LYMPHOGRANULOMA VENEREUM (LGV)

LGV is a sexually transmitted disease produced by infection with Chlamydia trachomatis and is characterized by a primary lesion followed by suppurative lymphadenitis and lymphangitis. LGV is endemic in East and West Africa, India, Malaysia, Korea, Vietnam, South America, and the Caribbean. It is more common in urban areas, among the sexually promiscuous and the lower socioeconomic classes.

Etiology:  
LGV is caused by C. trachomatis serotypes L1, L2 and L3. 

Pathogenesis and clinical features:  
Incubation period ranges from three days to five weeks. The disease occurs in three stages; primary, secondary and tertiary.

• Primary stage: It is characterized by a small, transient, nonindurated vesicles, which ulcerates rapidly and heals quickly without scarring. In men, it is usually found in the coronal sulcus, prepuce or glans. In women, it is usually found in the posterior wall of the vagina, vulva or cervix. In most cases it does undetected.

• Secondary stage: LGV is primarily an infection of lymphatics and lymph nodes. From the mucosal surface, the organisms enter the draining lymphatic and lymph nodes to cause lymphangitis and lymphadenitis. LGV is characterized by unilateral, tender swelling of the lymph nodes in the groin area (inguinal lymph nodes). The large area of swelling in the groin is called a bubo. In women, inguinal lymphadenitis is unusual, however, the iliac lymph nodes may be involved and lead to pelvic adhesions. The lymph nodes enlarge, suppurate, become adherent to skin and break down to form sinuses discharging pus.

• Tertiary stage: Chronic inflammation obstructs the lymphatic vessels, leading to edema, ulcerations, and fistula formation. Multiple sinuses may develop and discharge purulent or bloodstained material. Involvement of the rectal wall in women or homosexual men may result in ulcerative proctitis with bloodstained purulent rectal discharges. Chronic lymphatic obstruction may eventually result in genital elephantiasis.

Laboratory diagnosis:
Specimen collection: Discharge from the suppurating lymph node and serum for serology.

• Microscopy: It is usually identified by iodine-stained inclusion bodies in pus taken from infected lymph nodes.

• Antigen detection: Chlamydial antigen in the specimen can be demonstrated by Fluorescent Monoclonal Antibody Test or Enzyme immunoassay.

• Serology: Complement fixation test, which usually demonstrates a rising titer of antibody or a high convalescent titer of 1:64 is significant. A microimmunofluorescence test measures type-specific antibody.

• Culture: Cyclohexamide-treated McCoy cells are used to identify intracytoplasmic inclusions in cells stained with monoclonal fluorescent antibodies. The organism can be grown in chic yolk sac or in mice following intracerebral inoculation.

• Molecular techniques: DNA hybridization techniques and Nucleic acid amplification using polymerase chain reaction or ligase chain reaction are also useful.

• Skin test: A skin test (Frei's test) detecting delayed hypersensitivity to Chlamydial antigen was described in 1925 by Frei. Initially the antigen was prepared by diluting the pus from bubo five-fold in saline and then heating at 60oC for two hours. Later the antigen was extracted from growth in yolk sac, purified by fractional sterilization and inactivated by phenol or heat. 0.1 ml of this antigen (called Lygranum) was injected indradermally on the forearm. A control prepared from the uninfected yolk sac was given on the other arm. A positive reaction was indicated by the appearance of a nodule at the site of injection in two days that increases in size (7mm wide) in 4-5 days. Frei's test becomes positive 2-6 weeks after infection and remains positive for several years. This test has been abandoned in many countries.