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. 2011 May 26;118(5):1216–1224. doi: 10.1182/blood-2011-03-316430

Table 2.

Factors favoring mucormycosis over aspergillosis

Clues Comments
Epidemiologic and host clues
    Institution with high background rates of mucormycosis5 Unique geographic exposures vs institution-specific differences in immunosuppression and anti-infective practices
    Iron overload16,17 The most reliable method of diagnosis is unclear
    Hyperglycemia with or without DM5 Degree and duration are undefined
    Prior voriconazole or echinocandin use5,18,24 The magnitude and specificity of such association are debatable
Clinical, radiologic, and laboratory clues
    Community-acquired sinusitis5,24 Pansinusitis or ethmoid involvement are important clinical clues of mucormycosis
    Oral necrotic lesions in hard palate or nasal turbinates4
    Chest wall cellulitis adjacent to a lung infarct4 Mucormycosis can spread across tissue planes
    Acute vascular event (eg, MI, GI bleeding)4 Resulting from the acute hemorrhagic infarct caused by Mucorales
    Multiple (n > 10) nodules in CT and pleural effusion24
    Reverse halo sign in CXR or CT25 Halo sign is as common in IPM as in IPA
    Presumed (by CT findings) fungal pneumonia with adequate (eg, > 2 μg/mL) voriconazole levels19
    Presumed (by CT findings) fungal pneumonia with repetitively negative GM and G-glucan serum levels24

DM indicates diabetes mellitus; MI, myocardial infarction; GI, gastrointestinal; CXR, chest x-ray; GM, galactomannan; IPM, invasive pulmonary mucormycosis; and IPA, invasive pulmonary aspergillosis.