Felis ISSN 2398-2950

Allergic bronchitis

Introduction

• Chronic bronchial inflammation associated with mucus hypersecretion and bronchial smooth muscle hypertrophy and constriction.
• Signs: coughing and/or dyspnea.
• Treatment: oxygen, corticosteroids and bronchodilators - long- or short-term.
• Prognosis: variable - many cats suffer recurrences but some are well controlled.

Print off the owner factsheet on Feline asthma to give to your client.

Pathogenesis

Etiology

• Poorly understood.
• Possible mechanisms:
  • Type 1 hypersensitivity to inhaled allergens - especially smoke, dust, air-fresheners etc.
  • Neurogenic bronchoconstriction, eg infection, exercise, excitement/stress and air pollutants.
• Broncho-hypersensitivity - hyper-reactive airways resulting from previous airway damage by viral infection or irritants.

Predisposing factors

General

• Viral upper respiratory tract infections Viral-induced upper respiratory tract disease.
• Inhaled irritants:
  • Dust (flea powder, carpet cleaner).
  • Human dander.
  • Sprays (flea products, household polishes).
  • Cat litter.
  • Smoke (cigarette, atmospheric pollution).
  • Scents (perfumes, air fresheners, Christmas trees).
• Defective mucociliary clearance due to infection resulting in ciliary stasis and ciliary damage.

Pathophysiology

• Primary airway inflammation   →   airflow obstruction via smooth muscle constriction, hypertrophy, bronchial wall edema and mucus gland hypertrophy.
• Possible pathophysiology:
• Allergen-induced:
  • Foreign antigen cross-links IgE on previously sensitized mast cells   →   degranulation and release of inflammatory mediators and granulocyte chemotaxis.
  • T-lymphocytes and eosinophils are attracted   →   release of mediators   →   constriction of tracheal smooth muscle and ciliostasis   →   decreased mucus clearance   →   plug small airways.
  • Released mediators also   →   sloughing of pneumocytes and inflammation   →   exposes sensory nerve endings to allergens   →   hyper-reactivity   →   smooth muscle contraction and bronchoconstriction.
  • Thickened, obstructed airways   →   air trapping   →   ventilation/perfusion anomalies   →   clinical signs.
• Neurogenic:
  • Stimulation of upper respiratory tract receptors by mechanical or chemical irritants   →   cough reflex and bronchoconstriction.
  • Stimulation of receptors in distal airways by irritants, allergens, viruses or inflammatory mediators   →   vagal bronchoconstriction.
  • Airway collapse, pneumonia or pulmonary edema   →   stimulation of non-myelinated nerve endings (C-fibers) in lung parenchyma   →   rapid shallow breathing pattern.
  • Aberrations in sympathetic, parasympathetic and non-adrenergic-non-cholinergic (NANC) systems which regulate normal airway tone may   →   bronchoconstriction.

Timecourse

• Weeks to months depending on severity.

Diagnosis

Treatment

Prevention

Outcomes