Infectious laryngotracheitis is category 1 restricted matter.
Under Queensland legislation, if you suspect the presence of this disease in any species of animal, you must report it to Biosecurity Queensland on 13 25 23 or contact the Emergency Disease Watch Hotline on 1800 675 888.
Infectious laryngotracheitis (ILT) is a highly contagious respiratory disease in poultry that has been identified in most countries around the world and remains a threat to the intensive chicken industry. The first Australian outbreak of ILT was recorded in New South Wales in 1935, and the disease has since been reported in all other states of Australia. ILT is characterised by gasping, neck extension and conjunctivitis (inflammation of the membrane around the eye).
A herpes virus involved in respiratory disease and reduced egg production
Chickens, pheasants, partridges, peafowl, turkeys, ducks, geese
ILT has an incubation period of 3-14 days (though 5-12 days is most common).
Individual birds are infectious from about the end of the incubation period and up to another 2 weeks. Even the vaccine strains can be shed for this period after inoculation and may cause disease in susceptible birds, although usually milder than field strains. The viral shedding period depends on when the last birds in the building became infected.
Many birds develop a carrier state with the virus hiding away in the facial nerves until the bird immunity wanes. If some stress occurs, many of these birds can shed infectious virus and some may even show disease, again usually a milder form but posing a risk to susceptible birds in close contact.
ILT virus can live for 8-10 days in droppings and up to 70 days in carcasses at ambient temperatures of 13-23ºC. The virus lasts longer in winter due to the cool temperature. The virus may survive for up to 80 days in tracheal exudate (throat exudate) on non-conductive material such as wood, if not disturbed. This demonstrates the importance of sound clean-up procedures and good biosecurity measures.
There is a marked variation in the pathogenicity (potency) of various virus strains. Three major forms are known:
- Onset of disease is sudden with a rapid spread.
- High mortality of up to 70%.
- Some birds may die in good body condition before characteristic signs of difficulty in breathing with extension of the neck and gasping in an attempt to inhale are present.
- Other respiratory signs may include rales (rattles in the throat), coughing with expulsion of blood or blood-stained mucous, and the bird is very depressed.
- On post mortem, acute haemorrhagic inflammation of the trachea and larynx is present, and the lumen (centre) of the trachea is blocked by mucoid blood clots and sometimes yellow caseous exudate (cheesy plug-hard pus).
- Death is normally by suffocation.
- Onset of illness is slower and respiratory signs may extend over some days before deaths are seen.
- High morbidity (sickness) rate but a lower mortality rate of 10-30%.
- Less severe respiratory signs of rales, coughing with expulsion of caseous matter, mucoid nasal discharge, gasping and infra-orbital sinus swelling.
- Often conjunctivitis with severe lacrimation (eye discharge) and eyelids matted together.
- On post mortem, mucous, which may be bloodstained, is found with membranes in the upper respiratory tract.
- Death is normally by suffocation.
Mild or chronic
- Low morbidity (sickness) rate of 5%.
- The bird is drowsy with signs of conjunctivitis, squinting eyes and bronchitis combined with a cough.
- Often a concurrent infection with coryza.
- Egg production may drop 10%.
On post mortem, false membranes or plugs are seen in the upper respiratory tract, which may cause death.
Early signs may include bouts of hard swallowing, ruffled feathers on the back of the head, squinting and the watering of one or both eyes (conjunctivitis).
After the incubation period, increased mucous forms in the trachea (windpipe), often followed by tracheal haemorrhage. This causes the bird to cough and extend its head in a characteristic manner to breathe. In some cases, only mild respiratory signs are visible but one eye may completely close.
Classic signs are gasping, coughing, and extending the neck forward and upwards with each breath to clear the mucous in the trachea. In fact, many birds die from this disease due to suffocation, as the windpipe becomes completely blocked.
Water fowls (ducks and geese) show no signs but ducks have been known to carry ILT virus for up to 2 weeks.
Up to 70% mortality - in acute cases.
How it is spread
Wild birds may act as carriers. Darkling beetles (litter beetles) have also been found to act as vector for ILT virus.
The virus is released from the respiratory tract and followed by rapid airborne transmission among birds in close contact, such as cage or pen mates. The virus enters the bird through the eye, nose or mouth. The coughed-up mucous and blood contains the virus and is another way that the disease quickly spreads. In infected birds, the virus can become latent and re-excreted at a later date without clinical signs.
In the past, most outbreaks have been traced to the movement of poultry, people and equipment. However, if environmental conditions are suitable, windborne spread may also be a factor.
The virus depends on a transporting agent to spread. The virus is not transmitted through the egg, so chickens are not infected at hatching. The virus can be spread by:
- introduction of infected birds - including the introduction of affected birds, carrier birds or birds that are incubating the disease at the time of introduction. Carriers of ILT virus can shed the virus at times of stress, infecting susceptible in-contact birds
- people and contaminated equipment - with contaminated crates and feed trucks known to be sources of infection. People who are in contact with infected birds and, on the same day, with susceptible flocks may transfer the disease if they do not take suitable biosecurity measures
- airborne spread - depending on the prevailing conditions. There is rapid airborne transmission among birds in close contact. The virus often requires mechanical transfer to cover even short distances, such as from one building to another. However, birds in sheds close to roads may even be infected by discharges (nasal droplets, faeces etc.) from diseased birds being transported down the road. Contaminated feathers and shed dust can also act as virus transporting agents.
- litter and manure - the virus can survive in the birds' environment for periods of time, and transmission may occur when susceptible birds are placed in a recently contaminated but uncleaned environment.
Under conditions such as cloud cover, humidity, showers and gusty winds, the ILT virus can easily cover 500m, and possibly much further.
Monitoring and action
Acutely affected birds show free blood in the trachea, which is generally associated with a mucous plug that inhibits normal breathing. The symptoms rapidly spread throughout the flock.
Birds with subacute and mild infections may show only slight difficulty in breathing and perhaps a mild watering of one or both eyes. However, the disease can still be easily transmitted from one bird to another. A mild ILT infection may look like any other respiratory or viral infection. Laboratory diagnosis will always be required to determine whether the ILT virus is present.
Sunlight, heat and desiccation (drying) are the 3 natural enemies of the ILT virus.
Vaccinate birds, first with a mild vaccine strain then about 4-6 weeks later with a more virulent vaccine strain. This produces an immunity that lasts at least 1 year. Moulted flocks should be vaccinated again at the end of the moult.
Antibiotics have no effect on the virus. Vaccination and the vaccine's short incubation period could be used to halt an outbreak.
Focus control measures on:
- preventing the spread of disease to other birds
- vaccination to build up immunity in susceptible birds.
Once the disease is accurately diagnosed, use the vaccination immediately to stop the spread and reduce the virulence of the disease.
- Last reviewed: 1 Jul 2016
- Last updated: 12 Jul 2016