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Guideline for self-study of students for practical lesson. Guideline for self-study of students for practical lesson



Guideline for self-study of students for practical lesson

Module I. Dermatology and Venereology

Thematic module 8. Venereal Diseases

LESSON 21

Tertiary period of syphilis. Congenital syphilis.

Theme urgency

The tertiary period of syphilis develops in a small number of patients who were neglectful of treatment for syphilis or were not treated at all. Old and very young age, traumas (physical, psychic, medicamentous), chronic diseases and toxicosis, and alcoholism are conducive to the development of tertiary syphilis. This period of syphilis usually begins three or four years after infection; in the last decades, however, it has shown a tendency to develop in eight to ten years, and may even become manifest only in tens of years. Patients with tertiary syphilis are a rare occurrence in Ukraine. In tsarist Russia they were often registered, particularly in rural areas.

Syphilis acquired by the foetus in uterus from the mother is called congenital or prenatal syphilis.

The foetus is infected via the transplacental route by Treponema pallida, usually after the fourth month. The chances of infection are greatest in early syphilis, diminishing with time.

The clinical features of syphilis tend to become less severe during pregnancy. Repeated miscarriages, stillbirths, premature deliveries and neonatal deaths are good indications of syphilitic infection.

The only means of diagnosing syphilis in a pregnant woman, in the absence of clinical signs, is by a routine blood serological examination during the early and late stages of pregnancy. An early diagnosis followed by adequate treatment is the only effective way of preventing congenital syphilis.

Concrete Objectives:

Students must know:

1. Classification of tertiary period of syphilis.

2. Clinical features of tertiary period of syphilis.

3. Investigations of tertiary period of syphilis.

4. Diagnosis of tertiary period of syphilis.

5. Differential diagnosis of tertiary period of syphilis.

6. Classification of congenital syphilis.

7. Clinical features of congenital syphilis.

8. Investigations of congenital syphilis.

9. Diagnosis of congenital syphilis.

10. Differential diagnosis of congenital syphilis.

Students should be able to:

1. To collect the medical history of patient with tertiary period of syphilis.

2. To inspect the patient with tertiary period of syphilis.

3. To define tertiary period of syphilis and describe its respective clinical manifestations.

4. To differentiate eruptions of tertiary period of syphilis from those similar of others dermatoses.

5. To define congenital syphilis and describe its respective clinical manifestations.

6. To differentiate sings of congenital syphilis from those similar of acquire syphilis and others dermatoses.

Tasks for self-study during preparation for lesson.

3.1. Theoretical questions for the lesson:

1. The course of tertiary period of syphilis.

2. Tubercles syphilid.

3. Gumma syphilid.

4. Pathogenesis and classification of congenital syphilis.

5. Syphilitic affection of the placenta and the foetus in congenital syphilis.

6. Congenital infantile syphilis.

7. Congenital syphilis of early childhood.

8. Late congenital syphilis.

The subject-matter:

TERTIARY PERIOD OF SYPHILIS (SYPHILIS TERTIARIA)

In distinction from the secondary period, the clinical manifestations in tertiary syphilis are prevalently local, often with involvement not only of the skin and mucous membranes, but of the internal organs, nervous system and motor apparatus; a scar remains after the lesions resolve. The pathoanatomical essence of tertiary syphilids is an infectious granuloma whose localization in some cases leads to impaired function of the organ in which it has formed.

The tertiary period of syphilis is subdivided into active tertiary syphilis and latent tertiary syphilis.

Involvement of the skin and mucous membranes (tertiary syphilids) may be displayed by tubercles or gumma (gummata ) on the skin, in the subcutaneous tissue, muscles, bones, internal organs and nervous system.

Only a small number of the lesions form (tubercles form in dozens while gummata are usually solitary). They follow a malignant course and always leave scars (if localized in vitally important organs they create a threat to the patient's life). If no treatment is applied, the lesions heal very slowly. They are not very contagious (treponemas are few in number and contained deep in the infiltrate) and respond well to antisyphilitic treatment, particularly with iodine preparations and salts of heavy metals. It should be borne in mind that in the tertiary period standard serological reactions are negative in 25 to 35 per cent of patients. The results of blood tests for T. pallidum immobilization, which are very rarely negative in the tertiary period, are of immense diagnostic value in such cases.

Tubercular Syphilid (Syphilis Tuberculosa)

Tubercular syphilid is usually localized on a small skin area, asymmetrically as a rule. The tubercle is semispherical or flat, copper-red with a cyanotic hue, and the size of a cherry stone. It is hard and has discrete boundaries. The infiltrate of the syphilitic tubercle undergoes necrosis either of the dry type or with the formation of ulcers. In the first case atrophy remains after the tubercle resolved. In the second case the ulcers leave a slightly retracted focus of grouped scars surrounded by a pigmented ring. The tubercles erupt in bouts and are therefore found in different stages of resolution. As a result a 'tesselated scar' forms (particularly often after a grouped tubercular syphilid) which many years later confirms the fact that the patient had suffered from tertiary tubercular syphilis. Most frequent occurrences are grouped tubercular syphilid, in which the tubercles are arranged in a cluster, or group without coalescing, and serpiginous (creeping) tubercular syphilid, in which the tubercles coalesce, heal in the centre while new tubercles appear on the periphery of the focus. Tubercular syphilid, in which the tubercles coalesce into a single patch, and dwarf syphilitic tubercles resembling a millet grain in size are encountered less frequently. Tubercular syphilid causes no subjective disorders.

Tubercular syphilid has to be differentiated first of all from lupus vulgaris in which the tubercles (lupomas) are soft (because of this the 'probe' phenomenon or Pospelov's sign is positive, i.e. the lupoma is easily pierced with a blunt probe or its soft tissue is easily pitted) and coloured light-red with a yellowish tinge well demonstrated in diascopy ('apple-jelly' phenomenon, 'apple mousse' sign). In lupus vulgaris the tubercles are usually flatter, only slightly elevated above the skin surface, and tend to coalesce into foci of extensive affection with ultimate formation of a vast depigmented atrophic scar, in the thickness of which new lupomas often develop. When the lupomas necrotize, ulcers with irregular and eroded contours form, they are reddish-cyanotic with soft irregular edges and often with a granular floor. Lupus vulgaris lasts several years. The syphilitic tubercles are hard, ham-red or intensively red in colour and are usually grouped in a focus without coalescing. If the tubercles in syphilis ulcerate, the ulcers have regular round contours, sloping uneroded edges, a clean and smooth floor and a dense-elastic infiltrate in the base. The scars remaining after syphilitic tubercles are mottled in colour because of irregular pigmentation and uneven in relief ('tesselated scars'); new tubercles never form on them. The disease lasts weeks or months, rarely longer.

Serological reactions, which are positive in some patients, as well as the T, pallidum immobilization and immunofluorescence tests, which are positive in most patients, and, finally, the efficacy of trial antisyphilitic treatment help in recognizing tubercular syphilid.

CONGENITAL SYPHILIS

Syphilis of the Foetus

Damage to the foetus by the syphilitic infection is manifested by severe changes in the internal organs and bone system. They are revealed no earlier than the fifth month of intrauterine life and are linked with mass penetration of the placenta by treponemas. The greatest number of treponemas are found in the liver, spleen and adrenals. The foetal parenchymatous organs affected with syphilis become enlarged and firm, a fact associated with the development of diffuse proliferative infiltration and subsequent growth of connective tissue. Besides the liver and spleen, the lungs, kidneys, pancreas and gonads also have similar diffuse inflammatory changes in their tissue. The pronounced diffuse interstitial hyperplasia in the lungs may give rise to a specific condition called white pneumonia.

Affection of several vitally important parenchymatous organs leads to the death of the foetus. In such cases abortion occurs in the fifth or sixth months of pregnancy, or a stillborn child is delivered in the eighth month. The macerated wrinkled and flabby skin makes the stillborn infant look old.

Clusters of cell elements are seen around the vessels or within the parenchyma of the affected organ (miliary syphilomas) in some cases when the syphilitic process has a localized and focal character instead of a diffuse inflammatory one. In such a case the child may be born alive, but it is poorly resistant to infections because the defence forces of the body are weak; it dies (without treatment) within the first weeks or first months of life.

Intensified growth of bones usually takes place in the last months of intrauterine life in view of which the bones are involved later than the parenchymatous organs, usually in the sixth lunar month. Grade I, II and III specific osteochondritis of the long tubular bones develops often at the junction of the epiphyses and diaphyses where the bones grow in length; osteoperiostitis occurs in some cases.

Late Congenital Syphilis

Late congenital syphilis is diagnosed in children at the age of 4 to 15 years and later.

In its course, late congenital syphilis resembles acquired tertiary syphilis because patients develop gummata or gummatous infiltrations of the skin, mucous membranes and bones (gummatous periostitis and osteoperiostitis), joints, internal organs and nervous system (gummatous meningitis). Tubercular syphilids may appear on the skin.

Besides the listed symptoms of late congenital syphilis, which are identical with tertiary syphilids of acquired syphilis, there are groups of symptoms encountered only in late congenital syphilis. They are divided into three groups. The first group consists of authentic, or unconditional, signs pathognomonic for late congenital syphilis. The second group is composed of accessory signs, which suggest congenital syphilis when there are other signs confirming the syphilitic infection (the results of serological blood tests, medical history and results of examination of the mother). The third group is formed of dystrophies (stigmata), which are encountered in many chronic infectious diseases and are not specific for congenital syphilis. The combination of several dystrophies in the presence of other evidence of the infection (e.g. positive Wassermann's test in the blood of the child and mother), however, enables the physician to make the correct diagnosis of the disease.

Hutchinson 's triad (interstitial keratitis, syphilitic labyrinthitis and Hutchinson's teeth) is an unconditional, or authentic, sign of late congenital syphilis.

Interstitial keratitis is characterized by redness and opacification of the cornea, photophobia, lacrimation, and stable impairment of visual acuity. In most cases first one eye and some time later the other are affected. The process lasts for a long time and resolution is extremely slow.

Syphilitic labyrinthitis, or labyrinthine deafness, occurring suddenly in a state of apparent well-being is characterized by diminished hearing, usually bilateral, and tinnitus. The process is associated with infiltrative inflammation of the labyrinth and degeneration of the acoustic nerve. If labyrinthitis occurs in a child whose speech is still undeveloped, there may be difficulties in pronouncing sounds or the child may become a deaf-mute.

Hutchinson 's teeth are marked by dystrophy of the two permanent upper median incisors which are shaped like a chisel and have a notched cutting edge. Before the eruption of the permanent teeth, Hutchinson's teeth are identified on a radiograph. The complete Hutchinson's triad is a very rare occurrence.

The accessory signs of later congenital syphilis are: sabre shins, syphilitic chorioretinitis and gonitis, Robinson-Fourniet's radial scars, frontal bossing of the skull, deformity of the nose (saddleback, opera-glass, and ‘goat’ nose), certain dystrophies of the teeth (kidney-shaped or 'tobacco-pouch' tooth), and some forms of neurosyphilis.

Sabre shins are marked by night pains and anterior bending of the tibia as a consequence of osteoperiostitis suffered in infancy. Sabre forearms are encountered far less frequently.

Chorioretinitis is characterized by small 'salt-and-pepper' pigmented areas on the fundus of the eye. The process involves the vascular coat of the eye and the optic disk. Since chorioretinitis may also be of tuberculous etiology, it is considered not an authentic but an accessory sign of late congenital syphilis.

Syphilitic gonitis, or Clutton's synovitis, or joint (Clutton was the first to describe this condition) follows a chronic course with impaired mobility and restriction of movements usually at the knees and, less frequently, at the elbows or ankles. There is neither increase in local temperature nor tenderness.

Serological tests, which are positive in almost all cases with gonitis, and the results of ex juvantibus therapy help in making the diagnosis.

Robinson-Fourniet's scars are arranged radially around the corners of the mouth, on the chin, and around the lips, and form as the result of Hochsinger's diffuse papular infiltration suffered in infancy. In some cases these scars may be rounded or pitted (like a thimble). Similar small scars may remain after a child had candidiasis, pyoderma or burn, which sometimes leads to diagnostic errors.

Frontal bossing of the skull in congenital syphilis forms in the first months of life, whereas in rickets this deformity becomes apparent by the second or third year of life. It results from the deposition of a diffusely ossifying infiltrate in the frontal and parietal bones, leading to a bulging of the frontal eminences and the formation of a groove between them. Localized syphilitic hydrocephalus is a contributing factor. Some children with congenital syphilis have a steeple skull.

Syphilitic rhinitis suffered in early infancy may sometimes cause deficient development of the bony or cartilaginous part of the nose resulting in deformities of the nose, which are very typical of late congenital syphilis. They include saddleback (protruding nostrils), opera-glass and 'goat' nose . In acquired syphilis a gummatous process may also cause deformities of the nose.

Among the variety of dental dystrophies, the following are the accessory signs of later congenital syphilis. A kidney-shaped (tobacco-pouch) tooth (the four masticating cusps of the first molar are underdeveloped and occur as thin projections; the tooth itself is small, the diameter of the masticating surface is less than the diameter of the neck, which makes the tooth domed) and a 'pike' tooth (hypoplasia of the masticatory surface of the canine tooth, from which a thin conical outgrowth resembling the tooth of a fish protrudes).

Affections of the nervous system in late congenital syphilis are diverse and are always attended with a positive T. pallidum immobilization test, though Wassermann's reaction is negative in some cases. Dementia (as a consequence of syphilis of the cerebral vessels), Jacksonian epilepsy, hemiparesis, hemiplegia, speech disorders, persistent headache (as a manifestation of syphilitic hydrocephalus), and tabes dorsalis are among the forms of neurosyphilis. In children with tabes dorsalis various pupillary disorders (anisocoria, the Argyll Rober-tson pupil, etc.) are mostly revealed.

Among the numerous and diverse dystrophies encountered in children whose parents have various infectious (e.g. tuberculosis) and non-infectious (e.g. alcoholism) diseases, we shall dwell here only on those which are most common in late congenital syphilis, though they are not specific of syphilis alone. These dystrophies (stigmata) may also form in the early periods (sometimes in infants); they are caused by metabolic disorders, endocrine dysfunction, disorders of cardiovascular and nervous activity. The following stigmata of late congenital syphilis are most significant: (1) Avsitidiisky's sign consisting in thickening of the sternal end of the clavicle as the result of diffuse hyperostosis; (2) a high 'lancet-like' , or 'gothic' hard palate ; (3) infantile little finger (Dubois-Gissard's sign); the little finger is short (Dubois" sign) and the little finger is somewhat deformed and turned inward (Gissard's sign); (4) axiphoidia, i.e. absence of the sternal xiphoid process; (5) Carabelli's cusp, the presence of a fifth auxiliary cusp on the masticatory surface of the first upper molar; (6) diastema, gaps between the upper incisors; (7) hypertrichosis in boys and girls and growth of hair on the forehead almost to the eyebrows.

These dystrophies are of diagnostic importance if two or more of them are encountered in combination with other signs (at least with one true authentic sign of Hutchinson's triad, or with more than one accessory sign) of syphilis or with the findings of serological examination and medical history verifying the presence of the infection in the children and their parents.

Serological blood tests which are positive in 70 to 80 per cent of patients with active manifestations, and particularly the TPI, which is positive in almost 100 per cent of patients, help in the diagnosis of late congenital syphilis.

Literature.

The basic:

1. Lecture on the theme.

2. Guideline for self-study of students by preparation for practical lesson 21.

3. Yu. K.Skripkin and M.V. Milich. Skin and Venereal Diseases, English translation, Mir Publishers, 1981, p.467-472, 480-495.

The additional:

  1. Fitzpatrick et al. Dermatology in General Medicine, 4th ed. New York, McGraw-Hill, 1993.
  2. Fitzpatrick. Color Atlas and Synopsis of Clinical Dermatology, 3rd Edition, 1997.
  3. P.N Behl, A. Aggarwal, Govind Srivastava. Practice of Dermatology, 9th Edition, 2002 p.237-242.

 

Guideline for self-study of students for practical lesson


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