Aim The current study was conducted to determine the antimicrobial resistance profile and genetic relatedness of Aeromonas spp. isolated from healthcare and urban effluents, wastewater treatment plant (WWTP), and river water. Methods and results We detected the presence of genes conferring resistance to β‐lactam, quinolone, and aminoglycoside. Multilocus sequence typing (MLST) was carried out to differentiate the strains, and multilocus phylogenetic analysis (MLPA) was used to identify species. A total of 28 cefotaxime‐resistant Aeromonas sp. strains were identified, harboring uncommon Guiana‐Extended‐Spectrum (GES)‐type β‐lactamases (GES‐1, GES‐5, GES‐7, and GES‐16). Multidrug‐resistant Aeromonas spp. were found in hospital wastewater, WWTP, and sanitary effluent and A. caviae was identified as the most prevalent species (85.7%). Conclusion The release of untreated healthcare effluents, presence of antimicrobials in the environment, in addition to multidrug‐resistant Aeromonas spp., are all potential factors for the spread of resistance. Significance and impact of the sstudy We identified a vast repertoire of antimicrobial resistance genes in Aeromonas spp. from diverse aquatic ecosystems, including those that encode enzymes degrading broad‐spectrum antimicrobials widely used to treat healthcare‐associated infections. Hospital and sanitary effluents serve as potential sources of bacteria harboring antimicrobial resistance genes and are a threat to public health.

Background: Invasive candidiasis (IC) is a major cause of morbimortality in children. Previous studies described the clinical characteristics and risk factors for this infection; however, limited data are available on the predictors of mortality in these patients. In this context, we evaluated the risk factors associated with death due to IC in a pediatric tertiary care hospital in South of Brazil.Methods: This is a retrospective, cross-sectional, observational, and analytical study of a series of pediatric patients with clinical and laboratory diagnosis of IC from March 2014 to September 2017. Univariate and multivariate analysis were performed to estimate the association between the characteristics of the patients and death.Results: A total of 94 cases of IC were included. The incidence was 1.13 cases per 1000 patients/d, with a mortality rate of 14%. There was a predominance of non-albicansCandida(71.3%) in IC cases and, although there is no species difference in mortality rates, biofilm formation was associated with increased mortality. Clinical characteristics such as male sex, stay in the intensive care unit, and thrombocytopenia; comorbidities such as cardiological disease and renal insufficiency; and risks such as mechanical ventilation and dialysis were associated with increased mortality.Conclusion: Data from this study suggest that biofilm formation byCandidasp. is associated with increased mortality, and this is the first study to correlate the male sex and cardiological disease as risk factors for death in pediatric IC patients.

We investigated the molecular mechanisms underlying azole resistance in seven Candida tropicalis isolates that caused candidemia and candiduria in Paraná, Brazil (2016–2022). Biofilm production, antifungal susceptibility testing, multilocus sequence typing, amplification and sequencing of ERG11, and quantification of ERG11, MDR1, and CDR1 expression levels were performed. Notably, five isolates (71.4%) were from urine samples and two (28.6%) were from blood samples. All strains were biofilm producers, with levels ranging from moderate to strong. The minimum inhibitory concentration (MIC) values ranged from 8–>64 mg/L for fluconazole and 0.25–1 mg/L for voriconazole. All isolates had mutations in ERG11; Y132F and Y257N were predominant (71.4%), followed by Y132F and S154F (14.3%) and Y257H (14.3%). No differences in ERG11 expression were found between the susceptible and resistant groups, but MDR1 and CDR1 were more highly expressed in the susceptible isolates. All the isolates contained previously unassigned diploid sequence types. The emergence of C. tropicalis azole resistance has been previously described in Brazil; however, the presence of resistant isolates in urine highlights the need for surveillance resistant strains in both urinary and invasive contexts. In our study mutations in ERG11 were the main resistance mechanism identified in C. tropicalis.

Candida haemulonii is a complex formed by C. haemulonii sensu stricto, C. haemulonii var. vulnera, and C. duobushaemulonii. Members of this complex are opportunistic pathogens closely related to C. pseudohaemulonii, C. lusitaniae, and C. auris, all members of a multidrug-resistant clade. Complete genome sequences for all members of this group are available in the GenBank database, except for C. haemulonii var. vulnera. Here, we report the first draft genomes of two C. haemulonii var. vulnera (isolates K1 and K2) and comparative genome analysis of closely related fungal species. The isolates were biofilm producers and non-susceptible to amphotericin B and fluconazole. The draft genomes comprised 350 and 387 contigs and total genome sizes of 13.21 and 13.26 Mb, with 5,479 and 5,507 protein-coding genes, respectively, allowing the identification of virulence and resistance genes. Comparative analyses of orthologous genes within the multidrug-resistant clade showed a total of 4,015 core clusters, supporting the conservation of 24,654 proteins and 3,849 single-copy gene clusters. Candida haemulonii var. vulnera shared a larger number of clusters with C. haemulonii and C. auris; however, more singletons were identified in C. lusitaniae and C. auris. Additionally, a multiple sequence alignment of Erg11p proteins revealed variants likely involved in reduced susceptibility to azole and polyene antifungal agents. The data presented in this work will, therefore, be of utmost importance for researchers studying the biology of the C. haemulonii complex and related species.

Invasive infections caused by non-albicans Candida are increasing worldwide. However, there is still a lack of information on invasive candidiasis (IC) in the pediatric setting, including susceptibility profiles and clonal studies. We investigated the clinical, epidemiologic, and laboratory characteristics of IC, possible changes in antifungal susceptibility profiles over time, and the occurrence of clonality in our tertiary children's hospital. We analyzed 123 non-duplicate Candida isolates from sterile sites of pediatric patients in a tertiary hospital in southern Brazil, between 2016 and 2021. Data on demographics, comorbidities, and clinical outcomes were collected. Candida species distribution, antifungal susceptibility profiles, biofilm production, and molecular epidemiology of isolates were assessed using reference methods. The range of IC incidence was 0.88–1.55 cases/1000 hospitalized patients/year, and the IC-related mortality rate was 20.3%. Of the total IC cases, 42.3% were in patients aged < 13 months. Mechanical ventilation, parenteral nutrition, and intensive care unit (ICU) admission were common in this group. In addition, ICU admission was identified as a risk factor for IC-related mortality. The main site of Candida spp. isolation was blood, and non-albicans Candida species were predominant (70.8%). No significant clonal spread was observed among isolates of the three most commonly isolated species, and 99.1% of all isolates were biofilm producers. Non-albicans Candida species were predominant in this study. Notably, clonal expansion and emergence of antifungal drug resistance were not observed in our pediatric setting. The epidemiology of invasive candidiasis has changed over time and there is still a lack of information in the pediatric setting. Non-albicans Candida species predominated in this study, clonal expansion and emergence of antifungal drug resistance were not observed in our pediatric setting.

Invasive candidiasis (IC) contributes to the morbidity and mortality of hospitalized patients and represents a significant burden to the healthcare system. Previous Brazilian studies have reported the presence of endemic Candida parapsilosis sensu stricto genotypes causing candidemia and clonal transmission involving fluconazole-resistant isolates. We performed a 5-year retrospective analysis of IC cases in a Brazilian tertiary pediatric hospital and conducted a molecular investigation of C. parapsilosis sensu stricto. Non-duplicate C. parapsilosis sensu stricto genotyping was performed by microsatellite analysis. Antifungal susceptibility and biofilm formation were also evaluated. A total of 123 IC episodes were identified, with an IC incidence of 1.24 cases per 1000 hospital admissions and an overall mortality of 34%. The main species were the C. parapsilosis complex (35.8%), Candida albicans (29.2%), and Candida tropicalis (21.9%). All C. parapsilosis sensu stricto were recovered from blood cultures, and 97.5% were biofilm producers. Microsatellite typing identified high genotypic diversity among the isolates. We observed that all isolates were sensitive to amphotericin B, and although one isolate was non-sensitive to fluconazole, only a silent mutation on ERG11 gene was identified. No clear evidence of clonal outbreak or emergence of fluconazole-resistant isolates was found, suggesting that multiple sources may be involved in the epidemiology of IC in children.