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Antibiotics
Special Issues
Infection, Virulence and Drug Resistance of Fungal Pathogen
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Infection, Virulence and Drug Resistance of Fungal Pathogen

A special issue of Antibiotics (ISSN 2079-6382). This special issue belongs to the section "Fungi and Their Metabolites".

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 9033

Special Issue Editor

Prof. Dr. Changbin Chen

E-Mail Website
Guest Editor
The Center for Microbes, Development and Health, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai 200031, China
Interests: antifungal drug resistance; host-fungal interaction; mycobiota; Candida albicans

Special Issue Information

Dear Colleagues,

Billions of people suffer from the growing incidence of fungal infection every year. However, the current arsenal of antifungals is exceedingly limited due to a lack of new drug targets and the emergence of drug resistance. Furthermore, the rapid spread of the recently emerged “superbug” Candida auris further worsens the efficacy of first-line antifungal therapy. The diagnosis and treatment of human fungal infections remain a challenge, and tackling this challenge requires better understanding of the mechanisms contributing to fungal infection, pathogenicity, and antifungal drug resistance. Moreover, the importance of a One Health approach to prevent fungal infection is gaining attention, and the role of different factors, including nutrients, resident microbiota, and host innate/adaptive immunity, is highly appreciated. A number of cutting-edge technologies, including protein interactome, gene edition, drug repurposing, single cell omics, metabolomics, etc., provide robust and effective tools to unravel mechanisms and identify novel targets. This Special Issue seeks manuscript submissions that further our understanding of fungal infection, virulence, and drug resistance. Submissions on the characterization of new antifungals, technologies, and antifungal strategies and mechanisms that are harnessed to combat fungal infection are especially encouraged.

Prof. Dr. Changbin Chen
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antibiotics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Antifungal drug resistance
  • Host-fungal interaction
  • Mycobiota
  • Candida albicans

Published Papers (3 papers)

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Research

10 pages, 452 KiB  
Article
Does Systemic Methotrexate Therapy Induce Azole Resistance among Endogenous Candida Strains?
by Dawid Żyrek, Joanna Nowicka, Magdalena Pajączkowska and Ewa Morgiel
Antibiotics 2021, 10(11), 1302; https://0-doi-org.brum.beds.ac.uk/10.3390/antibiotics10111302 - 26 Oct 2021
Cited by 1 | Viewed by 1808
Abstract
Background: Research confirms that Candida spp. incubated with methotrexate develop multi-drug resistance to azoles, but it is not clear whether this phenomenon occurs in vivo in patients treated with cytostatics. The aim of the study was to assess whether systemic methotrexate therapy induces [...] Read more.
Background: Research confirms that Candida spp. incubated with methotrexate develop multi-drug resistance to azoles, but it is not clear whether this phenomenon occurs in vivo in patients treated with cytostatics. The aim of the study was to assess whether systemic methotrexate therapy induces resistance to azoles among endogenous Candida strains in patients with rheumatological diseases. Methods: The test group consisted of 52 rheumatological patients on methotrexate therapy, who have never been exposed to fluconazole. The control group was composed of 49 individuals who have never been exposed to either methotrexate or fluconazole. Oral swab and clinical information were obtained from each participant. The acquired material was cultured, then each strain was isolated and identified (MALDI TOF). Subsequently, minimal inhibitory concentration (MIC) for fluconazole was determined. Results: MIC values ranged from <0.125 to 64 µg/mL with the most common result <0.125 µg/mL. Samples obtained from 4 patients of the test group and 2 patients of the control group contained strains resistant to fluconazole. Conclusions: Despite slightly higher incidence of fluconazole-resistant strains among patients on systemic methotrexate therapy, we found no solid evidence to support the hypothesis that methotrexate induces resistance to azoles among endogenous Candida strains in patients with rheumatological diseases. Full article
(This article belongs to the Special Issue Infection, Virulence and Drug Resistance of Fungal Pathogen)
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13 pages, 1624 KiB  
Article
Two Sequential Clinical Isolates of Candida glabrata with Multidrug-Resistance to Posaconazole and Echinocandins
by Qiqi Wang, Yun Li, Xuan Cai, Ruoyu Li, Bo Zheng, Ence Yang, Tianyu Liang, Xinyu Yang, Zhe Wan and Wei Liu
Antibiotics 2021, 10(10), 1217; https://0-doi-org.brum.beds.ac.uk/10.3390/antibiotics10101217 - 07 Oct 2021
Cited by 4 | Viewed by 1905
Abstract
Candida glabrata is one of the most prevalent causative pathogens of invasive candidiasis, and multidrug-resistant strains are emerging. We identified two clinical isolates of C. glabrata, BMU10720 and BMU10722 sequentially isolated from one patient with multidrug-resistance to posaconazole (POS), caspofungin (CAS), micafungin [...] Read more.
Candida glabrata is one of the most prevalent causative pathogens of invasive candidiasis, and multidrug-resistant strains are emerging. We identified two clinical isolates of C. glabrata, BMU10720 and BMU10722 sequentially isolated from one patient with multidrug-resistance to posaconazole (POS), caspofungin (CAS), micafungin (MCF), and anidulafungin (ANF). Overexpression of ERG11 in BMU10720 and CDR1 in BMU10722 were detected at basal level. When exposed to POS, CDR1 was significantly up-regulated in both isolates compared with susceptible reference strain, while ERG11 was up-regulated considerably only in BMU10720. PDR1 sequencing revealed that both isolates harbored P76S, P143T, and D243N substitutions, while ERG11 was intact. Cdr1 inhibitor FK520 reversed POS-resistance by down-regulating ERG11 expression. FKS sequencing revealed that both isolates harbored S663P substitution in FKS2, and four single nucleotide polymorphisms (SNPs) existed in FKS2 genes between BMU10720 and BMU10722, while FKS1 was intact. Both FKS1 and FKS2 were up-regulated by CAS in BMU10720 and BMU10722. FK520 down-regulated FKS2 expression induced by CAS through inhibiting calcineurin, resulting in synergic effect with echinocandins as well as Congo Red and Calcofluor White, two cell wall-perturbing agents. In conclusion, the multidrug-resistance of C. glabrata isolates in our study was conferred by different mechanisms. CDR1 and ERG11 overexpression in one isolate and only CDR1 overexpression in the other isolate may mediate POS-resistance. S663P mutation in FKS2 and up-regulation of FKS2 may contribute to echinocandin-resistance in both isolates. Full article
(This article belongs to the Special Issue Infection, Virulence and Drug Resistance of Fungal Pathogen)
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12 pages, 911 KiB  
Article
Therapeutic Drug Monitoring of Isavuconazole: Serum Concentration Variability and Success Rates for Reaching Target in Comparison with Voriconazole
by Malene Risum, Mai-Britt Vestergaard, Ulla Møller Weinreich, Marie Helleberg, Nadja Hawwa Vissing and René Jørgensen
Antibiotics 2021, 10(5), 487; https://0-doi-org.brum.beds.ac.uk/10.3390/antibiotics10050487 - 23 Apr 2021
Cited by 22 | Viewed by 4634
Abstract
Isavuconazole (ISZ) is used in the treatment of aspergillosis and mucormycosis. The purpose of this study was to evaluate the therapeutic drug monitoring (TDM) of ISZ samples from a clinical setting performed at Statens Serum Institut. Materials/methods: Isavuconazole serum concentrations were determined by [...] Read more.
Isavuconazole (ISZ) is used in the treatment of aspergillosis and mucormycosis. The purpose of this study was to evaluate the therapeutic drug monitoring (TDM) of ISZ samples from a clinical setting performed at Statens Serum Institut. Materials/methods: Isavuconazole serum concentrations were determined by fluorescent detection on a UHPLC. Serum-ISZ (s-ISZ) results were included and compared to those of serum-voriconazole (s-VRZ) in a 33 month period from March 2017. Clinical data were obtained for patients receiving ISZ. The therapeutic range was initially 2–10 mg/L, but was adjusted to 2–5 mg/L during the study period except for selected patients with Mucorales infections who received off-label doses of ISZ. Results: A total of 273 s-ISZ and 1242 s-VRZ measurements from 35 and 283 patients, respectively, were included. Seventeen patients had received both ISZ and VRZ with TDM within the study period. The median s-ISZ was 4.3 mg/L (0.5–15.4 mg/L) with 83% of measurements within the therapeutic index. The median s-VRZ was 2.6 mg/L (0.2–21.9 mg/L) with 67% of measurements within the therapeutic index. The median intra-/interindividual coefficient of variation (CV) was 43.4%/54.8% for ISZ compared to 53.2%/83.3% for VRZ. For patients receiving ISZ, the adverse events were mostly gastroenteric and few drug–drug interactions were observed. Furthermore, immediate change from ISZ to VRZ treatment seemed to lead to prolonged metabolism of ISZ with detection up to 35 days after discontinuation. Conclusions: The majority of patients achieved s-ISZ levels well within the therapeutic range with less intra/interindividual CV than patients receiving VRZ. Full article
(This article belongs to the Special Issue Infection, Virulence and Drug Resistance of Fungal Pathogen)
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