To report the first case of cutaneous chronic active Epstein-Barr virus disease manifesting as persistent erythema multiforme in China. The 12-year-old female patient presented with recurrent erythema and blisters all over the body, accompanied by oral erosions for more than 5 months. Skin examination showed dark erythema scattered on the right upper eyelid and cheeks, as well as erosions and blisters arising in the dark erythema on the lower jaw; broad bean- to pigeon egg-sized blisters with clear fluids arising in erythema were scattered on the back, buttocks, and limbs, and some manifested as atypical targetoid lesions; there was a mung bean-sized erosion on the mucosa of the lower lip and the right buccal region each; the patient also presented with moon face and multiple striae atrophicae on the lower limbs. Histopathological examination of the skin lesions on the lower limb revealed basket-weave hyperkeratosis, epidermal necrosis, liquefaction degeneration of basal cells with subepidermal blister formation, and perivascular lymphocytic infiltration in the superficial dermis; direct immunofluorescence assay showed negative staining for IgG, IgM, IgA, and complement C3 among epidermal cells and at the basement membrane zone; enzyme-linked immunosorbent assay showed negative staining for serum antibodies against desmoglein 1/3 (Dsg1/3), BP180, and type Ⅶ collagen; immunohistochemical examination demonstrated partial positive staining for CD3, CD4, CD5, CD8, CD56, granzyme B, and Epstein-Barr virus-encoded RNA, positive staining for Ki67 (> 70%), but negative staining for CD20. The Epstein-Barr virus DNA level was measured to be 1.97 × 10 6 IU/ml in whole blood samples and 2.65 × 10 7 IU/ml in blister fluid samples. No mutation sites with functional significance were identified by whole-exome sequencing. Based on these findings, a diagnosis of cutaneous chronic active Epstein-Barr virus disease manifesting as persistent erythema multiforme was made. The patient was treated with methylprednisolone at a dose of 40 mg/d, intravenous drips of ganciclovir at 200 mg twice daily, etc., and discharged after improvement.

Candida auris ( C. auris) is a recently emerged multidrug-resistant fungal pathogen, featured by difficulty in identification, high mortality and easy spread in hospital environments. Furthermore, C. auris is resistant to various frontline antifungals. However, the mechanisms governing drug resistance remain unclear. This review summarized the mechanisms of triazole resistance in C. auris, including ERG11 missense mutations or overexpression, the activity of efflux pumps, missense mutations in TAC1 B, the gain of an extra copy of chromosomeⅤ, the role of Hsp90 and biofilm formation. In addition, the factors associated with the resistance to other drugs including echinocandins, polyenes, nucleoside analogues and acrylamide were also reviewed.