Relevance. The microbiota of the oral cavity is individual and the consistency of its composition provides a protective function that is regulated by the immune system. Dysbiotic changes in the oral microbiota composition lead to a devastation of local immunity and provide to the disease's development. Herpes virus infection аctivation suppresses the immune response which increases the level of oral mucosa bacteria colonization in particular during the acute course of infectious mononucleosis (IM).
Objective: to study the features of the oral microbiome composition and its sensitivity to antibacterial drugs in patients with infectious mononucleosis and acute tonsillitis.
Materials and methods. We examined 306 children aged 7 to 236 months. The main group (n = 280) – children with IM. Comparison group (n = 26) – children diagnosed with acute tonsillitis. The main group was divided into two subgroups: subgroup I – 234 children with MI caused by the Epstein-Barr virus (EBV), and subgroup II – 46 children with co-infection with the EBV virus and cytomegalovirus (CMV). The examination was performed according to the treatment protocol: general and biochemical analysis of blood, determination of IgM antibodies to Epstein-Barr virus and cytomegalovirus, bacteriological examination of oropharyngeal mucus, followed by determination of the sensitivity of the identified pathogens to antibacterial drugs.
The results. In oral microbiome of children with IM caused by EBV and CMV co-infection pneumococcus dominant. In children with acute tonsillitis, Staphylococcus aureus, S. pyogenes infection, and yeast-like fungi were predominant. S. pyogenes, in children with co-infection, has a high level of resistance to β-lactam antibiotics. Higher levels of antibiotic-resistant strains were found among Enterococcus spp. Isolates, especially in children with EBV-induced MI and co-infection of EBV and CMV.
Conclusions. The development of MI is accompanied by microecological dysbiosis of the mucous membranes of the oropharynx and tonsils, which do not provide enough level of colonization resistance, contributing to the spread of antibiotic resistance among resident and transient microbiota.
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