Sexually Transmitted Diseases - I. I. Mavrov 2005

Sexually Transmitted Infections
Urogenital Mycoplasmosis

Urogenital mycoplasmosis is a group of diseases caused by Mycoplasmas that affect the human Urogenital System. It plays a significant role in The Development of pathology in pregnant women, fetuses, and newborns, and frequently acts as an etiological factor in Infertility and Inflammatory Diseases of the urogenital Organs.

Etiology. Mycoplasmas are small-sized (125-250 nm), Cell wall-deficient bacterial Cells of variable shapes (small spheres, short filaments). They form characteristic pinpoint colonies on cell-free artificial culture media supplemented with horse serum (Figs. 31-33).

Mycoplasmas reproduce by several Methods: binary fission, multiple release of elementary bodies formed within filaments, and budding. They do not synthesize Fatty acids, sterols (such as Cholesterol), and certain Proteins, instead incorporating these components directly from their environment into their membranes.

The interaction between mycoplasmas and the host cell is driven by their adsorption onto The Cell surface and the penetration of membrane and other mycoplasmal components into the host cell. Viruses associated with urogenital and respiratory diseases can reside on the membranes of mycoplasmas inhabiting the urogenital or respiratory tracts. While The Nature of the interaction between mycoplasmas, host cells, and viruses remains poorly understood, available data indicate a potential exchange not only of low-molecular-weight substances but also of Biopolymers, including DNA and RNA (Figs. 34-36).

Mycoplasmas belong to the family Mycoplasmataceae, order Mycoplasmatales, Class Mollicutes. This family is divided into two genera: Mycoplasma (comprising about 100 species) and Ureaplasma (currently numbering only 3 species).

The majority of mycoplasmas are pathogenic. The mycoplasmal etiology of A number of urogenital and respiratory tract Infections caused by specific species has been established. Currently, five mycoplasma species are known to cause human disease: M. pneumoniae, M. genitalium, M. hominis, U. urealyticum, and M. incognita (recently isolated from AIDS patients). Pathogenic mycoplasmas as disease agents satisfy Koch's three postulates: a) the pathogenic microbe is isolated in all cases of the disease; b) the pathogenic microbe is isolated from sick organisms in a pure culture; c) Introduction of the pathogenic microbe into a susceptible Organism reproduces the disease.

Fig. 31. Colonies of Mycoplasma hominis on Agar medium resembling a "fried egg" appearance; detected in urethral discharge, x120.

Fig. 32. Colonies of Ureaplasma urealyticum on agar medium; isolated from ejaculate, x90.

Fig. 33. Colonies of Mycoplasma hominis and Ureaplasma urealyticum on serum agar medium, x90.

Fig. 34. Invagination of the cell cytoplasmic membrane beneath the terminal tip-like Structure of a mycoplasma. Ultrathin section, Electron Microscopy, x200,000. Specimen by G. G. Miller.

Fig. 35. Mycoplasma terminal tip-like structure in direct contact with the host cell cytoplasmic membrane. Ultrathin section, electron microscopy, x200,000. Specimen by G. G. Miller.

Fig. 36. Mycoplasma phagocytosing viruses. Electron microscopy, x70,000. Specimen by G. G. Miller.

U. urealyticum, M. genitalium, and M. hominis are the causative agents of inflammatory processes in the urogenital system. Urogenital mycoplasmoses are widespread diseases that, like other sexually transmitted infections, share common epidemiological patterns. The question of whether the recent increase in the incidence of these infections is linked to improved Laboratory Diagnostics or to a genuine spread is entirely logical. Evidently, both factors play a role.

Ureaplasmas were first isolated by M. Shepard (1954) from the Urethra of a patient with nongonococcal urethritis. Their distinctive feature is The ability to hydrolyze urea (they possess the enzyme for its hydrolytic Cleavage). They are selectively inhibited by erythromycin and potassium acetate, while being resistant to lincomycin, which suppresses the growth of other mycoplasma species. They grow as very small colonies (10 to 30 µm in diameter). When cultivation conditions are optimized, the size of ureaplasma colonies increases, approaching the dimensions of other mycoplasmas.

The biological uniqueness of ureaplasmas is reflected in their relatively rapid growth. The growth curve of ureaplasmas resembles that of mycoplasmas during the lag and early logarithmic phases; however, their logarithmic growth phase is considerably shortened, transitioning into the stationary phase within just 16-18 hours, whereas in mycoplasmas this phase lasts 78 hours or more. The optimal pH of the growth medium for ureaplasmas ranges from 6.0 to 6.5, which is slightly lower than that for other mycoplasmas (7.0-7.6). In insufficiently buffered nutrient media, alkalinization occurs, and ureaplasmas rapidly perish. After 24 hours of incubation, as much as 90% of the cell population dies. When isolating ureaplasmas from clinical specimens, samples are incubated for up to 3 days or more, as the lag phase of growth may be extended.

Ureaplasmas degrade urea into ammonia. Ureaplasma activity is driven by the enzyme urease synthesized in the Cytoplasm. They do not ferment sugars, do not reduce tetrazole and methylene blue, and lack catalase activity. Ureaplasmas are capable of synthesizing both saturated and Unsaturated fatty acids. They produce the pigment hypoxanthine, a product of purine METABOLISM, and possess a soluble ß-hemolysin active against rabbit and guinea pig erythrocytes.

A characteristic feature of ureaplasmas is their proteolytic activity directed against human IgA. A specific protease has been identified in all known reference and tested strains. Under the action of this enzyme, IgA is cleaved into fragments with molecular weights of 110 and 50 kDa. The enzyme is resistant to EDTA and sensitive to Trypsin. The ureaplasma membrane also contains the enzyme ATPase. Data have been obtained indicating differences in the membrane protein composition of various serotypes. Ureaplasmas comprise at least 11 different serotypes, which presumably possess varying pathogenic potential.

Ureaplasmas are found not only in humans. They have been detected in monkeys, cattle, goats, sheep, dogs, cats, mice, hamsters, and birds. Animal ureaplasmas are capable of causing mastitis and polyarthritis under natural and experimental conditions. They are found in semen and reproductive organs, causing seminal vesiculitis, endometritis, or salpingitis of varying severity, abortions, and fetal damage in animals. Experimental studies, as well as the fact that ureaplasmas cause various diseases in animals, do not provide sufficient grounds for direct analogies to humans. At the same time, experimental infections and knowledge of natural ureaplasmal diseases in animals contribute to understanding the pathogenetic mechanisms of this infection in humans.

Inflammatory processes in the urogenital system are also caused by M. genitalium, whose pathogenicity was confirmed by D. Taylor-Robinson et al. (1981). Serologically, this species differs from all previously known mycoplasmas and exhibits a more pronounced pathogenic potential. Its cells contain a terminal organelle 210-250 nm long and 35-60 nm wide. Using this structure, mycoplasma cells attach to erythrocytes and other cells (as well as to Glass and plastic). M. genitalium ferments glucose and does not affect Arginine and urea. They require cholesterol for growth, proliferate at temperatures of 30-37 °C, and are sensitive to thallium acetate.

Pathogenic strains also include certain strains of M. hominis, which are frequently encountered in urogenital infections. Like other mycoplasma species, it grows in semi-liquid, liquid, and semi-solid media consisting of 7 parts of a basal nutrient medium—which is a tryptic digest of bovine Heart Muscle—1 part of a 25% fresh Yeast extract, and 2 parts of unheated horse Blood serum.

M. hominis is characterized by significant variations in colony size, though morphologically they do not differ from the colonies of other mycoplasmas. The appearance of such colonies on solid nutrient media is commonly compared to a fried egg. The microstructural elements of the colonies are highly polymorphic, consisting mainly of spherical bodies of varying optical density, granular, filamentous, and sometimes branching structures.

Reproduction in M. hominis, as in other mycoplasma species, occurs through equal and unequal binary fission of the parent cell, budding, filament fragmentation, as well as by The formation of so-called elementary bodies, measuring 0.1–0.25 µm, within the cytoplasm or on the limiting membrane. According to theoretical calculations, the smallest of these are incapable of reproduction.

M. hominis degrades arginine, has no effect on glucose, weakly breaks down methylene blue, lacks phosphatase, lipase, and urease activity, does not induce tetrazolium reduction, hemolysis, or erythrocyte hemagglutination, and does not adsorb onto erythrocytes.

Mycoplasmas obtain Amino acids from their growth medium. The systems responsible for transporting amino acids across membranes are highly specific. Despite the fact that M. hominis does not interact with erythrocytes, it adsorbs onto various cells—such as gonococci, other Human and Animal tissue cells (diploid fibroblasts, human embryonic lung cells, African green monkey cells, muscle cell lines, human amnion, etc.)—as well as on human spermatozoa.

M. hominis is characterized by pronounced intraspecific heterogeneity caused by a wide spectrum and Variability of surface Membrane Proteins, which is manifested in various serological reactions.

There are several (7, and possibly 8) distinct serological types of M. hominis; their antigenic heterogeneity complicates serological Diagnosis and species identification. Other mycoplasmas are also detected in the urogenital canal, notably M. fermentans, M. salivarium, M. primatum, and M. pneumoniae.

M. fermentans is rarely detected in the urogenital system—accounting for less than 1% of all mycoplasma strains isolated from the urogenital tract. It ferments glucose and adsorbs human IgG, resulting in the formation of autoantibodies against aggregated immunoglobulin (i.e., rheumatoid factor), which can subsequently bind Complement components and IgM. These immune complexes circulate, become fixed in Tissues, and induce immunological reactions. The membranes of certain M. fermentans strains are highly toxic to mice and mouse thymocytes in vitro. M. incognita, a subspecies of M. fermentans, has been isolated from the urogenital tract of AIDS patients. In cases of coinfection, M. incognita enhances the virulence of the AIDS pathogen.

There is no evidence implicating M. salivarium and M. primatum in the development of pathological processes in human urogenital organs. At the same time, it is known that M. pneumoniae—the CAUSATIVE AGENT OF primary atypical Pneumonia in humans—can cause intrauterine, often generalized infections.

Most mycoplasma strains exhibit susceptibility to Tetracyclines, macrolides, and quinolones, while remaining resistant to sulfonamides and benzylpenicillin. Furthermore, mycoplasma strains resistant to tetracyclines and macrolides have emerged due to the presence of Plasmids.

A typical feature of all mycoplasmas is the absence of diaminopimelic acid, a component of the cell walls of many Bacteria. Mycoplasmas require sterols for growth and incorporate them into their membranes, whereas bacteria lack sterols entirely.

It has been established that Lipid Metabolism and its Functions vary among different mycoplasma strains. Based on this, they are divided into three groups: 1) enzymatically active mycoplasmas that do not require sterols; 2) enzymatically inactive mycoplasmas that do not require sterols; and 3) enzymatically active mycoplasmas that require sterols.

Mycoplasma proteins are readily separated by gel Electrophoresis. Recently, Disc electrophoresis in polyacrylamide gel has been successfully employed for differentiating individual mycoplasma species.

Mycoplasmas also differ in their neuraminidase activity, which is manifested in varying degrees of erythrocyte adsorption. The ability of individual mycoplasma species to utilize The amino acid arginine and their proteolytic enzyme activities also vary. These biochemical characteristics are of practical importance for the detection and identification of mycoplasmas.

Mycoplasmas differ significantly from bacteria in their resistance to chemical and physical agents, a property utilized in separating mycoplasmas from bacteria during cultivation and in selecting therapeutic measures.

Mycoplasmas are easily destroyed by ultrasound and by repeated freezing and thawing in distilled Water. Temperatures above 40 °C prove lethal within a few hours. When stored in a refrigerator, mycoplasmas remain viable for several weeks, and at -70 °C, for several years. They are rapidly inactivated by standard disinfectants and detergents.

Routes of transmission. Infection with urogenital mycoplasmal infection occurs predominantly through sexual contact. Indirect transmission is also possible, particularly in women and girls. The infection can be transmitted via various household items (bed linen, chamber pots) or medical instruments in obstetric-gynecological and urological settings (vaginal tips, rubber gloves, specula, etc.) if disinfection protocols are neglected. Infection of the upper genital tract (cervical canal, endometrium, fallopian tubes) can be mediated by spermatozoa acting as mycoplasma carriers. Intrauterine fetal infection and infection of newborns during passage through the mother's infected birth canal have also been established.

Epidemiology and general pathology. Currently, the incidence of diseases caused by mycoplasmas has increased significantly. The Role of mycoplasmas in sexually transmitted infections has grown notably, driven by numerous factors such as increased sexual activity, acceleration of growth and maturation, population migration, etc. Urogenital mycoplasmosis is among the most widespread Diseases of the human urogenital tract; it is frequently accompanied by lesions of the reproductive organs and often causes reproductive dysfunction or even disability, as affected individuals (both men and women) may require surgical intervention for complicated inflammatory processes of mycoplasmal etiology. It is distributed globally. Statistically reliable data on the prevalence of mycoplasma infections among various population groups across different Regions of the world are extremely scarce. However, numerous studies on this issue indicate a high prevalence of mixed mycoplasma infections in trichomonal, gonococcal, and chlamydial infections of the Urogenital apparatus, as well as in acute and chronic inflammations of the female external genitalia of undetermined etiology.

Microbiological and serological evidence of mycoplasma infection in patients with non-gonococcal urethritis, as well as those evaluated for prostatitis, cervicitis, and salpingitis, has been obtained by researchers worldwide. At the same time, examinations of healthy individuals with no history of disease frequently reveal mycoplasmas, demonstrating the existence of an asymptomatic carrier state. For instance, mycoplasmas are isolated from the urethra in 8–9% of clinically healthy men, and from the Vagina and cervix in 19–26% of observations. Ureaplasmas are isolated from the Pharynx in 5–10% of healthy individuals with no history of disease, and M. hominis in 1.5–3%. Meanwhile, most observations indicate that ureaplasmas are detected more frequently in women of childbearing age, relatively often in sexually active individuals, and in those with genital inflammatory diseases and pregnant women. These individuals evidently constitute the risk groups.

Analysis of data obtained from surveys and questionnaires administered to volunteers led to the Conclusion that ureaplasmas are more commonly found in women with multiple sexual partners. Epidemiological survey results demonstrate a high frequency of ureaplasma detection in women with symptoms of genital infection and reproductive dysfunction, and exceptionally rarely in nuns and virgins (H. Voung et al., 1981). Ureaplasmas are detected much more frequently in patients with Gonorrhea, Trichomoniasis, and gynecological disorders (58%) compared to a mere 4% in clinically healthy individuals. Notably, ureaplasmas were detected in 83–87% of women who had contact with men suffering from non-gonococcal urethritis and ureaplasma carriers. The detection rate of ureaplasmas in the urogenital organs of sexually active women ranges from 15% to 95%, increasing significantly with the number of sexual partners.

Ureaplasmas are also widespread among men. They are increasingly detected in men with nonspecific inflammatory processes of the urogenital tract. For example, ureaplasmas are isolated in 50–70% of individuals with non-gonococcal urethritis. It is possible that in the majority of cases, non-gonococcal urethritis is caused by these microorganisms, although the exact proportion remains unknown and may range from 20 to 40%.

Discrepancies in Data regarding the proportion of urogenital disorders caused by ureaplasmas depend to some extent on the laboratory methods employed. Furthermore, partner tracing (examination of sexual partners) is not always performed to clarify the etiological diagnosis. Therefore, fluctuations in the statistics on the spread of ureaplasmal infection reported by various authors are entirely natural and expected.

Judging the incidence of urogenital ureaplasmosis in men and women solely on The basis of detecting ureaplasmas in individuals with inflammatory diseases of the urogenital organs would be incorrect. It is well known that ureaplasmosis often proceeds (especially in women) with minimal symptoms or even completely clinically silent, without subjective discomfort. In such cases, patients do not seek medical attention and, consequently, go unrecorded.

Certain factors appear to activate the development of ureaplasmal infection in the urogenital tract. These include concurrent infections of various origins (bacterial, viral, chlamydial, fungal, etc.), hormonal shifts associated with the ovarian cycle phases, and other alterations in the physiological and immunological status of the organism. For the infectious process to develop, the breadth and magnitude of dissemination are far more critical than the mere presence or even persistence of ureaplasmas in the lower urogenital tract. From this perspective, the presence of a small number of ureaplasmas in the reproductive organs may not warrant concern. The detection of ureaplasmas in urine samples may also be transient and inconsequential. However, the penetration of ureaplasmas into deeper sections of the urogenital system can trigger acute urethral syndrome. These microorganisms are isolated from urine samples obtained via bladder catheterization in 54% of women presenting with urethral syndrome.

Latent, asymptomatic urogenital mycoplasmal infection can be reactivated during Pregnancy and Childbirth, under hypothermia, or during various stressful situations, leading to severe complications such as puerperal Sepsis, septic abortion, and inflammatory processes in the fetus, newborn, and maternal urogenital organs. Consequently, The high frequency of mycoplasma detection in patients with acute and chronic inflammatory diseases of the reproductive organs has sparked particular interest in studying urogenital mycoplasmal infection in the context of pregnancy, fetal, and neonatal pathology. Substantial statistical data indicate that ureaplasmas play an etiological role in first-trimester miscarriages and premature births. They have been isolated from the chorion and amnion of aborted fetuses, as well as from the Placenta in spontaneous abortions and premature deliveries. In most cases, the detection of these Microorganisms in the urine of pregnant women correlates with pregnancy complications, notably the birth of low-birth-weight infants. In such newborns, ureaplasma-induced infection typically manifests as respiratory tract pathology. Bronchopulmonary pathology of ureaplasmal origin in neonates stems from intrauterine infection, which is supported by evidence of pulmonary ureaplasmal infection in infants delivered via Cesarean Section, as well as in fetuses examined at various Cytology/cytology/21.html">Stages of intrauterine development.

Experimental studies and clinical observations demonstrate a causal link between Ureaplasma infection and the development of inflammatory processes in the reproductive organs, which impairs reproductive function to the point of infertility.

Male infertility caused by ureaplasmas may result not only from inflammation in the reproductive organs, but also from the Direct impact of ureaplasmas on spermatozoa. For instance, semen samples containing ureaplasmas exhibit a lower sperm concentration, reduced motility, and a higher percentage of atypical (pathological) forms compared to ureaplasma-free samples. The attachment of ureaplasmas to spermatozoa is now an established fact.

Our research has shown that in chronic inflammation of the Prostate Gland, including cases of male infertility, ureaplasmas were detected in the ejaculate (significant colonization) in 11.7% of patients. It was established that ureaplasmal prostatitis causes qualitative Changes in the ejaculate and affects its volume, concentration, sperm motility, and the proportion of pathological forms.

The attachment of ureaplasmas to the sperm HEAD leads to extensive destruction of the plasma and outer acrosomal membranes, as well as their degradation in the equatorial segment region. Although the inner acrosomal membrane may also be damaged, local destruction of the plasma and outer acrosomal membranes occurs as well, notably resulting from the binding of single ureaplasmas to the sperm head.

Damage to the outer acrosomal membrane in any of its regions leads to the premature release of acrosomal contents before the sperm fuses with the oocyte. A sperm with this type of pathology loses its fertilizing capacity, even if active motility is preserved. Consequently, ureaplasmas are capable not only of shielding the sperm membrane domains but also of destroying the acrosomes, thereby depriving spermatozoa of the ability to penetrate the egg membranes. The direct impact of ureaplasmas on sperm motility, caused by their tight adhesion, induces degenerative and qualitative changes in both the spermatozoa and the ejaculate, hindering normal conception.

The attachment of ureaplasmas to spermatozoa is viewed as a mechanism enabling these microorganisms to cross the cervical and tubal barriers into the upper female reproductive tract, where they induce inflammatory and obliterative processes that can disrupt oogenesis, prevent Fertilization, and cause Female Infertility. Ureaplasmas trigger inflammatory conditions in the FEMALE Reproductive System that impair—and can completely block—the passage of the mature oocyte into the uterine cavity. Furthermore, the presence of ureaplasmas in the endometrium can prove fatal to a successfully implanted fertilized egg, leading to its late-term abortion.

Urinary stone formation is observed in both natural and experimental mycoplasma infections. Specifically, ureaplasmas were isolated in 19% of such cases. The development of cystitis and stone formation induced by ureaplasmas was experimentally confirmed by inoculating the Urinary Bladder or renal medulla of rats (J. Téhier et al., 1984). Calculi formed in 60% of the infected animals as early as 4–5 days post-inoculation. Concomitant infection of rats with M. hominis also induced stone formation in 10% of the animals. Calculi measuring 1–10 mm in diameter were identified in the rat urinary bladder 6 weeks after infection. According to spectrochemical analysis, the mineral composition of these rat urinary calculi—specifically their phosphate, ammonium, and magnesium content—was similar to that of stones found in humans.

The etiological role of M. genitalium in the development of chronic and recurrent (though not acute) urogenital inflammatory processes has been established. M. genitalium was detected in 15% of patients with gonorrhea, 10% of individuals examined for urogenital chlamydial infection, and 27% of patients with chronic and recurrent non-gonococcal urogenital conditions. This pathogen was successfully isolated in 32% of cases from the urethra and rectum of men with non-gonococcal urethritis. M. genitalium is detected more frequently in homosexual men (30%) than in heterosexual men (11%). There are reports of this microorganism being detected in the human nasopharynx; however, its involvement in the Development of Respiratory diseases has not been proven.

Data obtained by us and other specialists (M. Sh. Kobakhidze, 1976) have shown that M. hominis is isolated significantly more often in patients (68.7%) than in healthy individuals (5.7%), and more frequently in female reproductive organ inflammatory processes (30–68.7%) than in male ones (22–40.5%).

M. hominis was detected by us in urethral discharges and prostatic secretions of 16.1% of patients with various post-gonococcal complications (prostatitis, vesiculitis, epididymitis). These patients exhibited decreased sexual potency and secondary infertility. In healthy individuals (control group), this mycoplasma species was detected in the urethra in 9.4% of cases.

A. Hafsteller (1977) identified the presence of M. hominis in men with urethroprostatitis and in women with adnexitis and cystitis. Mycoplasma cultures in such patients were obtained from urethral, vaginal, and cervical discharges, prostatic secretion, ejaculate, urine, and prostate biopsy material. Mycoplasmas were successfully isolated from urine in cases of Pyelonephritis, as well as from conjunctival smears and synovial fluid extracted from joints in Reiter's Syndrome.

In inflammatory diseases of the urogenital system, M. hominis is detected in 60–80% of cases, compared to 5–15% in healthy individuals. In vaginitis and cervicitis of unknown etiology, this mycoplasma species is found 2 to 6 times more often than in clinically healthy women. They are isolated in approximately 50% of female patients with pelvic inflammatory disease; a fourfold increase in antibody titers is observed in 25% of them, indicating that M. hominis is the cause of infection in at least 25% of cases.

A. V. Rudenko (1985) isolated M. hominis from patients with pyelonephritis, Glomerulonephritis, and cystitis. All strains obtained from clinical material in these pathological conditions induced generalized mycoplasmosis in animal models, characterized by destructive-inflammatory Kidney lesions and severe microcirculatory disturbances within the renal tissue.

Latent infection caused by M. hominis and its subclinical forms pose a potential hazard because, under certain conditions, they can reactivate and cause severe septic processes (Peritonitis, postpartum and post-abortion sepsis, etc.).

To date, the exact role of M. hominis in the development of secondary male infertility remains unclear. Literature data on this issue are highly contradictory: some researchers report such a link, while others do not.

Unlike in men, secondary infertility in women can develop As a result of inflammatory processes that disrupt oogenesis and hinder ovum transport. A very high detection rate of M. hominis (37%) is observed in women with salpingitis suffering from infertility. It has also been noted that treating women infected with these mycoplasmas using tetracycline-class Antibiotics a week prior to ovulation in some cases led to their clearance (sanation) and subsequent pregnancy (I. V. Rakovskaya, Yu. V. Vulfovich, 1990).

Numerous clinical data indicate that the isolation rate of mycoplasmas from the cervical canal in non-pregnant women of reproductive age does not exceed 13.3%; it increases to 23.6% in colpitis, and reaches 37.9% in cervical erosions and/or Endocervicitis.

During pregnancy, the isolation rate of mycoplasmas increases by 1.5–2 times. In women suffering from recurrent pregnancy loss, the isolation rate of mycoplasmas outside of pregnancy is 24.4%, and during pregnancy, mycoplasmas represent the most frequently encountered microorganisms within the microflora of the cervical canal and vagina (A. S. Ankyrskaya, 1985).

According to literature data, M. hominis is detected in 40–50% of pregnant women. The increased frequency and intensity of infection during pregnancy are likely explained by changes in the physiological and, specifically, hormonal status, which triggers the activation of endogenous mycoplasmal flora. Mycoplasmal infection of the endometrium can lead to detachment of the gestational sac and, consequently, to early-term pregnancy loss.

The presence of M. hominis in gynecological patients and pregnant women poses a particular risk due to potential fetal infection, which is associated with an increase in perinatal mortality.

A pronounced activation of mycoplasmas has been noted when they are associated with other microorganisms. The high frequency of mycoplasma isolation in trichomoniasis (40.5–68.7%), gonorrhea (22–30%), and chlamydiosis (10–15%) presumably indicates the role of mixed mycoplasma-gonococcal, mycoplasma-chlamydial, and mycoplasma-trichomonal infections in the etiology of various urogenital inflammatory processes. Among these, chlamydia-mycoplasma urogenital coinfection predominates (ureaplasmas were detected in 42–52% of cases of chlamydial urethritis in men and in 39% of cases of chlamydial cervicitis in women). We have also observed associations of mycoplasmas with viruses, yeast-like Fungi, and other microorganisms. Several researchers (D. Taylor-Robinson, 1979; W. McCormack, 1980) emphasize the particular significance of combined mycoplasma-viral infection, with viral co-occurrence being noted in more than half of diagnosed mycoplasmosis cases.

Other clinical syndromes linked to mycoplasmal infection have also been described, including erythema multiforme, Stevens-Johnson syndrome, Nervous system involvement (encephalitis, meningoencephalitis), Brain abscess, and postpartum septic Arthritis. Mycoplasmas isolated from the mitral valve and aorta of patients undergoing valve replacement can cause postoperative complications. These pathogens are also identified in individuals with hypogammaglobulinemia. The role of these microorganisms in certain autoimmune disorders and leukemias has been established, as well as in human immune system diseases accompanied by transient immunodeficiency and impaired tolerance to self-Antigens.

Urogenital mycoplasmosis has an incubation period whose duration remains a subject of debate. According to literature data, it can range from 3 days to 5 weeks, being shorter in patients with acute inflammatory manifestations than in those with sluggish or subacute forms of the disease.

As a rule, urogenital mycoplasmosis predominantly presents with mild or oligosymptomatic forms, making it difficult to determine the exact duration of the incubation period. The conflicting data regarding the incubation period are largely due to the fact that in many patients—especially married individuals—the precise time of infection cannot always be reliably determined.

The Pathogenesis of urogenital mycoplasmoses remains poorly understood, with only fragmentary data available regarding the interaction between mycoplasmas and host cells. The Mechanism of interaction between ureaplasmas and susceptible cells may involve the persistence of these microorganisms on The cell membrane, though it has not yet been established whether they act strictly as membrane parasites or invade the cytoplasm.

The waste products of these bacteria, such as peroxides and terminal Respiration products, can obviously be toxic to body cells. However, for peroxides to exert their damaging effect on The cell wall, close contact with mycoplasmas is required.

Lipid Peroxidation resulting from The activity of peroxidase locally produced by a mycoplasma colony can lead to cell wall damage. M. hominis utilizes arginine as a substrate and metabolizes it into ammonia and carbon dioxide. Ureoplasmas break down urea into end products. The concentration of ammonia generated in this process can be toxic to the macroorganism. However, regarding M. hominis, the idea that a decrease in arginine content within the macroorganism has a greater toxic effect than the accumulation of ammonia remains highly controversial. M. hominis and ureoplasmas produce neither exotoxins nor endotoxins. And although it has been established that M. hominis can enter the bloodstream (in women with elevated body Temperature following an abortion), these microorganisms primarily attach to and multiply On the surface of the epithelium lining the urogenital and respiratory tracts, and are therefore regarded as surface parasites.

Mycoplasmas can also attach to spermatozoa, erythrocytes, fibroblasts (in monolayer culture), macrophages, and tracheal epithelium. Firm attachment of mycoplasmas to the host cell wall creates favorable conditions for colony formation while simultaneously supplying them with nutrients; the colony affects the host cell wall through the continuous production of its metabolites.

Mycoplasmas utilize Components of the host cell wall, specifically cholesterol and fatty acids. The mechanism of mycoplasma attachment remains insufficiently elucidated. For instance, when a mycoplasma attaches to the urethral epithelium, the bond is very strong and is not disrupted by the pressure of urine flow. However, electron microscopy studies have established that a definite space exists between the mycoplasmas and the host cell wall, meaning there is no tight, direct adhesion.

The potential pathogenic effect of mycoplasmas on the body has been studied using a fallopian tube epithelial cell culture. Following the attachment of mycoplasmas to the ciliated epithelium, a deceleration of ciliary beat frequency is observed, followed by the development of ciliosis. If the infection progresses, destruction of the ciliated epithelium and desquamation of the superficial cell layer are noted.

When extrapolated to humans, the results obtained from experiments with fallopian tube epithelial cell culture suggest that mycoplasma infection of the fallopian tubes should impair ovum transport by reducing or completely blocking ciliary activity. Local destruction of the ciliated epithelium may also contribute to the occurrence of Ectopic Pregnancy.

The presence of lesions far from the portal of entry (joint alterations, encephalitis, etc.) suggests that mycoplasmosis is not merely a local disease. The generalization of the infection is also evidenced by the detection of mycoplasmas in the Bone Marrow of leukemia patients, in Lymph Nodes, lung tissue, testicular biopsies, prostate tissue, and tumor tissues. However, the role of mycoplasmas in the genesis of leukemia and tumors remains ultimately unresolved.

Clinical manifestations. Mycoplasmoses are classified according to their localization (mycoplasmal urethritis, balanitis, prostatitis, epididymitis, cervicitis, bartholinitis, endometritis, salpingitis, etc.).

In urogenital mycoplasmosis, a characteristic clinical picture is not observed, yet a great variety of forms is noted. Urogenital mycoplasmal infections can be acute, chronic, and asymptomatic. As a rule, the disease runs a torpid course, with symptoms developing over 2–3 months. Typically, torpid, pauci-symptomatic vulvovaginitis, urethritis, and cervicitis progress to chronic urogenital mycoplasmosis. Patients complain of periodic itching in the urogenital area and scanty mucous discharge that may spontaneously disappear, only to reappear and intensify after some time.

Acute urogenital mycoplasmosis is rarely observed. In most cases, transient lesions are noted, and with proper Treatment, patients generally recover completely. Mycoplasmoses frequently follow a chronic course, manifesting as vaginitis, cervicitis, and inflammatory processes in the fallopian tubes and Ovaries. Nongonococcal urethritis is among the chronic forms of DISEASES ASSOCIATED WITH mycoplasmal infection. Asymptomatic forms are not accompanied by reactive inflammatory phenomena in the urogenital mucosa.

Diagnostics

Every patient under observation must undergo a comprehensive clinical examination. This applies both to patients with overt signs of urogenital system disorders (in which case There is a risk of missing impairments in other organs and systems) and to patients with subjective and objective symptoms that do not even remotely resemble urogenital pathology, despite the process having advanced too far. When urogenital pathology is suspected, alongside general clinical data, it is necessary to collect additional Anamnesis and resort to special examination methods.

Various Laboratory examination methods are of decisive importance in establishing a diagnosis of urogenital mycoplasmosis. Specific diagnostic methods include microbiological, serological, immunofluorescence assays, and genetic probes.

Culture diagnostics. For microbiological analysis, samples are taken from the mucosa of the urethra, the cervical canal, the vagina, and paraurethral ducts. Samples for isolating mycoplasmas should be taken from the First and Second portions of morning urine (using a 3-glass test). When mycoplasmal or ureaplasmal prostatitis is suspected, expressed prostatic secretion is used for inoculation. In cases of male infertility, it is advisable to examine semen using a microbiological method. Biosubstrates obtained via laparoscopy and amniocentesis, as well as tissues from aborted and stillborn fetuses, are also subject to such examination.

Samples selected for cultivation are immediately placed in a transport medium of the following composition: PPLO broth without crystal violet – 70 ml, horse serum (preservative-free) – 20 ml, yeast extract (pH 6.0) – 10 ml, benzylpenicillin (500,000 IU/ml) – 0.2 ml, polymyxin B (50 µg/ml) – 0.1 ml, amphotericin B (5 µg/ml) – 0.1 ml; the pH of the medium is adjusted to 6.0–6.2. Samples must be delivered to the laboratory urgently; they can be stored at 4 °C for up to 24 h, whereas longer storage requires low-temperature freezing (–70 °C).

Liquid and solid media prepared on the basis of PPLO agar and broth are used for cultivating M. hominis. COMPOSITION OF THE basal medium (per 100 ml of working medium): PPLO broth medium – 70 ml, yeast extract – 10 ml, normal horse serum – 20 ml, benzylpenicillin – 1,000 IU/ml, thallium acetate at a dilution of 1:2,000. Solid agar medium has the same base as the liquid one, with The addition of 1.3% agar-agar (Fig. 37). A biphasic medium can be used (1 part agar medium layered with 2 parts liquid medium). When isolating mycoplasmas from clinical material, 0.2% L-arginine and an indicator (phenol red) are introduced into the medium. During arginine metabolism via Ornithine to ammonia, M. hominis alkalinizes the medium, changing the pink color to red. On agar medium, the bacteria form colonies 200–300 µm in size with a characteristic fried-egg Morphology.

Fig. 37. Mycoplasma colonies on solid nutrient medium, × 120.

SP-4 medium, used for cultivating spiroplasmas, is also recommended. It yields good results in detecting mycoplasmas in men with nongonococcal urethritis and in women with inflammatory diseases of the urogenital organs.

Several different media are proposed for the culture diagnostics of ureaplasmas. We suggest those that are quite effective and most accessible to laboratories in medical diagnostic institutions.

Liquid medium for cultivating ureaplasmas. To 2.94 g of PPLO broth (Difco) without crystal violet, add 143 ml of deionized water, adjust the pH to 6.5 ± 0.5 with 2N NaOH or 2N HCl, and sterilize by autoclaving for 15 min at 1.4 atm (1.1 atm). After cooling to 50 °C, prepare the medium: basal broth – 140 ml, horse serum (preservative-free) – 40 ml, yeast extract (pH 6.0) – 20 ml, L-Cysteine hydrochloride 2% – 1 ml, urea 10% – 0.4 ml, phenol red 1% – 0.2 ml, benzylpenicillin (500,000 IU/ml) – 0.4 ml; adjust the pH to 6.0.

A nutrient medium prepared on the basis of placental broth with enriched supplements (horse serum – 20 ml, yeast extract – 4 ml; pH 6.5) is also used.

Agar differential medium. To 2.4 g of trypticase soy broth (BBL), add 80 ml of deionized water, adjust the pH to 5.5 by adding 2N NaOH or 2N HCl, and then add 1.3 g of agar. Sterilize by autoclaving for 15 min at 1.1 atm. After cooling to 50 °C, add yeast extract (pH 6.0) – 2 ml, urea 10% – 2 ml, L-cysteine hydrochloride 2% – 0.5 ml, benzylpenicillin (500,000 IU/ml) – 0.2 ml, manganese sulfate 3% – 1 ml, or (preferably) CaCl₂ ∙ 2H₂O – 0.014 g.

Inoculated nutrient media are incubated at 37 °C. Ureoplasmas grow on agar medium within 48–72 h as small dark-brown or brownish-black colonies with a diameter of 15–30 µm.

The growth of ureoplasmas is inhibited by ammonium ions accumulating in dead cells, the concentration of which increases during culture growth. For this reason, the ureoplasma cultivation medium cannot support their growth even when a fresh portion of broth is added to it. At the same time, the filtrate of the growth medium, devoid of ammonium ions, can serve as a basis for preparing a new cultivation medium. On solid medium, ureoplasmas are cultivated more successfully in an atmosphere of gas mixtures containing 5% CO₂ and 95% N₂, or 5% O₂, 10% CO₂, and 85% N₂.

Serological studies. Laboratory diagnostics of mycoplasmosis involves antigen isolation, determination of serum Antibodies, and specific antigens using agglutination assays (RAGA), immunofluorescence assay (IFA), and enzyme-linked immunosorbent assay (ELISA).

In recent years, a test system based on DNA Amplification for the detection of mycoplasms—the Polymerase Chain Reaction (PCR)—has been developed and introduced into practice. The high sensitivity of this method makes it possible to detect mycoplasms in cases where other methods fail. However, to date, there are no clear criteria for obtaining critical quantitative indicators of mycoplasma or ureaplasma invasion massiveness that would indicate the manifestation of their pathogenicity. Therefore, to avoid errors in the Laboratory Diagnosis of mycoplasma or ureaplasma infection, a comprehensive set of diagnostic test systems must be used.

In cases where mycoplasms or ureaplasms are detected by microbiological methods, IFA, or PCR, and their antigens are identified in blood serum (via ELISA or RAGA), a generalized infectious process is diagnosed. Specific antibodies are detected in approximately 25% of cases (using ELISA or passive hemagglutination assay); their absence may be associated with either the low immunogenicity of the pathogen or an immunosuppressive state, the development of which is promoted by mycoplasma infection.

The detection of mycoplasms by microbiological methods in the absence of positive results in IFA or PCR is attributed to inadequate sampling, specifically a low cell count in the smear.

Positive PCR findings combined with negative microbiological, serological, and IFA results indicate a localized infection with low bacterial load. In such cases, if clinical symptoms are absent, it can be classified as asymptomatic carriage.

Negative microbiological results alongside positive IFA and PCR data may indicate the inadequacy of the culture media used.

If a mycoplasma, ureaplasma, their antigens, or corresponding antibodies are detected by only one of the aforementioned methods, a follow-up examination is performed after a specified period (1 month) to confirm asymptomatic carriage.

Urogenital mycoplasmosis in men

Most cases of urogenital mycoplasmosis in men present as a chronic syndrome characterized by scanty genital discharge and vague pain. Occasionally, the disease begins as acute urethritis. Discharge is present from the very beginning and remains a constant feature. Pruritus, discomfort, and pain in the urogenital region are frequently observed. In some cases, patients complain of pain in the Scrotum, Perineum, anus, as well as the lumbar and sacral regions.

The disease progresses slowly. For the infectious process to develop, the mere persistence of mycoplasms in the lower urogenital tract is less important than the extent and density of dissemination. The pathogenicity of various mycoplasma serotypes and their combined effects also play a certain role.

In men, mycoplasms can affect the urethra, prostate gland, Seminal Vesicles, epididymides, urinary bladder, Kidneys, and Urinary Tract.

Mycoplasma urethritis, like urethritis of other etiologies, may initially present with acute, subacute, or torpid inflammatory symptoms. Acute forms are rare. According to Siboulet (1971), acute mycoplasma urethritis was observed in 5% of patients. We diagnosed acute urethritis in 4.7% of male patients with mycoplasmosis.

The inflammatory process may involve either the entire urethra or its anterior portion. Clinically, acute mycoplasma urethritis is indistinguishable from acute gonococcal urethritis (hyperemia and edema of the Lips of the external urethral meatus, massive purulent urethral discharge, turbid urine in the first portion in anterior urethritis, and in both portions in total urethritis). Subjective sensations in such patients are similar to those experienced in acute gonorrhea.

In subacute and torpid forms, inflammatory signs in the urethra are significantly milder, discharge is scanty, mucous or mucopurulent, and appears only upon expression from the urethra or after prolonged urinary retention. The first portion of urine may be slightly turbid, opalescent, or even clear, containing mucous or mucopurulent threads.

In chronic mycoplasma urethritis, symptoms are very mild. Subjective sensations typically amount to minor itching, tickling, or burning in the urethra. Inflammatory phenomena around the urethral lips are absent, though the lips may occasionally stick together. Scanty mucous droplet discharge is revealed only upon expression, sometimes exclusively in the morning, and mucous threads are noted in the urine.

Balanitis and Balanoposthitis. Mycoplasma urethritis can be complicated by balanitis and balanoposthitis, which arise either from irritation by urethral discharge or primarily as a result of the direct action of mycoplasms on the Skin of the glans Penis.

Factors predisposing to the development of balanitis include reduced bodily resistance, a narrow corona of the glans, and sexual excesses (which compromise the integrity of the skin, facilitating subsequent penetration by mycoplasms).

In mycoplasma balanitis and balanoposthitis, patients complain of itching and discharge from the preputial sac, in which pathogens are frequently detected. After retracting the edematous corona of the glans, intensive inflammation and epidermal maceration are revealed in the coronal sulcus. The surface of the glans and the inner leaf of the foreskin appear edematous, loosened, and hyperemic. As the inflammatory process progresses, it may cause the detachment of the affected cornified layer of the skin of the glans penis, leading to the formation of superficial erosions, abrasions, and, in rare cases, ulcers. Long-standing balanitis may cause phimosis, and balanoposthitis may lead to paraphimosis.

M. fermentans has been isolated from cases of balanitis in men and fusospirillary vulvovaginitis in their female partners; There are also reports of this mycoplasma species being detected in ulcerative lesions of the penis.

Mycoplasma urethritis in men often follows a torpid course with few noticeable subjective symptoms, which is why many patients seek medical attention only when organs other than the urethra become involved in the pathological process. In some cases, only emerging complications compel the patient to consult a doctor.

Mycoplasma prostatitis and vesiculitis. Infection most frequently spreads to the prostate gland and seminal vesicles from the prostatic urethra directly through the excretory ducts. Mycoplasms may also penetrate the prostate from the anterior urethra via Blood and Lymphatic vessels.

The factors precipitating mycoplasma prostatitis and vesiculitis are identical to those causing inflammation of other etiologies (gonococcal, chlamydial, etc.). These include sexual excesses, alcohol consumption, constipation, prolonged or interrupted intercourse, etc.

Clinically, mycoplasma-induced lesions of the prostate gland and seminal vesicles do not differ from nongonococcal inflammatory diseases of these organs. G. Rossebauer et al. (1977) detected U. urealyticum in the ejaculate of 15% of male patients with prostatitis. We isolated M. hominis from the ejaculate of men with post-gonococcal urethritis complicated by prostatitis and vesiculitis. U. urealyticum was detected in prostatic secretion more frequently than in the urethra (I. I. Mavrov, A. Ye. Karpenko, 1984).

According to foreign authors and our own observations, chronic prostatitis arising primarily and pursuing a torpid course is among the most frequent complications of urogenital mycoplasma infection.

In some patients, subjective Complaints may be entirely absent, whereas in others, they are exceptionally numerous.

Chronic mycoplasmal prostatitis frequently causes increased nocturnal urination. The urine is sometimes clear with mucopurulent threads, or occasionally cloudy in the first or both portions. In some cases, as with prostatitis of other etiologies, patients complain of decreased potency.

Epididymitis. Among the complications of urogenital mycoplasmosis in men is epididymitis or orchiepididymitis. Epididymitis is more commonly observed in patients with protracted mycoplasmal urethritis, or in those who received no treatment at all, or whose treatment was untimely and improper.

Mycoplasmal epididymitis may occur when the inflammatory process spreads to the prostatic urethra, from where it penetrates into the Epididymis via the vas deferens. The onset of epididymitis is typically promoted by sexual activity during mycoplasmal urethritis, sexual disorders, unjustified instrumental examinations, rough massage of the prostate gland, and other pathogenetic factors.

In most cases, mycoplasmal epididymitis develops gradually and runs an insidious course without distinct symptoms. Some patients experience prodromal phenomena such as malaise, vague dragging pain in the groin, perineum, and the corresponding half of the scrotum. The pain gradually intensifies, though without reaching a high degree of intensity. Within 1–2 days, enlargement of the inflamed epididymis becomes very noticeable. Palpation reveals enlargement and induration of the entire epididymis; its surface may be nodular. Edema and hyperemia of the scrotal skin are mildly expressed. Body temperature rarely exceeds 38 °C and often remains normal.

Cystitis. Mycoplasmal cystitis is relatively rare and occurs only in the presence of factors that facilitate the penetration and entry of mycoplasmas into the urinary bladder and their subsequent multiplication. In healthy individuals, this is prevented by constant emptying of the bladder and the bacteriostatic properties of its mucosa. However, if complete emptying of the bladder is impossible (for example, in urethral meatal stenosis), favorable conditions arise for the development of chronic cystitis. Inflammatory changes in the bladder wall vary depending on the severity and duration of the disease. They may spread throughout the entire bladder or be confined only to a part of it, predominantly in the trigone (trigonitis). The disease occurs not only in men, but also in women and children.

Clinical signs of cystitis are typical: frequent urges to urinate, dysuria, Urinary Incontinence, and occasionally Hematuria. Objective Examination reveals suprapubic tenderness upon palpation and, at times, inflammatory changes of the external urethral meatus.

Pyelonephritis. Mycoplasma-induced inflammation in a number of cases simultaneously involves the kidney tissue and the renal pelvis. The course of mycoplasmal pyelonephritis is usually chronic, though it can occasionally be acute. The disease presents atypically or without characteristic signs, which is why it may remain unrecognized or be diagnosed late. Pyelonephritis caused by mycoplasmas is observed in men, women, and children alike. The causes of Chronic Pyelonephritis may include repeated penetration of mycoplasmas into the kidneys from foci of infection, anatomical and functional abnormalities that promote the development of an ascending mycoplasmal process, and a decrease in the immunological reactivity of the patients' bodies.

The clinical picture is varied and depends on the form of the disease (acute or chronic) and the degree of renal impairment. It should be emphasized that in mycoplasmal pyelonephritis, mucosal lesions of the urethra may be insignificant.

Urogenital Mycoplasmosis in Women

Women are most frequently asymptomatic carriers of mycoplasmas. Under The Influence of various stress factors, a latent infection can transform into a chronic relapsing form or an acute infection. In some cases, vaginitis, cystitis, and salpingitis develop. Factors that provoke the Development of the infectious mycoplasmal process include concurrent infections of various etiologies (bacterial, including chlamydial, viral, fungal), and hormonal fluctuations associated with ovulation, pregnancy, and other physiological changes.

Depending on the localization, a distinction is made between mycoplasmosis of the External female genitalia (vulvitis, subsequently vulvovaginitis, urethritis, paraurethritis, bartholinitis, etc.) and mycoplasmosis of the Internal Female Genitalia (adnexitis, endometritis, salpingitis, ovarian inflammation and abscesses, etc.).

Mycoplasmosis of the external female genitalia. Most frequently, the infection penetrates the vaginal vestibule and the urethra, affects the small vestibular glands and the Bartholin's gland, and subsequently spreads to the internal genitalia, primarily the vagina. Lesions of the external genitalia in women are not accompanied by subjective symptoms of mycoplasmosis; objective manifestations are mild and short-lived.

By analogy with other Sexually Transmitted Diseases (gonorrhea, trichomoniasis), a distinction is made between fresh torpid and chronic mycoplasmosis of the external female genitalia.

Fresh torpid urogenital mycoplasmal lesions in women are rarely observed. They briefly manifest as mild itching in the area of the external genitalia and scanty discharge that causes no concern. As a rule, patients do not seek medical attention; the infection is discovered during the examination of sources of infection, including sexual partners suffering from urogenital mycoplasmosis.

In a significant number of patients, the external urethral meatus is slightly edematous. Palpation of the urethra through the anterior vaginal wall sometimes reveals thickening, and in some cases, induration. In the area of the cervix and its external os, the mucous membrane is edematous and occasionally eroded.

Frequently, urogenital mycoplasmosis in women presents with no subjective or objective clinical signs, and only the examination of discharge or scrapings from the urogenital mucosa helps detect mycoplasmas. Such women become mycoplasma carriers.

Against the Background of adverse factors (decreased body defense mechanisms, hormonal disorders, etc.), various complications of vulvovaginitis and urethritis may arise (abscess of the Bartholin's gland, ascending mycoplasmal lesions of the internal female genitalia, urinary bladder, renal pelvis, etc.).

Mycoplasmosis of the internal genitalia. Ascending mycoplasmal infection in women manifests initially as vulvovaginitis, followed by endometritis, salpingitis, and adnexitis. Mycoplasmas penetrating into the uterine cavity through the cervical canal can cause endometritis. The role of mycoplasmas in endometritis is confirmed by the detection of these microorganisms in the uterine cavity during medical and spontaneous abortions, as well as stillbirths. Clinically, mycoplasmal endometritis proceeds similarly to endometritis caused by other infectious agents. Its main symptoms are menstrual irregularities and bleeding. Complications of mycoplasmal endometritis may include infertility and spontaneous miscarriages.

In mycoplasmal salpingitis, pathogens penetrate from the uterine cavity into the lumen of the fallopian tubes. The literature contains reports of isolating M. hominis in women with pelvic inflammatory disease (Pelvioperitonitis). During laparoscopy in 50 women with salpingitis (R. A. March et al., 1976), M. hominis was isolated directly from the fallopian tubes as the sole causative agent of salpingitis in four patients, whereas mycoplasmas were not detected in any of the women in the control group. In these four patients, the titers of the indirect (passive) hemagglutination assay (IHA) increased significantly during the course of the disease.

R. A. March and L. Westrum (1970) isolated M. hominis from the cervix in 64% of patients with salpingitis and in only 6% of women in the control group. When performing IHA, antibodies to mycoplasmas were found in 54% of patients and 10% of healthy women.

Although U. urealyticum was isolated directly from the fallopian tubes in two out of 50 women with salpingitis, it is unlikely to be the causative agent. This pathogen is isolated from the cervix with equal frequency in women with and without salpingitis. U. urealyticum does not infect the fallopian tubes in cell cultures of these organs and does not cause experimental salpingitis in monkeys (R. A. March et al., 1976), whereas M. hominis inoculated into the fallopian tubes of monkeys caused salpingitis and parametritis in them (B. R. Moller et al., 1978).

Mycoplasmal oophoritis and adnexitis are typically secondary, resulting from the invasion of pathogens from the fallopian tubes. This leads to mycoplasmal inflammation of the Ovary, up to the formation of abscesses, and causes adhesions between the ovary and the inflamed, thickened fallopian tube (adnexitis). Patients with adnexitis complain of lower back pain, menstrual irregularities, sometimes dysuric disorders, and pain during intercourse; they also frequently suffer from infertility.

Urogenital Mycoplasmosis in Children

Inflammatory diseases of the urogenital system caused by mycoplasmas pose a particular epidemiological danger due to the possibility of fetal infection. The clinical picture is often extremely severe, and the prognosis is not always favorable. In intrauterine mycoplasmosis, a generalized pathological process develops, affecting the respiratory organs (bronchopneumonia), eyes, Liver, kidneys, and Central Nervous System.

According to foreign authors, intrauterine mycoplasmosis develops in 5.5–23% of children. Characteristic features in such cases include premature and early rupture of amniotic membranes in pregnant women, fever during labor and the postpartum period. It is believed that in pregnant women, the mycoplasmal infection has an ascending character, spreading from the external genitalia and being aspirated by the fetus. Confirmation of this may be the predominance of pulmonary lesions in fetuses and newborns whose mothers had a urogenital mycoplasmal infection. The detection of mycoplasmas in the Tissues of the Spleen, kidneys, and brain of the fetus also suggests a hematogenous pathway of spread for this infection.

The intensity of genital tract colonization by mycoplasmas also causes infant infection during passage through the birth canal. It has been established that the frequency of pathogen isolation in children correlates with the percentage of infection in pregnant women. Mycoplasmas are detected in the pharynx, external genitalia, and umbilicus of infants, as well as in urine and vaginal secretions. In some cases, this carrier state is asymptomatic, while in others it manifests as vulvitis, pneumonia, or encephalitis.

In certain forms of mycoplasmosis, the primary local lesion is apparent only at the onset of the disease, after which the mycoplasmal process becomes generalized, leading to the development of meningitis and meningoencephalitis in children. In such cases, mycoplasmas can be isolated from abscesses of various localizations and from CEREBROSPINAL FLUID.

Mycoplasmal infections in pregnant women are associated with a reduction in neonatal body weight (on average 304 g lower than that of infants born to uninfected mothers). Notably, the birth weight of infants whose mothers were infected with ureaplasmas and treated with erythromycin was higher than that of infants born to untreated mothers.

The literature contains data on the association of generalized mycoplasmal infection with severe, often multiple Congenital Malformations that caused infant mortality. Some authors (S. M. Becker et al., 1976; A. S. Ankirskaya, 1977) note that 50.8% of children born to women with cervical mycoplasma colonization die in the perinatal period, and 12.5% exhibit congenital malformations, particularly of the central nervous system. Reports on congenital malformations associated with mycoplasmal infection are of particular significance, given that the etiology of such anomalies remains unexplained in 50% of cases.

Clinical and Laboratory studies have demonstrated that mycoplasmas acquired via vertical transmission spontaneously disappear in infants within a short period. Nevertheless, approximately 5% of children under one year of age remain infected. During Puberty, urogenital mycoplasmal infection is rarely observed in boys, whereas in premenarcheal girls, ureaplasmas are detected in 10% of cases and M. hominis in 5%.

Urogenital mycoplasmosis in children is frequently a contagious disease. For instance, in the presence of close contact between children and adolescents with infected individuals (within families or childcare collectives), the prevalence of mycoplasmal vulvovaginitis in girls reaches 3-30%. Each case of overt vulvovaginitis in pediatric settings (nurseries, kindergartens, etc.) corresponds to multiple cases of milder urogenital mycoplasmal infections.

The clinical course of urogenital mycoplasmosis in children is variable, characterized by frequent remissions and exacerbations. The infection may be entirely asymptomatic, presenting merely as a carrier state. Typically, the infection is activated by adverse factors such as stress or immunodeficiency. Episodes of dysuria and pyuria mimicking pyelonephritis may occur, predominantly in girls. Exacerbations can be triggered by concurrent urogenital infections or Upper Respiratory Tract infections.

It has been established that hormonal status influences the isolation rate of ureaplasmas. These microorganisms are most frequently isolated (42% of cases) from the vagina of newborns and girls under 30 days of age, and relatively rarely (5%) during the prepubertal period. However, establishing a direct correlation between hormonal status and ureaplasma detection in children is complex, and further research is required to elucidate underlying patterns.

Comprehensive clinical and laboratory evaluation of girls with recurrent vulvovaginitis revealed that ureaplasmas are the causative agent in 6% of cases. Mixed infections involving Chlamydia and ureaplasmas have also been documented (D. I. Mavrov, 1990). This condition is characterized by frequent, prolonged remissions during which clinical symptoms completely resolve. During exacerbations, all patients present with vaginal discharge; however, vaginoscopy reveals endocervical discharge in only isolated cases associated with ectopic lesions of the ectocervix. Urinary tract infections are diagnosed relatively frequently in patients with vulvovaginitis.

Genital mycoplasmas are most commonly transmitted through sexual contact. Nevertheless, according to certain observational studies, ureaplasmas are cultured in 40% of virgins, indicating that the carrier state cannot always be attributed to sexual transmission in sexually mature women. It is hypothesized that transmission occurs intrapartum from the mother, after which ureaplasmas persist asymptomatically and may manifest post-puberty even in the absence of sexual activity. This hypothesis is supported by the high isolation rate of ureaplasmas in newborns (42%), which is comparable to that observed in adult women who have never engaged in sexual intercourse (T. Iwasaka et al., 1986).

A potential site of mycoplasmal persistence is the vagina, where their invasiveness remains too low to manifest prior to puberty; another is the cervical canal, from which sampling is extremely difficult in pediatric patients. Evidence that the cervix serves as a favorable niche for the persistence and proliferation of ureaplasmas is provided by data from postmenopausal women, where they are detected in 25% of cases.

The lower segments of the Large Intestine (rectum) may also act as a reservoir for mycoplasmal persistence. M. hominis and U. urealyticum are frequently detected in the rectum (with ureaplasmas reaching up to 69%). It is highly probable that mycoplasmas initially colonize the rectum, which functions as an infectious reservoir, and subsequently translocate to the reproductive organs following the onset of puberty. Resolving these critical questions will likely require studies involving serotyping of ureaplasmas isolated from the gastrointestinal and urogenital tracts, followed by comparative analysis.

Treatment

Anti-mycoplasmal therapy must be comprehensive, pathogenetically substantiated, and encompass not only direct action against the pathogen but also measures to enhance host immune defenses.

Clinical experience in treating urogenital mycoplasmosis at the Institute of Dermatology and Venereology of the Academy of Medical Sciences of Ukraine has demonstrated that combination therapy incorporating agents that stimulate nonspecific host resistance yields superior outcomes, especially when antibiotic monotherapy proves insufficient. In urogenital mycoplasmosis, as in other infectious inflammatory Disorders of the urogenital tract, treatment must correspond to the clinical topographic diagnosis, disease stage, and individual pathological Features of the patient. A thorough anamnesis and comprehensive patient evaluation are essential.

Etiotropic treatment of urogenital mycoplasmoses is conducted using antibiotics active against mycoplasmas, taking into account the stage of the inflammatory process. When formulating a comprehensive therapeutic plan, it must be considered that mycoplasmosis is a multifocal disease; consequently, the goal is not only to eradicate the pathogen but also to eliminate the consequences of its impact, thereby achieving clinical cure. In cases of prolonged pathological processes, etiotropic treatment should be supplemented by measures to boost nonspecific bodily resistance. Active management of urogenital mycoplasmosis must be combined with dispensary care, including the screening and treatment of sexual partners.

Therapy for urogenital mycoplasmoses also includes immune priming, physiotherapy, local treatments, management of comorbid conditions and pelvic congestion, a rational lifestyle, and an appropriate diet (prohibiting alcohol and spicy foods).

Among therapeutic agents, tetracycline, its derivatives, and erythromycin are the most effective. Doxycycline, tetracycline, or erythromycin are administered orally for 10-14 days (doxycycline at 100 mg and tetracycline at 500 mg twice daily). For ureaplasmosis, erythromycin is indicated at 250 mg four times daily. Women are additionally advised to use tetracycline or erythromycin at 100 mg in the form of vaginal suppositories or antibiotic-impregnated tampons.

In some cases, high-dose oral administration of tetracycline or erythromycin (2 g/day for adults) may lead to clinical improvement without eradicating mycoplasmas from the urogenital tract (I. I. Mavrov, A. G. Kletnoy, 1984). These antibiotics are also administered intramuscularly or intravenously according to clinical indications.

Fluoroquinolones (ciprofloxacin, ofloxacin) are recommended. These agents are prescribed orally or parenterally for 10-14 days.

In the management of patients with urogenital mycoplasmal infection, daily intraurethral and intravesical instillations via catheter are employed for 10 days using 50 ml of a 2% gelatin solution, 500 IU of an oil-based vitamin A solution, 200 IU of Insulin, and 1 million IU of tetracycline.

Women are prescribed daily vaginal baths using the same solution for 10-12 days. For chronic prostatitis and vesiculitis in men, as well as endometritis and salpingitis in women, phonophoresis with tetracycline or erythromycin is indicated. Other local therapeutic methods (such as urethral bougienage and massage) and physical therapy (diathermy, ultrasound, UHF currents, etc.) utilized for chronic urogenital infections of various etiologies are also recommended.

The Selection of a specific local treatment modality in each individual case depends on the disease duration, the Nature of the pathological process, the patient's individual physiological characteristics, and their reactivity to particular stimuli. Local therapy also exerts a systemic effect.

To confirm the cure of a patient with mycoplasmosis, 7-8 days post-therapy, follow-up cultures should be obtained from various anatomical sites where mycoplasmas were previously detected (urethra, paraurethral ducts, vagina, cervix, etc.), along with analysis of fresh urine sediment, glandular secretions (prostate, seminal vesicles), and ejaculate.

If mycoplasmas are persistently detected, a second course of treatment is administered. Treatment is considered complete only when inflammatory signs have resolved and mycoplasmas are no longer detectable. Typically, one or two treatment courses are sufficient to suppress the mycoplasmal infection, provided that the sexual partner is treated concurrently. Post-treatment medical surveillance for 2-3 months is of paramount importance.

Prevention

Due to its widespread prevalence, numerous and often severe complications leading to impaired reproductive function, fetal and neonatal pathologies, pregnancy complications, disability, and urogenital mycoplasmosis represent a serious public health concern. Certain challenges remain in both the Diagnosis and treatment of this condition.

Prevention measures for urogenital mycoplasmoses are similar to those for other sexually transmitted infections. Preventive efforts utilize a dispensary-based approach aimed at detecting mycoplasmoses primarily among risk groups (sex workers, homosexual individuals); women of childbearing age suffering from chronic inflammatory diseases of the urogenital organs of unknown etiology; pregnant women with a complicated obstetric history and adverse pregnancy outcomes; and individuals requiring kidney or other internal organ transplantation.

To achieve scientifically grounded objectives in the prevention and control of urogenital mycoplasmoses, improving laboratory services plays a paramount role. The application of laboratory Methods for the etiological diagnosis of mycoplasma infections requires specialized training for laboratory physicians and adequate material and technical support.

Although mycoplasmoses are epidemiologically urogenital diseases, due to their diverse clinical manifestations, they must be monitored not only by venereologists but also by physicians of other specialties. The effectiveness of treatment and prevention programs largely depends on the coordinated efforts of specialists across various clinical fields.

Special attention is required for the prevention of intrauterine mycoplasmosis, which results from fetal infection with urogenital and/or respiratory mycoplasmas. Targeted screening of pregnant women at various stages is of great preventive significance. If mycoplasmas are detected, both partners must undergo treatment to prevent intrauterine fetal infection.

An important condition for prevention is health education, which informs the public about the forms and symptoms of mycoplasma infection, its transmission routes, and potential consequences. A normal sex life, adherence to personal hygiene, and The Use of individual preventive measures play a significant role in reducing morbidity.

The prevention of urogenital mycoplasmosis must be based on modern understanding of the etiology and epidemiology of this disease. It should be kept in mind that through close contact with infected family members, mycoplasma infection can be transmitted via shared bedding, toiletries, towels, etc. Occasionally, staff in preschool childcare facilities become a source of mycoplasma infection. Children's genital 'play' and masturbation also bear some significance.

Active case finding and engaging patients in treatment remain the cornerstone of successful control over urogenital mycoplasmoses. In the majority of men and women, the disease runs a chronic or latent course without clinical manifestations or subjective symptoms, which naturally leads such individuals to consider themselves healthy and prevents them from seeking medical help on their own initiative, thereby remaining potential sources of mycoplasma infection spread.