VG Med WF 135157c lungs finger in glove centrilobular nodules LLL allergic bronchopulmonary aspergillosis 9ABPA) CT lungs finger in glove centrilobular nodules LLL allergic bronchopulmonary aspergillosis 9ABPA) CT 40F Cough Asthma

Allergic Bronchopulmonary Aspergillosis (ABPA)

1. Challenge

Ashley Davidoff MD

40F Cough Asthma

2. Findings

Finger in glove
Centrilobular nodules LLL

ABPA Finger in Glove Sign LLL
77 year old female with history of asthma, allergic bronchopulmonary aspergillosis (ABPA) and COPD
CT in the axial plane of the left lower lobe shows inspissated and bronchiectatic segmental airways to the LLL, magnified in the lower image, (green arrowheads) reminiscent of the finger in glove appearance of ABPA)
Ashley Davidoff TheCommonVein.net 227Lu 135157cL

Finding	Definition	Comment
Finger-in-glove Sign	A radiological finding characterized by tubular or branching opacities that radiate from the hilum. This appearance is created by mucoid impaction within dilated bronchi, also known as a bronchocele.	This sign is classically associated with Allergic Bronchopulmonary Aspergillosis (ABPA). It results from an exaggerated immune and inflammatory response to Aspergillus fumigatus, leading to the production of thick mucus plugs within the bronchi. While it can be seen in other conditions such as cystic fibrosis and bronchial atresia, in the context of asthma, it is highly suggestive of ABPA. Citation: Martinez S, et al. Radiographics. 2008.
Centrilobular Nodules	Small (typically 5-10 mm) nodular opacities located in the center of the secondary pulmonary lobule. This location corresponds to the anatomic site of the small airways (bronchioles) and their accompanying arteries.	In ABPA, centrilobular nodules are a common finding and represent dilated bronchioles filled with mucus or inflammatory material. They can sometimes form branching patterns described as a “tree-in-bud” appearance, indicating impaction within the terminal bronchioles. The presence of these nodules points to small airways involvement in the disease process. Citation: Agarwal R, et al. Indian J Chest Dis Allied Sci. 2007.

3. Diagnosis

The clinical focus is on controlling the inflammatory cascade to prevent progressive and irreversible lung damage.

Allergic Bronchopulmonary Aspergillosis (ABPA)

Definition	Allergic bronchopulmonary aspergillosis (ABPA) is an immunological hypersensitivity disorder resulting from an exaggerated immune response to the fungus Aspergillus, most commonly Aspergillus fumigatus. It occurs almost exclusively in patients with asthma or cystic fibrosis. It is characterized by bronchospasm, eosinophilia, and immunologic evidence of an allergic reaction to Aspergillus antigens.
Cause	The etiological agent is Aspergillus, a ubiquitous mold found in soil, decaying vegetation, and dust. While most individuals inhale Aspergillus spores without consequence, those with predisposing conditions like asthma or cystic fibrosis may develop ABPA. The Etymology of Aspergillus: From Holy Water to Human Pathogen This image juxtaposes an ornate Christian liturgical implement, the Aspergillum, with the microscopic structure of the mold genus Aspergillus, explaining a remarkable moment of etymological crossover between biology and religion. The Aspergillum (Latin for “little sprinkler,” derived from aspergere meaning “to sprinkle”) is the brush or perforated ball used by a priest to sprinkle holy water (the rite of Asperges). The ubiquitous mold genus Aspergillus was named in 1729 by the Italian priest and biologist Pier Antonio Micheli. Viewing the asexual spore-forming structure (the conidial head) of the fungus under a microscope, Micheli was struck by its resemblance to the radiating bristles or perforations of the holy water sprinkler used in church ceremonies. This dual image illustrates how the physical shape of a religious artifact provided the name for one of the most clinically important fungi, which causes a spectrum of human diseases collectively known as Aspergillosis. Courtesy: Ashley Davidoff MD, TheCommonVein.com (135157d) and Wiki Commons In these patients, the fungus colonizes the mucus in the airways, triggering a hypersensitivity reaction rather than a direct tissue invasion.
Pathophysiology	The pathophysiology involves a combination of Type I and Type III hypersensitivity reactions to Aspergillus antigens. Inhalation of spores by susceptible individuals with impaired mucociliary clearance leads to colonization. This triggers a vigorous immune response involving IgE-mediated mast cell degranulation (Type I) and the deposition of immune complexes (Type III), resulting in eosinophilic inflammation, tissue necrosis, and excess mucus production. T-helper 2 (Th2) cells play a critical role, releasing cytokines like IL-4 and IL-5, which amplify the inflammatory cascade. This chronic inflammation leads to airway damage and remodeling.
Structural Result	The persistent inflammatory response in ABPA causes significant structural damage to the lungs. The hallmark structural change is the development of bronchiectasis, which is the abnormal and permanent widening of the airways. This process often leads to bronchial wall thickening and mucoid impaction. Over time, untreated or recurrent inflammation can progress to pulmonary fibrosis and scarring, which represent irreversible end-stage lung disease.
Functional Impact	Functionally, ABPA manifests as worsening airway obstruction and a decline in pulmonary function. Patients experience symptoms consistent with an asthma exacerbation, including bronchospasm and increased mucus production, leading to airflow limitation. Pulmonary function tests typically show an obstructive ventilatory defect. In advanced stages with fibrosis, a restrictive defect and reduced diffusion capacity for carbon monoxide (DLCO) may also develop. The disease can lead to chronic mucus production, severe persistent asthma, and progressive loss of lung function. Airway narrowing, gas trapping, and small airway disease are key components of the functional derangement.
Imaging	Radiologic findings are crucial for diagnosis. High-resolution computed tomography (HRCT) of the chest is the preferred modality. Characteristic findings include central bronchiectasis (predominantly affecting the inner two-thirds of the lungs), mucoid impaction, and bronchial wall thickening. High-attenuation mucus (HAM) within the impacted bronchi is a highly specific and pathognomonic sign of ABPA. Other findings may include fleeting pulmonary infiltrates (opacities that appear and resolve in different locations over time), atelectasis from bronchial plugging, and signs of small airways disease like tree-in-bud opacities.
Labs	Laboratory investigations are essential for confirming the diagnosis. Key diagnostic markers include a markedly elevated total serum IgE level (typically >1000 IU/mL), the presence of specific IgE and IgG antibodies against A. fumigatus, and peripheral blood eosinophilia (>500 cells/µL). A positive skin prick test to Aspergillus antigen indicates sensitization. Sputum cultures may grow A. fumigatus, but this only reflects colonization and is not diagnostic on its own.
Treatment	The primary goals of treatment are to control inflammation, manage symptoms, and prevent disease progression. Systemic oral corticosteroids, such as prednisone, are the cornerstone of therapy to suppress the allergic inflammatory response. Antifungal agents, most commonly itraconazole, are used as adjunctive therapy to reduce the fungal load in the airways, which can help lower the steroid dose and reduce the frequency of exacerbations. Inhaled corticosteroids are not effective as a primary treatment for ABPA. Biologic medications like omalizumab may be considered in some cases.
Prognosis	The prognosis for ABPA is variable and depends on early diagnosis and appropriate management. With timely treatment, long-term control and remission are achievable. Exacerbations are common, particularly within the first few years after stopping initial therapy. Delayed diagnosis or inadequate treatment can lead to progressive lung damage, including irreversible bronchiectasis and pulmonary fibrosis, resulting in chronic respiratory symptoms and a significant decline in lung function. Patients with serologic ABPA (without bronchiectasis at diagnosis) tend to have better long-term outcomes and maintain lung function better than those who present with established bronchiectasis.

4. Medical History and Culture

Etymology	Aspergillus: The genus Aspergillus was first described in 1729 by the Italian priest and biologist, Pier Antonio Micheli. The name derives from the resemblance of the fungus’s spore-forming structure (the conidiophore) to an aspergillum, a liturgical instrument used to sprinkle holy water (from Latin aspergere, “to scatter”). Aspergillosis: This term, denoting infection or disease caused by Aspergillus, combines the genus name with the suffix “-osis,” which in medical terminology signifies a process, condition, or state, often a diseased one. Its first known use in print dates to 1898. Bronchopulmonary: This is a compound word derived from broncho- (referring to the bronchi) and pulmonary (referring to the lungs). It signifies a condition pertaining to or affecting both the bronchi and the lungs.
AKA / Terminology	Hinson-Pepys disease. Allergic aspergillosis. Allergic bronchopulmonary mycosis.
Historical Notes	1729: Pier Antonio Micheli first identified and scientifically described the genus Aspergillus. In his seminal work, Nova plantarum genera, he challenged the theory of spontaneous generation by demonstrating that fungal spores reproduce the same type of fungus. 1863: The term ‘aspergillosis’ was first coined by J.B. Georg W. Fresenius when he described an infection in the Great bustard bird caused by Aspergillus fumigatus. 1952: The clinical entity of ABPA was first formally described by Hinson, Moon, and Plummer. They detailed cases of patients presenting with asthma, recurrent pulmonary infiltrates, and eosinophilia. 1967: The term bronchopulmonary dysplasia (BPD) was first used by Northway et al. to describe chronic lung injury in premature infants, a separate condition but etymologically related. 1986: A classification system for ABPA was proposed, introducing the concept of seropositive ABPA (ABPA-S) for patients with serologic evidence of the disease but without the established lung damage of central bronchiectasis, representing an earlier stage of diagnosis.
Cultural or Practice Insights	Aspergillus is a ubiquitous mold, commonly found in soil, decaying vegetation, and indoor environments; therefore, its spores are frequently inhaled without causing illness in most individuals. Disease manifestation is heavily dependent on the host’s immune status, ranging from hypersensitivity reactions like ABPA in atopic individuals (e.g., those with asthma or cystic fibrosis) to life-threatening invasive disease in the severely immunocompromised. The presence of Aspergillus in respiratory cultures can be a confounding factor for clinicians, as it may represent simple colonization rather than active infection, requiring careful correlation with clinical, radiological, and immunological findings. While many species of Aspergillus are pathogenic, others are beneficial and have been used for centuries in various cultural practices, such as the fermentation of soybeans for miso and soy sauce (Aspergillus oryzae) and the production of sake. The fungus is also a known agent of biodeterioration, posing a threat to cultural heritage items like old manuscripts, paintings, and textiles by degrading organic materials such as cellulose.
Notable Figures or Contributions	Pier Antonio Micheli (1679-1737): An Italian botanist and priest who is considered a founder of modern mycology. He was the first to scientifically describe the Aspergillus genus, noting its method of reproduction via spores. K.F.W. Hinson, A.J. Moon, and M. Plummer: This team of British physicians first characterized ABPA as a distinct clinical syndrome in 1952, differentiating it from simple asthma and invasive fungal infection. Jack Pepys: A prominent 20th-century allergist and immunologist who, along with Hinson, made foundational contributions to the understanding of ABPA as a hypersensitivity lung disease, leading to the eponym “Hinson-Pepys disease”. Ritesh Agarwal and Arunaloke Chakrabarti: Contemporary researchers from India who have published extensively on ABPA, contributing significantly to modern diagnostic criteria, classification, and understanding its global burden.
paintings	While no specific paintings of ABPA are known, the biodeterioration caused by Aspergillus species on historical artworks is a subject of study. For instance, studies have identified various Aspergillus species on easel paintings, showing how the fungus colonizes and damages cultural artifacts.
sculptures	The use of fungal mycelium, including that of Aspergillus species, is an emerging field in BioArt. Artists are experimenting with mycelium as a sustainable material for creating sculptures and even architectural prototypes, exploring themes of life, decay, and regeneration.
photography	In a project at the Technische Universität Berlin, artist Sunanda Sharma used photography and time-lapse footage to visualize the black pigmentation of Aspergillus niger, transforming the fungus from a pathogen into an aesthetic subject.
literature	The debilitating effects of chronic respiratory diseases like severe asthma, a prerequisite for ABPA, are a recurring theme in literature. For example, the character of Tiny Tim in Charles Dickens’ “A Christmas Carol” is often speculated to have suffered from a respiratory ailment that left him weak and breathless.
poetry	A poem could capture the immunological struggle and the feeling of airway constriction central to the ABPA experience. In bronchial halls where shadows creep, A silent, spore-borne vigil keep. Aspergillus, named for holy spray, Finds in the lung a place to stay. Not with the force of sharp invasion, But by allergic, slow persuasion. The IgE in arms does rise, Beneath the asthmatic’s wheezing skies. Eosinophils, a marching band, Infiltrate the promised land. A “finger-in-glove,” the shadow cast, Of mucus plugs, a mold unsurpassed. A tempest in the chest resides, Where hypersensitivity presides. A dance of fungus, host, and fate, Sealed within the airway gate.
Quotes and/or Teaching Lines	The “finger-in-glove” sign is a classic radiological descriptor for mucoid impaction in dilated central bronchi, a pathognomonic feature of ABPA. “ABPA is not a true infection but rather an immunologic reaction to the fungus Aspergillus fumigatus colonizing the airways.” This line emphasizes the hypersensitivity nature of the disease rather than tissue invasion. “High-attenuation mucus (HAM) on CT is a highly specific finding for ABPA.” This highlights a key radiological clue that can differentiate ABPA from other causes of bronchiectasis.

6. MCQs

Part A

Question	Answers
1. The immunopathogenesis of Allergic Bronchopulmonary Aspergillosis (ABPA) is complex and involves multiple hypersensitivity reactions. Which combination of Gell and Coombs hypersensitivity reactions is most characteristic of ABPA?	a) Type II and Type IV b) Type I and Type III c) Type I only d) Type IV only
2. A patient with asthma is being evaluated for ABPA. Which of the following immunological findings is considered a mandatory criterion for diagnosis according to the ISHAM-ABPA working group?	a) Total serum IgE > 2500 IU/mL b) Positive serum precipitins (IgG) to Aspergillus fumigatus c) Peripheral blood eosinophilia > 1000 cells/µL d) Elevated Aspergillus fumigatus specific-IgE (≥0.35 kUA·L⁻¹)
3. A 40-year-old female with a history of poorly controlled asthma presents with cough and expectoration of brownish plugs. According to the revised ISHAM-ABPA working group criteria, which of the following is considered a predisposing condition for ABPA?	a) Sarcoidosis b) Idiopathic Pulmonary Fibrosis c) Asthma d) Chronic Obstructive Pulmonary Disease (COPD)
4. What is the initial pharmacological agent of choice for inducing remission in a newly diagnosed, symptomatic patient with ABPA?	a) Itraconazole b) Omalizumab c) Systemic corticosteroids d) Inhaled corticosteroids
5. A CT scan of the chest in a patient with ABPA demonstrates tubular, branching opacities radiating from the hilum, particularly in the upper lobes. What does this “finger-in-glove” sign represent?	a) Arteriovenous malformations b) Interstitial fibrotic stranding c) Mucoid impaction within dilated bronchi d) Lymphangitic spread of a neoplasm
6. While several imaging findings are associated with ABPA, which of the following is considered pathognomonic when present?	a) Centrilobular nodules b) Central bronchiectasis c) High-attenuation mucus d) Fleeting parenchymal opacities
7. What is the most characteristic distribution of bronchiectasis in classic cases of ABPA?	a) Panlobular and lower lobe predominant b) Peripheral and subpleural c) Central (segmental and subsegmental bronchi) and upper lobe predominant d) Diffuse, involving all lung zones equally

Part B

1. The immunopathogenesis of Allergic Bronchopulmonary Aspergillosis (ABPA) is complex and involves multiple hypersensitivity reactions. Which combination of Gell and Coombs hypersensitivity reactions is most characteristic of ABPA?
a) Type II and Type IV	x	Type II (cytotoxic) reactions are not a primary mechanism in ABPA. While a cell-mediated Type IV reaction also occurs, the combination of Type I and III is most characteristic.
b) Type I and Type III	✓	The pathophysiology of ABPA involves a vigorous immunological response to Aspergillus antigens. This includes an IgE-mediated Type I hypersensitivity reaction, causing immediate bronchospasm and mast cell degranulation, and a Type III reaction, which involves the deposition of immune complexes (IgG and antigen) in the airway walls, leading to tissue damage. Agarwal R, Clin Exp Allergy, 2013
c) Type I only	x	While a Type I reaction is necessary, it does not encompass the full spectrum of immune-mediated damage seen in ABPA; the immune complex deposition of Type III is also a critical component.
d) Type IV only	x	A Type IV (delayed-type, cell-mediated) hypersensitivity reaction is involved, but it is not the sole or most defining reaction; the antibody-mediated Type I and III reactions are central to the diagnosis and pathology.

2. A patient with asthma is being evaluated for ABPA. Which of the following immunological findings is considered a mandatory criterion for diagnosis according to the ISHAM-ABPA working group?
a) Total serum IgE > 2500 IU/mL	x	The ISHAM working group recommends a cutoff of total serum IgE ≥500 IU·mL⁻¹, not >2500 IU/mL. While levels are often much higher, ≥500 IU·mL⁻¹ is the essential threshold.
b) Positive serum precipitins (IgG) to Aspergillus fumigatus	x	The presence of IgG antibodies (precipitins) to A. fumigatus is a supportive, not essential, criterion. A patient can be diagnosed with ABPA without it if other criteria are met.
c) Peripheral blood eosinophilia > 1000 cells/µL	x	A peripheral blood eosinophil count of ≥500 cells·μL⁻¹ is a supportive, not essential, criterion for the diagnosis of ABPA.
*d) Elevated Aspergillus fumigatus* specific-IgE (≥0.35 kUA·L⁻¹)**	✓	According to the 2024 ISHAM-ABPA working group consensus criteria, an elevated A. fumigatus-specific IgE (≥0.35 kUA·L⁻¹) is one of two essential components required for diagnosis, the other being a total serum IgE ≥500 IU·mL⁻¹. This demonstrates sensitization to the fungus, which is a prerequisite for the allergic cascade. Agarwal R, Lancet Infect Dis, 2024

3. A 40-year-old female with a history of poorly controlled asthma presents with cough and expectoration of brownish plugs. According to the revised ISHAM-ABPA working group criteria, which of the following is considered a predisposing condition for ABPA?
a) Sarcoidosis	x	Sarcoidosis is a granulomatous disease that can have overlapping imaging findings but is not a primary predisposing condition for ABPA.
b) Idiopathic Pulmonary Fibrosis	x	Idiopathic Pulmonary Fibrosis is a progressive fibrotic lung disease and is not a typical predisposing condition for ABPA.
c) Asthma	✓	Asthma is the most common predisposing condition for ABPA, occurring in the vast majority of patients. The diagnosis of ABPA is built upon the foundation of an underlying condition like asthma or cystic fibrosis. Agarwal R, Lancet Infect Dis, 2024
d) Chronic Obstructive Pulmonary Disease (COPD)	x	While COPD has been more recently included as a potential predisposing condition, asthma and cystic fibrosis remain the classic and most frequent underlying diseases.

4. What is the initial pharmacological agent of choice for inducing remission in a newly diagnosed, symptomatic patient with ABPA?
a) Itraconazole	x	Antifungal agents like itraconazole are typically reserved as second-line or steroid-sparing therapy for patients with recurrent exacerbations or who are steroid-dependent.
b) Omalizumab	x	Omalizumab (anti-IgE therapy) is a biologic agent used in refractory or steroid-dependent cases but is not the first-line treatment for an acute presentation.
c) Systemic corticosteroids	✓	Systemic corticosteroids, such as oral prednisolone, are the cornerstone of therapy for acute ABPA. Their primary role is to suppress the inflammatory and allergic responses, thereby reducing airway inflammation, decreasing serum IgE levels, and clearing pulmonary infiltrates to prevent irreversible lung damage like bronchiectasis and fibrosis. Agarwal R, Lancet Infect Dis, 2024
d) Inhaled corticosteroids	x	Inhaled corticosteroids, while used for underlying asthma, are not sufficient to control the intense systemic and airway inflammation of an acute ABPA exacerbation.

5. A CT scan of the chest in a patient with ABPA demonstrates tubular, branching opacities radiating from the hilum, particularly in the upper lobes. What does this “finger-in-glove” sign represent?
a) Arteriovenous malformations	x	Arteriovenous malformations are vascular anomalies that would enhance with intravenous contrast, unlike mucoid impaction.
b) Interstitial fibrotic stranding	x	Interstitial fibrosis appears as reticulation or honeycombing, which is a distinct pattern from the tubular opacities of mucoid impaction.
c) Mucoid impaction within dilated bronchi	✓	The “finger-in-glove” sign is the classic radiographic and CT manifestation of a bronchocele, which is a bronchus that has become dilated and filled with tenacious, thick mucus. In ABPA, this mucus is often laden with fungal hyphae and eosinophils. Patel Y, J Thorac Imaging, 2019
d) Lymphangitic spread of a neoplasm	x	Lymphangitic carcinomatosis typically presents as nodular thickening of the interlobular septa and bronchovascular bundles, not large, finger-like tubular opacities.

6. While several imaging findings are associated with ABPA, which of the following is considered pathognomonic when present?
a) Centrilobular nodules	x	Centrilobular nodules are a common but non-specific finding, also seen in infectious bronchiolitis and other conditions.
b) Central bronchiectasis	x	Central bronchiectasis is highly characteristic of ABPA but is not pathognomonic; it can be seen in other conditions such as cystic fibrosis and primary ciliary dyskinesia.
c) High-attenuation mucus	✓	High-attenuation mucus (HAM), defined as mucoid impaction that is visibly denser than adjacent paraspinal muscle on non-contrast CT, is a pathognomonic finding for ABPA. Its presence is attributed to the inclusion of calcium salts and metals within the inspissated, eosinophil-rich mucus. Agarwal R, Eur Respir J, 2007
d) Fleeting parenchymal opacities	x	Fleeting pulmonary opacities are characteristic but not pathognomonic, as they can occur in other eosinophilic lung diseases.

7. What is the most characteristic distribution of bronchiectasis in classic cases of ABPA?
a) Panlobular and lower lobe predominant	x	Lower lobe predominant bronchiectasis is more typically associated with aspiration, immunodeficiency states, or end-stage idiopathic pulmonary fibrosis (traction bronchiectasis).
b) Peripheral and subpleural	x	Peripheral and subpleural bronchiectasis is not the classic distribution for ABPA. Traction bronchiectasis associated with peripheral fibrosis (e.g., in usual interstitial pneumonia) has this appearance.
c) Central (segmental and subsegmental bronchi) and upper lobe predominant	✓	The classic description of bronchiectasis in ABPA is that it is predominantly central, involving the segmental and subsegmental bronchi, with relative sparing of the more peripheral airways. There is also a recognized predilection for the upper lobes. Panchal N, Allergy Asthma Proc, 2015
d) Diffuse, involving all lung zones equally	x	While the disease can be extensive, the classic pattern is not one of uniform diffuse involvement but rather a central and upper lobe predominance.

7. Memory Page

Asthmatic Spores of Aspergillus Allergic Bronchopulmonary Aspergillosis Finger in Glove Sign Bronchiectasis and Inspissated Thick, tenacious mucus containing eosinophils, Charcot-Leyden crystals, cellular debris, and colonizing Aspergillus hyphae.

Finger-in-Glove ABPA
Artistic rendering shows an asthmatic man with breathing difficulty. The lungs are overlaid with Aspergillus spores, and a CT scan reveals the classic finger-in-glove sign at the left base. The gloved hand reinforces the concept of mucus-impacted bronchi in ABPA.
Courtesy: Ashley Davidoff MD, TheCommonVein.com (135157c.MAD)

Finger-in-Glove Sign: The Pathognomonic CT Finding in Allergic Bronchopulmonary Aspergillosis (ABPA)
Ashley Davidoff MD, AI-assisted — Memory Image – TheCommonVein.com (135157c.MAD.gif02)

The Fungal Glove

A wheezing breath, a tightening chest,
The asthma patient finds little rest.
Within his airways, a shadow takes hold,
Not just of pollen, but of ancient mold.

Aspergillus spores, an innocent dust,
Ignite the deep tissues with allergic thrust.
The bronchi weep, they swell and they strain
Collecting thick mucus, a sticky, trapped rain.

The CT unveils what the dark lung concea
A tubular pattern, the truth it reveals.
It’s the Finger-in-Glove, a bizarre, branching sight
A bronchus distended, sealed up and white.

The hand of the fungus has grasped what it found,
A mold-laden mucus where air can’t be found.
A chilling reminder, dramatically made,
Of allergic defense in a life disobeyed
The glove is the airway, distended and weak,
The finger is sickness, a shape we must seek.

The Common Vein

VG Med WF 135157c lungs finger in glove centrilobular nodules LLL allergic bronchopulmonary aspergillosis 9ABPA) CT lungs finger in glove centrilobular nodules LLL allergic bronchopulmonary aspergillosis 9ABPA) CT 40F Cough Asthma

Allergic Bronchopulmonary Aspergillosis (ABPA)

1. Challenge

Ashley Davidoff MD

40F Cough Asthma

2. Findings

Finger in glove
Centrilobular nodules LLL

3. Diagnosis

Allergic Bronchopulmonary Aspergillosis (ABPA)

4. Medical History and Culture

6. MCQs

Part A

Part B

7. Memory Page

Asthmatic Spores of Aspergillus Allergic Bronchopulmonary Aspergillosis Finger in Glove Sign Bronchiectasis and Inspissated Thick, tenacious mucus containing eosinophils, Charcot-Leyden crystals, cellular debris, and colonizing Aspergillus hyphae.

The Fungal Glove

Etymology of Aspergillus

1. Challenge

2. Findings

2. Findings

3. Diagnosis

4. Medical History and Culture

6. MCQs

7. Memory Page

TCV

Allergic Bronchopulmonary Aspergillosis (ABPA)

1. Challenge

Ashley Davidoff MD

40F Cough Asthma

Related Links

2. Findings

Finger in glove Centrilobular nodules LLL

Related Links

3. Diagnosis

Allergic Bronchopulmonary Aspergillosis (ABPA)

Related Links

4. Medical History and Culture

Related Links

6. MCQs

Part A

Part B

Related Links

7. Memory Page

Asthmatic Spores of Aspergillus Allergic Bronchopulmonary Aspergillosis Finger in Glove Sign Bronchiectasis and Inspissated Thick, tenacious mucus containing eosinophils, Charcot-Leyden crystals, cellular debris, and colonizing Aspergillus hyphae.

The Fungal Glove

Etymology of Aspergillus

Related Links

1. Challenge

2. Findings

2. Findings

3. Diagnosis

4. Medical History and Culture

6. MCQs

7. Memory Page

TCV

Finger in glove
Centrilobular nodules LLL