Synonyms: Chronic Obstructive Pulmonary Disease
The chronic obstructive pulmonary disease denotes a complex range of chronic respiratory disorder originating primarily from lungs. The conditions which cause disruption of gaseous exchange in lungs include bronchitis, bronchiolitis, alveolitis, emphysema, fibrosis and neoplasia. Gerber (1973) opined that ‘heaves’ or ‘broken wind’ is symptom but not a disease as such above terms have seen discarded. Aristotle was perhaps the first man to describe the posterity, the characteristic abdominal expiratory effort associated with emphysematous condition in horses which is a chronic progressive condition affecting respiration, circulation and general condition characterized by an expiratory dyspnoea, chronic cough, intermittent nasal discharge, intestinal flatulence, unthriftyness and lack of stamina.
Distribution
The prevalence of the disease amongst horses in India is not exactly known. But, in a clinical survey in Northern Command over a period of five years a total number of 467 cases have been found to suffer from pulmonary disease out of 3161 horses.
Aetiology
Multifactorial aetiology has been suggested. The specific aetiology is still a point of discussion. Following factors have been included:
(a) Feeding: Feeding of dusty or mouldy hay, food grains may act as an inciting agent. Such induced condition has been ascribed as Farmer’s lung in horse.
(b) Inhalation of irritant fumes: McDonald (1971) stated that chlorine gas poisoning in farm animals may produce pulmonary emphysema. The fumes act by liberation of humoral substance from lung tissues or by direct action on nerve receptors or on contractile tissues are yet to be determined.
(c) Stabling: Jericho and Harrier (1975) reported that as a result of constant air pollution in barns, the inhalation always contain potentially irritating materials and the effect of such inhalation may cause emphysema in horse.
(d) Prostaglandins and drugs: Prostaglandin produced in the lungs are of two types e.g. Prostaglandin E and Prostaglandin F. Prostaglandin E causes bronchodilation and F causes bronchoconstriction. Drugs like aspirin inhibits both E and F series of Prostaglandin in lungs and may block the constrictor effect of F series on isolated bronchial muscles, thus may help in the development of the disease.
(e) Genetic factors: Little John (1977) observed that coat colour which is genetically transmitted, has significant relation with the distribution of respiratory diseases in horse. According to his opinion, all cases of emphysema are noted in chest nut coat colour. It was observed that mean globulin fraction of serum was significantly lower than those of normal horses and ponies. In India, Indian breed of horses are found to be most susceptible over Spanish and Italian.
(f) Infectious agents: The role of infectious agents in the aetiology of pulmonary disease is not perfectly defined. Gerber (1973) opined that chronic obstructive pulmonary disease result due to after effect of influenza virus where the horses continue to cough. McPherson and Lawson (19874) recorded pulmonary disease in mare after infectious respiratory disease caused by influenza A/equi-2 virus and Streptococcus zooepidemicus.
Susceptible Hosts
All horses irrespective of age and sex do suffer. According to Cook (1965) hunters and ponies are more likely to be affected than race horse. Mules are more susceptible.
Clinical Findings
This disease usually does not show any rise of temperature but moderate rise of temperature defined as ‘antecedent febrile illness’ have been recorded. In the initial stage, the horse maintains alertness, normal appetite and regular voidance of faeces. A short paroxysm of coughing may be observed in the morning after watering or following morning exercise. There may be moderate mucoid exudate discharge from nostrils. Development of dyspnoea following exercise will denote about emphysema. At this stage, double expiratory effort in breathing nasal discharge in affected horses. The discharge may be serous-mucoid-mucopurulent or blood stained in nature. Bilateral blood stained nasal discharge will positively indicate haemorrhage into the lungs. Race horses with early emphysema may develop exercise induced pulmonary haemorrhages, the so called ‘Bleeder’ and exhibit epistaxis.
Thorax on palpation may reveal a distinct apical impulse of the heart on the left side and if hypertrophy of the heart is marked it may be palpated on right. On percussion, the lung field is found to be expanded posteriorly due to distension of lungs and depression of the diaphragmatic cupola. Cook and Rossadale (1976) observed that auscultation near the nostril produces a clicking sound during early expiration caused by pulling away of the arytenoid cartilage from a sticky mucous covered pharynx.
Auscultation will disclose various sounds. The ventricular murmur is increased in magnitude in proportion to the severity of involvement. In early cases, dry rales are heard frequently and at times moist rales may be detected. In advance cases, sounds are characterised by sibilant, gurgling, wheezing and crepitant rales along with signs of pulmonary congestion.
Lesions
Gross lesion: On opening the thorax, lungs fail to collapse and are fully distended. The lungs are pale or greyish have lost their elasticity and drier than normal. Alveolar interstitial emphysema is prominent. The margins of the lobes are thickened and rounded. Chronic bronchiolitis is invariably present containing focal accumulation of tenacious, mucoid exudate.
Microscopic lesions: The normal pulmonary architecture is lost. The alveolar walls show atrophy. Alveoli are ruptured and there is union of adjacent alveoli to form a number of large, irregular air sacs. Much of the capillary network may disappear, resulting in marked decreased in the vascularity of the lung parenchyma. There is dilatation of bronchioles. A diffuse sign of bronchitis, bronchiolitis and peri bronchiolitis are visible.
Diagnosis
While reviewing the chronic obstructive pulmonary disease in man. Anon (1972) remarked that ‘it does not take a doctor to diagnose breathlessness’ in the same tune, it may be told that ‘it does not take a veterinarian to diagnose heaves in horse’. The diagnosis is based on clinical findings-expiratory dyspnoea.
(a) Administration of atropine: Sobti (1978) noted that administration of 8 to 16 mg atropine per 1000 pounds body weight subcutaneous injection will alleviate the dyspnoea in 20-30 minutes and persists for 3 to 4 hours.
(b) Exercise test: Horses suffering from this disease when subjected to exercise test, may show a very clear pathological increase in heart rate.
(c) Altered respiration function: In order to assess the respiratory function, partial pressure of arterial oxygen (PaO2) and maximum intrathoracic pressure change during breathing are done.
(d) Radiological examination: Plain radiography as well as use of radio-opaque tentallum powder blown into the airways may give reliable radiological evidence.
Treatment
- Treatment is mostly symptomatic aimed at correcting the signs.
- There should be provision of fresh air.
- Drugs used are bronchodilators e.g. Aminophylline, Deriphyllin, Salbutamol etc.
- Long term Cortico steroid may help in chronic cases.
- Systemic acidosis should be corrected with systemic alkalisers. (e.g Sodibi carbonate)
- Broad spectrum antibiotics e.g. Ampicillin, Erythromycin etc. may be used to check secondary bacterial invasion.
Control
- Avoid dusty feed.
- Avoid direct exposure to fumes, smoke and irritants.
- Avoid overworking. Light work should be given in susceptible hosts.
- Avoid exposure to allergens.
- Graded exercise should be practised.
