Purulent diseases – bronchiectasis, pulmonary abscess
Two chronic suppurative diseases of the lung, one in which the airways are permanently widened and fill with infected mucus, and one in which a pocket of lung dies and fills with pus.
- 12 min read
- 5 questions
- Checked 28 Oct 2026
Contents6 sections
At a glance
- Bronchiectasis is permanent widening of the bronchi, with a cycle of infection, neutrophilic inflammation and failed mucus clearance. It causes a daily productive cough, recurrent infections and sometimes haemoptysis.
- HRCT makes the diagnosis: dilated bronchi wider than the adjacent artery, which do not taper. The search for a cause includes immunoglobulins, tests for cystic fibrosis and ciliary dyskinesia, and Aspergillus.
- Treatment is daily airway clearance, prompt antibiotics for exacerbations guided by sputum culture, and in frequent exacerbators long-term azithromycin or inhaled antibiotics; treat the cause, and rehabilitate.
- A lung abscess is a cavity of pus within the lung, mostly after aspiration of mouth anaerobes, or behind an obstruction. It gives a foul sputum, a swinging fever and weight loss.
- The film shows a thick-walled cavity with an air–fluid level. Treat for 4 to 6 weeks with an antibiotic that covers anaerobes, drain if it fails, and look for a cancer or a foreign body.
Definition and overview
The syllabus groups the two as "purulent diseases" of the lung: both are chronic infections that produce pus, and both are treated for weeks.
Bronchiectasis
Bronchiectasis means abnormal and permanent dilatation of the airways. In practice it is a clinical syndrome, with a chronic productive cough and recurrent respiratory infections, in a patient whose CT shows dilated bronchi. Its core is a "vicious circle": neutrophilic inflammation damages the airway wall, the damage impairs mucociliary clearance, mucus stagnates and bacteria colonise, and infection drives further inflammation. Cystic fibrosis bronchiectasis is regarded as a separate entity.
Three CT patterns are described: cylindrical (tubular, the commonest), varicose (beaded) and cystic or saccular (the worst, with rounded sacs).
Point at a name or a part to light it.
Bronchiectasis is a permanent widening of the bronchi. A normal bronchus narrows as it divides; the commonest form, cylindrical, stays wide and even, varicose swells and narrows like beads, and cystic, the most severe, ends in sacs that often hold an air–fluid level. On CT, a bronchus that fails to taper over 2 cm beyond a division is the most sensitive sign.
Simplified: not to scale: the walls drawn thicker than life so they read; each bronchus drawn dividing twice, where the bronchial tree divides many more times before its alveoli; each drawn as a flat outline seen from the side, its wall the same all round; each form drawn on its own, where one patient often has more than one, in different lobes.
3 sources
- Kumar and Clark's Clinical Medicine, 10th edition. Elsevier, 2021. Chapter 28, Respiratory disease: bronchiectasis (pp. 982–983).
- Juliusson G, Gudmundsson G. Diagnostic imaging in adult non-cystic fibrosis bronchiectasis. Breathe (Sheff). 2019;15(3):190-197.
- Gramegna A, Amati F, Terranova L, et al. Neutrophil elastase in bronchiectasis. Respir Res. 2017;18:211.
Lung abscess
A lung abscess is localised suppuration and necrosis of the lung with a cavity, which is visible on the film or CT, often with a fluid level. A fluid level always means an air–liquid interface. It is primary when it arises in a previously normal lung with no obstruction or immune defect, usually after aspiration (a necrotising pneumonia in a healthy person is counted here too), and secondary when it complicates an obstructing tumour, bronchiectasis, an immune defect, a septic embolus or spread from elsewhere; sources draw the line slightly differently. By convention it is acute for up to 4 to 6 weeks and chronic after that. Cavities are also made by tuberculosis, cancer and vasculitis; they are not "abscesses" in this sense unless they are infected and fluid-filled.
Etiology and pathophysiology
Bronchiectasis
A cause is found in only about half of cases; the rest are labelled idiopathic. The causes are:
| Group | Examples |
|---|---|
| Post-infective | severe pneumonia, tuberculosis (the leading cause worldwide), whooping cough, measles, aspiration |
| Mechanical obstruction | foreign body, tumour, enlarged lymph nodes, post-tuberculous stenosis, inspissated mucus |
| Immune deficiency | primary (panhypogammaglobulinaemia, selective IgA or IgG subclass deficiency) or secondary (HIV, lymphoma, leukaemia) |
| Mucociliary clearance defects | cystic fibrosis; primary ciliary dyskinesia (Kartagener syndrome is the form with situs inversus, which includes dextrocardia, with sinusitis); Young syndrome (azoospermia and sinusitis) |
| Immune over-response | allergic bronchopulmonary aspergillosis (ABPA); graft-versus-host disease; after lung transplant |
| Associated diseases | COPD and asthma (an increasingly recognised overlap), rheumatoid arthritis, inflammatory bowel disease, α1-antitrypsin deficiency, idiopathic pulmonary fibrosis (traction bronchiectasis), congenital defects of the bronchial wall |
In primary ciliary dyskinesia the dynein arms of the cilia are defective, so mucus is not cleared. The same defect in the embryonic cilia that set left from right leaves the orientation of the organs random, so about half of the patients have situs inversus (Kartagener syndrome), and in the sperm tail it causes male infertility.
In the airway, an insult (infection, obstruction or a clearance defect) starts the cycle. Neutrophils release elastase and other enzymes that destroy the elastic tissue and muscle of the bronchial wall, which dilates and loses its tone. Cilia are lost, and the epithelium is replaced by a mucus-secreting one. Mucus stagnates, and the airways are colonised, mostly by H. influenzae and Pseudomonas aeruginosa, but also Strep. pneumoniae, Staph. aureus, Moraxella and non-tuberculous mycobacteria. The bronchial arteries enlarge and become fragile, which is the source of haemoptysis.
Lung abscess
Most primary abscesses follow aspiration of oropharyngeal contents in a patient who is at risk: alcohol use disorder, seizures, reduced consciousness, stroke, swallowing disorders, and poor dentition (gingivitis is the source of the organisms). The bacteria are the mouth anaerobes (Fusobacterium, Peptostreptococcus, Prevotella) with streptococci, including the Strep. anginosus (milleri) group. The aspirate settles in the dependent segments: in a supine patient the posterior segments of the upper lobes and the apical (superior) segments of the lower lobes, in an upright one the basal segments, and the right lung more often than the left (the right middle lobe and the apical or posterior segments of the right lower lobe are the classic sites).
The sequence is aspiration pneumonitis, then pneumonia over days, then necrosis with liquefaction over one to two weeks, and finally rupture into a bronchus, where the pus is coughed up and an air–fluid level appears.
The other causes are:
- necrotising pneumonia with Staph. aureus (including the Panton–Valentine leucocidin strains), Klebsiella pneumoniae, gram-negative enteric bacilli and H. influenzae;
- inadequately treated pneumonia;
- bronchial obstruction by an endoluminal cancer or an inhaled foreign body;
- septic emboli, from right-sided endocarditis, an infected intravenous line, pelvic septic thrombophlebitis, or septic thrombophlebitis of the internal jugular vein after a throat infection (Lemierre syndrome), giving multiple peripheral abscesses;
- tuberculosis and fungi; and
- spread from an amoebic liver abscess.
Clinical features
Bronchiectasis
The patient has a persistent cough with large amounts of purulent sputum every day, often worse in the morning, and recurrent chest infections, in which the sputum volume and purulence increase. Others are breathlessness and wheeze as the disease advances; pleuritic chest pain and fever in infection; fatigue; and haemoptysis, usually streaks with infection, but occasionally massive. There may be rhinosinusitis, which suggests ciliary disease or an immune defect. In severe cases the sputum separates in a glass into layers.
On examination coarse crackles are heard over the affected lung, sometimes with wheeze, though the examination may be normal. Clubbing is seen mostly in cystic fibrosis. Complications are massive haemoptysis (a medical emergency), pneumonia, empyema, pneumothorax, respiratory failure with cor pulmonale, and rarely amyloidosis or brain abscess. An exacerbation, by international consensus, is a deterioration over at least 48 hours in three or more of cough, sputum volume or consistency, sputum purulence, breathlessness or exercise tolerance, fatigue or malaise, and haemoptysis, such that a clinician judges that treatment should change. A severe exacerbation is one that needs admission or intravenous antibiotics.
Lung abscess
The illness is subacute and the patient is unwell for days or weeks: a swinging fever, night sweats, malaise and weight loss, with a cough that produces large amounts of foul-smelling sputum (anaerobes), sometimes with haemoptysis or pleuritic pain. There may be few signs: consolidation or an amphoric note over the cavity, a pleural rub, and clubbing in chronic suppuration. There is normocytic anaemia and a raised CRP and ESR, with a neutrophil leucocytosis. Poor teeth are a clue. Complications are empyema, bronchopleural fistula, pyopneumothorax, haemoptysis, brain abscess and, in chronic cases, amyloidosis.
Diagnosis and management
Bronchiectasis
HRCT of the chest is the investigation of choice: a bronchus wider than the adjacent artery (the signet ring sign), bronchi that do not taper (tram tracks), airways visible near the pleura, mucus plugging and thickened walls. The chest film may be normal, or show tram tracks, ring shadows and cysts. Further tests look for a cause, a reversible factor and a complication:
- sputum culture for bacteria, mycobacteria and fungi, repeated while stable, since the chronic organism guides treatment;
- spirometry, usually obstructive;
- immunoglobulins and vaccine responses (Hib, tetanus, pneumococcus);
- sweat test and genetics for cystic fibrosis: some textbooks test everyone under 40, while the guidelines test on clinical features (onset in childhood, male infertility, malabsorption, pancreatitis), with a low threshold because CFTR modulator drugs now exist;
- nasal nitric oxide to screen for primary ciliary dyskinesia, followed by specialist ciliary tests;
- total IgE, Aspergillus-specific IgE and IgG and a blood eosinophil count, or skin prick testing, for ABPA; and
- tests for rheumatoid arthritis, α1-antitrypsin deficiency and others, as the history suggests.
The Bronchiectasis Severity Index (age, BMI, FEV1, admissions, exacerbations, breathlessness, Pseudomonas colonisation, other colonisation, and radiological extent of 3 or more lobes or cystic change) and the FACED score (FEV1, age, chronic colonisation, extent, dyspnoea) estimate the outlook and guide how closely to follow the patient. On the Index, 0 to 4 points is mild disease, 5 to 8 moderate and 9 or more severe.
Management has these parts:
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Airway clearance daily: the active cycle of breathing technique, autogenic drainage or postural drainage, with devices that give a positive expiratory pressure (Flutter, Acapella). Nebulised hypertonic saline is a mucoactive option when clearance alone does not control symptoms; it improves symptoms and quality of life rather than exacerbation rates, and a bronchodilator first or a test dose guards against bronchospasm. Recombinant DNase is not used.
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Treat exacerbations promptly with an antibiotic chosen from previous sputum cultures, for about 2 weeks. H. influenzae responds to amoxicillin, co-amoxiclav or doxycycline; Pseudomonas to ciprofloxacin by mouth (500 mg twice a day, or 750 mg in more severe infection) or an intravenous antipseudomonal β-lactam, with dual therapy for multidrug-resistant organisms. Fluoroquinolones are kept for when other antibiotics are unsuitable.
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Reduce exacerbations in patients at high risk. UK guidance offers long-term antibiotics from three or more exacerbations a year; newer European guidance draws the line lower, at two or more in the previous year, one severe exacerbation, or one with severe daily symptoms:
- a long-term macrolide (azithromycin or erythromycin; a strong recommendation), which is immunomodulatory and antibacterial. First exclude active non-tuberculous mycobacterial infection (a negative sputum culture), check the QTc on the ECG and the liver and kidney function, and warn about hearing loss, tinnitus and imbalance; a baseline audiogram is not required; and
- long-term inhaled antibiotics (colistimethate first in UK practice, gentamicin second) for chronic Pseudomonas infection, a strong recommendation, with a macrolide as the alternative.
Separately, a first isolate of Pseudomonas with clinical deterioration is treated with an eradication course (ciprofloxacin for 2 weeks is first-line in UK practice; it is a conditional recommendation, on observational evidence).
Rotating oral antibiotics are no longer recommended. Long-term oral non-macrolide antibiotics are not suggested as first-line treatment, and against inhaled corticosteroids in patients who do not also have asthma or COPD (both conditional recommendations).
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A new class of drug: brensocatib, an inhibitor of dipeptidyl peptidase-1 (which activates neutrophil serine proteases). In its main trial (1721 patients, 52 weeks) the annual exacerbation rate was 1.02 on 10 mg and 1.04 on 25 mg against 1.29 on placebo (rate ratios 0.79 and 0.81), and lung function fell less on 25 mg; skin hyperkeratosis was commoner. It was licensed in the United States, the European Union and the United Kingdom in 2025 and 2026 (from age 12; in Europe for two or more exacerbations in the previous year), but the guidelines pre-date it.
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Treat the cause: immunoglobulin replacement for antibody deficiency; ABPA with steroids and itraconazole; stop the aspiration; remove the obstruction.
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Pulmonary rehabilitation, vaccination (influenza, pneumococcus, COVID-19), and stopping smoking. Look for and treat associated conditions: cardiovascular disease, osteoporosis, anxiety and depression, rhinosinusitis and reflux.
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Complications: massive haemoptysis calls for resuscitation, airway protection and bronchial artery embolisation, with surgery if that fails. Respiratory failure is treated with oxygen and non-invasive ventilation, and suitable patients are referred for transplantation. Surgery is for localised disease that does not respond.
Lung abscess
The film shows a thick-walled cavity, usually with an air–fluid level, in a dependent segment; CT is essential to show the cavity, a cause, and the pleura. Sputum and blood cultures are sent, though anaerobes are rarely grown, and a pleural fluid sample if there is an effusion. Bronchoscopy is done for a foreign body or a tumour, particularly in a smoker, and to take samples. Think of the differential diagnosis of a cavity: cavitating squamous-cell lung cancer, tuberculosis, granulomatosis with polyangiitis, fungal infection, an infected bulla or cyst, infarction, and an empyema with a bronchopleural fistula.
Treatment is a prolonged course of antibiotics guided by culture or clinical judgement, 4 to 6 weeks, or until the film shows a small scar or a clear lung. It begins intravenously and goes to oral drugs when the patient improves. For aspiration, co-amoxiclav is the usual choice, with clindamycin or metronidazole combined with another agent in penicillin allergy; metronidazole alone is not enough, because mouth streptococci are not covered. The evidence is observational, and no guideline fixes the regimen or the duration. Treat Staph. aureus, Klebsiella or Pseudomonas by their sensitivities. Postural drainage and physiotherapy help. Drainage (percutaneous, by CT or ultrasound) or surgery is for abscesses that fail to respond, are large, or have an associated empyema or bleeding, and resection is rarely needed. Treat the dental sepsis and the cause of aspiration, and remove an obstruction. An empyema is a separate problem.
Epidemiology
Bronchiectasis is more common than it was thought to be and is increasingly diagnosed, since CT is more available; little is known for certain, and the reported incidence varies widely. In UK primary-care data, the prevalence rose between 2004 and 2013, from about 350 to 566 per 100 000 in women and from about 300 to 486 per 100 000 in men, and it rises with age; mortality was about twice that of the general population. In low-income countries tuberculosis and childhood infections are the main causes, and the burden is higher; in rich countries more cases now come with COPD and asthma.
Lung abscess is uncommon today. The fall is usually attributed to earlier antibiotic treatment of pneumonia and better dental care, and primary abscesses are seen mostly in men with alcohol use disorder or impaired consciousness and swallowing. Septic embolic abscesses are linked to intravenous drug use.
Prognosis
The outlook for bronchiectasis is variable and depends on its cause and severity. A low FEV1, Pseudomonas aeruginosa infection, frequent exacerbations, breathlessness, hospital admissions, and extensive disease are associated with worse outcomes, and the severity indices are used to put them together. Good clearance, early treatment of exacerbations and treatment of the cause slow the decline. Severe disease ends in respiratory failure and cor pulmonale.
Most lung abscesses from aspiration heal with antibiotics alone, with good results in primary disease; the outlook is worse for a secondary abscess, in an immunocompromised or debilitated patient, with a large abscess, or with an infection caused by Staph. aureus or gram-negative organisms. Follow-up films are needed until the cavity has cleared, and a cavity that does not close in spite of treatment must be investigated for a tumour. Some abscesses leave bronchiectasis behind.
Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.
1Which finding on CT confirms bronchiectasis?
2A 25-year-old man has had a productive cough and sinusitis since childhood, with dextrocardia on the chest X-ray and bronchiectasis on CT. Which test screens for the likely cause?
3A patient with bronchiectasis has three exacerbations a year. Which long-term treatment is shown to cut the number?
4How long is a lung abscess usually treated with antibiotics?
5What is the commonest route to a primary lung abscess?