ASSOCIATION OF MYCOPLASMA INFECTION WITH UROGENITAL PATHOLOGY
UDC 616.97:616.993.1
ASSOCIATION OF MYCOPLASMA INFECTION WITH UROGENITAL PATHOLOGY
N.V. Chebotareva, Doctor of Medical Sciences,
Academy of Postgraduate Education under the Federal Research
and Clinical Center of the Federal Medical-Biological Agency
(125371, Russia, Moscow, Volokolamsk highway, 91)
E-mail: nchvg@mail.ru
G.E. Bagramova, Doctor of Medical Sciences,
Academy of Postgraduate Education under the Federal Research
and Clinical Center of the Federal Medical-Biological Agency
(125371, Russia, Moscow, Volokolamsk highway, 91)
E-mail: bagramova@mail.ru
N.A. Chebotareva, Resident of the Department of Pediatric Diseases, specializing in Dermatovenereology,
Federal State University of Education
(125371, Russia, Moscow, Radio street, 10A, building 2)
E-mail: nadia-2000@bk.ru
Abstract. This article considers the actual problem of practical health care: the role of mycoplasmas in the defeat of the upper and lower parts of the urogenital organs. Described associated with Mycoplasma inflammatory processes in men and women. Carried out molecular genetic studies, which helped to expand the understanding of the variability of the vaa gene in M. hominis, encoding the VAA block possessing antigenic properties and serving as a key protein in the adhesion of the microorganism. Key proteins in the adhesion of M. genitalium are MG191 and MG192.
Keywords: urogenital infection, Mycoplasma, adhesion of the microorganism.
Inflammatory diseases of the lower and upper genitourinary organs in association with mycoplasmas are most often detected in sexually active men and women of reproductive age [13]. Various organs of the human body can be colonized by 16 types of mycoplasmas [2]. That is why, in recent years, they have continued to attract the attention of scientists and doctors from various countries, especially M. hominis, U. urealyticum, and M. genitalium [13].
The distinctive features of mycoplasmas are their small size, lack of a rigid cell wall, large cell polymorphism, and binary division [15]. They differ from bacteria in their cytoplasmic membrane, which has three layers, and their ability to pass through bacterial filters [3].
The study of the morphology of Mycoplasma revealed their polymorphism: spherical, kokkobatsillary, branching, and other fancy shapes, as well as small elementary bodies ranging in size from 125 to 250 nm [7].
Mycoplasma are sensitive to the effects of chemical and physical factors. They die rapidly at high temperatures, but are resistant to low temperatures. They are not only adsorbed onto the membranes of epithelial cells, lymphocytes, and synovial tissues, where they persist, but they can also be introduced intracellularly and multiply. Hallmarks of mycoplasma include the absence of a cell wall and the ability to persist in the host cell membrane. Reproduction of mycoplasma occurs intracellularly. It has been proven that all mycoplasmas have the ability to influence not only the metabolism of host cells, but also their genetic information [15; 19].
Reproduction of mycoplasmas is diverse: from binary and asymmetric division to budding, branching, and segmentation. Unlike chlamydia, mycoplasmas grow on artificial nutrient media in the presence of protein and sterols [1; 15]. Faster growth occurs on liquid nutrient media containing urea. The urease enzyme they produce metabolizes it [11].
The greatest difficulties in obtaining a culture relate to M. genitalium, since its growth on a nutrient medium takes up to 1-1.5 months. This is due to the small size of the genome, which takes part in the enzymatic decomposition of the nutrient medium necessary for the replication of the microorganism [19].
One of the important links in the chain of protection from infectious microorganism agents is phagocytes. It would seem that, in the absence of a cell wall, mycoplasma should be simple and easy to digest by phagocytes. In fact, however, the biological properties of Mycoplasma either prevent phagocytosis or prevent the digestion of these organisms in phagocytes [13].
Mycoplasma also have a cytotoxic effect on lymphocytes and are able to suppress lymphocyte proliferation and activate T-killers. Often, Mycoplasma is located in invaginated cell membrane microfibers or is protected and inaccessible to the action of antibodies. The similarity of Mycoplasma membranes to membranes of host cells leads to their weak immunogenicity and long-term persistence, and the presence of common antigenic structures in Mycoplasma and cells of the body is the cause of autoimmune processes, leading to complications [13].
The genitourinary organs are most often inhabited by M. hominis, U. urealyticum and M. genitalium, which are mainly transmitted sexually [15]. Incubation time: from 5 days to 5 weeks. Risk factors for infection include: early onset of sexual activity, frequent change of sexual partners, age at the onset of sexual activity, pregnancy, and lack of barrier methods of protection [10].
M. genitalium is recognized as a pathogenic microorganism that can cause urethritis in men and women, cervicitis [15; 22]. M. genitalium has received its name because of its preferred localization in the genital area. The discovery of M. genitalium refers to 1981, when it was isolated from two men with non-gonococcal urethritis in a specialized clinic in London [20]. However, only 5 years later, with the appearance of its diagnosis by PCR, the opportunity arose to determine the role of M. genitalium in the development of pathology of the urinary organs [16; 23].
Using PCR, M. genitalium was detected in 13% of men with acute non-gonococcal urethritis; in 27% of those with chronic and recurrent forms [16]. M. genitalium is involved in the development of chronic prostatitis in men with Reiter's syndrome. High concordance from sexual partners when symptomatic urethritis is present indicates sexual transmission [15].
Mycoplasma genitalium in women is the cause of urethritis, cervicitis, endometritis, and tubal infertility [12].
When analyzing the detection of M. genitalium in patients with non-gonococcal urethritis, it turned out that it was most often found in residents of Central Africa (41.7%), England (33.3%), the USA (30.8%), and less often in Japan (13.2%). In patients with asymptomatic urethritis, it was found in 15% of patients in Central Africa, 9.8% in Sweden, and 9.1% in England [17]. It is noted that M. genitalium rarely combines with C. trachomatis.
In men who applied to an anonymous examination room, the detection rate of M. genitalium is 37% [12]. According to our data, it is 9.1% among people complaining of urethral discharge and 6.2% among people without complaints.
Thus, to date, M. genitalium is recognized as an absolute pathogen, but further research is required on its role in the development of pelvic inflammatory disease in women and complicated forms in men.
As for U. urealyticum and M. hominis, their detection in both healthy individuals and in some diseases of the urogenital tract makes it difficult to classify them as pathogenic or conditionally pathogenic flora. M. hominis and U. urealyticum are present on the mucous membranes and in secretions of the urogenital tract in 40-80% of practically healthy individuals of reproductive age in the amount of < 10.4 CFU/ml [8].
M. hominis and U. urealyticum are conditionally pathogenic microorganisms; however, the manifestation of pathogenic properties can occur under certain conditions. These may be: hormonal changes, prolonged use of oral contraceptives, shifted intrauterine devices, surgical intervention, abortion, pregnancy, impaired immune status [19].
The activity of these opportunistic microorganisms is enhanced by the presence of infection by pathogens – N. gonorrhoeae, Tr. vaginalis, M. genitalium, and herpes simplex virus (HSV). Obviously, this is due to damage to the mucous membranes of the urinary tract and creating conditions for colonization [13].
Experimental animal studies confirmed the role of Mycoplasma in the development of inflammatory diseases of the urogenital area. In particular, the inoculation of M. hominis into the fallopian tube of the apes led, within a few days, to the development of restricted forms of salpingitis and parametritis in all animals [14]. Antibodies to M. hominis can be detected in newborns. During passage through the birth canal, M. hominis frequently colonizes the nasopharynx and vagina. In a newborn born by caesarean section, antibodies are detected much less frequently. Antibodies in the newborn may be maternal, as evidenced by their disappearance after a few months from birth. It should be noted that after puberty (with no sex partners), antibodies reappear or appear for the first time. The presence of antibodies in the serum of healthy individuals complicates the interpretation of the role of Mycoplasma in diseases of the urogenital tract [7]. Colonization of M. hominis and U. urealyticum increases with the onset of sexual activity, and seeding increases as the number of sexual partners increases. In particular, if M. hominis can be detected in 18% of women and 14% of men when having 3-5 sexual partners, U. urealyticum – in 72% and 41%, respectively, then when having 6-14 sexual partners, the percentage of M. hominis detection in women is 31%, in men – 13%, and U. urealyticum – 76% and 56%, respectively [7]. U. urealyticum plays a more important role than M. hominis in the development of pathology of the urogenital tract in men. The frequency of their detection in patients with non-gonococcal urethritis is close to 50%. A tenfold increase in the concentration of ureaplasmas in the prostate secretion as compared to their concentration in the urine is established in 82 (13.7%) men out of 597 patients with abacterial prostatitis [4].
Evidence of the development of ureaplasmic urethritis was obtained in volunteers. U. urealyticum was isolated from prostate secretions and ejaculate in women with bacterial vaginosis [22].
Lately, the attention of foreign authors has been focused on molecular genetic studies, in particular the search and study of genes that encode key proteins engaged in the adhesive function and may determine virulence properties of Mycoplasma. The genome of Ureaplasma spp. was sequenced in 2000. Its size has been determined to be 751 bp. The genomes of M. genitalium and M. hominis have also been determined and amount to 665 and 580 bp, respectively [5]. Subsequently, serovars were studied, the division into which is based on the variability of the mba gene. The mba gene has an unstable and variable structure, with 5'-ends segments that are relatively conservative and 3'-ends regions that are variable and contain homogeneous repeating elements. It is assumed that these regions determine the pathogenic potential and contribute to the high variability of the genotypic and phenotypic properties of Ureaplasma spp. It has been established that the 3'-ends region of the mba gene can be different within the same strain [21].
As for the genetic classification of M. hominis, it is based on the variability of the vaa gene, encoding the VAA block possessing antigenic properties and which is a key protein involved in adhesion of the microorganism. Six gene variants of the vaa gene have been identified. Variability of the vaa gene set comprises eight gene modules that define a unique primary structure. Two modules are permanent, and six different sequences make up the structure of the gene, but not all modules are part of the structure of each gene [18].
It is the variability of the surface protein Vaa and the variability of the gene encoding it that affect the adhesive properties of M. hominis. It is hypothesized that the genetic variability of M. hominis determines various clinical manifestations in patients [9].
Regarding M. genitalium, it is known that the study of its genetic variability is based on the study of the structure and functioning of the MgPa operon encoding the proteins MG190 (mgpA), MG191 (mgpB or P40) and MG192 (mgpC or P110). It is the latter two proteins that are key surface proteins in the adhesion process of M. genitalium. The genes encoding them are variable and suggest that they determine antigenic variability [9].
Similar studies were conducted on the basis of the State Research Center of Dermatovenerology and Cosmetology, Russian Ministry of Health [6]. According to the authors, the genetic variant of M. hominis II (more often than other studied variants) leads to the development of inflammatory processes of the genitourinary organs in women, accompanied by clinical manifestations. The genetic variant of M. hominis more often leads to asymptomatic infection without clinical and laboratory signs of inflammation.
The study of K. I. Plakhova involved selected samples of M. genitalium, belonging to three different phylogenetic groups for the mp192 gene. Infection with any of them may be accompanied by inflammatory clinical manifestations of urethritis or cervicitis. The introduction of such studies into practice in the distant future will allow for personalized patient management.
According to some authors, the frequency of isolation of U. urealyticum in women with inflammatory diseases of the genitals is 80%, for infertility is 51%, and pregnancy pathology is 45%. In association with other pathogenic and/or opportunistic microorganisms, U. urealyticum can participate in the development of bacterial vaginosis, cervicitis, inflammatory diseases of the pelvic organs, complications of pregnancy, postpartum, and post-abortion complications [8].
The consequences of infection with ureaplasmas during pregnancy are premature termination of pregnancy, weakness of labor, and chorioamnionitis. In the postpartum period, there is a delay in uterine involution, and endometritis.
Detection of Mycoplasma in newborns with neonatal pathology reaches 58.6%. Newborns associated with the microorganism have a high incidence of pneumonia, tonsillitis, conjunctivitis, and other inflammatory processes [4]. Studies indicate the influence of ureaplasmas on the reproductive function of men [4]. This happens in the form of a direct effect on spermatozoa (their concentration in sperm decreases, motility decreases, and atypical forms appear). The indirect effect occurs due to the development of inflammatory processes, such as chronic prostatitis and epididymitis.
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Материал поступил в редакцию 01.07.25
АССОЦИАЦИЯ МИКОПЛАЗМЕННОЙ ИНФЕКЦИИ С УРОГЕНИТАЛЬНОЙ ПАТОЛОГИЕЙ
Н.В. Чеботарёва, доктор медицинских наук,
Академия постдипломного образования ФГБУ ФНКЦ ФМБА России
(125371, Россия, г. Москва, Волоколамское шоссе, д. 91)
E-mail: nchvg@mail.ru
Г.Э. Баграмова, доктор медицинских наук,
Академия постдипломного образования ФГБУ ФНКЦ ФМБА России
(125371, Россия, г. Москва, Волоколамское шоссе, д. 91)
E-mail: bagramova@mail.ru
Н.А. Чеботарёва, ординатор кафедры детских болезней по специальности дерматовенерология,
ФГАОУ ВО «Государственный университет просвещения»
(105005, г. Москва, ул. Радио, д. 10А, стр. 2)
E-mail: nadia-2000@bk.ru
Аннотация. В данной статье рассматривается актуальная проблема практического здравоохранения: роль микоплазм в поражении нижних и верхних отделов мочеполовых органов. Описаны ассоциированные с микоплазмами воспалительные процессы у мужчин и у женщин. Проведенные молекулярно-генетические исследования, позволили расширить представление о вариабельности гена vaa у M. hominis, кодирующего блок VAA, обладающего антигенными свойствами и являющегося ключевым белком в адгезии микроорганизма. Ключевыми в адгезии M. genitalium, являются белки MG191 и MG192.
Ключевые слова: урогенитальная инфекция, микоплазмы, адгезия микроорганизма.