Allergic bronchopulmonary aspergillosis is an allergic lung reaction to a type of fungus (most commonly Aspergillus fumigatus) that occurs in some people with asthma or cystic fibrosis.
The fungus Aspergillus fumigatus flourishes in soil, decaying vegetation, foods, dusts, and water. Certain people who inhale the fungus may become sensitized and develop a chronic allergic reaction. Other fungi, including Penicillium, Candida, Curvularia, and Helminthosporium, can cause an identical illness. In some people, the effects of the allergic reaction combine with the effects of the fungus to damage the airways and lungs.
The disorder differs from typical pneumonias caused by bacteria, viruses, and most fungi, in that the fungus does not actually invade the lung tissue and directly destroy it. The fungus colonizes the mucus in the airways of people with asthma or cystic fibrosis (both of whom tend to have increased amounts of mucus) and causes recurrent allergic inflammation in the lung. The tiny air sacs of the lungs (alveoli) become packed primarily with eosinophils. Increased numbers of mucus-producing cells may also appear. If the disease has caused extensive damage, inflammation may cause the central airways to widen permanently, a condition called bronchiectasis (see Bronchiectasis and Atelectasis: Bronchiectasis). Eventually, the lungs are likely to become scarred.
Other forms of aspergillosis can occur. Aspergillus can invade the lungs and cause serious pneumonia in people with an impaired immune system. This condition is an infection, not an allergic reaction (see Fungal Infections: Aspergillosis). Aspergillus can also form fungus balls (aspergillomas) in cavities and cysts of lungs damaged by another disease, such as tuberculosis; severe bleeding may result.
Symptoms and Diagnosis
The first indications of allergic bronchopulmonary aspergillosis are usually progressive symptoms of asthma, such as wheezing and shortness of breath, and a mild fever. The person usually does not feel well. Brownish flecks or plugs may appear in coughed-up sputum.
Repeated chest x-rays show areas that look like pneumonia, but they appear to migrate to new areas of the lung, most often in the upper parts. With long-standing disease, chest x-rays or computed tomography (CT) may show widened airways, which are often plugged with mucus; this appearance is similar to one that would be found in a person who has a lung tumor. The fungus itself, along with excess eosinophils, may be seen when the sputum is examined under the microscope. Blood tests reveal high levels of eosinophils and antibodies to Aspergillus. Skin testing can determine if the person is allergic to Aspergillus, but the test does not distinguish between allergic bronchopulmonary aspergillosis and a simple allergy to Aspergillus, which may occur in people who have allergic asthma without aspergillosis.
Because Aspergillus appears in many places in the environment, the fungus is difficult to avoid. Antiasthma drugs, especially corticosteroids, are used to treat allergic bronchopulmonary aspergillosis (see Asthma: Drugs Used to Treat Asthma). Antiasthma drugs also open up the airways, making it easier to cough up mucus plugs and clear out the fungus. The corticosteroid prednisone, taken initially in high doses, and then over a long period of time in lower doses, may prevent progressive lung damage. Most specialists recommend oral corticosteroids; the inhaled kind has not been shown to work well for this condition. The antifungal drug itraconazole is sometimes used in addition to corticosteroids to help eliminate the fungus from the lung.
Because the lung damage may worsen gradually without causing any noticeable changes in symptoms, chest x-rays, pulmonary function tests (see Diagnosis of Lung Disorders: Pulmonary Function Testing (PFT)), levels of eosinophils in the blood, and amounts of immunoglobulin E (IgE) antibody are regularly monitored. As the disease is controlled, the eosinophil and antibody levels usually fall, but they may rise again as an early sign of flare-ups.
Last full review/revision September 2006 by Lee S. Newman, MD, MA