Avian influenza

1. DEPARTMENT OF VETERINARY PATHOLOGY
COLLEGE OF VETERINARY & ANIMAL SCIENCE
NAVANIA ,VALLABHNAGAR ,UDIPUR
AVIAN INFLUENZA (FOWL PLAGUE)
GUIDED BY:- SUBMITTED BY:-
DR.ANITA RATHORE ASHISH KUMAR
DR.GOVERDHAN SINGH III YEAR B.V.Sc & A.H.
DR.KAMAL PUROHIT BATCH :- 2015-16

2. AVIAN INFLUENZA
 Avian influenza is a highly contagious viral disease of poultry caused by
Avian influenza virus type “A” (H₅N₁) of Orthomyxoviridae family.
characterized by high morbidity and mortality, serofibrinosis pericarditis ,
air sacculitis , pneumonia, sinusitis and caseous exudate in upper respiratory
tract. This disease is also known as Fowl plague and occurs in pandemic
form.
History :- the disease cause high mortality in fowl was firstly described in
1878 in Italy.
 in recently outbreak of highly pathogenic Avian Influenza in Hongkong in
Dec. 1997 to necessiating slaughter of entire chicken population of more
than 1.5 million.
The virus have 2 subtypes :- 1. low virulence virus (LPAI)
 2. high virulence virus (Capable to cause severe disease & inflicting upto
100% mortality. The term “Highly pathogenic avian influenza (HPAI) has
been used for these viruses.

3. MORPHOLOGY OF INFLUENZA VIRUS
 Ss RNA enveloped virus .
 8 segmented viral genome ( -ve sense)
Different surface projection or spikes ( 10-12 nm
in length) on lipid membrane of virion envelop.
The surface spikes ( surface antigen ) are of 2
different shapes 1. Haemagglutinin (it is rod shape
trimmer made of 3 structural subunits)
2. Neuraminidase ( shaped tetramer made of 4
subunits )
HA is responsible for attachment of virion to
cell surface receptors ( sialyl-oligosaccharide)
NA activity is responsible for releasing of new
virus from the cell by it’s action on the
neuraminic acid in the receptor

4. Classification of virus based on HA& NA
Type “A” Avian Influenza virus are divided into subtypes
according to the antigenic nature of HA & NA .
At present 15 distinct HAs & 9 NAs is seen .
Each virus possess 1 HA & NA subtype .
The standard nomenclature for virus includes :-
i. Antigenic type A , B , C
ii. Host of origin
iii. Geographical location
iv. Strain reference number
v. Year of isolation
vi. HA & NA subtype described in brackets i.e. ( HᵪNᵧ )

5. HOST :-Domestic birds includes chicken , turkey , geese ,
duck , guinea fowl , pheasants , quails , feral birds ( wild birds )
 Duck yield more viruses than any other groups , they act as
reservoir host but not shows clinical signs because they are
resistant to those strains which are virulent for chicken &
turkey.
Spread :- infected birds excrete virus from the respiratory
tract , conjunctiva & faeces.
 Mode of transmission includes :-
i. direct contact b/w infected & susceptible birds
ii. Indirect contact including aerosol ( droplet )
 Main route of spread is feaco-oral route.
 Virus can spread horizontally but can’t spread vertically.

6. Virus adsorbs to glycoprotein receptor containing sialic acid on the cell surface.
Virus enters in the susceptible host via faeco -oral route
Virus enters in the cell by receptor mediated endocytosis
Infectivity of virus depends on post translational cleavage of HA molecule , cleavage
done by host proteases at cleavage site , cleavage depend on basic amino acid
Trypsin like enzyme can cleave if only a single amino acid ( arginine) present at clevage
site whereas other proteases requires multiple basic amino acid
Pathogenesis

7. The ability of proteases in host cell to achieve cleavage of HA molecule is imp. In
deciding the virus replication & infectivity
These virus are cleaved in tissues where trypsin like enzyme are found i.e. respiratory
and digestive tract. Since they cannot cleaved elsewhere .
Highly pathogenic virus causes HAs with multiple basic amino acids at cleavage site
throughout whole body by proteases .
The virus replicate in many tissues and organs cause generalized disease. It leads to
death.
The HAs of low to moderate virulent influenza virus have a single basic amino acid
arginine .

8. First sign of highly pathogenic Avian Influenza in chicken & turkey is
sudden onset of high mortality which may approach 100% within
few days
Other clinical sign includes cessation of egg laying , respiratory signs
includes coughing excessive lachrymation , oedema of head & face ,
cyanosis of unfeathered skin & diarrhoea ,
Highly virulent Avian Influenza outbreak tends to self limiting
because few birds survive the disease to act as carrier.
The less virulent virus may cause drop ion egg production , anorexia ,
sinusitis ,low mortality .
For waterfowls a faecal – water- cloacal route.
CLINICAL SIGNS

9. GROSS LESIONS :-
1. With less pathogenic viruses
 mild lesions are observed in sinuses characterized by catarrhal , fibrinous ,
serofibrinous , mucopurulent , caseous inflammation .
 Other lesions are odema of tracheal mucosa with serous exudate , thickened
air sacs with fibrinous or caseous exudate or catarrh to fibbrinous enteritis .
2. High pathogenic viruses
 no prominent lesions because the birds die very quickly before gross lesions
can develop.
 However congestive hemorrhagic hematic change has been observed .
Initial change
 Odema of head with swollen sinuses & cyanotic , hemorrhagic wattles &
combs.
Lesions

10. Hemorrhage on intestine Hemorrhage on trachea
Swollen head ,comb &
wattles

12. Microscopic lesions
Changes includes edema , hyperemia , hemorrhage & foci of perivascular
lymphoid cuffing mainly in myocardium , spleen , lung & wattles.
Brain lesions:- includes foci of necrosis , perivascular cuffing , glial foci ,
lesions of mild to severe diffused , non suppurative encephalitis .
None lesions are pathognomic.
Zoonotic importance
A growing body of evidance suggest that pandemic ( strains of human)
influenza arises as a result of recombination between animal & human viruses.
Genetically rearrangement between the human & avian viruses is suggest as the
mechanisam from which new human pandemic strain arise.
The frequency of variation among influenza viruses is in two ways :-
antigenic shift & antigenic drift .
Antigenic drift :- minor antigenic change in HA & NA.
Antigenic shift :- major antigenic change in HA & NA.

13. Duck act as a “ melting pot “ , where various strains of influenza virus
can comes together & undergo genetic reassortment , resulting in new srain of
infuenza virus .
Antigenic shift origin traced to China.
China is known as large reservoir of different infuenza “ a” among the duck
specices .
H1N1 – swine – avian – human connecting public health significantly .
DIAGNOSIS
heamagglutination inhibition test
double immunodiffusion test to detect the Ab
to the nucleoprotein .

14. Differential diagnosis
Characteristics Avian influenza Ranikhet
I / p 36 hrs – 3 days 4 – 6 days
Course of disease Few hrs or more 3 days or more
Symptoms Dullness , oedema of face ,
diarrhoea
Respiratory symptoms ,
diarrhoea , nervous symptoms ,
oedema absent or less marked
Lesions ( gross ) 1.Hemorrhage on serous
surface of proventriculus ,
gizzard , intestine & muscles
2.Heart , lung & subcutis may
be infiltrated with serofibrinosis
exudate .
1. Hemorrhegic ulcers on
mucous surfaces not in
muscles.
2. absence.
Histopathology Perivascular cuffing in brain Endothelial cuffing is present
Hemagglutination Hemagglutinates RBCs of
many species , elution is very
slow ( in rabbit)
Elution after hemagglutination
is fast
Hemolysis negative May be positive
Embryopathology Haemorrhages in muscles ,
inclusion bodies is absent
s/c haemorrhages , inclusion
bodies is found

15. PREVENTION & CONTROL
Vaccine can prevent clinical signs & death
Specific protection is achieved through autogenous virus vaccine
Antibodies to the viral nuraminisidase may provide some
protection . Currently , only inactivated whole AI virus and fowl
pox –A-H5 vaccine are licensed in the USA
The use of AI vaccines requires approval of the state veterinarian
Treating LP-affected flocks with broad spectrum antibiotics to
control secondary pathogen & increasing house temp.

16. THANK
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