INTRODUCTION

Lymphogranuloma venereum (LGV) is a genital ulcer disease caused by the L1, L2, and L3 serovars of Chlamydia trachomatis [1]. This infection is found most frequently in tropical and subtropical areas of the world [2]. The diagnosis is difficult to establish on clinical grounds alone and frequently relies upon either serologic testing [3,4], culture, or more recently, nucleic acid amplification testing (NAAT) of direct specimens.

LGV will be reviewed here. Other manifestations of C. trachomatis infection are discussed separately. (See "Genital Chlamydia trachomatis infections in women" and "Genital Chlamydia trachomatis infections in men" and "Epidemiology, diagnosis, and management of trachoma".)

EPIDEMIOLOGY

Although previously rare, lymphogranuloma venereum (LGV) infection has been increasingly reported in developed countries since 2003. Large outbreaks have been reported in Western Europe and North America, primarily in men who have sex with men (MSM) [5-10], with the largest outbreak reports from New York City [11] and the United Kingdom (UK) [12]. The majority of these cases have presented as proctitis. A close epidemiologic link between the outbreaks in the Netherlands and New York City was suggested through molecular typing of the serovars.

The vast majority of MSM who have acquired LGV are also HIV-infected (76 percent in one report) [12]. This is a major public health concern since enhanced shedding of HIV during clinical proctitis could increase the risk of HIV transmission to uninfected men [12]. In the UK outbreak of 327 cases of LGV, 4 percent of the patients also had a new diagnosis of HIV infection [12]. Thirty-nine percent had a diagnosis of another sexually transmitted infection and approximately 19 percent were also infected with hepatitis C virus.

Prior to the outbreaks in MSM, LGV was primarily endemic in heterosexuals in areas of East and West Africa, India, parts of Southeast Asia, and the Caribbean where it is manifested as the classic form of disease with genital ulcers and lymphadenopathy (without proctitis) [2]. However, LGV is not the predominant cause of genital ulcer disease in a number of these regions despite a high frequency of exposure as evidenced by C. trachomatis antibodies [13,14]. This was illustrated in a survey of 196 patients with genital ulcers from Madagascar, 79 percent of whom had chlamydial antibodies [13]. LGV was confirmed by multiplex polymerase chain reaction (PCR) in only 16 (8 percent). This contrasted with much higher rates of infection with chancroid, syphilis, and HSV of 33, 29 and 10 percent, respectively. (See "Chancroid" and "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection" and "Pathogenesis, clinical manifestations, and treatment of early syphilis".)