AVIAN INFLUENZA (AI)

PENDAHULUAN

 Penyakit yang
sangat infeksius
penting pada
berbagai jenis
unggas
 Dapat bersifat
zoonosis
 Dampak kesehatan
& ekonomi yang
besar
ETIOLOGI

 Avian Influenz Virus (AIV)

 Family: Orthomyxoviridae
 The family contains five genera, classified
by variations in nucleoprotein (NP and M)
antigens: influenza A, influenza B,
influenza C, thogotovirus, and isavirus.
 Genus influenza A virus (IAV); infects birds
 Small pleomorphic (spherical/linear)
viruses, diameter 80-120 nm, 200 to 300
nm long
 Consist of a lipid envelope with large
spikes surrounding eight helically
symmetrical nucleocapsid segments
 A linear negative-sense, ssRNA genome, 10–14.6
kb in overall size
 Consist of 8 segments that encode at least 11
proteins; 9 structural proteins, polymerase basic
1 (PB1), PB1-F2, PB2, polymerase acid (PA),
hemagglutinin (HA), nucleoprotein (NP),
neuraminidase (NA), matrix 1 (M1), M2,
 2 non-structural proteins (NS), NS1 and NS2
and nuclear export protein (NEP).
 HA, NA play an important role in the variability
of IAV genomes - generate genetic drift and
genetic shift
 CONTD

 HA plays important roles in viral attachment and facilitates the fusion of

between viral envelope with membrane of the host cell
 HA as receptor binding site and the antigenic site, HA is the main target of
host's immune response
 NA is a major surface antigen, help release new viruses from host cell and
mediate dissemination of the viruses
 HA & NA subject of mutation and target of immune system
 PB1, PB2 and PA which together forming the RNP complex that are
responsible in replication and transcription of RNA
 IAV are classified into 18 HA subtypes (H1–H18) and 11 NA subtypes (N1–
N11)
 Because of their lipid envelope, influenza viruses are sensitive to heat (56°C,
30 minutes), acid (pH 3), and lipid solvents,
HOST AND TRANSMISSION

 All birds, mamalia, humans

 All known subtypes of influenza A can be found in birds, and wild
aquatic birds are the major reservoir for influenza A viruses
 Wild waterfowls- anatidae (ducks, swans, geese) from Anseriformes
order and laridae (gulls and terns) and scolopacidae (shorebirds) from
Charadriiformes
 Wild bird (wild water bird) are considered as major reservoirs of LPAI
viruses
 In some endemic areas like China, Indonesia, Vietnam and Egypt,
Anatidae, especially ducks have been identified as important reservoirs of
HPAI H5N1 outbreaks and distribution to for poultry species and humans
 Domestic ducks may also shed H5N1 asymptomatically and are
considered to play a key role in the persistence of H5N1 in Asia
 Avian influenza virus is shed in high concentrations in the feces of wild
birds, and can survive for long periods in cold water.
 Transmission: inhalation, ingestion
EKOLOGI VIRUS AVIAN INFLUENZA H5N1

RG Webster et al. 2006

GLOBAL DISTRIBUTION
 The first report about HPAI infection in wild birds was obtained in 1961
in South Africa
 In 1997, 2001, 2002 human infections with the HPAI A(H5N1) virus
were reported during an outbreak in poultry in Hong Kong SAR, China
 Since 2003, this avian virus has spread from Asia to Europe and Africa
 In May 2005, one of the largest HPAI H5N1 outbreak in wild waterfowl
happened at Qinghai Lake in Western China
 In 2013, human infections with the LPAI A(H7N9) virus were reported in
China. Since then, the virus has spread in the poultry population across the
country and resulted in several hundred human cases and many human
deaths
 In 2016-2017, H7N9-human deaths in China
 Indonesia, 30 province infected with HPAI H5N1
PATHOGENESIS

 Inhalation or ingestion
 Distribution of SA receptors in tissues may influence the
range of AI susceptible host
 In aquatic birds, replication usually happen in the enteric tract
(SA receptor on epithelial cells of the bird intestinal tract)
 Human, SA receptor predominantly found on epithelial cells
of Upper Respiratory Tract (URT)
 For wild aquatic birds, the virus is shed in the feces and
transmission is fecal–oral, but respiratory replication recently
has been documented, indicating the potential for inhalational
transmission.
 In poultry, replication is predominantly within the respiratory
tract, but it also can occur in the intestinal tract, suggesting
transmission may be by either ingestion or inhalation.
 In mammals, transmission is by aerosol,droplets, and fomites.
Based on pathogenicity, can be devided
into 2 AI:
1) Low-pathogenicity avian influenza
(LPAI), epithelial cells within the
respiratory and gastrointestinal tracts
2) High-pathogenicity avian influenza
(HPAI), HPAI infections usually
cause systemic infection, resulting in
multiple organ failure, destruction of
cardiovascular and nervous systems
and a death
HPAIv LPAIv
CLINICAL SIGNS

 Infects a wide range of host species

 The clinical signs of AI are varied from one species to the others
 The variation of AI clinical signs depends on the species, age
and type of bird, pathogenicity of the viruses
 In birds, the clinical manifestations of AI are ranging from
asymptomatic infections, mild respiratory infections to severe
systemic infections or sudden death.
 Predominantly, wild birds or waterfowls are infected by LPAI
viruses- asymptomatic form
 LPAI H5 and H7 can undergo viral mutation- HPAI H5 & H7 in
poultry animal
• HPAI- sudden death without prodromal
symptoms.
• If birds survive for more than 48 hours (which is
more likely in older birds), clinical presentations
including respiratory signs, such as nasal
discharges, coughing, rales and dyspnoea,
lacrimation, sinusitis, diarrhea, edema of the
head, face and neck, apathy, reduced
vocalisation, marked reduction in feed and
water intake, cyanosis of the unfeathered skin,
wattles and comb, incoordination and nervous
signs (tremors of the head and neck, inability to
stand, torticollis, and other unusual postures).
• In laying birds, additional clinical
features include a marked drop in
egg production, usually
accompanied by an increase in
numbers of poor quality eggs

• high morbidity is accompanied by

high and rapidly escalating
unexplained mortality
Kebengkakan pada Kebengkakan pada pial
jengger
tortikolis
Kelainan Postmortem :
1. Unggas yang mati dengan bentuk perakut AI tidak
memperlihatkan lesio
2. Dehidrasi
3. HPAI, pada kantung udara ditemukan eksudat fibrinous, juga
pada oviduct, peritoneum dan selaput perikardial .
Bentuk infeksi Mild sampai moderate :
4. Imflamasi dari conjunctiva, trakhea dan airsacs
5. Pembendungan pada otot
6. Ovari regressi pada ayam petelur
7. Edema pada kepala dengan ada pembendungan,
haemorrhagi dan cyanosis dari pial dan jengger, dan
sinusitis.
8. Ulserasi dan muncul vesikel pada pial
9. Petechial dan ecchymotic haemorrhagi pada lemak
abdominal, serosal dan permukaan mucosal , jantung
heart, , proventriculus dan usus kecil
10. Kaki terlihat edema dengan haemorrhagi
11. Paha kemerahan.
Perdarahan pada usus halus
                             

                          
Perdarahan pada Haemorrhagi pada
usus trakhea
Fowl cholera,
 chlamydiosis,
 mycoplasmosis,
 velogenic viscerotropic Newcastle disease,
 infectious laryngotracheitis,
 duck plague
 acute poisonings

DIFFERENTIAL DIAGNOSIS
  Samples taken from dead birds should include
intestinal contents (faeces) or cloacal swabs and
oropharyngeal swabs. Samples from trachea,
lungs, air sacs, intestine, spleen, kidney, brain,
liver and heart should also be collected and
DIAGNOSTIC processed either separately or as a pool.
TESTS  Samples from live birds should include both
oropharyngeal and cloacal swabs
 Isolasi pada TET
 HA/HI
 ELISA
 RT-PCR
 Vaksinasi
PENCEGAHAN
Surveilens
& KONTROL
Biosecurity