Shortly after Hinson et al proposed the term allergic bronchopulmonary aspergillosis (ABPA) in 1952, 23 Pepys et al at the Brompton Hospital, London, discovered several immunoserological features that confirmed the designation of allergy. 30,31 The initial proposal was based on only three patients: two women ages 45 and 55 years and a 37-year-old man. Their criteria for the diagnosis of ABPA were as follows: recurrent fever, radiologic evidence of recurrent collapse and consolidation in different areas; sputum containing plugs from which fungi could be cultured (all three had Aspergillus fumigatus ); and a blood eosinophilia of 1000/mm 3 . Interestingly, neither asthma nor bronchiectasis were considered diagnostic criteria, although each patient had evidence of asthma, and two had definite saccular bronchiectasis whose location, central or peripheral, was not emphasized. Hinson et al thought sensitization to the fungus was the pathogenic mechanism because of the eosinophilia, character of the sputum, and absence of significant fungal invasion in histologic examinations of biopsy and necropsy material. They attributed inconclusive results of skin tests to Aspergillus extracts in two of the patients and controls to the quality of the extracts. It remained for the Pepys group to develop fungal extracts that produced immediate and delayed skin tests and serum precipitating antibodies that showed clinical correlation. By 1971, they had published a series of 111 cases diagnosed as ABPA and proposed the immunopathogenic mechanism of a combination of IgE-mediated (Gell and Coombs Type I) and immune complex-mediated (Type III) factors. 30 Bronchiectasis of a central or proximal distribution was considered a complication of recurring local bronchial plugging and resultant immunologic inflammation. For the first 16 years after the initial report, it was believed to be a disease limited to the United Kingdom. Eventually, reports first by Patterson and Golbert 41 and then by Slavin et al 51 conceded it was present in North America but only as a rarity. By 1973, however, ABPA was termed no longer rare in the United States, 24 probably because of the more widespread application of potent Aspergillus extracts in both in vivo and in vitro tests and heightened awareness; the diagnosis was being reported worldwide. 43 The true prevalence of ABPA remains highly speculative: ABPA is not recognized in the international classification of diseases (including the ninth revision of 1996) and the diagnostic criteria lack clinical uniformity and standardized tests. Thus epidemiologic conclusions will be based on circuitous reasoning. In this article, an attempt is made to approach its prevalence by several routes. Statistical and epidemiological aspects of related or associated diseases such as asthma, cystic fibrosis, bronchiectasis, pulmonary eosinophilia, and aspergillosis are invoked. Sensitization rates to Aspergillus antigens are also assessed. Finally, we discuss whether ABPA represents a condition recently born or recently discovered.