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Feline Bronchial Asthma

Christine M. Serafin, DVM, DACVIM (SAIM)
The Animal Surgical Center of Michigan, Flint, Michigan, USA

Feline bronchial asthma is one of the most commonly present the antigen, bound to major histocompatibility
recognized diseases of the lower respiratory tract of cats complex class II receptors, to naïve CD4+ T helper cells,
and is estimated to affect up to 5% of the cat population. triggering these cells to differentiate into T helper 2 cells.
The broad range of clinical manifestations that charac- T helper 2 cells, in turn, produce interleukins (IL) 4, 5,
terizes this condition, its similarities to the human form and 13. IL‐4 in particular induces B cells to switch from
of the disease, the challenges inherent to its diagnosis, production of immunoglobulin (Ig) G to antigen‐specific
and the necessity for life‐long treatment warrant signifi- IgE that then binds to Fc receptors on the surface of mast
cant consideration of feline bronchial asthma in both cells. Allergen particles that are subsequently inhaled
human and veterinary respiratory medicine. cross‐link IgE molecules on the surface of mast cells,
initiating an intracellular cascade of events that culmi-
nates in mast cell degranulation. Histamines and leukot-
Etiology and Pathophysiology rienes released from degranulating mast cells promote
increased vascular permeability, smooth muscle con-
Feline bronchial disease is a general term that has been traction, and mucus production, generating the clinical
applied to inflammatory disease of the lower airways manifestations associated with asthma. IL‐4, IL‐5, and
that does not have an apparent etiology. Feline asthma is IL‐13 that are also released by mast cells recruit eosino-
considered to be a specific form of bronchial disease phils to the airways. Major basic protein, eosinophil
that is distinguished from other inflammatory airways peroxidase, and cationic proteins released by degranu-
diseases by reversible airflow limitation. This airflow lating eosinophils induce the tissue damage that charac-
obstruction is caused by smooth muscle hyperreactivity terizes asthma.
and hypertrophy, increased mucus production, inflam-
mation, and permanent airway remodeling. Airflow
restriction reverses either spontaneously or in response Epidemiology
to pharmacological intervention. Intermittent broncho-
constriction, predominantly eosinophilic lower airway Cats of any age can develop asthma but young to
inflammation, and an allergic immunopathogenesis middle‐aged cats are most often affected. A predilection
differentiate feline asthma from chronic bronchitis, for the Siamese breed has been proposed.
which is typified by neutrophilic airway inflammation in
response to a previous insult. Accordingly, asthma is
recognized by its three hallmark features: airway History and Clinical Signs
eosinophilic inflammation, hyperresponsiveness, and
permanent remodeling. A wide spectrum of clinical signs characterizes feline
Although the exact etiopathogenesis has not been asthma. Acute manifestations arise from bronchocon-
determined, type I hypersensitivity response is widely striction and can include severe dyspnea, orthopnea,
accepted to be the basis for the development of feline tachypnea, cyanosis, open‐mouth breathing, and wheez-
bronchial asthma. This response begins with dendritic ing. Episodes of dyspnea may occur on a daily basis or as
cells within the airways that process inhaled allergen. infrequently as once or twice yearly. Chronic manifesta-
These cells migrate to the regional lymph nodes and tions are typified by paroxysmal episodes of coughing.

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical