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M. R. Reddy
Respiratory Diseases among Layers and Broilers in India
Respiratory Disease:
An Interaction of Host-Pathogen-Environment
HOST
Respiratory
Disease
Contami-
nation
Sub-clinical
Infection
Stress
Temperature
Humidity
Ventilation
Ammonia
Dust
Stocking rate
Feeding Space
Litter condition
Water quality
Feed quality
Brooding
Debeaking
Handling
Hygiene
Multi-age
Pathotype
Strain/varient
Challenge dose
Mutation rate
Primary
infection
Intercurrent
Infection
Age
Meat /egg type
Genetic
potential
General health
Specific
immunity
Non specific
immunity
VIRAL
TRIAD
MDV
CAVIBD
IMMUNOSUPPRESSION Improper
NUTRITION
Managemental
(STRESS)
TOXICITY
(Drugs &
Mycotoxins) Poor vaccine Response
Severe vaccine reactions
Reovirus
ALVs
Respiratoty Disease outbreaks
ND, IB, MG, Colibacillosis
Features of Important Pathogens
Property IBV LP AIV ILTV MG/MS
Envelope Enveloped Enveloped Enveloped No Cell wall
Stability Frazile Frazile Frazile Frazile
Genome RNA
Unstatble
Mutations
RNA
Unstable
Mutations
DNA
Stable
DNA, RNA
Stable
Infection Acute
Self limiting
Acute
Self limitimg
Acute
Latent
Life long
Chronic
Persistent
Life long
Prevalence
In India
High
Endemic
High High High
Endemic
Vaccines Permitted
H120, M41
Not
permitted
Not
permitted
Permitted
Infectious Bronchitis
• IBV is highly infectious and contagious
• It causes respiratory, urinary and reproductive disorders
• Inspite of vaccination, outbreaks of IBV causes significant economic losses in India
• New varients keep emerging
• Mutations of the S1 gene results in new serotypes and cause tissue tropism
• In india Massachusetts type vaccines (H120, M41) are lisened to control IB
Prevalence of IBV in different regions
Region Samples processed IBV isolations Prevalence (%)
Central 166 88 53.01
East 21 17 80.95
North 86 41 46.59
South 246 106 43.09
Total 521 252 48.37
Prevalence of IBV in different type of birds
Bird type Samples
processed
IBV isolations Prevalence (%)
Layers 50 17 34.00
Br Parents 101 58 57.43
Broilers 370 177 47.84
Total 521 252 48.37
Flock wise frequency of IBV Isolation
Region Flocks IBV isolations Prevalence (%)
Central 69 53 77.94
East 4 4 100.00
North 51 32 62.75
South 132 68 51.52
Total 256 157 61.33
Flock wise frequency of IBV Isolation
Region Flocks IBV isolations Prevalence (%)
Layers 28 11 39.29
Br Parents 67 39 58.21
Broilers 161 107 66.46
Total 256 157 61.33
Nephropathogenic (54.3%)
1
2
3
Phylogenetic Analisis of Indian IBV isolates
1
Massachissets (20%)2
Novel strains (25.7%)3
IB Vaccination Strategy
1-5 day - Mass (H120)
30 day - Mass+local varient
12 wk - Mass+local varient
16 wk - IB killed
35 weeks onwords: (As required based on Seromonitoring
• Mycoplasmas are highly versatile and successful pathogen
• Chronic: Once infected, infection remains for life
• Mycoplasma lack a cell wall: resistant to penicillin group of antibiotics
• Antimicoplasmal drugs are bacteriostatic
• Antibodies can not eliminate infection
• Field infection (MG/MS) level is high due to vertical transmission and low level of
biosecurity
• Raising mycoplasma clean flocks is not practicable
AVIAN MYCOPLASMOSIS
Etiology
Significant pathogenic species:
M. gallisepticum - Chickens, Turkeys
M. synoviae - Chickens, Turkeys
M. melwagridis - Turkeys
M. iowae - Turkeys
Target organs:
– Respiratory system
– Synovial membranes
– Reproductive system
Pathogenesis
Inhalation
Attach to cilia & epithelial cells
Toxic substances/metabolites
cell damage and cilia destruction
Colonization
move down to lungs & air sacs
Cause damage
Airsacculitis
Blood
Ovary
Oviduct
Joints
E.coli
Colonization of
mucosal surface
is achieved using
Adhesions
Establish a very close
attachment
With epithelial cells
Capsule surrounding MG
Enhance adherence
Immune evasion and persistence
Mycoplasma
Attach
Macropages
Lymphoblasta
Lymphocytes
Destroy
surface receptors
Impaired
macrophage function
Immune response
Rapid change of surface antigens
• On/off switching (phase variation)
• Gain and loss of surface proteins
• Structural changes (size variation)
The capsule surrounding MG resist phagocytosis
Capsule block the effects of complement by masking antigens
Masking of immunogenic antigens –prevent direct
presentation to host immune system
Intracellular invasion
Factors that influence the disease in the field
Specific infectious agents
–Infectious bronchitis virus
–Newcastle disease virus
–H.paragallinarum
–P.multocida
Secondary bact. infections
–E. coli
Vaccine reactions
–Infectious bronchitis
–Newcastle disease
Immunosuppressive agents
–IBD, CAV, MD
–Mycotoxins
Environmental stresses
–Excessive ammonia
–Dust
–Overcrowding
–Chilling
–Humidity
–Poor Ventilation
–Handling (Vaccination, Debeaking)
–Heat weaning
–Feed change (Starter-grower)
–Poor hygiene
Eggshell apex abnormality (Feberwee et al., 2009)
Seroprevalance of Mycoplasma gallisepticum by ELISA
(Based on Flocks)
Region No. of
Flocks Tested
No. of Flocks Positive %
Positive
Central 22 17 77.3
East 10 07 70.0
North 26 22 84.6
South 28 21 75.0
Total 86 67 77.9
Seroprevalance of M. gallisepticum by ELISA
(Based on Flocks)
0
20
40
60
80
100
Layers Br Parents Broilers
91.7
77.5
30
Seroprevalence
Prevalance of M. gallisepticum
by Isolation and Identification
(Based on Flocks)
Region No. of
Flocks Tested
No. of Flocks Positive %
Positive
Central 22 7 31.8
East 10 1 10.0
North 15 2 13.3
South 27 7 25.9
Total 64 17 26.6
Prevalance of M. gallisepticum
by Isolation and Identification
(Based on Flocks tested)
0
20
40
31
20
10
MG prevelance
0
20
40
60
80
100
Central East North South
81.80
100
92.31 89.29Percentage
REGION
Seroprevalence of
M synoviae in different regions
based on flocks tested
45
50
55
60
54.55
60.00
53.33
51.72
Percentage
REGION
Prevalence of
M synoviae in different regions
based on flocks tested
Seroprevalence of M synoviae in different
types of birds based on flocks tested
0
20
40
60
80
100
97.22
85.00 80.00
Percentage
0
20
40
60
80 73.33
42.86
36.4
Percentage
FLOCK
Prevalence of M synoviae in different types of
birds based on flocks tested
OPTIONS FOR MG & MS CONTROL
Control
Living with
infection
Biosecurity
GMPs
Antibiotics Vaccines
Live
Vaccines
Killed
ts-11
6/85
Tiamulin
Tylosin
Tilmicosin
Tylvalosin
Lyncomycin
Tetracyclines
Enrofloxacin
Ciprofloxacin
MG MS
Live
Vaccines
MS-H
Minimum inhibitory concentrations of MG & MS
Antibiotic MIC (g/ml)
MG MS
Tylosin 0.02 0.04
Tiamulin 0.005 0.08
Lincomycin 2.50 0.63
Spectinomycin 1.25 1.25
Spiramycin 0.08 0.63
Erythromycin 0.02 40.0
Tetracycline 0.08 0.08
Other Control Measures
• Proper environmental control to reduce stress
– Temperature, Ventilation , Stoking density
• Proper control of other respiratory diseases
• Proper control of immunosuppressive diseases
• Strategic medication at recognized times of stress
– First week of life
– When heat weaned, feed changed
– Debeaking, Vaccination
– Peak egg production
• Biosecurity
– Isolation
– Hygine
– Traffic control
Low Pathogenic Avian influenza
• Influenza virus A, Orthomyxoviridae
• Enveloped, Negative stranded, segmented RNA viruses.
• 16 subtypes: Haemagglutinin (H)
• Nine neuraminidase (N) antigens.
• All H and N combinations have been isolated.
• Extreme antigenic variability exists.
TYPE-CTYPE-A TYPE-B
Influenza Virus
Sub Types (HN subtypes)
H/N H1 H2 H3 H4 H5 H6 H7 H8 H9 H10 H11 H12 H13 H14 H15 H16
N1 H1N1 H2N1 H3N1 H4N1 H5N1 H6N1 H7N1 H8N1 H9N1 H10N1 H11N1 H12N1 H13N1 H14N1 H15N1 H16N1
N2 H1N2 H2N2 H3N2 H4N2 H5N2 H6N2 H7N2 H8N2 H9N2 H10N2 H11N2 H12N2 H13N2 H14N2 H15N2 H16N2
N3 H1N3 H2N3 H3N3 H4N3 H5N3 H6N3 H7N3 H8N3 H9N3 H10N3 H11N3 H12N3 H13N3 H14N3 H15N3 H16N3
N4 H1N4 H2N4 H3N4 H4N4 H5N4 H6N4 H7N4 H8N4 H9N4 H10N4 H11N4 H12N4 H13N4 H14N4 H15N4 H16N4
N5 H1N5 H2N5 H3N5 H4N5 H5N5 H6N5 H7N5 H8N5 H9N5 H10N5 H11N5 H12N5 H13N5 H14N5 H15N5 H16N5
N6 H1N6 H2N6 H3N6 H4N6 H5N6 H6N6 H7N6 H8N6 H9N6 H10N6 H11N6 H12N6 H13N6 H14N6 H15N6 H16N6
N7 H1N7 H2N7 H3N7 H4N7 H5N7 H6N7 H7N7 H8N7 H9N7 H10N7 H11N7 H12N7 H13N7 H14N7 H15N7 H16N7
N8 H1N8 H2N8 H3N8 H4N8 H5N8 H6N8 H7N8 H8N8 H9N8 H10N8 H11N8 H12N8 H13N8 H14N8 H15N8 H16N8
N9 H1N9 H2N9 H3N9 H4N9 H5N9 H6N9 H7N9 H8N9 H9N9 H10N9 H11N9 H12N9 H13N9 H14N9 H15N9 H16N9
H5: HPAI, LPAI Notifiable
H7: HPAI, LPAI Notifiable
H9: Mostly LPAI Not notifiable
Avian influenza sub-types Important for Poultry
Poultry
•Chicken
•Ducks
•Turkey
•G. fowl
•Quails
•Emu
Wild birds
Water fowl
Feces
Secretions
Excretions
Dead bird
Vehicles
People
Raw mat.
Animals
Rodents
Insects
Litter
Dust
VIRUS
VIRUS
VIRUS
Feed
Water
Aerosols
Droplets
VIRUS
Portals of
Virus Exit
Source of
AI Virus
Modes of
Spread
Virus
Contaminant
s
Ingestion
(MOUTH)
Inhalation
(NOSE)
Conjunctiva
(EYE)
Portals of
Virus Entry
Avian Influenza Virus: Transmission
Avian Influenza: Pathogenesis
AI Virus
Feed/Water Dust/air
Ingestion Inhalation
Digestive
System
Respiratory
System
Blood circulatory system
Brain SkinVisceral Organs
Multiple Organ Failure
Death
LPAI
HPAI
Multi-organ Damage
Processes
• Direct virus replication in
cells/tissues/organs
• Indirect effects from
production of cellular
mediators such as
cytokines
• Ischemia from vascular
thrombosis
• Cardiovascular collapse
from coagulopathy or
disseminated
intravascular coagulation
TYPE OF IMMUNITY Killed vaccines
Local immunity
- Humeral (Antibody IgA) No
- Cell Mediated (Cytotoxic T cells) No
Systemic immunity
- Humeral (Antibody- IgY, IgM) Yes
- Cell Mediated (Cytotoxic T cells) No
Prevention and Control
1. Biosecurity
• Isolation of farms
• Movement control
• Wild bird control
• Dead bird dsposal
• Mannure disposal
• Disinfection
2. Vaccination
• Mass vaccination
• Inactivated -homologous
• Surveillance –genotyping
• Regular Updating of vaccines
Vaccines protect only homologous
subtypes/mutants of field virus
• No cross-neutralization/cross-protection among subtypes
– H9 vaccine do not protect H5 or H7
• No cross-protection among mutants of same subtype
– Parent H9 vaccine do not protect mutants of H9
Why AI Vaccines not giving satisfactory results
• High mutation rate of AI virus
• Only killed vaccines allowed
• Killed vaccines donot induce local respiratory immunity
• Killed vaccines donot induce cell mediated immunity
• Vaccine can not prevent infection
• ILT caused by enveloped DNA herpes virus.
• There are many pathotypes of the virus.
• Antigenic uniformity, strains differ in virulence
• Some are very mild and others can cause severe morbidity and mortality.
• Most common is Mild Form “ILT”
Infectious laryngotracheitis (ILT)
Mode of transmission
• Older carrier birds are a common source of infection.
• Aerosol, Direct contact, ingestion of contaminated feed, water, litter
• Clinical disease occurs 6-12 days after natural exposure to the ILT virus
Mild Form of ILT
• Swollen watery eyes
• Conjunctivitis
• Swollen sinuses
• Nasal discharge
• Production loss / layers (10-20%)
Severe Form of ILT
• Severe coughing
• Bloody exudates
• Neck extended
• Labored breathing
• Mortality high - can reach 50 - 70%,
(usually 10 - 20 %)
• Persists for 2 - 6 weeks
Mucous in trachea is seen first, followed
later bloodby then necrotic tissue
Chronic treacheal lesions
Vaccination
• ILT can be effectively controlled by vaccination
– 5-7 weeks of age
– Revaccinate at 15 weeks of age
• Most are modified live isolates and are administered by eye drop.
• Vaccinated and unvaccinated birds should not be mixed due to the possibility of
reversion to virulence.
• Vaccination can be administered in the face of outbreak to help reduce further
morbidity and mortality.
Why ILT vaccines not permitted
in India
• Reportable disease
• Virus latency – in infected and vaccinated birds
• Residual pathogenicity of vaccine strains
• Reactivation of vaccine strains
• Trade restrictions
Newcastle Disease
• ND is endemic and outbreaks are common particularly in summer
• NDV genome is stable and Single serotype exists
• In activated Vaccine: Pre lay and Mid lay recommended
• Seromonitoring of vaccinated flocks essential
• Booster vaccination with live vaccines at 6-8 weeks interval based on serology
• Avoid errors in vaccine admistration
Infectious coryza
• Infectious coryza outbreaks observed in the field inspite of vaccination
• Infected birds become carrier and act as reservoir of infection
• Three Serogroups (A,B,C) and Nine Serovars (A1, A2, A3, A4, B1, C1, C2, C3, C4)
• Cross protection within serovar B is only partial
• Correct other factors contributing outbreaks: Stress, errors in vaccine
administration etc
• Surveillance and vaccine updating essential
Conclusions
• Comprehensive Surveillance of LPAI and ILT to establish their widespred
prevalence in Indian Poultry
• Vaccines to control varient IBV, LPAI and ILT
• All the outbreaks are not due to vaccines but mostly related to other risk factors
• Avoid errors in management and biosecurity
• Correction of vaccination & Medication errors
• Vaccination Monitoring – Setting baselines

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Diseases Among Layers & Broilers in India - Knowledge Day 2016

  • 1. M. R. Reddy Respiratory Diseases among Layers and Broilers in India
  • 2. Respiratory Disease: An Interaction of Host-Pathogen-Environment HOST Respiratory Disease Contami- nation Sub-clinical Infection Stress Temperature Humidity Ventilation Ammonia Dust Stocking rate Feeding Space Litter condition Water quality Feed quality Brooding Debeaking Handling Hygiene Multi-age Pathotype Strain/varient Challenge dose Mutation rate Primary infection Intercurrent Infection Age Meat /egg type Genetic potential General health Specific immunity Non specific immunity
  • 3. VIRAL TRIAD MDV CAVIBD IMMUNOSUPPRESSION Improper NUTRITION Managemental (STRESS) TOXICITY (Drugs & Mycotoxins) Poor vaccine Response Severe vaccine reactions Reovirus ALVs Respiratoty Disease outbreaks ND, IB, MG, Colibacillosis
  • 4. Features of Important Pathogens Property IBV LP AIV ILTV MG/MS Envelope Enveloped Enveloped Enveloped No Cell wall Stability Frazile Frazile Frazile Frazile Genome RNA Unstatble Mutations RNA Unstable Mutations DNA Stable DNA, RNA Stable Infection Acute Self limiting Acute Self limitimg Acute Latent Life long Chronic Persistent Life long Prevalence In India High Endemic High High High Endemic Vaccines Permitted H120, M41 Not permitted Not permitted Permitted
  • 5. Infectious Bronchitis • IBV is highly infectious and contagious • It causes respiratory, urinary and reproductive disorders • Inspite of vaccination, outbreaks of IBV causes significant economic losses in India • New varients keep emerging • Mutations of the S1 gene results in new serotypes and cause tissue tropism • In india Massachusetts type vaccines (H120, M41) are lisened to control IB
  • 6.
  • 7.
  • 8. Prevalence of IBV in different regions Region Samples processed IBV isolations Prevalence (%) Central 166 88 53.01 East 21 17 80.95 North 86 41 46.59 South 246 106 43.09 Total 521 252 48.37
  • 9. Prevalence of IBV in different type of birds Bird type Samples processed IBV isolations Prevalence (%) Layers 50 17 34.00 Br Parents 101 58 57.43 Broilers 370 177 47.84 Total 521 252 48.37
  • 10. Flock wise frequency of IBV Isolation Region Flocks IBV isolations Prevalence (%) Central 69 53 77.94 East 4 4 100.00 North 51 32 62.75 South 132 68 51.52 Total 256 157 61.33
  • 11. Flock wise frequency of IBV Isolation Region Flocks IBV isolations Prevalence (%) Layers 28 11 39.29 Br Parents 67 39 58.21 Broilers 161 107 66.46 Total 256 157 61.33
  • 12. Nephropathogenic (54.3%) 1 2 3 Phylogenetic Analisis of Indian IBV isolates 1 Massachissets (20%)2 Novel strains (25.7%)3
  • 13. IB Vaccination Strategy 1-5 day - Mass (H120) 30 day - Mass+local varient 12 wk - Mass+local varient 16 wk - IB killed 35 weeks onwords: (As required based on Seromonitoring
  • 14. • Mycoplasmas are highly versatile and successful pathogen • Chronic: Once infected, infection remains for life • Mycoplasma lack a cell wall: resistant to penicillin group of antibiotics • Antimicoplasmal drugs are bacteriostatic • Antibodies can not eliminate infection • Field infection (MG/MS) level is high due to vertical transmission and low level of biosecurity • Raising mycoplasma clean flocks is not practicable AVIAN MYCOPLASMOSIS
  • 15. Etiology Significant pathogenic species: M. gallisepticum - Chickens, Turkeys M. synoviae - Chickens, Turkeys M. melwagridis - Turkeys M. iowae - Turkeys Target organs: – Respiratory system – Synovial membranes – Reproductive system
  • 16. Pathogenesis Inhalation Attach to cilia & epithelial cells Toxic substances/metabolites cell damage and cilia destruction Colonization move down to lungs & air sacs Cause damage Airsacculitis Blood Ovary Oviduct Joints E.coli Colonization of mucosal surface is achieved using Adhesions Establish a very close attachment With epithelial cells Capsule surrounding MG Enhance adherence
  • 17. Immune evasion and persistence Mycoplasma Attach Macropages Lymphoblasta Lymphocytes Destroy surface receptors Impaired macrophage function Immune response Rapid change of surface antigens • On/off switching (phase variation) • Gain and loss of surface proteins • Structural changes (size variation) The capsule surrounding MG resist phagocytosis Capsule block the effects of complement by masking antigens Masking of immunogenic antigens –prevent direct presentation to host immune system Intracellular invasion
  • 18. Factors that influence the disease in the field Specific infectious agents –Infectious bronchitis virus –Newcastle disease virus –H.paragallinarum –P.multocida Secondary bact. infections –E. coli Vaccine reactions –Infectious bronchitis –Newcastle disease Immunosuppressive agents –IBD, CAV, MD –Mycotoxins Environmental stresses –Excessive ammonia –Dust –Overcrowding –Chilling –Humidity –Poor Ventilation –Handling (Vaccination, Debeaking) –Heat weaning –Feed change (Starter-grower) –Poor hygiene
  • 19.
  • 20.
  • 21.
  • 22. Eggshell apex abnormality (Feberwee et al., 2009)
  • 23. Seroprevalance of Mycoplasma gallisepticum by ELISA (Based on Flocks) Region No. of Flocks Tested No. of Flocks Positive % Positive Central 22 17 77.3 East 10 07 70.0 North 26 22 84.6 South 28 21 75.0 Total 86 67 77.9
  • 24. Seroprevalance of M. gallisepticum by ELISA (Based on Flocks) 0 20 40 60 80 100 Layers Br Parents Broilers 91.7 77.5 30 Seroprevalence
  • 25. Prevalance of M. gallisepticum by Isolation and Identification (Based on Flocks) Region No. of Flocks Tested No. of Flocks Positive % Positive Central 22 7 31.8 East 10 1 10.0 North 15 2 13.3 South 27 7 25.9 Total 64 17 26.6
  • 26. Prevalance of M. gallisepticum by Isolation and Identification (Based on Flocks tested) 0 20 40 31 20 10 MG prevelance
  • 27. 0 20 40 60 80 100 Central East North South 81.80 100 92.31 89.29Percentage REGION Seroprevalence of M synoviae in different regions based on flocks tested 45 50 55 60 54.55 60.00 53.33 51.72 Percentage REGION Prevalence of M synoviae in different regions based on flocks tested
  • 28. Seroprevalence of M synoviae in different types of birds based on flocks tested 0 20 40 60 80 100 97.22 85.00 80.00 Percentage 0 20 40 60 80 73.33 42.86 36.4 Percentage FLOCK Prevalence of M synoviae in different types of birds based on flocks tested
  • 29. OPTIONS FOR MG & MS CONTROL Control Living with infection Biosecurity GMPs Antibiotics Vaccines Live Vaccines Killed ts-11 6/85 Tiamulin Tylosin Tilmicosin Tylvalosin Lyncomycin Tetracyclines Enrofloxacin Ciprofloxacin MG MS Live Vaccines MS-H
  • 30. Minimum inhibitory concentrations of MG & MS Antibiotic MIC (g/ml) MG MS Tylosin 0.02 0.04 Tiamulin 0.005 0.08 Lincomycin 2.50 0.63 Spectinomycin 1.25 1.25 Spiramycin 0.08 0.63 Erythromycin 0.02 40.0 Tetracycline 0.08 0.08
  • 31. Other Control Measures • Proper environmental control to reduce stress – Temperature, Ventilation , Stoking density • Proper control of other respiratory diseases • Proper control of immunosuppressive diseases • Strategic medication at recognized times of stress – First week of life – When heat weaned, feed changed – Debeaking, Vaccination – Peak egg production • Biosecurity – Isolation – Hygine – Traffic control
  • 32. Low Pathogenic Avian influenza • Influenza virus A, Orthomyxoviridae • Enveloped, Negative stranded, segmented RNA viruses. • 16 subtypes: Haemagglutinin (H) • Nine neuraminidase (N) antigens. • All H and N combinations have been isolated. • Extreme antigenic variability exists.
  • 33. TYPE-CTYPE-A TYPE-B Influenza Virus Sub Types (HN subtypes) H/N H1 H2 H3 H4 H5 H6 H7 H8 H9 H10 H11 H12 H13 H14 H15 H16 N1 H1N1 H2N1 H3N1 H4N1 H5N1 H6N1 H7N1 H8N1 H9N1 H10N1 H11N1 H12N1 H13N1 H14N1 H15N1 H16N1 N2 H1N2 H2N2 H3N2 H4N2 H5N2 H6N2 H7N2 H8N2 H9N2 H10N2 H11N2 H12N2 H13N2 H14N2 H15N2 H16N2 N3 H1N3 H2N3 H3N3 H4N3 H5N3 H6N3 H7N3 H8N3 H9N3 H10N3 H11N3 H12N3 H13N3 H14N3 H15N3 H16N3 N4 H1N4 H2N4 H3N4 H4N4 H5N4 H6N4 H7N4 H8N4 H9N4 H10N4 H11N4 H12N4 H13N4 H14N4 H15N4 H16N4 N5 H1N5 H2N5 H3N5 H4N5 H5N5 H6N5 H7N5 H8N5 H9N5 H10N5 H11N5 H12N5 H13N5 H14N5 H15N5 H16N5 N6 H1N6 H2N6 H3N6 H4N6 H5N6 H6N6 H7N6 H8N6 H9N6 H10N6 H11N6 H12N6 H13N6 H14N6 H15N6 H16N6 N7 H1N7 H2N7 H3N7 H4N7 H5N7 H6N7 H7N7 H8N7 H9N7 H10N7 H11N7 H12N7 H13N7 H14N7 H15N7 H16N7 N8 H1N8 H2N8 H3N8 H4N8 H5N8 H6N8 H7N8 H8N8 H9N8 H10N8 H11N8 H12N8 H13N8 H14N8 H15N8 H16N8 N9 H1N9 H2N9 H3N9 H4N9 H5N9 H6N9 H7N9 H8N9 H9N9 H10N9 H11N9 H12N9 H13N9 H14N9 H15N9 H16N9
  • 34. H5: HPAI, LPAI Notifiable H7: HPAI, LPAI Notifiable H9: Mostly LPAI Not notifiable Avian influenza sub-types Important for Poultry
  • 35.
  • 36. Poultry •Chicken •Ducks •Turkey •G. fowl •Quails •Emu Wild birds Water fowl Feces Secretions Excretions Dead bird Vehicles People Raw mat. Animals Rodents Insects Litter Dust VIRUS VIRUS VIRUS Feed Water Aerosols Droplets VIRUS Portals of Virus Exit Source of AI Virus Modes of Spread Virus Contaminant s Ingestion (MOUTH) Inhalation (NOSE) Conjunctiva (EYE) Portals of Virus Entry Avian Influenza Virus: Transmission
  • 37. Avian Influenza: Pathogenesis AI Virus Feed/Water Dust/air Ingestion Inhalation Digestive System Respiratory System Blood circulatory system Brain SkinVisceral Organs Multiple Organ Failure Death LPAI HPAI Multi-organ Damage Processes • Direct virus replication in cells/tissues/organs • Indirect effects from production of cellular mediators such as cytokines • Ischemia from vascular thrombosis • Cardiovascular collapse from coagulopathy or disseminated intravascular coagulation
  • 38.
  • 39. TYPE OF IMMUNITY Killed vaccines Local immunity - Humeral (Antibody IgA) No - Cell Mediated (Cytotoxic T cells) No Systemic immunity - Humeral (Antibody- IgY, IgM) Yes - Cell Mediated (Cytotoxic T cells) No Prevention and Control 1. Biosecurity • Isolation of farms • Movement control • Wild bird control • Dead bird dsposal • Mannure disposal • Disinfection 2. Vaccination • Mass vaccination • Inactivated -homologous • Surveillance –genotyping • Regular Updating of vaccines
  • 40. Vaccines protect only homologous subtypes/mutants of field virus • No cross-neutralization/cross-protection among subtypes – H9 vaccine do not protect H5 or H7 • No cross-protection among mutants of same subtype – Parent H9 vaccine do not protect mutants of H9
  • 41. Why AI Vaccines not giving satisfactory results • High mutation rate of AI virus • Only killed vaccines allowed • Killed vaccines donot induce local respiratory immunity • Killed vaccines donot induce cell mediated immunity • Vaccine can not prevent infection
  • 42. • ILT caused by enveloped DNA herpes virus. • There are many pathotypes of the virus. • Antigenic uniformity, strains differ in virulence • Some are very mild and others can cause severe morbidity and mortality. • Most common is Mild Form “ILT” Infectious laryngotracheitis (ILT)
  • 43. Mode of transmission • Older carrier birds are a common source of infection. • Aerosol, Direct contact, ingestion of contaminated feed, water, litter • Clinical disease occurs 6-12 days after natural exposure to the ILT virus
  • 44. Mild Form of ILT • Swollen watery eyes • Conjunctivitis • Swollen sinuses • Nasal discharge • Production loss / layers (10-20%)
  • 45. Severe Form of ILT • Severe coughing • Bloody exudates • Neck extended • Labored breathing • Mortality high - can reach 50 - 70%, (usually 10 - 20 %) • Persists for 2 - 6 weeks
  • 46.
  • 47. Mucous in trachea is seen first, followed later bloodby then necrotic tissue
  • 49. Vaccination • ILT can be effectively controlled by vaccination – 5-7 weeks of age – Revaccinate at 15 weeks of age • Most are modified live isolates and are administered by eye drop. • Vaccinated and unvaccinated birds should not be mixed due to the possibility of reversion to virulence. • Vaccination can be administered in the face of outbreak to help reduce further morbidity and mortality.
  • 50. Why ILT vaccines not permitted in India • Reportable disease • Virus latency – in infected and vaccinated birds • Residual pathogenicity of vaccine strains • Reactivation of vaccine strains • Trade restrictions
  • 51. Newcastle Disease • ND is endemic and outbreaks are common particularly in summer • NDV genome is stable and Single serotype exists • In activated Vaccine: Pre lay and Mid lay recommended • Seromonitoring of vaccinated flocks essential • Booster vaccination with live vaccines at 6-8 weeks interval based on serology • Avoid errors in vaccine admistration
  • 52. Infectious coryza • Infectious coryza outbreaks observed in the field inspite of vaccination • Infected birds become carrier and act as reservoir of infection • Three Serogroups (A,B,C) and Nine Serovars (A1, A2, A3, A4, B1, C1, C2, C3, C4) • Cross protection within serovar B is only partial • Correct other factors contributing outbreaks: Stress, errors in vaccine administration etc • Surveillance and vaccine updating essential
  • 53. Conclusions • Comprehensive Surveillance of LPAI and ILT to establish their widespred prevalence in Indian Poultry • Vaccines to control varient IBV, LPAI and ILT • All the outbreaks are not due to vaccines but mostly related to other risk factors • Avoid errors in management and biosecurity • Correction of vaccination & Medication errors • Vaccination Monitoring – Setting baselines