Pathogenesis of purulent gynecological diseases

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

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

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

Currently, the theory of the ascending (intrakanalikulyarnom) path of infection prevails.

Damaged tissues (micro- and macro damage for invasive interventions, operations, childbirth, etc.) are the entrance gates of infection. Anaerobes penetrate from the neighboring ecological niches of the mucous membranes of the vagina and the cervical canal, and also partly from the colon, external genitalia, skin; proliferate, spread and condition the pathological process. The ascending path of infection is also characteristic of other forms of microorganisms.

In the presence of IUDs, microorganisms can also spread by the type of capillary effect along threads that hang in the vagina. The ways of spreading strict anaerobes with the help of spermatozoa or trichomonads are described, in such cases they are relatively easy to enter the uterus, fallopian tubes and abdominal cavity.

According to the research, chlamydia from the cervical canal penetrate into the mucous membrane of the uterus body and intrakanalykulyarnym way from the endometrium into the fallopian tubes. In the presence of cervicitis of chlamydia, 41% of patients were found in the endometrium, in the presence of salpingitis - in 21% of cases, with the clinical manifestations of endometritis in women either absent or mild.

Based on ultrastructural studies in the experiment, it was suggested that a serious accumulation of mucus, accompanied by swelling and loss of ciliary epithelium, plays a major role in the damage of the tubes as a result of infection with Chlamydia trachomatis.

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

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

To the specific pathogens, later endogenous flora of the lower genital tract can be joined - 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.

In the experiment it was shown that Tumor-Necrosis-Factor (TNF), excreted mainly by macrophages under the influence of Chlamydia trachomatis, is an essential component of the pathogenesis of inflammation.

TNF (cytokines) found FMGuerra-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 gonorrhea PA Rice et al. (1996) assign a place to lipo-oligosaccharides and pentidoglucones. These amines also stimulate the chemotaxis of polymorphous cell leukocytes whose metabolites can damage the tissue. The authors emphasize that the study of immunological mechanisms of inflammation should receive more attention. LSvenson (1980) believes that N. Gonorrheae causes damage to epithelial cells and is more virulent than C. Trachomatis.

Immunopathological disorders in the development of inflammation - an extremely complex and dynamic process. Disorders in general terms are 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 that are nonspecific 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 a rise in the serum content of antibodies of different classes and the most diverse antigen specificity, including due to a pathological rise in the synthesis and secretion of numerous autoantibodies.

After a lapse of 7-10 days or more from the debut of the disease, the main value begins to have specific immune responses (development of antibodies to the pathogen and its life products), as well as antigen-specific T cells. As the acute infectious process decays, a smooth decrease in the production of heteroclonal antibodies and a simultaneous increase in the production (titer) of antibodies to specific antigens of the pathogen of infection usually occur. At the same time, an increase in the synthesis of specific antibodies of IgM class is first observed, which after another 2 weeks is replaced by the synthesis of antibodies of class Ig G of the same antigenic orientation. Specific antibodies contribute to the elimination of the pathogen from the body mainly through 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, which selectively destroy the body's own cells containing pathogens, occurs. The latter is achieved either by triggering a genetically determined program of cell death (apoptosis), or by ejection of cytolytic factors by T-lymphocytes and natural killers, damaging the membranes of those cells of the body where presentation of fragments of antigens of pathogens occurs.

After the end of the acute period, the disease can go into a chronic sluggish form with an erased symptomatology or a clinical cure occurs, accompanied by complete elimination of the infectious agent. However, most often there is a persistence of the pathogen in the host organism against the backdrop of establishing new, close to neutral relationships between micro- and macroorganisms. The latter is typical for almost all human viruses (with very few exceptions), as well as for many non-viral forms of microflora such as chlamydia, mycoplasmas, etc. The corresponding phenomena manifest themselves as persistent or latent infection and are relatively rarely accompanied by reactivation of infectious pathology.

Survival of microorganisms in a constantly operating system of immunological surveillance requires sophisticated tactics of escaping from control of the host's immune system. This tactic is based on the use of a number of adaptive mechanisms that allow, first, to perform general (generalized) inhibition of immunity, the intensity of which becomes insufficient to eliminate the pathogen, and secondly, to include some additional mechanisms that allow the microorganism to remain "invisible" to effector mechanisms immunity, or induce their tolerance, and, third, to distort the immune responses of the host organism, reducing their antimicrobial activity. The strategy of persistence of microorganisms necessarily includes, on the one hand, general immunosuppression (of varying degrees of severity), which can be lifelong, and on the other, 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 with abscessing, purulent bodies.

Inflammatory process of the mucous membrane of the tube (endosalpingitis) passes to the muscular membrane, where there are hyperemia, microcirculation disorders, exudation, perivascular infiltrates, interstitial edema are formed.

Further, the serous cover of the tube (perisalpingite), the ovarian epithelium envelope (periophoritis), then the inflammation spreads to the peritoneum of the small pelvis.

Ovary is involved in the inflammatory process is not always, because the embryonic epithelium covering it serves as a rather powerful barrier to the spread of infection, including purulent.

However, after the rupture of the follicle, its granulosa is infected, a purulent oophoritis, then a pyovar. Due to the adhesion of the pili and the development of adhesions in the ampullar part of the tube, sachet "tumors" arise with serous (hydrosalpinx) or purulent (pyosalpin) contents. Inflammatory formations in the ovaries (cysts, abscesses) and the hydrosalpinks and pyosalpinks that merge with them form a so-called tubo-thoracic "tumor", or an inflammatory tubo-ovarian formation.

Chronization, progression and periodic exacerbation of the inflammatory process occur against the background of disintegration of the muscular tissue of the fallopian tubes, as well as deep functional and structural changes in the vessels of the uterine appendages until the development of adenomatous proliferation.

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

Most patients in the ovaries show cystic changes of a different nature - from small single to large multiple cysts. In some patients, the inner lining of the cysts is not preserved or is represented by an indifferent epithelium. The main weight is follicular cysts, as well as cysts of the yellow body.

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

With frequent recurrences of chronic purulent salpingitis, the risk of infection of cystic lesions increases significantly. This is facilitated by the formation of a single tubo-ovarian conglomerate, which often has a common cavity. The defeat of the ovaries almost always takes the form of an abscess arising from the suppuration of the cysts. Only such a mechanism allows itself to imagine the possibility of developing large and moreover multiple ovarian abscesses.

Our studies have shown that modern antibiotic therapy has led to significant changes in the clinic and the morphology of purulent inflammation. Less and less common are exudative forms of inflammation. In patients with 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 polyethiologic nature of the microbial factor. Morphological specificity is difficult to determine by the structural changes in the walls of the fallopian tubes and the cellular composition of the inflammatory infiltrate. The only exception is tuberculosis salpingitis, in which always detect specific granulomas in the mucosa and the walls of the tubes.

The second way - the spread of microorganisms from extragenital foci, including from the intestine - is extremely rare, but it should be remembered about this possibility.

TN Khung up with et al. Report a case of pelvic abscess (bilateral purulent salpingitis and abscess of the Douglas space) in virgo caused by Salmonella, which is confirmed by a rare variant of pelvic infection with the participation of gastrointestinal microorganisms in patients with gastroenteritis. A similar case of a tubo-ovarian abscess caused by Salmonella is described by E.Kemmann and L.Cummins (1993). The obvious infection occurred nine months before the operation for an abscess.

Modern antibacterial therapy has limited the possibilities of hematogenous and lymphogenic pathways of the pathogens of purulent infection, which currently have significance only in the generalization of the infectious process.

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

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

Thus, in conclusion, it can be said that the variety of damaging agents and factors, the change in the pathogens of inflammatory processes, the use of various methods of treatment, of which antibiotic therapy should be particularly emphasized, led to a change in the classical clinical and pathomorphological pattern of purulent inflammation.

It should be emphasized that the basis of purulent inflammation almost always is the irreversible nature of the process. Its irreversibility is due not only to the above-mentioned morphological changes, their depth and severity, but also to functional disorders in which the only rational 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, which largely determines the individual characteristics of the course and outcome of the disease.

In 80% of women with chronic inflammation of the appendages of the uterus without exacerbation, according to immunocytobiochemical studies, a persistent, latent, current inflammatory process is diagnosed, and a quarter of patients have a risk or an immunodeficiency state that requires immunocorrective therapy. The outcome of long-term recurrent inflammatory processes are purulent inflammatory diseases of the uterine appendages.

Thus, arguing about the concept of the etiology and pathogenesis of purulent diseases in gynecology, we can draw certain conclusions.

1. At present, the pyogenic microflora of any genital localization is predominantly associative, while gram-negative and anaerobic microorganisms are the main destructive factors. At the same time, the gonococcus as a causative agent of the purulent process in the tubes and less frequently in the uterus and ovary not only has not lost its significance, but has also increased its aggression level due to concomitant microflora, and primarily STIs.
2. In modern conditions, the progression of suppuration and subsequent destruction of tissues against active antimicrobial therapy is characteristic, therefore, the degree and severity of intoxication, as well as the possibility of development of septic complications, in the inflammatory process of the genitalia of one or another localization significantly increases due to the increased virulence and resistance of the 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 prolonged treatment, but in many cases the cause of new relapses, exacerbations and a more severe course of the postoperative period.
4. In the short term, we should not expect a decrease in the number of suppurative processes of the genitals and postoperative purulent complications. This is due not only to an increase in the number of patients with immunopathology and extragenital pathology (obesity, anemia, diabetes mellitus), but also with a significant increase in operative activity in obstetrics and gynecology. It is, in particular, a significant increase in the number of abdominal births, endoscopic and general surgical operations.

[1], [2], [3], [4], [5], [6]