bubble_chart Overview

Lymphogranuloma Venereum (LGV), also known as the fourth venereal disease, is one of the first-generation sexually transmitted diseases. Its pathogen has recently been identified as the trachoma-like chlamydia, primarily transmitted through sexual contact, and occasionally through contamination or laboratory accidents. Complications include genital ulcers, local lymphadenopathy, advanced stage elephantiasis, and rectal strictures. Due to the extensive development of chemotherapy, this disease is now extremely rare.

bubble_chart Epidemiology

LGV is primarily transmitted through sexual contact, with the peak incidence occurring between the ages of 20 and 30, coinciding with the peak of sexual activity. The infection rate of this disease is much lower than that of gonorrhea and syphilis. Early manifestations are more common in men than in women, while women often present with advanced-stage complications. The primary lesion in the genital area is usually mild and easily overlooked. It is not until the appearance of subacute or chronic bubo or the advanced-stage anorectal syndrome in women that people become alarmed and seek medical attention. Initially, the disease was mistakenly thought to be seasonal bubo or tropical bubo, leading to its consideration as a tropical or subtropical disease. However, it has also been found to occur in temperate or cold regions. Extensive research has confirmed that this disease is associated with sexual transmission.

bubble_chart Pathogen

In the 1930s, researchers collected samples from local lesions for smear examination and extracted fluids from the brain, spinal cord, testes, and lymph nodes of experimental monkeys to make smears for Giemsa staining. They discovered small deep sky-blue bodies that remained a non-fading light blue after several minutes of acetone treatment (while the blue granules seen in normal tissue cells showed decolorization after acetone treatment). Using the collodion thin membrane filtration method, the pathogen was determined to have a diameter of about 0.3 micrometers. Under electron microscopy, the pathogen appeared spherical with a diameter of 400 micrometers.

In the 1960s, studies using electron microscopy and cell culture methods confirmed that this body shared some characteristics with the pathogens of prickly-ash-like sore (trachoma) and psittacosis but differed from typical viruses. It was sensitive to broad-spectrum antibiotics and sulfonamides. It has now been identified as a subgroup of Chlamydia trachomatis, with serotypes L1~L3, most of which are caused by L2. Like other chlamydiae, it has a unique life cycle, can proliferate in the yolk sac of chicken embryos, and some strains can cause rapid death of the embryos. It can also grow in tissue or cell cultures. Glycogen-containing inclusion bodies appear in the cytoplasm of infected cells. The susceptibility of cells to LGV is not enhanced by pretreatment with DEAE-dextran. The three serotypes L1, L2, and L3 share cross-antigens with variants D and E of prickly-ash-like sore (trachoma). Recently, non-LGV strains of chlamydia causing proctitis have been found, especially among male homosexuals. With the development of monoclonal antibody technology, serotypes such as Ia, Da, L2a, D, and I have been identified. Specific types (D, G, L1, L2) have been found to be associated with rectal infections in homosexual men.

LGV has a heat-labile internal toxin, as well as heat-stable and heat-labile antigens, with the heat-stable antigen not being destroyed by heating at 100°C. This is an antigen shared with Chlamydia psittaci. Injecting LGV into the brains of mice or monkeys can cause encephalitis, but it does not infect birds when injected into their brains.

After infection with LGV, complement-fixing antibodies appear in the serum. Humans are the only natural hosts of this disease, which tends to invade the skin and lymph nodes. The serotypes of LGV are more invasive, causing more systemic lesions, unlike other serotypes of Chlamydia trachomatis which are mainly confined to mucous membranes. LGV pathogens can invade macrophages. Cell-mediated and humoral immunity can limit but not completely eliminate the spread of local and systemic infections. Even in advanced stages, the pathogen can still be isolated from infected tissues.

The pathogen of this disease has low resistance and can be killed by common disinfectants. It survives for 2-3 days outside the body and can be inactivated at 50°C for 30 minutes or at 90-100°C for 1 minute. It cannot survive in 70% ethanol, 2% lysol, 2% chloramine, ultraviolet light, or dry room warming.

bubble_chart Pathological Changes

Primary chancre: Non-specific inflammatory changes.

Lymph node: Specific pathological changes - granulomas with stellate abscess formation, central necrotic tissue, infiltration of polymorphonuclear leukocytes and macrophages, surrounded by epithelioid cells, with visible plasma cells. The abscess is triangular or quadrangular, which is of diagnostic significance. Late stage [third stage] is characterized by extensive fibrosis and large areas of coagulative necrosis.

bubble_chart Clinical Manifestations

1. Incubation period: There is a history of unclean sexual intercourse, with an incubation period of 7 to 10 days.

2. Early symptoms: The initial lesion often occurs on the male penis, glans, coronal sulcus, and foreskin, or on the female vaginal vestibule, labia minora, vaginal opening, and around the urethral opening. It manifests as very small blisters or ulcers, typically 5-6 mm in size, usually single but sometimes multiple, with no obvious symptoms. They do not heal for several days but leave no scars after healing. They can also occur in the perianal area, mouth, and other locations.

3. Intermediate stage [second stage] symptoms: 1 to 4 weeks after the appearance of the initial lesion, male inguinal lymph nodes swell (the four properties of bubo nature of disease), with pain, tenderness, adhesion, and fusion. The "groove sign" may be observed (the inguinal ligament separates the swollen lymph nodes above and below, creating a groove-like appearance on the skin). After several weeks, the lymph nodes soften, rupture, and discharge yellow serous or bloody pus, forming multiple fistulas resembling a "watering can." This condition does not heal for months and leaves scars after healing. In females, the initial lesion often occurs in the lower vagina, spreading to the iliac and rectal lymph nodes, causing lymphadenitis, proctitis, and clinical symptoms such as hematochezia, bloody mucus stool, abdominal pain, diarrhea, tenesmus, and lower back pain. This leads to perianal swelling, fistulas, rectal stricture, and elephantiasis-like swelling of the labia.

4. Advanced stage symptoms: After several years or decades, long-term recurrent inguinal lymphangitis (or lymphadenitis) can lead to genital elephantiasis, rectal stricture, and other complications.

5. Systemic symptoms: During the period of lymph node swelling and suppuration, systemic symptoms such as shivering, high fever, arthralgia, lack of strength, and hepatosplenomegaly may occur. Other manifestations include polymorphic erythema, nodular erythema, conjunctivitis, aseptic arthritis, and pseudomeningitis.

bubble_chart Auxiliary Examination

The diagnosis of this disease relies on the isolation of the pathogen and serological examination, with genetic diagnosis being crucial for confirming the disease.

1. Chlamydia culture: Pus from fluctuant lymph nodes is aspirated and inoculated into mouse brain tissue, chicken embryo yolk sac, or McCoy cells (which have replaced the former two) to isolate the pathogen, but the sensitivity is not high.

2. Serological examination: The most helpful serological method currently is the complement fixation test. This test is very sensitive, showing positive results 4 weeks after infection, and is diagnostically significant when high levels of antibodies (1:64) are detected. However, this test is not specific for sexually transmitted lymphogranuloma and must be analyzed in conjunction with clinical findings.

3. Microimmunofluorescence test and enzyme-linked immunosorbent assay (ELISA) have also been applied, offering certain sensitivity and specificity, and can be used for differentiation and screening purposes.

4. Genetic diagnosis.

bubble_chart Diagnosis

1. History of unclean sexual intercourse, incubation period of 7 to 10 days.

2. Early stage presents as genital vesicles, erosions, and ulcers, with inguinal lymphadenopathy appearing 1 to 4 weeks later. Males may exhibit the "groove sign," and multiple fistulas resembling a "watering can" pattern, with scarring after healing. Females may develop perirectal inflammation, and in advanced stages, elephant hide swelling and rectal stricture may occur.

3. When lymph nodes are involved, systemic symptoms such as shivering, high fever, and arthralgia may occur.

4. Pathological changes include stellate abscesses in the lymph nodes.

5. Complement fixation test becomes positive 4 weeks after infection, with a titer of 1:64 or higher.

6. Chlamydia (L1, L2, and L3 serotypes) can be isolated through tissue culture.

7. PCR test for Chlamydia DNA is positive.

bubble_chart Treatment Measures

1. Doxycycline 100mg, twice daily for 21 days.

2. Tetracycline 500mg, four times daily for 14 days.

3. Minocycline 100mg, twice daily for 15 days, double the first dose.

4. Azithromycin 250mg, twice daily for 7 days.

5. Noroxin: 250mg, twice daily for 14 days.

6. Compound formula: Co-trimoxazole 2 tablets, twice daily for 14 days. {|105|}

bubble_chart Differentiation

1. Genital Herpes: The differentiation between this disease and sexually transmitted disease lymphogranuloma venereum is shown in Table 1.

Table 1 Differentiation between sexually transmitted disease lymphogranuloma venereum and genital herpes

	sexually transmitted disease lymphogranuloma venereum	genital herpes
number	1-2 rarely multiple	several
location	coronal sulcus, frenulum	variable
ulcer	deep, dark red	superficial small blisters erosion, bright red
infiltration	mostly visible	none──present
subjective symptoms	none	pain or burning sensation
chance of infection	present	none
past history	none	often recurrent
bubo	sexually transmitted disease lymphogranuloma venereum	none
pathogen	chlamydia	herpes simplex virus

2. Hard chancre: syphilis inguinal lymphadenitis is hard, painless, does not ulcerate, and can be distinguished by the presence of syphilis spirochetes.

3. Soft chancre: inguinal lymphadenitis is more painful, with more pus, and the pathogen is Haemophilus ducreyi.

Differentiation of various sexually transmitted disease lymphadenitis

item	sexually transmitted disease lymphogranuloma venereum	syphilis	soft chancre
pathogen	chlamydia	syphilis spirochete	Haemophilus ducreyi
incubation period	1 day	21 days	3～5 days
distribution	1 or 2 sides	both sides	1 or 2 sides
number	multiple	several	single or multiple
size	egg or larger	thumb-sized	egg or larger
pain	+	-	+
redness and suppuration	+	-	+
groove sign	+	-	+
multiple fistulas	++	-	+
systemic symptoms	++	-	+
syphilis serological test	-	+	-