Respiratory problems are a common presentation in companion parrots. Clinical signs vary depending on the cause and can include sneezing, coughing, nasal and ocular discharge, voice changes and noisy breathing. Severely affected birds can also develop open-mouth breathing, tachypnoea and tail bobbing. Some parrots can mimic human coughs and sneezes but do not have respiratory problems, and others may hyperventilate when stressed or upset. Therefore, it is important to distinguish whether birds presenting with respiratory signs are clinically unwell. Early recognition of clinical signs combined with rapid diagnosis and appropriate therapy can improve patient outcomes. Several common causes of respiratory signs in companion parrots are discussed below; however, this list is not exhaustive.
Aspergillosis is the most common mycotic respiratory disease in psittacine birds (Martel, 2016). It is usually considered an opportunistic disease. Many birds exposed to Aspergillus spores do not develop disease; however, infection can occur if a bird is exposed to an overwhelming number of spores or is immunosuppressed. Immunosuppression is usually the result of stress or poor husbandry.
Several Aspergillus species have been reported to cause disease; however, the most common is Aspergillus fumigatus. Common sources of infection include damp or mouldy feeds, such as seeds or nuts, poor cage hygiene and poor ventilation. The most commonly affected parrot species appear to be African grey parrots, blue-fronted Amazon parrots and Pionus parrots (Oglesbee, 1997).
Clinical presentation of aspergillosis can be classified into two forms: acute and chronic. The acute form is thought to be caused by inhaling an overwhelming number of spores (Carrasco and Forbes, 2016) and usually results in acute depression, dyspnoea and anorexia (Martel, 2016). Obstructive granulomas within the trachea can cause a change in voice and obstruct the airway, causing acute dyspnoea and death. The chronic form is generally associated with immunosuppression (Carrasco and Forbes, 2016). Clinical signs are generally non-specific, including anorexia, lethargy, vomiting, polydipsia, polyuria, weakness and a fluffed appearance (Figure 1).
Diagnosis can be difficult as no one specific test provides certainty of infection. Aspergillosis can cause profound heterophilic leucocytosis, anaemia and elevation of liver enzymes and bile acids on blood work. However, some birds do not mount an immune response, and haematology can be normal (Doneley, 2016a). Serology can show whether the bird has been in contact with the fungus but will not be able to suggest whether it is an active infection, long-term exposure or past infection. Endoscopy is a useful tool to visualise the air sacs and lungs and to identify any fungal plaques. Samples can be taken during endoscopy for cytology and culture. Radiographs can also aid in diagnosis; however, radiographic features are usually only seen at the later stage of infection. Bronchopneumonia with a prominent parabronchial pattern and thickening of the air sac walls can be observed on the images. In some cases, distinct nodular lesions can also be seen (McMillan and Petrak, 1989).
Aspergillosis can cause profound heterophilic leucocytosis, anaemia and elevation of liver enzymes and bile acids on blood work. However, some birds do not mount an immune response
Treating aspergillosis requires prolonged antifungal therapy that can last for six months or longer (Martel, 2016). Combination therapy using both systemic and topical (or nebulised antifungal) medication is preferred. Surgical debulking of the granulomatous material may be needed. Patients often need supportive care for several days while anorexic or dyspnoeic. It is also important to correct the husbandry of the patients to prevent recurrence.
Avian chlamydiosis (Chlamydophila psittaci)
Avian chlamydiosis is a zoonotic infectious disease affecting birds, mammals and humans. It is caused by Chlamydophila psittaci, an obligatory intracellular bacterium. The disease is referred to as psittacosis when it passes from parrots to humans. It can spread rapidly within a closed group of animals through a faecal-oral route or by inhalation. The disease can be shed in faeces, urine, and nasal and oropharyngeal discharge (Doneley, 2016b). Vertical transmission has also been documented (Olsen et al., 1990).
Clinical signs of chlamydiosis in birds are often non-specific but can include lethargy, anorexia, ocular and nasal discharge (Figure 2), sneezing, feather colouration changes, bright-green urates and green-yellow diarrhoea. In some cases, neurological signs or even sudden death can be seen. Affected birds can also become lifelong carriers and develop latent infection without any clinical signs but continue shedding the pathogen when stressed or immunocompromised.
Psittacosis may be suspected on radiography if the bird has hepatosplenomegaly and air sacculitis. Haematology often shows anaemia, marked leucocytosis and heterophilia. Samples from conjunctival, choanal and cloacal swabs or faeces can be used for PCR. Multiple samples should be collected over three to five days as the pathogenis shed intermittently (Crosta et al., 2016). Cytology of swabs or tissue can aid in diagnosis as Chlamydophila psittaci shows up with the use of Gimenez or Machiavello stains (Doneley, 2016b). Serology tests for the Chlamydophila antigen and antibody are also available. However, it is important to note that a positive result for the Chlamydophila antibody does not necessarily indicate the bird is a carrier of the infection as the bird can be in the latent stage and a high antibody titre may persist after treatment. It is therefore recommended to use the Chlamydophila antibody test in conjunction with a PCR to confirm an active infection.
Affected birds should be treated with a six-week course of tetracyclines, and good biosecurity should be practised to prevent the spread of the disease. The patient should also be retested two to three weeks after the treatment ends.
It is […] recommended to use the Chlamydophila antibody test in conjunction with a PCR to confirm an active infection
Rhinoliths are firm plugs of debris that block the nares, resulting in breathing difficulties. They usually form secondary to sinusitis or rhinitis. Hypovitaminosis A also plays a significant part in this condition as it leads to keratinisation of the mucous membrane lining of the respiratory tract (Orosz, 2014). Rhinoliths can cause progressive and permanent damage to the soft tissue and bone of the nasal passages if not removed.
Removal involves gentle traction under sedation or general anaesthesia, with nasal flushing as required, ensuring the patient has a protected airway. Systemic therapy is not often required but should be started based on cytology and the results of culture and sensitivity. If the anatomy of the nasal passage is permanently altered (Figures 3A and 3B), the patients will be more prone to mucus accumulation and opportunistic infections. Regular nasal flush and nebulisation may be needed to prevent recurrence. Hypovitaminosis A should also be corrected, usually by transitioning the parrot to a pellet-based diet rather than a seed-based diet.
Avian species do not have a diaphragm, so they rely on the movement of the ribcage and sternum to create negative air pressure for gas exchange. They also have a system of air sacs that facilitate airflow through the lungs to increase oxygen exchange capacity and efficiency. Due to the absence of a diaphragm, any condition that puts pressure on the air sacs can reduce inspiratory volume and cause dyspnoea. Common non-respiratory-system problems that can cause hyperpnoea or dyspnoea include egg binding in female birds, coelomic organ enlargement, cardiac disease, ascites, intracoelomic masses and obesity (Figure 4).
Psittacine birds are sensitive to airborne toxins due to their efficient gas exchange system. They can absorb higher amounts of toxins from the air, and therefore reach a toxic dose earlier than mammalian species. Signs of toxicity can include open-beak breathing, cyanosis, bright-red mucous membrane, dyspnoea, nasal discharge, sneezing and coughing, etc. The most common household respiratory toxin encountered by birds is polytetrafluoroethylene (PTFE) from overheated non-stick cookware. Once clinical signs are present, the prognosis is usually very poor (Lightfoot and Yeager, 2008). Acute death can also occur after the exposure. Cigarette or bonfire smoke, candles and aerosols can have variable effects on birds depending on the level and chronicity of exposure, and a thorough history for patients presenting with dyspnoea should investigate the presence of these within the home.
Cigarette or bonfire smoke, candles and aerosols can have variable effects on birds […] and a thorough history for patients presenting with dyspnoea should investigate the presence of these within the home
Investigation of respiratory problems in psittacine birds should follow a similar diagnostic approach to that of dogs and cats. Culture, sensitivity and PCR tests are useful for diagnosing infectious diseases. Respiratory problems in psittacine birds are usually husbandry related; therefore, husbandry review and client education are important for prevention.