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

Author:

Mantecón‐Vallejo María de los Ángeles1,Mesquida Aina23,Ortiz María de Valle4,Buzón‐Martín Luis5,Ossa‐Echeverri Sergio4,Fisac‐Cuadrado Lourdes4,Megías‐Lobón Gregoria1,Ortega‐Lafont María Pilar1,Muñoz Patricia2367,Escribano Pilar238ORCID,Guinea Jesús2368ORCID

Affiliation:

1. Clinical Microbiology Department Complejo Asistencial Universitario de Burgos Burgos Spain

2. Clinical Microbiology and Infectious Diseases Hospital General Universitario Gregorio Marañón Madrid Spain

3. Instituto de Investigación Sanitaria Gregorio Marañón Madrid Spain

4. Intensive Care Unit Complejo Asistencial Universitario de Burgos Burgos Spain

5. Internal Medicine Department Complejo Asistencial Universitario de Burgos Burgos Spain

6. CIBER Enfermedades Respiratorias‐CIBERES (CB06/06/0058) Madrid Spain

7. Medicine Department, Faculty of Medicine Universidad Complutense de Madrid Madrid Spain

8. School of Health, HM Hospitals Universidad Camilo José Cela Madrid Spain

Abstract

AbstractBackgroundFluconazole‐resistant Candida parapsilosis (FRCP) is a matter of concern in Spain.ObjectivesWe here report a FRCP spread across a 777‐bed referral hospital located in Burgos, Spain, during the COVID‐19 pandemic.Patients/MethodsIn 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.ResultsWe 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).ConclusionsWe 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.

Publisher

Wiley

Subject

Infectious Diseases,Dermatology,General Medicine

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