Date: 26 November 2013
The patient was a 37-year old man in whom P.carinii pneumonia developed in August 1987, followed by esophageal candidiasis and upper gastrointestinal bleeding in September. Chronic perineal herpes led to the formation of rectourethral fistula and multiple episodes of urosepsis, for which he was given long-term ciprofloxacin therapy to suppress bacterial colonization of the bladder. He discontinued heavy alcohol use in September 1987 and smoked marijuana occasionally.On April 23 1989, the patient was admitted to the hospital with a two-month history of increasing dry cough with shortness of breath. He reported transient fever (temperature to 41°C). He was admitted with leukopenia, with his neutrophil count falling to 16 x 106/l on the second hospital day. A chest film showed bilateral fluffy lower-lobe infiltrates (this image). Zidovudine was discontinued. The patient had a rapidly downhill course despite intravenous treatment with trimethioprim-sulfamethoxazole. A bronchoscopy on the sixth hospital day revealed what appeared to be a foreign body in the left lower-lobe bronchus. It was removed, together with much necrotic, mucoid debris. On microscopic examination, the “foreign body” was necrotic, containing large numbers of hyphae and conidia in a manner typical of an aspegilloma or fungal cast. The culture grew A.fumigatus.
Clinical and radiologic improvement followed bronchoscopy, and itraconazole therapy was begun because of the concern about invasive aspergillosis in the setting of marked neutropenia. The patient tolerated the medication well at a dose of 200 mg twice daily, and the chest film became normal over the subsequent six weeks, after which itraconazole was discontinued. A sputum specimen cultured for fungus four weeks after the start of therapy was negative. After the initial improvement with itraconazole, the patient had recurrent urosepsis, associated with dehydration and marked confusion. Nine weeks after the discontinuation of itraconazole, he died of progressive dementia complicated by recurrent pneumonia and sepsis. There was no postmortem examination.
This patient was described (pt 11) and this chest radiograph reproduced in Denning DW, Follansbee S, Scolaro M, Norris S, Edelstein D, Stevens DA. Pulmonary Aspergillosis in the Acquired Immunodeficiency Syndrome. N Engl J Med 1991; 324: 654-662.
Copyright: n/a
Notes: n/a
Images library
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Title
Legend
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Conidial head and brown conidia in a section of a fungus ball caused by Aspergillus niger (H&E, x 400).
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Double diffusion test for aspergillosis. Central well contains Aspergillus fumigatus antigen and wells in the top and bottom contain control antiserum.
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Allergic Bronchocentric Granulomatosis. low power. Sections show muscle, lung with acute inflammation and evidence of organisation with early fibrosis. The bronchial wall can be seen with chronic inflammation and many eosinophils.There is a thickened basement membrane. No definite granulomata are seen.
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Allergic Bronchocentric Granulomatosis. Sections show muscle, lung with acute inflammation and evidence of organisation with early fibrosis. The bronchial wall can be seen with chronic inflammation and many eosinophils.There is a thickened basement membrane. No definite granulomata are seen.
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Allergic Bronchocentric Granulomatosis. Higher power. Sections show muscle, lung with acute inflammation and evidence of organisation with early fibrosis. The bronchial wall can be seen with chronic inflammation and many eosinophils.There is a thickened basement membrane. No definite granulomata are seen.
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Allergic Bronchocentric Granulomatosis. Higher power. Sections show muscle, lung with acute inflammation and evidence of organisation with early fibrosis. The bronchial wall can be seen with chronic inflammation and many eosinophils.There is a thickened basement membrane. No definite granulomata are seen.
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Allergic Bronchocentric Granulomatosis. Low power. Sections show muscle, lung with acute inflammation and evidence of organisation with early fibrosis. The bronchial wall can be seen with chronic inflammation and many eosinophils.There is a thickened basement membrane. No definite granulomata are seen.
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Allergic Bronchopulmonary Aspergillosis (ABPA). PT JC
CXR prior to bronchoscopy had shown an opacity just superior to the right hilum, which was felt to represent possibly a fungal plug. Patient was therefore bronchoscoped.
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Secondary metabolites, Structural diagram. Trivial name – 2-hydroxy-3-methyl-1,4-benzoquinone
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Secondary metabolite structure: trivial name – 13-O-Methylviriditin
