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INFECTIOUS
LARYNGEOTRACHEITIS
Laryngeotracheitis
 Infectious laryngeotracheitis (ILT),
 Avian diphtheria
History:-
 First described 1925 in Canada
 Australia and Great Britain in 1935
 Isolated (1930)
 Caused by alpha herpes virus (Beaudette 1937)
Etiology
 Alpha herpes virus commonly known as
infectious laryngotracheitis virus (ILTV)
 Double stranded DNA (155kb)
 Enveloped
 Size: 195-250 nm
Aetiology strain differentiation
 Based on virus neutralization (VN),
immunofluorescence (IF) and cross-
protection studies, ILTV strains are
considered to be Antigenically homogeneous.
 Infectious laryngotracheitis virus is an acute,
highly contagious infection of chickens and
pheasants.
 Result in severe production losses due to
mortality and/or decreased egg production.
 Characterized by severe dyspnoea,
coughing, expectoration of bloody exudate
and severe necrotizing laryngitis and/or
tracheitis.
Survival out the Host
 Virus survives for 47 days at room
temperature on swabs, for 8-10 days in
droopings at 10-23c° and for 21-27 days in
carcass.
 Virus is destroyed in 44 hours in the trachea
tissue of an unrefrigerated chicken carcass.
Susceptible Hosts
 Primarily in chickens
 Usually older birds
 Pheasants & pheasant crosses are rarely affected.
 Virus has been isolated from trachea of Peafowl.
 Other birds resistant (ducks, pigeons, doves,
sparrows, crows, starlings, guinea fowl).
Physical/Chemical Susceptibility
 Susceptible to heat
 Susceptible to many chemicals
 Chloroform, ether, iodophors, cresols,
 Hydrogen peroxide fumigant (5%)
Structure Of Virus
Transmission
 Between flocks
 Mechanical carriage of infective foci such
contaminated implements, feathers, litter,
clothing, poultry dust and faeces, broken
eggs and faeces dried on egg trays and
equipment are a good source of infection.
 Purchased sick and carrier birds.
Transmission
Horizontal transmission
 Aerosolization of virus
 Birds, feed, water
 Contaminated litter
 Fomites (equipment, boots, clothes)
No vertical or egg transmission known
Factors influencing susceptibility
 More prevalent in cold months.
 Clinical disease is more severe in hotter
climates.
 Occurs from year to year on the same
premises or in the same general areas.
 Seen mainly in mature age.
 Male are more susceptible
Pathogenesis
 Virus present in trachea for 6-10 days PI
 Inflammation and necrosis (tracheal cores)
 Produce intranuclear inclusions in the
epithelium of infected birds.
 Necrotic cells, blood, inflammatory debris,
cellular edema
 High virus shed during infection
 Leads to Death b/c of asphysia
Clinical Signs
 Acute respiratory disease
 Conjunctivitis – almond eye (often first signs)
 Nasal discharge
 Moist rales, coughing, gasping
 Dyspnea
 Expectoration of blood (only in severe infections)
 Decreased production
 Egg production 5-15%: no problems with shell quality
 Unthrifty birds
 Recovery in ~7-28 days (usually 10-14 days)
 Duration ~2-6 weeks in flock
Clinical Signs
 Incubation 6-12 days post infection (PI)
 2-4 days experimentally
 Severe
 90-100% morbidity
 5-70% mortality
 Mild (‘silent LT’)
 As low as 5% morbidity and 1% mortality
Clinical Signs
Clinical Signs
Clinical Signs
Gross Necropsy
 Conjunctivitis and sinusitis
 Hemorrhage, edema
 In mild cases, may be only sign (inflammation)
 Laryngotracheitis
 Mucus, hemorrhage
 Tracheal plug
 Lungs are normal or show congestion
Gross Necropsy
Diagnosis
 Clinical signs
 Histopathology
 Virus isolation
 Detection of LT antigens
 Detection of LT viral DNA
 Electron microscopy
 Serology
Gross Necropsy
 Type A intranuclear inclusions
 3 day PI (only found for ~ 1-5 days)
 Syncytia (multi-nucleated giant cells)
 Epithelial edema, enlargement, and decilliation
 Inflammatory cells mucosa
 Loss of goblet cells
 Separation of epithelial layers
 Sloughing into lumen
Histopathology
Differential Diagnosis
 Pox (diptheretic or wet)
 Infectious bronchitis
 New castle disease
 Coryza
 CRD
 Avitaminosis
Prevention and Control
 Avoid mixing of vaccinated or recovered chickens
with susceptible chickens
 Contaminated litter
 Fomites
 Anything that has contacted infected/vaccinated
birds
 Boots, hands, clothes, equipment, vehicles
 People, rodents, wild birds, and dogs may
 mechanically carry LT
Prevention –
MLV (Vaccine Program)
 Broiler vaccination 2-4 wks of age
 Frequently given in drinking water
 May be as early as 10-12 day.
 Immunity to 8-15 wks post vaccination
 Breeders: (re)vaccinate at 10-12 wks of age
 Eyedrop
 Layer vaccination ~ 7 & 15 weeks of age
THANKS

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Infectious Laryngotracheitis (ILT) Virus

  • 2. Laryngeotracheitis  Infectious laryngeotracheitis (ILT),  Avian diphtheria History:-  First described 1925 in Canada  Australia and Great Britain in 1935  Isolated (1930)  Caused by alpha herpes virus (Beaudette 1937)
  • 3. Etiology  Alpha herpes virus commonly known as infectious laryngotracheitis virus (ILTV)  Double stranded DNA (155kb)  Enveloped  Size: 195-250 nm
  • 4. Aetiology strain differentiation  Based on virus neutralization (VN), immunofluorescence (IF) and cross- protection studies, ILTV strains are considered to be Antigenically homogeneous.
  • 5.  Infectious laryngotracheitis virus is an acute, highly contagious infection of chickens and pheasants.  Result in severe production losses due to mortality and/or decreased egg production.  Characterized by severe dyspnoea, coughing, expectoration of bloody exudate and severe necrotizing laryngitis and/or tracheitis.
  • 6. Survival out the Host  Virus survives for 47 days at room temperature on swabs, for 8-10 days in droopings at 10-23c° and for 21-27 days in carcass.  Virus is destroyed in 44 hours in the trachea tissue of an unrefrigerated chicken carcass.
  • 7. Susceptible Hosts  Primarily in chickens  Usually older birds  Pheasants & pheasant crosses are rarely affected.  Virus has been isolated from trachea of Peafowl.  Other birds resistant (ducks, pigeons, doves, sparrows, crows, starlings, guinea fowl).
  • 8. Physical/Chemical Susceptibility  Susceptible to heat  Susceptible to many chemicals  Chloroform, ether, iodophors, cresols,  Hydrogen peroxide fumigant (5%)
  • 10. Transmission  Between flocks  Mechanical carriage of infective foci such contaminated implements, feathers, litter, clothing, poultry dust and faeces, broken eggs and faeces dried on egg trays and equipment are a good source of infection.  Purchased sick and carrier birds.
  • 11. Transmission Horizontal transmission  Aerosolization of virus  Birds, feed, water  Contaminated litter  Fomites (equipment, boots, clothes) No vertical or egg transmission known
  • 12. Factors influencing susceptibility  More prevalent in cold months.  Clinical disease is more severe in hotter climates.  Occurs from year to year on the same premises or in the same general areas.  Seen mainly in mature age.  Male are more susceptible
  • 13. Pathogenesis  Virus present in trachea for 6-10 days PI  Inflammation and necrosis (tracheal cores)  Produce intranuclear inclusions in the epithelium of infected birds.  Necrotic cells, blood, inflammatory debris, cellular edema  High virus shed during infection  Leads to Death b/c of asphysia
  • 14. Clinical Signs  Acute respiratory disease  Conjunctivitis – almond eye (often first signs)  Nasal discharge  Moist rales, coughing, gasping  Dyspnea  Expectoration of blood (only in severe infections)  Decreased production  Egg production 5-15%: no problems with shell quality  Unthrifty birds  Recovery in ~7-28 days (usually 10-14 days)  Duration ~2-6 weeks in flock
  • 15. Clinical Signs  Incubation 6-12 days post infection (PI)  2-4 days experimentally  Severe  90-100% morbidity  5-70% mortality  Mild (‘silent LT’)  As low as 5% morbidity and 1% mortality
  • 19. Gross Necropsy  Conjunctivitis and sinusitis  Hemorrhage, edema  In mild cases, may be only sign (inflammation)  Laryngotracheitis  Mucus, hemorrhage  Tracheal plug  Lungs are normal or show congestion
  • 21. Diagnosis  Clinical signs  Histopathology  Virus isolation  Detection of LT antigens  Detection of LT viral DNA  Electron microscopy  Serology
  • 23.  Type A intranuclear inclusions  3 day PI (only found for ~ 1-5 days)  Syncytia (multi-nucleated giant cells)  Epithelial edema, enlargement, and decilliation  Inflammatory cells mucosa  Loss of goblet cells  Separation of epithelial layers  Sloughing into lumen Histopathology
  • 24. Differential Diagnosis  Pox (diptheretic or wet)  Infectious bronchitis  New castle disease  Coryza  CRD  Avitaminosis
  • 25. Prevention and Control  Avoid mixing of vaccinated or recovered chickens with susceptible chickens  Contaminated litter  Fomites  Anything that has contacted infected/vaccinated birds  Boots, hands, clothes, equipment, vehicles  People, rodents, wild birds, and dogs may  mechanically carry LT
  • 26. Prevention – MLV (Vaccine Program)  Broiler vaccination 2-4 wks of age  Frequently given in drinking water  May be as early as 10-12 day.  Immunity to 8-15 wks post vaccination  Breeders: (re)vaccinate at 10-12 wks of age  Eyedrop  Layer vaccination ~ 7 & 15 weeks of age