Sexually Transmitted Diseases - I. I. Mavrov 2005

Other bacterial infections of the urogenital organs
Infections caused by group B streptococci

Group B streptococci (Streptococcus agalactiae), first isolated from chronic mastitis in cows, have in recent years attracted close research attention as causative agents of human urogenital infections. They are isolated from the male Urethra and female birth canals. Asymptomatic carriage in both sexual partners is frequently observed, with both urethral and pharyngeal forms of carriage having been documented.

Etiology. Streptococci belong to the family Streptococcaceae, genus Streptococcus. These spherical or oval microorganisms, approximately 2 µm in diameter, typically form chains. Cocci reproduce by division perpendicular to the longitudinal axis of the chain. The Cells forming the chain often display a distinct paired arrangement. Streptococci responsible for urogenital diseases produce a capsule composed of hyaluronic acid, which impedes phagocytosis.

Most strains of group B streptococci possess two Polysaccharides, one of which is a group-specific polysaccharide common to all strains (a rhamnose-glucosamine polysaccharide). Type-specific polysaccharides, located superficially as capsular substances, are chemically glucose-galactose-N-acetylglucosamine polysaccharides that are serologically distinct, allowing group B streptococci to be divided into five serotypes. They readily hydrolyze sodium hippurate and may produce an orange pigment. St. agalactiae belongs to ß-hemolytic streptococci, which cause complete lysis of erythrocytes; ß-streptococci are generally susceptible to penicillin, ampicillin, Aminoglycosides, and Other Antibiotics, while rarely showing susceptibility to bacitracin.

Group B streptococci are members of the normal microflora of the Urogenital System. However, their role is highly significant in The Development of neonatal Sepsis and meningitis, as well as infections of the urogenital and respiratory tracts, joints, and other pathologies.

Modes of transmission. Group B streptococci can be transmitted sexually, with intrauterine infection and transmission during childbirth also being possible. Nosocomial transmission of S. agalactiae has likewise been reported.

Epidemiology and Pathogenesis. Group B streptococci are found in humans much more frequently than previously assumed. They are prominent pathogens in neonatal infections. During childbirth, approximately 75% of newborns become infected with streptococci if the mother is a carrier, yet only 1–2% of cases develop into sepsis. Sepsis caused by these pathogens carries a 50% neonatal mortality rate, and the majority of surviving children experience severe Brain damage (C. Baker, 1980).

Infections caused by S. agalactiae in the first months of a child's life manifest either early (acute respiratory distress, apnea, septicemia, meningitis) or late (otitis, Arthritis, Osteomyelitis). In adults, the incidence of Urogenital infections caused by group B streptococci correlates with the presence of other sexually transmitted urogenital pathogens, notably Gonorrhea. In recent years, alongside the rise in Sexually Transmitted Diseases, the incidence of ß-streptococcal infections has also increased. Therefore, The Role of sexual transmission warrants thorough investigation, along with the development of targeted therapies and Prevention strategies. According to I. Knox (1979), approximately half of the male partners of pregnant women whose vaginal flora exhibits ß-streptococcal colonization harbor the same bacterial strain in the urethra.

The risk of infection depends on numerous factors, among which the degree of vaginal and urethral colonization is particularly crucial. Vaginal colonization by group B streptococci is associated with an increased probability of Premature Rupture of membranes and/or preterm delivery. The duration of the "dry period" during labor, as well as maternal bacteremia, significantly increases the risk of vertical transmission to the child. The serotype of the pathogen colonizing the reproductive tracts of sexual partners is also of considerable significance.

Group B streptococci are typically present in the vaginal flora of 1/3 of healthy women. The colonization of ß-group B streptococci is influenced by the maturation or regeneration of the urethral and vaginal epithelium, as well as by hormonal contraceptives. It has been found that oral contraceptive use, on the one hand, completely neutralizes all cyclic variations in epithelial susceptibility to ß-group B streptococcal adhesion and, on the other hand (more importantly), drastically increases the adhesion rate of the pathogen to the barrier epithelium of the vaginal mucosa (T. N. Bulgakova et al., 1989).

Consequently, since colonization of mucous membranes is preceded by pathogen adhesion to the barrier epithelium, adhesion levels reflect the potential tissue susceptibility to infection. In this regard, it is essential to periodically monitor the urogenital microflora profile of female patients undergoing contraceptive therapy.

One of the factors determining individual epithelial susceptibility to ß-group B streptococcal adhesion may be the Fibronectin content On the surface of epithelial cells (A. A. Totolian, K. B. Grabovska, 1990; G. Hlinkova, A. Motlova, 1985). The role of group B streptococcal surface Antigens in genital tract epithelial adhesion is complex: the more virulent the streptococcal strain, the less actively it adheres to the epithelium, and conversely, as virulence decreases during the Selection of cells that do not produce the type-specific antigen, the adhesive Properties of the microbes increase.

The high adhesive activity of virulent group B ß-streptococci is a key factor in the development of mixed urogenital infections, including viral-bacterial co-infections. The latter promotes the activation of persistent avirulent ß-streptococci, which manifest their pathogenicity As a result of virus-specific modifications of host Cell membranes, thereby facilitating the dissemination of the infectious process.

Clinical presentation. Clinical manifestations of urogenital streptococcal infection vary widely in severity. The disease is predominantly asymptomatic. When symptoms do occur, they resemble those caused by other sexually transmitted pathogens (gonococci, chlamydia, Mycoplasmas, Viruses, etc.), including serous, purulent, or bloody discharge, dysuria, and inflammation of the reproductive tract. Alongside Urinary Tract infections, group B streptococci can cause bronchopneumonia, neonatal sepsis, meningitis, arthritis, and other disorders.

Carriage of group B ß-streptococci is also observed; however, colonization does not invariably lead to neonatal infection or, still less, to fatal disease.

Diagnosis. Detecting infections caused by group B ß-streptococci is generally straightforward. These microorganisms are typically isolated on Blood Agar and differentiated using Gram staining and the catalase test. For the initial screening of S. agalactiae, the hippurate Hydrolysis test and the cAMP test are employed. Identification is typically achieved within 24 hours.

Laboratory diagnosis is primarily based on isolating the pathogen from clinical specimens (genital swabs, blood, CEREBROSPINAL FLUID) followed by identification. Serological assays targeting Antibodies against capsular polysaccharides help determine the group affiliation of the pathogen. The antigen is extracted via Hydrochloric acid hydrolysis. Precipitation Reactions of the resulting extract—either in capillaries or agar gel—using group- and type-specific sera confirm not only the group affiliation but also the antigenic profile of the isolated pathogen.

Currently, coaglutination assays utilizing group-specific diagnostic kits are widely used to detect ß-streptococcal infections. To clarify the etiology of group B streptococcal infections, Methods for detecting group antigens in biological fluids are applied, utilizing rapid coaglutination and latex agglutination tests.

Treatment and prophylaxis. Penicillin therapy can alleviate symptoms, but the infection may still persist. Therefore, a combination of penicillin and aminoglycosides is indicated to enhance the bactericidal efficacy of penicillin. Combining aminoglycosides with furagin is also advisable, while erythromycin and ampicillin are frequently recommended as well. The administration of erythromycin or ampicillin (orally or intravenously) prevents the transmission of group B streptococci from mothers to infants. Antibiotics should be prescribed at dosages that establish effective therapeutic levels in Tissues. Pathogenetic and symptomatic treatments, as well as therapies aimed at stimulating host defense mechanisms, are administered according to clinical indications.

Comprehensive treatment regimens for streptococcal infections and their complications are prescribed in accordance with General Principles of etiological and Pathogenetic Therapy for inflammatory urogenital and systemic infections.

Preventing the spread of group B streptococcal infections involves: pathogen detection; timely diagnosis of group B ß-streptococcal carriage, particularly in pregnant and parturient women; eradication of carriage and treatment of pronounced clinical disease forms; and the development of specific prophylactic methods aimed at inducing type-specific Immunity.

It is vital to adhere strictly to asepsis and antisepsis rules during local therapy, various instrumental Procedures (urethroscopy, cystoscopy, sample collection for laboratory testing, etc.), and neonatal care. If a sexual partner has a streptococcal infection, all sexual contacts must be thoroughly evaluated and, regardless of the absence of apparent clinical symptoms in exposed individuals, prophylactic treatment must be prescribed.