Respiratory diseases with a possible allergic aetiology are a
poorly defined group of conditions in animals, and include
pulmonary infiltration with eosinophilia (PIE) in dogs,
feline asthma syndrome, acute bovine pulmonary emphysema
and oedema (atypical interstitial pneumonia, fog
fever) in cattle, and recurrent airway obstruction and summer
pasture-associated obstructive pulmonary disease in
horses. All are believed to involve an allergic reaction to
either inhaled allergens (see below) or migrating pulmonary
parasites.
Inflammatory lung disease has been recorded in pigs and
other species following inhalation of irritant gases.
Allergic pulmonary disease may involve neutrophilic or
eosinophilic migration into the lung parenchyma and airways,
and mast-cell degranulation with release of inflammatory
mediators such as histamine. Airway mucosal
inflammatory mechanisms may be activated leading to the
release of prostaglandins and leukotrienes. The symptoms
of allergic pulmonary disease can vary from mild intractable
coughing to severe respiratory distress and death.
Allergens causing recurrent airway obstruction, RAO
(chronic obstructive pulmonary disease, COPD) in horses
include mould spores from hay and bedding. Poor quality
and ‘heated’ hay and straw carry the greatest concentration
of these spores. Control of RAO is effected by avoiding
these allergens, which is best achieved by keeping susceptible
animals permanently at pasture. If affected horses need
to be stabled, an alternative to straw, such as shredded paper
or shavings, should be used for bedding. Adequate ventilation
of the stable is essential and each horse should be
housed separately. Good quality hay should be fed and
should be soaked before feeding to dampen down any dust.
Better alternatives to feeding hay include the use of vacuum-
packed haylage, silage, or hydroponic grass. Summer
pasture-associated obstructive pulmonary disease
(SPAOPD) is similar to RAO except that it occurs in pastured
horses and is probably caused by pollen allergens.
Treatment of RAO and SPAOPD should ideally be directed
at preventing further exposure to the allergens rather than
the use of long-term therapy. However, short-term therapy
may be helpful when clinical signs are severe, and longterm
treatment may be necessary when management
changes are ineffective at controlling the disease.
Drugs that may be usefully employed include bronchodilators
such as clenbuterol or ipratropium and mucolytics such
as dembrexine. Corticosteroids are also used. To reduce the
risk of side effects, corticosteroids are administered by
mouth or nebulisation. Oral prednisolone on an alternate
day regime is advised. An initial dose of 1 to 2 mg/kg is
administered every morning. After two weeks of therapy,
response to treatment should be assessed and the dosage
reduced until the minimum effective dose is reached. Corticosteroid
therapy should eventually be discontinued if
possible.
In severe cases and in horses with acute exacerbations of
disease, dexamethasone therapy may be necessary, but this
drug carries a greater risk of undesirable side effects. An
initial dose of intravenous dexamethasone (0.1 mg/kg) may
be administered once daily for 2 to 3 days, followed by a
reducing dosage over the next 7 to 10 days (depending on
the clinical response). The efficacy of orally administered
dexamethasone preparations has not been evaluated.
Inhaled corticosteroid therapy has also been used for treatment
for RAO in horses.
Acute bovine pulmonary emphysema and oedema is probably
initiated by ingestion of large quantities of DL-tryptophan
in grass aftermath, although some cases have
occurred due to migrating lungworms or inhalation of toxic
gases. Fibrosing alveolitis involves a chronic allergic reaction
to mould spores.
The most common allergens implicated in feline asthma
syndrome have not been definitively identified but may
include human and equine dander (epithelium) and house
dust mite. In cats presented in status asthmaticus emergency
therapy is required. Cats in respiratory distress often resent
restraint making oxygen suplementation difficult. Reversal
of severe bronchoconstriction can be achieved with intravenous
aminophylline (2 to 5 mg/kg), intravenous atropine
(20 to 40 micrograms/kg), or epinephrine 20 micrograms/
kg by subcutaneous, intramuscular, or intravenous injection
using epinephrine 100 micrograms/mL. The intravenous
injection should be given with extreme caution. Corticosteroids
have limited use in status asthmaticus.
For cats presented with acute bronchospasm associated with
feline asthma, therapy may include intravenous aminophylline,
atropine (15 micrograms/kg by intravenous injection
or 40 micrograms/kg by intramuscular injection), or dexamethasone
(0.2 to 1.0 mg/kg by slow intravenous injection).
These drugs should give a rapid response and reversal of bronchospasm. The rapidity of the response can assist in
making a diagnosis of this condition.
Routine management of feline asthma is effected by oral
prednisolone. Initial treatment is 1 mg/kg once daily and
then reduced over the subsequent 3 weeks to 200 micrograms/
kg on alternate days, or to a dose sufficient to control
the symptoms. Medication may be withdrawn at 6 to 8
weeks and re-introduced as required. Continuous medication
may be necessary, particularly if the suspected airborne
allergen cannot be identified or avoided. The potential longterm
effects of corticosteroids should be considered (see
section 7.2). Zafirlukast (see section 5.3.5) is reported to be
a beneficial adjunct to standard feline asthma prophylactic
therapy. Cyproheptadine (see section 5.3.3) may be used
prophylactically in asthmatic cats. However, cyproheptadine
should only be used if other control methods have
failed. The delivery of glucocorticosteroids by inhalation
for the treatment of feline asthma and feline bronchial disease
is being evaluated and has shown promising results to
date. Inhalational drugs may be delivered using an AeroKat spacer (distributed by BreathEazy).