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Newcastle Disease
ND is a fatal and contagious disease of many avian
species predominantly the poultry sector that
creates a constant threat to the poultry industry in
the Egypt.
The disease is complicated due to different
pathotypes and strains of the virus that induce
variation in the severity of disease characterized by
fatal respiratory and neurological pathogenesis
The OIE definition for reporting an outbreak of ND is:
Criteria for virulence
The virus has (ICPI) in day-old chicks
(Gallus gallus) of 0.7 or greater.
Multiple basic amino acids have been demonstrated in the virus
(either directly or by deduction) at the C-terminus of the F2 protein
and phenylalanine at residue 117, which is the N-terminus of the F1
protein.three arginine or lysine residues between residues 113 and
116. (OIE .,2012).
The NDV
Order :
mononegivir
als
Family :
paramyxovi
rida
Sub family :
paramyxovi
rinae
Genus :
Avulavirus
Serotypes:
APMV-1
(APMV-1 to
APMV-12)
• Genetic
analysis
classify NDV
to class I,
class II
• Class I
a virulent
strains
• Class II
both virulent
and a virulent
Molecular structure of NDV
Main Structure genome of NDV
contains six genes
that code for the six
major structural
proteins
Genome sequence of
NDV are (15,186-
15,198 nt long)
•NDV is an enveloped,
single stranded non-
segmented, negative
sense RNA virus with
helical capsid symmetry
F M LNP P HN
L, NP, P (V)
2013
NDV genotypes (I- XVIII)
Class II
Genotype I
Genotype II
Genotype III
Genotype IV
Genotype V
Genotype VI
Genotype VII
VII A
VII G
VII B
VII F
VII C
VII D
VII E
Genotype VIII
Genotype IX
Genotype X
Genotype XI
Genotype XII
GENOTYPE XIII
Genotype IVX
Genotype XV
Genotype XVI
Genotype XVII
Genotype XVIII
NDV World Panazootics
Genotype
II,III,IV…………. 1st
panazootic
(started in
southeast Asia in
the mid-1920)
Genotype V
……………………..2nd
panazootic
(started in the
Middle East in
the late 1960s
and to have
spread to most
countries by the
early 1970)
Genotype
VI……………
.ppmv-3rd
panazootic ( in
the Middle East
in the late 1970,
spread to Europe
in the 1980),
Genotype VII
and VIII ……. 4th
panazootic
(since the early
1990s to current
date in Asia,
Europe and
Africa including
Egypt )
Genotype VII(a-h)
new sub-genotypes
of vNDV suggests
that a new, fifth,
panazootic of NDV
already originated
in Southeast Asia,
extended to the
Middle East, and
was entering into
Eastern Europe.
(Miller et
al., 2015)
History OF NDV IN Egypt
diseas
e
record
ed in
Egypt
for the
first
time
in year
1942
(Daub
ney
and
Manc
El-
Nassa
ri,
1957;
Eissa,.
1960
pigeo
n
(Ahm
ed
and
Reda,
1967),
Lanca
ster
and
Alexa
nder,
.1975
(velog
enic
NDV)
Khafa
gy,
1983;
Amal
Eid,
1984;
and
Bakhi
t and
Abd
El-
Hami
d,
1990)
Hassa
n et
al.,
2004).
(Abde
l
mone
im et
al.,
2006;
Amer
et al.,
2006).
Mah
moud
et al.
(2006)
Ramz
y et
al.
(2009)
Moha
med
et al.
(2009)
Saad
et al.
(2010)
Moha
med
et al.
(2011)
Radw
an et
al.,
2013)
Hussi
en et
al.
(2014)
Ismail
et al.
(2014)
Shala
by et
al.
(2014)
Mosta
fa et
al . (
2014)
Awad et
al.
(2015)
Abdel
Aziz
et al.
(2016)
Economic Significance
 Mortality (reach up to 100% in fully susceptible flocks)
 Decrease in egg production by up to 40% for a period, but
when returns to normal it takes 4 weeks
 soft egg shell (5%).
 BROILER -condemnation in slaughter house( MG-Ecoli)
 Vaccination and control measures
 Zoonotic (pink eye)
cancer therapy
Biologic Properties
 Hemagglutination Activity
(binding of theHN protein to the sialic acid receptors on
the surface of theRBCs)
HA Test
Neuraminidase Activity
 Prevent Clumping- elution
The fusing activity
infectivity of the virus depends on the proteolytic
cleavage by a host protease of the precursor F0 protein
into theheterodimer (F1 and F2)
Pathotyping
 MDT after allantoic sac inoculation, of less than60 hours, 60–90
hours, and greater than 90 hours (lentogenic ,mesogenic, and
velogenic)
 The intracerebral pathogenicity index (ICPI) in day-old chicks
 (ICPI> 0.7 M0.7-1.5 V 1.5-2)
 Molecular bases of pathogenicity
Lentogenic F0 cleavage site:
monobasic amino acid motif → cleaved by extracellular trypsin-like
proteolytic enzymes on the surface of mucous membranes → local
and asymptomatic infection
Velogenic F0 cleavage site: :
multiple basic amino acid motif (at least 2, like arginine [R] or
lysine [K] residues) → cleaved by intracellular proteolytic enzymes
→ generalized infection
Intracerebral Pathogenicity Index ICPI
Twisting of the head and neck, Paralysis of both wings and
both legs closed eyes, ruffled feathers an dropping wings
Epidemiology
 Host range and susceptibility
 Over 250 species
• Chicken are highly susceptible then TurkeyND in
• Pigeons , caused by paramyxovirus serotype 1
(PPMV-1)
• Quail
NDV GEO DIST
2014-2015
Role of waterfowls and wild birds in
Epidemiology
 ducks and geese are a potential reservoirs of NDV
 House sparrows
Sources of infection and mode of
transmission
• movement of live birds – feral birds, pet/exotic birds,
game birds, racing pigeons, and commercial poultry
• contact with other animals
• movement of peoples and equipment
• movement of poultry products
• airborne spread
• contaminated poultry feed and water
• contaminated vaccines ( incomplete inactivation
and/or decontamination of the vaccines)
Methods of infection
 The inhalation of virus via aerosol form or ingestion
of contaminated feed or litter.
Incubation Period
For natural exposures to NDV varies between 2 and 15
Days,
Averaging around 5–6 days
Experimental infection 2-4 day
Pathotypes on the basis of the clinical signs in
infected chickens
as following
 Viscerotropic velogenic (Doyle's form): a highly pathogenic
form in which haemorrhagic intestinal lesions
 Neurotropic velogenic (Beach's form): a form that
accompanied with high mortality, usually following respiratory
and nervous signs.
 Mesogenic (Beaudettes form): a form that causes respiratory
signs, occasional nervous signs, but low mortality.
 Lentogenic or respiratory ( Hitchner's form) : a form that
associated with mild or subclinical respiratory infection.
 Asymptomatic: a form that usually consists of a subclinical
enteric infection
Environmental effects
 Rainy season
More favorable for the occurrence and spread of the
disease.
 Extreme weather can increase the intensity of the
disease.
Neural form of the disease is more common in
summer
Clinical Signs
Non vaccinated chickens infected with virulent viscerotropic
isolates become listless and depressed 2 days after infection
ending with 100% mortality by the third or fourth day.
Nervous signs (torticollis, head shaking)
PM lesion
 V NDV
Gross lesion in internal organs of nonvaccinated group after infection by NDV
strain EG/18/2015
Sever hemorrhages on tips of proventriculus glands and greenish contents
of gizzard
1. Hemorrhages of intestinal cell wall intestinal ulceration
(button shaper of payer's patches ) in mucosa of small
intestine.
2.Intestinal ulceration and sever boudenal ulceration
(button shape of payer's patches ) in mucosa of small
intestine.
3. Ulceration in mucosa of small intestine ( elliptical
ulceration).
1 2
3
Petechial hemorrhage in the spleen
Sever congestion in trachea Sever hemorrhage of cecal tonsils
Congested and enlarged liver and distended gall bladder
Laboratory diagnosis
 Isolation and Identification of NDV
 Sampling
1. Tracheal, oropharyngeal and cloacal swabs (or faeces) .
2. Organs samples also collected in some studies (lung, kidneys, intestine
(including contents), caecal tonsils, spleen, brain, liver and heart tissues).
RRT-PCR /(RT-PCR) Isolation
ECE lesion
+ve -ve +ve -ve after 2
passages
Differentiation between
vaccinal and virulent
NDV (not used as routine test)
Any type
Reported to
GOVs
HI /or NT
Typing using standard
reference antisera (not applicable)
Genomic sequence
of F gene
Viral detection protocol in different birds
Chicken embryo was congested and with
subcutaneous hemorrhage on the head
Rapid HA Test
Isolation
chicken embryo after inculcation in ECE 9-11 day age
Blood samples collected (10 -20 samples /
flocks). For serology
HI TEST
Protective titer in broiler
In layer ,Breeder
Molecular diagnosis of NDV
 rRT-PCR Assay
 Fusion gene protein cleavage site analysis
sequence
 Phylogenetic Analyses
Differential diagnosis
 High mortality, High morbidity and Respiratory
Manifestation
 AI,MG ,
 Drop in egg production and egg abnormalities
 EDS,IB
 Nervous signs
 Head swelling
 Hemorrhage (coccidiosis ,mycotoxin)
 Diarrhea
Prevention and control
 Biosecurity
Vaccination
Live lentogenic vaccines
Live mesogenic vaccines
Inactivated vaccines
Recombinant (live &inactivated)
Virus
strains
Pathotype ICPI IVPI Derivation Use in
chicken
Routes
Strain H Mesogenic 1.4 0.0 laboratory
attenuated by
egg passage
Secondary im, sc
Mukteswar Mesogenic 1.4 0.0 laboratory
attenuated by
egg passage
Secondary im, sc
Komarov Mesogenic 1.4 0.0 laboratory
attenuated by
intracerebral
passage in
ducklings
Secondary im, sc,
io
Roakin Mesogenic 1.45 0.0 Field isolates Secondary im, ww
La Sota Lentogenic 0.4 0.0 Field isolates Secondary in, io,
dw, sp,
aer
F (Asplin) Lentogenic 0.25 0.0 Field isolates Primary in, io,
dw, sp,
aer
Hichner B1 Lentogenic 0.2 0.0 Field isolates Primary in, io,
dw, sp,
aer, bd
mass application of live vaccines it is difficult
to produce protective antibodies in high percentages of
birds in a flock. Ocular delivery provides the best
response(93%), while vaccine delivery in water or spray
may produce protective antibodies in only 53% to 60%
of the birds
Inactivated vaccines
Recombinant vaccines
Emergency vaccination

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Newcastle Disease

  • 1.
  • 2.
  • 3. Newcastle Disease ND is a fatal and contagious disease of many avian species predominantly the poultry sector that creates a constant threat to the poultry industry in the Egypt. The disease is complicated due to different pathotypes and strains of the virus that induce variation in the severity of disease characterized by fatal respiratory and neurological pathogenesis
  • 4. The OIE definition for reporting an outbreak of ND is: Criteria for virulence The virus has (ICPI) in day-old chicks (Gallus gallus) of 0.7 or greater. Multiple basic amino acids have been demonstrated in the virus (either directly or by deduction) at the C-terminus of the F2 protein and phenylalanine at residue 117, which is the N-terminus of the F1 protein.three arginine or lysine residues between residues 113 and 116. (OIE .,2012).
  • 5. The NDV Order : mononegivir als Family : paramyxovi rida Sub family : paramyxovi rinae Genus : Avulavirus Serotypes: APMV-1 (APMV-1 to APMV-12) • Genetic analysis classify NDV to class I, class II • Class I a virulent strains • Class II both virulent and a virulent
  • 6. Molecular structure of NDV Main Structure genome of NDV contains six genes that code for the six major structural proteins Genome sequence of NDV are (15,186- 15,198 nt long) •NDV is an enveloped, single stranded non- segmented, negative sense RNA virus with helical capsid symmetry F M LNP P HN
  • 7.
  • 8. L, NP, P (V)
  • 9. 2013 NDV genotypes (I- XVIII) Class II Genotype I Genotype II Genotype III Genotype IV Genotype V Genotype VI Genotype VII VII A VII G VII B VII F VII C VII D VII E Genotype VIII Genotype IX Genotype X Genotype XI Genotype XII GENOTYPE XIII Genotype IVX Genotype XV Genotype XVI Genotype XVII Genotype XVIII
  • 10. NDV World Panazootics Genotype II,III,IV…………. 1st panazootic (started in southeast Asia in the mid-1920) Genotype V ……………………..2nd panazootic (started in the Middle East in the late 1960s and to have spread to most countries by the early 1970) Genotype VI…………… .ppmv-3rd panazootic ( in the Middle East in the late 1970, spread to Europe in the 1980), Genotype VII and VIII ……. 4th panazootic (since the early 1990s to current date in Asia, Europe and Africa including Egypt ) Genotype VII(a-h) new sub-genotypes of vNDV suggests that a new, fifth, panazootic of NDV already originated in Southeast Asia, extended to the Middle East, and was entering into Eastern Europe. (Miller et al., 2015)
  • 11. History OF NDV IN Egypt diseas e record ed in Egypt for the first time in year 1942 (Daub ney and Manc El- Nassa ri, 1957; Eissa,. 1960 pigeo n (Ahm ed and Reda, 1967), Lanca ster and Alexa nder, .1975 (velog enic NDV) Khafa gy, 1983; Amal Eid, 1984; and Bakhi t and Abd El- Hami d, 1990) Hassa n et al., 2004). (Abde l mone im et al., 2006; Amer et al., 2006). Mah moud et al. (2006) Ramz y et al. (2009) Moha med et al. (2009) Saad et al. (2010) Moha med et al. (2011) Radw an et al., 2013) Hussi en et al. (2014) Ismail et al. (2014) Shala by et al. (2014) Mosta fa et al . ( 2014) Awad et al. (2015) Abdel Aziz et al. (2016)
  • 12. Economic Significance  Mortality (reach up to 100% in fully susceptible flocks)  Decrease in egg production by up to 40% for a period, but when returns to normal it takes 4 weeks  soft egg shell (5%).  BROILER -condemnation in slaughter house( MG-Ecoli)  Vaccination and control measures  Zoonotic (pink eye) cancer therapy
  • 13. Biologic Properties  Hemagglutination Activity (binding of theHN protein to the sialic acid receptors on the surface of theRBCs) HA Test Neuraminidase Activity  Prevent Clumping- elution The fusing activity infectivity of the virus depends on the proteolytic cleavage by a host protease of the precursor F0 protein into theheterodimer (F1 and F2)
  • 14. Pathotyping  MDT after allantoic sac inoculation, of less than60 hours, 60–90 hours, and greater than 90 hours (lentogenic ,mesogenic, and velogenic)  The intracerebral pathogenicity index (ICPI) in day-old chicks  (ICPI> 0.7 M0.7-1.5 V 1.5-2)  Molecular bases of pathogenicity Lentogenic F0 cleavage site: monobasic amino acid motif → cleaved by extracellular trypsin-like proteolytic enzymes on the surface of mucous membranes → local and asymptomatic infection Velogenic F0 cleavage site: : multiple basic amino acid motif (at least 2, like arginine [R] or lysine [K] residues) → cleaved by intracellular proteolytic enzymes → generalized infection
  • 15. Intracerebral Pathogenicity Index ICPI Twisting of the head and neck, Paralysis of both wings and both legs closed eyes, ruffled feathers an dropping wings
  • 16.
  • 17. Epidemiology  Host range and susceptibility  Over 250 species • Chicken are highly susceptible then TurkeyND in • Pigeons , caused by paramyxovirus serotype 1 (PPMV-1) • Quail
  • 18.
  • 20.
  • 21.
  • 23. Role of waterfowls and wild birds in Epidemiology  ducks and geese are a potential reservoirs of NDV  House sparrows
  • 24. Sources of infection and mode of transmission • movement of live birds – feral birds, pet/exotic birds, game birds, racing pigeons, and commercial poultry • contact with other animals • movement of peoples and equipment • movement of poultry products • airborne spread • contaminated poultry feed and water • contaminated vaccines ( incomplete inactivation and/or decontamination of the vaccines)
  • 25. Methods of infection  The inhalation of virus via aerosol form or ingestion of contaminated feed or litter. Incubation Period For natural exposures to NDV varies between 2 and 15 Days, Averaging around 5–6 days Experimental infection 2-4 day
  • 26. Pathotypes on the basis of the clinical signs in infected chickens as following  Viscerotropic velogenic (Doyle's form): a highly pathogenic form in which haemorrhagic intestinal lesions  Neurotropic velogenic (Beach's form): a form that accompanied with high mortality, usually following respiratory and nervous signs.  Mesogenic (Beaudettes form): a form that causes respiratory signs, occasional nervous signs, but low mortality.  Lentogenic or respiratory ( Hitchner's form) : a form that associated with mild or subclinical respiratory infection.  Asymptomatic: a form that usually consists of a subclinical enteric infection
  • 27. Environmental effects  Rainy season More favorable for the occurrence and spread of the disease.  Extreme weather can increase the intensity of the disease. Neural form of the disease is more common in summer
  • 28. Clinical Signs Non vaccinated chickens infected with virulent viscerotropic isolates become listless and depressed 2 days after infection ending with 100% mortality by the third or fourth day.
  • 29.
  • 30.
  • 31.
  • 34. Gross lesion in internal organs of nonvaccinated group after infection by NDV strain EG/18/2015 Sever hemorrhages on tips of proventriculus glands and greenish contents of gizzard
  • 35.
  • 36. 1. Hemorrhages of intestinal cell wall intestinal ulceration (button shaper of payer's patches ) in mucosa of small intestine. 2.Intestinal ulceration and sever boudenal ulceration (button shape of payer's patches ) in mucosa of small intestine. 3. Ulceration in mucosa of small intestine ( elliptical ulceration). 1 2 3
  • 37. Petechial hemorrhage in the spleen Sever congestion in trachea Sever hemorrhage of cecal tonsils
  • 38. Congested and enlarged liver and distended gall bladder
  • 39. Laboratory diagnosis  Isolation and Identification of NDV  Sampling 1. Tracheal, oropharyngeal and cloacal swabs (or faeces) . 2. Organs samples also collected in some studies (lung, kidneys, intestine (including contents), caecal tonsils, spleen, brain, liver and heart tissues).
  • 40. RRT-PCR /(RT-PCR) Isolation ECE lesion +ve -ve +ve -ve after 2 passages Differentiation between vaccinal and virulent NDV (not used as routine test) Any type Reported to GOVs HI /or NT Typing using standard reference antisera (not applicable) Genomic sequence of F gene Viral detection protocol in different birds
  • 41. Chicken embryo was congested and with subcutaneous hemorrhage on the head Rapid HA Test Isolation chicken embryo after inculcation in ECE 9-11 day age
  • 42. Blood samples collected (10 -20 samples / flocks). For serology HI TEST Protective titer in broiler In layer ,Breeder
  • 43. Molecular diagnosis of NDV  rRT-PCR Assay  Fusion gene protein cleavage site analysis sequence  Phylogenetic Analyses
  • 44. Differential diagnosis  High mortality, High morbidity and Respiratory Manifestation  AI,MG ,  Drop in egg production and egg abnormalities  EDS,IB  Nervous signs  Head swelling  Hemorrhage (coccidiosis ,mycotoxin)  Diarrhea
  • 45. Prevention and control  Biosecurity Vaccination Live lentogenic vaccines Live mesogenic vaccines Inactivated vaccines Recombinant (live &inactivated)
  • 46.
  • 47. Virus strains Pathotype ICPI IVPI Derivation Use in chicken Routes Strain H Mesogenic 1.4 0.0 laboratory attenuated by egg passage Secondary im, sc Mukteswar Mesogenic 1.4 0.0 laboratory attenuated by egg passage Secondary im, sc Komarov Mesogenic 1.4 0.0 laboratory attenuated by intracerebral passage in ducklings Secondary im, sc, io Roakin Mesogenic 1.45 0.0 Field isolates Secondary im, ww La Sota Lentogenic 0.4 0.0 Field isolates Secondary in, io, dw, sp, aer F (Asplin) Lentogenic 0.25 0.0 Field isolates Primary in, io, dw, sp, aer Hichner B1 Lentogenic 0.2 0.0 Field isolates Primary in, io, dw, sp, aer, bd
  • 48. mass application of live vaccines it is difficult to produce protective antibodies in high percentages of birds in a flock. Ocular delivery provides the best response(93%), while vaccine delivery in water or spray may produce protective antibodies in only 53% to 60% of the birds