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George Arzey, Senior Veterinary Officer, Elizabeth Macarthur Agricultural Institute, Menangle NSW

Posted Flock & Herd April 2013


Considering that the avian respiratory system served dinosaurs well 175-250 million years ago, at a period when low environmental oxygen and high temperature affected the planet (1, 2); this combination of flow-through ventilation (uni- and bidirectional) and crosscurrent exchange allows birds to extract up to 160% more oxygen from the air than mammals can (i.e. up to 260% of mammalian levels (3). it could be argued that such a system has plenty of spare capacity to accommodate the humble lifestyle of the domestic chicken.

Diagram of air sacs

The structural efficiency of the bird's respiratory system to oxygenate does not necessarily match the system's ability to protect against infection and contaminants. The air flow through the lungs to air sacs during inspiration and then from air sacs through the lungs during expiration provides a double opportunity for gas absorption but also an opportunity for respiratory infection in air-sacs (mainly the caudal air sac (4), the more prominent site of respiratory infection) to cross the thin barriers into the lungs.

A dominant role is played by the upper respiratory system, nasal cavity and pharynx in removing larger particles down to about 4nm. Smaller particles are not entrapped and require further filtration mechanisms present in the trachea, primary and secondary bronchi (4).

The rigidity of the lungs and the comparative relative scarcity of respiratory macrophages in birds compared with mammals may have some influence on the ability to defend, although this aspect is debatable.

The system in birds may also depend on other structures through possible impact on the air sacs in cases such as peritonitis, ascites and tumour formation in the abdomen.

It is useful to remember this point when a differential diagnosis is considered since respiratory distress may indicate malfunction of other systems and structures that are not physiologically part of the respiratory system.


Small poultry flocks are not usually kept in cages or under intensive husbandry and are less likely to encounter repeated long term insults like dust or high ammonia levels. However they are, for example, more likely to suffer insults from lime, a product that is sometimes most generously spread in a pen or poultry yards in the belief that it is the panacea for every real and imaginable malady.

It is apparent from some studies (5) that differences in the disease profile of hens in different housing systems may be encountered and that viral respiratory diseases are less likely to be encountered in small free range flocks than in intensive flocks. However the diagnosis of diseases in NSW, especially in small free range flocks, is somehow biased towards viral diseases especially notifiable viral diseases. This may be because the common bacterial diseases are not notifiable. As such, the owner is required to pay for their diagnosis and they are of much less public and industry interest than avian influenza, Newcastle disease and ILT.


Respiratory signs in poultry include runny watery eyes, swollen sinuses, nasal discharge, wheezing, sneezing, gurgling/rattling, gasping and mortality. Cyanosis, considering the spare capacity of the avian respiratory system is indeed a sign of a significantly acute or long standing significant respiratory malfunction.

The differential diagnosis of respiratory diseases of poultry includes the following diseases and conditions;

The range of aetiological agents involved in respiratory signs and the complexity of the system makes it a challenge to identify the agent(s) involved. An analysis of diagnostic submissions to the SDVL lab between January and August 2012 reveals that out of 23 submissions from small poultry flocks, in only 6 (26%) was the aetiology identified. In 4/6 of these cases ILT was diagnosed, in 1/6 LPAI (H4N6) and in 1/6 Pasteurella multocida was cultured (Arzey, unpublished data).

The reasons for the low success rate of conclusive diagnosis are;

  1. Inappropriate/insufficient specimens
  2. Depth of knowledge of the species and the disease
  3. Availability of limited history
  4. Submitting veterinarian requesting limited diagnosis (exotic disease exclusion)
  5. Limitation on the scope of exploration at the lab (financial and time constraints)
  6. Transport and accessibility to the laboratory
  7. Already on medication
  8. Multiple aetiology/disease syndromes
  9. Late stage when investigation start.

All the above may explain the low diagnostic rate but to be truthful; I have to mention that in my early years as Veterinary Officer Seven Hills, charged with the diagnosis of each mortality in the poultry research flocks at Seven Hills, I anxiously carried specimens across Sydney to the poultry lab at Glenfield expecting to find out the answers to most of the cases of morbidity and mortality that I encountered on the station's flock. I soon found out that the lab was a very useful place to visit but not the citadel of answers or a fountain of diagnostic solutions that I expected it to be and that Dr Quincy ME was only a figment of popular TV series.

With respect to diagnosis of respiratory diseases of poultry several questions can be asked;

  1. Who can diagnose a case in a flock?
  2. What does 'no diagnosis' mean?
  3. How do you progress cases of 'no diagnosis'?

Historical events in NSW and other States also indicate that the diagnosis of diseases in flocks may require persistence and repeated attempts to diagnose. It took more than 4 weeks to diagnose Newcastle disease at Dean Park in 1998 despite repeated submission to laboratories and the involvement of at least 3 veterinarians in the case.

One of the lessons to remember, not only from this episode, is that in many cases when a flock is investigated, repeated investigations are required to arrive at a diagnosis. This is particularly relevant to respiratory diseases where the multiplicity of causative agents and their interactions with other factors can complicate the diagnosis.


1. LP avian influenza

Table of Avian influenza subtypes
Key - D-ducks, C - chickens, T- turkeys PM- Pasteurella multocida,
MH-M haemolytica, EPD- Egg production drop

The table above demonstrates that the consistency of respiratory signs in LPAI incidents is low and maybe associated with concurrent bacterial or other viral infections (H10 in NSW with no respiratory signs and H10 in Qld with respiratory signs. H9N2 in two turkey flocks, one with and another without respiratory signs). Perhaps it is useful to consider also that 10/14 of the flocks where LPAI was reported were duck or a mixed duck/chicken enterprises and 100% of the FR flocks infected with LPAI in Australia between 1976 and 2012 were mixed ducks/chicken enterprises.

2. Newcastle Disease

Neurotropic velogenic - high mortality; respiratory and nervous signs predominate;

Mesogenic - low mortality; respiratory signs usually predominate.

During the ND outbreaks in Australia between 1998 and 2002 the mostly reported clinical signs were depression, nervous signs; ataxia, paralysis, opisthotonus and head nodding, increased mortality and changes to egg shell colour. However, respiratory signs including sinusitis and runny eyes were clearly evident in a significant number of layer flocks without nervous signs or prior to the emergence of nervous signs.

Country differences between the clinical manifestations of velogenic NDV have been reported and in Australia with the Australian origin (Ao) NDV, regional differences in the appearance of respiratory signs were evident between Sydney and the Mangrove Mountain (Arzey Unpublished data).

Gross pathology is not consistently present in the respiratory tract of poultry infected with NDV but tracheal haemorrhages and congestion could be evident similar to some cases of ILT. Unlike ILT, airsaculitis could be present.

Pathological changes were absent or subtle in many chickens during the 1998-2002 AoND outbreaks.

3. ILT

Cause - Gallid herpes virus

ILT may appear in 2 forms; the severe form with dyspnoea, gasping, coughing, blood stained mucus, cheesy core and mortality and the milder form where clinical signs include watery eyes, swelling of the sinuses, nasal discharge, possibly haemorrhagic, conjunctivitis and mortality. In mild forms conjunctivitis may be the only gross pathology present. In either the severe or the milder forms, ILT requires consideration of viral and bacterial differential diagnosis unless gross pathology and clinical history can provide a few more clues. The presence of cheesy cores in the tracheal lumen is almost pathognomonic of ILT.

Perhaps the case below illustrates some of the issues and particularly that lack of a diagnosis may simply be because at different stages of the disease typical pathology or the agent may no longer be present.

A case submitted to SDVL;

"Old English Game birds owned by a show breeder. Has been struggling with a low mortality, high morbidity respiratory infection in his birds. Began about 2 weeks after bringing birds back from a show. Some birds get very mild signs and then recover while other birds get a chronic problem. Some birds need euthanasia because of severe respiratory signs. Signs include red comb and wattles, upper respiratory noise, stretching necks out, sneezing and coughing. No response to antibiotics prescribed by a private veterinarian (1 live bird brought into LHPA. Lethargic)".

Lab report -"The lesions are aetiologically nonspecific. Possible agents include viruses such as Infectious bronchitis, Mycoplasma & 2nd Bacterial infection. Infectious coryza can't be definitely excluded, however one would have expected to see more severe inflammation of the infraorbital sinus".

ILT PCR was negative but what does this mean considering the meagre number of specimens from the flock -1, the possibility that the virus was no longer present and that the window of opportunity for a typical pathology is narrow with ILT,

4. Fowl pox

The disease occurs in the cutaneous (classical) form and the diphtheritic (wet pox) form and the combination of both in the same flock or even in the same bird. The wet pox form is more associated with respiratory signs than the classical cutaneous form. In the wet pox form yellowish lesions appear on the mucous membranes of the mouth, oesophagus, or the trachea and respiratory signs can be evident and may either resemble ILT or Coryza/CRD. Flock mortality ranges from low to 50% depending on the species of birds, their age, the virulence of the virus and the nature of the lesions.

Case 12/6899 perhaps can be used as an example for a respiratory disease that involves fowl pox and when difficulties have been experienced with the diagnosis.

Excerpt of lab report;

Excerpt of laboratory report
(Avian influenza and NDV was excluded on the basis of PCR negative results).

This case demonstrates that in some instances the disease may 'wave Hello' at the investigator and still some important aspects can be missed.

When respiratory signs are present in a flock with pox like lesions, e.g. on the North Coast, in April, the chances are that it is pox and not NDV or AI. Presence of mortality may indicate the virulence of the virus or the presence of complications and superimposed infections.

5. Pneumonitis infection (Turkey Rhinotracheitis/Swollen Head Syndrome)

Not reported in Australia but how hard do we look?

Affects - turkeys and chickens.

Clinical signs and lesions:

In young turkeys - sneezing. Rales and nasal discharge, conjunctivitis, swelling of the infraorbital and submandibular areas can be seen.

In laying turkey flocks a drop in production may occur along with respiratory distress. Morbidity is high whereas mortality may vary being usually higher in young poults.

In chickens

Pneumovirus may be involved in the so called "swollen head syndrome" (SHS)- affected chickens may show swelling of the periorbital and infraorbital sinuses, torticollis, cerebral disorientation and depression. Marked egg production losses can be associated with SHS.

At necropsy the lesions seen may vary due to other microorganisms that may complicate the original picture. In cases of SHS, apart from oedema of the head, also purulent or caseous subcutaneous exudate can be found. Rhinitis, tracheitis and sinusitis are frequently noted in both chicken and turkeys.

E coli infection is often involved.

6. Infectious bronchitis (IB)


Corona-virus is the causal agent. Several different serotypes of IB virus are known to exist.

Species affected:

Chickens are the main species susceptible to IB virus although reported occasionally in pheasants where it causes high mortality.

Clinical signs:

In young chicks less than 6-8 weeks of age IB virus infection causes a cheesy exudates in the bifurcation of the bronchi, thereby causing asphyxia, and severe respiratory distress, similar to ILT. Runny eyes and swollen sinuses may also be present.

In older chickens IB does not cause mortality. Respiratory signs may be present but are usually relatively mild or absent. Egg production is affected and deformed eggs with pale shell eggs, soft-shelled, misshapen eggs and wrinkled shells will often be laid. The internal quality of the egg, especially the albumen more watery than normal may be observed.

Image of chicken head

7. Marek's disease and leucosis

Although not the primary manifestation of Mareks disease, tumour formation localized in some areas or organs, or those affecting some of the nerves may lead to presence of respiratory signs.


These include: Coryza (Haemophilus paragalinarum), Mycoplasma/CRD, Pasteurella multocida- F cholera, E. coli, Streptococcosis, Chlamydiosis, Ornithobacterium rhinotracheale.

Unlike some of the viral diseases that are species specific (eg ILT), most of the bacterial diseases listed above can affect a wide variety of avian species although some species maybe more susceptible than others (e.g. F cholera - turkeys).

There are some aspects like age of the bird that are useful in differential diagnosis (F cholera rarely in birds younger than 16 weeks of age).

It is almost impossible to arrive at a presumptive diagnosis of any of the above bacterial diseases on the basis of the mere appearance of respiratory signs. Other clues like level of mortality, % morbidity, presence of other clinical signs and clinical history are important for an initial stab at diagnosis. Gross pathology may provide further clues but caution should be practised since obvious pathology like perihepatitis and pericarditis usually associated with E.coli are also encountered in Pastuerellosis, Streptococcosis, Chlamydiosis, CRD and Ornithobacterium rhinotracheale. Gross pathology may not be present in acute cases especially when the organism excretes endotoxins or its presence may actually be a result of secondary infection.

Earlier accounts of some diseases like F cholera (9), indicated that different clinical signs predominated in different geographical areas of Australia. In Qld the respiratory manifestations of F cholera were more commonly observed while in Victoria it was the encephalitic form.

In all the bacterial infections that are listed above respiratory signs ranging from runny eyes and nostrils to wheezing, sneezing, gasping and mortality may be encountered. However, for example, the presence of significant mortality among chickens would suggest that Infectious Coryza, CRD and possibly Chlamydiosis or Ornithobacterium rhinotrachelis are not serious contenders on the differential diagnosis list.

While a unilateral swelling of the face in chickens may indeed indicate presence of Haemophilus paragallinarum, the absence of such a swelling but presence of runny nostrils does not indicate that it is CRD or other bacterial infection in preference to Coryza.

Successful culture of some organisms may also present a challenge for both the submitter and the laboratory. For the submitter; to submit the appropriate range of specimens and for the laboratory- to ensure that the growth requirements provided are optimal and do not restrict the rate of successful culture. Distances to the laboratory and transport conditions are also an important aspect in the rate of successful diagnosis. For example, Haemophilus can be inactivated rapidly outside the live bird, and at a temperature of 370C the window of opportunity for survival is only 24 hours. At 40C the survival of H. paragallinarum may not be beyond 48 hours. Doing a post-mortem in the middle of summer and leaving the designated lab tissues unchilled for longer than 10 minutes maybe all that is required to ensure that a positive case of infectious coryza is not diagnosed.

Mycoplasma requires very specific transport and storage conditions including temperature and time. Tissues must be transported on dry ice until ready to be cultured.

Both E. coli-colibacillosis and Streptococcosis are considered secondary pathogens and likely to be associated with damage to the respiratory tract by other organisms and /or stress factors. However, it is important to consider that especially Colisepticemia as a result of inhaled E. coli contaminated dust can easily occur and furthermore, lesions of Colisepticemia have been produced readily and quickly following inoculation of pathogenic E. coli into the air sacs of healthy chickens.

Dismissing E. coli as a primary pathogen requires careful considerations.

Chlamydiosis is often excluded in cases involving respiratory signs of poultry. The disease is believed to be rare in chickens world-wide but more common in ducks and turkeys. Is this really the case?

There have been two scientifically documented cases of infection in Australian poultry flocks, which were associated with clinical signs and increased mortality (6,7). Several cases in poultry have been reported over the years in both commercial and small flocks of chicken in NSW. On average, between 1990 and 2007, each year 1 cases of Chlamydiosis was reported in commercial and backyard chickens in NSW. Some of the cases in poultry were associated with the diagnosis of infection in the owners. Additional human cases were traced to non-clinical presence of Chlamydiosis in flocks.

Mortality varied between flocks ranging from no increase in mortality to 7% - 10% mortality in commercial young pullets. Morbidity also varied and in some cases up to 20% morbidity was reported. Clinical signs vary between cases and included; conjunctivitis (dry and wet), birds continuously scratching their eyes, blindness, periorbital swelling, nasal discharge, cough and gasping. On autopsy significant variation was noted and the following were observed; Interstitial pneumonia, tracheitis, airsaculitis, pericarditis, perihepatitis and splenomegaly. These cases could have been easily confused with E coli, Coryza, ILT and other respiratory diseases.

PCR is often offered as a diagnostic test in lieu of the more expensive IFAT but "this test is not species-specific and has not been fully assessed for diagnosis of chlamydiosis in poultry, nor has it been validated for its capacity to detect Chlamydophila spp in specimens other than conjunctival swabs" (8). Over the years our Chlamydia cases were diagnosed by histo, (elementary bodies), egg isolation and more recently because of OH&S issues the IFAT (Immunofluorescent Antibody test) has been used to confirm infection in chickens.

For IFAT, impression smears on special slides are required.


In cases of Aspergillosis, signs can vary but when respiratory signs are present they may be associated with nervous signs including torticollis and imbalance. Gasping may be present with or without nasal excretion and runny eyes. Unlike ILT, the mortality in adult poultry is low and the disease can be easily confused with IB and other respiratory pathogens if an autopsy is not done.

On autopsy small white caseous nodules should be present in lungs and air sacs, especially in turkeys and to a lesser degree in chickens. In chickens diffuse grey yellow discolorations of the lungs is more likely with mucopurelent exudates present in the air sacs. Ascites may also be present with pulmonary Aspergillosis in chickens.

Image of chicken lungs <em>post-mortem</em>


It is not intended to cover these causes in detail and the reason that the three are mentioned is to remind investigators that respiratory signs can be associated with parasitic infection or with non-infectious causes. Physical and nutritional causes of respiratory signs in poultry may be more common than the parasitic ones.

It is believed that Gape worms have not been reported in poultry in Australia although the parasite was reported in imported aviary birds. The appearance of laboured breathing and eventually suffocation can be associated with the presence of gape worms in the trachea which leads subsequently to the development of inflammatory reactions and the presence of nodules in the trachea or other parts of the respiratory system.

Trichomoniasis is uncommon in poultry but not in pigeons. It produces small caseous nodules along the oral cavity, oesophagus, proventriculus as well as the conjunctiva sinuses and larynx.

Vitamin A deficiency results in the formation of dry diphtheritic membranes in the trachea and small nodules and pustules in the trachea and oesophagus. Clinical signs may resemble Coryza, Fowl pox.


More likely to be encountered in confined flocks but small flocks housed in poorly ventilated, wet, over crowded facilities overnight may suffer from Ammonia exposure.

Exposure to high concentration of ammonia may result in damage to the upper respiratory tract with possible photophobia and excess lacrimation. and constant attempts to rub the eyes. The damage to the respiratory tract may increase the likelihood of secondary infection.

Lime toxicity is likely to manifest itself as ulcerative changes along the GI tract. However, it may impact on the respiratory tract ; runny eyes as well as severe conjunctivitis can be encountered.


  1. Science.discovery.com Accessed 13/12/12
  2. Codd et al Avian like breathing mechanics in maniraptoran dinosaurs Proc R Soc. B 2008; 275; 157- 161s
  3. Wedel MJ, Evidence for bird-like Air-sacs in Saurischian dinosaurs. The J of Experimental Zoology 311A 2009;1-18
  4. Fedde MR Relationship of structure and function of the avian respiratory system to disease susceptibility. Poultry Science 1998, 77: 1130-1138
  5. Fossum et al Causes of mortality in laying hens in different housing systems in 2001 to 2004. Acta Veterinaria Scandinavica, 2009, 51;3
  6. Arzey & Arzey, (1990), Chlamydiosis in layer chickens. AVJ, 67(12) 461
  7. Barr et al, Isolation of Chlamydia psittaci from commercial broiler chickens Australian Veterinary Journal 63(11): 377-378
  8. Robertson et al Investigations of the prevalence of Chlamydiosis in the Australian chicken meat industry. 2011,RIRDC Publication number 11/073 rirdc.infoservices.com.au
  9. Hungerford TG Diseases of Poultry Published by Angus and Robertson 1969, page 286-299


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