Morphology and culture. These organisms are slender bacteria, 0.2 im wide and 5-15 im long; they feature 10-20 primary windings and move by rotating around their lengthwise axis. Their small width makes it difficult to render them visible by staining. They can be observed in vivo using dark field microscopy. In-vitro culturing has not yet been achieved.
Pathogenesis and clinical picture. Syphilis affects only humans. The disease is normally transmitted by sexual intercourse. Infection comes about because of direct contact with lesions containing the pathogens, which then invade the host through microtraumata in the skin or mucosa. The incubation period is two to four weeks. Left untreated, the disease manifests in several stages:
■ Stage I (primary syphilis). Hard, indolent (painless) lesion, later infiltration and ulcerous disintegration, called hard chancre. Accompanied by regional lymphadenitis, also painless. Treponemes can be detected in the ulcer.
■ Stage II (secondary syphilis). Generalization of the disease occurs four to eight weeks after primary syphilis. Frequent clinical symptoms include mi-cropolylymphadenopathy and macular or papulosquamous exanthem, broad condylomas, and enanthem. Numerous organisms can be detected in seeping surface efflorescences.
■ Latent syphilis. Stage of the disease in which no clinical symptoms are manifested, but the pathogens are present in the body and serum antibody tests are positive. Divided into early latency (less than four years) and late latency (more than four years).
■ Stage III (tertiary or late syphilis). Late gummatous syphilis: manifestations in skin, mucosa, and various organs. Tissue disintegration is frequent. Lesions are hardly infectious or not at all. Cardiovascular syphilis: endarteritis obliterans, syphilitic aortitis. Neurosyphilis: two major clinical categories are observed: meningovascular syphilis, i.e., endarteritis obliterans of small blood vessels of the meninges, brain, and spinal cord; parenchymatous syphilis, i.e., destruction of nerve cells in the cerebral cortex (paresis) and spinal cord (tabes dorsalis). A great deal of overlap occurs.
■ Syphilis connata. Transmission of the pathogen from mother to fetus after the fourth month of pregnancy. Leads to miscarriage or birth of severely diseased infant with numerous treponemes in its organs.
Diagnosis. Laboratory diagnosis includes both isolation and identification of the pathogen and antibody assays.
Pathogen identification. Only detectable in fluid pressed out of primary chancre, in the secretions of seeping stage II efflorescences or in lymph node biopsies. Methods: dark field microscopy, direct immunofluorescence (Fig. 4.23).
Antibody assays. Two antibody groups can be identified:
■ Antilipoidal antibodies (reaginic antibodies). Probably produced in response to the phospholipids from the mitochondria of disintegrating somatic cells. The antigen used is cardiolipin, a lipid extract from the heart muscle of cattle. This serological test is performed according to the standards
322 4 Bacteria as Human Pathogens — Treponema pallidum -
322 4 Bacteria as Human Pathogens — Treponema pallidum -
S Fig.4.23 Serous transudate from moist mucocutaneous primary chancre. Direct immunofluorescence.
of the Venereal Disease Research Laboratory (USA) and is known as the VDRL flocculation reaction.
■ Antitreponema antibodies. Probably directed at T. pallidum.
— Treponema pallidum particle agglutination (TP-PA). This test format has widely replaced the Treponema pallidum hemagglutination assay (TPHA). The antigens (ultrasonically-treated suspension of Treponema pallidum, Nichols strain, cultured in rabbit testicles) are coupled to particles or erythrocytes.
— Immunofluorescence test (FTA-ABS). In this fluorescence treponemal antibody absorption test the antigen consists of killed Nichols strain treponemes mounted on slides and coated with patient serum. Bound antibodies are detected by means of fluorescein-marked antihuman IgG antibodies. Selective antitreponeme IgM antibodies can be assayed (= 19S-FTA-ABS) using antihuman IgM antibodies (i capture test).
— Treponema pallidum immobilization test (TPI test). Living treponemes (Nichols strain) are immobilized by antibodies in the patient serum. This test is no longer used in routine diagnostics. It is considered the gold standard for evaluation of antitreponeme antibody tests.
The antibody tests are used as follows:
— Primary diagnostics: TP-PA or TPHA, VDRL, FTA-ABS (all qualitative).
— Special diagnostics: VDRL (quantitative); 19S-FTA-ABS.
Therapeutic success can be determined by the quantitative VDRL test. A rapid drop in reagins indicates an efficacious therapy. The 19S-FTA-ABS can be used to find answers to specialized questions. Example: does a positive result in primary diagnostic testing indicate a serological scar or a fresh infection?
Therapy. Penicillin G is the antibiotic agent of choice. Dosage and duration of therapy depend on the stage of the disease and the galenic formulation of the penicillin used.
Epidemiology and prevention. Syphilis is known all over the world. Annual prevalence levels in Europe and the US are 10-30 cases per 100 000 inhabitants. The primary preventive measure is to avoid any contact with syphilitic efflorescences. When diagnosing a case, the physician must try to determine the first-degree contact person, who must then be examined immediately and provided with penicillin therapy as required. National laws governing venereal disease management in individual countries regulate the measures taken to diagnose, prevent, and heal this disease. There is no vaccine.
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