Lymphogranuloma venereum

Lymphogranuloma venereum
Lymphogranuloma venereum in a young adult who experienced acute onset of tender, enlarged lymph nodes in both groins
Specialty	Infectious diseases

Lymphogranuloma venereum (LGV; also known as climatic bubo,^[1] Durand–Nicolas–Favre disease,^[1] poradenitis inguinale,^[1] lymphogranuloma inguinale, and strumous bubo)^[1] is a sexually transmitted infection caused by the invasive serovars L1, L2, L2a, L2b, or L3 of Chlamydia trachomatis.^[2]

LGV is primarily an infection of

In developed nations, it was considered rare before 2003.^[3] However, a recent outbreak in the Netherlands among gay men has led to an increase of LGV in Europe and the United States.^[4][5]

LGV was first described by Wallace in 1833^[6] and again by Durand, Nicolas, and Favre in 1913.^[7][8] Since the 2004 Dutch outbreak many additional cases have been reported, leading to greater surveillance.^[9] Soon after the initial Dutch report, national and international health authorities launched warning initiatives and multiple LGV cases were identified in several more European countries (Belgium, France, the UK,^[10] Germany, Sweden, Italy and Switzerland) and the US and Canada. All cases reported in Amsterdam and France and a considerable percentage of LGV infections in the UK and Germany were caused by a newly discovered Chlamydia variant, L2b, a.k.a. the Amsterdam variant. The L2b variant could be traced back and was isolated from anal swabs of men who have sex with men (MSM) who visited the STI city clinic of San Francisco in 1981. This finding suggests that the recent LGV outbreak among MSM in industrialised countries is a slowly evolving epidemic. The L2b serovar has also been identified in Australia.^[11]

Signs and symptoms

The clinical manifestation of LGV depends on the site of entry of the infectious organism (the sex contact site) and the stage of disease progression. ^{[citation needed]}

• Inoculation at the mucous lining of external sex organs (penis and vagina) can lead to the inguinal syndrome named after the formation of buboes or abscesses in the groin (inguinal) region where draining lymph nodes are located. These signs usually appear from 3 days to a month after exposure.^{[citation needed]}
• The rectal syndrome (lymphogranuloma venereum proctitis, or LGVP) arises if the infection takes place via the rectal mucosa (through anal sex) and is mainly characterized by proctocolitis or proctitis symptoms.^[12]
• The pharyngeal syndrome is rare. It starts after infection of pharyngeal tissue, and buboes in the neck region can occur.^{[citation needed]}

Primary stage

LGV may begin as a self-limited painless genital ulcer that occurs at the contact site 3–12 days after infection. Women rarely notice a primary infection because the initial ulceration where the organism penetrates the mucosal layer is often located out of sight, in the vaginal wall. In men fewer than one-third of those infected notice the first signs of LGV. This primary stage heals in a few days. Erythema nodosum occurs in 10% of cases.^{[citation needed]}

Secondary stage

The secondary stage most often occurs 10–30 days later, but can present up to six months later. The infection spreads to the lymph nodes through

Over the course of the disease, lymph nodes enlarge, as may occur in any infection of the same areas as well. Enlarged nodes are called buboes. Buboes are commonly painful. Nodes commonly become inflamed, thinning and fixation of the overlying skin. These changes may progress to necrosis, fluctuant and suppurative lymph nodes, abscesses, fistulas, strictures, and sinus tracts. During the infection and when it subsides and healing takes place, fibrosis may occur. This can result in varying degrees of lymphatic obstruction, chronic edema, and strictures. These late stages characterised by fibrosis and edema are also known as the third stage of LGV, and are mainly permanent.^{[citation needed]}

Diagnosis

The diagnosis usually is made

For identification of serotypes, culture is often used. Culture is difficult. Requiring a special medium, cycloheximide-treated McCoy or HeLa cells, and yields are still only 30 to 50%. DFA, or direct fluorescent antibody test, PCR of likely infected areas and pus, are also sometimes used. DFA test for the L-type serovar of C. trachomatis is the most sensitive and specific test, but is not readily available.^{[citation needed]}

If polymerase chain reaction (PCR) tests on infected material are positive, subsequent

Recently a fast realtime PCR (TaqMan analysis) has been developed to diagnose LGV.^[13] With this method an accurate diagnosis is feasible within a day. It has been noted that one type of testing may not be thorough enough.^{[citation needed]}

Treatment

Treatment involves antibiotics and may involve drainage of the buboes or abscesses by needle aspiration or incision. Further supportive measure may need to be taken: dilatation of the rectal stricture, repair of rectovaginal fistulae, or colostomy for rectal obstruction.^{[citation needed]}

Common antibiotic treatments include tetracycline (doxycycline)^[14][15] (all tetracyclines, including doxycycline, are contraindicated during pregnancy and in children due to effects on bone development and tooth discoloration), and erythromycin.^{[citation needed]} Azithromycin is also a drug of choice in LGV.

Further recommendations

As with all

Prognosis is highly variable. Spontaneous remission is common. Complete cure can be obtained with proper antibiotic treatments to kill the causative bacteria, such as tetracycline, doxycycline, or erythromycin. Prognosis is more favorable with early treatment. Bacterial superinfections may complicate course. Death can occur from bowel obstruction or perforation, and follicular conjunctivitis due to autoinoculation of infectious discharge can occur.^{[citation needed]}

Long-term complications

Genital elephantiasis or esthiomene, which is the dramatic end-result of lymphatic obstruction, which may occur because of the strictures themselves, or fistulas. This is usually seen in females, may ulcerate and often occurs 1 to 20 years after primary infection. Fistulas of, but not limited to, the penis, urethra, vagina, uterus, or rectum. Also, surrounding edema often occurs. Rectal or other strictures and scarring. Systemic spread may occur, possible results are arthritis, pneumonitis, hepatitis, or perihepatitis.^{[citation needed]}

Notes