Pathophysiology

In normal animals, the dorsal cricoarytenoideus muscles contract to abduct the corniculate processes of the arytenoids during inspiration, causing opening of the rima glottidis. This muscle is innervated by the recurrent laryngeal nerve, a branch of the vagus that originates near the thoracic inlet and loops around the subclavian artery on the right side, or the aorta on the left side, and returns craniad to the larynx. Laryngeal paralysis is recognized as a congenital disorder or heritable disease in some breeds and as an acquired form in older, large breed dogs. Some breeds that develop congenital laryngeal paralysis are affected by a generalized polyneuropathy (Table 5.1), and in the acquired idiopathic form, several studies have now confirmed the generalized nature of the neurologic deficits. Electromyographic studies and nerve conduction velocities in peripheral limb musculature of dogs with acquired laryngeal paralysis are suggestive of axonal disease (Jeffrey et al. 2006; Thieman et al. 2010). It has been recognized that affected older, large breed dogs often display clinical signs and physical examination findings of esophageal dysfunction and decreased proprioceptive placing, supporting a more generalized neurologic defect (Stanley et al. 2010). Laryngeal sensation is also abnormal. This syndrome has been labeled geriatric‐onset laryngeal paralysis–polyneuropathy (GOLPP).

Laryngeal paralysis can also result from trauma during surgery that disrupts neural transmission (thyroidectomy, repair of a patent ductus arteriosus, or tracheal ring placement), bite wounds, strangulation, or crush injuries. A mediastinal mass, granuloma, or hemorrhage compressing the recurrent laryngeal nerve can also lead to unilateral or bilateral laryngeal paralysis.

In animals with laryngeal paralysis, active contracture to open the glottis is depressed or lost, and this can be unilateral or bilateral. When unilateral, it appears that the left side is affected more commonly or earlier than the right side (Johnson 2016). Inspiration against a narrowed glottis results in a pressure drop across the larynx, and turbulent velocity of airflow causes irritation of the mucosa. This leads to mucosal edema and further obstruction of airflow. The larynx serves as an important protective mechanism against pulmonary inhalation of damaging substances. During swallowing, the palate contracts to close off the nasopharynx, the lateral walls of the pharynx propel the bolus toward the esophagus while the laryngeal folds and cartilages adduct, and the epiglottis moves caudally to block the larynx and prevent aspiration. Defects in any part of the process can lead to tracheal or lower airway injury from aspiration. It appears that some dogs with laryngeal dysfunction experience sensory as well as motor loss and this likely contributes to silent aspiration of oropharyngeal or gastroesophageal contents that leads to cough. It is common for dogs with laryngeal paralysis to accumulate secretions around the glottis, resulting in gagging or retching.

Cats are also affected by congenital or acquired laryngeal paralysis, but it is less commonly recognized clinically because they are less physically active and regulate activity to avoid respiratory distress associated with inspiratory obstruction of airflow.

History and Signalment

Laryngeal paralysis results in inspiratory difficulty, reduced vocalization or a change in sound of the bark/meow, excessive or loud panting, gagging, and retching. Exercise intolerance may be the first abnormality noted and can be mistaken as a sign of aging in large or Retriever breeds. Signs are worsened by heat, stress, excitement, or exercise, and severely affected animals can suffer syncope or cyanosis. Careful questioning of the owner is recommended to uncover concurrent esophageal or gastrointestinal dysfunction, because the combination of regurgitation or vomiting with laryngeal disease or laryngeal surgery enhances the risk for aspiration pneumonia.

The acquired form of laryngeal dysfunction results in clinical signs late in life (10–14 years of age), and traumatic or iatrogenic injury to the larynx during surgery can result in development of signs at any age. Purebred animals with congenital disease are young when signs are first recognized, although the disease in Shepherds and some Leonbergers has a slightly later onset (Table 5.1).

Pathophysiology

Norwich Terrier upper airway syndrome (NTUAS) is a congenital and likely heritable condition affecting many Norwich Terriers in the USA and Europe. Although these dogs are not phenotypically brachycephalic, they have laryngeal malformation with collapse that is likely the primary defect. Narrowing of the laryngeal aditus creates a large pressure gradient across the airway opening that leads to secondary changes of laryngeal ventricular eversion, tonsillar enlargement, redundant supra‐arytenoid folds, inflammation, and laryngeal collapse (Figure 5.3). A mutation in the gene for ADAMTS3 metallopeptidase enzyme, responsible for promotion of lymphangiogenesis, could make Norwich Terriers predisposed to develop this exuberant soft tissue swelling because of lymphedema (Marchant et al. 2019). Rarely, soft palate elongation or minor tracheal collapse can be observed in affected dogs. Some dogs have concurrent malformations in the nasopharynx, which might be congenital or could develop due to foreign body entrapment above the palate associated with mishandling of material in the oral cavity associated with airway obstruction.

History and Signalment

Affected dogs often have a history of noisy breathing, snoring, excessive panting, or exercise intolerance; however, some dogs display no clinical signs despite substantial upper airway changes. Severely affected dogs can be presented to the veterinarian for collapse or cyanosis due to airway obstruction. Cough is occasionally part of the clinical history and could be related to laryngeal irritation or low‐grade aspiration injury.

Physical Examination

Upper airway auscultation can reveal stertor and stridor in some dogs, although the absence of these abnormalities does not indicate the lack of pathology. In one small study, 4 of 12 dogs with respiratory complaints had a normal physical exam, as did 4 of 4 dogs lacking respiratory complaints (Johnson et al. 2013). However, 6 of these 8 dogs without physical examination abnormalities had severe manifestations of disease identified during laryngoscopic examination.

Diagnostic Findings

Cervical radiographs can reveal an indistinct quality to the larynx suggestive of edema or inflammation, but the diagnosis and grading of laryngeal abnormalities requires laryngoscopy. Function is often preserved, except in cases where severe perilaryngeal swelling appears to impinge on abduction of the arytenoids.

Treatment

Although controversial, laryngeal ventriculectomy is often performed in severely affected Norwich Terriers as a palliative measure to increase the laryngeal opening and reduce the effects of airflow dynamics on the remainder of the larynx. Some surgeons advocate tonsillectomy for the same reason. In severely obstructive cases, resection of the dorsal periarytenoid tissue has partially alleviated clinical signs. In most cases postoperative glucocorticoids are employed; inhaled preparations are preferred and can be required for several months to years whether or not surgery is performed. The efficacy of this treatment is unknown.

Prognosis

Despite severe airway obstruction, many dogs remain overtly healthy and active throughout life. When surgical intervention has been performed, most owners indicate an improvement in respiration, although many dogs are variably clinical for disease. Clinical understanding of this affliction is important for veterinarians because it is common knowledge among breeders and owners of Norwich Terriers. Genetic investigations are ongoing. Importantly, laryngeal narrowing has critical implications for anesthesia because these dogs often require smaller endotracheal tubes than might be expected based on their size, and some dogs can require use of a stylet to secure an airway.

Pathophysiology

Normally the epiglottis sits immediately below the soft palate and is somewhat parallel to the tongue. During swallowing, it moves back to cover the larynx, and during inspiration, it moves upward to contact the palate and direct air through the nasopharynx to the larynx. In dogs with retroversion, the epiglottis is overly mobile and travels caudally to obstruct the larynx during inspiration (Figure 5.4). The cause for this is unknown, but it could represent malacic change (similar to laryngomalacia in humans), fracture of the epiglottis, or denervation to the hyoepiglottic muscles, which control movement of the epiglottis. Mild variants of this anatomic abnormality are often encountered during laryngeal exam, and it appears that additional pathology such as tracheal collapse, an elongated soft palate, airway inflammation, or obesity is required to result in clinical manifestations of upper airway obstruction.

History and Signalment

Episodic or persistent respiratory distress characterized by inspiratory difficulty is often in the history of affected dogs. Generally, animals are older (>8 years of age), females are affected more often than males, and many are over‐weight. This is a disease primarily of small to medium‐sized breed dogs, with Yorkshire Terriers and Cocker Spaniels represented more commonly, along with brachycephalic breeds (Skerrett et al. 2015).

Physical Examination

Intermittent or persistent stridor is the most common finding, although some dogs can appear normal at rest and only develop stridor with excitement.

Diagnostic Findings

Cervical radiographs or fluoroscopy can reveal malpositioning of the epiglottis in relation to the larynx and oropharynx. Caution is warranted in over‐interpreting pharyngeal collapse, because this is common in brachycephalic breeds, even those lacking specific respiratory findings. Retroversion of the epiglottis can be visualized during laryngoscopy when the examiner has knowledge of the normal upper airway. A light plane of anesthesia is employed, and it is important that the tongue is not retracted too far cranially during the examination so that the epiglottis is allowed to rest in its normal position.

Treatment

Weight loss and environmental modifications are pivotal to reduce stress on the respiratory system. When the dog has continued airway obstruction, temporary or permanent epiglottopexy is typically performed by suturing the base of the tongue to the ventral surface of the epiglottis. Breakdown of the suture site is not uncommon. Partial or complete epiglottectomy can also be performed, but the client needs to be aware that dogs that have had surgical interventions are at risk for aspiration events post‐operatively. Dogs that have persistent clinical signs require permanent tracheostomy.

Prognosis

It is unclear whether surgical intervention improves survival (Skerrett et al. 2015) and many dogs can continue to suffer from airway obstruction. Given that retroversion is often part of other upper airway obstructive diseases, further research is needed to determine optimal management strategies for these dogs.

Pathophysiology

The etiology of tracheal collapse is unknown, but a study performed in a small number of dogs reported a reduction in chondrocytes and a lack of glycosaminoglycan and chondroitin sulfate in tracheal cartilage (Dallman et al. 1988). The lack of structural integrity in the cartilage is purported to result in weakening of cartilage rings, with flattening of the tracheal rings in a dorsoventral direction. An elongated dorsal tracheal membrane prolapses into the lumen of the airway, lending a dynamic component to the collapse. Repetitive contact between the membranous muscle and the ventral floor of the trachea leads to mechanical irritation of the mucosa, which enhances tracheal edema and inflammation. The cervical trachea collapses during inspiration, while the intrathoracic portion of the trachea collapses during forced expiration or cough because of the pressure gradients that develop during the respiratory cycle (Figure 5.5). Many dogs with tracheal collapse have collapse of both the cervical and intrathoracic trachea. In some dogs, the lobar bronchi also are collapsed, with the right middle and left cranial lobar bronchi affected most commonly (Johnson and Pollard 2010; Bottero et al. 2013), although it is unknown whether this is caused by the same pathology that has been described in dogs with tracheal collapse. When bronchial collapse is found in conjunction with tracheal collapse, it is termed tracheobronchomalacia. In some dogs only lobar or lower or smaller airway collapse is detected and this is termed bronchomalacia when luminal diameter is reduced by at least 50%.

Airway collapse can be static or dynamic. The most severe form of cervical tracheal collapse tends to be static in nature, often causing respiratory difficulty on both inspiration and on expiration. Lobar bronchial collapse can be static but also somewhat dynamic, with collapse evident at rest but with some degree of opening during inspiration and closure on expiration. Smaller airway or segmental lobar changes in luminal diameter tend to be dynamic. An endoscopic classification of bronchomalacia differentiated among dynamic, dynamic plus static, and static bronchial collapse to develop functional classes of airway collapse for future studies and to aid in understanding of the disease (Bottero et al. 2013), although this has not been widely applied in clinical practice.

The role of inflammation in the development of airway collapse and in the perpetuation of clinical signs remains unclear. Mechanical trauma due to airway wall apposition can be a cause of inflammation or can result from recurrent dynamic collapse. Neutrophilic or lymphocytic inflammation is commonly found in affected dogs and likely contributes to coughing. Similarly, the role of airway infection in tracheobronchomalacia is unknown, with some studies finding a majority of dogs with intracellular bacteria or evidence of infection (Bottero et al. 2013; Lesnikowski et al. 2020) while others report an absence of infection (Singh et al. 2012). Use of different sampling methods and different definitions of infection (intracellular bacteria, culture results, clinical features, etc.) likely play a role in these various findings.

Finally, the role of cardiomegaly and left atrial enlargement in bronchial collapse remains controversial. One case‐controlled study that used bronchoscopic assessment of the severity and distribution of lobar bronchial collapse in dogs with and without left atrial enlargement concluded that airway collapse was independent of cardiomegaly and was often associated with airway inflammation (Singh et al. 2012). A study using computed tomography (CT) to define bronchial collapse based on a reduced bronchial‐to‐aorta ratio reported an inverse relationship between left atrial size and vertebral heart score with bronchial diameter, suggesting that the heart was involved in airway collapse (LeBastard et al. 2021). However other CT studies have demonstrated bronchial narrowing in the absence of cough in brachycephalic dogs (Yoon et al. 2020) and in other dogs lacking respiratory signs (Cote et al. 2022), raising questions about the role of various thoracic conformations and application of imaging ratios in the clinical syndrome of airway collapse.

History and Signalment

Tracheal collapse is seen most commonly in small or toy‐breed dogs, such as the Yorkshire Terrier, Pomeranian, Poodle, Maltese, and Chihuahua, while bronchomalacia can be seen in any size of dog. Tracheal collapse is diagnosed rarely in large breed dogs, but bronchial collapse is relatively common. Bronchomalacia is much less common in cats than in dogs and is rarely responsible for clinical signs, although static bronchial collapse can be found in some cats with chronic bronchial disease. At the time of presentation to the veterinarian, dogs with airway collapse can range from 1 to 15 years of age, depending on the degree of airway collapse and the presence of contributing clinical conditions.

Most dogs with tracheal collapse have a chronic history of waxing and waning respiratory difficulty or cough that has grown progressively worse over time or has become refractory to treatment. This likely is the reason that several studies refer to tracheal collapse as a progressive disease. Some dogs will have both respiratory difficulty and cough. Exacerbation of cough after eating and drinking or with excitement is common in dogs with tracheal or airway collapse, and this likely reflects some degree of laryngeal dysfunction or aspiration injury. Some dogs cough excessively on waking or in the middle of the night and this could also reflect micr‐aspiration. The cough is often described as paroxysmal, dry, or as a “honking” cough. Owners sometimes mistake the cough for vomiting or will report gagging or retching in association with the cough as the animal attempts to clear secretions from the airways. Worsened signs, exercise intolerance, and respiratory distress tend to occur during physical exertion, with heat stress, or in humid conditions. This could be the result of airway collapse alone, chronic bronchitis, infectious airway disease, and/or concurrent upper airway obstruction (edema, ventricular eversion, or laryngeal paralysis). Cyanosis or syncope can occur in severely affected animals due to complete airway obstruction, vagally mediated syncope, or pulmonary hypertension.

Physical Examination

Dogs with airway collapse are usually systemically healthy, they are often overweight, and they cough readily on tracheal palpation. The respiratory pattern can appear normal at rest, until coughing or stress leads to a debilitating paroxysmal event that causes air hunger or cyanosis. Caution is warranted when auscultating or palpating the trachea, because a severe paroxysm of cough could induce a crisis of coughing or cough syncope. Marked expiratory effort or an abdominal press on expiration can indicate bronchial collapse or concurrent bronchitis.

Auscultation over the trachea can reveal musical or wheezing sounds caused by turbulent airflow through the narrowed lumen. Stridor over the upper airway could represent laryngeal paralysis, but can also be heard in dogs with severe cervical tracheal collapse that results in a narrowed and fixed tracheal diameter. In dogs with cranial lung herniation or severe kinking of the cervical trachea, ballooning of the thoracic inlet can be seen during cough or forced expiration.

Lung sounds can be difficult to assess in dogs with tracheal or airway collapse due to tachypnea, obesity, or referred upper airway sounds. Inspiratory and/or expiratory crackles can be an indication that bronchomalacia is present, especially when combined with expiratory effort. An end‐expiratory snap over the thorax can be an indicator that intrathoracic tracheal or bronchial collapse is present. Careful cardiac auscultation should be performed, because 20% or more of middle‐aged, small breed dogs have mitral valve insufficiency in addition to airway collapse. Usually the murmur is low grade (2–3/6) and heart rate is low or a respiratory arrhythmia is present, allowing differentiation between congestive heart failure‐related respiratory signs and airway collapse. Hepatomegaly is a common finding in dogs with tracheal collapse and could be related to fatty infiltration of the liver, intermittent hypoxia, or a non‐specific hepatopathy.

Diagnostic Findings

Although the diagnosis of tracheal collapse can be strongly presumed based on the signalment, history, and physical examination findings, a complete diagnostic work‐up should be performed to define concurrent disorders and provide appropriate therapy. Recognition of bronchial collapse is more problematic and requires advanced diagnostic capabilities, including fluoroscopy and bronchoscopy. Routine hematologic testing occasionally detects predisposing conditions or concurrent diseases in dogs with tracheal collapse, although this is rare. Increased liver enzymes are not uncommon in dogs with airway collapse, and elevations in serum bile acids have also been reported (Bauer et al. 2006). Whether this is related to transient hypoxia to the liver or fatty infiltration is unclear.

Radiographs are essential both to examine airway diameter and to detect concurrent pulmonary or cardiac disorders. Cautious interpretation of the cardiac silhouette is warranted, because the dog breeds commonly affected by airway collapse often have a larger cardiac silhouette than expected, particularly when they are small breed chondrodystrophic dogs. Also, fat around the pericardial space and reduced lung expansion from obesity can lead to the false impression of cardiomegaly. However, right‐sided heart enlargement can be present in dogs with tracheobronchomalacia, concurrent pulmonary disease, or other factors that predispose to the development of pulmonary hypertension.

It is important to note that airway collapse is often a dynamic process and radiographs can give a false impression of the presence or absence of collapse. In the cervical region, overlying structures such as the esophagus and neck muscles can obscure details on airway diameter. Evaluation of left and right lateral views may improve distinction of structures; however, differences in positioning and in the phase of respiration can make it difficult to compare these views directly. Obtaining inspiratory and expiratory phases of respiration can be helpful, because the cervical region should collapse on inspiration while intrathoracic airways should collapse on expiration; however, the difficulty in timing these radiographs precisely limits the actual value. In comparison to fluoroscopy, radiographs under‐estimate the severity of tracheal collapse and are less able to detect intrathoracic airway collapse, which is often more severe than cervical collapse (Macready et al. 2007) (Figure 5.6). Therefore, while radiographs are useful as a screening tool for collapsing airways, they cannot be relied on for the diagnosis and likely will provide inaccurate information regarding the location and severity of tracheobronchial collapse. Fluoroscopy, where available, is beneficial in providing information on the degree of dynamic airway obstruction, and it also allows correlation of airway collapse with cardiac and respiratory cycles. Additional findings such as cranial lung herniation during cough can be detected (Figure 5.7).

Bronchoscopy can document tracheal collapse and is useful for grading the degree of collapse (Figure 5.8). In addition, bronchoscopy readily identifies bronchomalacia, which can be static or dynamic (Figure 5.9). Bronchoalveolar lavage or an endotracheal wash sample can be used to document bacterial or Mycoplasma infection and to detect inflammation by cytologic examination. Bronchomalacia can accompany eosinophilic or neutrophilic inflammatory disease as well as lower respiratory tract infection, therefore the importance of collecting an airway sample is readily apparent. Interestingly, airway collapse is often associated with BAL lymphocytosis, which is an unusual type of inflammatory airway disease (Johnson and Vernau 2019).

The risk of anesthesia for bronchoscopy can be significant in dogs with airway collapse, especially in obese animals with severe tracheal sensitivity or in hyperexcitable dogs. A slow recovery from anesthesia is advisable to minimize stress, and an oxygen‐enriched environment should be available. One milliliter of 1% lidocaine sprayed into the distal trachea at the end of bronchoscopy can help decrease the cough reflex.

CT with imaging during inspiration and expiration can also provide information on airway collapse, however it does not assess the presence or absence of infection or inflammation. Therefore, it provides less clinical guidance for treatment strategies.

Treatment

Animals that have marked respiratory difficulty and coughing can require emergency management. Stress should be minimized, and oxygen supplementation can be beneficial to assist in calming. Cough suppression and sedation can be achieved with butorphanol (0.2–0.4 mg/kg subcutaneously [SC] every 4–6 hours), and the addition of acepromazine (0.01–0.2 mg/kg SC) can have a synergistic effect in producing sedation. Caution should be employed when using the drugs together or when an opioid is considered, because over‐sedation can require intubation, which will exacerbate airway inflammation. To decrease laryngeal or tracheal inflammation, a single dose of dexamethasone SP (0.05–0.20 mg/kg intravenously [IV]) can be administered.

Outpatient management should be designed to treat disorders identified in the diagnostic work‐up whenever possible. Almost all affected dogs would benefit from weight loss (see Chapter 3). While this can be very beneficial in reducing and even eliminating cough, it can take a long time to accomplish this, and both the dog and the owner often cannot tolerate the length of time required without using additional measures. If physical examination findings suggest bronchomalacia (crackles, expiratory effort), a trial on extended‐release theophylline (5–10 mg/kg orally [PO] twice a day [BID]) can be considered to improve expiratory airflow and lessen the tendency for small airways to collapse. This drug is not indicated for use in dogs with cervical tracheal collapse, and beta‐2‐agonists are not beneficial. Airway infection is rarely found, but when present it should be treated with appropriate antibiotics as determined by airway sampling. If the dog is too unstable to obtain an airway sample, a trial on doxycycline (3–5 mg/kg PO BID) can be employed to treat potential Mycoplasma infection and to provide mild anti‐inflammatory effects. If chronic bronchitis is diagnosed, glucocorticoids should be employed (see later in this chapter). These measures and appropriate client communication can generally help manage clinical signs and owner expectations.

Dogs with tracheal collapse and bronchomalacia can have local airway inflammation from chronic airway injury. When this is suspected or confirmed on bronchoscopy, a short course (5–7 days) of prednisone can be beneficial, although side effects such as weight gain and panting can worsen airway collapse. If the animal responds well to oral glucocorticoids and ongoing control of inflammation is anticipated or if oral glucocorticoids are contra‐indicated due to obesity, heart disease, diabetes, or renal disease, inhaled glucocorticoids would be preferred to limit side effects. Dogs with bronchomalacia and airway inflammation can experience at least a 50% reduction in cough within 2 weeks of instituting inhaled fluticasone propionate (see Chapter 2).

Finally, narcotic cough suppressants are typically required to control cough when inflammation and infection have been managed. These drugs should be administered often enough to reduce cough without inducing severe sedation. Suggested drugs include hydrocodone (0.22 mg/kg PO two to four times a day [QID–BID]) initially or butorphanol (0.55 mg/kg PO QID–BID). Starting with a frequent dosing interval and gradually extending the time between doses and/or reducing the dose appears to be most effective in controlling signs while avoiding the development of tolerance.

Ancillary measures include avoidance of collars and decreased exposure to heat and humidity. Use of management strategies that limit aspiration injury, as described for laryngeal paralysis, can also be helpful in reducing cough. Use of omeprazole to limit acid injury to the airways has to be balanced against the tendency for some dogs to vomit when taking this drug. Upper airway surgery, if needed, can also reduce clinical signs.

Dogs that fail medical management require additional intervention. In dogs with cervical tracheal collapse, placement of tracheal ring prostheses (Figure 5.10) will result in a dramatic reduction in clinical signs (Buback et al. 1996). The primary complication of surgery is development of laryngeal paralysis from damage to the recurrent laryngeal nerve during or after surgery, and tracheostomy can be required for management. When intrathoracic tracheal collapse is detected and medical management has been exhausted, placement of an intraluminal stenting device (Figure 5.11) can be life‐saving. Stents are indicated particularly for dogs that have difficulty breathing, rather than for dogs with a primary complaint of cough. It is critical that a stent of appropriate type and size is used to attain a successful outcome and that an experienced clinician places the stent (Weisse 2009). The most problematic form of tracheal collapse is grade 4 cervical collapse, where the ventral surface of the trachea bulges inward toward the dorsal surface, creating a double lumen or W‐shaped trachea, sometimes referred to as a tracheal malformation (Figure 5.8d). This configuration is often encountered at the thoracic inlet and, while it can sometimes be managed with external ring prostheses, stenting is also performed in some cases. Improving stent contact with the tracheal walls through ballooning is frequently used in these cases in an attempt to improve integration of the stent with the tracheal epithelium.

Bronchial collapse or bronchomalacia is not necessarily a contraindication for placement of extrathoracic rings or for stent placement in the trachea, although dogs that continue to cough due to lower airway collapse are at greater risk for breaking the stent. Research into the manufacture of bronchial stents and methods to improve tracheal contact is ongoing.

Post‐procedure management is typically provided in an intensive care setting. Antibiotics are often required for aspiration events, and cough suppressants can be needed to prevent damage to the stent. Longer‐term complications of stent placement include migration, granuloma formation, or breakage of the stent. Owners need to be aware that multi‐drug therapy and continued monitoring will be required after stent placement.

Prognosis

Tracheal collapse with or without lower airway collapse or bronchomalacia is a common cause of cough in small breed dogs. Bronchomalacia is also frequently encountered in large breed dogs with infectious or inflammatory airway disease, however, because airway collapse typically requires bronchoscopy for identification, the condition is under‐diagnosed. Most dogs with tracheobronchomalacia can be managed successfully with an individualized treatment plan designed to control abnormalities noted during diagnostic testing; however, the underlying pathology of airway collapse is irreversible. Recurrent clinical signs should be anticipated and for dogs that are refractory to therapy, more aggressive interventions including stenting should be investigated.

Pathophysiology

Canine infectious respiratory disease (CIRD) complex is associated with multiple pathogens, including parainfluenza virus (CPIV), canine adenovirus (CAV‐2), and canine distemper virus (CDV), as well as newer viruses such as canine respiratory coronavirus (CRCoV), canine herpesvirus (CHV‐1), and canine influenza virus (CIV). Canine pneumovirus (CnPnV) and reovirus are of questionable pathogenicity. Subtypes of influenza viruses infecting dogs include H3N8, which crossed species from horses to dogs in 2004 (Crawford et al. 2005), and H3N2, which likely originated in Southeast Asia before causing outbreaks in the midwest (Chicago, Illinois) and southern (Atlanta, Georgia) United States, with subsequent spread of the organism to multiple states. Outbreaks of viral diseases in shelters result in spillover of pathogens into the community and vice versa. Vaccination has reduced the incidence of some viral infections; however, additional pathogens are continually added to the list of organisms involved in CIRD (Table 5.2). Lack of vaccines for CHV‐1 and CRCoV results in a large population of dogs at risk for infection.

Viral infection of epithelial cells damages mucosal cells and alters local immunity, which predisposes the animal to infection with both primary respiratory pathogens (Bordetella and Mycoplasma) and other commensal and pathogenic bacteria, including Streptococcus equi subsp. zooepidemicus. Infection is prevalent in animals that are housed in shelter environments or held in close confinement, because the viruses are highly contagious and easily spread by aerosolization or fomites.

History and Signalment

Clinical signs of naso‐ocular discharge, cough, and possibly anorexia or lethargy are usually seen 2–10 days post‐exposure to an infected animal, and the dose of pathogens encountered might play a role in the severity of clinical disease. Young animals in shelters are quickly exposed to most organisms and will readily spread the disease to animals of any age in the general population. While infection with viral organisms usually results in a mild cough, infection with Bordetella classically results in a dry, paroxysmal, “seal bark” cough, and involvement of aerobic bacteria (particularly Streptococcus equi subsp. zooepidemicus) or Mycoplasma can lead to development of pneumonia with a moister cough.

CHV‐1 was initially recognized as a cause of fading puppy syndrome, neonatal death, and abortion, but more recently has been associated with both ocular and disseminated disease of respiratory origin. Immunocompromise, in particular, can enhance the severity of infection. Disease associated with CHV‐1 tends to result in dramatic ocular involvement with marked conjunctivitis, ulcerative keratitis, and blepharospasm, as well as nasal signs and even pneumonia.

CDV is an epitheliotropic virus that can result in respiratory, gastrointestinal, and ultimately neurologic disease, which can be fatal. Although vaccination has substantially reduced the occurrence of this infection, genetic variants of the virus can develop in regions of low vaccination prevalence and vaccine breakthrough can occur when outdated or poorly stored products are used.

In general, viral infections are typically self‐limiting, with resolution of signs in 7–10 days, although Bordetella, Mycoplasma, and CIV infections can result in chronic cough that requires specific investigation and treatment.

Physical Examination

Most dogs with CIRD remain systemically healthy, although neonates and immuno‐compromised patients are susceptible to the development of pneumonia and resultant signs of illness. Most dogs display obvious tracheal sensitivity but have a normal respiratory pattern and normal lung sounds unless bronchopneumonia develops. Increasing severity of disease is recognized by the development of tachypnea, harsh lung sounds, fever, anorexia, and lethargy. With bacterial infection, a moist and productive cough can develop, tachypnea can be observed, and crackles or wheezes are sometimes auscultated. Physical examination abnormalities are usually confined to the respiratory tract, although CHV‐1 can cause surface ocular disease, and chorioretinitis can be detected in dogs with CDV.

Diagnostic Findings

In privately owned pet animals that are systemically healthy, the diagnosis of CIRD is usually based on history and clinical signs. In an outbreak situation or in an ill animal, it is important to identify the infecting organism(s) in order to limit spread of disease and provide appropriate treatment. A CBC can show lymphopenia suggestive of a viral insult, or alterations in neutrophils due to bacterial infection (leukocytosis with a left shift or neutropenia associated with acute infection). If marked conjunctivitis or blepharospasm is noted, a fluorescein stain should be applied to the eyes to detect the classic dendritic ulcer of CHV‐1. Thoracic radiographs would be expected to show a diffuse interstitial infiltrate in viral pneumonia and alveolar infiltrates in the presence of bacterial infection.

In animals with primarily upper respiratory tract signs, a nasal, ocular, or pharyngeal swab can be assessed for organisms through culture or molecular assay. It is important to note that these tests can confirm the molecular presence of an organism, but do not prove causation of clinical signs of disease, and a majority of PCR positive dogs can be apparently healthy (Jaffey et al. 2021). Many of these tests can be impacted by recent vaccination and other limitations of the assays must be considered. For example, CRCoV is difficult to culture and molecular identification (reverse transcription polymerase chain reaction: RT‐PCR) or paired serology 2–3 weeks apart is usually required to identify exposure to the organism. Additionally, the value of a positive test is limited because detection of this virus bears little relation to the presence or absence of clinical signs.

The timing of viral shedding in relationship to the onset of clinical signs alters the value of viral culture. Experimental CHV‐1 infection in dogs results in peak ocular manifestations of disease by day 7–10, yet viral shedding peaks at day 5 and declines substantially by day 10 (Ledbetter et al. 2009). In the case of CIV, diagnosis based on virus isolation is also problematic. Clinical signs begin 2–3 days post‐infection, but the virus is shed only for a maximum of 5–7 days, making it unlikely that culture or PCR will detect virus unless the dog is presented very early in the course of disease. Documentation of CIV infection (or exposure to CIV) is best made through assessment of hemagglutination inhibition serum titers for virus‐specific antibodies. When possible, acute and convalescent serum samples (preferably 14 days after clinical signs are detected) should be evaluated to detect a greater than fourfold increase in titer. Usually only convalescent serum is available, but if the dog has not been vaccinated for CIV, a positive titer indicates that the dog has been exposed to the virus and is likely infected. Acute and convalescent serum samples can also be useful in the diagnosis of CPIV and CAV‐2, although testing is not usually performed because dogs fully recover from infection and vaccinal titers can confuse interpretation.

If CDV is suspected, a conjunctival or genital scrape can be evaluated for inclusion bodies using direct immunofluorescence antibody testing. This is most helpful in the acute (<3 weeks) stage of disease, although evaluation of lower respiratory secretions (BAL or tracheal wash fluid) might allow detection of virus for a longer period of time (up to 1–2 months) post‐infection. While a positive test can be diagnostic, a negative test does not rule out disease.

If an animal with evidence of lower respiratory tract involvement in CIRD is stable for anesthesia and a definitive diagnosis is required, collection of airway samples would be recommended for virus isolation, bacterial cultures (aerobic, anaerobic, and Mycoplasma), cytology with immunocytochemistry or immunofluorescence, and PCR or quantitative RT‐PCR.

Treatment

In uncomplicated cases of CIRD complex, supportive care results in resolution of signs. Physical activity is restricted, collars are avoided, and nutrition and hydration are provided. If bacterial infection is considered unlikely, cough suppressants can be used to break the cycle of repetitive airway injury; however, there is a risk for development of pneumonia if bacteria are trapped in the lungs. Many dogs are initially treated with antibiotics for presumed primary or secondary infection. Doxycycline and chloramphenicol are reasonable antibiotics to use because of their efficacy against Mycoplasma species. Bordetella has in vitro susceptibility to a number of antibiotics, but often the bacterium is not sensitive in vivo because it infects cilia lining the respiratory tract, which are not readily accessed by systemically administered agents. Nebulization of an aminoglycoside can be required to reduce bacterial numbers while the immune system assists in clearing the organism (see Chapter 3). Shelter dogs with signs of CIRD had lower vitamin D levels than healthy dogs in the shelter population (Jaffey et al. 2021); however it is unclear if this is a cause or effect of the respiratory illness. Therefore, no specific recommendations can be provided for supplementation in diseased animals. Specific antiviral therapy is not currently available or recommended for affected dogs.

Prognosis

Most dogs that become infected with organisms involved with CIRD survive, although fatalities can be seen, particularly with distemper virus and influenza virus. CIV and Bordetella infections can result in chronic signs in some cases. Subclinical shedders represent a source of environmental exposure for susceptible dogs, particularly in the case of Bordetella, which can survive in the environment. Importantly, prolonged shedding of H3N2 influenza virus can occur beyond 3 weeks, despite the fact that the dog is free of obvious clinical signs (Newbury et al. 2016).

In a dense population of dogs, appropriate infection control measures should be in place to limit the spread of respiratory disease. Reducing crowding, improving air exchanges, and using rigorous hygiene practices are all helpful. Most viruses are readily destroyed by bleach or quaternary ammonia compounds, and workers should be alert for the possibility of spreading disease while working among animals. When disease is detected in a population, limiting contact of susceptible dogs with those showing clinical signs is important; however, dogs can spread infection in the absence of clinical signs. Ideally, sick dogs should be kept completely isolated from the rest of the population, and full clothing coverage, gloves, and booties should be used in environments containing sick animals. New dogs that enter the environment should be held in isolation until the incubation period (~7–10 days) for infectious diseases has passed.

Prevention

Vaccination against the commonly encountered pathogens reduces but does not eliminate clinical disease. The 2022 American Animal Hospital Association (aaha.org) Canine Vaccination Guidelines recommend core vaccinations against CDV, canine parvovirus, CAV‐2, and possibly CPIV, as well as rabies vaccination. Given the commonality of CPIV infection, vaccination should likely be considered core. Non‐core vaccines should also be considered in select instances. Use of a mucosal vaccine for Bordetella (some of which also include CPIV or CAV‐2) can be used in susceptible dogs that will be exposed to a dense population of dogs, because it provides protection within 48–72 hours of administration. Subcutaneous vaccination also provides adequate protection, but it takes longer for the dogs to develop an immune response. Intranasal vaccination can occasionally have untoward side effects and dogs that are prone to respiratory disease might best be managed with oral or subcutaneous vaccines. Vaccination in the face of an outbreak has not appreciably lessened clinical disease.

Subcutaneous vaccines are available against H3N8 and H3N2 and a bivalent vaccine is available, although dogs can still develop a mild form of disease if exposed. The initial vaccine series is typically two injections separated by 2 weeks and must be administered 4–5 weeks prior to potential exposure to closely housed dogs. These vaccines will result in seroconversion, negating one of the diagnostic methods possible for influenza. Therefore, risk factors for disease must be considered when deciding whether to vaccinate against the influenza virus.

Pathophysiology

Parasites implicated in respiratory disease include lungworms Filaroides hirthi (canine), Aelurostrongylus abstrusus (feline), Capillaria aerophila (dogs and cats), Oslerus osleri (canine), Crenosoma vulpis (canine), Paragonimus kellicotti (dogs and cats), and larval migration of Toxocara, Ancylostoma, or Strongyloides. Specific features of life cycle, transmission, and diagnosis of each parasite are summarized in Table 5.2.

History and Signalment

Parasitic bronchitis occurs more commonly in young, outdoor animals and particularly those that hunt, because ingestion of an intermediate host is often involved in transmission. However, it can be encountered in any cat or large or small breed dog regardless of activity, because the mechanism for transmission of many of these parasites is incompletely understood. Most airway parasites are associated with cough; however, O. osleri and Paragonimus can lead to difficulty breathing. With infection by Oslerus, this is due to obstruction of the trachea by parasitic nodules, while Paragonimus leads to difficulty breathing when rupture of a parasitic cyst results in pneumothorax.

Physical Examination

Tracheal sensitivity is generally present with most parasitic infections, and wheezing can be heard because of airway inflammation or obstruction. Tachypnea can be the primary sign observed in young kittens infected with Aleurostronglyus. Infection by Paragonimus and resultant pneumothorax can be detected by the presence of tachypnea and an absence of breath sounds dorsally due to air accumulation. Percussion can detect hyper‐resonance in the dorsal thorax.

Diagnostic Findings

Blood work can reveal eosinophilia and fecal examinations can be diagnostic (Table 5.3), although because parasites are shed intermittently, a negative fecal does not rule out infection. Filaroides, Capillaria, and Aelurostrongylus can result in a nodular pattern, mixed interstitial‐alveolar densities, or in a bronchial pattern (Figure 5.15). O. osleri results in nodules within the trachea near the carina, and C. vulpis can rarely cause nodular proliferations. These can be seen radiographically or during bronchoscopy and appear as round, soft tissue densities (Figure 5.16). In animals with larval migration, radiographic infiltrates are often concentrated in the caudal lobes. Parasitic larvae can be found in the airways (Figure 5.17), in biopsy samples, or in bronchoalveolar lavage fluid cytology. PCR is available for some parasites.

Paragonimus forms nodular densities or either air‐ or fluid‐filled cysts. Nodules are typically thin‐walled in the dog and thick‐walled in the cat. Pneumothorax is evident radiographically as loss of vascular and bronchial markings in the periphery (see Chapter 7).

Treatment (Table 5.3)

Most airway parasites can be treated medically with oral or topical anti‐parasiticides, although O. osleri can be particularly refractory to therapy. When rupture of a Paragonimus cyst is identified, a chest tap is needed to alleviate respiratory difficulty and lung lobectomy is usually required.

Prognosis

Most animals will recover from parasitic bronchitis. Mortality can occur with rupture of Paragonimus cysts or because of airway obstruction associated with refractory infection by O. osleri.

Pathophysiology

Non‐specific inflammation of the larynx is common secondary to any infectious or inflammatory disease of the lower airway, and it can also be encountered in animals with vomiting disorders that result in acid injury to the upper airway. Brachycephalic breeds are particularly prone to development of inflammatory lesions or vocal fold granulomas, likely associated with trauma from airflow obstruction along with gastroesophageal reflux disease. Laryngeal inflammation can also occur secondary to trauma associated with choke chain injury, an insect bite, or inhalation of noxious fumes. Less commonly, primary inflammation of the larynx is encountered. In the cat, this lesion can appear similar to a neoplasm, and biopsy differentiation is crucial. The etiology of inflammation is usually not determined, however trauma and gastroesophageal reflux disease should be considered.

History and Signalment

Animals with primary or secondary laryngitis can be of any age or breed. Owner complaints are similar to those seen with other laryngeal diseases and include inspiratory difficulty, dysphonia, inappetence or difficulty swallowing, and retching.

Physical Examination

Stridor or loud inspiratory sounds over the larynx are signs of upper airway obstruction, and cervical palpation will sometimes reveal an unusual larynx (firm or asymmetric) in some dogs or cats.

Diagnostic Findings

Cervical radiographs can reveal caudal retraction of the hyoid apparatus (Figure 5.1), although this is a very non‐specific finding that can be artifactual due to increased respiratory effort. Increased soft tissue density in the region of the larynx or a possible mass lesion should be evaluated by visual inspection and biopsy under anesthesia. Careful pre‐anesthetic planning is advised in case an obstructive lesion is discovered that requires a tracheostomy. A wire or stylet should be available to facilitate intubation if necessary. Secondary laryngitis is associated with hyperemia and mucosal edema, while primary or granulomatous laryngitis is typically associated with a mass effect on the larynx. A tissue sample for histopathology can be acquired using 2 or 3 mm cup biopsy forceps (Sontec Instruments, Centennial, CO, or Karl Storz Veterinary Endoscopy, Goleta, CA) and will reveal lymphocytic or granulomatous inflammation in the absence of neoplastic change.

Treatment

Secondary laryngitis will usually resolve with treatment of the underlying airway or gastrointestinal condition. Primary inflammatory laryngitis can require debulking surgery, laryngectomy, and/or tracheostomy to alleviate respiratory distress. Some cases respond adequately to glucocorticoids alone or in combination with surgery (Tasker et al. 1999).

Pathophysiology

Chronic bronchitis is defined by the presence of a daily cough that occurs for at least 2 months of the year and lacks a specific cause. Cough is related to activation of irritant receptors in the airways by products of inflammatory cells and excessive airway mucus. While the specific cause is unknown, recruitment of inflammatory cells could result from exposure to environmental pollutants, second‐hand smoke, or inhaled irritants. Neutrophilic infiltration of the airway results in release of proteases, elastases, and oxidizing products that perpetuate inflammation and airway damage. Histologic examination of mucosal biopsy specimens from dogs with chronic bronchitis reveals hypertrophy and hyperplasia of mucous glands and goblet cells, fibrosis of the lamina propria, and epithelial erosion with squamous metaplasia. These changes contribute to obstruction of airflow through accumulation of mucus within the airway and lead to clinical signs of cough and exercise intolerance. Bronchoconstriction is not a component of this disease in dogs.

Focal or generalized bronchomalacia can sometimes accompany chronic bronchitis and other forms of inflammatory airway disease, perhaps because inflammatory mediators lead to weakening of cartilage or have effects on airway smooth muscle tone. It is also possible that chronic airway collapse stimulates some degree of inflammation through repetitive airway injury caused by apposition of airway walls. Chronic bronchial inflammation can lead to bronchiectasis in some cases.

History and Signalment

Chronic bronchitis is a disease of middle‐aged to older dogs, and both large and small breed dogs are affected. The predominant clinical complaint is persistent coughing, which can be a dry, hacking cough or moist and productive, when copious amounts of respiratory secretions are produced. A “goose honk” cough might predominate in dogs that have concurrent tracheal or airway collapse. Dogs are typically healthy and relatively active, although in the later stages of disease, exercise intolerance or heavy breathing can be reported.

Physical Examination

Dogs with chronic bronchitis are often overweight but appear otherwise healthy. Some dogs will pant excessively, while dogs severely affected by bronchitis can have prolonged expiration or an expiratory push. Tracheal sensitivity is usually present because of non‐specific airway inflammation. Thoracic auscultation can be normal or sometimes will reveal coarse, diffuse crackles associated with mucus accumulation or opening and closing of small airways. These findings in conjunction with expiratory effort are difficult to differentiate from those associated with bronchomalacia. Expiratory wheezes are considered the hallmark of chronic bronchitis, although these are not commonly ausculted. Careful cardiac auscultation is advised to detect concurrent valvular insufficiency, which is a common concurrent condition in older small breed dogs.

Diagnostic Findings

The diagnosis of chronic bronchitis is one of exclusion, because infectious bronchitis (Mycoplasma or Bordetella) and airway collapse cause similar historical and physical examination findings. Clinicopathologic abnormalities are typically absent in dogs with chronic bronchitis. Arterial blood gas analysis (if performed) generally shows only mild to moderate hypoxemia, and hypercarbia is not detected until late in the disease if respiratory failure ensues.

Thoracic radiography is an important part of the diagnostic work‐up to confirm the likelihood of chronic bronchitis and to rule out other conditions. Classically, a generalized increase in bronchial infiltrates is expected in dogs with chronic bronchitis. End‐on bronchi (doughnuts) and airways seen in longitudinal section (tram lines) represent airway walls thickened by inflammation (Figure 5.18). However, radiographs are insensitive for detecting chronic bronchitis, and in a case‐controlled evaluation using film radiography, only increased thickness of airway walls and increased numbers of visible airway walls differed between normal dogs and dogs with bronchitis (Mantis et al. 1998). Digital radiography might be more able to detect bronchial abnormalities, however it is important to realize that normal thoracic radiographs do not rule out the diagnosis of chronic bronchitis. CT has been suggested as a means for identifying thickening of airway walls by comparing bronchial wall thickness to pulmonary artery diameter in the cranial lung lobes, with a ratio exceeding 0.6 deemed consistent with the diagnosis of chronic bronchitis (Szabo et al. 2015). However, another study reported that <15% of dogs with chronic bronchitis had a ratio greater than 0.6 and interobserver variability was relatively high, calling into question the value of CT in the diagnosis of bronchitis (Mortier et al. 2018). Different interpretations might be partly explained by the lack of pulmonary inflation during CT in the latter study. In a dog suspicious for bronchitis, the primary value of CT would be to document the sequela of bronchiectasis and airway plugging or to use inspiratory and expiratory CT to determine the presence of airway collapse.

Collecting airway samples by tracheal wash or bronchoscopy is recommended to characterize the cellular infiltrate in the airway and to rule out infectious causes of cough prior to initiating anti‐inflammatory therapy. Bronchoscopy is particularly useful when typical radiographic findings of bronchitis are lacking, because visual findings and airway cytology can be diagnostic; however, careful case selection is important to avoid complications. Obese dogs with marked expiratory effort seem more likely to have anesthetic difficulties, and judicious therapeutic trials using theophylline and weight loss might be considered for these dogs. Dogs with chronic bronchitis have airway hyperemia, the airway mucosa has a cobblestone or irregular appearance, and most dogs have increased mucus lining the airway (Figure 5.19). In animals with long‐standing bronchitis, fibrotic inflammatory nodules can be seen protruding into the bronchial lumen.

Chronic bronchitis can be confirmed with airway sampling via tracheal wash or bronchoscopy. Cytologically, chronic bronchitis is characterized by an increase in total cell numbers and a predominance of non‐degenerate neutrophils (Figure 5.20). Some dogs have a high proportion of lymphocytes in airway washings, and it is unclear whether this represents a variant of chronic bronchitis or is related to bronchomalacia (Johnson and Vernau 2019). Increased mucus is present in many airway samples, and Curschmann’s spirals (bronchial casts of airway mucus) are sometimes noted. Epithelial cells and squamous metaplasia can also be seen on cytologic examination.

Although suppurative inflammation is typically present on cytologic examination, bacterial infection is not a significant problem in the majority of dogs with chronic bronchitis. A light growth of bacteria is not unexpected, because the trachea and large airways of dogs are not sterile. Because Mycoplasma is part of the normal oral flora but also can exacerbate lower airway injury, special culture techniques should be performed in bronchitic animals to rule out Mycoplasma infection.

Treatment

Prognosis

When a diagnosis of chronic bronchitis is made, owners should understand that this is a chronic disease that can be controlled but never fully cured. Reduction in cough by 50% should be considered a successful outcome, particularly in dogs that have concurrent airway collapse or bronchiectasis. The majority of animals have residual cough and exhibit clinical signs periodically throughout life. Bronchoscopic changes and the presence of fibrosis or chronic inflammation on biopsy specimens confirm the irreversibility of airway disease. The goals of therapy are to control inflammation, thus limiting clinical signs, to diagnose and treat infection if it occurs, and to prevent worsening airway disease that might lead to debilitating sequelae such as bronchiectasis and cor pulmonale.

Pathophysiology

Feline bronchial disease is a disorder associated with airway inflammation (eosinophilic or neutrophilic) in the absence of infection that results in excessive mucus production, epithelial hyperplasia, and in the asthmatic form of disease, airway smooth muscle constriction. Over time, inflammation leads to airway remodeling, which results in a physically smaller airway lumen and fixed airway obstruction, that leads to the clinical signs of cough and/or respiratory distress seen in affected cats. Acute respiratory distress is associated with bronchoconstriction of hyper‐responsive airways and is considered one of the hallmarks of the asthmatic phenotype. Chronic cough is sometimes considered more suggestive of bronchitis, although attempts to define inflammatory airway disease as two distinctive syndromes with specific etiologies have not been successful to date.

Disease prevalence has not been established in the cat population, but inflammatory airway disease is encountered frequently and is the most common cause of cough in various studies of feline lower respiratory tract disease. While etiologic factors that induce airway inflammation have not been elucidated in the naturally occurring disease, sensitization to antigen or allergen results in similar clinical and radiographic features of disease in experimental models. Studies in naturally occurring disease have produced conflicting results regarding the role of allergens in disease. In a study of 10 cats with naturally occurring respiratory signs, there were significantly more serum and intradermal responses to a wide variety of allergens (grass, weed, mold, and trees) than in cats lacking observable respiratory tract disease (Moriello et al. 2007). A non‐controlled study in cats with respiratory signs suggested an allergic etiology in 15 of 18 (78%) cats based on 2+ or 3+ serum allergen‐specific IgE results (van Eeden et al. 2020). Two case‐controlled studies identified positive serum allergen responses in both healthy cats and those with various forms of inflammatory airway disease (Buller et al. 2020; Hörner‐Schmid et al. 2023), suggesting that allergy might play a role in some but not all cats. Some studies suggest responsiveness to a mite allergen, however allergy testing in general is fraught with inconsistent results (see Chapter 2). Other factors that have been suggested to play a role in the initiation or perpetuation of airway inflammation include genetic susceptibility, exposure to environmental pollutants or irritants, oxidant‐mediated damage, and gastroesophageal reflux.

History and Signalment

Any age cat can develop inflammatory airway disease, although middle‐aged females (2–8 years) seem to be more frequently represented. Siamese cats may have an increased incidence of disease and might also suffer from a more chronic form of bronchial disease. Coughing and/or respiratory distress are the most frequently encountered complaints in cats with bronchial disease, and the duration of illness, severity of signs, and presence of other clinical abnormalities are variable. The cough is often described as a dry, “hacking” cough, and paroxysms of coughing with marked abdominal effort can be reported. Some cats may be observed to cough just once a day, but this low frequency does not necessarily correlate with the degree of airway inflammation present. Owners can report audible breathing sounds or wheezes that become progressively worse over time. Exercise intolerance can be evident, and the cat may limit its activity to lessen stress on the respiratory system. Cats that develop bronchoconstriction usually display acute respiratory distress, tachypnea, and occasionally cyanosis.

Environmental history is important in cats with bronchial disease, and astute owners are sometimes able to identify trigger events that result in bronchoconstriction. Coughing and respiratory difficulty can worsen in association with use of aerosol sprays, the presence of cigarette smoke, or increased dust in the environment because the airways of cats with inflammation are primed to respond to any irritant. Avoidance of recognized triggers can lessen bronchoconstrictive episodes and reduce cough.

Physical Examination

Cats with airway disease can appear normal at rest and have normal pulmonary auscultation. However, these cats will often display increased tracheal sensitivity, and post‐tussive crackles can sometimes be auscultated. Harsh lung sounds, crackles, or expiratory wheezes can be heard intermittently in affected cats, and the expiratory phase of respiration may be prolonged. In cats in the midst of a bronchoconstrictive episode, air trapping can occur distal to obstructed airways, leading to a barrel‐shaped chest. Auscultation in this area of the lung will be relatively quiet, and increased resonance is found on percussion. The remainder of the cat’s physical examination is typically normal.

Diagnostic Findings

Cats with bronchial disease or feline asthma can have a normal leukogram or a neutrophilic leukocytosis on a CBC, and peripheral eosinophilia is a variable finding. A biochemical profile may reveal hyperproteinemia as a non‐specific indicator of chronic inflammation. Specific tests are required to rule out parasitic bronchitis with Aelurostrongylus (see parasitic bronchitis), feline heartworm disease (see Chapter 8), and infectious bronchitis (Mycoplasma or Bordetella).

The classic radiographic finding in feline bronchial disease is thickening of airways (Figure 5.21); however, radiographs can appear relatively normal, might not match the severity of the clinical presentation, or can appear similar to those found with infectious causes of cough. Radiographic findings and severity scores of cats with eosinophilic, mixed, or neutrophilic inflammatory airway disease were similar in one study (Lee et al. 2020). Cats with acute bronchoconstriction sometimes lack pulmonary infiltrates but show other radiographic signs of airway obstruction, including flattening of the diaphragm, air trapping, or hyperlucency (Figure 5.22). An alveolar pattern (patchy or lobar involving the right middle lung lobe or other lung lobes) can be observed when a mucus plug obstructs a large airway and causes distal atelectasis (Figure 5.23).

Airway sampling through transoral tracheal wash or bronchoscopy can be used to evaluate specimens from feline airways and rule out an infectious cause of cough through culture and cytology (see Chapter 2). Pretreatment with terbutaline (orally or subcutaneously) prior to airway sampling improves the safety of the procedure, perhaps by lessening the bronchoconstrictive response to the lavage process. An eosinophilic tracheal wash specimen is supportive of the diagnosis of feline bronchial disease in a cat with cough and tends to be found in somewhat younger cats (Lee et al. 2020); however, non‐degenerate neutrophils predominate in many cases of feline bronchial disease and mixed inflammation is also common (Figure 5.24). When bronchoscopy is performed and multiple lung lobes are sampled for cytology, differing types of inflammation (eosinophilic and neutrophilic) are found in a single cat in almost 50% of cases (Ybarra et al. 2012).

Bacterial cultures should be submitted to rule out infection, although low numbers of bacteria can be isolated from the airways of both healthy and diseased cats because the airways are not sterile. The role of Mycoplasma as a cause for cough is somewhat controversial, but cats that have this organism isolated in conjunction with neutrophilic inflammation often respond to doxycycline, avoiding the need for long‐term glucocorticoid therapy. Therefore, obtaining specific culture for Mycoplasma as well as aerobic bacterial culture is advised. PCR is also available for detecting Mycoplasma organisms, either as a general class of bacterium or for M. felis.

Treatment

In the animal that presents with cyanosis and open mouth breathing, diagnostic tests should be kept to a minimum until respirations are stabilized. An oxygen‐enriched environment should be provided. Terbutaline, a beta‐2‐agonist, is an effective bronchodilator with minimal cardiac side effects that can be administered subcutaneously or intravenously (0.01 mg/kg) and quickly relieves bronchoconstriction by functionally opposing smooth muscle contraction. Alternatively, albuterol, an inhaled beta‐2‐agonist, could be administered via facemask and spacing chamber. Respiratory rate and effort should be monitored visually during the first 15–30 minutes after treatment to determine therapeutic response. If the cat fails to improve, a second dose of terbutaline can be administered. If the cat remains in respiratory distress and bronchial disease remains highest on the differential list (based on a history of cough), short‐acting glucocorticoids (i.e. dexamethasone) should be administered. Glucocorticoid therapy is not recommended initially because it will reduce ingress of eosinophils into the airway, thus changing the cytology of subsequent tracheal wash or bronchoalveolar lavage. If the cat fails to respond to bronchodilators and glucocorticoids, an alternate etiology of respiratory distress is likely. Because congestive heart failure can also result in tachypnea and respiratory distress, consideration should be given to administering furosemide in certain cases (see Chapter 1).

Prognosis

Feline bronchial disease is associated with substantial morbidity and occasional mortality in the feline population. Cats with poorly controlled inflammation are at risk for airway remodeling, emphysema, bronchiectasis, and pneumothorax. Clinical signs of many cats are well controlled with medication; however, it must be given life‐long in most cats. Cats that experience bronchoconstrictive attacks appear to be most likely to die from the disease or from euthanasia due to the cost of repeated veterinary visits.