Excerpt from Syphilis

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Background

Treponema pallidum is the microaerophilic spirochete that causes syphilis, a chronic systemic venereal disease with multiple clinical presentations (ie, the great imitator). Syphilis is characterized by episodes of active disease (primary, secondary, tertiary stages) interrupted by periods of latency. Since the diagnosis frequently is suspected after examination of skin lesions, dermatologists are recognized as experts in the diagnosis and treatment of syphilis. Syphilis is transmitted in 2 ways, either from intimate contact with infectious lesions (most common) or blood transfusions (blood collected during early syphilis), or it is transmitted transplacentally from an infected mother to her fetus.

Pathophysiology

In acquired syphilis, the organism rapidly penetrates intact mucous membranes or microscopic dermal abrasions and, within a few hours, enters the lymphatics and blood to produce systemic infection. The CNS is invaded early in the infection; during the secondary stage, examinations demonstrate that more than 30% of patients have abnormal findings in the cerebrospinal fluid (CSF). During the first 5-10 years after infection, the disease principally involves the meninges and blood vessels, resulting in meningovascular neurosyphilis. Later, the parenchyma of the brain and spinal cord are damaged, resulting in parenchymatous neurosyphilis.

Regardless of the stage of disease and location of lesions, 2 histopathologic hallmarks of syphilis have been noted including obliterative endarteritis and plasma cell–rich mononuclear infiltrates. Endarteritis is caused by the binding of spirochetes to endothelial cells, mediated by host fibronectin molecules bound to the surface of the spirochetes. The resultant endarteritis heals with scar tissue formation.

The mononuclear infiltrates reflect a delayed-type hypersensitivity response to T pallidum, and in certain individuals with tertiary syphilis, this response by sensitized T lymphocytes and macrophages results in gummatous ulcerations and necrosis. Antigens of T pallidum induce host production of treponemal antibodies and nonspecific reagin antibodies. Immunity to syphilis is incomplete. For example, host humoral and cellular immune responses may prevent the formation of a primary lesion (chancre) on subsequent infections with T pallidum, but they are insufficient to clear the organism. This may be because the outer sheath of the spirochete is lacking immunogenic molecules, or it may be because of down-regulation of helper T cells of the TH1 class.

Frequency

United States

The incidence of syphilis had been declining in recent years, with 53,000 reported cases (11,387 primary and secondary cases) in 1996, compared with 113,000 cases (33,962 primary and secondary cases) reported in 1992. However, the number of cases of primary and secondary syphilis increased yearly from 2000-2003. In 2003, 7177 cases were reported to the US Centers for Disease Control and Prevention. Most of this increase has been noted in men, particularly in men who have sex with other men. The overall cases reported in women decreased. More than 80% of cases were reported in the southern United States. Trends for congenital syphilis cases closely parallel those for acquired syphilis cases in women, namely, a decreased incidence over the past decade.

International

Syphilis remains prevalent in many developing countries and in some areas of North America, Asia, and Europe, especially Eastern Europe. In some regions of Siberia, as of 1999, prevalence was 1300 cases per 100,000 population.

Mortality/Morbidity

• Although rarely seen by clinicians since the use of penicillin became widespread in the 1950s, the primary complications of syphilis in adults include neurosyphilis, cardiovascular syphilis, and gumma. Death resulting from syphilis continues to occur. One study found that of 113 recorded deaths resulting from sexually transmitted diseases, 105 were caused by syphilis, with cardiovascular and neurosyphilis accounting for the majority of these deaths.
• These figures have continued to increase since the emergence of the AIDS epidemic, since genital ulcer diseases (including syphilis) are cofactors for the sexual transmission of HIV. Additionally, untreated patients who are HIV seropositive have an increased risk for rapid progression to neurosyphilis and for its complications. In addition, patients with HIV are at greater risk for development or relapse of early symptomatic neurosyphilis for up to 2 years after treatment with intramuscular or intravenous penicillin.
• Congenital syphilis is the most serious outcome of syphilis in women. It has been shown that a higher proportion of infants are affected if the mother has untreated secondary syphilis, compared to untreated early latent syphilis. Since T pallidum does not invade the placental tissue or the fetus until the fifth month of gestation, syphilis causes late abortion, stillbirth, or death soon after delivery in more than 40% of untreated maternal infections. Neonatal mortality usually results from pulmonary hemorrhage, bacterial superinfection, or fulminant hepatitis.

Race

In the United States, syphilis is more prevalent among persons of minority race and ethnicity. The reported prevalence of syphilis is somewhat higher among blacks than other ethnic groups. However, this rate has declined significantly in the past few years. From 2000-2003, the primary and secondary syphilis rate declined from 12 cases per 100,000 population to 7.8 cases per 100,000 population in this ethnic group. In 2002, 49.8% of all reported cases were in blacks, compared with 39.2% of cases in 2003.

Sex

The male-to-female ratio has increased over the past 3 years, largely due to the increased rate of disease among men who have sex with other men. In 2003, it was approximately 5:1.

Age

The incidence of syphilis peaks at age 15-34 years.

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