Community acquired Aspergillus pneumonia and/or pneumonitis

Invasive aspergillosis in immunocompromised patients may be acquired in the community (Patterson et al.,1997; Einsele et al., 1998; Cornillet et al., 2006). Recent reports of invasive aspergillosis in newly hospitalized chronic obstructive pulmonary disease (COPD) patients, many of whom, but not all, were treated with corticosteroids, emphasizes the high frequency of Aspergillus acquisition in the community (Bulpa, Dive, & Sibille, 2007; Guinea et al., 2010; Xu et al., 2012). Virtually cases all cases of allergic bronchopulmonary aspergillosis (ABPA), Aspergillus bronchitis and chronic pulmonary aspergillosis (CPA) are, or presumed to be, acquired out of hospital (Rocchi 2015). This is hardly surprising given the ubiquitous nature of Aspergillus fumigatus and other species (Warris & Verweij, 2005; Hedayati, Mayahi, & Denning, 2010). It would therefore not be surprising that susceptible patients may develop community acquired Aspergillus pneumonia.

Reports of community acquired Aspergillus pneumonia and/or pneumonitis are uncommon. The terminology is also variable. There appear to be 3 common features to these reports: A remarkable exposure to airborne spores, prior influenza or other viral infection and/or underlying pulmonary disease, usually emphysema or chronic obstructive pulmonary disease (COPD). Only a few cases are described. 

Clancy and Nguyen (1998) presented one case and summarized the prior literature. They only included cases that fulfilled the following criteria: (1) onset of respiratory symptoms within 14 days of presentation to physician; (2) no underlying medical condition or immunosuppression medication; (3) hyphal elements within the lung parenchyma on histopathology of a biopsy or autopsy; and (4) respiratory tract or tissue culture positive for Aspergillus spp. All 12 cases they identified were infected with A. fumigatus and ranged in age from 14 months to 67 years. One had underlying COPD and one cirrhosis, three were heavy smokers and three heavy drinkers. Three were noted to have overt ‘fungal’ exposures – hay and artificial manure and A. fumigatus was isolated from these sources. Three patients had serologic evidence of prior influenza or other viral infection. Illness developed over 2 to 14 days before seeking medical help and clinical features were not different from bacterial pneumonia. Eight patients had bilateral diffuse infiltrates, three localised infiltrates on their initial chest radiographs, with progression to diffuse infiltrates in all over the next few days. One had a normal chest X-ray with development of a localized and then diffuse infiltrate. Four patients had cavitary lesions. Microscopy for hyphae was positive in one patient and sputum cultures were positive for Aspergillus in 7 of 10 patients (criteria for inclusion in the series). All 12 patients died, despite amphotericin B therapy in six. 

Two other series require mention – both reporting a slowly progressive ‘necrotising pneumonia’ (Kennedy, Malone, & Blyth, 1970; Binder, et al., 1982). Kennedy et al report 4 cases of a necrotising pneumonia in 4 patients in Edinburgh, none immuncompromised but 2 with overt prior pulmonary disease and one a heavy smoker. Gradually evolving large cavitary lesions over weeks with positive sputum cultures for A. fumigatus and detectable Aspergillus precipitating antibody in serum characterized the antemortem diagnostic findings, although Streptococcus pneumoniae and Haemophilus influenzae were also cultured. Two patients died, one of co-existing lung carcinoma. Binder et al present 4 additional cases of a chronic necrotizing pneumonia (chronic necrotizing pulmonary aspergillosis) attributable to A. fumigatus or in one case A. flavus. Progressive cavitation over weeks characterized the patients’ course, with significant co-existing or additional bacterial infections. Three of three tested patients had strongly positive Aspergillus precipitins. The three patients with amphotericin B improved, the other died. 

Since that time additional cases attributable to exposure related to damp and decomposing bark have been described (Conrad, et al., 1992; Arendrup, et al., 2006; Butler et al., 2013) and other cases attributable to other ‘vegetal’ (Batard, et al., 2003) or decomposing plant materials (Siddiqui et al., 2007) and gardening (Zuk, et al.,1989; Meeker, et al., 1991; Russell, et al., 2008). The radiological patterns described are primarily those of a miliary, bilateral diffuse pattern, with high level exposure, but unilateral, usually upper lobe cavitary disease is also well described.  Many of the cases with overwhelming infection are probably patients with immune deficiency, not previously recognized. The most common of these is probably chronic granulomatous disease, but it is likely other entities are responsible. The interplay between excess exposure and the ability of the lung to withstand infection probably determines the pattern of infection. So “mulch pneumonitis” describes severe infections in CGD, in which the causative fungus (and possibly other external agents) is not always identified. This emphasises the likely publication bias of diagnosed cases, with positive cultures, autopsy or biopsy histology and a lack of cases diagnosed by indirect means such as seroconversion with antibody, Aspergillus antigen or DNA detection in respiratory fluids or glucan 1,3-Beta D-glucan detection in serum. Non-fulminatant cases and those with cavitation usually have detectable positive Aspergillus antibody in serum (Kennedy et al., 1970; Binder et al., 1982; Arendrup et al., 2006) and some with very severe disease are also seropositive. 

Late diagnosis and lack of antifungal therapy are associated with early death and/or progressive disease. Amphotericin B therapy is probably ineffective for severe cases (Clancy & Nguyen, 1998; Batard et al., 2003; Siddiqui et al., 2007; Russell et al., 2008). Voriconazole is recommended for treatment in the acute phase, with the addition of corticosteroids for those with overwhelming infection and/or pneumonitis, in the current state of our relative ignorance of this condition. More slowly progressive infection may respond to itraconazole.

Case histories:


Pt DSM, Community acquired Aspergillus pneumonia 02/02/2010 Pt DSM Community acquired primary Aspergillus pneumonia 05/03/2010
Pt DSM, Community acquired Aspergillus pneumonia 02/02/2010 Pt DSM Community acquired primary Aspergillus pneumonia 05/03/2010 July 2011 primary Aspergillus pneumonia












David W. Denning FRCP FRCPath FIDSA FMedSci
Professor of Medicine and Medical Mycology
Director, National Aspergillosis Centre
Education and Research Centre
University Hospital of South Manchester (Wythenshawe Hospital)
Southmoor Road
Manchester M23 9LT UK

October 2015