Felis ISSN 2398-2950

Allergic bronchitis

Synonym(s): Feline asthma, Bronchial asthma, Eosinophilic bronchitis

Contributor(s): Philip K Nicholls, Elizabeth Rozanski, Penny Watson

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

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Dye J A, McKiernan B C, Rozanski E A et al (1996) Bronchopulmonary Disease in the cat - Historical, Physical, Radiographic, Clinicopathologic, and Pulmonary Functional Evaluation of 24 Affected and 15 Healthy Cats. JVIM 10 (6), 385-400 PubMed.

Other sources of information

  • Johnson L (1997) Bronchial Disease. In: August Consultations, Feline Internal Medicine 3.


ADDED