ArticleAntimicrobial agents and chemotherapy2015
Acquired Multidrug Antifungal Resistance in Candida lusitaniae during Therapy.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 81 citations in OpenAlex.
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- Drivers of diversification in fungal pathogen populations.PLoS pathogens · 2024Review
- Epidemiology of Candidemia in Mashhad, Northeast Iran: A Prospective Multicenter Study (2019-2021).Journal of fungi (Basel, Switzerland) · 2024Article
- Phenotypical Differences at the Physiological and Clinical Level between Two Genetically Closely RelatedJournal of fungi (Basel, Switzerland) · 2024Article
- Novel antifungals and treatment approaches to tackle resistance and improve outcomes of invasive fungal disease.Clinical microbiology reviews · 2024Review
- Identification of Virulence Factors in Isolates ofMicroorganisms · 2024Article
- Antifungal susceptibility testing following the CLSI M27 document, along with the measurement of MFC/MIC ratio, could be the optimal approach to detect amphotericin B resistance inAntimicrobial agents and chemotherapy · 2024Article
- Long-term stability of acquired drug resistance and resistance associated mutations in the fungal pathogenFrontiers in cellular and infection microbiology · 2024Article
- The rapid emergence of antifungal-resistant human-pathogenic fungi.Nature reviews. Microbiology · 2023Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida lusitaniae is usually susceptible to echinocandins. Beta-1,3-glucan synthase encoded by FKS genes is the target of echinocandins. A few missense mutations in the C. lusitaniae FKS1 hot spot 1 (HS1) have been reported. We report here the rapid emergence of antifungal resistance in C. lusitaniae isolated during therapy with amphotericin B (AMB), caspofungin (CAS), and azoles for treatment of persistent candidemia in an immunocompromised child with severe enterocolitis and visceral adenoviral disease. As documented from restriction fragment length polymorphism (RFLP) and random amplified polymorphic DNA (RAPD) analysis, the five C. lusitaniae isolates examined were related to each other. From antifungal susceptibility and molecular analyses, 5 different profiles (P) were obtained. These profiles included the following: profile 1 (P1) (CAS MIC [μg/ml], 0.5; fluconazole [FLC] MIC, 0.25), determined while the patient was being treated with liposomal AMB for 3 months; P2 (FLC MIC [μg/ml], 0.25; CAS MIC, 4), while the patient was being treated with CAS for 2 weeks; P3 (CAS MIC [μg/ml], 0.5; FLC MIC, 32), while the patient was being treated with azoles and CAS initially followed by azoles alone for a week; P4 (CAS MIC [μg/ml], 8; FLC MIC, 8), while the patient was being treated with both drugs for 3 weeks; and P5 (AMB MIC [μg/ml], 0.125; CAS MIC, 8), while the patient was being treated with AMB and FLC for 2 weeks. CAS resistance was associated with resistance not only to micafungin and anidulafungin but also to AMB. Analysis of CAS resistance revealed 3 novel FKS1 mutations in CAS-resistant isolates (S638Y in P2; S631Y in P4; S638P in P5). While S638Y and -P are within HS1, S631Y is in close proximity to this domain but was confirmed to confer candin resistance using a site-directed mutagenesis approach. FLC resistance could be linked with overexpression of major facilitator gene 7 (MFS7) in C. lusitaniae P2 and P4 and was associated with resistance to 5-flurocytosine. This clinical report describes resistance of C. lusitaniae to all common antifungals. While candins or azole resistance followed monotherapy, multidrug antifungal resistance emerged during combined therapy.
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