What disease(s) are we really talking about?
Although feline asthma is among the most commonly diagnosed respiratory conditions in cats, there is still a lot of confusion about how to define or classify this condition or how to differentiate it from other lower respiratory tract problems.
In recent years a number of different terms have been proposed to help classify disorders of the lower respiratory tract of cats. In many cases, these are still very general terms that primarily describe localization (e.g. bronchi) or relevant diagnostic test results (e.g. inflammatory cells in an airway wash). In other cases, there has been an attempt to describe the etiology (e.g. allergy) or make distinctions based on clinical signs (e.g. bronchitis when cough is predominant, asthma when reduced airflow or dyspnea). From this larger discussion of terminology it has been suggested, and largely accepted, that feline non-infectious lower airway (or bronchial) diseases can be divided into two general categories of chronic bronchitis and asthma.There seems to be general agreement that a diagnosis of asthma should imply certain characteristic features including: 1) chronicity with variable and recurrent clinical signs, 2) reduction in airflow, 3) bronchial hyperresponsiveness, 4) increased mucous production, 5) lower airway inflammation, and 6) lack of a specific infectious etiology. Some authors also remain adamant that asthma in cats has allergic basis and is associated with spontaneous bronchoconstriction, unlike other lower airway inflammatory diseases. Overall, however, there is currently no widely accepted, standardized specific criterion for making a specific diagnosis of feline asthma (as opposed to chronic bronchitis).
From a practical standpoint, there is so much overlap in the clinical and diagnostic features of feline asthma and feline chronic bronchitis that distinguishing the two conditions in a clinical setting can be quite challenging. For an individual veterinarian, cat, or client it may also not make that much difference given our current level of understanding of the two conditions and currently available therapeutic options.
Numerous factor have been implicated in the development of asthma in humans, including allergies, environmental irritant substances/pollutants, exercise, stress, and medications. Almost all of these factors have also been reported to cause lower respiratory tract disease in cats, but in general, feline asthma has been considered to be an allergic condition, while respiratory problems secondary to the other factors are often classified as separate conditions.
Cases of true allergic disease, or asthma, likely represent type I hypersensitivity reactions. Initiation of the process occurs when potential allergens are inhaled, taken up and processed by dendritic cells in the airways, and then presented in conjunction with MHC II molecules to naïve CD4+ lymphocytes. In susceptible individuals, when these lymphocytes are activated in the presence of appropriate co-stimulatory molecules, the immune response is polarized towards a Th2 response. The cytokines produced by this (especially IL4, IL5, and IL13) orchestrate an inflammatory response in which allergen-specific IgE is produced and eosinophils, basophils, and mast cells all become involved. When the cat is re-exposed to the allergen, IgE bound to mast cells becomes cross-linked and results in degranulation, leading to further exacerbation of the inflammatory cascade.
Tissue responses and injury resulting from degranulation of mast cells and eosinophils include smooth muscle contraction, increased vascular permeability, edema, damage to / sloughing of the protective epithelial lining of the airways, enhanced local neural responsiveness. Long term changes can include epithelial metaplasia and proliferation, hyperplasia of mucous glands with excess mucous production, impaired mucociliary clearance, hypertrophy and hyperplasia of smooth muscle, fibrosis, and emphysematous changes in the pulmonary parenchyma.
In non-allergic bronchitis, similar tissue injury can be seen as a result of the oxidative damage caused by neutrophilic inflammation.