What causes vulvovaginitis?

Vulvovaginitis in girls develops as a result of overstraining of the child’s body’s defense systems, mediated by a number of factors:

• suppression of immunity;
• dysbacteriosis of the mother's birth canal;
• violation of the normal period of adaptation of the newborn;
• disruption of the development of microbiocenoses of the child's mucous membranes:
• frequent acute respiratory viral infections;
• hypertrophy of the elements of the lymphoid apparatus of the nasopharynx.

To a significant extent, the child’s health is affected by environmental problems and changes in the quality of food, which contains an ever-increasing amount of substances of unnatural origin (synthetic components).

Relapses of non-specific bacterial vulvovaginitis in girls in 82% of cases occur against the background of exacerbation of extragenital pathology, which is one of the leading causal risk factors for the development of vulvovaginitis, a powerful source of infection. In the anamnesis of patients with vulvovaginitis, systemic blood diseases, exudative diathesis, glomerulonephritis, cystitis, pyelitis, enterobiasis are found with equal frequency. In 5-8% of cases, vulvovaginitis in girls is accompanied by diabetes mellitus, thyrotoxicosis, endogenous obesity.

It has been established that vulvovaginitis is more common in children with chronic diseases of the nasopharynx, since children who frequently suffer from respiratory diseases experience depression of cellular immunity and an increase in the frequency of delayed-type hypersensitivity reactions.

Before birth and in the neonatal period, the vaginal mucosa of a girl mainly consists of 3-4 layers of intermediate-type squamous epithelium. However, under the influence of estrogens and progesterone, which come from the maternal-placental bloodstream or with mother's milk, epithelial cells have the ability to produce glycogen and thereby support the vital activity of lactic acid bacteria. Only after 3-4 hours of the neonatal period, when the process of epithelial desquamation and cervical mucus clouding intensifies, lactobacilli, bifido- and corynebacteria, and isolated coccal flora can be detected in the vagina.

The accumulation of lactic acid during the life of lactoflora causes a shift in the acid-base balance of the vaginal environment of a newborn girl to the acidic side (pH 4.0-4.5). Bifidobacteria, as well as lactobacilli, protect the vaginal mucosa from the effects of not only pathogenic but also opportunistic microorganisms and their toxins, prevent the breakdown of secretory immunoglobulin (IgA), stimulate the formation of interferon and lysozyme. The resistance of the body of a newborn girl is facilitated by the high content of IgG received through the placenta from the mother. A significant drop in estrogen levels occurs within 10 days from the moment of birth. It is during this period that the elimination of estrogens causes the so-called "sexual crisis" and the appearance of menstrual-like discharge in approximately 10% of newborns. Epithelial cells lose their ability to proliferate and synthesize glycogen. By the end of the first month of a girl's life, the thin and easily damaged vaginal epithelium is represented only by basal and parabasal cells. The reaction of the vaginal contents becomes alkaline, the pH increases to 7.0-8.0. Lacto- and bifidobacteria disappear.

How is vulvovaginitis classified?

Classification of vulvovaginitis is based on various principles. Depending on the patient's age, there are:

• vulvovaginitis of infancy (0-12 months);
• vulvovaginitis during childhood (1-8 years);
• prepubertal vulvovaginitis (from 8 years to menarche);
• vulvovaginitis of puberty (with menarche). According to the clinical course, the following are distinguished:
• acute vulvovaginitis;
• chronic vulvovaginitis:
  • in the acute stage;
  • in remission.

According to the species composition and pathogenicity of microorganisms, the following are distinguished:

• non-specific vulvovaginitis (bacterial, caused by opportunistic microorganisms) against the background of chronic inflammatory diseases of the ear, throat, nose, respiratory and urinary systems, intestinal dysbacteriosis;
• atopic vulvovaginitis (allergic genesis);
• against the background of systemic extragenital diseases (diabetes mellitus, hepatocholecystitis, leukemia, hypercorticism;
• against the background of prolapse or decreased ovarian function;
• bacterial vaginosis (non-specific vaginitis);
• against the background of mechanical, chemical and thermal damage to the vulva and vagina;
• against the background of helminthic invasion;
• against the background of a foreign body;
• against the background of lichen planus;
• against the background of scleroderma or vulvar dystrophy (lichen sclerosus).

Specific vulvovaginitis in girls can occur with the following diseases:

• gonorrhea;
• urogenital trichomoniasis;
• urogenital chlamydia;
• urogenital mycoplasmosis;
• tuberculosis;
• fungal infections (Candida fungi);
• genital herpes;
• papillomavirus infection;
• childhood viral infections (measles, scarlet fever, diphtheria, chickenpox).