The objective of the present study was to elucidate the specific features of the clinical course of acute otitis media as well as the peculiarities of the vestibular function and the microbial paysage associated with this pathological condition under the present-day conditions. The study included 135 patients presenting with acute otitis media (AOM) at different stages of the disease. The discharge obtained from the tympanic cavity of all the patients was examined with the use of polymerase chain reaction in real time, audiological and vestibulogical methods. The distinctive features of acute otitis medium associated with Streptococcus pneumoniae infection were found to be the intense pain syndrome with the symptoms of intoxication, well apparent inflammatory changes in the tympanic membrane as revealed by otoscopy, the increased frequency of sensorineural impairment of hearing, and the characteristic type B tympanometric curve. Typical of AOM associated with Haemophilus influenza infection are the mild pain syndrome, weak changes in the tympanic membrane as revealed by otoscopy, conductive hearing loss, and the type C tympanometric curve.

The article presents information about the advantages and possibilities of modern methods of pathomorphological assessment used in otorhinolaryngology that not only allow to differentiate various forms of pathological processes, but also provide insight into the change in their physiological functions, as well as the opportunity to follow the stages of regeneration processes. Special attention is paid to the possibilities of the immunohistochemical method of assessment.

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Despite the ever growing progress in antibiotic therapy and the advent of the new methods for this purpose, the number of patients suffering from chronic focal infection of the ENT organs has not decreased during the last decades which turns the problem of chronization of inflammation into a serious challenge for the physicians as exemplified by chronic inflammation in the mucous membrane of the middle ear. Pathological changes in the middle ear make up a large fraction of ENT diseases of importance not only for otorhinolaryngologists but also for the specialists in the related medical disciplines. The present article is an overview of etiological, pathogenetic, and pathomorphological aspects of chronization of the inflammation process that are known to occur in the mucous membrane of the middle ear. In the overwhelming majority of the cases, the main cause of the conversion of acute inflammation in the middle ear into the chronic condition is the inadequate (incorrect), inopportune or incomplete treatment of the acute inflammatory process in the middle ear.

Objective. To determine the clinical and morphological  criteria of chronic inflammation development in the middle ear mucosa and the study of local immunity.Material and methods. 67 patients  aged from 19 to 67 years (men-28,  women-39) with complaints of pain, congestion in the ear, constant or intermittent  mucopurulent discharge from the ear, and hearing loss were examined. The disease  duration ranged from 3 days to 20 years or more. We have investigated the mucosa of the pathologically changed parts of the tympanic cavity. The sections were  stained  with hematoxylin  and eosin,  and trichromatic color by Mallory. For the  immunohistochemical  study monoclonal antibodies  to T lymphocytes  (CD4 T-lymphocytes-helper cells, CD8 T-lymphocytes-suppressors), B-lymphocytes  (CD20) were used. The calculation of the immunohistochemical  reaction was performed with a standard increase of 40 in 12 fields of view.Conclusions. On Week 3 of the disease is a clear imbalance in the local immune defense occurs, which is a turning point in the course of the disease. In the period since 6 months and suppression of the immune response was detected. Thus, we believe that in conditions of a purulent inflammatory process the beginning of the process of chronic inflammation (development of granulation tissue) in the mucous membrane of the middle ear occurs on Week 3 from the onset of the disease, which is by 2–2.5  times later than in aseptic conditions.