Acute pulmonary aspergillosis in immunocompetent subjects after exposure to bark chippings

Arendrup, Maiken Cavling; O’Driscoll, B R; Petersen, Eskild A.; Denning, David W.

doi:10.1080/00365540600606580

Cited by 27 publications

(30 citation statements)

References 20 publications

(15 reference statements)

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“…This fungus causes different pathologies including occupational rhinitis in people working in damp and mouldy places [6], allergic aspergillosis and invasive forms of aspergillosis in immunosuppressed patients [7]. Several cases of acute pulmonary aspergillosis in immunocompetent patients have been reported [8], [9], [10]. The factors that enable A. fumigatus to cause invasive disease are not currently understood [11].…”

Section: Introductionmentioning

confidence: 99%

Trypacidin, a Spore-Borne Toxin from Aspergillus fumigatus, Is Cytotoxic to Lung Cells

et al. 2012

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Inhalation of Aspergillus fumigatus conidia can cause severe aspergillosis in immunosuppressed people. A. fumigatus produces a large number of secondary metabolites, some of which are airborne by conidia and whose toxicity to the respiratory tract has not been investigated. We found that spores of A. fumigatus contain five main compounds, tryptoquivaline F, fumiquinazoline C, questin, monomethylsulochrin and trypacidin. Fractionation of culture extracts using RP-HPLC and LC-MS showed that samples containing questin, monomethylsulochrin and trypacidin were toxic to the human A549 lung cell line. These compounds were purified and their structure verified using NMR in order to compare their toxicity against A549 cells. Trypacidin was the most toxic, decreasing cell viability and triggering cell lysis, both effects occurring at an IC50 close to 7 µM. Trypacidin toxicity was also observed in the same concentration range on human bronchial epithelial cells. In the first hour of exposure, trypacidin initiates the intracellular formation of nitric oxide (NO) and hydrogen peroxide (H2O2). This oxidative stress triggers necrotic cell death in the following 24 h. The apoptosis pathway, moreover, was not involved in the cell death process as trypacidin did not induce apoptotic bodies or a decrease in mitochondrial membrane potential. This is the first time that the toxicity of trypacidin to lung cells has been reported.

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Section: Introductionmentioning

confidence: 99%

Trypacidin, a Spore-Borne Toxin from Aspergillus fumigatus, Is Cytotoxic to Lung Cells

et al. 2012

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“…In previous cases, massive inhalation of spores was thought to be the likely route of infection [3]. There is diagnostic difficulty in these cases and diagnosis is often made at post-mortem, because blood and sputum cultures have poor sensitivity [1,3].…”

Section: Discussionmentioning

confidence: 99%

Acute Aspergillus pneumonia associated with mouldy tree bark-chippings, complicated by anti-glomerular basement membrane disease causing permanent renal failure

Butler

Brockley

Denning³

et al. 2013

Medical Mycology Case Reports

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A non-immunocompromised man developed acute Aspergillus pneumonia after spreading mouldy tree bark mulch. Despite normal renal function at presentation, he developed rapidly progressive glomerulonephritis with acute kidney injury due to anti-glomerular basement membrane antibodies (anti-GBM) 4 weeks later. He remained dialysis dependent and died of sepsis 10 months later. We hypothesise that he contracted invasive pulmonary Aspergillosis from heavy exposure to fungal spores, leading to epitope exposure in the alveoli with subsequent development of GBM auto-antibodies.

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“…Hospital water could be a major source of filamentous fungi, in particular Aspergillus fumigatus [8-10]. We have recently noted 'primary' A. fumigatus infection after exposure to bark chippings presumably heavily contaminated with fungus in normal people [11]. …”

Section: Discussionmentioning

confidence: 99%

Invasive pulmonary aspergillosis 10 years post bone marrow transplantation: a case report

Rashid

Denning

2009

J Med Case Reports

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IntroductionInvasive pulmonary aspergillosis is a leading cause of mortality and morbidity in bone marrow transplant recipients. Establishing the diagnosis remains a challenge for clinicians working in acute care setting. However, prompt diagnosis and treatment can lead to favourable outcomesCase presentationWe report a case of invasive aspergillosis occurring in a 39-year-old Caucasian female 10 years after an allogeneic haematopoietic bone marrow transplant, and 5 years after stopping all immunosuppression. Possible risk factors include bronchiolitis obliterans and exposure to building dust (for example, handling her husband's dusty overalls). There are no similar case reports in the literature at this time.ConclusionHigh clinical suspicion, especially in the setting of failure to respond to broad-spectrum antibiotics, should alert clinicians to the possibility of invasive pulmonary aspergillosis, which, in this case, responded to antifungal therapy.

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Acute pulmonary aspergillosis in immunocompetent subjects after exposure to bark chippings

Cited by 27 publications

References 20 publications

Trypacidin, a Spore-Borne Toxin from Aspergillus fumigatus, Is Cytotoxic to Lung Cells

Trypacidin, a Spore-Borne Toxin from Aspergillus fumigatus, Is Cytotoxic to Lung Cells

Acute Aspergillus pneumonia associated with mouldy tree bark-chippings, complicated by anti-glomerular basement membrane disease causing permanent renal failure

Invasive pulmonary aspergillosis 10 years post bone marrow transplantation: a case report

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