DFA test for the L-type serovar of C. trachomatis is the most sensitive and specific test, but is not readily available.If polymerase chain reaction (PCR) tests on infected material are positive, subsequent restriction endonuclease pattern analysis of the amplified outer membrane protein A gene can be done to determine the genotype.Recently a fast realtime PCR (TaqMan analysis) has been developed to diagnose LGV. With this method an accurate diagnosis is feasible within a day. It has been noted that one type of testing may not be thorough enough. Treatment
Treatment involves antibiotics and may involve drainage of the buboes or abscesses by needle aspiration or incision. Further supportive measure may need to be taken: dilatation of the rectal stricture, repair of rectovaginal fistulae, or colostomy for rectal obstruction.Common antibiotic treatments include tetracycline (doxycycline) (all tetracyclines, including doxycycline, are contraindicated during pregnancy and in children due to effects on bone development and tooth discoloration), and erythromycin. Azithromycin is also a drug of choice in LGV. Further recommendations
As with all STIs, sex partners of patients who have LGV should be examined and tested for urethral or cervical chlamydial infection. After a positive culture for chlamydia, clinical suspicion should be confirmed with testing to distinguish serotype. Antibiotic treatment should be started if they had sexual contact with the patient during the 30 days preceding onset of symptoms in the patient. Patients with a sexually transmitted disease should be tested for other STDs due to high rates of comorbid infections.
Lymphogranuloma venereum (LGV; also known as climatic bubo, Durand–Nicolas–Favre disease, poradenitis inguinale, lymphogranuloma inguinale, and strumous bubo) is a sexually transmitted disease caused by the invasive serovars L1, L2, L2a, L2b, or L3 of Chlamydia trachomatis.LGV is primarily an infection of lymphatics and lymph nodes. Chlamydia trachomatis is the bacterium responsible for LGV. It gains entrance through breaks in the skin, or it can cross the epithelial cell layer of mucous membranes. The organism travels from the site of inoculation down the lymphatic channels to multiply within mononuclear phagocytes of the lymph nodes it passes. In developed nations, it was considered rare before 2003. However, a recent outbreak in the Netherlands among gay men has led to an increase of LGV in Europe and the United States.LGV was first described by Wallace in 1833 and again by Durand, Nicolas, and Favre in 1913. Since the 2004 Dutch outbreak many additional cases have been reported, leading to greater surveillance. Soon after the initial Dutch report, national and international health authorities launched warning initiatives and multiple LGV cases were identified in several more European countries (Belgium, France, the UK, Germany, Sweden, Italy and Switzerland) and the US and Canada. All cases reported in Amsterdam and France and a considerable percentage of LGV infections in the UK and Germany were caused by a newly discovered Chlamydia variant, L2b, a.k.a. the Amsterdam variant.