Clonal spread of fluconazole‐resistant C. parapsilosis in patients admitted to a referral hospital located in Burgos, Spain, during the COVID‐19 pandemic

• Published in: Mycoses 2024-01, Vol.67 (1), p.e13685-n/a
• Main Authors: Mantecón‐Vallejo, María de los Ángeles, Mesquida, Aina, Ortiz, María de Valle, Buzón‐Martín, Luis, Ossa‐Echeverri, Sergio, Fisac‐Cuadrado, Lourdes, Megías‐Lobón, Gregoria, Ortega‐Lafont, María Pilar, Muñoz, Patricia, Escribano, Pilar, Guinea, Jesús
• Format: Article
• Language: English
• Subjects: Amphotericin B; Antibiotics; Azoles; Candida parapsilosis; Candidemia; Cardiovascular system; COVID-19; Echinocandins; EUCAST; Fluconazole; Genetic markers; Genotypes; Intensive care units; Microsatellites; Pandemics; resistance; Y132F
• ISSN: 0933-7407; 1439-0507
• DOI: 10.1111/myc.13685

Background Fluconazole‐resistant Candida parapsilosis (FRCP) is a matter of concern in Spain. Objectives We here report a FRCP spread across a 777‐bed referral hospital located in Burgos, Spain, during the COVID‐19 pandemic. Patients/Methods In April 2021, an FRCP isolate (MIC = 64 mg/L, E‐test®) from a hospitalised patient was detected. Up to June 2022, all C. parapsilosis isolates (n = 35) from hospitalised patients (n = 32) were stored and genotyped using microsatellite markers, and their antifungal susceptibilities were studied (EUCAST); FRCP isolates were molecularly characterised. Results We detected 26 FRCP isolates collected between 2021 (n = 8) and 2022 (n = 18); isolates were susceptible to amphotericin B, echinocandins and ibrexafungerp. FRCP isolates were grouped into three genotypes: CP‐707 and CP‐708 involved isolates harbouring the Y132F + R398I ERG11p substitutions (n = 24) and were clonally related; the remaining CP‐675 genotype involved isolates harbouring the G458S ERG11p substitution (n = 2). FRCP genotypes were genetically related to the FRCP genotypes found in Madrid and were unrelated to fluconazole‐susceptible ones. Patients harbouring FRCP were mainly (n = 22/23) admitted to intensive care units. Most patients had received broad‐spectrum antibiotics (n = 22/23), and/or antifungal therapy with azoles (n = 14/23) within the 30 days prior to FRCP isolation. Thirteen patients were colonised, 10 of whom were infected and presented candidaemia (n = 8/10), endovascular infection (n = 1/10) or complicated urinary infection (n = 1/10). Overall nonattributable 30‐day mortality was 17% (n = 4/23). Conclusions We report an outbreak caused by FRCP affecting patients admitted to the ICU of a referral hospital located in Burgos. Patients harbouring FRCP had a higher fluconazole use than those carrying susceptible isolates.