Table 2.
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.