AVIAN INFLUENZA
Avian influenza (AI) is highly contagious disease caused by influenza virus A.
Most viruses cause only mild disease in poultry, and are called low pathogenic avian influenza viruses.
Highly pathogenic avian influenza viruses can develop from certain LPAI viruses,
can kill up to 90-100% of the flock,
and cause epidemics that may spread rapidly, devastate the poultry industry and
result in severe trade restrictions.
Also known as Grippe Aviaire and
Fowl Plague
OIE listed diseases
ETIOLOGY:
Influenza A virus10 : SS –ve, RNA virus
Family: Orthomyxoviridae
The surface of the virus is covered by two types of glycoprotein projections:
1) Hemagglutinin (HA) - rod-shaped trimers
A total 16 hemagglutinin (H1-16) subtypes are identified based on
hemagglutinin inhibition tests
Primary determinant of high pathogenicity in chickens
Responsible for attachment of the virus to cell receptors and eventually
for the fusion of the virus and cell membranes
This allow the virus
genome to enter the cell and replication to take place
2) Neuraminidase (NA) - mushroom-shaped tetramers
A total 9 neuraminidase (N1-9) subtypes are identified based on neuraminidase
inhibition tests
Responsible for release of virus by cells via action on neuraminic acid
The highly lethal systemic disease caused by AI viruses is referred as
Highly Pathogenic Avian Influenza (HPAI), while milder infection caused by AI
viruses is referred as Low Pathogenic Avian Influenza (LPAI).
A virus is defined as HPAI or
LPAI by its ability to cause severe disease in intravenously inoculated
young chickens in the laboratory, or by its possession of certain genetic
features that have been associated with high virulence in HPAI viruses.
All HPAI viruses are notifiable AI viruses
All H5 and H7 LPAI viruses are notifiable because these subtypes can
mutate to the highly pathogenic virus when allowed to circulate in poultry
populations.
Antigenic Drift and Shift
Antigenic Drift
Antigenic drift in influenza viruses arises from point mutations in the
HA and/or NA genes that results in minor antigenic changes in the coding
proteins
Antigenic Shift
Antigenic shift arises from genetic re-assortment between the gene segments
of two influenza viruses that infect the same cell and result in the
acquisition of novel HA and/or NA antigen combinations in a virus that can
infect a population with no pre-existing immunity
H5, H7 and H9 subtypes of avian influenza A viruses are known to infect
both birds and people and associated with most HPAI outbreaks.
HOST
Wide variety of wild and domestic birds
Hong Kong (1997): First documented case of direct human infection with
avian influenza virus (H5N1);
Asian outbreak of HPAI H5N1; 79 human fatalities in 2006
TRANSMISSION
Virus excreted from respiratory tract, conjunctiva, feces
Direct and indirect contact (aerosol, contaminated fomites)
Wild birds (esp. ducks) are the primary source for domestic poultry
PATHOGENESIS
Following aerosol infection virus entry in to the body
⇓
With help of HA virus binding to host-cell receptors
⇓
Following binding, the virus is internalized by
endocytosis
⇓
Acidification of the endosome environment induces
conformational changes in the HA trimer
⇓
Mediating fusion between the viral envelope and the
endosomal membrane
⇓
Which allows delivery of the viral ribonucleoprotein
into host cells
⇓
Virus genome enters the cell and replication begin
⇓
To become infectious virus particle, the cleavage of
the HA protein into the HA1 and HA2 proteins is essential
The cleavage of the HA protein is depend on number of basic amino acids in the HA1 near the cleavage site
LPAI are released from the host cell with an uncleaved HA protein and they are not infectious → HA of LPAI viruses have only two non-consecutive basic amino acids at the carboxy-terminus of the HA1 that is only cleavable by trypsin-like proteases found in respiratory and intestinal epithelial cells → so cleavage HA occurs only respiratory and intestinal epithelial cells → virus replication occurs only in limited organs → virus replication induced necrosis of apoptosis of infected cells → limited organs affected → lower virulence
HA of HPAI virus have multiple basic amino acids at cleavage site → so cleaved intracellularly
by ubiquitous furin-like proteases found in most host tissues → HA is cleaved
inside the cell before virus assembly and is infectious when it is released from
the host cells → so virus can attached to most cells of the body tissue → virus
can replicate in the most of the body tissue → virus replication induced
necrosis of apoptosis of infected cells → produced lesions in most body tissue
→ high mortality
CLINICAL SIGNS
Clinical signs of disease are extremely variable and depend on other
factors including host species,
Age,
Sex,
Concurrent infections,
Acquired immunity, and
Environmental factors.
Low Pathogenic Avian
Influenza (LPAI)
Wild birds produce no clinical signs
In chickens and turkeys, clinical signs reflect abnormalities in the respiratory, digestive, urinary, and reproductive organs.
Mild to severe respiratory signs such as coughing, sneezing, rales, and excessive lacrimation.
Ruffled feathers, listlessness, decreased activity, lethargy, decreased feed and water consumption, and occasionally diarrhea
Decreased egg production
High Pathogenic Avian
Influenza (HPAI)
Sudden death without signs of illness
Nervous disorders (i.e., head and neck tremors, inability to stand, torticollis, opisthotonus)
Respiratory signs
Oedema
of the head and face
Subcutaneous haemorrhage with cyanosis of the skin, particularly of the head and wattles
Diarrhoea
Macroscopic Pathology
Highly variable
Low Pathogenic Avian Influenza (LPAI)
Catarrhal to fibrinous sinusitis,
Tracheitis,
Air sacculitis,
Peritonitis and enteritis,
Oophoritis and
Salpingitis
High Pathogenic Avian Influenza (HPAI)
Edema of the head and sinusitis
Cyanotic, congested and hemorrhagic wattles, combs, conjunctiva and legs
Petechiae on the inside of the keel, abdominal fat, serosal surfaces and peritoneum
Hemorrhage in lung, ovary, intestinal mucosa, and proventricular mucosa
Necrotic foci in pancreas, spleen, and heart, and occasionally in liver and
kidney.
Microscopic Pathology
Edema, congestion, hemorrhage, perivascular lymphoid cuffing, and
necrosis in the myocardium, spleen, lungs, brain, wattles, liver, kidney,
pancreas, skeletal muscle, and lymphoid necrosis
DIAGNOSIS
Based on clinical signs
Gross and microscopic lesions
Samples to be collected: tracheal, oropharyngeal, or cloacal swabs of either live or dead birds
RT-PCR
Virus isolation
Serological test includes
Agar Gel Immuno -
Diffusion (AGID)
ELISA
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Sources:
https://books.google.com/books?id=QN0h7-MGKy8Chttps://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1009&context=cfsph_factsheetshttps://www.coursehero.com/file/28665437/influenzaapdf/https://scholar.cu.edu.eg/?q=mmamer/files/1-avian_influenza.doc https://www.nature.com/articles/nrmicro1208
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