Management of Suspected Airway Disease in Dogs


RCVS Specialist in Small Animal Medicine
Davies Veterinary Specialists
Manor Farm Business Park
Higham Gobion, Hitchin

Do you think you have seen a dog with ‘hay fever’ or ‘asthma’? It is well accepted that allergic responses can trigger respiratory tract signs in humans and allergic triggers are suspected to underlie feline allergic bronchitis (‘feline asthma’). In dogs, however, the potential for allergy as a trigger for respiratory signs is less generally accepted and gains little mention in standard veterinary text books, which understandably concentrate on the more readily characterised disorders such as chronic bronchitis, neoplasia and infection. Since allergic disease is accepted as a cause of dermatological signs and gastrointestinal signs, for example, there is no reason to suppose that allergy could not trigger airways signs in dogs, as it does in humans and other veterinary species. Published reports support this conclusion (Corcoran and others 1991, Clerx and others 2000).

Clinical signs associated with inflammation and irritation of the anatomic regions of the airway are outlined in table 1. With all signs, of course, a wide differential diagnosis must be considered. Additional features that might indicate a possible allergic trigger include a seasonality or variability in clinical signs. As with ‘hay fever’ in humans, pollen may be an aeroallergen for dogs and clinical signs may be worse only at certain times of the year. Similarly, signs may be triggered by exposure to allergen in certain areas of the normal environment. Allergic disease is typically characterised by the presence of eosinophils in inflammatory infiltrates of tissue, representing an inappropriate acute response to benign antigens as a result of immune sensitisation. In nature these responses are typically directed at parasites such as intestinal helminths, and an important tenet of clinical management of all cases where allergy is suspected is to ensure that there is no associated parasitism either through diagnostic testing, therapy or both. Suspected and known causes of hypersensitivities in humans and animals include fungi, drugs, bacteria, food proteins, pollens, dust mite proteins and animal dander (Clercx and others 2000). For allergic airway disease, there are no specific diagnostic tests available to identify either allergy or the triggering allergen, other than exposure:withdrawal:exposure regimes. Unfortunately, unlike the skin, the airways are not amenable to localized exposure testing, and this could, potentially, trigger serious and life-threatening responses. It is unusual, therefore, to be able to definitively identify possible triggers. The suspicion of allergy, however, is increased upon identification of an eosinophilic component in diagnostic samples such as nasal flushes, pharyngeal swabs and broncho-alveolar lavage, although the presence of eosinophils should not be considered an absolute prerequisite.

Therapeutic options for suspected airway diseases include allergen avoidance, irritant avoidance, anti-inflammatory therapy and palliative therapy such as bronchodilation. Allergen avoidance may be possible if a specific trigger can be recognised, and a process of trial and error in exposing the patient to various regions of its normal environment may help. Similarly, a small proportion of cases appear to respond to exclusion diets, and there is a justification for a diet trial in most cases (Corcoran and others 1991). In all cases of inflammatory airway disease, additional irritants should be avoided if at all possible, including tobacco smoke, house dust and other noxious and irritating substances a dog might be exposed to through typical indiscriminate sniffing. Anti-inflammatory drugs, particularly corticosteroids, are an important tool in managing airway inflammation and can be administered orally or by inhalation (see on). Similarly, bronchodilators (methylxanthines, beta-2 agonists) may be administered to relieve bronchospasm when there is small airway involvement and both oral and inhaled medications may be used.

In this article, I will use some case examples to illustrate where allergy appeared to play a role in the generation of a variety of clinical signs related to the airway and a range of options for therapy.


‘Jethro’ a seven year old male English bull terrier

Jethro presented with a complicated medical history including chronic allergic skin disease, hypoadrenocorticism and lungworm, which had been appropriately treated. The presenting complaint was of expiratory dyspnoea and coughing. On examination Jethro was bright and alert and in good to slightly obese body condition. There were marked crackles over both lung fields and Jethro demonstrated a wheezy cough during the consultation. Haematology showed a mild neutrophilia, lymphocytosis and monocytosis, consistent with chronic inflammation. Thoracic radiographic examination showed a generalized bronchointerstitial pattern (figure 1). An echocardiographic examination was unremarkable. No lungworm larvae were found in faeces. A bronchoscopic examination showed excess airway mucus and dynamic small airway collapse. A BAL grew no organisms and on cytology there was mild neutrophilic inflammation. Possible underlying causes for the bronchitis were considered to be allergy, infection or irritation. Notwithstanding the lack of a specific identified trigger, anti-inflammatory and bronchodilator therapy was indicated and, to avoid complicating the management of Jethro’s other medical conditions, he was considered a good potential candidate for inhalation therapy. Jethro was weaned onto inhaled budesonide (Pulmicort, AstraZeneca) 100µg twice daily and salbutamol (Ventolin, Allen and Hanburys) 100µg three to four times daily, according to instructions shown in box 1. [Note that Pulmicort is presently unavailable and fluticasone (Flixotide, Allen and Hanburys) appears an acceptable alternative]. Jethro was re-examined five weeks later, when the owners reported that there had been no difficulty in getting Jethro to accept inhaled treatment. They reported minimal coughing and markedly improved exercise tolerance. Examination revealed some expiratory effort and occasional crackles were audible over the ventral lung fields. A repeat thoracic radiograph showed a marked reduction in the lung pattern previously noted (figure 2). The owners were advised that they could withhold salbutamol unless needed for bronchospasm relief and to maintain once daily budesonide inhalation for continued suppression of inflammation in the airway.


Corrie, a five year old female neutered border collie

Corrie presented with a history of exercise intolerance and occasional wheezing and low grade coughing. The owner was a keen hill walker and had noticed a reduction in Corrie’s normal stamina on long walks, although Corrie was well able to tolerate ‘normal’ exercise. She was otherwise considered to be well with no other clinical signs. Clinical examination was unremarkable. Haematology and biochemistry screens were unremarkable. Faecal parasitology was negative. Thoracic radiographs showed a mild generalized bronchial pattern and, on bronchoscopic examination, there was hyperaemia of the bronchial mucosa. A BAL revealed a mild, mixed neutrophilic-eosinophilic inflammation with no organisms. An allergic bronchitis was suspected and, to explore possible triggers, a turkey and rice exclusion diet (James Wellbeloved turkey and rice kibble) was started. Within two weeks the owner reported a marked improvement in clinical signs and, after a further two weeks, re-introduction of a normal diet was associated with a noted deterioration. An exclusion diet was maintained and Corrie was considered well and normal for four years. She represented after four years because of a recurrence of coughing and exercise intolerance, and repeat investigations suggested a recurrence of eosinophilic-neutrophilic bronchitis. This did not respond to dietary management at this point, so therapy with inhaled budesonide and salbutamol was initiated and a good response was identified by the owner, with reduced coughing and panting and improved exercise tolerance.


Ellie, a two and one half year old female golden retriever

Clinical signs in this dog were difficult to define. The owner complained that there was exercise intolerance, abnormal breathing and a dark tongue colour on exercise. Ellie was also reported to have a tendency to gag and cough after drinking. Previous history included a possible, but unconfirmed, myopathy and von Willebrand’s disease. On examination Ellie was bright, alert and responsive and in good general condition. Rectal temperature and pulse rate and strength were normal. There was a tachypnoea with shallow breathing at a rate of 50 breaths per minute, with a suspicion of increased inspiratory and expiratory noise. Haematology and biochemistry panels were unremarkable and no parasites were apparent on faecal examinations. Thoracic radiographs showed a very mild bronchial pattern. A bronchoscopic examination was unremarkable but there was a nodular change with hyperaemia in the nasopharynx, the mucosa of which bled readily. A BAL grew no organisms but cytology showed a mild excess of mucus with neutrophils, lymphocytes, eosinophils and alveolar macrophages, consistent with a possible allergic bronchitis. It was suspected that there was an associated allergic pharyngitis. Initial treatment was prednisolone 0.5 mg/kg BID, but there was no perceived response to this after 10 days and the owner was reluctant to continue this management. The owner was, however, keen to try inhalation therapy, which was started with budesonide 100µg BID and salbutamol 100µg QID. After 10 days the owner reported a very good acceptance and tolerance of the therapy by Ellie and a noticeable improvement in her demeanour, breathing and exercise tolerance, with a reduction in signs of swallowing and coughing after drinking. The owner was extremely happy to see improvement after a number of months of anxiety.


Bailey, a one year old male golden retriever

Bailey presented with a history of fever, tachypnoea and malaise, with coughing. On examination he appeared anxious and was tachypnoeic (40 breaths per minute), pyrexic (39.2 Celsius) with reluctance to rise. Haematology was unremarkable apart from a mild monocytosis; biochemistry screens were unremarkable and urinalysis was normal. A thoracic radiograph showed a moderate-to-severe patchy broncointerstitial pattern. Bronchoscopy revealed mucosal hyperaemia and a BAL showed a predominance of eosinophils with some neutrophils and alveolar macrophages, consistent with eosinophilic bronchopneumopathy. Pending results, Bailey was supported in the practice and showed signs of spontaneous recovery. Following discharge to the normal home environment, however, there was a rapid deterioration in signs with worsening malaise, dyspnoea and fever. Suspecting a possible environmental trigger, further careful questioning of the owner was undertaken and it was established that Bailey was exposed to cats and relatively high levels of house dust because of home renovation works. After a further period of stabilization, we explored this possibility by an unscientific exposure to cat dander by temporarily placing Bailey in a room with cats present, and on the two occasions this was attempted there was a doubling of resting respiratory rate from 20 to 40 per minute within ten minutes of starting, suggesting a possible allergy to cat dander. Bailey was subsequently treated by removing him from sources of cats and minimising house dust exposure, and with inhaled budesonide 100µg BID and salbutamol 100µg four times daily, supplemented initially by prednisolone 1mg/kg orally twice daily, reducing to 0.25mg/kg every other day. A good initial response was seen and Bailey was ultimately managed with long term inhaled therapy and allergen avoidance alone. Careful explanation of allergy and possible triggers greatly facilitated environmental control in this case.


These four cases illustrate the principles behind diagnosis and management of suspected allergic airway disease in dogs as well as the range of possible presentations. When managing these cases careful explanation of the principles underlying therapy is essential to engender owner compliance in potentially daunting therapy. Experience suggests, however, that with support and encouragement owners and their dogs can achieve effective management in many cases. Inhaled therapy, in particular, offers many potential benefits in dogs, as has been clearly demonstrated in cats.



C. Clercx, D. Peeters, F. Snaps, P. Hansen, K. McEntee, J. Detilleux, M. Henroteaux, M.J. Day. (2000) Eosinophilic bronchopneumopathy in dogs. Journal of Veterinary Internal Medicine 14, 282-291

B.M. Corcoran, K.L. Thoday, J.I. Henfrey, J.W. Simpson, A.G. Burnie and C.T. Mooney (1991) Pulmonary infiltration with eosinophils in 14 dogs. Journal of Small Animal Practice 32, 494-502


Owner instructions for inhalation therapy Equipment

Pulmicort Evohaler, budesonide 50 micrograms/metered inhalation
Flixotide Evohaler fluticasone proprionate 50 micrograms/metered inhalation

Ventolin Evohaler, salbutamol 100 micrograms/metered inhalation

Aerodawg inhaler and mask


Initial dose

Flixotide (anti-inflammatory): 1-2 actuations (100 micrograms) twice daily (medium sized dog)
Ventolin (bronchodilator): 1-2 actuation 3-4 times daily if needed for bronchospasm relief (medium sized dog)



Follow instructions on inhaler regarding storage and preparation for drug delivery. Place mask on spacer and inhaler into other end. Hold mouth closed and gently place device over nostrils, allowing breathing via spacer. When breathing is calm and steady, initiate dose by pressing inhaler. Allow 30 seconds of breathing to inhale dose from spacer. Rest for 30 seconds, repeat for second dose, if necessary.



A period of acclimatisation to the technique may be necessary before this procedure will be tolerated. Start by introducing the mask to patient, placing it on their body then on the head in a gentle fashion, so he/she learns not to be afraid of the device. At the same time, let them see and get used to the presence of the spacer and inhaler. Initially from a distance, and then moving closer, activate the inhaler so that he/she becomes used to the noise associated with this. This process should last a few days. When they appear comfortable with the mask, place it over the nose with the mouth closed so that they get used to breathing through it. Then add the spacer and repeat. Once they are comfortable with breathing through the mask and spacer, and used to the sound of the inhaler, try adding the inhaler and initiating a dosing. Individuals will vary with how quickly the procedure will be tolerated, but patience and gentle handling, with calm reassurance of the animal should be rewarded with acceptance.


Rhinitis Sneeze, nasal discharge (serous or mucoid). May be accompanying conjunctivitis
Pharyngitis Snorting, reverse sneezing, excessive swallowing, gulping and gagging.
Tracheobronchitis Coughing (often harsh and dry). Expiratory dyspnoea (if small airways involved). Exercise intolerance. Heat intolerance. Increased panting.
Pneumonitis Coughing (often deep and soft), inspiratory and expiratory dyspnoea, malaise, fever.

Table 1
Signs associated with possible allergic airway disease


Figure 1
A right lateral radiographic projection of the thorax of a seven year old English bull terrier with inflammatory airway disease, showing a diffuse bronchointerstitial lung pattern.


Figure 2
A follow-up radiograph of the same dog in figure 1, five weeks after commencing treatment with inhaled corticosteroid (budesonide) and bronchodilator (salbutamol). There is a marked reduction in the severity of the changes seen.