Coagulase-negative staphylococci (CoNS) for a long time were considered avirulent constituents of the human and warm-blooded animal microbiota. However, at present, S. epidermidis, S. haemolyticus, and S. hominis are recognized as opportunistic pathogens. Although linezolid is not registered for the treatment of CoNS infections, it is widely used off-label, promoting emergence of resistance. Bioinformatic analysis based on maximum-likelihood phylogeny and Bayesian clustering of the CoNS genomes obtained in the current study and downloaded from public databases revealed the existence of international linezolid-resistant lineages, each of which probably had a common predecessor. Linezolid-resistant S. epidermidis sequence-type (ST) 2 from Russia, France, and Germany formed a compact group of closely related genomes with a median pairwise single nucleotide polymorphism (SNP) difference of fewer than 53 SNPs, and a common ancestor of this lineage appeared in 1998 (1986–2006) before introduction of linezolid in practice. Another compact group of linezolid-resistant S. epidermidis was represented by ST22 isolates from France and Russia with a median pairwise SNP difference of 40; a common ancestor of this lineage appeared in 2011 (2008–2013). Linezolid-resistant S. hominis ST2 from Russia, Germany, and Brazil also formed a group with a high-level genome identity with median 25.5 core-SNP differences; the appearance of the common progenitor dates to 2003 (1996–2012). Linezolid-resistant S. hominis isolates from Russia demonstrated associated resistance to teicoplanin. Analysis of a midpoint-rooted phylogenetic tree of the group confirmed the genetic proximity of Russian and German isolates; Brazilian isolates were phylogenetically distant. repUS5-like plasmids harboring cfr were detected in S. hominis and S. haemolyticus.

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Nosocomial infections caused by gram-positive organisms, including Staphylococcus aureus and enterococci (Enterococcus faecium and Enterococcus faecalis) are steadily increasing in almost all clinics around the world. Cancer patients have a higher risk of hospital-acquired infections than non-cancer patients. Cancer patients are immunosuppressed due to increased use of broad-spectrum antibiotics and chemotherapy drugs, radiation therapy, surgery and use of steroids. This paper presents an analysis of resistance of gram-positive bacterial pathogens to antimicrobial agents to determine treatment strategy for cancer patients.

The aim of the study was to determine the main Candida species isolated from blood of cancer patients, to compare the taxonomic structure of strains obtained from children and adults with candidemia. In total, during the study period, candidemia was microbiologically proven by blood culture in 81 patients (duplicates were excluded). Patients in the intensive care unit (ICU) accounted for 35,8%. The total number of isolates elaborated was 82 strains of 10 Candida species. In general, in the taxonomic structure of candidemias, C. parapsilosis (61.0%) predominates, C. albicans (20.7%) is in the second place, followed by C. glabrata and C. lusitaniae (3.7% each); C. krusei, C. guilliermondii and C. tropicalis (2.4% each). C. parapsilosis was statistically significantly often isolated from blood compared to C. albicans (61.0% versus 20.7%, respectively, p<0.0001). Candidemia was statistically significantly more often detected in adults than in children (63.0% versus 37.0%, respectively, p<0.002). Moreover, in adults, C. parapsilosis was statistically significantly more often isolated from blood than C. albicans (70.6% versus 15.7%, respectively, p<0.0001). In children, there were no significant differences in the frequency of isolation of C. parapsilosis and C. albicans: the proportion of C. parapsilosis was 45.2%, C. albicans - 29.0%. Rare species were identified in 7.8% of cases in adults, and in 12.9% of cases in children without statistical difference (p>0.05). The proportion of Candida non-albicans during the study period was 79.3%, and C. parapsilosis is the main species in this group (76.9%).

Colorectal cancer (CRC) is one of the leading causes of death from cancer in many countries of the world, both in men and women, and these rates are on the rise. The probability of suffering from CRC is about 4–5 % and the risk for developing CRC is associated with personal features or habits such as age, chronic disease history and lifestyle, but in most cases colorectal cancer develops as a result of the degeneration of adenomatous formations or along the jagged path. Immune dysregulation, dysbiosis, and epithelial destruction contribute to colorectal cancer carcinogenesis. The gut microbiota has a relevant role, and dysbiosis situations can induce colonic carcinogenesis through a chronic inflammation mechanism. Some of the bacteria responsible for this multiphase process include Fusobacterium spp., Bacteroides fragilis and enteropathogenic Escherichia coli. moreover, CRC is caused by mutations that target oncogenes, tumour suppressor genes and genes related to DNA repair mechanisms.Considering that the average time for the development of adenocarcinoma from precancer takes about 10 years, changes in the microbiota can be a prospective marker for screening precancerous conditions of the colon, as well as the detection of changes in DNA.The work will discuss the relationship between changes in the microbial composition of the colon with the genetic mutations identified by molecular genetic sequencing.