eMedicine Specialties > Pulmonology > Infectious Lung Diseases

Aspergillosis

Author: Eloise M Harman, MD, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Florida College of Medicine
Contributor Information and Disclosures

Updated: Dec 29, 2009

Introduction

Background

Aspergillus species are ubiquitous molds found in organic matter. Although more than 100 species have been identified, the majority of human illness is caused by Aspergillus fumigatus and Aspergillus niger and, less frequently, by Aspergillus flavus and Aspergillus clavatus. The transmission of fungal spores to the human host is via inhalation. Also see the eMedicine articles Aspergillosis (dermatology focus), Aspergillosis (pediatric focus), and Aspergillosis, Thoracic (radiology focus).

Aspergillus may cause a broad spectrum of disease in the human host, ranging from hypersensitivity reactions to direct angioinvasion. Aspergillus primarily affects the lungs, causing 4 main syndromes, including allergic bronchopulmonary aspergillosis (ABPA), chronic necrotizing Aspergillus pneumonia (or chronic necrotizing pulmonary aspergillosis [CNPA]), aspergilloma, and invasive aspergillosis. However, in patients who are severely immunocompromised, Aspergillus may hematogenously disseminate beyond the lung, potentially causing endophthalmitis, endocarditis, and abscesses in the myocardium, kidney, liver, spleen, soft tissue, and bone. Aspergillus is second to Candida species as a cause of fungal endocarditis. Aspergillus -related endocarditis and wound infections occur in the context of cardiac surgery.

ABPA is a hypersensitivity reaction to A fumigatus colonization of the tracheobronchial tree and occurs in conjunction with asthma and cystic fibrosis (CF). Allergic fungal sinusitis may also occur alone or with ABPA. Bronchocentric granulomatosis and malt worker's lung are 2 hypersensitivity lung diseases that are caused by Aspergillus species, but they are rare.

An aspergilloma is a fungus ball (mycetoma) that develops in a preexisting cavity in the lung parenchyma. Underlying causes of the cavitary disease may include treated tuberculosis or other necrotizing infection, sarcoidosis, CF, and emphysematous bullae. The ball of fungus may move within the cavity but does not invade the cavity wall; however, it may cause hemoptysis.

CNPA is a subacute process usually found in patients with some degree of immunosuppression, most commonly that associated with underlying lung disease, alcoholism, or long-term corticosteroid therapy. Because it is uncommon, CNPA often remains unrecognized for weeks or months and can cause a progressive cavitary pulmonary infiltrate.

Invasive aspergillosis is a rapidly progressive, often fatal infection that occurs in patients who are severely immunosuppressed, including those who are profoundly neutropenic, those who have received bone marrow or solid organ transplants, and patients with advanced AIDS1 or chronic granulomatous disease. This infectious process is characterized by invasion of blood vessels, resulting in multifocal infiltrates, which are often wedge-shaped, pleural-based, and cavitary. Dissemination to other organs, particularly the central nervous system, may occur.

Pathophysiology

Aspergillus causes a spectrum of disease, from colonization to hypersensitivity reactions to chronic necrotizing infections to rapidly progressive angioinvasion, often resulting in death. Rarely found in individuals who are immunocompetent, invasive Aspergillus infection almost always occurs in patients who are immunosuppressed by virtue of underlying lung disease, immunosuppressive drug therapy, or immunodeficiency.

Aspergillus hyphae are histologically distinct from other fungi in that the hyphae have frequent septae, which branch at 45° angles. The hyphae are best visualized in tissue with silver stains. Although many species of Aspergillus have been isolated in nature, A fumigatus is the most common cause of infection in humans. A flavus and A niger are less common. Likely, this relates to the ability of A fumigatus, but not most other Aspergillus species, to grow at normal human body temperature.

Human host defense against the inhaled spores begins with the mucous layer and the ciliary action in the respiratory tract. Macrophages and neutrophils encompass, engulf, and eradicate the fungus. However, many species of Aspergillus produce toxic metabolites that inhibit macrophage and neutrophil phagocytosis. Corticosteroids also impair macrophage and neutrophil function. Underlying immunosuppression (eg, HIV disease, chronic granulomatous disease, pharmacologic immunosuppression) also contributes directly to neutrophil dysfunction or decreased numbers of neutrophils. In individuals who are immunosuppressed, vascular invasion is much more common and may lead to infarction, hemorrhage, and necrosis of lung tissue. Persons with CNPA typically have granuloma formation and alveolar consolidation. Hyphae may be observed within the granulomata.

Frequency

United States

  • Although allergy to Aspergillus, as manifested by a positive skin test reaction to Aspergillus antigen, is present in approximately 25% of people with asthma and 50% of patients with CF, ABPA is much less common. From surveys and an ABPA registry, 0.25-0.8% of people with asthma and approximately 7% of patients with CF are estimated to have ABPA. The incidence of ABPA in people with asthma who are steroid-dependent or have associated central bronchiectasis is higher, estimated at 7-10%.
  • CNPA is rare. Frequently undetected in life and found at autopsy, the frequency of chronic necrotizing Aspergillus pneumonia may be underestimated.
  • The frequency of invasive aspergillosis reflects disease states and treatments that result in prolonged neutropenia and immunosuppression. Invasive aspergillosis is estimated to occur in 5-13% of recipients of bone marrow transplants, 5-25% of patients who have received heart or lung transplants, and 10-20% of patients who are receiving intensive chemotherapy for leukemia. Although it has been described in individuals who are immunocompetent, invasive aspergillosis is exceedingly uncommon in this population.
  • Aspergilloma is not rare in patients with chronic cavitary lung disease and CF. In one survey of patients with cavitary lung disease due to tuberculosis, 17% developed aspergilloma.

International

  • The incidence of ABPA in people with asthma appears to be higher in Great Britain compared with the United States.

Mortality/Morbidity

  • Invasive aspergillosis is associated with significant mortality, with a rate of 30-95%.
  • Chronic necrotizing Aspergillus pneumonia has a reported mortality rate of 10-40%, but rates as high as 100% have been noted because it often remains unrecognized for prolonged periods.
  • Aspergilloma is associated with hemoptysis, which may be severe and life threatening.
  • ABPA may cause problems with asthma control. Repeated episodes of ABPA may cause widespread bronchiectasis and resultant chronic fibrotic lung disease.

Age

  • The age distribution of aspergillosis is consistent with that of the various comorbid conditions with which it is associated.

Clinical

History

The 4 most common manifestations of Aspergillus lung disease (ie, ABPA, CNPA, aspergilloma, and invasive aspergillosis) have quite different clinical manifestations.

  • ABPA is a syndrome occurring in asthmatic persons and patients with CF that results from a hypersensitivity reaction to Aspergillus colonization of the tracheobronchial tree. 
    • This syndrome may cause fever and pulmonary infiltrates that are unresponsive to antibacterial therapy.
    • Patients often have a cough and produce mucous plugs, which may form bronchial casts. They may have hemoptysis.
    • People with asthma who have ABPA may have poorly controlled disease and difficulty tapering off oral corticosteroids.
    • ABPA may occur in conjunction with allergic fungal sinusitis, with symptoms including chronic sinusitis with purulent sinus drainage.
  • Aspergilloma may manifest as an asymptomatic radiographic abnormality in a patient with preexisting cavitary lung disease due to sarcoidosis, tuberculosis, or other necrotizing pulmonary processes.
    • In patients with HIV disease, aspergilloma may occur in cystic areas resulting from prior Pneumocystis carinii pneumonia.
    • Of patients with aspergilloma, 40-60% experience hemoptysis, which may be massive and life threatening. Less commonly, aspergilloma may cause cough and fever.
  • CNPA manifests as a subacute pneumonia unresponsive to antibiotic therapy, which progresses and cavitates over weeks or months. 
    • Patients with CNPA have underlying disease, such as steroid-dependent chronic obstructive pulmonary disease (COPD) or alcoholism, with symptoms that may include fever, cough, night sweats, and weight loss.
    • Usually, patients have received prolonged courses of antibiotic therapy and sometimes empiric antituberculous therapy without response prior to diagnosis via biopsy or culture.
  • Invasive aspergillosis typically manifests with fever, cough, dyspnea, pleuritic chest pain, and, sometimes, hemoptysis in patients with prolonged neutropenia or immunosuppression.
    • For patients at risk for Aspergillus infection after organ transplantation, the most common transplant type at risk is bone marrow. However, invasive aspergillosis may be observed in patients who have received lung, heart, and other solid organ transplants. Of these solid organ transplants, lung transplant recipients are at significant risk. After bone marrow transplantation, invasive aspergillosis has a bimodal distribution, occurring early with prolonged neutropenia before engraftment and later in the context of high-dose corticosteroid therapy for graft versus host disease.
    • In patients with leukemia and lymphoma, aspergillosis may occur after chemotherapy-induced bone marrow suppression, with resultant prolonged neutropenia, manifesting with persistent fever and pulmonary infiltrates despite broad-spectrum antibiotic therapy. Radiographic and CT scan images may reveal characteristic patterns, including nodules, cavitary infiltrates, and focal infiltrates.
    • Invasive aspergillosis is being increasingly observed in patients with COPD on long-term corticosteroid therapy.2,3

Physical

Physical findings in patients with aspergillosis are nonspecific.

  • In ABPA, the patient may have fever. Wheezing may be noted upon auscultation of the chest. The patient may produce mucous plugs upon coughing.
  • In invasive aspergillosis and chronic Aspergillus pneumonia, the patient is febrile and may have evidence of lung consolidation. Patients may have hemoptysis. Patients with invasive aspergillosis may be tachypneic and have rapidly progressive worsening hypoxemia.
  • In patients with aspergilloma, signs of the underlying lung disease may be noted, including clubbing in patients with CF. Hemoptysis is frequently present.

Causes

Invasive aspergillosis rarely occurs in patients who are immunocompetent.

  • ABPA is found in people with asthma and/or CF who are allergic to Aspergillus. The thick mucus found in the airways of these patients may make clearing inhaled Aspergillus spores difficult. Additionally, evidence of genetic susceptibility has been reported. Patients who have certain HLA alleles, particularly HLA-DR2, have increased susceptibility to ABPA, whereas HLA-DQ2 appears to be protective.4
  • Risk factors involved in the development of CNPA include underlying pulmonary disease (including COPD, interstitial lung disease, and previous thoracic surgery) and altered immune status due to chronic corticosteroid therapy, alcoholism, collagen-vascular disease, or chronic granulomatous disease.
  • Aspergilloma typically develops in the context of preexisting cavitary disease. Aspergillomas may develop in patients with invasive aspergillosis or chronic necrotizing Aspergillus pneumonia.
  • Invasive aspergillosis occurs almost exclusively in patients who are immunocompromised.
    • Neutropenia and corticosteroid therapy are major risk factors.
    • In addition to patients who have undergone transplantation, patients profoundly neutropenic after receiving chemotherapy for hematologic malignancies or lymphoma, children with chronic granulomatous disease, and patients with late-stage HIV disease also are at risk.
    • Specific risk factors for invasive aspergillosis after bone marrow transplantation include prolonged neutropenia, graft versus host disease, high-dose corticosteroid therapy, disruption of normal mucosal barriers, mismatched or unrelated donor transplants, and the presence of central venous catheters.
    • Invasive Aspergillus infection in patients without malignancy or prior chemotherapy (who probably are nevertheless not immunocompetent) is most commonly seen in those with critical illness and COPD who are taking long-term corticosteroid therapy.5

More on Aspergillosis

Overview: Aspergillosis
Differential Diagnoses & Workup: Aspergillosis
Treatment & Medication: Aspergillosis
Follow-up: Aspergillosis
References
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Further Reading

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Keywords

aspergillosis, fungus, fungal infection, inhalational fungal disease, mold infection, invasive pulmonary aspergillosis, allergic bronchopulmonary aspergillosis, ABPA, chronic necrotizing pulmonary aspergillosis, CNPA, chronic necrotizing Aspergillus pneumonia, aspergilloma, mycetoma, fungus ball, disseminated aspergillosis, fungal endocarditis, Aspergillus fumigatus, A fumigatus, Aspergillus niger, A niger, Aspergillus flavus, A flavus, Aspergillus clavatus, A clavatus, bronchocentric granulomatosis, malt worker's lung

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Contributor Information and Disclosures

Author

Eloise M Harman, MD, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Florida College of Medicine
Eloise M Harman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American Medical Women's Association, American Thoracic Society, Phi Beta Kappa, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Oleh Wasyl Hnatiuk, MD, Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences
Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

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Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine
Disclosure: Keck School of Medicine, USC None None

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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