Webinar 6- Respiratory Disease

One of the most common and frustrating health issues in backyard poultry is respiratory disease. There are a number of potential reasons for such a high prevalence of respiratory disease in backyard holdings:

  • Many holdings have multiple ages of birds
  • Many holdings have several poultry species
  • Birds are regularly bought in from multiple sources (such as markets) with little or no history
  • Very few backyard keepers vaccinate for respiratory disease
  • Many of these birds are free range and as such come into regular contact with wild birds

Before discussing the common respiratory diseases of backyard chickens it is worth discussing the unique physiology and anatomical features the avian respiratory system.

Anatomy

Like mammals when birds breathe air flows from their nares and into their sinuses where the air is warmed (many respiratory pathogens can infect the sinuses causing sinusitis).The air then enters the pharynx via the slit like opening in the hard palate (the choanae). Next the air enters the opened glottis into the trachea. Just as in mammals the upper respiratory tract is lined by ciliated epithelial cells which help move mucus and debris up out of the airway protecting the lower airway (lungs and air sacs) from pathogens.

Unlike mammals birds have fixed lungs which do not expand or reduce with breathing. Instead in order to move air through their lungs birds have expandable air sacs which fill with air whilst inhaling and deflate when the bird exhales.

Birds have nine air sacs in total (a single intraclavicular air sac and paired cervical, cranial thoracic, caudal thoracic and abdominal air sacs). The intraclavicular air sac, the cervical air sacs and the cranial thoracic air sacs make up the cranial air sacs whilst the caudal thoracic and abdominal air sacs make up the caudal air sacs. These air sacs are extremely thin and are not vascularised. The air sacs should be cling film-like (transparent with no thickening, mucus or vasculature).

Birds do not have diaphragms to move air into and out of the respiratory system.Instead the air sacs inflate and deflate due to the movement of the musculature of the abdominal wall.

The fact that most birds fly means that they have a relatively high oxygen demand compared to mammals. Often flight occurs at high altitudes where the partial pressure of oxygen is low therefore their lungs must be capable of highly efficient gaseous exchange. To ensure this highly efficient exchange birds have arranged their air sacs to ensure unidirectional air flow through their lungs. Furthermore avian lungs have tube-like structures called parabronchi with poorly developed alveoli to facilitate this uni-directional air flow. When the bird inhales fresh air flows into the cranial air sacs via parabronchi of the lungs (where it undergoes gas exchange) and directly into the caudal air sacs. At the end of inspiration the cranial air sacs contain air low in oxygen and high in carbon dioxide whilst in contrast the caudal air sacs contain oxygen rich air. During exhalation the carbon dioxide rich air from the cranial air sacs is directly expelled whilst the oxygen rich air from the caudal air sacs exit the respiratory system via the lungs where it loses oxygen and gains carbon dioxide.

Inhalation:

Exhalation:

Pathogenesis

There are many potential pathogens that can cause respiratory disease most of which behave similarly and go on to produce similar clinical signs. (Each of these pathogens are discussed below in detail). These pathogens are often spread via the faeco-oral and aerosol routes. Fomites are also generally important in their spread.

The majority of these pathogens once inhaled attach to and damage the epithelial cells of the upper respiratory tract causing sinusitis and tracheitis. The damaged trachea and sinuses are then easy places for environmental organisms (such as E. coli) which are normally removed by the respiratory system to become established. This can result in a muco-purulent sinusitis and tracheitis.

As a result of the damage to the trachea the cilia are no longer able to waft mucus (often containing pathogens such as E. coli) up the trachea. This damage to the muco-cilliary escalator means that debris including many pathogens which are normally removed by this protective mechanism can reach the air sacs and lungs unimpeded.

Unfortunately the air sacs are very thin and have virtually no blood supply meaning once pathogens reach them they can establish themselves very easily causing air sacculitis. Subsequently this air sacculitis can then cause peritonitis by crossing the very thin poorly vascularised air sacs.

The ciliated epithelial cells of the trachea are similar to cells found in egg shell gland of the oviduct and the kidneys. This means that many respiratory pathogens can cause poor quality eggs shells, a loss of egg shell colour and nephritis.

Clinical signs

Many birds with respiratory disease may present with:

  • Dyspnoea
  • Lethargy
  • Weight loss
  • Sneezing (correctly called snicking since sneezing requires a diaphragm)
  • Naso-occular discharge
  • Facial swelling due to swollen infraorbital sinuses hence the condition is commonly called ‘bulgy eye’ in game birds
  • Pale eggs with poor shell quality
  • Polyuria (appearing as diarrhoea)

Differential diagnosis:

  • Infectious Bronchitis Virus (IB)
  • Mycoplasma gallisepticum (Mg)
  • Mycoplasma synoviae (Ms)
  • Mycoplasma meleagridis (Mm)
  • Avian RhinoTracheitis virus (ART/TRT)
  • Infectious LaryngioTracheitis (ILT)
  • Riemerella (Ducks)
  • Syngamus trachea
  • Aspergillus fumigatus
  • Avian paramyxovirus including Newcastle’s Disease (NDV)
  • Avian Influenza (AI)

Infectious Bronchitis:

IB is caused by a coronavirus. This virus is predominantly a pathogen of chickens. The virus is predominantly shed from the respiratory tract but faecal shedding is also common. The virus is very resistant and can survive in the environment for weeks. The virus will infect and damage the ciliated epithelial cells of the respiratory tract and after a short incubation period of 1-3 days the virus can cause snicking, sinusitis and a naso-occular discharge . The damage to the cilia allows environmental commensals such as E. coli to reach the air sacs where they may go on to cause air sacculitis and even peritonitis.Like many respiratory pathogens IB will infect the cells of the egg shell gland and will often lead to poor quality egg shells and a loss of shell colour. This damage to the egg shell gland can be temporary or permanent and there is no way of telling whether or not it will resolve.

In severe cases certain strains of IB (IB-QX) can cause such severe damage to the oviduct if the bird is infected pre-puberty that permanent adhesions form in the oviduct (often this results in huge fluid filled cysts) thus forever impeding the transport of the egg from the oviduct to the vent. In these cases the egg yolk ends up freely in the abdomen. These birds are called internal layers. The yolk will slowly be absorbed from the abdomen but if the bird lays internally every day then the yolks will be laid faster than they will be absorbed thus building up a mass of egg yolk in the abdomen. This mass has the potential to provide a rich nutrient medium for bacteria which can go on to cause egg peritonits. Due to the build up of yolks in the abdomen the bird adopts a penguin-like stance to assist in breathing.

IB can also infect the cells of the kidney leading to nephritis. In severe cases this renal damage can cause these birds to suffer dehydration, polyuria (manifesting itself as diarrhoea) and even visceral and articular gout.

Like all coronaviruses IB mutates frequently and immunity against one serotype doesn’t necessarily confer immunity against other strains, meaning birds can be infected with different strains throughout life.

The variability of IB strains presents a problem for vaccination and necessitates the designer of an IB vaccine program to be aware of the strains circulating locally in their area. Successful vaccination depends upon identifying the circulating IB strains in your area and ensuring that birds receive initially live vaccines for the relevant strains followed by a killed inactivated vaccine. Because this virus can infect young chicks it is often recommended to give the first vaccine before seven days of age.

A cockerel with an occular discharge

Above: Pale eggs (Note some breeds normally lay pale eggs)

Above: The distended abdomen of a pullet with a large fluid filled cyst caused by IB Qx

Mycoplasma gallisepticum (Mg)

Mg is a relatively common respiratory pathogen found in backyard chickens and turkeys. The bacteria is shed in the respiratory secretions of infected birds. This aerosolised bacteria is the inhaled by other birds. Like IB, Mg infects the cells of the respiratory tract leading to tracheitis and sinusitis which appears as peri-occular swelling often containing caseous material (due to secondary bacteria). Similarly Mg also infects the cells of the egg shell gland leading to a reduction in the quality and colour of the egg shell.

Mg often infects birds concurrently with ART.

One of the biggest issues with Mg and other Mycoplasma species is that once infected with it, birds remain carriers for life. Often during periods of stress such as re-homing, these latent carriers recrudesce and develop clinical signs once again. This recrudescence can allow these carriers to infect other new flock mates.

It is possible to vaccinate against Mg using either two killed vaccines given at least four weeks apart or using a live attenuated vaccine to begin with followed by a single killed vaccine at least four weeks later.

Note: Mg can be transmitted vertically and via copulas. This is important as many people buy eggs on eBay for hatching and can bring in disease.

Above:A hen with peri-occular swelling caused by sinusitis caused by Mg

Mycoplasma synoviae (Ms)

Ms is primarily a pathogen of turkeys causing mostly synovitis but it can cause respiratory disease. The spread of Ms is as for Mg.

Whilst Ms is primarily a turkey pathogen it has been shown to cause disease in chickens but its effects are marginal if any.

There are currently no Ms vaccines available against Ms in the UK.

Mycoplasma meleagridis (Mm)

Mm infects only turkeys and is associated with lameness due to synovitis and bone deformation. The spread of Mm is similar to that of Mg and Ms.

There are currently no Mm vaccines available in the UK.

Avian RhinoTracheitis (ART)

ART is caused by a pneumovirus. ART was previously known as TRT (Turkey RhinoTracheitis) as in the past it was thought to only infected turkeys; however it is now a frequently found pathogen of chickens.

The virus is shed from the respiratory tract secretions and is inhaled by other birds in the flock. (Fomites can also spread the virus). After an incubation period of 6-8 days affected birds show typical respiratory signs. Although ART can cause egg shell gland damage this damage is not thought to be permanent as with IB.

ART is frequently found along with Mg and together they cause sinusitis and egg shell gland damage. ART doesn’t become latent and once recovered birds shouldn’t become infected again.

Vaccination is possible with a live attenuated vaccine being given followed by a killed vaccine at least four weeks later.

Infectious LaryngioTracheitis (ILT)

ILT is caused by a herpes virus. The virus is spread via the aerosol route. After an incubation period of 6-12 days the virus causes a haemorrhagic tracheitis. This tracheitis can lead to a plug of mucus and clotted blood in the trachea which can lead to severe difficulty breathing and affected birds will often gasp. This plug can obstruct the tracheal bifurcation causing death by asphyxiation. Like all herpes viruses ILT becomes latent in the nervous system and can reappear later in life.

There is a vaccine against ILT which is in the form of a live attenuated vaccine. This vaccine is rather virulent and can cause clinical signs in its own right therefore its use should be considered very carefully on a holding. Certainly I cannot recommend it unless the condition is already present on the farm. This vaccine can be used in the face of an outbreak.

Above: Haemorrhagic tracheitis caused by ILT

Riemerella

Riemerella is a bacteria related to Pasturella but is mostly associated with respiratory disease in waterfowl (usually young ducks). The bacteria is either inhaled or gets in through skin wounds. After infection affected birds can show signs in as little as two days. These birds become dull and hunched up with respiratory signs and in severe cases neurological signs may be observed.

On PM affected birds will have pathology of the respiratory tract along with possible meningitis, septicaemia and salphingitis.

Many recovered birds become internal layers due to the salphingitis.

There are no licensed vaccines currently in the UK at this time.

Syngamus tracheaor Bronchialis-‘Gape worm’

Gape worms are a rather rare but over diagnosed cause of respiratory disease in backyard fowl and are mostly found in gamebirds

The adult worms live in the trachea in permanent copulas thus the conjoined male and female have a Y-shaped appearance. The presence of the worms in the trachea leads to difficulty breathing causing the birds to gape. Gape worms can obstruct the airway leading to what appears to be sudden death.

The female lays her eggs in the trachea where they are coughed and swallowed. Gape worm often uses earth worms as an intermediate host but can complete its life cycle directly.

Gape worms are readily carried by wild birds and these can act as a source of infection. These worms can be treated with Flubenvet in feed for seven days . The worm has a pre-patent period of just under two weeks and as such infected flocks need to be dewormed fourteen days after the end of the first treatment.

Above: Gape worms in the trachea

Aspergillus

Aspergillus fumugatis is a fungus normally found in the environment. For the most part it is relatively harmless; however ifbirds are exposed to high levels of spores or if the bird is immuno-compromised then the bird can go on to develop caseous fungal plaques in its air sacs and lungs leading to gasping. These fungal plaques can in extreme cases establish themselves in the nervous system leading to nervous signs.

Transmission is from the environment only and the infection cannot be transmitted from infected birds.

The levels of spores in the environment often build up where wet bedding is dried providing the heat and humidity necessary for fungal proliferation thus contaminating the environment. One common place for these conditions to be found is in incubators and brooding houses hence young chicks are most commonly infected. In the past Aspergillosis was called ‘brooder pneumonia’.

There is no effective treatment and euthanasia is recommended.

Prevention is based upon ensuring that litter is kept dry and that poor quality bedding isn’t used. Note hay is a common source for high levels of spores so never use hay to bed poultry.

. Above: An air sac with multifocal fungal plaques

Avian paramyxovirus

Avian paramyxoviruses can cause respiratory disease in all domestic fowl. The virus is spread by the aerosol and faeco-oral routes. Fomites are an important method for spreading paramyxoviruses. In general the virus is resistant and can survive for several weeks in the environment. Wild birds can carry paramyxoviruses and can act as a source of infection for domestic fowl.

Strictly speaking the term Newcastle disease only applies to highly pathogenic paramyxovirus strains. Whether or not a paramyxovirus is classed as Newcastle disease depends upon its pathogenicnity as determined by the VLA. There are three grades of pathogenicnity of the virus: lentogenic (low level pathogenicnity), mesogenic (moderate pathogenicnity) and velogenic (highly pathogenic). The viral serotypes will often have tissue tropism: pneumotrophic (the respiratory tract), viserotrophic (the viscera including the digestive tract) and pneumotrophic (the nervous system).

Depending on the serotype the clinical signs can vary from mild respiratory signs right through to diarrhoea, neurological signs (torticollis) and even sudden death. ND can damage the egg shell gland leading to egg shell quality deterioration. ND will cause typical respiratory disease pathology but unlike other pathogens the virulent viserotrophic strains can cause haemorrhages of the proventiculus.

Like other respiratory pathogens vaccinations against ND can be given (a live attenuated vaccine followed by a killed vaccine at least four weeks later).

If you suspect NDV please contact AHVLA.

Avian Influenza (AI)

AI is caused by a orthomyxovirus. There are many serotypes of AI varying in pathogenicity. The UK is currently free from highly pathogenic AI.

The virus is spread by the faeco-oral and respiratory routes and depending on the strain it can cause clinical signs varying from sudden death right through to mild respiratory signs. Post mortem findings tend to be generalised and are not diagnostic.

The virus can be carried by Fomites surviving for several weeks in the environment. Water fowl may carry AI however they tend not to show clinical signs readily.