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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Neurosyphilis is caused by Treponema pallidum, the bacteria that cause syphilis. It usually occurs about 10 - 20 years after a person is first infected with syphilis. Not everyone who has syphilis will develop this complication. Treponema pallidum is usually transmitted via direct contact with the infected lesion (sexual contact) or blood transfusion (rare). The incubation period varies with the size of innoculum (9-90 days). Following transmission, Treponema pallidum uses the intact or abraded mucous membrane to enter the body. It then disseminates to the lymphatics and blood stream to gain access to any organ of the body. Syphilis uses fibronectin molecules to attach to the endothelial surface of the vessels in organs resulting in inflammation and obliteration of the small blood vessels causing vasculitis (endarteritis obliterans). Organism has slow replication rate (30-33 hrs) and evades the initial host immune response. It may seed to different organs of the body especially the cardiovascular system and central nervous system resulting in tertiary syphilis. Different stages of syphilis results from the interaction between the antigen and the host immune response. The initial infection in primary syphilis is limited due to Th1 response and lack of the antibody response. It is speculated that there is a shift from Th1 to Th2 response during secondary syphilis. Cytotoxic T cells and an incomplete humoral immunity response is mainly responsible for persistence of infection and tissue damage in tertiary syphilis. Ineffective type 4 delayed hypersensitivity reaction containing macrophages and sensitized T cells is mainly responsible for the gumma formation in various organs. There is no known genetic association of syphilis. However, neurosyphilis may be associated with the gene polymorphism for IL-10 production with increased levels seen in the patients with neurosyphilis. In neurosyphilis, the brain tissue and preganglionic portion of the dorsal roots of spinal nerves is infiltrated with lymphocytes and plasma cells, and invasion of treponema pallidum spirochetes to brain tissue and posterior columns of the spinal cord makes them atrophic. The demyelination of the axones of the neurons is the main cause of symptoms and it affects the neurons in the brain, dorsal root ganglia and posterior columns of the spinal cord.
The forms of presentation of neurosyphilis can be grouped in two categories:[3]
Other less important forms are:
In neurosyphilis, the brain tissue and preganglionic portion of the dorsal roots of spinal nerves is infiltrated with lymphocytes and plasma cells, and invasion of treponema pallidum spirochetes to brain tissue and posterior columns of the spinal cord makes them atrophic.[4]
The pathogenesis of neurosyphilis may be described in the following steps:[4][5][1][6][7][8][9][10][11][12][13]
Treponema pallidum is usually transmitted via direct contact with the infected lesion (sexual contact) or blood transfusion (rare).
The incubation period varies with the size of innoculum (9-90 days).
Different stages of syphilis results from the interaction between the antigen and the host immune response.[4][5]
Acute response
Chronic
There is no known genetic association of syphilis. However, neurosyphilis may be associated with the gene polymorphism for IL-10 production with increased levels seen in the patients with neurosyphilis.[13]
Neurosyphilis is associated with increased transmission of HIV. The underlying mechanism may be related to the accumulation of dendritic cells containing CCR5 co-receptors at the site of infection, the same receptor entity binding the HIV.[11]
Primary syphilis
Secondary syphilis
Tertiary syphilis