".
••In latent casesIn latent cases → no signs and lesions but there is immune
reaction.

52. Morbidity and mortality:Morbidity and mortality:
••In gosling infected in hatcheryIn gosling infected in hatchery → 100% mortality.
••In 2In 2--3 wk gosling3 wk gosling → high morbidity & 10% mortality. Poor
management, bacterial, fungal, viral infection influences the
mortality level.
••In gosling over 4 wk of ageIn gosling over 4 wk of age → rare shows signs. Older birds
respond immunologically. “Late form” reported in 1-3 month
birds.

56. Gross Lesions:Gross Lesions: Most commonly in heart.
Heart:Heart: pale myocardium, rounded at its apex.
Liver, spleen, pancreas:Liver, spleen, pancreas: Swollen and congested.
In more prolonged course:In more prolonged course: Pericarditis, perihepatitis, and
liver dystrophy.
Straw colored fluid in abdominal cavity, pulmonary edema,
catarrhal enteritis. Hemorrhages in thigh and pectoral
muscles.
Diphtheritic and ulcerative lesions in mouth, pharynx, and
esophagus.

58. PreventionPrevention:: vaccination of dams with live vaccine.

59. Duck Parvovirus (DPV)
It is an acute, systemic Parvovirus infection of young Muscovy
ducklings characterized by high mortality, enteric signs, locomotor
signs, nervous signs and abnormal feathering and stunting with
mortality 80%.
The disease emerged in Muscovy ducks in western France in 1989.
Goose Parvovirus (GPV) vaccine failure led to isolation and
characterization of new virus that was found to be related to, but
distinct from, goose Parvovirus.
DPV differentiated from GPV by cross-neutralization tests. Only
Muscovy ducks are susceptible to DPV, but goose and other type
of ducks are resistant. DPV is move severe in young duckling (<5
wks) but the latter are susceptible immunologically when infected.
Transmitted horizontally, vertically and during hatching.

60. Clinical symptoms and P.M. lesions: Similar to GPV infection.
Differential diagnosis from reovirus infection by absence of
exudative pericarditis, tenosynoviris or splenic lymphoid
hyperplasia.
Prevention:
-Through good biosecurity.
-Immunization of breeders to prevent vertical transmission and
provide MDA during the initial period of greatest susceptibility.
Day-old vaccination to provide active immunity followed decline of
MDA. Two inoculations with bivalent, oil emulsion vaccine
containing DPV and GPV in breeders. Duckling is given killed DPV
vaccine in combination with live attenuated GPV vaccine.
Control: No treatment.