Lymphogranuloma venereum (LGV) is caused by one of three invasive serovars (L1, L2 or L3) of Chlamydia trachomatis, though L2 is the most common strain involved.
L2 is the main serovar causing the current outbreaks in Europe and North America.
Since 2003 there have been increasing LGV outbreaks across Europe mainly amongst HIV-positive MSM
Most UK cases are among MSM involved in dense sexual networks/party scene not linked to LGV-endemic countries
LGV remains endemic in tropical areas including Southern Africa, West Africa, Madagascar, India, South-East Asia and the Caribbean.
LGV proctitis in MSM
Pharyngeal LGV infection
Asymptomatic LGV infection
Secondary lesions, lymphadenitis or lymphadenopathy or bubo
Tertiary stage or the genito-anorectal syndrome
Historically LGV was a diagnosis of exclusion. Anorectal syndrome, particularly in MSM, is diagnosed based on clinical suspicion (e.g. proctocolitis, inguinal lymphadenopathy, genital ulcer) after the exclusion of other causes.
Microscopy: Rectal polymorphonuclear leucocytes (PMNLs) from rectal swabs is predictive of LGV proctitis, especially in HIV-positive MSM, with levels of >10 and >20 PMNLs per high-power field both shown to be significant.
Nucleic acid amplification tests (NAATs) have high sensitivity and specificity and if positive for C.trachomatis DNA may then be tested for LGV specific DNA from genital, rectal and throat swabs, urine, bubo pus, lymph node aspirates and biopsy specimens.
Other tests: Culture has sensitivity of 75-85%, less for buboes and is labour intensive and rarely available. Chlamydia serology cannot necessarily distinguish past from current LGV infection, does not have high sensitivity/specificity and is only available in specialised laboratories.
Collection of specimens
Chlamydiae are intracellular organisms so samples should aim to contain cellular material, which can be obtained from: