Candida auris is an emergent yeast pathogen, easily transmissible between patients and with high percent of multidrug resistant strains. Here we present a draft genome sequence of the first known Russian strain of C. auris, isolated from a case of candidemia. The strain clustered within South Asian C. auris clade and seemingly represented an independent event of dissemination from the original species range. Observed fluconazole resistance was probably due to F105L and K143R mutations in ERG11.

Severe COVID-19 alters the biochemical and morphological characteristics of blood cells in a wide variety of ways. To date, however, the vast majority of research has been devoted to the study of leukocytes, while erythrocyte morphological changes have received significantly less attention. The aim of this research was to identify erythrocyte morphology abnormalities that occur in COVID-19, compare the number of different poikilocyte types, and measure erythrocyte sizes to provide data on size dispersion. Red blood cells obtained from 6 control donors (800–2200 cells per donor) and 5 COVID-19 patients (800–1900 cells per patient) were examined using low-voltage scanning electron microscopy. We did not discover any forms of erythrocyte morphology abnormalities that would be specific to COVID-19. Among COVID-19 patients, we observed an increase in the number of acanthocytes (p = 0.01) and a decrease in the number of spherocytes (p = 0.03). In addition, our research demonstrates that COVID-19 causes an increase in the median (p = 0.004) and interquartile range (p = 0.009) when assessing erythrocyte size. The limitation of our study is a small number of participants.

Coronavirus disease (COVID-19) has become a global pandemic. COVID-19 patients need immediate diagnosis and rehabilitation, which makes it urgent to identify new protein markers for a prognosis of the severity and outcome of the disease. The aim of this study was to analyze the levels of interleukin-6 (IL-6) and secretory phospholipase (sPLA2) in the blood of patients regarding the severity and outcome of COVID-19 infection. The study included clinical and biochemical data obtained from 158 patients with COVID-19 treated at St. Petersburg City Hospital No. 40. A detailed clinical blood test was performed on all patients, as well as an assessment of IL-6, sPLA2, aspartate aminotransferase (AST), total protein, albumin, lactate dehydrogenase (LDH), APTT, fibrinogen, procalcitonin, D-dimer, C-reactive protein (CRB), ferritin, and glomerular filtration rate (GFR) levels. It was found that the levels of PLA2, IL-6, APTV, AST, CRP, LDH, IL-6, D-dimer, and ferritin, as well as the number of neutrophils, significantly increased in patients with mild to severe COVID-19 infections. The levels of IL-6 were positively correlated with APTT; the levels of AST, LDH, CRP, D-dimer, and ferritin; and the number of neutrophils. The increase in the level of sPLA2 was positively correlated with the levels of CRP, LDH, D-dimer, and ferritin, the number of neutrophils, and APTT, and negatively correlated with the levels of GFR and lymphocytes. High levels of IL-6 and PLA2 significantly increase the risk of a severe course by 13.7 and 2.24 times, and increase the risk of death from COVID-19 infection by 14.82 and 5.32 times, respectively. We have shown that the blood levels of sPLA2 and IL-6 increase in cases which eventually result in death and when patients are transferred to the ICU (as the severity of COVID-19 infection increases), showing that IL-6 and sPLA2 can be considered as early predictors of aggravation of COVID-19 infections.

Aim. Using a collection of samples from the biobank ofCityHospital № 40 ofSt. Petersburg, to study the cytokine profile in patients with coronavirus disease 2019 (COVID-19) and sepsis, in comparison with patients with abdominal inflammation and septicemia.Material and methods. The study included serum samples from 181 patients with sepsis and COVID-19 (127 patients with a diagnosis confirmed by polymerase chain reaction (PCR); 54 patients with a negative PCR test, but with a characteristic computed tomographic lung performance) and 47 patients with abdominal sepsis. The content of cytokines was determined using a multiplex immunofluorescence analysis based on the Luminex xMAP technology using the HCYTOMAG60K panel — a soluble CD40 ligand (sCD40L), interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin 6 (IL-6), interleukin 8 (IL-8), monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor alpha (TNFα), vascular endothelial growth factor (VEGF). Other laboratory parameters (C-reactive protein (CRP), ferritin, procalcitonin) were taken from patient records. Normality of distribution was assessed by the Shapiro-Wilk test. To compare groups, the Mann-Whitney test for independent samples, Wilcoxon test for dependent samples, and the Kruskal-Wallis test with Bonferroni correction for multiple comparisons were used.Results. In patients with sepsis and COVID-19 infection, no differences in the concentrations of cytokines, ferritin and CRP were found between the groups with detected and not detected virus by PCR test. Based on this, this group was considered homogeneous when studying the cytokine profile. It was shown that in patients with sepsis and COVID-19, significantly higher levels of sCD40L (p<0,0001) and VEGF (p=0,037) and relatively low levels of CRP (p<0,0001), IL-6 (p<0,0001), IL-8 (p<0,0001), TNFα (p<0,00058).Conclusion. These results indicate that sepsis in patients with COVID-19 courses with less elevation in inflammatory cytokine than in abdominal sepsis. At the same time, a critically high level of sCD40L indicates the significant endothelial damage.

Early recognition of rupture-prone atherosclerotic lesions in patients with high-graded carotid stenosis is an important clinical problem for preventing ischemic stroke. Various pathophysiological mechanisms are responsible for the progression and instability of plaques, such as changes in lipid composition, infiltration by immunoinflammatory cells and degradation of the extracellular matrix of the vascular wall by matrix metalloproteinases, enhanced inflammatory response and plaque neovascularization. These features are the main cause of plaque rupture and, as a consequence, neurologic symptoms. Therefore, matrix metalloproteinases and inflammatory factors can serve as possible markers for patients with severe unstable stenosis of carotid arteries. Due to the heterogeneity of atherosclerotic lesions, only one biomarker is not enough to reliably predict the development of a stroke. The use of a combination of biomarkers is better correlated with clinical data and, therefore, exceeds the analysis of individual factors. To increase the overall sensitivity and specificity and more reliable diagnosis of stroke in patients with symptomatic and asymptomatic carotid stenosis, the biomarker panel should include independent biomarkers. Further preclinical experiments and clinical trials are needed to assess the significance and precise definition of the threshold levels of such biomarkers before they can be used in clinical practice.