Penyakit penting pada unggas

akibat infeksi virus( IB, ILT EDS)

Sri Murtini
Beberapa penyakit viral penting dalam
industri peternakan diIndonesia :
• Infectious Bronchitis
• Infectious Laryngotracheitis
• Eggs Drops Syndrom
INFECTIOUS BRONCHITIS

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 Deskripsi Penyakit
• Penyakit pernapasan akut pada ayam yang sangat
menular.
• Semua usia ayam rentan terinfeksi, khususnya pada
ayam petelur .
• Infeksi pada anak ayam /ayam muda menyebabkan
pertumbuhan terhambat & kecenderungan mudah
terinfeksi penyakit lain.
• Ayam baik pedaging maupun petelur yang terinfeksi
mengalami penurunan produksi dan mempengaruhi
kualitas telur.
• Kalkun lebih tahan terhadap penyakit ini.
 Etiologi
Virus ini adalah anggota dari :
• Spesiesnya: Avian coronavirus, Genus
Gammacoronavirus, subfamily Coronavirinae, Famili
Coronaviridae, dalam ordo Nidovirales.
• Coronavirus memiliki genom RNA untai tunggal,
tidak tersegmentasi, sense positif.
• Ada beberapa serotipe dan strain virus infeksius
bronkitis (IBV) yang berbeda di seluruh dunia
 Patogenesa infeksi IBV

• IBV biasanya ditularkan ke inang melalui inhalasi,

kemudian menempel pada epitel pernapasan dan
masuk melalui endositosis yang diperantarai reseptor
• IBV memasuki saluran pernapasan bagian atas, target
sel infeksi : epitel, yang bersilia dan termasuk
kelenjar yang mensekresi lendir , menyebabkan
ciliostasis dan akumulasi lendir
• Replikasi virus di puncak epitel pernapasan 3-7 hari
pasca infeksi (dpi) tergantung pada strain IBV yang
menginfeksi
 Patogenesa infeksi IBV
• tanda-tanda gangguan pernapasan muncul
dalam 2 dpi dan puncak sekitar 6 dpi
• Manifestasi klinis pernapasan ini termasuk
bersin, terengah-engah, batuk, ronki trakea,
sekret hidung, konjungtivitis, dan dispnea
• manifestasi klinis non-pernapasan seperti
depresi, penurunan berat badan, lesu dan
meringkuk bersama-sama
 Gejala klinis
• Ayam petelur penurunan produksi dan kualitas
telur
• Beberapa jenis virus adalah nefropatogenik
dan dapat menyebabkan nefritis interstisial
dan kematian.
• Tingkat keparahan gangguan pernapasan yang
diinduksi IBV meningkat akibat bakteri, yang
menyebabkan airsacculitis kronis
 Clinical Signs
CHICKS –
The nature and severity of the disease are influenced by the age
and immune status of the flock and virulence of the causal
strain.
The main clinical signs were restless and huddled together, difficult
in breathing, gasping, coughing, sneezing, tracheal rales, nasal
discharge, wet eye and swollen sinus, ruffled feathers, morbidity
up to 100%
• Facial swelling may also occur occasionally, particularly with
concurrent bacterial infection of the sinuses.
• Depressed and cold decrease of feed intake and conversion, loss
of body weight
• increased water intake, wet droppings, depression,
lethargy and poor growth in broilers
• Morbiditas dan mortalitas yang terkait dengan infeksi
saluran pernapasan IBV tergantung pada usia infeksi;
ayam muda sangat terpengaruh dibandingkan dengan
ayam dewasa
• Pada pemeriksaan post-mortem, perdarahan dan
akumulasi eksudat kaseosa, serosa dan catarrhal di
trakea, saluran hidung dan sinus jelas, serta
perubahan besar pada kantung udara (yaitu,
akumulasi busa atau keruh eksudat)
 Clinical Signs
LAYERS -
• Rales and seldom have nasal or ocular discharge.
• Egg production may drop 20-50%.
• mainly affects egg quality (thin, rough, fragile,
misshapen egg shells and thin watery egg) and
causes decrease in egg production In some cases the
virus infection may cause severe damage to the
oviduct and result in decreased or permanent loss of
egg production
 Method of Spread
• Airborne aerosol from infected birds ( respiratory tract).
• Direct contact with short time carriers.
• fecal transmission and fomites.
• Virus shedding lasting for several weeks after infection and persistent
carriers may be present.
• Disease also transmitted through materials, equipment and movement of
field worker from the infected flocks to health farm also movement of live
birds.
• Wild birds may play a crucial role as reservoirs and long-distance carriers
of IBV.
 Mortality
• Respiratory IB usually not significant but in recent year high mortality nots
- although tracheal plugs at the bifurcation cause asphyxiation.
• Some serotypes can cause serious airsacculitis.
• Depends on secondary infection such as Mycoplasma.
• Nephrotropic strains may cause high mortality in chicks and layers. Causes
urolithiasis.
• Nephrotropic strains include Holt and Gray.
Nephropathogenic strains can produce
interstitial nephritis with high mortality
(up to 60%) in young chickens. In most
outbreaks, although secondary bacterial
infections may cause higher losses.
 Postmortem Lesions
CHICKS AND BROILERS
• Infected chickens have serous, catarrhal or caseous exudates may be seen
in the trachea, nasal cavity and sinuses
• Congested blood vessels in trachea and caseous plugs of mucus in the
primary bronchi (Tracheal plugs at the bifurcation)may followed secondary
infection and cause asphyxiation. Lungs may appear congested and
airsacculitis is common Slight airsacculitis - severity varies with serotype of
IBV.Ark causes airsacculitis.
• Nephropathogenic strains, the kidneys become pale and swollen and urate
deposits may form in the kidneys and ureters
 Postmortem Lesions
PULLETS AND LAYERS
• Hyperemia of trachea
• Serous & catarrhal exudate of trachea
• the ovarian follicle may be flaccid, Deposition of yolk material in the
peritoneal cavity (egg peritonitis) is common Salpingitis & permanently
damaged oviduct.
• Infection of 2-3 week old pullets with IBV may cause infertility,
salpingitis, and internal laying.
• Swollen kidneys with urates
• Necropsy finding of bird infected with QX strain frequently showed either
cystic oviduct with watery contents that could exceed one liter or partially
atrophic oviduct with large cystic dilatation .
 Differential Diagnosis
• Newcastle Disease
• Laryngotracheitis (ILT) - slow moving
• Infectious Coryza(Haemophilus gallinarum) - swollen head
• Avian Influenza
• turkey rhinotracheitis (TRT) also causes a swollen head
syndrome
 Diagnosis
• History of fast spreading respiratory disease
• ELISA - uses Mass. antigen but get cross reaction with other
serotypes.
• HI - IBV is treated with neuraminidase enzyme before testing
because IBV is not naturally hemagglutinating.
• VN - rises in titer between paired serum samples (2 wks.
apart)
• Agar-gel precipitation test (AGPT)
 Diagnosis
• Isolation and identification of virus-
embryonating eggs – stunting, curled, and
hemorrhagic - vaccine strains are embryo
adapted and often affect embryos on the 1st or
2nd passage whereas field strains may require
additional passages before lesions appear.
• Identification of IBV serotype - PCR, monoclonal
antibody test, etc.
• Detection of virus genome (RT-PCR)
Stunted, Curled Embryos
 Prevention
Establish and enforce a biosecurity program.
Vaccination - complete prevention of IB is
difficult because of variation of field strains
and the ability of the virus to change. There is
little cross protection between serotypes.
 Prevention (Cont.)
VACCINES:

LIVE - Monovalent - usually Mass

Bivalent - Mass. & Connecticut 

Other attenuated strains such as Holland

andArk. 99 are used as vaccines.
 Prevention (Cont.)
VACCINES:

KILLED - used in breeders and layer pullets to

prevent production losses and produce
consistently high antibody titers.
 Prevention (Cont.)
• Management Procedures
• Ideal management includes strict isolation,
high biosecurity, and repopulation with only
day-old chicks following the cleaning and
disinfection of the poultry house and
equipment in contact with poultry or poultry
litter and removal of the feces from the
premises.
Treatment:
 None for the virus (acyclovir,
amantadine)
 Broad spectrum antibiotics for
secondary bacterial involvement
 Infectious Bronchitis Virus (IBV)

• Young chickens
• Broiler chickens
• Layers

healthy chicks

IBV-infected egg defect IBV-infected normal

embryo embryo
 Avian infectious laryngotracheitis virus

• Acute disease of chicken, pheasants (3-9 month)

• Respiration problems, bloody mucous secretion
• Conjunctivitis - panophtalmitis
• Mild - peracute disease
• Antigenic uniformity, strains differ in virulence
• Impact of environment (iritation of resp.tract, low
temperature, concurrent infections)
 Laryngotracheitis –
Incidence and Distribution
• Worldwide distribution
• Intensive rearing
• Control
• Layers and breeders
• Typically well vaccinated/controlled
• Broilers
• Short life cycle; often not vaccinated unless regional
• May be endemic in some flocks
 Infectious Laryngotracheitis
• Penyebab : Herpesvirus
• Sensitivity: mild (halogen-detergents + iodophors, heating,
freezing (-18°, -25° C !)
• Acute respiratory disease
• Conjunctivitis
Laryngitis
Tracheitis
(Histopathology: intranuclear inclusion body in
epithelial cells by 3 day PI)
 Laryngotracheitis – Etiology

• Alphaherpesvirus
• Morphology/composition
• Similar to other Alphaherpes viruses
• Double stranded DNA (155kb)
• Enveloped
• Glycoprotein spikes (humoral and cell mediated immunity)
• Shape: Icosahedral
• Size: 195-250 nm
• Similar to MDV
 Laryngotracheitis –
Hosts
• Primarily in chickens
• Usually older birds
• Respiratory tract: viremia unlikely
• Pheasants & pheasant crosses (sporadic)
• Peafowl (rare isolate)
• Turkeys (experimental)
• Other birds resistant (ducks, pigeons, doves,
sparrows, crows, starlings, guinea fowl) May still carry
virus mechanically
 Laryngs
(left - normal) (medium - hyperemic) (right - fibrin)
 Laryngotracheitis – Pathogenesis
• Portal of entry : Upper respiratory/ocular
Ingestion → nasal epithelium
• Horizontal transmission
• Aerosolization of virus
• Birds, feed, water
• Contaminated litter
• Fomites (equipment, boots, clothes, tires)
• Moves slowly through flock
• No vertical or egg transmission known
 Laryngotracheitis – Pathogenesis
• Virus present in trachea for 6-10 days PI
• Inflammation and necrosis (tracheal cores)
• Necrotic cells, blood, inflammatory debris
• High virus shed during infection
• Leads to :
Death (asphyxiation)
Latent carriers
• Latent carriers :
Trigeminal ganglion + tracheal epithelium
Persistent infection & intermittent shedding
• Laryngotracheitis – Pathogenesis
• Spread to trigeminal ganglion 4-7 days PI
• Found to be latent for up to 15 months
• Stress may cause virus to recrudesce
Movement, reproduction, etc.
Carriers in flock for 16 months
• racheal swabs ~ 2%
• Organ cultures ~ 50%
 REPLIKASI VIRUS
PROSES REPLIKASI TERJADI DI NUCLEUS
Virus penetrasi ke sel inang pada bagian clathrin- and caveolae-independent
endocytosis.
Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke nuklues
Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui peranan
faktor sel inang ,
DNA virus tersebut ditranskripsi menjadi mRNAs virus .
mRNAs virus ditranslasi menjadi protein virus

Replication ini diduga dimediasi oleh protein Rep protein, yang akan memproduksi
DNA utas tunggal berbentuk bulat

DNA utas tunggal yang disintesa :

a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untuk proses
trankripsi dan replikasi
b) akan dibungkus oleh kapsid protein dan meghasilkan virus baru , virus tersebut
dilepaskan dari sel melalui budding
 Laryngotracheitis –
Economic Significance
• Not determined
• Mortality
• Decreased production
• Meat, eggs, breeder potential, increased down time
• Uniformity, feed conversion
• Processing issues
• Vaccination (vaccines, labor)
• Waste disposal & storage
• Labor (service responsibilities, transport, cleaning and
 Avian infectious laryngotracheitis virus

• Virus latency – in infected and vaccinated animals

• Rezidual pathogenicity of vaccine strains
• Cell immunity – non-transmissible to the newborns
 Avian infectious laryngotracheitis virus

Samples: 4-6 living animals

trachea, larynx - chilled, not frozen

Diagnostics
• I.N. inklusions - trachea
• IF test – trachea
• Izolation on EE (CAM), IFA identification
• Differentiation of vaccine and field strains by REA
 Adenoviruses
Adenoviruses aden = gland (Greek)
first isolated from adenoid tissue
Key Features:

1. Icosahedral capsid (80 nm)

2. Larger dsDNA genome (35 kbp): 30-40 genes

3. Encodes own DNA polymerase and factors that regulate cellular processes

4. Many animals are infected by multiple serotypes

5. Mainly associated with mild respiratory disease

6. Highly immunogenic. Fairly resistant

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 Adenoviruses

Adenovirus Structure

fibre
penton
hexon

DNA

terminal protein

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 Adenoviruses

Importance of Adenoviral capsid

1. Fibre and penton bind to proteins on the cell surface- determine tissue
infectivity.

2. Adenoviruses can cause red blood cells to clump (haemagglutination).

Mediated by the fibre. Used for diagnosis- haemagglutination-inhibition
(HI) test.

3. Hexon is the most abundant capsid protein and the major target for the
infected animal’s immune system. Immunity is long-lasting.

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 Adenoviruses
Avian Adenoviruses
1. Egg drop syndrome
(EDS76)- first reported in
1976. Infects pouch shell
gland with soft-shelled and
shell-less eggs produced,
with no clinical signs.
Effectively eradicated from
most countries.
2. Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marble
spleen disease of pheasants. Also causes immunosuppression. Controlled
by vaccination.

3. Avian adenovirus 1- causes bronchitis in quails. Control by isolation and

decontamination.
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• Egg drop syndrome virus, which is classified in
the genus Atadenovirus, likely originated in
ducks and spread to chickens through a
contaminated vaccine. Duck atadenovirus A
also is included in the genus Atadenovirus.
 Egg Drop Syndrome ‘76
• Cause • Adenovirus Infection Type
• Age group affected 3
• Transmission • Chicken layers + ducks
• Clinical Signs + • Pharynx and feces
Lesions
• Loss of color in pigmented
eggs, drop in egg
production, thin to shell
less eggs, rough shell,
• Diagnosis inactive and atrophied
• Vaccine oviducts, edema in uterus
 Egg Drop Syndrome ‘76
Egg drop syndrome, pertama kali dilaporkan pada
tahun 1976,
ditandai dengan produksi telur bercangkang lunak
dan
tanpa cangkang oleh ayam yang tampaknya sehat.
Ayam petelur komersial meskipun sudah
divaksinasi terhadap infeksi adenovirus, Egg drop
syndrome, pada delapan hari pascainfeksi, virus
tetap tumbuh masif di daerah kantong sel kelenjar
oviduk bersamaan dengan terjadinya perubahan
cangkang telur.
 EGG DROP SYNDROME VIRUS

• Progeny from these infected eggs can

hatch and appear clinically normal but
latently infected. When a latently
infected individual reaches peak lay,
the virus is reactivated.
• The virus can be transmitted vertically
and should an unprotected flock
become infected during lay, the egg
drop can be profound.
 Transmisi
• Transmission is possible horizontally via the faecal
/oral route. Classically an infected flock will initially
show a loss of shell pigmentation, followed by thin
shelled, soft shelled, and shell-less eggs.
• There is an apparent drop in egg production,
though overall production may be normal, but there
will be fewer normal eggs. It has been calculated
that the loss equates to about 10 to 16 eggs per hen
when a naïve flock is infected (Pattison et al. 2008).
 Diagnosa dan pencegahan
• Confirmation of a challenge is possible with rising
antibody titres on paired serology or PCR testing
(assuming isolation of the virus is not required).
• No treatment is available, but even in small flocks,
vaccination should be considered.
• The only licenced EDS vaccines in internationally are
polyvalent inactivated vaccines.
• Replacement pullets for an infected site should be
injected with this vaccine intramuscularly between 14
and 16 weeks of age.
• In chicken flocks previously free of infection with this virus, the first clinical signs
of infection are loss of color in pigmented eggs and soft-shelled, thin-shelled,
and shell-less eggs. Thin-shelled eggs may have a rough or even sandpaper-like
surface. Because birds tend to eat the shell-less eggs, affected eggs may be
overlooked, but egg production numbers decrease by a maximum of 40%.
• In flocks in which there is antibody, the disease is seen as a failure to achieve
production targets. There is also an enzootic form of the disease, similar but
more difficult to detect
• Characteristic lesions in infected birds occur in the pouch shell gland and oviduct,
where epithelial cells become necrotic and contain intranuclear inclusion bodies.
• There is associated inflammatory infiltration. These findings are virtually
pathognomonic, but diagnosis may be confirmed by virus isolation or serology.
• Hemagglutination-inhibition or neutralization assays are specific for this virus
and do not cross-react with antibodies from aviadenovirus infections.
This disease has been eradicated from primary
breeder flocks in most countries.
layer flocks is further managed by:
(1) preventing contact with other birds, especially
waterfowl;
(2) disinfecting all equipment regularly; (3) 
chlorination of water. 
Inactivated vaccines are available for use in
chickens before they begin laying eggs, but they
only reduce, rather than eliminate, virus
transmission.