Sexually Transmitted Diseases - I. I. Mavrov 2005

Sexually Transmitted Diseases
Urogenital Chlamydiosis

A group of diseases and syndromes caused by *Chlamydia trachomatis* is characterized by direct multifocal lesions of the Genitourinary system with subsequent complications (impairment of reproductive function, potential risk of becoming a source of chlamydial infections in other sites, including perinatal ones).

Etiology. The CAUSATIVE AGENT OF urogenital chlamydiosis is *Chlamydia trachomatis*, which are non-motile, coccoid, Gram-negative obligate intracellular microorganisms. Being unable to independently synthesize ATP, they act as energy parasites within the host Cell; however, unlike Viruses, they contain both DNA and RNA. Urogenital infections are caused by *Ch. trachomatis* serotypes D-K.

The biological uniqueness of chlamydia—consisting in obligatory intracellular energy-dependent parasitism and a unique developmental cycle occurring against the Background of a complex of bacterium-like characteristics (preservation of morphological identity throughout The life cycle, division of vegetative forms, presence of a Cell wall, DNA and RNA content, enzymatic activity, presence of a common genus-specific antigen, susceptibility to broad-spectrum Antibiotics, etc.)—determines, According to the unanimous opinion of specialists, the independent taxonomic position of these microorganisms within the prokaryotes. At the same time, the issues regarding their Classification remain debatable.

In the classification system of chlamydia, the order Chlamydiales is distinguished as an independent order that includes a single family, Chlamydiaceae, represented by the single genus *Chlamydia*, which combines two species of microorganisms: *Ch. trachomatis* and *Ch. psittaci*. The species *Ch. trachomatis* includes human pathogens responsible for trachoma, urogenito-ocular infections, lymphogranuloma venereum, as well as the agent of mouse pneumonitis. The species *Ch. psittaci* encompasses pathogens causing psittacosis (ornithosis), Pneumonia, abortion, polyarthritis, enteritis, Conjunctivitis, and encephalitis in domestic and wild animals. These microorganisms primarily affect animals, but zoonotic chlamydial infections also occur in humans.

Chlamydial infection primarily affects the genitourinary system. At the same time, establishing the etiological factor leading to respiratory tract lesions is of utmost importance. Therefore, the ISOLATION OF A new strain, *Ch. pneumoniae*, is of great theoretical and practical interest. It is the causative agent of chlamydial pneumonia in humans. Patients with elevated levels of Antibodies to this strain can be considered a risk group for myocardial infarction, with the risk being higher than in groups with other risk factors for cardiovascular disease. All chlamydiae develop in the yolk sac of chicken embryos and cause their death when the number of microorganisms becomes significant. *Ch. trachomatis* also multiplies in cell cultures of various lines, especially after treating the Cells with cycloheximide, cytochalasin B, or iododeoxyuridine. The multiplication process differs among various immunological types of *Ch. trachomatis*. The growth of strains isolated from trachoma patients (serotypes A-C) differs from that of strains obtained from inguinal lymphogranuloma (serotypes L₁-L₃) or urogenital infections (serotypes D-K). Multiplication in the Cell Cytoplasm corresponds to a developmental cycle that results in The formation of compact inclusions with a Glycogen matrix containing the chlamydiae.

The main morphological forms of chlamydia are elementary bodies and reticulate (initial) bodies, with intermediate forms appearing during the developmental cycle, defined as transitional or intermediate bodies. These forms exhibit ultrastructural, biological, and functional differences that are similar among different chlamydiae under identical environmental conditions.

All chlamydiae undergo a series of successive changes during reproduction. The mature, infectious form is the elementary body, about 0.3 µm in diameter, with an electron-dense nucleoid. This infectious particle enters the host cell via phagocytosis. A vacuole is formed from the host cell surface membranes around this small particle. The small particle transforms into a large one, about 0.5–1.0 µm in diameter (the initial or reticulate body), which lacks an electron-dense nucleoid. Inside the membrane-bound vacuole, it increases in size, becoming an intermediate body, and undergoes multiple divisions. Ultimately, the entire vacuole fills with small particles formed from the large bodies through transverse fission and transforms into an "inclusion" within the cytoplasm of the host cell. Newly formed small particles (elementary bodies) can leave the host cell and infect other cells. The developmental cycle lasts 24–48 hours.

Fully formed mature intracellular inclusions appear as compact masses located near The Nucleus and stain purple with Giemsa stain (where mature particles are densely packed) (see insert VIII, 3-4). When stained with a diluted aqueous Lugol's solution, inclusions formed by the same chlamydiae (agents of lymphogranuloma venereum, trachoma, and conjunctivitis) turn brown due to the glycogen-like matrix surrounding the particles.

The outer cell envelope of chlamydia is similar to that of Gram-negative Bacteria. It contains Lipids (in relatively large amounts) and peptidoglycan, which apparently includes muramic acid. Chlamydiae contain a high amount of lipids, particularly Phospholipids. In elementary bodies, protein accounts for about 60%, comprising at least 18 Amino acids.

Chlamydiae exhibit specific staining properties that vary at different Selection/3.html">Stages of development. Elementary bodies stain purple with Giemsa stain and red with Macchiavello stain, contrasting well with the blue cytoplasm of the host cell. Reticulate bodies stain blue with Giemsa stain. Gram staining yields negative or variable results, making this method ineffective for identifying chlamydia.

Chlamydiae possess Two Types of Antigens, presumably localized in The Cell wall. Group antigens are found in all members of the genus *Chlamydia*. They are lipopolysaccharides resistant to heat and the action of Nucleases and proteases, but they are inactivated by periodate and lecithinase and partially destroyed by deoxycholate Treatment. Like other Gram-negative bacterial lipopolysaccharides, they contain 2-keto-3-deoxyoctonate. Specific antigens remain bound in the cell wall after most of the group antigens are extracted using organofluorine compounds or deoxycholate. Some specific antigens are Proteins purified by immunoadsorption. Specific antigens are best detected by immunofluorescence. They are present in a limited number of chlamydiae, although a single species may contain several specific antigens.

The Toxic Effect of chlamydiae is associated with The properties of their antigens. Specific neutralization of toxicity by antisera allows for the grouping of chlamydiae based on their antigens. Fifteen serological types of *Ch. trachomatis* (A, B, Ba, D-K, L₁-L₃) have been identified. The last three are immunological types of lymphogranuloma venereum.

Chlamydiae possess endogenous METABOLISM, can independently generate СО₂ from glucose, Pyruvate, and glutamate, and contain dehydrogenases. However, energy-rich intermediates from the host cell are required to drive their biosynthetic activity.

Cell wall synthesis inhibitors, such as penicillin or cycloserine, lead to the formation of morphologically defective forms of chlamydia, yet they yield no significant therapeutic results in clinical practice. Protein Synthesis Inhibitors (Tetracyclines, macrolides) are effective both experimentally and clinically. Because chlamydiae synthesize dihydrofolic acid during their life cycle, they are inhibited by sulfonamides, which block this synthesis. Aminoglycosides exhibit a weak inhibitory effect on chlamydiae.

Chlamydiae are rapidly inactivated by elevated temperatures. Their pathogenicity is completely lost upon heating at 60 °С for 10 min. At the same time, chlamydiae retain virulence for several years at temperatures ranging from -50 to -70 °С. Lyophilization significantly reduces their infectivity, although air-drying may allow some microorganisms to retain it for a prolonged period.

Inactivation of chlamydiae is rapidly achieved by ether (within 30 min) or phenol (0.5% solution for 24 h). They are highly sensitive to 70% ethanol, 2% lysol solutions, 0.05% silver nitrate, 0.1% potassium iodate, 0.5% potassium permanganate, and 25% hydrogen peroxide, and are inactivated at room Temperature within two days.

Particular attention should be paid to laboratory data obtained when evaluating the antichlamydial efficacy of chlorine-containing preparations widely used for disinfecting medical personnel's hands and Water decontamination. It was found that the commonly used 0.5% chloramine B solution is unable to inactivate urogenital chlamydial strains even with a 10-minute exposure. Only a 2% concentration of the preparation ensures the disinfection of material within 1 min. It was also established that at room temperature (18-19 °С), chlamydiae can remain viable in dechlorinated water for up to 5 days; consequently, their reliable inactivation in shared water reservoirs can be achieved only through hyperchlorination, maintaining a residual active chlorine concentration of at least 3 mg/L in the water (V. O. Martynova, 1989). These data must be taken into account not only in laboratory practice but also when developing specific preventive measures against urogenital and related infections of chlamydial etiology.

Routes of transmission. Infection occurs sexually. Non-sexual transmission of chlamydial infection (via contaminated, infected hands, linen, etc.) has no significant epidemiological importance, although it must also be taken into account. A high frequency of chlamydial infection (over 50%) in newborns passing through infected birth canals has been clearly established, as well as intrauterine transmission of the infection.

Epidemiology and general pathology. Chlamydial infections were described many millennia ago. Data concerning them can be found in the Old Testament, as well as in ancient Chinese and ancient Egyptian sources, which predominantly refer to trachomatous conjunctivitis and trachoma. The first data on the Morphology of chlamydia (cytoplasmic inclusions) were obtained in 1907 with the discovery by Z. Halberstädter and S. Prowazek of the first representative of this group of microorganisms—the causative agent of trachoma. Soon, similar cytoplasmic inclusions were found in mucous membrane scrapings from eye infections in newborns, as well as in cervical infections in their mothers and non-gonococcal urethritis in men. In 1957, a culture of chlamydia was isolated from trachoma patients in China. Shortly thereafter, it was also obtained from genital secretions. Thanks to cell culture techniques, research on chlamydia began to develop at an accelerated pace.

In recent decades, interest in chlamydial infections, particularly urogenital ones, has noticeably increased. Data from foreign and domestic authors indicate that chlamydial infection is prevalent primarily among sexually active men and women, most frequently in individuals aged 20 to 40 years. There is a trend toward an increasing incidence among younger women, which is associated with Changes in the Sexual Behavior of this population group.

Since cases of urogenital chlamydial infection are not subject to mandatory registration with public health authorities, accurate epidemiological data on the prevalence of these diseases are still provided only by select centers.

Infection with *Ch. trachomatis* is currently likely the most frequent among Sexually Transmitted Infections. According to available data, in economically developed countries, one-third of the population is infected 2-3 times over the course of their lifetime. In Germany, about one million infected individuals are registered annually, compared to 4 million in the USA. Direct and Indirect costs associated with this, for example, in the USA, amount to 1.4 billion dollars, with 80% of this sum attributed to women. Chlamydiae are detected in 30-60% of all women with Gonorrhea, while gonococci are found in 20-40% of women diagnosed with a chlamydial infection. Among men with gonorrhea, 25-40% also test positive for chlamydia. The prevalence of urogenital chlamydial infection is approximately 4-6 times higher than that of gonorrhea.

The portal of entry for the infection is the human genitourinary system. A necessary condition for the onset of the infectious process is the penetration and multiplication of chlamydiae within the epithelial Cells of the genitourinary mucosa. Due to the pathogen's preferential tropism for columnar epithelium (in natural infection), the primary focus of infection typically develops in the Urethra of both men and women, as well as in the cervix, frequently serving as a source of ascending infection of the reproductive Organs and extragenital infections of various localizations.

Upon interacting with susceptible cells, chlamydiae act as active parasites, utilizing various virulence factors. Having penetrated the cell, viable chlamydiae exert their highly specific activity directed against the Lysosomes surrounding the phagocytic vacuole—a bounded area of the cytoplasmic membrane formed when the phagocyte engulfed the pathogen. Thus, chlamydiae neutralize the host cell's most critical defense mechanism, phagocytosis, thereby securing their ability to replicate further within the cytoplasmic inclusion of the host Organism's cells.

In the Pathogenesis of urogenital chlamydiosis, alongside the direct action of the pathogen on the infected epithelial cells lining the Urinary Tract, the damage to surrounding Tissues by hydrolytic lysosomal Enzymes released from infected cells during microbial Replication, and the Toxic effects of autolysis products from destroyed cells, the intrinsic toxic activity characteristic of all chlamydiae plays a significant role.

As the pathogen multiplies and exerts its pathogenic effects, a pathological process develops in the tissues, dynamically reflecting the scale of local and systemic defensive and compensatory Reactions of the host organism. Edema and mucosal hyperemia appear at the site of the primary lesion, accompanied by a compromised epithelial layer with partial epithelial desquamation, subepithelial and deeper lymphoid infiltration, inflammatory exudate formation, and functional impairment.

The localization, severity, and duration of these pathological manifestations, along with their sequelae, determine the clinical symptomatology and reflect The Nature and course of the infectious process. Urogenital chlamydial infection is rarely confined to the primary focus. The primary mechanism for expanding its "territory" involves the sequential involvement of the urogenital mucosal epithelium via ascending transcanalicular spread. While acknowledging the potential role of prior sensitization, particularly in ascending infections, it must be emphasized that the varying intensity of the pathological process during initial urogenital infection depends on the virulence of the infecting strain and the reactivity of the patient's immune system.

In both men and women, chlamydial infection most commonly manifests after an incubation period ranging from 5 to 30 days, potentially triggering a wide spectrum of pathologies. The primary reservoir of urogenital chlamydiosis is infected human urogenital organs, which serve as the natural habitat for these pathogenic microorganisms that typically replicate within columnar epithelial cells of the mucous membranes.

In men, the urethra is primarily affected, followed by secondary involvement of other organs (Prostate Gland, Seminal Vesicles, Epididymis). Chlamydial urethritis is the most prevalent manifestation, accounting for 35–60% of nongonococcal urethritis cases in men, with approximately 20% of these cases remaining clinically asymptomatic.

According to our data and observations by other researchers, chlamydial urethritis in men occurs in more than 60% of cases following casual sexual contact. Chlamydiae are isolated in 60–70% of patients with post-gonococcal urethritis developing after successful gonorrhea treatment.

Chlamydial urethritis frequently coexists with prostatitis, signs of which are detected in over 46% of patients during targeted examination. Furthermore, vesiculitis is diagnosed concurrently with chlamydial prostatitis in 15.7% of patients.

Chlamydial epididymitis is a frequent manifestation of urogenital chlamydiosis in men and may result from inadequate treatment of a chlamydial infection. According to several authors (A. Bruce et al., 1983) and our own clinical observations, a chlamydial etiology of acute orchiepididymitis was observed in 35–56% of patients across various age groups.

Delayed or insufficiently prolonged therapy frequently leads to Chronic Pyelonephritis, though the inflammatory process can also present acutely. The spread of infection from the Urinary Bladder to the renal pelvis through the ureteral lumen can occur due to impaired urinary dynamics and urine stasis within the bladder and along the entire length of the Ureters. Infection may also reach the renal pelvis via vesicoureteral reflux. When inflammation is present at the ureterovesical junction, a portion of the bladder contents can be forced back into the renal pelvis during bladder contraction.

Chlamydiae inhabiting the urogenital tract and causing local Inflammatory Diseases are also causative agents of oculogenital chlamydiosis, pneumonia, and other conditions. A direct link between chlamydial infections and reproductive dysfunction in both men and women has been firmly established.

Our research has demonstrated that 31.2% of men suffering from chlamydiosis experience sexual dysfunction (diminished erection or orgasm, premature ejaculation) and Infertility, accompanied by pronounced seminal pathology. Chlamydial epididymitis is frequently associated with oligo- and azoospermia. Chlamydiae can attach to spermatozoa and not only ascend into the fallopian tubes, causing tubal occlusion, but also reach the peritoneal cavity, leading to pelvic inflammatory disease and visceral involvement.

In our patients, chlamydiae served as the etiological and pathogenetic basis for several extragenital disorders, including ocular lesions (conjunctivitis), Joint Diseases (Reiter's Syndrome), Nervous system disorders (encephalitis), and Inner ear pathologies (cochlear neuritis, vestibular apparatus dysfunction), among others.

Currently, Ch. trachomatis is widely recognized as a major pathogen responsible for numerous obstetric and gynecological inflammatory diseases.

Chlamydiae can also induce inflammatory processes outside the reproductive tract, such as perihepatitis (Fitz-Hugh-Curtis syndrome), perisplenitis, and perinephritis in conjunction with salpingitis, pelviperitonitis, and other conditions. Chlamydiae are detected in 5–10% of patients in gynecological wards, 1–8% of pregnant women, and 20–30% of women presenting at outpatient clinics for sexually transmitted infections. As a rule, the prevalence of chlamydial infections is exceptionally high among women with multiple sexual partners. For instance, the incidence of chlamydial cervicitis among promiscuous women is 20–25 times higher than among women with a single mutually faithful sexual partner.

A high detection rate of chlamydia is observed in high-risk groups with frequent partner changes (39% in adolescent girls, 47% in pregnant adolescent girls), as well as in 30–40% of women suffering from nongonococcal urogenital inflammatory disorders. The course of the chlamydial process is frequently asymptomatic or paucisymptomatic. In infected women, the cervical canal is most commonly targeted, which can lead to ascending infection involving the Uterus, fallopian tubes, Ovaries, and Peritoneum. Chlamydiae account for up to 80% of all cases of infectious cervicitis. Frequently, patients with chlamydial cervicitis also harbor other microorganisms (gonococci, ureaplasmas), and bacterial vaginitis (Gardnerellosis, streptococcal, staphylococcal, etc.) may occur concurrently. A chlamydial etiology is identified in 12–60% of female patients presenting with nongonococcal inflammatory Diseases of the reproductive organs.

Chlamydial infection frequently affects the cervix and urethra simultaneously. Notably, more than 90% of women with positive urethral test results remain entirely asymptomatic. A low-lying external urethral meatus and a narrow Vagina—particularly in nulliparous women—create favorable conditions for primary infection, which is frequently compounded by chlamydial involvement of the paraurethral ducts and crypts. From the urethra, chlamydiae are capable of ascending into the bladder, causing cystourethritis.

The potential for chlamydiae to be transferred via cervical secretions to the rectum has also been documented. According to literature data and our own clinical observations, chlamydial proctitis is frequently clinically asymptomatic and is typically uncovered only through targeted laboratory screening.

Chlamydial infection can lead to endometritis and salpingitis, and may occasionally cause late Postpartum Endometritis. In cases of endometritis or salpingitis, chlamydiae can be detected in external genital secretions as well as during diagnostic laparoscopy. Chlamydiae are a frequent cause of salpingitis, accounting for up to 20% of all cases according to published data. However, because the Clinical symptoms of chlamydial salpingitis are non-specific and subtle, a significant number of cases likely remain undiagnosed.

Chlamydial infection localized in the female urogenital tract contributes to Pregnancy complications and serves as a source of various chlamydial infections in newborns. Infection of the reproductive tract in pregnant women holds significant epidemiological importance as a reservoir for perinatal infections. Intrapartum transmission to the newborn can occur, resulting in conjunctivitis in approximately 40% of cases and pneumonia in 15%. Infants may also develop otitis media or nasopharyngeal infections. Furthermore, maternal cervical chlamydial infection can trigger chorioamnionitis. The possibility of intrauterine transmission has also been definitively proven; such cases are associated with Premature Rupture of membranes, preterm birth, low birth weight, and increased rates of perinatal morbidity and infant mortality.

Oculogenital chlamydiosis in adults, presenting typically as follicular conjunctivitis, generally occurs As a result of transferring the pathogen from the urogenital tract to the eyes via contaminated hands or personal items (handkerchiefs, towels, etc.). Chlamydial eye infection frequently serves as the initial indicator of an asymptomatic urogenital infection in the patient or their sexual partner. The urogenito-ocular route of transmission can also occur in shared water bodies or through unconventional sexual practices. Direct eye-to-eye transmission from an infected person to a healthy individual is less common.

In sporadic Reiter's syndrome, chlamydiae are sexually transmitted, causing urogenital manifestations (urethritis, prostatitis, cystitis, epididymitis, vesiculitis, cervicitis, adnexitis, etc.), joint pathology, and occasionally self-limiting, transient conjunctivitis. The spread of chlamydiae from the urogenital tract to the joints is considered "metastatic," while joint pathology is closely linked to genetic predisposition. Biologically and antigenically, chlamydiae act as the primary triggers for this condition, often differing from the majority of urogenital strains isolated from uncomplicated urogenital infections.

Chlamydiae are not part of the normal human microflora. Their detection invariably indicates an active infectious process across various organs and systems of the body.

Currently, accumulating data point to a potential etiological role of chlamydiae in the pathogenesis of cardiovascular diseases, specifically atherosclerosis and myocardial infarction. Studies by several researchers (Z. Campbell et al., 1998) have shown that chlamydiae can colonize endothelial cells in structurally normal vascular walls across various vascular beds. Presumably, immune-mediated inflammation triggered by chlamydial antigens localized within the coronary artery walls can lead to rapid luminal narrowing and myocardial ischemia. The predominance of IgM responses and a high frequency of immune complexes containing antibodies in patients with acute myocardial infarction suggest a close pathogenetic link between this condition and an immune reaction to chlamydial antigens (I. I. Mavrov, A. P. Byelozorov, 2001).

Chlamydiae are established etiological agents for a wide array of diseases characterized by polymorphic clinical manifestations. They can cause otitis media, nasopharyngeal inflammation, and persistent esophageal inflammatory changes leading to esophagitis in both children and adults. In some cases, patients with complicated chlamydiosis exhibit clinical signs of Central Nervous System involvement—such as meningitis, meningoencephalitis, cranial and peripheral neuropathies—alongside symptoms of asthenia and somatogenic depression (chronic fatigue, irritability) (I. I. Mavrov, A. G. Kletnoy, 2001).

Urogenital chlamydiosis and its epidemiologically linked extragenital manifestations are characterized not only by overt symptoms but also by an asymptomatic course. For instance, asymptomatic chlamydial urethritis is detected during routine preventive screening in approximately 5% of seemingly healthy men. Similarly, asymptomatic cervical chlamydial infection, devoid of any clinical signs of cervicitis, is identified in 1–4% of women examined in control groups.

There is a certain correlation between marital status and the prevalence of urogenital chlamydial infection. Naturally, in the absence of behavioral risk factors such as promiscuity, married individuals have a reduced or limited exposure to sexually transmitted infections, including chlamydiosis. At the same time, unlike other nongonococcal urogenital infections, urogenital chlamydiosis does not always show a strict correlation with marital status.

Specialists do not share a consensus regarding The impact of factors such as contraceptives, the Menstrual cycle, and pregnancy on the multiplication rate of chlamydia and, consequently, on the clinical severity of urogenital chlamydiosis. At the same time, it is known that under experimental conditions, steroid hormonal preparations are capable of activating chlamydial infection. Oral contraceptive use between the 1st and 4th weeks of the menstrual cycle increases the frequency of chlamydia isolation from the cervix.

In our opinion, an important factor capable of influencing the activation and spread of chlamydial infection is mixed urogenital infections and various etioepidemiological combinations, which, much like their clinical manifestations, require further targeted study. Urogenital chlamydioses, including mixed infections, are defined in human infectious pathology by direct multifocal lesions of the Urogenital System and their consequences affecting reproductive function, as well as the potential hazard of becoming a source of chlamydial infections in other sites, particularly perinatal ones.

Of epidemiological interest are reports of chlamydiosis in prepubertal children—specifically urethritis in boys and vaginitis, cervicitis, and proctitis in girls—when sexual transmission has been ruled out and the source of infection has been identified. Such cases may result from a persistent infection acquired during the perinatal period, either through passage down infected birth channels or via intrauterine infection.

According to several authors, children born to mothers with chlamydia-infected genital tracts exhibited not only manifest forms of chlamydial conjunctivitis, nasopharyngitis, and pneumonia, which typically emerge shortly after birth, but also asymptomatic infections of various localizations. Subsequent monitoring of these infants over several months in the absence of clinical symptoms revealed chlamydia isolated from the eyes, nasopharynx, vagina, and rectum. Consequently, perinatal persistent chlamydial infection is likely the cause of subsequent urogenital inflammatory processes in adolescents in whom sexual transmission is not confirmed.

Natural, genetically determined Immunity to human chlamydial infection is absent. It is also evident that lasting immunity does not develop after recovery from the disease. The macroorganism's Immune Response varies across different forms of chlamydial infection. In clearly localized forms of urogenital infection with a limited spread of the inflammatory process, intensive antigenic stimulation of The Immune System by chlamydia is unlikely due to their low immunogenic activity. However, in response to urogenital tract infection by chlamydia, the macroorganism engages a series of cellular and humoral immunity mechanisms, also utilizing non-specific defense factors.

In most cases, the level of immune responses in this pathology is insufficient for complete suppression of reproduction and elimination of the pathogen, yet the immune mechanism limits the pathological process, frequently helping to establish a relative equilibrium between the infectious agent and the macroorganism (persistent infection), and in some instances, presumably ensures spontaneous recovery from the infection.

Clinical manifestations. The clinical course of urogenital chlamydiosis is highly diverse, ranging from acute to asymptomatic forms. In both men and women, chlamydia causes inflammatory lesions of the urogenital system that clinically resemble non-gonococcal and other inflammatory processes of the urogenital organs.

Urogenital chlamydial infection most frequently acquires a subacute, chronic, or persistent form, and less commonly causes acute inflammatory processes. The clinical picture of the disease depends on the time elapsed since infection, the Topography of the lesion, and the severity of local and systemic macroorganism reactions. These factors account for the variety of clinical manifestations of manifest forms of chlamydial infection, as well as its asymptomatic course.

Depending on the localization in men, chlamydial inflammation can affect the urethra, prostate gland, or epididymis; in women, it involves the cervical canal and other Regions of the Urogenital apparatus. In most cases, various Organs of the urogenital system are affected simultaneously.

Individuals with urogenital chlamydial infection can be divided into several groups. Patients with acute chlamydiosis typically present with hyperemia of the urogenital mucous membranes and mucopurulent discharge from the urethra or vagina. In some cases, frequent urges to urinate are noted. In patients with an inert and protracted disease course, these symptoms are significantly milder, but mucopurulent discharge is always present. As a rule, these patients seek medical attention on their own initiative.

There are individuals who lack clinical symptoms, observe no discharge from urogenital organs, and report no other Complaints. Upon the most thorough Clinical examination of the urogenital apparatus, changes are generally undetected. Chlamydia is discovered in these individuals solely through laboratory testing, representing cases of chlamydial infection carriage.

A distinction is made between primary chlamydial infection and recurrent infection (reinfection). In the majority of patients, chlamydiosis occurs in combination with other diseases (such as gonorrhea or Trichomoniasis).

Certain specific features regarding the manifestations, course, and spread of chlamydial infection, as well as The Development of complications, necessitate a separate examination of urogenital chlamydioses in men, women, and children.

Diagnostics

Due to the similarity of clinical manifestations of inflammatory processes in the urogenital system of various etiologies, as well as the frequency of mixed infections in the same localization, gonorrhea, trichomoniasis, and mycoplasmosis must first be ruled out. Laboratory investigations are a crucial component of the comprehensive examination of patients. They are used to establish the etiological Diagnosis, determine treatment tactics, evaluate the effectiveness of etiotropic therapy, and carry out epidemiological surveillance.

Currently, Laboratory Diagnosis of urogenital chlamydiosis involves the indication (detection) of chlamydia directly within infected cells, the Isolation of the pathogen, and the detection of chlamydial antibodies.

Indication of chlamydia directly in infected cells. This method involves detecting cytoplasmic inclusions formed by chlamydia through the staining of the microorganism's morphological structures. The test material consists of scrapings from accessible mucous membranes of the urogenital organs (urethra, cervix, cervical canal, etc.) and other organs (such as the conjunctiva and rectum) in extragenital forms of chlamydial infection. Smear-imprints of discharges, secretions, and tissues obtained during surgical interventions are investigated less frequently.

Determination of the morphological structures of microorganisms. Detecting chlamydial cytoplasmic inclusions in epithelial cells from preparations stained using the Romanowsky-Giemsa method is a classical diagnostic approach for chlamydioses.

Cytoplasmic inclusions are compact or loose granular masses containing morphological structures of the pathogen at various stages of its reproduction. They are frequently identified near the nucleus, often displacing it to the cell periphery, and exhibit a diverse shape, differing in color and internal Structure from the nucleus and cytoplasm. Small early inclusions containing large bodies 0.5-1.2 µm in diameter stain blue-purple, whereas large inclusions with predominantly small mature pathogen structures stain pink-red. Frequently, chlamydial inclusions of varying maturity and density are found within a single cell. When the microorganism's morphological structures are dispersed, a vacuole containing them becomes visible.

To avoid diagnostic errors, cytoplasmic inclusions must be clearly differentiated from other structural entities that may appear in the studied preparations. These include black or dark green pigment granules, sometimes appearing in the nucleus cytoplasm as granular masses: granular structures of traumatized nuclei that resemble the nuclear material of undamaged cells in color, shape, and size; mucin grains that stain red or blue and lie separately from one another in the cytoplasm; eosinophilic granules of destroyed eosinophils located individually or On the surface of epithelial cells; diffuse eosinophilic multidimensional cytoplasmic granularity; cellular detritus adsorbed onto the surface or phagocytosed by an epithelial cell; and accompanying microflora, which often includes gonococci, streptococci, pneumococci, diphtheroids, and other microorganisms typically found not only on The surface of epithelial cells but also in other areas of the preparation.

The detection of cytoplasmic inclusions in scraping preparations allows for the diagnosis of roughly 10-15% of all chlamydial infection cases running both a manifest and asymptomatic course.

Detection of microorganism antigens. The direct fluorescent antibody method is used to diagnose urogenital chlamydial infection; it is based on the classical work of Coons and Kaplan (1950) and is widely employed in diagnosing many viral and bacterial infections. Its essence lies in combining fluorochrome-labeled antibodies with a specific antigen and observing the reaction product under a luminescent Microscope.

The detection of chlamydial cytoplasmic inclusions in epithelial cell scraping preparations using fluorescent antibodies is a highly sensitive and specific diagnostic method for urogenital chlamydial infection. To prevent diagnostic errors, high-quality Reagents must be used, along with proper control and rigorous evaluation of results.

The fluorescent antibody technique for detecting chlamydial antigens within cytoplasmic inclusions is applied in direct and indirect modifications. The direct immunofluorescence assay (DFA) requires a fluorescent chlamydial antisera, whereas the indirect immunofluorescence assay (IFA) requires human or animal serum containing chlamydial antibodies along with a corresponding species-specific fluorescent antiserum.

Enzyme-linked immunosorbent assay (ELISA) is utilized to detect chlamydial antigens in the test material. Its diagnostic sensitivity is 92%, and its Specificity is 94%.

Immunological Methods are used to detect chlamydial antibodies via enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination assay (IHA), indirect immunofluorescence assay (IFA), and Complement fixation test (CFT).

Molecular biological Research Methods demonstrate high diagnostic accuracy. Polymerase Chain Reaction (PCR) exhibits high sensitivity (95-97 %) and specificity (95-98 %).

Immunochromatographic rapid tests have been developed and are widely used (test duration ranges from 10 to 30 minutes). These include the "Chlamydia Stat-Pak assay" (Chemo Diagnostic Systems, USA) and "Chlamydia-Check 1" (Veola-Lab., France). However, their sensitivity and specificity are significantly lower than those of traditional test systems.

Diagnostic isolation of chlamidia. The diagnosis is confirmed by isolating the causative agent. These methods require specialized equipment and appropriately qualified personnel.

Diagnostic isolation of chlamidia in urogenital chlamydial infection is performed using epithelial cells from the yolk sac membranes of developing chicken embryos and in cell culture.

The critical conditions for obtaining accurate results include reliably freeing the test material from accompanying bacterial flora and preventing the inactivation of chlamidia during TRANSPORT AND STORAGE. This is achieved by treating the samples with antibiotics that do not affect the viability of chlamidia while exerting a bactericidal effect on the accompanying microflora, as well as by using transport media, low temperatures, and minimizing the time between sample collection and inoculation into chicken embryos or cell culture.

Chlamidia are isolated more successfully (especially when infecting chicken embryos) from heavily infected primary material obtained from patients who have not received antichlamydial therapy. Nevertheless, these methods provide valuable diagnostic information even in chronic and asymptomatic forms of chlamydial infection.

Isolation of chlamidia in chicken embryos. For a long time, isolation in 6-8-day-old developing chicken embryos inoculated via the yolk sac was the only reliable method for the etiological diagnosis of chlamydial infections, and it remains a highly specific diagnostic method for urogenital chlamydial infection, its extragenital manifestations, and lymphogranuloma venereum.

In terms of sensitivity, this method is comparable to diagnostic chlamidia isolation in cell culture and slightly inferior to the fluorescent antibody technique used to detect microorganism antigens in infected cells (A. A. Shatkin, 1979; V. R. Martinova et al., 1979; Schachter et al., 1970, 1978, etc.).

The Criteria for the diagnostic isolation of chlamidia are the presence of the microorganism's morphological structures and the presence of genus-specific antigen. Specific embryo mortality is typically observed in subsequent passages.

This method is labor-intensive and time-consuming (ranging from 7-12 days to 3-4 weeks, accounting for 2-3 blind passages), which limits its Practical Application given the availability of rapid Methods for the etiological diagnosis of the infection. At the same time, it is widely used to establish the chlamydial etiology of various pathologies, to obtain laboratory cultures of chlamidia, and in various scientific studies.

Isolation of chlamidia in cell cultures. Most Representatives of the species Ch. trachomatis, with the exception of the causative agent of lymphogranuloma venereum, are unable to infect cells and multiply in various cell cultures under standard conditions. This circumstance long restricted The Use of cell culture methods for diagnosing urogenital chlamidiosis and chlamidiosis of other localizations. This limitation has been overcome through additional methodological techniques that enhance microorganism adsorption onto the cell surface, activate its uptake by the cell, and suppress the cell's normal metabolism. For this purpose, widely used techniques—either independently or in various combinations—include centrifuging the infectious material onto a cell monolayer, irradiating cells with X-rays, treating the cell monolayer with DEAE-dextran (an oligosaccharide that promotes macromolecule uptake), or treating cells with 5-iodo-2-deoxyuridine or cycloheximide (antimetabolites with cytostatic activity).

Currently, McCoy, HeLa-229, and L-929 cells are most frequently used for the diagnostic isolation of chlamidia from the urogenital organs.

Urogenital chlamidiosis in men

Chlamydial urethritis (urethritis chlamydialis). In men, it typically follows a chronic course, though acute and subacute forms also occur. The onset of the disease and the subsequent inflammatory process are, in most cases, characterized by subtle subjective symptoms. The most frequent signs of the disease include discomfort, itching, urethral pain, frequent urges to urinate, and urethral discharge. When the urethra and other organs are affected simultaneously, patients also complain of pain in the scrotal, perineal, and anal regions, in the lumbar and sacral areas, along the sciatic nerve, and in the lower extremities.

The most typical symptom of urethritis is mucous, mucopurulent, or purulent urethral discharge. In acute cases, the discharge flows freely or appears upon pressing the canal. In most patients with an acute or subacute onset, The amount of discharge decreases within a few days. Chlamydial urethritis with mild subjective complaints is usually accompanied by very scanty discharge in the form of a "morning drop." Often, discharge appears after prolonged urine retention, sometimes during defecation or at the end of urination.

Typically in chlamydial urethritis, when urethral discharge is scant, the urine in the First and Second portions remains clear, containing single or multiple mucopurulent threads. When discharge is abundant, the urine appears cloudy in the first or both portions.

Patients exhibit varying degrees of inflammation of the urethral Lips (hyperemia, pastosity, agglutination). Signs of inflammation can frequently be detected in the paraurethral ducts as well.

Chlamydial paraurethritis (paraurethritis chlamydialis). The paraurethral ducts (paraurethral glands) serve as a reservoir for chlamidia and a source of reinfection for both the patient and a healthy sexual partner. Paraurethritis rarely causes subjective complaints, but it poses an epidemiological risk. Detecting it is an important objective of clinical examination.

Urethroscopy reveals no specific mucosal changes in the urethra characteristic of chlamydial infection. Patients typically present with a soft infiltrate, residual signs of a soft infiltrate, a transitional infiltrate, and littritis. In isolated cases, a hard infiltrate may develop. Limited granulations and lesions of the seminal colliculus are frequently detected in the prostatic urethra.

The inflammatory process may also involve the Bulbourethral Glands. Chlamydial cowperitis often causes no subjective sensations, though patients occasionally complain of periodic pain in the Perineum and thighs. In such cases, the Bulbourethral gland is typically palpated as a dense, pea-sized nodule.

Chlamydial prostatitis (prostatis chlamydialis) runs a chronic, torpid course with periodic exacerbations. Acute inflammation of the prostate gland is extremely rare. As a rule, patients complain of urethral discharge—sometimes occurring during defecation (defecatory prostatorrhea) or at the end of urination (Micturition prostatorrhea)—vague discomfort, itching in the urethra and rectum, and intermittent pain in the perineum, Scrotum, groin, suprapubic region, sacral area, and along the sciatic nerve. Some patients note the sticking together of the lips of the external urethral meatus following prolonged urine retention. Frequency of urination may increase, sometimes at night. Urine in the first and second portions is most often clear, containing admixtures of mucous or mucopurulent threads and flakes, though it is sometimes cloudy in the first or both portions.

Based on the nature and severity of the chlamydial lesion in the prostate, catarrhal, follicular, and parenchymatous prostatitis are distinguished. During digital rectal examination in catarrhal prostatitis, the prostate is not enlarged, has a normal consistency, and is tender. In catarrhal prostatitis, the ducts of adjacent glandular lobules of the prostate are inflamed, and their lumens contain significant amounts of leukocytes, mucus, and desquamated epithelium.

When the inflammatory process encompasses individual lobules of the glandular parenchyma, follicular prostatitis develops. In these cases, the prostate is likewise not enlarged, but Palpation reveals tender and occasionally firm nodules of varying sizes.

A significant enlargement of the entire gland or one of its lobes, along with changes in its configuration and consistency in parenchymatous prostatitis, is determined by palpation. In this condition, the prostate gland is typically firm and tender.

Chlamydial prostatitis accompanied by posterior urethritis may develop insidiously. In some cases, prostatitis can be diagnosed solely through microscopic examination of prostatic secretions, which reveals elevated leukocyte counts and, quite frequently, chlamydiae. Patients typically report frequent urination, sometimes accompanied by terminal Hematuria. Aside from mild burning or a tickling sensation in the perineum, a slight feeling of pressure in the rectal area, and frequent nocturia, there are usually no other clinical signs of prostatitis.

It is important to bear in mind that prostatitis may also be caused by a mixed infection involving chlamydia alongside other pathogens (such as gonococci, Mycoplasmas, trichomonads, viruses, or other bacteria).

Chlamydial vesiculitis (vesiculitis chlamydialis) generally accompanies prostatitis or epididymitis. Inflammation of the seminal vesicles can be bilateral and is typically characterized by mild symptoms. Patients complain of discomfort and pelvic pain, a feeling of fullness in the perineum, and dull pain radiating to the sacrum, groin, or testicles. Urination may be accompanied by discomfort, though frequency is not increased. Chlamydial vesiculitis is typically chronic. Digital rectal examination reveals swollen seminal vesicles that are slightly tense and tender upon palpation.

A chronic, torpid course of the disease is characterized by weak erections, premature ejaculation, spermatorrhea, general malaise, lethargy, apathy, and other symptoms. Much like inflammation of the prostate gland, involvement of the seminal vesicles is frequently caused by mixed infections, such as chlamydial-gonococcal, chlamydial-mycoplasmal, or chlamydial-trichomonal coinfections.

Chlamydial epididymitis (epididymitis chlamydialis) most commonly develops against the background of a primary urethral infection, as well as prostatitis and vesiculitis. Chlamydiae spread to the epididymis via a canalicular route, damaging the epithelium lining the lumen of the vas deferens. Occasionally, signs of deferentitis and funiculitis are also observed. The inflamed vas deferens can be palpated as a slightly tender cord-like structure. In cases of funiculitis, the Spermatic Cord is thickened and tender upon palpation.

Epididymitis caused by chlamydiae can present in acute, subacute, and chronic forms. The chronic form may occur either as an independent manifestation of a chlamydial infection or as a consequence of an acute or subacute inflammatory process.

The inflammatory process may extend to the tunica vaginalis or involve the entire testicle, leading to orchiepididymitis. Acute orchiepididymitis presents with Asymmetry, Swelling of the hyperemic and warm scrotum on the affected side, which is exquisitely tender upon palpation. The enlarged half of the scrotum contains an extremely tender, oval-shaped mass, usually with a uniformly tense surface that gives a false sense of fluctuation.

In patients with torpid unilateral orchiepididymitis combined with prostatitis, vesiculitis, and deferentitis, sexual potency is frequently impaired, and spermogram abnormalities are detected.

Urogenital Chlamydiosis in Women

Chlamydial urethritis (urethritis chlamydialis) frequently affects the cervix and urethra simultaneously. More than 90% of women with positive culture results from urethral specimens remain entirely asymptomatic. When the infection does lead to urethral syndrome, chlamydial urethritis is accompanied by mild subjective complaints. Patients may experience urethral itching, pain at the onset of urination, and occasionally urinary urgency. Mild irritation of the external urethral meatus is observed without spontaneous discharge; however, scant, predominantly mucous, nearly colorless secretions can be obtained following urethral massage. These symptoms are generally short-lived, yet in the majority of patients examined during remission, urethroscopy reveals structural changes in the urethral mucosa, such as soft infiltration, residual signs of soft infiltration, and coarse mucosal folds.

Chlamydial paraurethritis and vulvitis (paraurethritis chlamydialis; vulvitis chlamydialis). Chlamydial urethritis is most frequently accompanied by paraurethritis of the same etiology. A chronic inflammatory process in the paraurethral ducts is indicated by hyperemia of their openings and the presence of mucous or mucopurulent discharge that can be expressed as a droplet.

The Vestibule of the vagina may also be involved in the chlamydial pathological process, with a predilection for the area around the external urinary meatus or between the Clitoris and urethra. Subjective symptoms in patients are generally mild, most commonly presenting as itching or burning in the external genitalia. When pressure is applied laterally to chlamydia-infected folds, mucous secretions are released.

Chlamydial bartholinitis (bartholinitis chlamydialis). In this condition, symptoms are mild and non-specific. Patients report secretions and periodic itching of the external genitalia.

Because chlamydiae proliferate within the surface columnar epithelium of the excretory ducts of Bartholin's glands, a characteristic sign of duct involvement is a pea-sized hyperemic spot with a dark red dot in the center, corresponding to the opening of the gland's excretory duct. Palpation of the inflamed Bartholin gland allows a drop of slightly turbid mucus to be expressed from the duct opening. When obstructed, the excretory duct transforms into a large cyst filled with clear fluid. In some cases of chlamydial bartholinitis, the surrounding tissue becomes involved in the inflammation, resulting in a painful infiltrate located laterally near the vaginal introitus.

Chlamydial vaginitis (vaginitis chlamydialis) is a rare manifestation of chlamydial infection and virtually never occurs in women with normal hormonal levels. Chlamydiae do not multiply within the normally functioning, keratinized stratified squamous epithelium of the vagina and, in an extracellular state, are highly sensitive to the acidic environment of vaginal secretions. Chlamydial vaginitis may develop in children (vulvovaginitis), elderly women, and during pregnancy, when Structural and functional changes in the epithelium occur due to specific hormonal shifts.

Secondary chlamydial vaginitis accompanies Endocervicitis and arises as a result of the macerating effect of cervical canal secretions, as well as other contributing factors, such as trauma or decreased estrogenic activity.

Chlamydial cervicitis (cervicitis chlamydialis). The symptoms of chlamydial cervicitis are non-specific and mild. Patients occasionally report a sensation of moisture in the genital area and a feeling of pelvic heaviness with mild lower back pain during menstruation. Clinically, it manifests as scant cervical discharge, observed in only 60% of cases. Additionally, intermenstrual bleeding, itching, and dysuria are sometimes noted as associated symptoms.

Chlamydial infection is more prevalent in women with cervical ectropion. During colposcopy, some researchers have identified a typical edematous-exophytic-follicular form of cervicitis, confirmed by cytologic and histologic analysis. Chlamydial infections are associated with an increased frequency of dysplastic changes in the cervical epithelium; however, the carcinogenic potential of chlamydiae has not been proven.

The inflammatory process within the cervical canal—where chlamydiae proliferate within the columnar epithelium—is accompanied by cervical secretions, typically mucopurulent in nature. These secretions cause maceration of the stratified squamous epithelium of the vaginal portion of the cervix, leading to its partial desquamation. The cervix becomes edematous and hyperemic, erosions form around the external os, and an ectopia of the columnar epithelium extending from the canal is observed. Prolonged chlamydial cervicitis can lead to hypertrophic erosions. In some cases, millet-sized vesicles containing turbid fluid appear in the area of the os.

Chronic chlamydial infection of the cervix may also present with signs of non-specific inflammation, which do not necessarily involve the formation of hypertrophic erosions, lymphoid follicles, or mucopurulent discharge. In certain patients with persistent chlamydial infection of the cervical canal, the pathogen can be detected despite the complete absence of clinical signs of the disease at the time of examination.

Chlamydial endometritis and salpingitis (endometritis chlamydialis, salpingitis chlamydialis). Chlamydial infection can ascend the reproductive tract, involving the endometrium. This leads, notably, to late postpartum endometritis.

Clinically, chlamydial endometritis presents similarly to endometritis of other etiologies, accompanied by general malaise, fever, lumbosacral pain, lower abdominal pain, and menstrual irregularities. Mucopurulent cervical discharge is typically observed. A chronic course of inflammation with subsequent involvement of the fallopian tubes is also possible.

Chlamydial salpingitis is quite common in urogenital chlamydiosis. Chlamydiae spread sequentially from the cervical canal into the uterine cavity and reach the fallopian tubes, provoking an inflammatory process that affects the mucosal, muscular, and serosal layers.

As with gonorrhea, chlamydial infection frequently leads to bilateral involvement of the fallopian tubes. When the infection spreads through the abdominal ostium of the fallopian tube, the Ovary is typically drawn into the inflammatory process.

There is no classic clinical picture of chlamydial salpingitis: mild lower abdominal pain accompanied by low-grade fever, alongside subtle findings regarding the uterine adnexa during pelvic examination, are more indicative of a chlamydial infection than any other etiology. Blood tests rarely show leukocytosis, whereas an elevated ERYTHROCYTE SEDIMENTATION RATE (ESR) is much more common. The disease tends to follow an indolent course.

Virtually every case of salpingitis is accompanied by cervicitis. In contrast to the subtle Clinical presentation of the disease, diagnostic laparoscopy reveals distinct pathological changes in the fallopian tubes. These often lead to infertility and Ectopic Pregnancy. In such cases, Chlamydia are directly detected in smears obtained from closed fallopian tubes. This likely confirms that the infection ran an asymptomatic or mildly symptomatic course, going unnoticed by the patient, which prevented timely diagnosis and appropriate treatment.

It is currently considered proven that chlamydial salpingitis may also affect other organs, resulting from both the canalicular spread of the infection through the abdominal opening of the fallopian tubes and the successive involvement of all layers of the tube wall followed by the peritoneum. It is hypothesized that chlamydial salpingitis leads to tubal occlusion; however, the exact incidence of such complications remains to be established. Presumably, any form of this disease can result in the ectopic implantation of a fertilized ovum, leading to intrauterine fetal demise.

Chlamydial salpingo-oophoritis (salpingoophoritis chlamydialis). The most common symptoms of the disease include a dull aching pain in the lower abdomen and lumbosacral region, which intensifies with tension of the abdominal wall, and intermenstrual bleeding. In some patients, body temperature rises to 37–37.5 °C. According to the literature, In addition to superficial ovarian lesions that cause adhesions to surrounding tissues and organs, the inflammatory chlamydial process can also extend deep into the ovarian parenchyma, damaging its internal structure.

Chlamydial Pelvioperitonitis (pelvioperitonitis chlamydialis). This develops as a complication of salpingitis and salpingo-oophoritis. Besides the urogenital peritoneum, other peritoneal areas may also be involved. Laparoscopy and precise etiological diagnosis have established a frequent association between acute chlamydial Peritonitis and acute fibrinous perihepatitis, referred to by some authors as Fitz-Hugh-Curtis syndrome.

In the acute stage of the disease, against the background of symptoms characteristic of salpingitis, there is a sudden onset of sharp pain initially localized in the lower abdomen. Patients exhibit abdominal Muscle guarding, fever (up to 38–40 °C), tachycardia, marked leukocytosis, and an elevated ESR. Constipation and flatulence are also frequently observed.

There is no doubt that chlamydial pelvioperitonitis is a frequent yet insufficiently studied complication of salpingitis and salpingo-oophoritis. Cases of chlamydial salpingitis, peritonitis, and ascites following therapeutic abortion or appendectomy have been described as a result of the reactivation of a subclinical urogenital infection.

Urogenital Chlamydiosis in Children

Physicians often overlook inflammatory diseases of the urogenital organs of chlamydial etiology in children, yet they are by no means rare.

Transmission can occur vertically (intrauterine), during the passage of the newborn through the mother's chlamydia-infected birth canal, and subsequently through poor hygiene and household contact (shared bedding, toiletries, etc.), as well as through sexual contact in adolescents with urogenital chlamydiosis.

According to literature data, the overall percentage of infants infected with intrauterine chlamydial infection reaches 6.3–9.8%. Between 30% and 70% of children are infected during passage through the birth canal, and 10–20% of them develop pneumonia and conjunctivitis (V. I. Cherepova, 1988; D. I. Hess, 1993).

Infection of the vagina frequently occurs in newborn girls born to mothers with chlamydial cervicitis. Vulvovaginitis of chlamydial origin is observed in both early childhood and older children, often concurrently with ophthalmochlamydiosis. We have diagnosed vulvovaginitis in girls aged 3 to 14 years without any indication of chlamydial infection at other anatomical sites.

Analysis of the available data suggests that urogenital Chlamydial infection in children can remain asymptomatic for a prolonged period, becoming activated under The Influence of various factors, including other pathogenic agents.

In the manifest course of postgonococcal chlamydial urethritis in boys, mucosal or mucopurulent urethral discharge appears, along with erythema and edema of the external urethral meatus, as well as mild dysuria. Most commonly, manifest chlamydial infection in girls is localized in the external genitalia and vagina, and less frequently in the urethra and rectum. Occasionally, the endocervical canal is involved in the inflammatory process.

The clinical symptoms of chlamydial infection in girls involving the external genitalia and vagina do not differ from the known manifestations of other inflammatory processes at the same sites. In pronounced vaginitis, erythema of the mucosa of the external genitalia is noted, along with mucous, mucopurulent, or purulent vaginal discharge that becomes profuse upon pressure on the perineum or lower abdomen. The inflammatory process also affects the vaginal vestibule and hymen, manifesting as erythema and tenderness. Mildly symptomatic chlamydial vaginitis is characterized by remissions and exacerbations.

Several studies on vulvovaginitis in premenarchal girls (R. Bump, 1987; D. I. Mavrov, 1988) have established that *Chlamydia* are frequently the cause of postgonococcal vulvovaginitis. Furthermore, in children with recurrent vulvovaginitis typically unresponsive to traditional therapy, *Chlamydia* were identified in 47% of examined cases as the sole pathogens. Specific etiotropic anti-chlamydial treatment led to the eradication of the causative agent, and the symptoms of vulvovaginitis resolved.

It must be specifically emphasized that in all cases, specimens for examination were collected from the vagina rather than the infantile uterine cervix. Evidently, *Chlamydia* are capable of infecting the atrophic squamous epithelium of the prepubertal vagina, which has not yet been exposed to estrogen influence, and causing true vaginitis. This situation differs significantly from that in adult women, in whom The Effect of estrogens on the reproductive organs is quite pronounced. In such cases, *Chlamydia* exhibit a tissue tropism for columnar epithelium, and lower genital tract infection is confined to the cervix. Such hormone-dependent localization of infection in the female reproductive tract is also generally accepted for gonococci.

Therefore, chlamydial infection must be ruled out in every child presenting with vulvovaginitis. This primarily applies to patients with gonococcal vulvovaginitis, as chlamydiosis accompanies gonorrhea in 27–33% of such cases (R. Bump, 1987). Since chlamydial infections have now surpassed gonorrhea in prevalence among Sexually Transmitted Diseases, The problem of diagnosing chlamydiosis not empirically, but on The basis of laboratory testing, becomes increasingly evident.

If a child is diagnosed with chlamydial vulvovaginitis, the source of infection must invariably be identified. Although perinatal infection of the newborn's eyes and rectum, followed by prolonged carriage of *Chlamydia* in these organs and subsequent autoinfection of the genitalia, is possible, a diagnosis of chlamydial vulvovaginitis in a child should raise suspicion of sexual abuse.

To date, the detection of *Chlamydia* in the anogenital area as a potential "marker" of child sexual abuse has been well-documented. Specifically, *Chlamydia* have been detected in 4–6% of girls who experienced sexual abuse, even though none of them exhibited symptoms of vulvovaginitis. In such cases, the presence of *Chlamydia* assists in establishing the fact of sexual abuse.