Tree-in-bud (TIB) appearance on HRCT consists of 2-4 mm centrilobular nodules with branching linear opacities. It usually represents impacted/inflamed terminal bronchioles with endobronchial spread of material, most often infection. See the
radiologic-pathologic overview.
Differential diagnosis
1. Infectious bronchiolitis - most common
- Tuberculosis, especially endobronchial or post-primary TB
- Nontuberculous mycobacteria: MAC, M. abscessus, particularly if middle lobe/lingula bronchiectasis is present
- Bacterial bronchopneumonia / bronchiolitis: including Staphylococcus, Pseudomonas, H. influenzae
- Viral bronchiolitis: RSV, influenza, parainfluenza, adenovirus
- Less commonly fungal airway infection in immunocompromised patients
Clues: upper-lobe TIB, cavitation, necrotic nodes favor TB; cylindrical bronchiectasis with right-middle-lobe/lingular disease favors NTM.
2. Aspiration-related bronchiolitis
- Recurrent aspiration due to dysphagia, GERD, altered sensorium, neuromuscular disease, esophageal disorder, or poor dentition.
Clues: dependent or basal predominance, often right lower lobe; may coexist with patchy consolidation and bronchiectasis. Recurrent aspiration produces basilar TIB opacities.
Murray & Nadel's Textbook of Respiratory Medicine, p. 945.
3. Bronchiectasis with mucus impaction
- Cystic fibrosis
- Primary ciliary dyskinesia
- Allergic bronchopulmonary aspergillosis
- Post-infective bronchiectasis
- Immunodeficiency-associated bronchiectasis
Clues: airway dilatation, bronchial wall thickening, mucus plugging, recurrent infection.
4. Noninfectious inflammatory small-airway disease
- Diffuse panbronchiolitis
- Follicular bronchiolitis, including rheumatoid arthritis and Sjögren syndrome
- Constrictive/obliterative bronchiolitis
- Inhalational bronchiolitis
Clues: mosaic attenuation and expiratory air trapping point toward bronchiolar obstruction; clinical autoimmune disease may suggest follicular bronchiolitis.
5. Vascular causes - uncommon
- Tumor emboli or carcinomatous endarteritis
- Septic pulmonary emboli, though these more typically create peripheral nodules, sometimes cavitating
6. Neoplastic airway spread - rare
- Endobronchial spread of adenocarcinoma
- Bronchovascular/interstitial tumor infiltration
- Lymphoma or leukemic pulmonary infiltration
Clues: persistence/progression despite appropriate antimicrobial treatment, known malignancy, lymphangitic features, or atypical distribution.
Practical pattern-based approach
| HRCT association/distribution | More likely cause |
|---|
| Upper-lobe TIB + cavity | TB or other mycobacterial infection |
| Middle lobe/lingula TIB + bronchiectasis | NTM, especially MAC |
| Lower-lobe/dependent TIB + consolidation | Aspiration |
| Diffuse TIB + bronchiectasis/mucus plugs | Chronic airway infection, CF, ABPA, ciliary disorder |
| TIB + mosaic attenuation/air trapping | Small-airway inflammatory or constrictive bronchiolitis |
| Persistent unilateral focal TIB | Local obstruction, foreign body, endobronchial lesion, focal infection |
Next clinical correlation: symptoms, fever, chronic cough/sputum, weight loss/night sweats, aspiration risk, immune status, and prior CTs. Common work-up includes sputum Gram stain/culture, AFB smear/culture with NAAT when TB is possible, and bronchoscopy if disease is focal, progressive, or sputum testing is unrevealing.