Pathogenesis of purulent gynecologic diseases

Currently, inflammatory diseases of the pelvic organs have a multimicrobial origin, and are based on a complex interaction between synergistic infectious agents.

The female body, unlike the male, has an open abdominal cavity, which communicates with the external environment through the vagina, cervical canal, uterine cavity and fallopian tubes, and under certain conditions, infection can penetrate into the abdominal cavity.

Two variants of pathogenesis are described: the first is ascending infection with flora from the lower parts of the genital tract, the second is the spread of microorganisms from extragenital foci, including from the intestines.

Currently, the prevailing theory is about the ascending (intracanalicular) route of infection.

Damaged tissues (micro- and macrodamage during invasive interventions, operations, childbirth, etc.) are the entry points for infection. Anaerobes penetrate from adjacent ecological niches of the mucous membranes of the vagina and cervical canal, and also partly from the large intestine, external genitalia, skin; they multiply, spread and cause the pathological process. The ascending route of infection is also characteristic of other forms of microorganisms.

In the presence of an IUD, microorganisms can also spread by the capillary effect along the threads hanging in the vagina. Pathways for the spread of strict anaerobes by sperm or trichomonads have been described, in which case they relatively easily enter the uterus, fallopian tubes, and abdominal cavity.

According to research data, chlamydia from the cervical canal penetrate into the mucous membrane of the uterine body and intracanalicularly from the endometrium into the fallopian tubes. In the presence of cervicitis, chlamydia were detected in the endometrium of 41% of patients, in the presence of salpingitis - in 21% of cases, while clinical manifestations of endometritis in women were either absent or weakly expressed.

Based on ultrastructural studies, the experiment suggested that severe mucus accumulation accompanied by edema and loss of ciliary epithelium plays a major role in tubal damage resulting from Chlamydia trachomatis infection.

In complicated forms of inflammation and unfavorable course of the process, researchers especially often isolated C. trachomatis from the fallopian tubes, from where it was isolated together with Escherichia coli and Haemophilus influenzae as part of a polymicrobial infection. Based on this, the authors conclude that C. trachomatis can be considered as a "means of advancement" in cases of complicated and severe infection.

It is indicated that the formation of tubo-ovarian abscesses currently occurs as a result of secondary invasion of C. trachomatis after primary lesion of the fallopian tube and ovary by gonococcus. It distinguishes two phases of such lesion: the first is lesion of the fallopian tube with its occlusion, the second is secondary infection of the tube against the background of existing changes.

The specific pathogens may later be joined by the endogenous flora of the lower genital tract - gram-positive and gram-negative aerobic bacteria, as well as anaerobes, which leads to the progression of the disease and the appearance of complications of the purulent process.

The experiment showed that Tumor-Necrosis-Factor (TNF), released mainly by macrophages when exposed to Chlamydia trachomatis, is an essential component of the pathogenesis of inflammation.

TNF (cytokines) were found by FM Guerra-Infante and S. Flores-Medina (1999) in the peritoneal fluid of patients with acute inflammation, with the most frequently isolated microorganisms being Chlamydia trachomatis.

In the mechanism of damage to the endothelium of the fallopian tubes by gonococci, PA Rice et al. (1996) attribute a place to lipooligosaccharides and pentidoglycans. These amines also stimulate chemotaxis of polymorphonuclear leukocytes, the metabolites of which can damage tissue. The authors emphasize that more attention should be paid to the study of immunological mechanisms of inflammation development. LSvenson (1980) believes that N. gonorrheae causes damage to epithelial cells and is more virulent than C. trachomatis.

Immunopathological disorders during inflammation development are an extremely complex and dynamic process. The disorders are generally presented as follows: at the beginning of an acute bacterial or viral inflammatory process, the main role belongs to cytokines (some interleukins, interferons, TNF - tumor necrosis factor and others), as well as polysaccharides and muramylpeptides of the bacterial wall, which are non-specific activators of B-lymphocytes and plasma cells. Therefore, in the first 1-2 weeks from the beginning of the generalized infectious process, polyclonal activation of the B-cell link is observed, accompanied by an increase in the serum content of antibodies of different classes and very different antigen specificity, including due to a pathological increase in the synthesis and secretion of numerous autoantibodies.

After 7-10 days or more from the onset of the disease, specific immune reactions (production of antibodies to the pathogen and its waste products) and antigen-specific T cells begin to play a major role. As the acute infectious process subsides, there is usually a gradual decrease in the production of heteroclonal antibodies and a simultaneous increase in the production (titers) of antibodies to specific antigens of the infectious agent. At first, an increase in the synthesis of specific antibodies of the Ig M class is observed, which after another 2 weeks is replaced by the synthesis of antibodies of the Ig G class of the same antigen orientation. Specific antibodies contribute to the elimination of the pathogen from the body mainly due to the mechanisms of opsonization, activation of the complement system and antibody-dependent lysis. At the same stages, activation and differentiation of antigen-specific cytotoxic T lymphocytes occurs, ensuring the selective destruction of the body's own cells containing pathogens. The latter is achieved either by launching a genetically determined cell death program (apoptosis), or by the release of cytolytic factors by T-lymphocytes and natural killers that damage the membranes of those cells in the body on which the presentation of fragments of pathogen antigens occurs.

After the acute period is over, the disease may become chronic, sluggish, with erased symptoms, or clinical recovery occurs, accompanied by complete elimination of the infectious agent. However, most often, the pathogen persists in the host organism against the background of the establishment of new, nearly neutral relationships between the micro- and macroorganism. The latter is typical for almost any human virus (with very rare exceptions), as well as for many non-viral forms of microflora such as chlamydia, mycoplasma, etc. The corresponding phenomena manifest themselves in the form of persistent or latent infection and are relatively rarely accompanied by reactivation of the infectious pathology.

The survival of microorganisms in the conditions of a constantly operating system of immunological surveillance requires sophisticated tactics of escaping from the control of the host immune system. This tactic is based on the use of a number of adaptive mechanisms that allow, firstly, to carry out generalized inhibition of immunity, the intensity of which becomes insufficient for the elimination of the pathogen, secondly, to include some additional mechanisms that allow the microorganism to remain "invisible" to the effector mechanisms of immunity, or to induce their tolerance, and, thirdly, to distort the immune reactions of the host organism, reducing their antimicrobial activity. The strategy of microorganism persistence necessarily includes, on the one hand, general immunosuppression (of varying degrees of severity), which can be lifelong, and on the other hand, leads to a distortion of the effector links of immunity.

Endosalpingitis is morphologically characterized by the presence of an inflammatory infiltrate, consisting mainly of polymorphonuclear leukocytes, macrophages, lymphocytes, plasma cells, and, in the case of abscess formation, purulent bodies.

The inflammatory process of the mucous membrane of the tube (endosalpingitis) spreads to the muscular membrane, where hyperemia, microcirculation disorders, exudation occur, perivascular infiltrates and interstitial edema are formed.

Next, the serous covering of the tube (perisalpingitis) and the covering epithelium of the ovary (perio-oophoritis) are affected, and then the inflammation spreads to the peritoneum of the small pelvis.

The ovary is not always involved in the inflammatory process, since the germinal epithelium covering it serves as a fairly powerful barrier to the spread of infection, including purulent infection.

However, after the rupture of the follicle, its granular membrane becomes infected, purulent oophoritis occurs, then pyovar. As a result of the gluing of the fimbriae and the development of adhesions in the ampullar part of the tube, saccular "tumors" with serous (hydrosalpinx) or purulent (pyosalpinx) contents arise. Inflammatory formations in the ovaries (cysts, abscesses) and the hydrosalpinx and pyosalpinx that merge with them form the so-called tubo-ovarian "tumor", or inflammatory tubo-ovarian formation.

The chronicity, progression and periodic exacerbation of the inflammatory process occur against the background of disintegration of the muscle tissue of the fallopian tubes, as well as deep functional and structural changes in the vessels of the uterine appendages up to the development of adenomatous proliferation.

When hydrosalpinx is formed, not only deep morphological but also no less severe functional changes in the tube are observed, therefore any reconstructive operations in these cases are doomed to failure.

Most patients have cystic changes of various nature in the ovaries - from small single to large multiple cysts. In some patients, the internal lining of the cysts is not preserved or is represented by indifferent epithelium. The bulk of these are follicular cysts, as well as corpus luteum cysts.

The chronic stage is characterized by the presence of infiltrates - tubo-ovarian formations - with the outcome in fibrosis and sclerosis of tissues. In the acute stage, tubo-ovarian formations significantly increase in volume, which gives the right to equate this process in practice with acute.

With frequent relapses of chronic purulent salpingitis, the risk of infection of cystic formations increases significantly. This is facilitated by the formation of a single tubo-ovarian conglomerate, often having a common cavity. Ovarian damage almost always occurs in the form of an abscess, which occurs as a result of suppuration of cysts. Only such a mechanism allows one to imagine the possibility of the development of large and multiple ovarian abscesses.

Our studies have shown that modern antibacterial therapy has led to significant changes in the clinical picture and morphology of purulent inflammation. Exudative forms of inflammation are becoming less common. In patients with a chronic purulent process, the role of the primary pathogen is not significant. Morphological changes consist primarily in the erasure of any differences due to the polyetiology of the microbial factor. Morphological specificity is difficult to determine by the features of structural changes in the walls of the fallopian tubes and the cellular composition of the inflammatory infiltrate. An exception is tuberculous salpingitis, in which specific granulomas are always found in the mucous membrane and walls of the tubes.

The second path - the spread of microorganisms from extragenital foci, including from the intestines - is extremely rare, but it is necessary to remember this possibility.

T.N. Hung up et al. reported a case of pelvic abscess (bilateral purulent salpingitis and abscess of the Douglas pouch) in virgo caused by Salmonella, which confirms a rare variant of occurrence of pelvic infection with the participation of gastrointestinal microorganisms in patients with gastroenteritis. A similar case of tubo-ovarian abscess caused by Salmonella is described by E. Kemmann and L. Cummins (1993). Obvious infection occurred nine months before surgery for the abscess.

Modern antibacterial therapy has limited the possibilities of hematogenous and lymphogenous routes of spread of pathogens of purulent infection, which are currently significant only in the generalization of the infectious process.

The presence of other routes of infection besides the ascending route is reported by WJHueston (1992), who observed a patient with a tubo-ovarian abscess that developed 6 years after hysterectomy, which excludes the most common ascending route of infection. The patient did not have concomitant appendicitis or diverticulitis. The author suggested that the source of abscess formation was subacute inflammation in the appendages preceding the operation.

A similar case was described by N.Behrendt et al. (1994). Tuboovarian abscess developed in a patient 9 months after hysterectomy for uterine myoma. Before the operation, the patient had used an IUD for 11 years. The causative agent of the abscess was Actinomyces Israilii.

Thus, in conclusion, it can be said that the diversity of damaging agents and factors, the change of pathogens of inflammatory processes, the use of various methods of therapeutic intervention, of which antibiotic therapy should be especially noted, have led to a change in the classical clinical and pathomorphological picture of purulent inflammation.

It should be emphasized that purulent inflammation is almost always based on the irreversible nature of the process. Its irreversibility is caused not only by the above-mentioned morphological changes, their depth and severity, but also by functional disorders, for which the only rational method of treatment is surgical.

The course of the purulent process is largely determined by the state of the immune system.

Immune reactions are the most important link in the pathogenesis of the purulent process, largely determining the individual characteristics of the course and outcome of the disease.

In 80% of women with chronic inflammation of the uterine appendages outside of exacerbation, according to immunocytobiochemical studies, a persistent, latent inflammatory process is diagnosed, and a quarter of patients have a risk or presence of an immunodeficiency state, which requires immunocorrective therapy. The outcome of long-term recurrent inflammatory processes are purulent inflammatory diseases of the uterine appendages.

Thus, when discussing the concept of etiology and pathogenesis of purulent diseases in gynecology, certain conclusions can be drawn.

1. At present, the pyogenic microflora of any genital localization is predominantly associative in nature, with gram-negative and anaerobic microorganisms being the main destructive factors. At the same time, gonococcus as a causative agent of the purulent process in the tubes and, less frequently, in the uterus and ovary, has not only not lost its significance, but has also increased the degree of its aggression due to the accompanying microflora, and, first of all, STIs.
2. In modern conditions, the progression of suppuration and subsequent tissue destruction against the background of active antibacterial therapy is characteristic, therefore, with an inflammatory process of the genitals of one or another localization, the degree and severity of intoxication, as well as the possibility of developing septic complications, increases significantly due to the increasing virulence and resistance of microflora.
3. Insufficiency of the immune system in patients with purulent diseases of the pelvic organs is not only a consequence of a severe inflammatory process and long-term treatment, but also in many cases the cause of new relapses, exacerbations and a more severe course of the postoperative period.
4. In the near future, we should not expect a decrease in the number of purulent processes in the genitals and postoperative purulent complications. This is due not only to the increase in the number of patients with immunopathology and extragenital pathology (obesity, anemia, diabetes mellitus), but also to a significant increase in surgical activity in obstetrics and gynecology. In particular, this concerns a significant increase in the number of abdominal deliveries, endoscopic and general surgical operations.

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