Understanding a cat's cough
Q: Please update me on common respiratory diseases in cats.
Drs. Carol Norris Reinero, Leah A. Cohn and Ray Dillon gave excellent lectures on common respiratory diseases in cats at the 2009 American College of Veterinary Internal Medicine Forum in Montreal, Canada. Some relevant points are provided below.
AsthmaDr. Carol Norris Reinero of the University of Missouri defines asthma as a chronic inflammatory disorder of the lower airways that also has airway hyper-responsiveness and airflow limitation (leading to clinical respiratory signs) as well as airway remodeling as prominent features. Genetics and environmental exposures are thought to play important roles in asthma development.
Asthma in cats has been suggested to be related to dietary hypersensitivity. With the waxing and waning signs that normally occur with this disease in many cats, it might appear that a change of diet could alter clinical signs. However, no scientific evidence supports a dietary causation of feline allergic airway disease.
Allergic asthma is typically associated with an eosinophilic inflammatory response. However, the presence of a peripheral eosinophilia has not been correlated with the degree of airway eosinophilia. Normal thoracic radiographs have been reported in up to 23 percent of asthmatic cases. A characteristic bronchial or bronchointerstitial pattern can be seen with other respiratory diseases in cats, including chronic bronchitis, heartworm-associated respiratory disease and lungworm infection (Aelurostrongylus abstrusus). There is ongoing debate on what should be considered a reference range for the various cell types in bronchoalveolar lavage fluid and how to best discriminate feline asthma from feline chronic bronchitis, but eosinophilic airway inflammation supports a diagnosis of feline asthma (especially once parasitic diseases have been ruled out).
Feline asthma is routinely treated with injectable or oral glucocorticoids. In healthy cats, inhaled glucocorticoids have minimal systemic effects on the adaptive immune system, although they can still suppress the hypothalamic-pituitary-adrenocortical axis. Inhaled glucocorticoids have reduced eosinophilic airway inflammation in experimental feline asthma. It is commonly accepted that glucocorticoids effectively control lower airway inflammation and should be titrated to the lowest effective dose to control clinical signs of disease. Bronchodilators are important in the medical management of asthma. Albuterol (also called salbutamol in Europe), a short-acting beta2 agonist, is frequently given by metered dose inhalation using a spacer in cats. Chronic use of inhalant racemic albuterol induces neutrophilic airway inflammation de novo in healthy cats and exacerbates eosinophilic airway inflammation in experimentally asthmatic cats (the so-called beta agonist paradox). Thus, inhalant racemic albuterol should be used as rescue therapy and not as monotherapy for daily treatment.
If an underlying allergic trigger can be identified as a cause for asthma, allergen avoidance or allergen-specific immunotherapy can be tried. It is challenging to identify clinically relevant allergens in cats, as the timing and amount of allergen exposure, different numbers and types of allergens, concurrent medications and other environmental factors may influence test results. Both intradermal skin testing and serum allergen-specific IgE determination can be used; in experimentally asthmatic cats with known/controlled aeroallergen exposure, the former is sensitive and the latter (by the high affinity Fc epsilon receptor-based ELISA) is highly specific. Abbreviated protocols for allergen-specific immunotherapy called rush immunotherapy (RIT) have shown great promise in experimental feline asthma. Ongoing studies are focusing on cross-protection with RIT using one allergen unrelated to the allergen used for experimental sensitization and challenge.
Dr. Leah A. Cohn of the University of Missouri indicates that natural influenza virus infections and experimental infections can be transmitted by direct inoculation of the virus parenterally or through the respiratory tract in domestic cats. It is thought that initial viral replication occurs in the respiratory and gastrointestinal tract with subsequent viremia. Some cats can remain well despite infection; these cats most likely have exposure to lesser viral loads. In those with greater exposure, extensive pulmonary damage and multifocal organ hemorrhage and necrosis are responsible for death. Neurologic signs including ataxia and seizures in naturally infected cats likely result from nonsuppurative encephalitis. More common signs are nonspecific and include fever, depression, third eyelid prolapse, conjunctivitis, increased respiratory effort, nasal discharge and icterus. Sometimes, sudden death is observed within days of infection.