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Allergic bronchitis
Introduction
- Chronic bronchial inflammation associated with mucus hypersecretion and bronchial smooth muscle hypertrophy and constriction.
- Cause: poorly understood - possible mechanisms: Type 1 hypersensitivity to inhaled allergens, neurogenic bronchoconstriction; bronchial hypersensitivity.
- Signs: coughing and/or dyspnea.
- Diagnosis: radiography, bronchoscopy, cytopathology, bacteriology, transtracheal wash, hematology, biochemistry, fecal analysis.
- Treatment: oxygen, corticosteroids and bronchodilators - long- or short-term.
- Prognosis: variable - many cats suffer recurrences but some are well controlled.
Presenting signs
- Chronic coughing (paroxysmal, non-productive, dry, retching, gagging).
- Tachypnea and dyspnea.
- Exercise intolerance.
- Recurrent bouts of bronchopneumonia Pneumonia.
- Cachexia, debility.
Acute presentation
- Severe signs → cyanosis and exhaustion + possible death (life-threatening bronchoconstriction).
Age predisposition
- Any age.
Breed/Species predisposition
Special risks
- Anesthesia General anesthesia: overview.
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.
- Bronchial 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
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Treatment
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Prevention
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Outcomes
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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.