Sexually transmitted diseases - Lymphogranuloma Venereum (LVG)

Lymphogranuloma venereum (LGV), widely known as lymphopathia venerea, lymphogranuloma inguinale, tropical bubo, climatic bubo, poradenitis inguinales, strumous bubo, and Durand-Nicolas-Favre disease is a sexually transmitted disease caused by the Chlamydia trachomatis LGV strain, the persistent serotypes L1, L2, or L3 of Chlamydia trachomatis. It starts as an acute genital infection that eventually develops into a chronic crippling illness like genital elephantiasis or anorectal stricture. Further, the organism may possibly spread systemically to cause constitutional symptom.

The disease was initially described by Wallace in 1833 as a pathological and clinical entity and was restated by Durand, Nicolas, and Favre in 1913.

The disease is relatively rare in the United States and other industrialized nations infecting only an average of 250 to 400 people a year, mostly males between the age of 15 and 24. It is however highly prevalent in the tropical areas which include Southeast Asia, Africa, Central and South America and the Caribbean, thus the coined term “tropical hubo.”

Lymphogranuloma venereum (LGV) is transmitted primary through direct sexual contact with the genitals, mouth or rectum. Other cases are transmission by fomites, nonsexual personal contact, as well as laboratory accidents. When it enters the body, it is being reproduced in the lymph nodes. It is most closely associated with anal sex and same sex intercourse predominantly male to male. Newborns can also acquire the disease from infected mothers during birth.
The World Health Organization lists the following as the major sources of the disease:

• C trachomatis
• Serovars units L1, L2, and L3.
• Unprotected sex
• Anal intercourse
• Residing in or visiting tropical/developing countries
• Prostitution

LGV develops in 3 major stages. Majority of LGV infections in the primary and secondary stages may perhaps be considered undetected.

In the primary stage, LGV begins as a self-limited painless genital ulcer that appears at the contact site 3-12 days or longer. It is very rare for women to notice the primary infection because the primary ulceration where the organism penetrates the mucosal layer is situated out of sight in the vaginal wall. Same applies to most men and there are fewer than 1/3 of those afflicted notice the first manifestations of LGV. This primary stage however heals in after several days.

In the secondary stage, the disease usually occurs around 10-30 days later most often, but can occur up to 6 months later. The said infection then attacks to the lymph nodes through multi layered lymphatic drainage pathways. The regular presenting clinical manifestation of LGV among men whose primary exposure was genital is unilateral, majority of cases, lymphadenitis and lymphangitis, sometimes tender inguinal and/or femoral lymphadenopathy due to the drainage pathway for their likely infected areas. Lymphangitis of the dorsal penis may perhaps occur and coincides string or cord. The infected person may experience lymphadenitis and lymphangitis noted above or may have proctitis, inflammation limited to the rectum (the distal 10--12 cm) that may be associated with anorectal pain, rectal discharge or tenesmus, or proctocolitis, inflammation of the colonic mucosa extending to 12 cm above the anus and is associated with symptoms of proctitis with diarrhea or abdominal cramps and or inflammatory involvement of perirectal or perianal lymphatic tissues if the initial route of the bacterium was anal sex. In females, commonly cervicitis, salpingitis, or perimetritis may occur as well as the lymphangitis and lymphadenitis in deeper nodes. Due to lymphatic drainage pathways, several end up with an abdominal mass which infrequently suppurates and only 20-30% end up with inguinal lymphadenopathy.

Other systemic signs may include fever, malaise, and decreased appetite may occur as well. Researchers claim that diagnosis is often more difficult in women and homosexual men who perhaps doesn't have the inguinal symptoms.

During the whole course of the disease, the lymph nodes enlarge and are called buboes. They tend to become painful at first. Secondly, manifestations of inflammation, thinning, cracking and fixation of the overlying skin. And the last in the progression are necrosis, suppurative and fluctuant lymph nodes, abscesses, strictures, fistulas, and sinus tracts all may occur. Fibrosis may occur during the infection and when it subsides and healing takes place. This is due to varying degrees of lymphatic obstruction, chronic edema, and strictures. These later phases characterised by edema and fibrosis are more relatively known as the third stage of LGV and are critically permanent.

In the later stage or the third stage, the disease is already characterized by proctocolitis. The symptoms include anal pruritus, fever, rectal pain, constipation, bloody mucopurulent rectal discharge, tenesmus, pencil-thin stools, and weight loss. Often, the diagnosis is loosely a consideration on the basis of physical findings. Moreover, clinical findings of large fluctuant buboes or draining sinuses can be suggestive of the diagnosis of LGV.

The long term complications are just the worsening and relative degradation of the affected areas.