Recurrent Airway Obstruction

Also known as: RAO, chronic obstructive pulmonary disease, COPD, heaves.

Do not confuse with: summer pasture associated obstructive pulmonary disease.

Description

Recurrent airway obstruction (RAO) is an inflammatory, obstructive respiratory disease of horses. Disease is induced by the exposure of susceptible animals to organic dust, which gives neutrophil influx to the airways, bronchospasm and mucus accumulation¹. This causes a cough, nasal discharge, and respiratory difficulty. When exposure to the allergen is eliminated, obstruction and clinical signs resolove or attenuate. However, animals are susceptible to reccurent episodes of airway obstruction throughout their lives, and so management is essential.

Since disease required exposure to organic dust, recurrent airway obstruction occurs in stabled horses that are, for example, bedded on straw and fed hay. The condition is therefore most prevalent in the northern hemisphere because horses tend to be stabled for large parts of their lives². Summer pasture-associated obstructive pulmonary disease (SPAOD) is a similar condition that occurs when horses kept on pasture are sensitive to environmental allergens, and may be considered the same disease as RAO but with different inciting factors¹.

Pathogenesis

When a horse with a history of RAO is moved from pasture to a stable, the hay it is fed and the straw it is bedded on harbour organic dusts. These dusts contain components which are capable of causing inflammation of the lungs, such as specific allergens, endotoxin, moulds and small particulate matter¹. Although small particles and endotoxin are known to cause pulmonary inflammation, there is evidence to suggest that there is an allergic component to recurrent airway obstruction. For example, bronchoalveolar lavage fluid in RAO has been shown to have increased levels of IgE specific for various moulds^haliwell, and the cytokine response appaears to be skewed towards TH2^lavoi: both of these facts are suggestive of an allergic mechanism.

On exposure to dust, neutrophils accumulate in the lung and quickly invade the lumen of the airway¹. Aiway obstruction then develops due to several mechanisms. Mucus becomes more viscous and accumulates in the luman, and bronchospasm is initiated by the actions of inflammatory mediators on airway smooth muscle and cholinergic nerves^Olszewski. Oedema of the airway wall also contributes to narrowing, and in horses suffering chronic disease, the wall remodels to give mucus metaplasia, smooth muscle hypertrophy and peribronchial fibrosis^{1, allen}.

Signalment

RAO usually becomes apparent in middle-aged and older horses, and persists for life^allen. There is some evidence that there may be a genetic component to the disease, as many horses do not suffer RAO when they are housed in environments that can provoke clinical disease in others^marti.

Diagnosis

Clinical Signs

Mildly affected horses generally present with a history of occasional coughing and exercise intolerance. Signs become more obvious as the disease progresses. Tachypnoea is often seen, and there may be a mucopurulent nasal discharge. Severely affected animals show signs of respiratory distress at rest. These can include flared nostrils, wheezing, paroxysmal bouts of coughing and a laboured abdominal component to expiration. Chronically, marked dyspnoea increases energy expenditure and the animal may lose condition, as well as developing a "heave line" due to hypertrophy of the external abdominal oblique muscle^{allen, merck, ivis}.

merck Characteristic auscultatory findings include a prolonged expiratory phase of respiration, wheezes, tracheal rattle, and over-expanded lung fields. Wheezes are generated by airflow through narrowed airways, and are most pronounced during expiration. Crackles may be present and are associated with excessive mucus production. Mild to moderately affected horses may present with minimal clinical signs at rest, but coughing and exercise intolerance are noted during performance. Horses with RAO are not typically febrile unless secondary bacterial pneumonia has developed.

ivis On physical examination, clinical sings are restricted to the respiratory system. The nostrils may be flared and there may be a milky mucus discharge from the nose. Compression of the cranial trachea may reveal an increased sensitivity of the cough reflex. Abnormal lung sounds are heard to varying degrees depending on the severity of airway obstruction. In some severely affected animals, the lungs can be quite silent despite very strong inspiratory and expiratory efforts. This is because the airways are so obstructed that there is insufficient air movement to generate audible breath sounds. Usually however, breath sounds are increased at all levels of the airways but particularly over the peripheral lung fields. Wheezing is heard quite commonly but it is wise to listen for several breaths at many points over the lung because wheezing can be intermittent. Wheezes referred from deeper in the lung may be heard over the trachea and sometimes simply by listening at the nostrils. In horses that are less severely affected, ventilation may have to be increased by use of a rebreathing bag or exercise in order to hear abnormal lung sounds. Percussion will reveal increased size of the lung field in severely affected animals.

Pathology

COPD (Image sourced from Bristol Biomed Image Archive with permission)

COPD scanning electron micrograph (Image sourced from Bristol Biomed Image Archive with permission)

References

1. Robinson, N E (2001) Recurrent Airway Obstruction. In Equine Respiratory Diseases, IVIS.
2. Robinson N E et al (1995) The pathogenesis of chronic obstructive pulmonary disease of horses. The British Veterinary Journal, 152, 283-306.
3. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
4. Allen, K and Franklin, S (2007) RAO and IAD: respiratory disease in horses revisited. In Practice, 29(2), 76-82.
5. Halliwell R E W et al (1993) Local and systemic antibody production in horses affected with chronic obstructive pulmonary disease. Veterinary Immunology and Immunopathology, 38, 201-215.
6. Lavoie J P et al(2001) Neutrophilic Airway Inflammation in Horses with Heaves Is Characterized by a Th2-type Cytokine Profile. American Journal of Respiratory and Critical Care Medicine, 164, 1410-1413.
7. Marti, E et al (1991) The genetic basis of equine allergic diseases 1. Chronic hypersensitivity bronchitis. The Equine Veterinary Journal, 23, 457-460.
8. Olszewski M A et al (1999) Pre- and postjunctional effects of inflammatory mediators in horse airways. American Journal of Physiology, 277, 327-333.
9. McGorum, B et al (2007) Equine respiratory medicine and surgery, Elsevier Health Sciences.
10. Durham, A (2001) Update on therapeutics for obstructive pulmonary diseases in horses. In Practice, 23(8), 474-481.