The clinical spectrum of pulmonary aspergillosis

Abstract

The clinical presentation of Aspergillus lung disease is determined by the interaction between fungus and host. Invasive aspergillosis develops in severely immunocompromised patients, including those with neutropenia, and increasingly in the non-neutropenic host, including lung transplant recipients, the critically ill patients and patients on steroids. A high index of suspicion is required in patients without the classical risk factors as early presentation is usually silent and non-specific, pyrexia uncommon and timely treatment is crucial for survival. Invasive aspergillosis has also been diagnosed in normal hosts after massive exposure to fungal spores. Chronic pulmonary aspergillosis affects patients without obvious immune compromise, but with an underlying lung condition such as COPD or sarcoidosis, prior or concurrent TB or non-tuberculous mycobacterial disease. Aspergillus bronchitis may be responsible for persistent respiratory symptoms in patients with Aspergillus detected repeatedly in sputum without evidence of parenchymal Aspergillus disease, especially in patients with bronchiectasis and cystic fibrosis. Allergic bronchopulmonary aspergillosis affects patients with asthma and cystic fibrosis, and is important to recognise as permanent lung or airways damage may accrue if untreated. Changes in the classification of Aspergillus allergic lung disease have been proposed recently. Cases of extrinsic allergic alveolitis and chronic pulmonary aspergillosis have been observed after Aspergillus exposure. Asymptomatic colonisation of the respiratory tract needs close monitoring as it can lead to clinical disease especially with ongoing immunosuppression. The various syndromes should be viewed as a semicontinuous spectrum of disease and one form may evolve into another depending on the degree of ongoing immunosuppression.

Calcineurin Orchestrates Lateral Transfer of Aspergillus fumigatus during Macrophage Cell Death

“…A spectrum of immunocompromised states predisposes individuals to highmortality invasive or chronic forms of pulmonary aspergillosis (PA) (7). Organ transplant recipients are at high risk of PA, with lung transplant recipients being particularly susceptible and having a mortality greater than 40% (8,9).…”

Pulmonary solid tumor with coexisting pulmonary aspergillosis: case reports and literature review

“…This kind of airway mucosa Aspergillus infection are not fully recognized or described in current classifications or guidelines (27,28). The most reliable criterion of invasive fungal airway disease was the demonstration of submucous tissue invasion and damage caused by hyphae (28,29). However, bronchoscopic histopathological biopsy of case 1∼3 showed Aspergillus hyphae merely invaded necrotic tissue of mucous layer, the degree of damage did not involve bronchus submucous layer.…”

“…For case 1, 2 and 3, they are all probably a kind of chronic necrotizing infection of bronchial mucosa instead of acute invasive infection. This kind of airway mucosa Aspergillus infection are not fully recognized or described in current classifications or guidelines (27,28). The most reliable criterion of invasive fungal airway disease was the demonstration of submucous tissue invasion and damage caused by hyphae (28,29).…”

Un nouveau concept

“…Ces différents agents fongiques sont susceptibles d'augmenter la mortalité et la morbidité des patients [8][9][10] ; (3) les traitements antibiotiques pourraient faciliter le développement des infections fongiques pulmonaires chez ces patients. De même, l'utilisation de traitements immunosuppresseurs (corticosté-roïdes au long cours ou autres) favorise le développement d'infections fongiques invasives et graves, en particulier dans un contexte de transplantation, mais éga-lement sur fond de pathologie chronique telle que la BPCO où des cas d'aspergillose semi-invasive ont été rapportés [11][12][13] ; (4) enfin, les champignons sont capables d'interagir notamment avec des bactéries [14]. Ils peuvent aussi former des biofilms et induire une résistance aux traitements anti-infectieux.…”