Treponema pollidum is the causative organism of syphilis, a notorious venereal disease.Treponema pollidum is a slender ﬁexuous helix 6 to 14μm long. Its width 0.13μm in dried, electron-microscope preparations, but is about 0.2μm in the wet, living state, when it is just great enough for resolution with the light microscope. It has 6 to l2 coils that are remarkably evenly disposed at 1.0μm intervals and its two ends are tapered. Because of its weak refractility and slender thickness, about the limit of resolution by the light microscope, it is best observed in wet living preparations with the dark ground microscope. ln dried preparations it needs to be thickened by silver impregnation methods to become visible. It is actively but rather lazily motile and there are three movements that propel it:-
Occasionally the organisms can be seen to divide by binary ﬁssion. As the spirochaete slowly moves across the dark ﬁeld of the microscope it often displays a characteristic tendency to bend at right angles near its midpoint. These features are best observed in exudates taken freshly from the patient and they enable the physician to make an immediate and reliable diagnosis on the spot.Experience is needed to identify most non-pathogenic commensal spirochaetes but generally they lack the regular spacing of the spiral coils at 1μm intervals and their lashing rapid motility easily distinguishes them from Treponema pallidum. When dark ﬁeld microscopy is not available the organism can be detected in wet ﬁlms of the exudate mixed with India ink. Treponema pallidum cannot be stained by simple aniline dyes or by Gram’s method. In ﬁlms stained by Giemsa’s prolonged method for 24 hours the organism appears as a delicate pink thread in contrast to the deep purple colour of coarser spirochaetes.
Under the electron microscope the protoplasmic core of Treponema pallidum is seen to be enveloped by a cell wall inside which it is contained by the cytoplasmic membrane. Between these two layers lie a number of axial filaments. lt is frequently possible to see that two of the ﬁlaments are anchored by the insertion of their terminal knobs into the tapering tip at on end of the spirochaetal cytoplasm . A second pair are similarly anchored into the other tip of the spirochaete. Each pair is twisted spirally around the organism, those from one end overlapping those from the other for most of the length of the organism. Thus when a cross-section is made in the middle of a spirochaete the microtome knife transects four ﬁlaments.
TREPONEMA PALLIDIUM PATHOGENICITY IN ANIMAL.
All attempts to cultivate Treponema pallidum in artiﬁcial culture media, chick embryos or tissue cultures have failed and it is conceded that the organism cannot as yet be cultivated on artiﬁcial media. lt is however, possible to propagate the spirochaetes by inoculating living treponemes from pathological lesions into the testes, scrotum, skin, or eye of the rabbit. The experimental disease in the rabbit resembles the early course of the natural disease in man. A primary lesion rich in spirochaetes develops but the later manifestations in the rabbit differ from human tertiary syphilis in that a large number of the organisms persist in the tissues without the development of any progressive disease. The Nichol's strain used in the TPI test has been kept for many years( > 25 years) by rabbit to rabbit intra-testicular passage since its ﬁrst isolation from the brain of a fatal case of general paralysis of the insane (GPI). Treponemes from rabbit ‘syphilomas' of the testis preserved in the proper suspending ﬂuids under anaerobic conditions remain actively motile for from four to seven days at 25°C or for two days at 37°C. Frozen in a medium containing 15 per cent glycerol at —65°C they remain viable for years and provide a reliable source of antigens for immunological tests. Drying rapidly kills the spirochaetes as does exposure to heat at 41-5 to 42°C. They do not survive at 0 to 4°C for more than one or two days. They are rapidly immobilized by trivalent arsenicals, bismuth and mercurials. Minute concentrations of penicillin kill them, though rather slowly.
ANTlGENlC STRUCTURE OF TREPONEMA PALLIDUM.
It is not known whether cardiolipin is contained in Treponema pallidum itself or whether it is released as a hapten from tissues damaged by infection. Since positive STS occur in other conditions than syphilis (‘biological false positives’) it seems that there may be a variety of disease processes presumably liberating antigenic materials which can generate anti-cardio- lipin antibodies. Although the STS provide and sensitive screening methods they obviously are not suﬁiciently speciﬁc for complete diagnostic reliability.
The second antigen is contained solely within the treponemes themselves where it can be demonstrated by speciﬁc immune ﬂuorescence(Fluorescent Treponemal Antibody or FTA test) and by the fact that when exposed to speciﬁcally protective antisera the spirochaetes lose their active mobility and are immobilized (Treponema pallidum Immobilization or TPI test). Both these phenomena are used for speciﬁc conﬁrmation of syphilis in sera that react positively with cardiolipin antigens. False positive reactions are not known to occur in these Treponema pallidum antibody tests.
A third antigen is known to be present in both Treponema pallidum and also in the non-pathogenic Reiter's treponeme that grows in artiﬁcial culture media. This treponemal group antigen is shared by other treponemes and can be detected by complement ﬁxation tests with antisera to the individual spirochaete strains. The Reiter complement ﬁxation test is a valuable screening test often added to the STS but it is not as speciﬁc as the Treponema pallidum antibody tests.
HOW SYPHILIS AFFECTS THE BODY?
Most cases of syphilis are contracted during sexual intercourse. The treponemes are present in superﬁcial genital lesions and pass from one partner to the other through intact mucous membranes or through minor skin abrasions. Occasionally the source of the infection is extra-genital and in a small percentage of cases the primary lesion is found around the mouth. More rarely infection has been reported in lesions on the hands of medical or nursing staff after investigating or treating cases of syphilis.
An important reason why, in developed communities, syphilis is almost exclusively spread by sexual intercourse, i.e. why it is a venereal disease, is the extreme delicacy of Treponema pallidum. This organism dies very rapidly when outside the body, e.g. almost instantly when dried or within an hour when kept moist. Thus under normal conditions of social life there is scarcely any possibility for it to be spread by forms of indirect contact with fomites, clothing etc.
When the spirochaete has penetrated its new host it begins to multiply at the site of its entrance (its generation time is less than 5 hours) and during the next 10 to 90 days the initial sore of primary syphilis appears. It is a focus of inﬂammatory tissue inﬁltrated with lymphocytes and monocytes and is ﬁrst noticed as a small red papule. The lesion is usually solitary and gradually enlarges; the centre breaks down to form a superﬁcial ulcer about 1 or 2cm in diameter. The base of the ulcer is indurated and the lesion is referred to as a ‘hard chancre’ or as the ‘primary sore’. It is the classical lesion of primary syphilis and in the male is often situated on the prepuce or the corona of the penis and in the female on the labia, the vaginal W811, or the cervix of the uterus.
There are very large numbers of treponemes in the primary sore and in the serum that exudes from it. In the early days of infection the spirochaetes invade the local lymph nodes where they cause an adenitis which in the male is in the inguinal region; and in the female is within the pelvis. The affected nodes have a ﬁrm rubbery consistency on palpation: from them the spirochaetes are soon conveyed to the blood stream in large numbers. This generalization of the infection throughout the body continues for 2 to 12 weeks after clinical infection. Towards the end of this time in an untreated case the primary chancre begins to subside spontaneously and leaves only a small scar.
Damage to the cardiovascular system with destruction of elastic tissue and the formation of aneurysms in large arteries, as well as gummata in the brain, bone. skin and internal organs,are some of the principal pathological effects. In the central nervous system tabes dorsalis characterized by a chronic progressive destruction of nerve ﬁbres in the spinal column is one important effect as also is meningovascular syphilis where continuing damage to brain cells results in general paralysis of the insane. The lesions of tertiary syphilis contain very few spirochaetes and the extensive tissue damage that occurs is possibly the result of a delayed hypersensitive reaction to the products of the persisting treponemes.
MOTHER TO CHILD INFECTION OF SYPHILIS
Treponema pallidum can cross the placental barrier and a syphilitic mother, especially in the secondary stage, may transmit the infection to her foetus. The lesions of congenital syphilis are essentially similar to those already described but when the infection is massive the child may be still-born or survive only a short time. The most important defects in late congenital syphilis are mental deﬁciency, chronic meningitis, blindness and deafness.
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