Lady Windermere Syndrome: CT Findings, Causes and Prognosis

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Key facts for practice and radiology board exams

Lady Windermere syndrome is the nodular bronchiectatic form of Mycobacterium avium complex (MAC) pulmonary disease, centred on the right middle lobe and the lingula, in an older woman with no previously recognised lung disease. On CT it is cylindrical or varicose bronchiectasis plus bronchial wall thickening plus clustered centrilobular nodules with tree-in-bud, in those two segments. Imaging satisfies only one of the three diagnostic criteria, so the report has to ask for sputum mycobacterial culture, not just describe bronchiectasis.

The eponym is weak evidence. It rests on six chest radiographs in a 1992 Chest paper and an untested hypothesis that these women voluntarily suppressed their cough [1].
The host phenotype is real. Patients are taller and leaner than matched controls, with scoliosis in 51 percent, pectus excavatum in 11 percent, mitral valve prolapse in 9 percent and CFTR mutations in 36 percent, with no demonstrable immune defect [4].
Bronchiectasis separates MAC from tuberculosis. Present in 94 percent of MAC versus 27 percent of tuberculosis, and involving a mean of 4.6 versus 1.8 lobes [8].
Cavitation is the prognostic switch. Disease-attributable death was 3.3 percent in non-cavitary nodular bronchiectatic disease versus 21.3 percent with cavitation over a median 56 months [12]. Report it explicitly.
One positive sputum culture is not disease. Two or more cultures of the same species are required; with two or more, the probability of clinically significant MAC disease reaches 98 percent [7].
Meeting criteria is not an automatic trigger to treat. The 2020 guideline makes treatment a conditional suggestion and accepts watchful waiting, which is what serial CT is for [7].

In this article

Key facts for practice and radiology board exams
What is Lady Windermere syndrome?
Who was Lady Windermere, and why the eponym is a problem
Who actually gets it: the body morphotype
CT findings of nodular bronchiectatic NTM disease
The three radiological phenotypes of MAC lung disease
Lady Windermere syndrome versus pulmonary tuberculosis on CT
From CT to diagnosis: the criteria your report triggers
How serious is Lady Windermere syndrome?
Treatment in 2026 and what imaging contributes
Middle lobe and lingular bronchiectasis: the differential
Reporting checklist
Frequently asked questions
References

The video walks through the full PACS image set for this case. The written reference below covers the CT pattern, the differential, the diagnostic criteria and the prognosis.

What is Lady Windermere syndrome?

It is a radiological phenotype of nontuberculous mycobacterial (NTM) lung disease, almost always caused by Mycobacterium avium complex, in which bronchiectasis and small nodules are confined to, or clearly dominated by, the right middle lobe and the lingula. The patient is characteristically a slender woman in her sixties or older, a lifelong non-smoker, with months of cough and no previously diagnosed lung disease.

Two labels describe the same thing, and the second is the one to use in a report. Lady Windermere syndrome is the eponym. Nodular bronchiectatic NTM pulmonary disease is the descriptive term used by the 2020 ATS, ERS, ESCMID and IDSA guideline, and it is the one that maps onto a treatment decision [7]. The disease is not rare and is not static: in a United States Medicare population aged 65 and over, incident NTM pulmonary disease averaged 20.1 per 100,000 per year between 2010 and 2019, rising fastest among women at 6.5 percent per year [15].

Axial CT chest showing right middle lobe cystic bronchiectasis and small nodules in Lady Windermere syndrome — Axial CT at the level of the heart: clustered cystic and varicose bronchiectasis with small nodules in the right middle lobe. This distribution, in an older woman who has never smoked, is the pattern the eponym describes.

Who was Lady Windermere, and why the eponym is a problem

Reich and Johnson described the pattern in Chest in 1992. Out of 29 patients with MAC pulmonary disease identified from a community population, six had a previously undescribed picture: all were women, all tended to be elderly, none had a predisposing pulmonary disorder, disease began in the dependent lingula or the middle lobe, and hilar adenopathy, volume loss and cavitation were uniformly absent. To explain it they proposed that habitual voluntary suppression of cough had left those poorly draining segments unable to clear secretions, and they named the pattern after a character in Oscar Wilde to suggest that the patients’ fastidiousness was its root cause [1].

Three things follow from that, and they matter when you write the word in a report.

The cough-suppression mechanism was a hypothesis, not a finding. It has never been tested prospectively, and the anatomical alternative is at least as good: the middle lobe and lingular bronchi are long and narrow, take off at acute angles, and have poor collateral ventilation, which is the same reason middle lobe syndrome exists at all.
The literary reference does not hold up. A 2008 report in the Singapore Medical Journal pointed out that the syndrome does not correspond to the character in the play and called the eponym inappropriate for an increasingly important condition [2]. The original author published a defence of it in Lung in 2018 [3], which tells you the question is still open.
The name blames the patient. It attributes a chronic mycobacterial infection to a woman’s manners. The evidence points instead to a body morphotype and to airway clearance biology, and there is a serious literature asking whether post-menopausal endocrine change contributes [6].

Who actually gets it: the body morphotype

The best characterisation comes from a prospective National Institutes of Health cohort of 63 patients with pulmonary NTM disease, 95 percent of them women and 68 percent lifetime non-smokers. Compared with age-matched and ethnicity-matched female controls from NHANES, patients were significantly taller (164.7 versus 161.0 cm) and leaner (body mass index 21.1 versus 28.2) [4]. A second cohort confirmed the same body and immune phenotype [5].

Feature	Frequency in pulmonary NTM disease	Why it matters
Female sex	95 percent of the NIH cohort	Skews the pre-test probability before you look at the lungs
Lifetime non-smoker	68 percent	Removes the usual explanation for bronchiectasis
Scoliosis	51 percent	Look at the coronal reformats, not just the lung windows
Pectus excavatum	11 percent	Reduced anteroposterior thoracic dimension, visible on the same CT
Mitral valve prolapse	9 percent	Part of the same connective tissue morphotype
CFTR mutation	36 percent	Heterozygous CFTR dysfunction, not cystic fibrosis
Demonstrable immune defect	None found	Normal IFN-gamma and IL-12 signalling, normal lymphocyte subsets

Morphotype of pulmonary nontuberculous mycobacterial disease, from the prospective NIH cohort [4].

The practical point for a radiologist: if you are reporting a chest CT on a tall, thin, older woman with scoliosis or pectus and you find middle lobe or lingular bronchiectasis with nodules, you are not looking at an incidental finding. You are looking at the phenotype.

CT findings of nodular bronchiectatic NTM disease

Five findings travel together. None of them is specific on its own, which is why the combination and the distribution carry the diagnosis.

CT finding	What it looks like	Note
Bronchiectasis	Cylindrical or varicose, occasionally cystic, with bronchial wall thickening	Present in 94 percent of MAC cases and typically multilobar [8]. Criteria and pitfalls on the tram-track sign page
Centrilobular nodules	Clusters of 2 to 5 mm nodules, often with a tree-in-bud pattern	Represent bronchiolar impaction. Nodules that connect to a dilated bronchus favour MAC over tuberculosis [9]
Middle lobe and lingular predominance	Disease centred on these two segments, often bilateral	Bronchiectasis in the middle lobes is significantly more common in NTM than in non-NTM bronchiectasis [10]
Mucus plugging	Tubular or branching intraluminal soft tissue, sometimes a finger-in-glove appearance	Significantly more frequent in bronchiectasis with NTM than without [10]
Cavitation	Thin or thick walled, most often upper lobe, superimposed on the nodular bronchiectatic pattern	Changes the phenotype, the regimen and the prognosis. Always state it [7,12]

The five CT findings of nodular bronchiectatic NTM lung disease.

Two supporting observations from a Hannover series that scored 128 CTs in adults with bronchiectasis, 36 of whom met ATS criteria for NTM disease: patients with NTM had significantly more middle lobe bronchiectasis, more extensive bronchiolitis and more small and large nodules, with larger cavities and thicker, more extensive walls, while peripheral ground-glass and interstitial change pointed away from NTM. After microbiological cure, bronchiolitis was the only score item that fell significantly, so resolving tree-in-bud is the imaging surrogate of treatment response, and the bronchiectasis itself does not reverse [10].

Axial CT chest showing clustered cystic bronchiectasis with adjacent nodular opacities in the right upper lobe — Clustered cystic bronchiectasis with adjacent nodular opacities, here in the right upper lobe. NTM disease is not confined to the middle lobe and lingula, and upper lobe involvement with cavitation defines the more aggressive fibrocavitary phenotype.

The three radiological phenotypes of MAC lung disease

The 2020 guideline treats the fibrocavitary and nodular bronchiectatic forms differently, so deciding which one you are looking at is a reporting task, not an academic one [7].

Phenotype	Typical patient	CT pattern	Consequence
Nodular bronchiectatic (the Lady Windermere pattern)	Older, slender, non-smoking woman with no prior lung disease	Middle lobe and lingular bronchiectasis, bronchial wall thickening, centrilobular nodules and tree-in-bud, no cavity	Slowly progressive. Standard three-drug oral regimen. Disease-attributable death 3.3 percent [12]
Fibrocavitary (classic)	Older man with COPD, prior tuberculosis or smoking history	Upper lobe cavitation, pleural thickening, volume loss, resembles reactivation tuberculosis	Faster progression. Add parenteral amikacin or streptomycin. Disease-attributable death 21.3 percent [7,12]
Hot tub lung (hypersensitivity reaction)	Younger adult, mean age 46, with hot tub, spa or circulating bath exposure	Diffuse centrilobular nodules and ground-glass opacity, no middle lobe bronchiectasis	Improves with avoidance of exposure, with or without corticosteroids. Antimycobacterial therapy generally not required [11]

Radiological phenotypes of MAC lung disease and what each one changes.

A fourth combination is worth flagging because it is missed: cavitation superimposed on nodular bronchiectatic disease. In the Osaka cohort, cavitary nodular bronchiectatic disease behaved like fibrocavitary disease rather than like an advanced stage of the non-cavitary form, and concurrent chronic pulmonary aspergillosis occurred in 17.3 percent of patients with cavitary MAC disease [12]. If a cavity develops a mural nodule, an air crescent or new pleural thickening on follow-up, raise aspergillosis explicitly.

Hot tub lung overlaps radiologically with subacute hypersensitivity pneumonitis, including the head cheese sign. The discriminator is the exposure history and the absence of middle lobe bronchiectasis, not the CT pattern alone.

Lady Windermere syndrome versus pulmonary tuberculosis on CT

This is the decision that matters most in tuberculosis-endemic practice, because MAC is intrinsically resistant to isoniazid and pyrazinamide. Starting empirical anti-tuberculous therapy in a patient with MAC disease wastes months and selects for resistance in the drugs that do work.

Feature	Favours MAC (nodular bronchiectatic)	Favours tuberculosis
Bronchiectasis	94 percent of cases, mean 4.6 lobes involved [8]	27 percent of cases, mean 1.8 lobes [8]
Interlobular septal thickening	12 percent [8]	51 percent [8]
Distribution	Middle lobe and lingula dominant, often bilateral	Apical and posterior upper lobe, superior segment of lower lobe
Relationship of nodules to airways	Granular and larger shadows connected to the bronchiectasis [9]	Nodules and consolidation without that connection
Calcification within the lesion	Uncommon	More frequent [9]
Calcified mediastinal or hilar nodes	Uncommon	More frequent [9]
Pleural effusion	Uncommon	More frequent [9]
Nodules, consolidation, cavitation	Similar frequency in both, so these do not discriminate [8]	Similar frequency in both [8]

CT discriminators between MAC lung disease and pulmonary tuberculosis [8,9].

Neither pattern is diagnostic. Both need culture, and a positive acid-fast bacilli smear does not settle the question, because NTM and M. tuberculosis both stain. Ask for speciation, not just smear. The other end of the mycobacterial spectrum, the miliary pattern, points away from both of these phenotypes.

From CT to diagnosis: the criteria your report triggers

Imaging is one of three criteria, and all three are required. These criteria were carried forward unchanged into the 2020 ATS, ERS, ESCMID and IDSA guideline [7].

Criterion	Requirement
Clinical	Pulmonary symptoms, with other diagnoses reasonably excluded
Radiological	Nodular or cavitary opacities on the chest radiograph, or multifocal bronchiectasis with multiple small nodules on CT
Microbiological	At least two separate expectorated sputum cultures positive for the same species, collected at least a week apart; or one positive culture from bronchial wash or lavage; or a biopsy showing granulomatous inflammation or acid-fast bacilli plus a positive culture from sputum, wash or tissue

Diagnostic criteria for NTM pulmonary disease. All three categories must be met [7].

One positive sputum culture is not disease. NTM are environmental organisms and can contaminate a specimen. With two or more positive cultures of the same species, the probability of clinically significant MAC disease reaches 98 percent [7].
Bronchoalveolar lavage outperforms sputum in the nodular bronchiectatic form, which is exactly the group with a dry-sounding cough and little expectoration [7].
Species matters. A single M. kansasii isolate in the right context may justify treatment, whereas M. gordonae usually needs repeated positives over months before it is believed [7].
Meeting the criteria is not the same as needing antibiotics. The guideline suggests treatment over watchful waiting only conditionally, and singles out smear-positive sputum and cavitary disease as where the case is strongest [7].

How serious is Lady Windermere syndrome?

It is a chronic infection that is measured in years, not weeks, and the honest answer has two layers: disease-attributable mortality is low in the non-cavitary form, while all-cause mortality in this elderly population is not.

Outcome measure	Figure	Source
Disease-attributable death, non-cavitary nodular bronchiectatic disease	3.3 percent over a median 56.4 months	Osaka cohort, 125 patients [12]
Disease-attributable death, cavitary disease	21.3 percent over the same period	Osaka cohort [12]
Sputum conversion with a standardised rifampicin, ethambutol and clarithromycin regimen	80.0 percent	Osaka cohort [12]
Refractory disease despite treatment	45.6 percent	Osaka cohort [12]
Emergent clarithromycin resistance	16.8 percent	Osaka cohort [12]
Concurrent chronic pulmonary aspergillosis in cavitary disease	17.3 percent	Osaka cohort [12]
All-cause mortality after a pulmonary MAC isolate	19 percent at 1 year, 68 percent at 10 years	Danish national cohort, 28 years of follow-up [14]
Effect of treatment duration on mortality	Treatment of 18 months or longer, adjusted hazard ratio 0.32	Korean cohort [13]

Outcome data in MAC pulmonary disease.

Read those two mortality figures together rather than separately. The Danish 10-year figure of 68 percent is all-cause death in people whose median age at isolation is well over 60 and who usually carry structural lung disease or other comorbidity: most of them die with MAC rather than of it [14]. The Osaka figures isolate the contribution of the infection itself, and they say the same thing the CT says: cavitation is the variable that matters [12].

Treatment in 2026 and what imaging contributes

The backbone has not changed since the 2020 guideline, and knowing it tells you which findings in your report will actually alter a prescription [7].

Macrolide-susceptible MAC: a three-drug, macrolide-based regimen. Azithromycin is preferred over clarithromycin, with ethambutol and a rifamycin. Two drugs are not equivalent to three.
Duration: at least 12 months after sputum culture conversion, so typically 15 to 18 months in total. Longer treatment tracks with better survival [13].
Cavitary, advanced bronchiectatic or macrolide-resistant disease: add parenteral amikacin or streptomycin to the initial regimen. This is the recommendation your description of a cavity triggers.
Refractory disease: amikacin liposome inhalation suspension is added when sputum has not converted after at least six consecutive months of guideline-based therapy.
Airway clearance is treatment, not an adjunct. The 2025 European Respiratory Society bronchiectasis guideline strongly recommends airway clearance techniques for most patients with bronchiectasis and pulmonary rehabilitation for those with breathlessness or reduced exercise capacity [17].

One development to watch. The phase 3b ENCORE study tested adding amikacin liposome inhalation suspension to azithromycin and ethambutol in newly diagnosed, antibiotic-naive MAC lung disease. The sponsor reported positive topline results in March 2026, with culture conversion by month 6 of 87.8 percent versus 57.0 percent, and the United States Food and Drug Administration granted priority review of the supplemental application in September 2026 with a target action date of 28 January 2027. If it is approved, inhaled amikacin moves from a last resort to an option at the start of treatment. The peer-reviewed publication is not out yet, so treat these numbers as sponsor-reported until it is.

Radiology contributes three things to that pathway: the initial pattern recognition that prompts culture at all, the presence or absence of cavitation that sets the regimen, and the serial comparison that distinguishes progression from stability in patients who are being watched rather than treated. For serial CT, compare against the same prior each time rather than the most recent one, because year-on-year change in this disease is small.

Middle lobe and lingular bronchiectasis: the differential

Before the report says MAC, walk the rest of the list. Distribution narrows it faster than anything else.

Cause of bronchiectasis	Typical distribution	Discriminating clue
Nodular bronchiectatic NTM disease	Right middle lobe and lingula	Clustered centrilobular nodules and tree-in-bud in the same segments
Primary ciliary dyskinesia	Middle lobe and lingula, lower lobes	Situs inversus in about half (Kartagener), chronic sinusitis, onset in childhood
Post-tuberculous	Upper lobes, superior segments	Volume loss, calcified nodes, fibrotic bands, pleural thickening
Allergic bronchopulmonary aspergillosis	Central and upper lobe	Mucoid impaction, high-attenuation mucus, asthma, raised IgE
Recurrent aspiration	Dependent lower lobes, posterior segments	Tree-in-bud in dependent segments, oesophageal dilatation, hiatus hernia
Cystic fibrosis	Upper lobe predominant	Younger patient, hyperinflation, mucus plugging, sinus disease
Middle lobe syndrome	Right middle lobe alone	Chronic collapse without an obstructing lesion. NTM is a recognised cause, so culture before calling it idiopathic
Mounier-Kuhn syndrome	Trachea and central bronchi	Tracheobronchomegaly with tracheal diverticula
Williams-Campbell syndrome	Fourth to sixth order bronchi	Cartilage deficiency with expiratory collapse on dynamic CT

Pattern-based differential for bronchiectasis, with the middle lobe and lingular causes first.

The bronchiectasis signs themselves, including the signet ring sign and the tram-track sign, are covered separately with their CT criteria and their false positives.

Reporting checklist

State the distribution: which lobes and segments, and whether the middle lobe and lingula dominate.
Grade the bronchiectasis: cylindrical, varicose or cystic, and how many lobes.
Say whether centrilobular nodules and tree-in-bud are present, and whether they connect to the dilated bronchi.
State cavitation explicitly, present or absent, with wall thickness and size. This changes the regimen and the prognosis.
Note mucus plugging, consolidation and lobar volume loss.
Look for a fungal ball, air crescent or new pleural thickening in any cavity, and raise chronic pulmonary aspergillosis if present.
Check the chest wall and spine on the same study for scoliosis and pectus excavatum, and say so: they support the phenotype.
Compare with the oldest relevant prior, not only the most recent one, and quantify change.
Recommend the next step in words: three sputum samples for acid-fast bacilli smear and mycobacterial culture with speciation, collected over at least one week, or bronchoalveolar lavage if the patient cannot expectorate.
Do not report the eponym alone. Write the pattern, then the eponym in parentheses if you want it.

Frequently asked questions

What is Lady Windermere syndrome?

It is the nodular bronchiectatic form of Mycobacterium avium complex lung disease, confined to or dominated by the right middle lobe and the lingula, in an older woman with no previously recognised lung disease. On CT it is a combination of cylindrical or varicose bronchiectasis, bronchial wall thickening, clustered centrilobular nodules with a tree-in-bud pattern, and often a small amount of mucus plugging, in those two segments. The term is a descriptive eponym, not a separate disease: the modern label is nodular bronchiectatic nontuberculous mycobacterial pulmonary disease.

How serious is Lady Windermere syndrome?

It is a chronic, slowly progressive infection rather than an acute threat, and the single finding that changes the outlook is cavitation. In a Japanese cohort of progressive MAC pulmonary disease followed for a median of 56 months, disease-attributable death occurred in 3.3 percent of patients with non-cavitary nodular bronchiectatic disease and in 21.3 percent of those with cavitary disease. All-cause mortality is higher still, because these patients are typically in their sixties or older and die with the disease as often as from it: a Danish cohort with 28 years of follow-up reported 19 percent all-cause mortality at one year and 68 percent at ten years after a pulmonary MAC isolate. Longer treatment is associated with better survival.

Why is it called Lady Windermere syndrome?

Reich and Johnson coined the term in Chest in 1992 after finding six women, out of 29 patients with MAC pulmonary disease in a community population, whose disease was confined to the lingula or the middle lobe with no cavitation, no adenopathy and no volume loss. They proposed that habitual voluntary suppression of cough had left those poorly draining segments unable to clear secretions, and named the pattern after a character in Oscar Wilde to suggest that fastidiousness was the root cause. The hypothesis has never been tested prospectively, and a 2008 report in the Singapore Medical Journal argued that the name does not correspond to the character in the play and that the eponym is inappropriate.

Is Lady Windermere syndrome contagious?

Mycobacterium avium complex is acquired from the environment, chiefly from water, and there is no evidence of person to person spread, so patients do not need respiratory isolation and contacts do not need screening. That reassurance does not extend to every nontuberculous mycobacterium. Whole genome sequencing has shown indirect person to person transmission of Mycobacterium abscessus between patients with cystic fibrosis, so speciation matters before you tell a ward there is nothing to worry about.

What is the difference between Lady Windermere syndrome and tuberculosis on CT?

Bronchiectasis is the discriminator. In a CT comparison of 77 immunocompetent patients, bronchiectasis was present in 94 percent of MAC cases against 27 percent of tuberculosis cases, and it involved a mean of 4.6 lobes in MAC against 1.8 in tuberculosis, while interlobular septal thickening favoured tuberculosis at 51 percent against 12 percent. Nodules, consolidation and cavitation occurred at similar rates in both. Practical rule: apical posterior upper lobe and superior segment disease with calcified nodes, calcification within the lesion and pleural effusion favours tuberculosis, whereas multilobar bronchiectasis centred on the middle lobe and lingula, with nodules that connect to the dilated bronchi, favours MAC.

What are the diagnostic criteria for nontuberculous mycobacterial lung disease?

The criteria carried forward into the 2020 ATS, ERS, ESCMID and IDSA guideline need all three of the following. Clinical: pulmonary symptoms, with other diagnoses reasonably excluded. Radiological: nodular or cavitary opacities on the chest radiograph, or multifocal bronchiectasis with multiple small nodules on CT. Microbiological: at least two separate expectorated sputum cultures positive for the same species, or one positive culture from a bronchial wash or lavage, or a biopsy showing granulomatous inflammation or acid-fast bacilli with a positive culture from sputum, wash or tissue. A single positive sputum culture does not make the diagnosis, whereas two or more positive cultures carry up to a 98 percent probability of clinically significant MAC disease.

Does a positive culture mean treatment has to start?

No. The 2020 guideline suggests treatment rather than watchful waiting in patients who meet the diagnostic criteria, but it is a conditional recommendation with very low certainty, and it singles out smear positive sputum and cavitary disease as the situations where the argument is strongest. Treatment means at least three drugs for at least 12 months beyond culture conversion, with real toxicity. For a minimally symptomatic older patient with limited non-cavitary disease, serial CT is a legitimate alternative, which is why a structured comparison with the previous study belongs in every follow-up report.

How is MAC lung disease treated in 2026?

For macrolide susceptible disease the backbone is a three-drug, macrolide-based regimen, with azithromycin preferred over clarithromycin, plus ethambutol and a rifamycin, continued for at least 12 months after sputum culture conversion. Cavitary, advanced bronchiectatic or macrolide resistant disease also gets parenteral amikacin or streptomycin in the initial phase. Amikacin liposome inhalation suspension is added for refractory disease, defined as failure to convert after six months of guideline based therapy. In March 2026 the sponsor reported positive topline results from the phase 3b ENCORE study in newly diagnosed MAC lung disease, and the FDA granted priority review of the supplemental application in September 2026, so the point at which inhaled amikacin enters the regimen may move earlier.

What is hot tub lung?

Hot tub lung is a hypersensitivity pneumonitis type reaction to aerosolised MAC from hot tubs, spa pools, showers or circulating home baths, and it is the main NTM mimic that does not look like Lady Windermere syndrome. Patients are younger, around 46 years on average, present with dyspnoea and cough, and the HRCT shows diffuse centrilobular nodules and ground-glass opacity rather than middle lobe bronchiectasis. In the largest series, 21 patients all improved with avoidance of exposure, 62 percent received corticosteroids, and only one received antimycobacterial therapy alone, so recognising it prevents a year of unnecessary triple therapy.

What should the radiology report say?

Name the pattern rather than just the bronchiectasis. State the distribution and whether the middle lobe and lingula dominate, grade the bronchiectasis, say whether centrilobular nodules and tree-in-bud are present and whether they connect to the dilated bronchi, and state explicitly whether there is cavitation and how thick the wall is, because cavitation changes both the regimen and the prognosis. Note mucus plugging, consolidation, volume loss and any fungal ball or pleural thickening that suggests chronic pulmonary aspergillosis. Then recommend the step that actually moves the diagnosis forward: three sputum samples for acid-fast bacilli smear and mycobacterial culture with speciation, collected over at least a week, or bronchoalveolar lavage if the patient cannot expectorate.

References

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