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Invasive external otitis caused by Aspergillus.

Abstract

Invasive external otitis occurs almost exclusively in patients with longstanding diabetes. Except for occasional cases, the etiologic agent has been Pseudomonas aeruginosa. We report a case caused by Aspergillus species in a diabetic patient with acute leukemia. Persistent infection was documented by culture and histology after a course of intravenous amphotericin B (total dose, 2 g). Clinical resolution occurred in association with a 3-month course of oral itraconazole. Four previously reported cases of invasive aspergillus otitis are reviewed.

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BibTeXRIS

P Phillips, G Bryce, J Shepherd, D Mintz. Invasive external otitis caused by Aspergillus.. https://doi.org/10.1093/clinids%2F12.2.277

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Variable number of tandem repeats of TNF receptor type 2 promoter as genetic biomarker of susceptibility to develop invasive pulmonary aspergillosis.

Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin alpha (LT-alpha) are pivotal mediators of inflammatory responses in fungal infection diseases. We hypothesized that polymorphisms in genes of these cytokines or their receptors might increase the susceptibility of hematologic patients to develop invasive pulmonary aspergillosis (IPA). One hundred two hematologic patients and 124 age-matched controls were enrolled in the study, and the following standard single nucleotide polymorphisms were investigated: TNF-alpha -308 and +489, LT-alpha +252 and Tumor Necrosis Factor Receptor 2 (TNFR2) +676. Variable number of tandem repeats (VNTRs) at position -322 of the TNFR2 gene were also studied. Genotypic and allelic frequencies were similar between patients and controls. IPA was diagnosed in 54 of the 102 patients according to consensus criteria published by the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group. TNF-alpha and LT-alpha polymorphisms were not associated with presence of IPA. Susceptibility to IPA was strongly associated with VNTR at position -322 in the promoter region of the TNR2 gene (p = 0.029) but was not associated with the presence of TNFR2 +676 polymorphism. A genetic difference in TNFR2 promoter VNTR may play a major role in susceptibility to IPA infection.

Aspergillosis↗