Allergic Fungal Airway Disease: Pathophysiologic and Diagnostic Considerations

Kerry Woolnough; Abbie Fairs; Catherine H. Pashley; Andrew J. Wardlaw


Curr Opin Pulm Med. 2015;21(1):39-47. 

In This Article

Abstract and Introduction


Purpose of review Fungal spores are ubiquitously present in indoor and outdoor air. A number can act as aeroallergens in Immunoglobulin E (IgE)-sensitized individuals and some thermotolerant fungi germinate in the lung where they can cause a combined allergic and infective stimulus leading to a number of clinical presentations characterized by evidence of lung damage. We discuss which biomarkers are useful in helping to guide diagnosis, prognosis and treatment of allergic fungal airway disease (AFAD).

Recent findings Diagnostic biomarkers, such as specific IgEs and fungal culture, for AFAD are limited by sensitivity, although this may be improved with novel agents such as specific IgEs to fungal components and quantitative PCR. Total IgE and hypereosinophilia are nonspecific and do not clearly relate to disease activity. High attenuation mucus and proximal bronchiectasis are specific, albeit insensitive markers of AFAD. Biomarkers that predict prognosis and treatment response are yet to be defined.

Summary This review summarizes the fungi involved and the current debate regarding the diagnostic criteria to define fungal-associated lung disease. We advocate the phasing out of the term allergic bronchopulmonary aspergillosis and the use of a more inclusive term such as AFAD, together with a more liberal set of criteria based largely on IgE sensitization to thermotolerant fungi, which identifies those patients at risk of developing lung damage.


Fungi can act as aeroallergens in those that are Immunoglobulin E (IgE)-sensitized and can cause a range of airway diseases by colonizing the lung. Allergen exposure to fungal spores, such as Alternaria alternata during the late summer and autumn months,[1] has been associated with acute bronchospasm, asthma admissions and deaths.[2,3] Most fungi that act as aeroallergens do not grow at body temperature and so cannot germinate in the airway. Adverse events are therefore related to the level of spore exposure. However, thermotolerant fungi including some saprophytes that are important in vegetation decomposition, such as Aspergillus fumigatus, grow at body temperature, enabling them to colonize the lung. Depending on the host airway response, fungal colonization can exacerbate asthma, or cause chronic sinusitis, fungal bronchitis, chronic necrotizing pneumonia, fungal empyema, allergic alveolitis or, in people with pre-existing lung cavities, the development of a fungal ball (aspergilloma) (Fig. 1).[4–9] Lastly, severely immunocompromised individuals can develop systemic infection. This review will focus on the clinical aspects of the involvement of thermotolerant fungi in allergic airway disease.

Figure 1.

The spectrum of lung disease caused by fungi is dependent on the presence of pre-existing lung conditions and on whether the host is immunocompetent.