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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:
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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.
Sinus
Trachea
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).
Air sac
Lungs (Should be a
salmon-pink
colour)
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:
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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:
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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 penguinlike 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 trachea or 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 if birds are exposed to high levels of spores or if the bird is immunocompromised 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.
There is no vaccine against AI currently available in the UK.
Note AI is a notifiable disease and if you suspect it in a flock please call AHVLA.
Diagnosis of Respiratory Disease
Diagnosis of the exact agent(s) involved in a case of respiratory disease is very difficult by
clinical signs alone given that many respiratory pathogens tend to cause similar clinical signs.
Unlike many conditions in cases of respiratory disease post mortems are not very specific
except for diagnosing gape worm.
Serology is often the best method for a retrospective diagnosis of IB, ART, Mg, Ms and Mm.
It is worth waiting at least two weeks after clinical signs before submitting blood for serology as the
birds will need time to seroconvert (Send in blood in plain tubes- see blood sampling in the practical
techniques section). It is often worth taking paired blood samples for serology to look for rising
titres. Note if vaccines have been given this needs to be taken into account of before interpreting
serology results.
Chicken vet offers serology for the diagnosis of respiratory disease along with full veterinary
interpretation.
To diagnose ILT it is best to use histopathology of the trachea to look for eosinophillic intranuclear inclusion bodies which are almost pathogonomic for this condition. Serology can prove
unreliable.
Aspergillus can be cultured from suspicious lesions on a suitable fungal medium.
As time goes on PCR testing is becoming much more popular for diagnosis respiratory
disease however for backyard flocks this seems rather expensive.
If you suspect NDV or AI please contact DEFRA.
Pathology:
The pathology of respiratory disease tends to be similar for most pathogens and is rarely
diagnostic. The severity of the lesions will depend upon the immune status of the bird and upon the
combination of pathogens present.
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Conjunctivitis
Sinusitis (can vary from a mild mucoid exudate through to inspisated pus)
Tracheitis
Airsacculitis (cloudy air sacs, neovascularisation and pus/mucus)
Egg peritonitis
Septicaemic signs (fevered carcase, inflamed liver, spleen and kidneys)
White urate deposits in the kidneys and ureters
Fevered
breast
muscle
Egg peritonitis
Enlarged
liver
Treatment
Irrespective of the underlying pathogens the treatment for respiratory disease is mostly the
same.
When approaching a case of respiratory disease it is important to ascertain the severity of
the condition. A mild respiratory disease case where the bird is snicking(sneezing) but is otherwise
fine will likely recover without the need for antibiotics. Mintamix is a plant extract based
decongestant which will help birds breathe. If the bird is unwell, the clinical signs severe or the signs
are not resolving then antimicrobials may be indicated. Even if the cause is viral you will want to
protect against secondary bacterial infection.
There are a number of antimicrobials available but it is important to use those which have
activity against Mycoplasma and secondary pathogens if you are unsure about the diagnosis.
For the majority of conditions many vets will use Fluroquinolones (Enrofloxacin) which is a
broad spectrum powerful antimicrobial (which will kill Mycoplasma) however there is concern about
overuse leading to resistance and its harmful effects on the intestinal flora.
Doxycycline and Tetracyclines are broad spectrum antimicrobials which have activity against
Mycoplasma and secondary pathogens such as E. coli. Generally either antimicrobial is given for five
days at 20mg/Kg in drinking water. It is worth noting that there is considerable resistance to
Tetracyclines.
Macrolides such as Tylosin (Tylan- Zero egg withdrawal) are commonly prescribed as they
are effective against Mycoplasma but they have a narrow spectrum of activity against other
secondary pathogens. Tylan can be given up to 200mg/Kg for five days.
Tiamulin (Denagard- zero egg withdrawal) is licensed against Mycoplasma but like Tylosin
has poor activity against secondary pathogens. A typical course of Denagard is 2ml/Litre of drinking
water for five days.
Aminoglycosides such as Lincospectin can be used effectively (for up to seven days at
50mg/Kg) as they have activity against both Mycoplasma and E. coli.
When treating respiratory disease it is often advised to treat the entire group of birds as
many of them will likely have subclinical disease.
Many antimicrobials destroy the gut flora and it is recommended about a week after the end
of treatment to give a probiotic such as Beryl’s to repopulate the intestine with ‘friendly bacteria’.
Prevention:
Prevention of respiratory disease like other diseases is based upon biosecurity. Always
obtain birds from a reliable source (local markets and eBay are bad sources). Ideally quarantine new
birds for three weeks before introducing them to an existing flock. If your client has high value birds
then testing them before admitting them to the flock may be a good idea.
Trying to keep wild birds and vermin away by keeping feed stored in metallic containers and
not placing feed on the ground or in the sight of wild birds.
Minimising stress will reduce the chances of respiratory disease taking hold and should help
reduce the chances of recrudescence in latent carriers. This means avoiding stresses such as poor
diet, over stocking, extremes of temperature, draughts and poor ventilation. Note poor ventilation
can lead up to high ammonia levels which can damage the cilia leaving the respiratory tract more
vulnerable to infection.
Vaccination is possible for respiratory disease but it is not straight forward.
Vaccination:
It is firstly important to decide whether or not a client needs to vaccinate against respiratory
disease. A client with a few backyard birds probably doesn’t need to vaccinate as the stocking
density and hopefully stress levels are low. For clients keeping and breeding several hundred birds it
is definitely worthy vaccinating. The problem clients are those with say 30-100 birds and you will
have to use information about their holding’s disease history to ascertain the disease risk.
Once you have decided to vaccinate a holding you next need to decide which respiratory
diseases you need to vaccinate for (Ideally include at least IB). Before instigating a vaccination
program it is probably worth carrying out serology on the holding to determine which pathogens are
present. For most respiratory diseases a vaccination with a killed vaccine repeated one month later
followed by annual boosters is the most practical option.
Many of these vaccines come in 1,000 dose packs so there will be considerable waste
however these 1,000 dose packs are relatively cheap costing approximately £30-40 per pack but if
you have to give several vaccines the costs will mount.
There is a single killed vaccine available containing: IB, ART and NDV.
Vaccinated birds should be boosted with killed vaccines annually.
Key points to remember
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Warn owners that many of these diseases can become latent and can recrudesce at a later
date especially when their birds are stressed
If there is egg shell gland damage it may not resolve fully
Mycoplasma can be transmitted vertically
IB immunity is serotype specific
Vaccination is neither straight forward nor will it give 100% protection