[ABILITY OF STAPHYLOCOCCUS OF VARIOUS STRAINS TO CREATE BIOFILMS AND THEIR EFFECT ON HUMAN BODY CELLS].

The urgency of the staphylococcus research is due to its ability to cause severe infections: softtissue infections, endocarditis, sepsis, toxic shock syndrome, and food poisoning. Coagulase-positive Staphylococcus aureus is the main infection agent of intrahospital infections. This agent has many factors of pathogenicity, which are well known. Among the coagulase-negative staphylococcus (CNS) strains, S. haemolyticus and S. epidermidis are clinically important, because they cause infections in patients with weak immune system. The mechanisms of the CNS pathogenicity are insufficiently understood. The goal of this work was to evaluate the potential pathogenicity of clinical strains of CNS from their capacity to create biofilms and the character of their interaction with human body cells by the example of the HT-29 cell culture. The research was carried out in laboratory strain S. aureus ATCC 29213 and clinical strains S. haemolyticus SH39, S. epidermidis SE36-1 isolated from the neonatal autopsy materials. The visual tests of biofilm formation by each strain and testing of the impact of the strains on the cell culture HT-29 was carried out in this work. The two species of CNS form biofilms at a higher rate than S. aureus. Upon incubation for 2 h of HT-29 cells with staphylococcus strains tested in this work, adhesion of bacteria on cell surface was observed. The adhesion was most pronounced in case of S. aureus ATCC 29213 and S. haemolyticus SH39. Upon 3 h of incubation with S. aureus ATCC 29213 and S. haemolyticus SH39, destruction of cell HT-29 monolayer was observed. The incubation for 24 h with the 3 strains tested in this work caused complete destruction of cell HT-29 monolayer. The maximal toxic effect on HT-29 cells was inherent in the strain S. haemolyticus SH39. The aggregate of the results obtained in this work indicates the presence of the pathogenicity factors in the strains S. haemolyticus SH39, which require additional research.

[Microbiological and molecular genetic characteristics of coagulase-negative staphylococcal isolates from neonates in intensive care unit].

The problem of hospital-acquired infections due to coagulase-negative staphylococci (CoNS) in neonatal intensive care units is crucial over the last 20 years in the world. Neonates with very low or extremely low body weight belong to a special group of risks by the CoNS infection. However, in Russia CoNS up to now are frequently considered as contaminants and not as the main etiologic factors of pneumonia and sepsis in extremely premature infants. It was shown that hospital strains of CoNS causing fatal infections in extremely premature infants are always present in intensive care units.

[Strain differentiation of Staphylococcus aureus by means of direct MALDI TOF mass spectrometry profiling].

Staphylococcus aureus--one of the most interesting for clinical studies of microbial species with extensive strain diversity, primarily due to the variability of virulence factors and pathogenicity. The aim of this study was approbation of a method for the rapid strain differentiation of S. aureus on the basis of bacterial cell direct protein profiling approach by means of MALDI TOF MS. Beta-lactamase and alpha-hemolysin productions, cording by the blaZ and hla genes, respectively, were selected as markers for the strain differentiation. Mathematical analysis of MALDI mass spectra from 53 isolates allowed the construction of two independent classification models that can differentiate the strains on the presence/absence of blaZ or hla genes. A number of the most significant peaks (masses), which can be considered as markers of the strain differences in S. aureus, were identified using a statistical contribution of each mass peak in the models. These diagnostic models differ the sensitivity and the specificity, which were 97.5% and 82.5% for the classification of strains on the basis of beta-lactamase production, and 90.0% and 88.7% by the presence of alpha-hemolysin.