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- CF, complement fixation
- LGV, lymphogranuloma venereum
- MIF, microimmunofluorescence
- NAAT, nucleic acid amplification test
- PCR, polymerase chain reaction
- RFLP, restriction fragment length polymorphism
- STBRL, sexually transmitted bacteria reference laboratory
Lymphogranuloma venereum (LGV) is caused by the invasive L1, L2, and L3 serovars of Chlamydia trachomatis. In contrast with serovars A-C that cause ocular infections and the more common D-K serovars of C trachomatis associated with genital infections, the L1-3 strains cause considerable disturbance in the local lymph nodes creating the characteristic clinical picture of painful swelling in the inguinal lymph glands. Recent whole genome sequence comparisons of oculo-genital and LGV strains have thus far failed to identify novel virulence factors that would account for the pathology of LGV.
Historically patients were unlikely to acquire the disease in the United Kingdom and most cases were diagnosed in those who had travelled to Asia, Africa, South America, or the Caribbean. Clinical LGV infection has three stages. The first stage arises at the site of inoculation and is usually a small ulcer somewhere on the external genitalia. This stage is transient and frequently passes unnoticed. If rectal transmission occurs, the first manifestation may be an acute proctitis, and this has been the most common presenting symptom of recent cases in the United Kingdom. Classically most patients present at the second stage, when the regional lymph nodes involved become firm, swollen, and painful, although this has been uncommon in UK acquired infections. Fever and malaise commonly accompany local symptoms. The primary ulcerative lesions often resolve before or during this stage but proctitis is likely to persist. Late stage disease results from lymphatic damage during the second stage and is characterised by lymphoedema and sometimes secondary ulceration. Scarring, strictures and fistulae involving the inguinal glands, genitalia, anus, …
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