Equine asthma (EA) is a condition of chronic lower airway inflammation in response to inhaled aero-allergens. Affected horses present with varying clinical signs depending on severity of airway inflammation and modelling.

This condition, which is arguably one of the most common, non-infectious lower airway diseases affecting horses globally, causes a spectrum of disease from mild subclinical poor performance without overt signs of airway disease in its mildest form, through to severe respiratory embarrassment and distress at rest in its most severe form. Therefore, classification into mild, moderate and severe is based on clinical signs and presentation, cytological airway inflammation/leukocyte profile and mucus production.

Importantly, while horses with mild and moderate EA may recover completely, horses with severe EA typically have more advanced airway modelling and do not completely recover, although successful management is achievable.

While respirable dust is considered the most common inciting trigger, other aero-allergens exist too, including pasture-associated allergens, which can trigger development of EA. Irrespective of the therapeutic interventions in place to manage EA in any of the three forms, it is important to note that airway inflammation will be ongoing and/or recurrent if environmental modifications are not in place to reduce, or eliminate, exposure to the inciting aero-allergens.

Types of equine asthma

EA can be classified as mild, moderate or severe; both mild and moderate EA result in clinical signs that are only evident during exercise, while severe EA results in respiratory signs at rest.

In all cases, reduced performance (either clinical or subclinical) and a degree of exercise intolerance with prolonged exercise recovery periods typically feature, as well as variable cough^1-3.

The concept that mild EA may be present in horses with no overt respiratory signs, but as a cause of poor performance in high-performing animals, has been widely accepted over the past decade, although this milder form of asthma can be easily overlooked given the absence of signs directly localising to the respiratory tract⁴.

Similarly, moderate EA results in reduced or poor performance, although clinical signs of coughing and/or respiratory dysfunction, such as increased respiratory effort with exercise or protracted exercise recovery times, help to localise the reduced performance to the respiratory tract. This, therefore, delineats mild from moderate EA.

Clinical diagnosis of all forms of EA is based on an increased tracheobronchial mucus score visualised endoscopically and aberration in the leukocyte profile obtained in bronchoalveolar lavage fluid³. Within the mild-moderate EA, various different forms of lower airway inflammation occur; these include airway hyper-responsiveness associated with increased numbers of metachromatic cells, such as mast cells and eosinophils, more commonly seen in young horses, or neutrophilic inflammation, typically affecting older horses³.

Two key clinical differences are important to note between mild-moderate EA and severe EA: mild-moderate EA is a reversible condition where severe EA is not, and severe EA results in clinical signs of respiratory dysfunction at rest (increased respiratory rate, effort; in chronic cases, the presence of a “heave line”). Severe EA typically affects horses aged seven years or older, and while it is irreversible, clinical remission is achievable and is the goal of treatment^3,5,6. In this form of EA, chronic airway inflammation leads to remodelling within the distal airways, including fibrosis, leading to bronchiolar collapse, air trapping and hyperinflation of alveoli^2,3,7. This chronic remodelling leads to development of exaggerated respiratory effort, both during exercise and at rest, with expiration more pronounced than inspiration due to the air-trapping.

While abnormal auscultation findings are inconsistent and less common in cases of mild-moderate EA, identification of crackles and wheezes is more common in severe EA.

A fourth variation of EA is summer pasture-associated recurrent airway obstruction (SPRAO), which, while it can be severe, is typically reversible. This form is seasonal and associated with pasture exposure rather than stable or feed dust. The two main temporal forms seen globally are during warm weather in humid climates, such as SPRAO in North America; or during dusty and dry periods where stubble burning or crop harvesting is occurring, such as SPRAO in the UK⁴.

A response to altered environment (such as stabling rather than pasture turnout) is typically effective at improving clinical signs and aids in differentiation of EA diagnostically.

Causes of EA

EA is an immune-mediated inflammatory response to inhaled aero-allergens that is localised to the lower respiratory tract. The stable environment contains high levels of respirable aero-allergens compared to outdoor environments, and both stable bedding and feed dusts are high in aero-allergens.

The inflammation is commonly neutrophilic, although other forms such as metachromatic and eosinophilic also occur; and when dysregulated, can be proinflammatory in itself⁸. The inciting aero-allergens (with the exception of SPRAO) are respirable organic particles such as endotoxins and exotoxins, mould spores, dust mites, ammonia and pollen, all of which are commonly found in bedding materials and routine horse feeds^{8, 9}. Exposure in susceptible horses triggers components of both a type I and type III hypersensitivity, leading to airway hyper-responsiveness with obstruction to the lower airways and altered gas exchange, and consequently, exercise-induced hypoxaemia and reduced performance³.

With chronicity and severity, the increased mucus secretion and accumulation induce more severe bronchoconstriction and bronchiolitis that leads to airway remodelling and irreversible pulmonary changes^4,10.

Early intervention is aimed at controlling neutrophilic inflammation, because while these cells are important first-line responders in the face of inflammation, a dysregulated response can be detrimental. Neutrophils release reactive oxygen species and neutrophil extracellular traps that – particularly during a dysregulated response – can cause exacerbation of tissue damage and, consequently, bronchoconstriction, mucus hypersecretion and airway remodelling^8,11.

SPRAO, while not fully understood, is thought to be triggered by exposure to grass pollens and a Th2 response with subsequent Th17 response. Irrespective, it is the triggered neutrophilic inflammation that, with chronicity, results in the disease⁴.

Management of EA

Environmental modifications

Irrespective of any therapeutic interventions, environmental management is the cornerstone of maintaining remission in horses with EA.

In the absence of effective environmental modifications and management, recurrence of EA is likely as soon as any therapeutic interventions are discontinued, assuming clinical control is achieved; in more severe cases, it may not be despite therapy if the environmental triggers remain.

Aero-allergens within the stable bedding and feed are considered the primary triggers for horses with EA due to their contribution to the increased dust in the respirable zone for stabled horses. The concentration of dust was found to be nearly 10-fold higher in stabled environments compared with pasture environments¹².

Likewise, in one study, 81% of the elevated respirable dust measurements occurred during mucking out of the stable or, interestingly, mucking out of the adjacent stable^{9, 13}. This highlights the importance of ensuring horses are removed from the barn when any stable activity is occurring, to reduce exposure to respirable aero-allergens.

Stables that have an open upper door – particularly if externally positioned – are preferred, as they allow respite from the dust⁹. Likewise, the respirable dust is typically lower in stand-alone stables compared to barns with multiple stables, where the respirable dust concentration may be increased 45-fold in barns of 16 or more horses, according to one study¹³.

The bedding used also plays a role, with sawdust and shavings associated with high levels of aero-allergens compared to low-dust bedding such as wood chips, paper or peat¹⁴.

High-dust bedding matter, such as straw and shavings, are associated with increased coughing and increased rates of requirement for therapeutic intervention, compared with low-dust alternatives such as wood chips or peat⁹.

Similarly, hay is another common source of respirable dust, with feeding of dry hay – particularly from round bales – associated with increased airway neutrophil and mucus accumulation¹⁵. However, soaking and steaming hay can be an effective means of reducing respirable dust, with reductions in dust concentrations of 93% to 95% reported for soaking hay for 10 to 30 minutes, or steaming for 80 minutes^13,16. Protracted soaking periods, such as overnight, have not been found to further improve the respirable dust content when compared to short 10 to 30-minute soaking periods; however, they do considerably reduce the nutrient content, which needs to be considered¹⁶.

In summary, it needs to be emphasised to horse owners and keepers that environmental management is a critical component of achieving and maintaining remission from severe EA, or reversing mild-moderate EA.

The optimum environment (with the exception of SPRAO) is pasture housing and feeding of pelleted rations if supplementary feeding is required. However, if additional fibre is needed, soaked or steamed hay is a good alternative to reduce respirable dust^13,15. If stabling cannot be avoided, bedding should be dampened regularly to reduce respirable aero-allergens; a low-dust bedding, such as woodchip or peat, should be used¹⁶; and horses should be removed from the stable during periods of mucking out, including of adjacent or neighbouring stables¹³.

Compliance is often difficult, but emphasising the known increases in respirable dust concentration associated with common practices such as mucking stables, feeding hay and common bedding substrates – in comparison with the alternatives of turnout during cleaning, soaking or steaming hay, and low-dust stable bedding alternatives – may help to highlight the importance of this component of EA management.

Therapeutic interventions

Alongside environmental modification and management, therapeutic interventions are commonly required as part of reversing the inflammation in mild-moderate cases of EA, or to induce remission during exacerbations of severe EA or SPRAO.

Therapeutic interventions can be broadly divided into bronchodilators and anti-inflammatory medications, both of which can be administered either systemically or via inhalation. As the clinical signs seen in horses with EA – particularly severe EA – are largely reflective of bronchoconstriction, bronchodilators are considered an essential part of rescue therapy for horses with severe EA. However, their role is in relief of bronchoconstriction, with no effect on treatment of the underlying lower airway inflammation. Consequently, their use should be alongside anti-inflammatory treatment in the form of corticosteroid administration and environmental management, unless corticosteroid administration is contraindicated, in which case they may be used as sole therapy.

In the face of an acute exacerbation of severe EA, bronchodilator administration results in rapid bronchodilation and relief of airway spasm. Intravenous N-butylscopolamine (buscopan) and atropine are administered respectively^{2, 6}. Alongside alleviation of bronchospasm, bronchodilation enables clearance of mucus plugs and obstruction from the lower airways². Due to the limited systemic side effects in comparison to atropine, N-butylscopolamine is now considered the preferred rescue therapy. However, due to their short duration of action and effects beyond the respiratory tract, these bronchodilators are appropriate for rescue therapy rather than short-term therapeutic intervention, with medications such as the beta2-agonists salbutamol (via inhalation) and clenbuterol (via oral administration) considered more appropriate for short-term therapy¹⁷.

In comparison to N-butylscopolamine, salbutamol provides a similar potency of bronchodilation without cardiovascular or gastrointestinal effects¹⁸. Efficacy of bronchodilators is typically most predominant in the first two to four weeks of treatment, with some horses becoming refractory to prolonged treatment¹⁷ and, as such, their use is most appropriate early and in conjunction with corticosteroid treatment and environmental modification.

Alongside bronchodilator therapy, anti-inflammatory therapy is indicated to reduce airway inflammation. Systemic administration of corticosteroids continues to provide the most profound and rapid alleviation of inflammation – particularly during acute exacerbations of severe EA^2,19,20.

However, systemic administration carries the increased risk of systemic side effects, including suppression of the HPA-axis, immunosuppression and an anecdotal risk of laminitis development. Preferably, inhalational administration can replace systemic administration of corticosteroids within one to two weeks of treatment to reduce systemic side effects.

The options available for inhalational corticosteroid therapy include fluticasone propionate via a metered dose inhaler (MDI), inhaled ciclesonide via a soft-mist inhaler, inhaled budesonide via nebulisation, or an MDI and inhaled beclomethasone. The latter is less often used clinically due to its reduced affinity for glucocorticoid receptors and suspected reduced potency in comparison to fluticasone²¹.

Previous recommendations have also included nebulised dexamethasone; however, recent studies suggest this is not efficacious^22,23 and is no longer recommended in the management of severe EA. Fluticasone via MDI has been shown to have a similar efficacy to systemic dexamethasone for management of mild-moderate EA²¹; however, systemic dexamethasone continues to be superior in the face of an acute exacerbation of severe EA.

Ciclesonide administered via the soft-mist inhaler provides delivery of this potent pro-drug to the airways. It is converted to des-ciclesonide on contact with the respiratory epithelium, resulting in potent glucocorticoid effects with minimal systemic side effects and no evidence of HPA-axis suppression²⁰.

Inhaled budesonide has also been shown to provide potent effects similar to systemic dexamethasone at high doses (1,800µg every 12 hours), and may be a suitable alternative to dexamethasone for clients already in possession of a nebuliser.

Dietary supplementation should also be considered as an adjunct therapy alongside environmental modifications and/or bronchodilators and anti-inflammatories – particularly in cases that are more challenging to manage or maintain in remission. Omega-3 polyunsaturated fatty acids can help to reduce airway inflammation and may be a suitable dietary supplementation in challenging cases³.

In summary, systemic administration of dexamethasone, unless contraindicated in an individual, should make up part of the initial treatment regimen in cases of severe EA, alongside environmental modification and bronchodilator therapy.

Transition to inhaled corticosteroids within one to two weeks is preferable to prolonged systemic treatment due to reduced systemic side effects.

In cases of mild-moderate EA, reversal of airway inflammation using inhaled corticosteroids alone or in combination with bronchodilators should be achievable in most cases.

Prevention of EA

True prevention of EA in predisposed animals is not always achievable. However, ensuring environmental management to reduce or eliminate risk factors for development of EA (primarily exposure to increased concentrations of respirable aero-allergens) not only improves animal welfare, but also reduces the risk of the development of EA. This is considered the most effective means of prevention of EA.

Likewise, in horses previously diagnosed with any form of EA, prevention of exacerbations or recurrences involves vigilant environmental management and avoidance of increased concentration of aero-allergens.

In horses with known history of SPRAO, avoidance of pasture during high-risk periods, such as warm weather, can also help to reduce recurrence. Additionally, avoidance of comorbidities such as insulin dysregulation and obesity, along with having their own benefits, may also reduce the risk of EA development.

Conclusion

In summary, EA can be a severe and debilitating condition affecting equids globally.

The management is centred around environmental modifications to reduce exposure to respirable aero-allergens through alteration in stable management practices, bedding substrate and feeding practices.

Alongside this critical step, various therapeutic interventions can be used to help reduce airway inflammation with the goal of reversal of mild-moderate EA and induction of remission in severe EA.  In horses with a previous history of EA in any form, ongoing, lifelong environmental management is critical.

A very strong argument exists that prioritising good ventilation, high stable hygiene practices (removing horses from the stables or barn during cleaning, and use of low-dust bedding substrate) and feeding of low-dust feed alternatives such as haylage or pelleted feeds during stabling improves welfare in all stabled horses, in addition to reducing the risk of EA development or exacerbation.

Use of some of the drugs in this article is under the veterinary medicine cascade.

• Appeared in Vet Times (2025), Volume 55, Issue 14, Pages 8-14