Republished: 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.

Zinc and Manganese Chelation by Neutrophil S100A8/A9 (Calprotectin) Limits Extracellular Aspergillus fumigatus Hyphal Growth and Corneal Infection

“…CP is likely also important in the immunosuppressed condition where hyphae are present as leucopenic mice have reduced CP expression in the lung and increased fungal burden (32), and patients who develop Aspergillus pulmonary infections are often either neutropenic or have neutrophil dysfunction (52). …”

Ecology of aspergillosis: insights into the pathogenic potency of Aspergillus fumigatus and some other Aspergillus species

“…Invasive pulmonary aspergillosis is the most common form of invasive aspergillosis, implying fungal invasion in the lung tissue. Patients at risk are predominantly haematopoietic stem‐cell transplant recipients and patients with haematological malignancies undergoing intensive chemotherapy; however, cases involving non‐neutropenic patients have also been reported (Kosmidis and Denning, ,b). Acute invasive rhinosinusitis is an underdiagnosed form of invasive aspergillosis which most commonly involves the maxillary sinus, followed by the ethmoid, sphenoid and frontal sinuses; this type of infection is aggressive and often fatal (Drakos et al ., ; Middlebrooks et al ., ).…”

“…After fungal germination, polymorphonuclear neutrophils provide the dominant host defence, rendering neutropenic patients at an elevated risk for developing aspergillosis (Kosmidis and Denning, ,b). In the phagocytes, NADPH‐oxidase catalyses the conversion of oxygen to superoxide anion and the generation of ROS displaying antimicrobial activity (Segal, ).…”

“…A locally invasive version of the disease, chronic necrotizing pulmonary aspergillosis, is mainly observed in humans with mild immunodeficiency or with a chronic lung disease. Non‐invasive forms of Aspergillus ‐induced lung disease include aspergilloma and allergic bronchopulmonary aspergillosis (ABPA) (Kosmidis and Denning, ,b).…”

The Role of PET in Monitoring Therapy in Fungal Infections

“…Patients in intensive care units in whom indwelling catheters remain for a long period of time and in whom the prolonged use of antibiotics changes the gut flora are at risk for acquiring IFIs. Patients with burns and premature babies are also at risk [30][31][32].…”