T. pallidum is a fastidious organism whose only natural host is man. The usual source of infection is contact with a cutaneous or mucosal lesion in a sexual partner in the early (primary or secondary) stages of syphilis. The organism is transmitted from such lesions during sexual activity through minute breaks in the skin or mucous membranes of the uninfected partner. In congenital cases, T. pallidum is transmitted across the placenta from mother to fetus, particularly during the early stages of maternal infection.
Once introduced into the body, the organisms rapidly disseminate to distant sites through lymphatics and the blood, even before the appearance of lesions at the primary inoculation site. This widespread dissemination accounts for the protean manifestations of the disease (
Fig. 18.19 ), which in adults can be divided into primary, secondary, and tertiary stages.
Primary syphilis. Several weeks after infection (mean, 21 days), a primary lesion, termed a chancre, appears at the point of spirochete entry. Systemic dissemination of organisms occurs during this period, while the host mounts an immune response. Two types of antibodies are formed: antibodies that cross-react with host constituents (nontreponemal antibodies) and antibodies to specific treponemal antigens. This humoral response, however, fails to eradicate the organisms.
Secondary syphilis. The chancre of primary syphilis resolves spontaneously over a period of 4 to 6 weeks and is followed in approximately 25% of untreated patients by the development of secondary syphilis. The manifestations of secondary syphilis, discussed in greater detail later, include generalized lymphadenopathy and mucocutaneous lesions. The mucocutaneous lesions of both primary and secondary syphilis are teeming with spirochetes and are highly infectious. Like the chancre, the lesions of secondary syphilis resolve even without antimicrobial therapy, at which point patients are said to be in early latent-phase syphilis.
Tertiary syphilis. Patients with untreated syphilis next enter an asymptomatic, late latent phase of the illness, defined as being more than 1 year after the initial infection. In about one third of cases, new symptoms develop over the next 5 to 20 years. This late symptomatic phase, or tertiary syphilis, is marked by the development of lesions in the cardiovascular system, central nervous system, or, less frequently, other organs. Spirochetes are much more difficult to demonstrate during the later http://ebooksmedicine.net
Neurosyphilis: Meningovascular Tabes dorsalis General paresis
Aortitis: Aneurysms Aortic regurgitation Gummas: Hepar lobatum Skin, bone, others
Infantile:
Childhood: Hutchinson teeth Eighth nerve deafness
Fig. 18.19 Proteanmanifestationsofsyphilis.
stages of disease, and patients are accordingly much less likely to be infectious than are those in the primary or secondary stages of disease.
T. pallidum also may be transmitted across the placenta from an infected mother to the fetus at any time during pregnancy, leading to the development of congenital syphilis. The likelihood of transmission is greatest during the early (primary and secondary) stages of disease, when spirochetes are most numerous. Because the manifestations of maternal disease may be subtle, routine serologic testing for syphilis is mandatory in all pregnancies. The stigmata of congenital syphilis typically do not develop until after the fourth month of pregnancy. In the absence of treatment, as many as 40% of infected infants die in utero, typically after the fourth month. The incidence of congenital syphilis is expected to rise because infection rates in women have increased in recent years.