Syphilis is usually transmitted by direct and intimate contact with moist infectious lesions of the skin and mucous membranes. Sexual contact is by far the commonest means of infection, but transfer of the disease by kissing or biting occasionally occur. Indirect transmission –i.e., by contaminated objects- is exceptional, since the organisms quickly die if allowed to dry.
Albert Heyman in Spirochetal Infections explains that the disease can be spread by inoculation with infected blood, as in transfusion syphilis. Infection is transmitted to the fetus through the placenta. Treponema pallidum is apparently capable of penetrating the intact mucous membrane, but a small
abrasion is probably required for inoculation to occur through the skin. Once the spirochete has penetrated the epithelium, it enters the lymphatics and can be demonstrated in the regional lymph nodes a few hours after experimental inoculation.From the lymph nodes, the organism spreads rapidly throughout the body by way of the blood stream. This spirochetemia may occur several weeks before appearance of the primary lesion at the site of inoculation. The early seeding of T. Pallidium in various tissues is the basis for many of the later manifestations of the disease.
About 3 to 6 weeks after the organism has entered the body, a primary lesion, the chancre, develops at the site of inoculation. The chancre is usually a single ulceration of the skin of mucous membrane; it heals spontaneously. About 6 weeks after its appearance, a generalized skin eruption, known as secondary syphilis, develops. In this stage, systemic manifestations are common. The signs of secondary syphilis also
disappear spontaneously.This sequence of events in early syphilis is variable. Infection without noticeable lesions probably occurs in a high percentage of cases, and many individuals with late syphilis are unable to recall either primary or secondary manifestations.
Following healing of the primary and secondary manifestations, the patient may show no outward signs of the infection (latent syphilis). Nevertheless, chronic, progressive, inflammatory changes may be taking place in the visceral organs or in the cardiovascular syphilis or central nervous system. Clinical evidence of cardiovascular syphilis or neurosyphilis may not develop for 10 to 20 years or more after the onset of the disease. Occasionally, the tissues of the host seem to become sensitized to the spirochetes, and large destructive lesions, called gummas, result. These lesions, which contain very few spirochetes, can occur in almost every organ of the body but are most frequent in the skin or bones.
Many patients with latent syphilis do not develop late manifestations and show no evidence of syphilis at autopsy. A study of patients with untreated early syphilis followed for a number of years showed that approximately one-third of them achieved spontaneous curs with the development of negative serologic tests. An equal number died of causes other than syphilis or developed latent syphilis with no clinical evidence of the disease other than a positive serologic test. The remaining third developed serious lesions of the cardiovascular or central nervous system or benign gummatous lesions of the skin or bones.