Salpingo-oophoritis

Etiology and routes of transmission

In modern gynecology, the development of specific salpingooophoritis is most commonly associated with sexually transmitted infections. One of the main pathogens is Chlamydia trachomatis, a small, spherical, Gram-negative bacterium belonging to the family Chlamydiaceae.

A key feature of Chlamydia is obligate intracellular parasitism. The pathogen exhibits a high tropism for columnar epithelial cells. Entering the body sexually, the infection affects the endocervix and urethra, and then ascends to the upper reproductive tract, invading the endosalpinx (the mucous membrane of the fallopian tubes). Hematogenous dissemination (spread via the bloodstream within monocytes) is less common, but can lead to multifocal lesions.

Pathogenesis of inflammation and adhesions

The mechanism of damage to the uterine appendages is closely linked to the unique 48–72-hour life cycle of Chlamydia. It proceeds in two stages:

1. Elementary bodies (EBs) — the infectious form. They attach to the host cell membrane, penetrate inside, and block the protective fusion of the phagosome with the lysosome (incomplete phagocytosis).
2. Reticulate bodies (RBs) — the vegetative form. Inside the cell, EBs transform into RBs, which actively replicate by binary fission. They then transform back into EBs, rupture the host cell, and emerge to infect new tissues.

The continuous destruction of endosalpingeal cells triggers a chronic inflammatory response. The main pathogenetic link in this process is the formation of scarring and adhesions in the affected tissues. With inadequate therapy, the pathogen is able to alter its antigenic structure, form L-forms, and enter a state of persistence (dormancy).

Clinical presentation and complications

The incubation period of the infection ranges from 5 to 30 days. Specific signs of salpingooophoritis are absent. The disease is characterized by polymorphism of symptoms, as well as a protracted, mild, or completely asymptomatic course. Acute forms of appendage inflammation are usually registered only in mixed (coinfection) cases.

Often, the ascending process is preceded by lower genital tract involvement: asymptomatic cervicitis (sometimes with mucopurulent discharge) or urethritis with itching and the "morning drop" sign.

Sequelae of pelvic inflammatory disease:

• Extensive adhesions in the area of the uterine appendages.
• Pelvioperitonitis and peritonitis.
• Infertility.
• Ectopic pregnancy.

Laboratory diagnostics

Due to scant symptoms, diagnosis based solely on the clinical presentation is impossible. The basis of diagnosis is the detection of the pathogen or its antigens in scrapes from the cervical canal and urethra.

• Microscopy: Giemsa-stained smears have low sensitivity (detecting the pathogen in only 25–30% of cases).
• High-sensitivity methods: PCR (molecular biological method), direct immunofluorescence (DIF), and enzyme-linked immunosorbent assay (ELISA).
• Gold standard: Culture method (isolation of parasites on a cell culture).
• Serology (blood test): an elevated IgM titer indicates the acute phase, while an increase in IgA and subsequently IgG indicates transition to the chronic stage. A decrease in IgA and IgG titers serves as a criterion for treatment efficacy.

Principles of treatment and criteria for cure

Therapy for specific salpingooophoritis must be comprehensive. Examination and treatment of all sexual partners are mandatory, as well as the use of barrier contraception during therapy.

Pelvic inflammatory disease treatment regimen (14–21 days):

• Etiotropic therapy: macrolides, tetracyclines (doxycycline), or fluoroquinolones (ofloxacin) are used. The drug of choice is often azithromycin (1.0 g orally once weekly for 3 weeks).
• Pathogenetic therapy: to correct the immune status, interferon preparations (viferon, kipferon), endogenous interferon inducers (cycloferon, tilorone), antioxidants, and vitamins are prescribed.
• Rehabilitation: correction of vaginal microbiocenosis with eubiotics and physiotherapy.

Criteria for cure: complete resolution of clinical manifestations and laboratory eradication of the pathogen. Follow-up tests are performed 7–10 days later, and then repeated 3–4 weeks after the end of the course.

Class and exam questions

What else to study on this topic

• The life cycle of Chlamydia trachomatis and mechanisms of cellular persistence.
• Criteria for cure of gonorrhea and types of provocative tests (biological, dietary, physical).
• Extragenital manifestations of urogenital infections (Reiter's syndrome).
• The impact of STIs on newborns (blennorrhea neonatorum, conjunctivitis, pneumonia).
• The body's immune response during intracellular bacterial parasitism.

Other topics in the "Gynecology" section

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