Tracheitis

Tracheitis is the inflammation of the tracheal mucosa and submucosa, often extending to the larynx and bronchi. It can be acute or chronic, infectious or non-infectious, and may be primary or secondary to other respiratory diseases. In veterinary medicine, tracheitis is commonly seen in dogs and cats, frequently as a component of infectious tracheobronchitis (kennel cough) or as a result of mechanical irritation, such as from intubation or tracheal collapse. The condition is characterized by coughing, often paroxysmal and non-productive, and may progress to pneumonia if lower airways are involved. Classification includes acute infectious tracheitis, chronic tracheitis secondary to collapse, and eosinophilic tracheitis (rare). Systemic relevance includes potential for sepsis in severe bacterial cases and respiratory distress if airway obstruction occurs.

Primary infectious agents include: Viruses: Canine parainfluenza virus (CPIV), canine adenovirus type 2 (CAV-2), canine distemper virus (CDV), canine herpesvirus, feline herpesvirus-1 (FHV-1), feline calicivirus (FCV). Bacteria: Bordetella bronchiseptica (primary pathogen in dogs and cats), Streptococcus equi subsp. zooepidemicus, Mycoplasma spp., Pasteurella multocida (cats), Escherichia coli, and opportunistic pathogens secondary to viral damage. Fungi: Rare, but Aspergillus spp. can cause tracheobronchitis in immunocompromised animals. Parasites: Oslerus osleri (dog lungworm) can cause tracheal nodules and inflammation. Non-infectious causes: Inhalation of irritants (smoke, dust, chemicals), gastroesophageal reflux (aspiration), tracheal collapse (chronic irritation), foreign bodies, trauma (including endotracheal intubation), and allergic or eosinophilic inflammation. Autoimmune or immune-mediated causes are rare. Virulence factors: Bordetella bronchiseptica produces toxins (e.g., tracheal cytotoxin) that impair ciliary function; viruses cause epithelial necrosis and ciliostasis, predisposing to secondary bacterial infection. Transmission is via aerosolized respiratory secretions, direct contact, or fomites.

Tracheitis is common in dogs and cats worldwide. In dogs, infectious tracheobronchitis is highly contagious and often outbreaks in kennels, shelters, and boarding facilities. Young dogs (<1 year) are more susceptible, but all ages can be affected. Certain breeds, such as brachycephalic dogs (e.g., Bulldogs, Pugs) are predisposed to tracheal collapse, which can lead to chronic tracheitis. Cats are commonly affected by FHV-1 and FCV, especially in multi-cat environments. No sex predilection is reported. Seasonal patterns may correlate with increased respiratory infections in colder months. Geographic variation exists: Bordetella bronchiseptica is ubiquitous, while Oslerus osleri is more common in certain regions (e.g., southeastern United States). Incidence rates are not well-documented but are high in high-density populations. Breed-specific genetic factors: Brachycephalic airway syndrome predisposes to tracheal hypoplasia and collapse, increasing risk of chronic tracheitis.

The tracheal mucosa is lined by ciliated pseudostratified columnar epithelium with goblet cells. Infectious agents initially adhere to epithelial cells, causing ciliary dysfunction and epithelial necrosis. Viral replication leads to inflammation with infiltration of neutrophils, macrophages, and lymphocytes. This results in mucosal edema, hyperemia, and increased mucus production. Bacterial pathogens, particularly Bordetella, colonize damaged epithelium and release toxins that further impair mucociliary clearance. The inflammatory response triggers cough reflex via irritant receptors. In chronic cases, such as tracheal collapse, repeated mechanical trauma leads to squamous metaplasia, fibrosis, and cartilage degeneration. Eosinophilic tracheitis involves infiltration of eosinophils, possibly due to allergic triggers. Systemic inflammatory response may occur if infection spreads to lower airways (bronchitis, pneumonia) or if bacteremia ensues. Secondary complications include bronchopneumonia, atelectasis, and in severe cases, respiratory failure.

Intrinsic factors: Young age (immature immune system), immunocompromised status (e.g., FIV, FeLV in cats; chronic corticosteroid use), anatomical abnormalities (brachycephalic syndrome, tracheal hypoplasia, collapsing trachea), and concurrent respiratory diseases (e.g., chronic bronchitis). Extrinsic factors: High-density housing (kennels, shelters), poor ventilation, stress, transport, vaccination status (incomplete or absent), exposure to irritants (cigarette smoke, dust), and iatrogenic factors (endotracheal intubation, tracheostomy). In cats, stress is a major trigger for FHV-1 reactivation. Dietary factors are not directly implicated, but obesity can exacerbate respiratory compromise.

Peracute/acute: Sudden onset of paroxysmal, dry, hacking cough, often worse with exercise or excitement. Cough may be productive (mucoid or purulent) if secondary bacterial infection. Fever, lethargy, anorexia, and nasal discharge may be present. In severe cases, respiratory distress, cyanosis, and open-mouth breathing. Subacute/chronic: Persistent cough lasting >2 weeks, often with gagging or retching. In tracheal collapse, cough is often 'goose-honking' and exacerbated by pressure on the trachea. Cats may show sneezing, ocular discharge, and conjunctivitis if viral etiology. Physical examination: Pharyngeal irritation, tracheal sensitivity on palpation, increased bronchovesicular sounds, crackles or wheezes if lower airways involved. Terminal: Severe respiratory distress, collapse, and signs of systemic illness (septic shock).

1. Bronchitis (acute or chronic): Cough similar, but auscultation reveals bronchial sounds; radiographs show bronchial pattern. 2. Bronchopneumonia: Fever, productive cough, crackles, consolidation on radiographs, leukocytosis. 3. Tracheal collapse: Chronic cough, 'goose-honking', radiographs show narrowing on expiration. 4. Foreign body: Acute onset, often with gagging, unilateral nasal discharge, radiographs or bronchoscopy reveal object. 5. Laryngeal paralysis: Inspiratory stridor, cough, exercise intolerance; laryngeal examination confirms. 6. Heartworm disease (dogs): Cough, exercise intolerance, eosinophilia, heartworm antigen test positive. 7. Feline asthma (cats): Chronic cough, eosinophilic inflammation, bronchial pattern on radiographs. 8. Neoplasia (tracheal or pulmonary): Progressive cough, hemoptysis, weight loss; imaging and biopsy. 9. Fungal infection (e.g., aspergillosis): Chronic cough, nasal discharge, fungal culture or serology. 10. Parasitic infection (Oslerus osleri): Cough, nodules on tracheal mucosa on bronchoscopy.

Step 1: History and physical examination, including tracheal palpation and auscultation. Step 2: Minimum database: CBC, serum biochemistry, urinalysis, and fecal examination (for lungworms). Step 3: Thoracic radiographs (three views) to assess tracheal lumen, pulmonary pattern, and evidence of pneumonia. Step 4: If infectious tracheobronchitis suspected, consider PCR or viral isolation from nasal/pharyngeal swabs. Step 5: If chronic or unresponsive, perform bronchoscopy with tracheal wash for cytology and culture. Step 6: If tracheal collapse suspected, perform fluoroscopy or dynamic radiographs. Step 7: Advanced imaging (CT) if mass or foreign body suspected. Step 8: In cats, test for FIV/FeLV and herpesvirus/calicivirus. Step 9: Consider echocardiography if cardiac disease is a differential. Step 10: If eosinophilic tracheitis suspected, evaluate for underlying allergic triggers.

Hematology: In viral tracheitis, CBC may be normal or show mild lymphopenia. In bacterial infection, neutrophilia with left shift may be present. Eosinophilia may be seen in parasitic or eosinophilic tracheitis. Serum biochemistry: Usually unremarkable; may show mild elevations in acute phase proteins (e.g., CRP). Urinalysis: Typically normal. Blood gas analysis: May show hypoxemia if severe respiratory distress. Specific biomarkers: CRP may be elevated in bacterial infections; procalcitonin is not routinely used. Serology/PCR: For viral agents (CPIV, CAV-2, CDV, FHV-1, FCV) and Bordetella. Fecal examination for Oslerus larvae (Baermann technique). Endocrine assays: Not indicated unless concurrent disease.

Radiography: Thoracic radiographs may show normal trachea or diffuse bronchial pattern. In tracheal collapse, lateral view may show narrowing of the tracheal lumen on expiration (cervical or thoracic). In chronic bronchitis, bronchial pattern with 'doughnut' opacities. Ultrasonography: Not typically used for trachea, but can evaluate cervical trachea for masses. Computed Tomography (CT): Provides detailed assessment of tracheal lumen, wall thickness, and extraluminal masses. Magnetic Resonance Imaging (MRI): Rarely used but can evaluate soft tissue structures. Endoscopy: Bronchoscopy is the gold standard for direct visualization of tracheal mucosa, detection of foreign bodies, collapse, and sampling. Fluoroscopy: Dynamic evaluation of tracheal collapse during respiration. Echocardiography: Not directly relevant but may rule out cardiac causes of cough.

Tracheal wash cytology: In infectious tracheitis, may show neutrophilic inflammation with intracellular bacteria (if bacterial). In eosinophilic tracheitis, >20% eosinophils. In chronic irritation, goblet cell hyperplasia and mucus. Histopathology (biopsy): Mucosal erosion, ulceration, inflammatory infiltrate (neutrophils, lymphocytes, plasma cells), fibrosis, and squamous metaplasia in chronic cases. Special stains: Gram stain for bacteria, Giemsa for protozoa, PAS for fungal elements.

Emergency stabilization: If respiratory distress, provide oxygen supplementation, and in severe obstruction, consider tracheostomy. Fluid therapy: IV crystalloids (e.g., LRS) at maintenance rates (60 ml/kg/day for dogs, 40-60 ml/kg/day for cats) with adjustments for dehydration. Primary medical therapy: For infectious tracheitis, antimicrobials if bacterial infection confirmed or suspected (e.g., doxycycline 5-10 mg/kg PO q12h for 7-14 days; amoxicillin-clavulanate 12.5-25 mg/kg PO q12h). For viral etiology, supportive care and antitussives (e.g., hydrocodone 0.22 mg/kg PO q6-8h) may be used cautiously. For tracheal collapse, manage with weight loss, cough suppressants, bronchodilators (e.g., theophylline 10-20 mg/kg PO q12h), and corticosteroids (e.g., prednisone 0.5-1 mg/kg PO q12h tapering). For eosinophilic tracheitis, corticosteroids (e.g., prednisone 1-2 mg/kg PO q12h) and possibly antihistamines. Surgical/interventional: For tracheal collapse, placement of intraluminal stents in severe cases. For foreign bodies, bronchoscopic removal. Supportive care: Humidification, rest, and avoidance of irritants. Dietary: If obese, weight reduction. Physical rehabilitation: Not typically required.

Short-term: For acute infectious tracheitis, prognosis is excellent with appropriate therapy, usually resolving in 1-2 weeks. Medium-term: For chronic tracheitis secondary to collapse, prognosis is guarded; many dogs require lifelong management. Long-term: For eosinophilic tracheitis, prognosis is good with corticosteroid therapy but may require long-term treatment. Mortality is low unless severe pneumonia or respiratory failure occurs. Negative prognostic indicators: Presence of pneumonia, systemic signs, immunocompromise, and lack of response to therapy.

Re-check at 7-14 days for acute cases to ensure resolution. For chronic cases, re-check every 3-6 months. Serial lab monitoring: CBC and biochemistry if on long-term corticosteroids. Repeat imaging: Radiographs or bronchoscopy if clinical signs persist. Dose-titration: Taper corticosteroids slowly over weeks. Long-term management: For tracheal collapse, maintain ideal body weight, use harness instead of collar, and avoid triggers.

Pearls: Always consider tracheal collapse in small breed dogs with chronic cough. Use antitussives cautiously; they may suppress protective cough. In cats, stress reduction is key to prevent FHV-1 recurrence. Pitfalls: Overuse of antibiotics for viral tracheitis; failure to diagnose underlying cause (e.g., foreign body, collapse); using cough suppressants in cases with productive cough; ignoring concurrent cardiac disease.

Antimicrobials: Doxycycline (5-10 mg/kg PO q12h) for Bordetella and Mycoplasma; Amoxicillin-clavulanate (12.5-25 mg/kg PO q12h) for broad-spectrum coverage; Azithromycin (5-10 mg/kg PO q24h) for 3-5 days. Antitussives: Hydrocodone (0.22 mg/kg PO q6-8h) or Butorphanol (0.05-0.1 mg/kg PO q6-12h) for non-productive cough. Bronchodilators: Theophylline (10-20 mg/kg PO q12h) or Aminophylline (10 mg/kg PO q8h). Corticosteroids: Prednisone (0.5-1 mg/kg PO q12h) for inflammation, tapering over 2-4 weeks. For eosinophilic tracheitis, higher doses (1-2 mg/kg) may be needed. Antihistamines: Cetirizine (0.5-1 mg/kg PO q24h) for allergic component. Fluid therapy: LRS at maintenance rates. Dosage adjustments: In renal/hepatic impairment, reduce doses of doxycycline and theophylline. Contraindications: Avoid corticosteroids in infectious tracheitis unless severe inflammation. Drug interactions: Theophylline interacts with fluoroquinolones and cimetidine.

ACVIM consensus statements on canine infectious respiratory disease complex (CIRDC) recommend vaccination against CPIV, CAV-2, and Bordetella. Studies show that doxycycline is effective against Bordetella. For tracheal collapse, a study by Johnson et al. (2010) reported that stent placement improves clinical signs but has complications. Eosinophilic tracheitis is rare; case reports suggest good response to corticosteroids. ISCAID guidelines for antimicrobial use in respiratory tract infections recommend avoiding antibiotics in mild viral cases. Plumb's Drug Handbook provides dosing references. Overall, evidence is limited for many therapies, and treatment is often empirical.