Taylor & Francis Group
Browse
umyc_a_1666598_sm5422.docx (13.16 kB)

Characterization of a Candida albicans isolate from a recurrent cervical lymphadenitis patient

Download (13.16 kB)
journal contribution
posted on 2019-10-17, 19:31 authored by Chengzhen Zhang, Wenjuan Wang, Qingtao Kong, Fang Liu, Jiangye Chen, Hong Sang

Candida albicans is the most frequently isolated opportunistic fungal pathogen in humans. However, patients with cervical lymphadenitis caused by Candida infection are rarely reported, and few studies have focused on the mechanisms underlying chronic Candida infection. In this study, we isolated a C. albicans strain (JL01) from a recurrent cervical lymphadenitis patient. The clinical isolate was identified by morphological observation and confirmed by DNA sequencing of the internal transcribed spacer (ITS) regions. Strain JL01 is resistant to azole antifungal drugs, but sensitive to amphotericin B. The strain is able to adapt to oxidative and osmotic stresses but is defective in filamentous and invasive growth. The strain displays attenuated virulence in a murine systemic infection model. RNA-sequencing analysis revealed that JL01 has a distinct gene expression profile compared with C. albicans reference strain SC5314; hundreds of transcripts were significantly dysregulated, including those related to morphogenesis and pathogenesis. Taken together, our clinical, virulence, morphological, and biological analyses suggest that the azole resistance, oxidative and osmotic stress tolerance, invasive defect, hypovirulence, and impaired interaction with the host immune system of strain JL01 may correlate with its ability to cause cervical lymphadenitis in the patient. Our research may contribute to elucidating the mechanism(s) underlying the drug resistance and immune escape of C. albicans in chronic fungal infection.

Funding

This work was supported by the National Natural Science Foundation of China (grant 81871630 to H.S. and grant 31370105 to J.C.) and the Foundation of Nanjing General Hospital (grant 2017011 to Q.K.) and CXTDA (grant 2017038).

History