Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic disorder caused by an IgE-mediated response to Aspergillus. It usually occurs in patients with asthma and may complicate the course of patients with cystic fibrosis. Steroids are the mainstay of therapy. The disease is exceedingly rare in HIV-infected individuals. We report a case of an HIV-positive man who was diagnosed with ABPA. His symptoms improved with discontinuation of highly active anti-retroviral therapy (HAART) and allergen avoidance without specific therapeutic intervention.
The patient is a 41-year old HIV-positive Caucasian male (absolute CD4 count 154 cells/ μl). He had a history of seasonal allergies without asthma and presented with one year of cough, thick purulent sputum, episodic hemoptysis, wheezing, dyspnea, fever, weight loss and malaise. The onset of his symptoms coincided with his re-location to an apartment that was heavily contaminated with mould. Chest imaging demonstrated bilateral patchy alveolar infiltrates and mild central bronchiectasis. Pulmonary function tests demonstrated mild obstructive disease (FEV1/ FVC ratio 70 %, FEF 25–75 49%) and air trapping (residual volume 161 %) with slight response to bronchodilators. A bronchoscopic evaluation showed mildly erythematous airways without structural abnormalities. Cultures of bronchoalveolar lavage fluid were negative. The diagnosis of ABPA in this patient was confirmed by strongly positive intracutaneous testing to Aspergillus antigen extract, systemic eosinophilia (1,000/ μl), a markedly elevated total IgE level (5,700 kU/ l) and detection of precipitating antibodies against Aspergillus fumigatus (Af), as well as elevated specific IgE to Af. His symptoms started to improve significantly when HAART was discontinued, and he moved out of his apartment. Follow-up chest imaging studies demonstrated interval improvement of alveolar infiltrates. Since the patient was only minimally symptomatic at the time of diagnosis, it was decided to observe him clinically without further therapeutic intervention.
The differential diagnosis of bilateral alveolar infiltrates in this patient is broad. A bacterial process seems unlikely, given the chronic presentation of the disease, with the possible exception of Nocardia, which may have a more insidious onset and has a variable radiographic appearance. Tuberculosis has to be considered, particularly since HIV-infected patients with lower CD4-counts commonly have atypical radiographic manifestations. Pneumocystis carinii pneumonia seems to be unlikely, since it usually presents with interstitial infiltrates and a non-productive cough. Hemoptysis would be highly unusual in this setting. An infection with endemic fungi, i.e. histoplasmosis and coccidiomycosis, has to be considered also, particularly in light of the chronic disease presentation. An allergic etiology was suspected in this patient because of the clear relationship between the severity of symptoms and his exposure to mould. Allergic bronchopulmonary aspergillosis is exceedingly rare in HIV-infected individuals and has only been reported in one case report. The diagnosis in this patient was confirmed by the presence of all but one diagnostic criterion: a positive skin test, elevated IgE-levels, eosinophilia, bronchiectasis, Aspergillus immonoprecipitants, elevated specific IgE against Aspergillus, and pulmonary infiltrates. The patient did not report a history of asthma, but admitted to frequent wheezing and had evidence of mild airway obstruction on PFTs. It is interesting to observe that the patient’s symptoms improved with allergen avoidance. Discontinuation of HAART therapy may have contributed to his recovery by altering T-cell immunity, which is considered to play an important role in the pathophysiology of ABPA.
ABPA is an extremely rare cause of bilateral pulmonary infiltrates in HIV-infected individuals. The diagnosis in this patient could be confirmed by the presence of all but one diagnostic criterion. Allergen avoidance and discontinuation of HAART coincided with symptomatic improvement.
M.M. Weder, None.