Fusarium spp. causing invasive disease in humans: A case series from north India.

Owing to their inherent resistance to different classes of antifungals, early identification of Fusarium spp. is crucial. In this study, 10 clinical isolates were included from patients with invasive fusariosis involving lungs, sinuses, or both. Clinico-radiological data were collected. Samples were processed by standard laboratory procedures. Three gene regions (ITS, TEF1, and RPB2) were amplified by PCR for multilocus sequencing. Fusarium MLST, FUSARIUM-ID, and FUSARIOID-ID databases were used for final identification. Antifungal susceptibility testing was performed by broth microdilution following CLSI M38-A3 and Sensititre™ YeastOne™ YO9 plate. Pulmonary involvement was seen in all patients, and sino-nasal involvement was present in six. Radiologically, consolidations and cavitations were present in eight and six cases, respectively. Halo sign was present in six; reverse halo sign was also found in three of them. Direct microscopy showed septate hyphae that were morphologically different from those found in aspergillosis. Results of the molecular identification were as follows: two Fusarium irregulare, one Fusarium pernambucanum, one Fusarium incarnatum, one Fusarium sp. FIESC 30, two Fusarium keratoplasticum, one Fusarium falciforme, one Fusarium pseudonygamai, and one Fusarium delphinoides. For both Fusarium solani (FSSC) and Fusarium incarnatum-equiseti (FIESC) species complexes, amphotericin B had the lowest minimum inhibitory concentrations (MICs). Importantly, for terbinafine, all FIESC isolates had low MICs, while FSSC isolates had high MICs. In some cases, early identification of Fusarium spp. is possible by means of morphology of hyphae on direct microscopy and findings on radiology. Molecular identification, at least to the species complex level, is crucial for the choice of antifungals.