Lymphogranuloma venereum

INTRODUCTION

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

LGV infection has been rarely reported in developed countries. As an example, LGV was the cause of only 1 percent of 531 cases of genital ulcer disease in Singapore compared to 72 percent for HSV [4]. However, the true incidence of disease is often difficult to determine because of variable reporting practices and the lack of a standardized diagnostic test or surveillance definition. Furthermore, 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 [12]. The majority of these cases have presented as proctitis. Early in the Netherlands and New York outrbreaks the chlamydia serovar was the same, suggesting a close epidemiological link.

A major public health concern is that consistently, two-thirds to three-quarters of the LGV cases in MSM are also HIV-positive. In the UK outbreak, 4 percent of the cases represented new diagnoses of HIV, which were made coincident with the LGV infection [12].

Prior to the recent outbreaks in MSM, LGV was primarily endemic in heterosexuals in areas of East and West Africa, India, parts of Southeast Asia, and the Caribbean [1]. 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".)