Introduction: The epidemiology of candidemia has shifted in the past few decades; drug-resistant non-albicans Candida species have become more prevalent worldwide. The aim of this retrospective study was to determine the epidemiology of Candida species isolated from hospitalized neonates, children and adults, and to investigate a potential changing susceptibility pattern in a large general tertiary hospital. Methods: All unique Candida strains isolated from candidemia cases between 1 January 2020 and 15 October 2024 were identified, and their susceptibility profile was characterized. The distribution pattern in different ward types (medical, surgical, pediatric and ICU) was recorded. Cumulative annual susceptibility profiles were compared. Results: Candidemia incidence increased during the COVID-19 pandemic, from 0.63/1000 patient-days in 2020 to 0.96/1000 patient-days in 2022, and has since slightly decreased (0.83 and 0.89 in 2023 and 2024, respectively). Candidemia-associated mortality was high (>50%) in 2020 and peaked during the pandemic. During the study period, Candida parapsilosis remained the most frequent Candida spp. However, since the first isolation of Candida auris from the bloodstream in late 2022, and despite intense infection control measures taken, its frequency sharply climbed to the second position after only C. parapsilosis in the first 10 months of 2024 (33.6% vs. 25.2% for C. parapsilosis and 21.0% for C. albicans). While C. albicans has remained highly susceptible to fluconazole (1% resistance rate), C. parapsilosis manifested significant resistance to fluconazole during 2022–2024 (52%). C. auris was universally resistant to azoles and one isolate also resistant to echinocandins. Conclusions: A high prevalence of azole resistance of C. parapsilosis, the most frequently isolated Candida species, persists, and a significant rise of C. auris was recorded in nosocomial bloodstream infections with severe implications on public health.

Emerging infectious diseases have inflicted a significant health and socioeconomic burden upon the global population and governments worldwide. West Nile virus, a zoonotic, mosquito-borne flavivirus, was originally isolated in 1937 from a febrile patient in the West Nile Province of Uganda. It remained confined mainly to Africa, the Middle East, and parts of Europe and Australia until 1999, circulating in an enzootic mosquito-bird transmission cycle. Since the beginning of the 21st century, a new, neurotropic, more virulent strain was isolated from human outbreaks initially occurring in North America and later expanding to South and South-eastern Europe. Since 2010, when the first epidemic was recorded in Greece, annual incidence has fluctuated significantly. A variety of environmental, biological and socioeconomic factors have been globally addressed as potential regulators of the anticipated intensity of the annual incidence rate; circulation within the zoonotic reservoirs, recruitment and adaptation of new potent arthropod vectors, average winter and summer temperatures, precipitation during the early summer months, and socioeconomic factors, such as the emergence and progression of urbanization and the development of densely populated areas in association with insufficient health policy measures. This paper presents a review of the biological and socioenvironmental factors influencing the dynamics of the epidemics of West Nile virus (WNV) cases in Greece, one of the highest-ranked European countries in terms of annual incidence. To date, WNV remains an unpredictable opponent as is also the case with other emerging infectious diseases, forcing the National Health systems to develop response strategies, control the number of infections, and shorten the duration of the epidemics, thus minimizing the impact on human and material resources.

Background/Objectives: Systemic and tissue inflammation play a crucial role in the pathophysiology of cardiometabolic disorders. Presepsin is a newly discovered marker of acute phase inflammation that is produced by monocytes or macrophages in response to bacterial infection and is a soluble fraction of the lipopolysaccharide (LPS) receptor. LPS is an endotoxin that, through the breakdown of the intestinal barrier, penetrates the systemic circulation and is an important bacterial mediator in the pathogenesis of sepsis and septic shock. Methods: A narrative review of the existing literature. Results: A growing body of evidence demonstrates that intestinal dysbiosis is involved in the pathogenesis of diabetes mellitus (DM) and cardiovascular (CV) disease, leading to increased circulating LPS concentrations in people with cardiometabolic disorders, even in the absence of infection. These data provide the theoretical background for a link between presepsin, DM, and CV pathology. Preliminary studies suggest that presepsin levels are downregulated in patients with well-controlled type 2 DM and correlate with continuous glucose monitoring metrics in infection-free individuals with type 1 DM. However, prospective data on the association between presepsin and the risk of diabetic complications are currently lacking. Presepsin has also been found to be elevated in infection-free individuals with myocardial infarction, heart failure, and myocarditis compared to controls and has been shown to correlate with mortality risk in subjects at high CV risk. Conclusions: The clinical utility of presepsin in the monitoring of patients with cardiometabolic disorders warrants further investigation by future studies.

Background/Objectives: Intestinal dysbiosis and systemic inflammation are involved in the pathophysiology of obesity and its complications. Presepsin is a recently discovered inflammation marker, being the soluble form of the bacterial lipopolysaccharide (LPS) receptor. Due to the imbalance of the gut flora and subsequent disruption of the intestinal barrier, circulating LPS levels have been found to be elevated in patients with metabolic diseases, even in the absence of infection. However, to date, no studies have evaluated whether obesity is associated with elevated presepsin levels. Methods: The present study included 81 participants (61.7% women, 27 with obesity, 34 with overweight, and 20 controls with normal body mass index), all free of infection and diabetes mellitus. Presepsin was measured in serum by ELISA, and its concentrations were compared between the groups. Results: The obesity group had higher presepsin levels compared to controls (8.09 vs. 4.45 ng/mL, p = 0.06). When participants with a history of cardiovascular disease were excluded from the analysis and adjusting for multiple confounders through a regression model, the obesity group had higher presepsin values than the overweight and control groups (5.84 vs. 3.32 ng/mL, p = 0.016). In contrast, the overweight group had lower concentrations than both the obesity group (p = 0.005) and the controls (p = 0.031). We did not find an association between presepsin and 25-hydroxy vitamin D levels (p = 0.368). Conclusions: Although the cross-sectional character of the study cannot demonstrate causal relationships, the results could potentially suggest that systemic inflammation is implicated in the pathogenesis of obesity through the disruption of the intestinal barrier. However, the findings should only be seen as hypothesis-generating. The reduction in presepsin in the overweight state is an interesting finding that deserves further investigation.

Systemic inflammation has been recognized as the cause and consequence of metabolic dysregulation in diabetes mellitus (DM). Presepsin has recently emerged as a promising biomarker for the detection of bacterial infections and sepsis. There is evidence that gut dysbiosis results in the increased circulating concentrations of Gram-negative bacteria lipopolysaccharide, the linkage of presepsin, which in turn promotes insulin resistance and correlates with the risk of diabetic complications. Thus, we hypothesized that presepsin could reflect the magnitude of systemic inflammation and metabolic decompensation in patients with DM even in the absence of infection. In this cross-sectional pilot study, we included 75 infection-free individuals with well-controlled (n = 19) and uncontrolled (n = 23) type 2 diabetes (T2D), well-controlled (n = 10) and uncontrolled (n = 10) type 1 diabetes (T1D), and normoglycemic controls (n = 13). Presepsin levels were compared between the groups and potential associations with demographic, clinical, and laboratory parameters were explored. We observed that the duration of DM was associated with presepsin values (p = 0.008). When the participants were classified into the type of DM groups, the presepsin levels were found to be lower in the patients with T2D compared to those with T1D (p = 0.008). However, significance in that case was driven by the difference between the well-controlled groups. After adjusting for the effects of DM duration, presepsin was significantly lower in the well-controlled T2D group compared to the well-controlled T1D group [1.34 (2.02) vs. 2.22 (4.20) ng/mL, p = 0.01]. Furthermore, we adjusted our findings for various confounders, including age, body mass index, and waist circumference, and found that the difference in the presepsin values between the adequately controlled groups remained significant (p = 0.048). In conclusion, our findings suggest that presepsin could potentially serve as a surrogate marker of inflammation and metabolic control in people with DM.

Background/Objectives: Inflammation is a hallmark of diabetes, with interleukin-6 (IL-6) emerging as a key mediator linking immune activation with metabolic regulation. Although IL-6 has been studied in both type 1 (T1D) and type 2 diabetes (T2D), its relationship with glycemic control across diabetes subtypes remains unexplored. Methods: We conducted a cross-sectional pilot study including 82 participants divided into the following subgroups: healthy controls (n = 14), individuals with T1D [n = 11 with glycated hemoglobin (HbA1c) < 7%; n = 11 with HbA1c ≥ 7%] and T2D (n = 21 with HbA1c < 7%; n = 25 with HbA1c ≥ 7%). Demographic, anthropometric, and laboratory parameters were collected. Group comparisons were performed, adjusted for age and body mass index (BMI) to account for significant demographic differences between groups. Correlations between IL-6, high-sensitivity C-reactive protein (hs-CRP), ferritin, and presepsin were evaluated using Spearman’s rank correlation. Results: IL-6 levels were approximately four-fold higher in T1D individuals with HbA1c ≥ 7% compared with controls [fold-change 4.06 (95% CI: 1.36–12.1), p = 0.013], with optimally managed T1D showing a non-significant trend (p = 0.079). No significant differences were observed in T2D groups. Advancing age demonstrated a borderline association with IL-6 (p = 0.068), whereas BMI was not significantly related. IL-6 correlated positively with hs-CRP (ρ = 0.463, p < 0.001), but not with ferritin or presepsin. Conclusions: IL-6 concentrations were significantly elevated in individuals with suboptimally managed T1D compared with controls, independent of age and BMI, suggesting that poor metabolic control amplifies systemic inflammation in autoimmune diabetes. These findings support IL-6 as a biomarker of inflammatory burden in T1D and provide a rationale for larger, longitudinal studies to determine its clinical utility.