SPIROCHETAL DISEASES the United States,3.8 in 1958 and 10.3 in 1968; Poland, 18.6 in 1958 and 53.8 in 1968; France, 3.3 in 1958 and 8M in 1968; greater Bombay, 177.7 in 1967.
It has been shown (United States) that for each reported case of early infectious syphilis three additional cases are diagnosed and treated by private physicians but not reported to the health authorities. A decline in late cardiovascular and neurosyphilis and in congenital syphilis has been observed since the mid-1940s. This decline has occurred despite the experience that late syphilis can be expected to increase after periods of the high incidence of early syphilis. The prevention of the lob, forms of syphilis by the penicillin treatment of early syphilis is one of the great achievements of the chemotherapy era. Host-Treponerne Relationship.
Man is the only natural host of T. pallidum Hormonal and genetic factors may affect susceptibility to infection. The host-treponeme interaction is best portrayed by the rhythm and features of the development of lesions during the course of untreated syphilis. Natural Course of Syphilis. Following implant-station and local multiplication of T. pallidum and extension of the infection to lymph nodes, treponemes spread rapidly to all body tissues via venous blood, the pulmonary circulation, and the arterial system. Human syphilis, therefore, ceases rapidly to be a local disease (even incubating infection can cause blood-transfusion syphilis).
SPIROCHETAL DISEASES agent does not grow in the bloodstream, but on passage through the small vessels, numerous metastatic foci are set up in the body, e.g., in the skin, mucous ‘ membranes, and nervous system. After the appearance of the initial lesion some three weeks following infection, multiplication continues for several weeks in these metastatic foci. Some eight to nine weeks after the original implantation the first generalized mucocutaneous outbreak occurs.
The primary lesion heals spontaneously within a few weeks and the secondary eruption within a few weeks or months. The treponemes in the metastatic foci of internal organs are presumably killed in most instances, but sometimes they become only temporarily inactivated (latent), giving rise to further manifestations. SPIROCHETAL DISEASES In the untreated disease further secondary episodes occur in 25 percent of patients within the first four years, mostly within two years. With increasing duration of infection, the hematogenous “showers” of treponemes generating this contagious epi-sores become less frequent and less rich in treponemes.
The cutaneous lesions tend to group and localize, or may occur solitarily until the mucocutaneous system no-longer responds to tree-names with pathologic changes. The further course of the untreated infection is illustrated by data from the University Clinic, Oslo, whereby the turn of the century some 1100 patients with diagnosed early syphilis remained untreated under hospitalized conditions and were subjected to follow-up studies.
In the last representative follow-up investigation 50 to 60 years after the original infection (Gjestland), late “benign” syphilis had occurred in 15 percent, cardiovascular syphilis in 10 percent, and neurosyphilis in6.5 percent of these patients. Ten percent died as a direct consequence of their disease. In about two thirds, latency continued indefinitely after the subsidence of the secondary attacks. They went through life without major physical or mental consequences of their disease. These features of the host-treponerne relationship in syphilis raise the question of the mechanisms concerned in the pathogenesis of lesions and their nature in both early and late disease and point to the remarkable role of the defense forces of the host against the invading pathogen during the natural course of the infection.
The immune response of the host directed against the pathogen is signaled by the modification of the natural course of syphilis as outlined above. The underlying warning repo-anemia, the decrease in demonstrable treponemes in late lesions, and the presence of presumed resistance to superinfection after the initial phase of the disease point in the same direction. Moreover, a varying degree of cross-resistance to syphilis in persons infected with yaws and pinta suggests the broader role of immunity in treponematoses. Knowledge is, however, meager or absent concerning the effector mechanisms in the protective host responses and the role of humoral and cell-mediated immunity. The humoral response involves the formation of two main antibody types, reagin* and treponemal antibody.
Reagin develops early, four to five weeks after infection, and forms more rapidly than treponemal antibody described below. It declines when the disease moves toward latency and may fall below detectable levels in late disease. It is affected considerably by therapy in the early phase of syphilis. A rising titer is a precursor of the clinical outbreak, and reagin is, therefore, a useful gauge of disease activity, but of limited value as an indicator of community. All SPIROCHETAL DISEASES evidence contradicts a protective role of reagin which is directed against cardiolipin present in the tissues of the antibody-producing host. Reagin is presumably an autoantibody formed in response to small amounts of cardiolipin “leaking” from host cells in the pathologic process (WHO, 1970). It is not known if reagin has a pathogenic significance.
“The term reagin is used throughout this article_ ft is widely accepted by physicians, clinicians, and epidemiologists to denote antibodies to cardiolipin-type antigens formed in syphilis and other treponematoses. Reagin is often referred to by immunologists and allergists to describe antibodies concerned in the immediate types of skin hypersensitivity and anaphylactic reactions.