Chlamydial genital tract infections

Lymphogranuloma venereum: Clinical presentations

The clinical course of LGV is classically considered as occurring in three stages.

Primary stage

After an incubation period ranging as wide as 3 to 30 days, a lesion reportedly appears on the glans of the penis or, in women, on the vaginal wall, labia or, occasionally, the cervix. Rarely lesions may occur at extra-genital sites such as the anus, fingers or tongue. The initial lesion is usually transient, barely perceptible and painless; occurring as a papule, a shallow ulcer / erosion, a herpes [cold-sore] - like lesion or as a non specific urethritis reflecting an intra-urethral lesion. This so-called primary lesion is seen in only 4% or so of LGV patients, either because being painless the patient doesn't seek medical attention, or because the lesions described are not real components of LGV [Schachter & Osoba, 1983]. This would explain the apparent unique ability of this biovar to replicate in dead, keratinized epithelium. Syphilis, chancroid, Donovan's disease, Herpes simplex, trauma and abrasions are all potential causes of such indeterminate lesions. There can, however, be no doubting the next stage.

Secondary stage

Occurs from one to several weeks after infection. Most patients attend clinics because of the marked lymphadenopathy [lay reader: swollen lymph glands] associated with this stage. The lymphadenopathy is usually unilateral, involving the retro-peritoneal lymph nodes in women or the inguinal lymph nodes in men. In the so-called bubonic form, both the inguinal and femoral lymph nodes may be involved giving rise, because of the separating Pupart's ligament, to the "groove sign" considered a characteristic of this disease, but one which is only seen in a small proportion of patients [Schachter & Osoba, 1983]. Other lymph nodes may become involved by lymphatic drainage of infection from the infected node, giving rise in some cases to a whole chain of swollen nodes. The infected nodes become abscesses which eventually suparate and may give rise to draining fistulae [lay reader: channels]. In a small proportion of patients chronic lymphadenopathy may persist for years. Swollen buboes may need aspiration to avoid rupture.

Tertiary stage

Progressive spread of the disease leads to increasing and devastating tissue destruction [Lynch et al., 1999]. LGV proctitis initially occurs, followed by rectal damage, strictures and, in women, the formation of recto-vaginal fistulae. Two separate reports of LGV rectovaginal fistula have occurred recently in the world literature [Lynch et al., 1999; Papagrigoriadis & Rennie, 1999] after a gap of almost thirty years [Lynch et al., 1999]. There may be substantial urethral destruction also. Epithelial tissue is destroyed and replaced with granulation tissue and infiltrating plasma cells which histologically and on endoscopic examination may mimic Chron's disease [Papagrigoriadis & Rennie, 1999]. Rectal infection with the LGV biovar of C. trachomatis is relatively common in homosexual men and is accompanied by signs of more systemic cachexic illness [fever, chills, weight loss, constipation] than is usually seen with chlamydial proctitis due to the usual oculo-genital serovars D thru K. In Seattle 7 chlamydial isolates from the rectum among a total of 767 rectal isolates of C. trachomatis obtained from men over a 10 year period were found to be caused by LGV serovar, L1. Sequencing studies on the nucleic acid of the omp1 gene of 6 of these isolates showed that they all shared the same unusual sequence different from the reference LGV strains, suggesting a single source outbreak had occurred. All 5 patients from whom these isolates were obtained were homosexual men who had symptomatic proctitis characterized by rectal pain, discharge, tenesmus, abnormalities seen on anoscopy, and leukocytes seen on gram stains of rectal specimens. It was thought that the clinical manifestations of rectal infection with serovar L1 infection might be less severe than those of L2 infections [Bauwens et al., 1995].

NEXT LGV: Laboratory diagnosis

References

Bauwens, J. E., Lampe, M. F., Suchland, R. J., Wong, K. Stamm, W. E. *(1995). Infection with Chlamydia trachomatis lymphogranuloma venereum serovar L1 in homosexual men with proctitis: molecular analysis of an unusual case cluster. Clinical Infectious Diseases *20, 576 - 581.

Lynch, C. M., Felder, T. L., Schwandt, R. A. & Shashy, R. G. (1999). Lymphogranuloma venereum presenting as a rectovaginal fistula. Infectious Diseases in Obstetrics & Gynecology 7, 199 - 201.

Htun, Y., Morse, S. A., Dangor, Y., Fehler, G., Radebe, F., Trees, D. L., Beck-Sague, C. M. & Ballard, R. C. (1998). Comparison of clinically directed, disease specific, and syndromic protocols for the management of genital ulcer disease in Lesotho. Sexually Transmitted Infections 74, Suppl 1: S23 - 28.

Papagrigoriadis, S., Rennie, J. A. (1998). Lymphogranuloma venereum as a cause of rectal strictures. Postgraduate Medical Journal 74, 168 - 169.

Schachter, J. & Osoba, A. O. (1983). Lymphogranuloma venereum. British Medical Bulletin 39, 151 - 154.