Etiology and Epidemiology
The causative agent is Chlamydia trachomatis, specifically its aggressive serovars L1, L2, L2a, L2b, and L3. Humans are the sole reservoir of infection. Transmission occurs primarily through sexual contact, although fomite transmission via contaminated objects is occasionally possible.
Susceptibility to the microorganism is high. Geographically, the pathology is most prevalent in tropical and subtropical regions, including Southeast Asia and Central and South America.
Pathogenesis
Specific L-serovars of chlamydia possess high invasiveness and dual tissue tropism. They selectively infect both the epithelium (epitheliotropism) and lymphoid tissue (lymphotropism).
The mucosal membranes of the genitalia serve as the portals of entry. Following successful penetration into the mucosa, the pathogen migrates to regional lymph nodes (usually the inguinal group), where intensive replication occurs. Soon, the active inflammatory process extends beyond the affected node, involving the surrounding connective tissue and leading to periadenitis.
Clinical Presentation
The latent incubation period lasts from 3 to 30 days. The disease manifests with a primary lesion on the external genitalia, presenting as small papules, erosions, or superficial ulcers that the patient may not even notice.
During the active phase, lymphatic system involvement comes to the forefront. Buboes form—painful, firm tumor-like masses consisting of coalesced inflamed lymph nodes and adjacent tissues. Subsequently, these nodes undergo purulent necrosis. The buboes spontaneously rupture, forming chronic, non-healing fistulae accompanied by severe destructive soft tissue changes.
This local destructive process is accompanied by systemic symptoms of toxicity. Patients often report fever, severe headache, and arthralgia. A skin rash may appear in some patients. In adverse courses, the infection may generalize, causing severe extragenital manifestations such as pneumonia.
Complications and Clinical Course
Lymphogranuloma venereum typically has a chronic, protracted course. Men are infected and affected more frequently than women, and the infection runs a significantly more severe course in males.
Local complications regularly include regional lymphadenitis, deep abscesses, and proctitis (inflammation of the rectum). Over time, chronic inflammation and fibrosis lead to severe anatomical defects:
- Rectal involvement: Fibrotic changes, massive adhesions, and papillomatous growths can lead to bowel obstruction.
- Lymphedema (elephantiasis): Adhesive processes completely block normal lymphatic drainage. In men, this results in scrotal and penile elephantiasis; in women, the vulva is massively affected.
In rare cases, the process extends beyond the pelvic region and generalizes, posing a life-threatening risk of conditions such as meningitis and pericarditis.
Following recovery, the body develops long-lasting immunity involving both cellular and humoral defense mechanisms.
Laboratory Diagnostics and Treatment
To microbiologically confirm the diagnosis, purulent discharge from ruptured buboes, lymph node biopsies, or blood serum samples are collected.
Comprehensive laboratory diagnostics include:
- Bacterioscopy — searching for intracellular inclusions of the pathogen in smears.
- Biological method — culturing chlamydia in the yolk sacs of chicken embryos, specialized cell cultures, or via intracerebral inoculation of mice.
- Serology — complement fixation test (CFT) using paired sera. The reaction is considered positive from the 2nd to 4th week of the disease, with a diagnostically significant antibody titer of 1:64 or higher.
- Allergy testing — intradermal skin test using a specific chlamydial allergen (Frei test).
Etiotropic treatment involves antibiotics from the macrolide and tetracycline classes. Maximum therapeutic efficacy is achieved only when administered in the early stages of the disease. Prevention is exclusively nonspecific and identical to standard measures for preventing sexually transmitted infections.