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

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.

[Aneurysmal subarachnoid haemorrhage: Results after introducing endovascular therapy in a medium-low volume centre]. / Hemorragia subaracnoidea aneurismática: resultados tras la introducción de la terapia endovascular en un centro de medio-bajo volumen.

OBJECTIVE: To evaluate the impact of introducing endovascular therapy for patients with aneurysmal subarachnoid haemorrhage (aSAH) in a medium-low volume centre. MATERIAL AND METHODS: A retrospective observational study was conducted by comparing the clinical outcome of patients with aSAH before and after introducing endovascular therapy in our centre. The main variables analysed were: type of treatment, hospital and late mortality, intra-procedural morbidity, rate of re-bleeding and vasospasm, and clinical outcome according to the Glasgow Outcome Score (GOS). RESULTS: Seventy-one patients were treated in two periods: 2010-2011 (32 patients; 19 clipped, 6 coiled, 7 untreated), and 2012-2013 (39 patients, 3 clipped, 34 coiled, 2 untreated). No significant differences were found in age, sex, clinical grade at admission, type and location of aneurysm, Fisher score, or in hospital mortality (28.1% vs 25.6%, P=.35), GOS (except for GOS 5: 43.37% vs 53.8%, P=.045), rate of hydrocephalus and rate of vasospasm. The second cohort obtained better results for aggregated GOS 1+2+3 (36.3% vs 43.75%, P=.034) and for GOS 4+5 (61.5% vs 56.25%, P=.078). The percentage of patients left untreated was significantly lower in the second period (5.1% vs 21.8%, P<.01), as well as the rate of re-bleeding (0% vs 9.4%, P<.01). Patients were treated earlier (2.51 vs 3.95 days), and hospital and total stay were lower (15.2 and 24.6 vs 10.3 and 18 days) in the second period, these differences not reaching statistical significance. CONCLUSIONS: Endovascular therapy allowed treating more patients with aSAH, and with a lower re-bleeding rate. This led to a modest reduction in morbidity and mortality.