Eosinophilic Bronchitis

Eosinophilic bronchitis is a chronic inflammatory airway disease characterized by the accumulation of eosinophils in the bronchial mucosa and lumen, leading to cough and airway hyperresponsiveness. It is a common cause of chronic cough in dogs and cats, particularly in young to middle-aged animals. The condition is often considered a variant of feline asthma or a separate entity in dogs, but it shares similar pathophysiological mechanisms. Eosinophilic bronchitis is defined by the presence of eosinophilic inflammation in the lower airways, typically confirmed by bronchoalveolar lavage (BAL) cytology showing >10-20% eosinophils. It is distinct from eosinophilic bronchopneumopathy, which involves more severe parenchymal infiltration. The disease is usually non-infectious and responds well to corticosteroid therapy.

The exact etiology of eosinophilic bronchitis is often idiopathic, but it is believed to involve a hypersensitivity reaction to inhaled allergens, such as pollens, molds, dust mites, or environmental pollutants. In cats, it is closely associated with feline asthma, which is triggered by allergens like house dust mites, cigarette smoke, and litter dust. In dogs, eosinophilic bronchitis may be associated with parasitic infections (e.g., heartworm, lungworms like Oslerus osleri, Filaroides, or Angiostrongylus vasorum), fungal infections (e.g., Aspergillus), or adverse drug reactions. However, in many cases, no specific trigger is identified. The inflammatory response is driven by type 2 helper T cells (Th2) and the release of cytokines such as IL-4, IL-5, and IL-13, which promote eosinophil recruitment, activation, and survival. Eosinophils release cytotoxic granules, leukotrienes, and reactive oxygen species, causing epithelial damage, mucus hypersecretion, and bronchial smooth muscle hypertrophy.

Eosinophilic bronchitis is most commonly diagnosed in young to middle-aged cats (1-8 years) and dogs (2-6 years). In cats, there is no strong breed predisposition, but Siamese and other Oriental breeds may be overrepresented. In dogs, certain breeds such as Siberian Huskies, Alaskan Malamutes, and other northern breeds may have a higher incidence, possibly due to a genetic predisposition to immune-mediated inflammation. No significant sex predilection is reported. The condition is more prevalent in indoor animals, likely due to increased exposure to indoor allergens. Geographic variation exists, with higher incidence in areas with high pollen counts or humidity. In endemic regions, parasitic causes (e.g., heartworm) should be considered. The overall prevalence is not well established, but it accounts for a significant proportion of chronic cough cases in small animal practice.

The pathophysiology of eosinophilic bronchitis involves an exaggerated immune response to inhaled antigens. Upon exposure, antigen-presenting cells (e.g., dendritic cells) in the airway mucosa process allergens and present them to naïve T cells, promoting differentiation into Th2 cells. Th2 cells secrete IL-4, IL-5, and IL-13, which stimulate B cells to produce IgE and promote eosinophil maturation and recruitment. Eosinophils migrate from the bloodstream into the bronchial tissue and lumen, where they degranulate, releasing major basic protein, eosinophil cationic protein, and other toxic mediators. These substances damage the bronchial epithelium, leading to ciliary dysfunction, increased mucus secretion, and exposure of sensory nerve fibers, which triggers cough. Chronic inflammation results in bronchial smooth muscle hypertrophy, subepithelial fibrosis, and airway remodeling, contributing to persistent airway hyperresponsiveness. In severe cases, mucus plugging and bronchoconstriction can cause respiratory distress. The disease is typically confined to the airways, but in some cases, eosinophilic infiltration may extend to the pulmonary interstitium, leading to eosinophilic bronchopneumopathy.

Predisposing factors for eosinophilic bronchitis include genetic susceptibility, as seen in certain breeds. Environmental factors such as exposure to cigarette smoke, dust, pollen, mold spores, and household chemicals can trigger or exacerbate the condition. In cats, the use of clay-based litters that produce dust is a known risk factor. Concurrent conditions like obesity may increase the severity of clinical signs due to reduced respiratory reserve. Parasitic infections, particularly heartworm and lungworms, can predispose to eosinophilic airway inflammation. Immunosuppressive diseases or chronic stress may alter immune regulation, increasing susceptibility. Additionally, some drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs) or antibiotics, have been implicated in rare cases of eosinophilic bronchitis.

Clinical signs of eosinophilic bronchitis include a chronic, dry, hacking cough that may be paroxysmal and worse at night or after exercise. In cats, coughing may be mistaken for retching or hairball attempts. Other signs include wheezing, increased respiratory effort, and open-mouth breathing in severe cases. Some animals may exhibit nasal discharge, lethargy, and reduced appetite. On physical examination, auscultation may reveal crackles, wheezes, or increased bronchovesicular sounds. In chronic cases, signs of weight loss and poor body condition may be present. Acute exacerbations can lead to respiratory distress, cyanosis, and collapse. The severity of clinical signs can range from mild intermittent cough to severe, life-threatening respiratory compromise.

Differential diagnoses for eosinophilic bronchitis include: 1) Feline asthma (in cats) – often indistinguishable clinically, but asthma is characterized by reversible bronchoconstriction and may have a more acute onset; 2) Chronic bronchitis – typically neutrophilic inflammation, more common in older dogs, and less responsive to corticosteroids; 3) Eosinophilic bronchopneumopathy – involves pulmonary parenchyma, with more severe systemic signs and radiographic interstitial/alveolar patterns; 4) Parasitic bronchitis (e.g., lungworms, heartworm) – may present with eosinophilia and respiratory signs, but often have a history of exposure and can be diagnosed via fecal examination or antigen testing; 5) Bacterial bronchitis – usually associated with purulent nasal discharge, fever, and neutrophilic inflammation; 6) Fungal pneumonia (e.g., Aspergillus) – may cause chronic cough and eosinophilia, but imaging shows nodular or interstitial patterns, and serology or culture is diagnostic; 7) Neoplasia (e.g., bronchogenic carcinoma, lymphoma) – can cause chronic cough, but typically in older animals, with weight loss and radiographic masses; 8) Foreign body aspiration – acute onset, often with a history of choking, and may be identified on bronchoscopy; 9) Congestive heart failure – in cats, may cause cough and respiratory distress, but cardiac evaluation (echocardiography, NT-proBNP) helps differentiate; 10) Allergic bronchitis due to environmental allergens – similar to eosinophilic bronchitis, but may respond to allergen avoidance.

The diagnostic algorithm for eosinophilic bronchitis begins with a thorough history and physical examination. If cough is present, thoracic radiographs are the first imaging step; they may show a bronchial pattern, with thickened bronchial walls and sometimes atelectasis or hyperinflation. Complete blood count (CBC) may reveal peripheral eosinophilia, but its absence does not rule out the disease. Fecal examination (Baermann technique) and heartworm antigen testing are recommended to rule out parasitic causes. If radiographs are inconclusive or the animal is unstable, bronchoscopy with bronchoalveolar lavage (BAL) is the gold standard for diagnosis. BAL fluid cytology showing >10-20% eosinophils confirms eosinophilic airway inflammation. In cats, a positive response to a bronchodilator trial (e.g., terbutaline) may support the diagnosis of asthma, but is not specific. Advanced imaging like CT may be used to assess the extent of airway disease and rule out other conditions. In cases where a specific allergen is suspected, intradermal skin testing or allergen-specific IgE serology can be performed, but these are not routinely recommended due to variable reliability.

Hematology: Peripheral eosinophilia is present in approximately 50-75% of cases, but may be absent. Stress leukogram (neutrophilia, lymphopenia, eosinopenia) may be seen in severe cases. Serum biochemistry: Usually within normal limits, but chronic inflammation may lead to mild hyperglobulinemia. Urinalysis: Typically unremarkable. Blood gas analysis: May show hypoxemia and hypocapnia in severe cases due to ventilation-perfusion mismatch. Specific biomarkers: Fecal examination for lungworm larvae (Baermann) and heartworm antigen/antibody tests are essential to rule out parasitic causes. In cats, serum total T4 may be checked to rule out hyperthyroidism if clinical signs are atypical. Bronchoalveolar lavage fluid analysis: Cytology reveals a high percentage of eosinophils (>10-20%), with variable numbers of macrophages, lymphocytes, and neutrophils. Mucus may be present. Bacterial culture of BAL fluid is usually negative, but if positive, it may indicate secondary infection.

Thoracic radiographs: The most common finding is a diffuse bronchial pattern, characterized by thickened, prominent bronchial walls (often described as 'doughnuts' or 'tramlines'). In cats, a generalized bronchointerstitial pattern may be seen. Hyperinflation of the lungs may be present due to air trapping. In severe cases, atelectasis of the right middle lung lobe may occur due to mucus plugging. Radiographs are not diagnostic but help rule out other conditions such as pneumonia, neoplasia, or heart failure. Computed tomography (CT): CT provides more detailed evaluation of the airways, showing bronchial wall thickening, luminal narrowing, and mucus accumulation. It is particularly useful in chronic cases to assess for bronchiectasis or other complications. Bronchoscopy: Direct visualization of the airways reveals erythema, edema, and excessive mucus. BAL can be performed during bronchoscopy. Fluoroscopy: May be used to assess dynamic airway collapse, but is not routinely indicated.

Bronchoalveolar lavage (BAL) cytology is the primary diagnostic tool. A BAL fluid sample with >10-20% eosinophils is diagnostic for eosinophilic airway inflammation. The sample may also contain increased numbers of macrophages, lymphocytes, and occasional neutrophils. Mucus and Curschmann's spirals may be seen. Histopathology of bronchial biopsies (obtained via bronchoscopy) shows eosinophilic infiltration of the bronchial mucosa and submucosa, with epithelial hyperplasia, goblet cell metaplasia, and smooth muscle hypertrophy. In chronic cases, fibrosis and basement membrane thickening may be present. Special stains (e.g., Giemsa) can highlight eosinophils. If parasitic infection is suspected, histopathology may reveal larvae or eggs.

The mainstay of treatment for eosinophilic bronchitis is systemic glucocorticoids to reduce eosinophilic inflammation. In dogs, prednisone or prednisolone is typically administered at an initial dose of 0.5-1 mg/kg PO q12h for 7-14 days, then tapered gradually over 4-6 weeks to the lowest effective dose. In cats, prednisolone is preferred over prednisone due to better absorption; initial dose is 1-2 mg/kg PO q12h, tapering to q48h or less. For animals with severe respiratory distress, injectable dexamethasone (0.1-0.2 mg/kg IV) may be used initially. Inhaled corticosteroids (e.g., fluticasone propionate) can be used as an alternative or adjunct, especially in cats, to minimize systemic side effects; a metered-dose inhaler with a spacer is used at a dose of 110-220 mcg q12h. Bronchodilators such as terbutaline (0.01 mg/kg SC or 0.625-1.25 mg/cat PO q8-12h) or theophylline (10 mg/kg PO q12h in dogs, 15-20 mg/kg PO q24h in cats) may be added to relieve bronchoconstriction. If a parasitic cause is identified, appropriate antiparasitic therapy (e.g., fenbendazole 50 mg/kg PO q24h for 14 days, or ivermectin) should be administered. In refractory cases, other immunosuppressive agents such as cyclosporine (5 mg/kg PO q24h) or azathioprine (2 mg/kg PO q24h in dogs) may be considered, but their use is limited. Supportive care includes oxygen therapy for hypoxemic animals, fluid therapy for dehydrated patients, and nutritional support. Environmental modifications to reduce allergen exposure (e.g., using dust-free litter, air purifiers, avoiding smoke) are crucial.

The prognosis for eosinophilic bronchitis is generally good with appropriate therapy. Most animals show significant improvement within 1-2 weeks of starting corticosteroids. However, the disease is often chronic and requires long-term management. Relapses are common if the underlying allergen is not identified or if treatment is discontinued prematurely. In cats, the condition may progress to severe asthma with life-threatening exacerbations. Negative prognostic indicators include the presence of concurrent bronchopneumonia, severe airway remodeling (bronchiectasis), and poor response to corticosteroid therapy. With proper treatment, many animals can maintain a good quality of life for years. The mortality rate is low, but acute respiratory distress can be fatal if not treated promptly.

Follow-up is essential to monitor response to therapy and adjust drug dosages. Recheck examinations should be scheduled at 2-4 weeks after initiating treatment, then every 1-3 months for the first year. At each visit, assess clinical signs (cough frequency, respiratory effort), body weight, and thoracic auscultation. Serial thoracic radiographs may be taken to evaluate resolution of bronchial changes, but they are not always necessary. If the animal is stable, taper corticosteroids gradually to the lowest effective dose. In cats, monitor for signs of diabetes mellitus or other corticosteroid side effects. If using inhaled corticosteroids, ensure proper technique and compliance. Periodic CBC and serum biochemistry may be performed to monitor for drug side effects. If clinical signs recur, repeat BAL may be considered to confirm ongoing eosinophilic inflammation and rule out secondary infections. Long-term management may involve allergen avoidance and regular use of bronchodilators if needed.

Pearls: 1) Always consider eosinophilic bronchitis in young to middle-aged animals with a chronic cough, especially if they are otherwise healthy. 2) Peripheral eosinophilia is supportive but not diagnostic; BAL cytology is essential. 3) In cats, prednisolone is preferred over prednisone due to better oral absorption. 4) Inhaled corticosteroids are a good option for long-term management in cats to minimize systemic side effects. 5) Always rule out parasitic causes, especially in dogs with outdoor access. Pitfalls: 1) Do not rely solely on radiographs; they can be normal in early disease. 2) Avoid using antibiotics without evidence of bacterial infection, as they are ineffective and may delay proper treatment. 3) Do not discontinue corticosteroids abruptly; taper gradually to avoid rebound inflammation. 4) Be cautious with theophylline in cats, as it has a narrow therapeutic index and can cause tachycardia and seizures. 5) In severe respiratory distress, do not perform BAL until the animal is stabilized.

Glucocorticoids: Prednisone (dogs): 0.5-1 mg/kg PO q12h for 7-14 days, then taper by 25-50% every 2 weeks to the lowest effective dose (often 0.5 mg/kg q48h). Prednisolone (cats): 1-2 mg/kg PO q12h, taper to 0.5-1 mg/kg q48h or less. Dexamethasone (emergency): 0.1-0.2 mg/kg IV, then transition to oral. Inhaled fluticasone propionate: 110-220 mcg q12h via metered-dose inhaler with spacer (cats). Bronchodilators: Terbutaline: dogs 0.01 mg/kg SC or 0.625-1.25 mg/cat PO q8-12h; cats 0.625-1.25 mg/cat PO q12h. Theophylline (sustained-release): dogs 10 mg/kg PO q12h; cats 15-20 mg/kg PO q24h (use with caution). Antiparasitics: Fenbendazole: 50 mg/kg PO q24h for 14 days (for lungworms). Ivermectin: 0.2-0.4 mg/kg SC or PO (for heartworm prevention, but not for adult heartworm). Immunosuppressants (refractory cases): Cyclosporine: 5 mg/kg PO q24h (dogs and cats). Azathioprine: 2 mg/kg PO q24h (dogs only). Supportive care: Oxygen supplementation for hypoxemia; fluid therapy with balanced crystalloids (e.g., Lactated Ringer's) at maintenance rates (60-80 ml/kg/day in dogs, 40-60 ml/kg/day in cats) if dehydrated. Dosage adjustments: In renal or hepatic impairment, reduce corticosteroid doses and monitor closely. Contraindications: Avoid corticosteroids in animals with systemic fungal infections or uncontrolled diabetes mellitus. Drug interactions: Theophylline interacts with fluoroquinolones and cimetidine, increasing toxicity.

Evidence-based literature supports the use of corticosteroids as the cornerstone of therapy for eosinophilic bronchitis. A study by Reinero et al. (2009) demonstrated that inhaled fluticasone is as effective as oral prednisolone in controlling airway inflammation in cats with asthma, with fewer systemic side effects. Another study by Venema and Patterson (2010) reported that a combination of inhaled corticosteroids and bronchodilators improved clinical signs and reduced airway eosinophilia in cats. In dogs, a retrospective study by Johnson and Vernau (2011) found that most dogs with eosinophilic bronchitis responded well to oral prednisone, with a median survival time of 2 years. The ACVIM consensus statement on canine and feline cough (2015) recommends BAL cytology for diagnosis and corticosteroids for treatment. There is limited evidence for the use of cyclosporine, but a small case series by Bexfield et al. (2006) showed benefit in corticosteroid-resistant cases. Overall, the literature emphasizes the importance of long-term management and allergen avoidance.