Tuberculous Vaginitis: Clinical Manifestations, Diagnosis, Treatment

Genital tuberculosis ranks second in prevalence after pulmonary tuberculosis. The disease tends to affect the female genitalia in approximately 1.5–2 % of cases.

It is a specific inflammation of the vaginal mucosa caused by M. tuberculosis. Genital tuberculosis typically develops through hematogenous spread; in rare instances, it may spread via lymphatic pathways.

Complaints

Patients may be concerned about nagging lower abdominal pain, pathological vaginal discharge, vaginal bleeding, or infertility.

Clinical presentation

A gynecological speculum examination may reveal a superficial tuberculosis-induced vaginal ulcer with undermined edges. The ulcer bed is infiltrated, and the base is covered with a yellowish or reddish-gray scale. At the edges of the ulcer can be found milky, whitish nodules, which when pressed with a spatula pale. An additional rectal examination is essential to rule out any rectovaginal fistulas.

Tubercular ulcers are a long-term condition. Patients may report general symptoms such as low-grade fever, weakness, decreased energy, fatigue, poor appetite and sleep, night sweats, weight loss, and dry skin.

Diagnosis of Vaginal Tuberculosis

Histological and cytological examination helps identify specific tuberculous inflammation in obtained samples. A bacteriological or culture test for M. Tuberculosis may use vaginal or ulcer discharge, menstrual blood, or aspirated material as samples. Genital tuberculosis may produce negative bacterial test results, even if the diagnosis has been confirmed microscopically. A nucleic acid amplification test (NAAT) allows for a rapid identification of M. Tuberculosis in samples. Xpert MTB/RIF is a NAAT that helps to both determine and identify the M. Tuberculosis complex. It is also useful in finding any genetic mutations that may indicate rifampicin resistance, one of the most effective tuberculosis medicines. A tuberculin skin test or interferon-gamma release assay (IGRA) is also an option.

1. Histological examination

Microscopic examination of tissues (biopsy specimens) to detect specific tuberculous granulomas (inflammatory foci containing Pirogov — Langhans cells).

2. Cytological examination

Analyzis of the cellular composition of smears or aspirates to detect signs of tuberculous involvement.

3. Bacteriological method (culture)

Cultivation of mycobacteria on nutrient media from samples such as vaginal discharge, menstrual blood, ulcer exudates, or biopsy specimens. May give false negative results.

4. Nucleic acid amplification tests (NAATs)

Molecular‑genetic methods (e.g., PCR) for rapid detection of M. Tuberculosis DNA in samples.

5. Xpert MTB/RIF

An automated NAAT that detects M. Tuberculosis and determines rifampicin resistance by identifying genetic mutations.

6. Standardized tuberculin test

Tuberculin is administered to assess the immune response. This is an auxiliary method and cannot be used as the sole means to confirm or exclude tuberculosis.

7. Interferon‑gamma release assay (IGRA)

Blood is tested for levels of interferon-γ produced in response to mycobacterial antigens. An alternative to skin testing.

Combining methods increases diagnostic accuracy, especially when cultures are negative. Histological methods and NAATs (Xpert MTB/RIF) are the most informative.

Treatment of Vaginal Tuberculosis

The core of therapy for vaginal tuberculosis is long‑term, multidrug anti‑tuberculosis chemotherapy, administered in specialized medical facilities. Treatment is selected individually, taking into account the pathogen’s drug susceptibility, the presence of concomitant diseases, and potential side effects.

1. Medical Therapy

Typically, a combination of 3–4 drugs from the following groups is prescribed:

• The main antituberculosis agents:
  • Isoniazid (4–6 mg/kg/day) — highly effective bactericidal agent;
  • Rifampicin (8–12 mg/kg/day) — key component of therapy, active against intracellular mycobacteria;
  • Pyrazinamide (20–30 mg/kg/day) — particularly active in the acidic environment of inflammatory lesions;
  • Ethambutol (15–25 mg/kg/day) — used to prevent resistance.
• Alternative medications (in case of resistance or intolerance):
  • Rifabutin, rifapentine (rifampicin substitutes);
  • Fluoroquinolones (levofloxacin, moxifloxacin);
  • Aminoglycosides (kanamycin, amikacin);
  • Capreomycin (for multidrug‑resistant TB);
  • Bedaquiline (used in newer short‑course regimens).

Treatment regimens:

• Standard regimen (drug‑sensitive TB): 2 months of intensive therapy (isoniazid + rifampicin + pyrazinamide + ethambutol), followed by 4 months of continuation therapy (isoniazid + rifampicin);
• Drug‑resistant TB: Individualized regimens including second‑line drugs; 18–24 months;
• New short‑course regimens: Bedaquiline + Pretomanid + Linezolid + Moxifloxacin (for MDR‑TB without fluoroquinolone resistance) or Bedaquiline + Pretomanid + Linezolid (for XDR‑TB) — 6 months.

2. Surgical Therapy

Indicated in cases of:

• Ineffective conservative therapy;
• Strictures, fistulas, abscesses;
• Prominent scarring resulting in impaired function.

3. Adjunctive Therapy

• Immunomodulators (as indicated);
• Physiotherapy (if not contraindicated);
• Local therapy (antiseptic and anti‑inflammatory agents);
• Microbiota correction (prebiotics and probiotics following the main treatment course).

4. Monitoring Treatment Effectiveness

• Regular molecular,microbiological, and histological studies;
• Assessment of symptom dynamics, physical examination;
• Pelvic ultrasound/MRI to evaluate treatment response;
• Monitoring of side effects (liver function tests, ophthalmologic monitoring during ethambutol therapy).

Treatment must be carried out under close supervision by a phthisiatrician and a gynecologist.