SYPHILIS
Dr. S. LALITHA PANKAJAM
Department of Pathology
SYPHILIS
Syphilis is a venereal (sexually - transmitted) disease caused by
spirochaetes, Treponema pallidum. Other treponemal diseases are yaws,
pinta and bejel. The word ‘syphilis’ is derived from the name of the
mythological handsome boy, Syphilus, who was cursed by Greek god
Apollo with the disease.
Causative Organism :
T. pallidum is a coiled spiral filament 10 μm long that moves
actively in fresh preparations. The organism cannot be stained by the
usual methods and can be demonstrated in the exudates and tissues by:
1. Dark ground illumination (DGI) in fresh preparation.
2. Fluorescent antibody technique.
3. Silver impregnation techniques.
4. PCR as a research method.
The organism has not been cultivated in any culture media but
experimental infection can be produced in rabbits and chimpanzees. The
organism is rapidly destroyed by cold, heat, and antiseptics.
Immunology :
T. pallidum does not produce any endotoxin or exotoxin. The
pathogenesis of the lesions appears to be due to host immune response.
There are two types of serological tests for syphilis : Treponemal
and Non - Treponemal.
A. Treponemal serological tests : These tests measure antibody
to T. pallidum antigen and are as under:
i) Fluorescent treponemal antibody - absorbed (FTA - ABS) test.
ii) Agglutinin assays e.g. micro - haemagglutination assay for T.
pallidum (MHA - TP), and Serodia TP - PA which is more sensitive.
iii) T. pallidum passive haemagglutination (TPHA) test.
B. Non - treponemal serological tests - These tests measure non -
specific reaginic antibodies IgM and IgG immunoglobulins directed
against cardiolipin - lecithin - cholesterol complex and are more
commonly used.
These tests are as under :
i) Reiter protein complement fixation (RPCF) test : test of
choice for rapid diagnosis.
ii) Venereal Disease Research Laboratory (VDRL) test :
Wassermann described a complement fixing antibody against antigen of
human syphilitic tissue. This antigen is used in the Standard Test for
Syphilis (STS) in Wassermann complement fixing test and Venereal
Disease Research Laboratory (VDRL) test.
Mode of Transmission :
Syphilitic infection can be transmitted by the following routes :
1. Sexual intercourse resulting in lesions on glans penis, vulva,
vagina and cervix.
2. Intimate person - to - person contact with lesions on lips,
tongue or fingers.
3. Transfusion of infected blood.
4. Materno - foetal transmission in congenital syphilis if the
mother is infected.
STAGES OF ACQUIRED SYPHILIS :
Acquired syphilis is divided into 3 stages depending upon the
period after which the lesions appear and the type of lesions. These are :
Primary, Secondary and Tertiary syphilis.
1. PRIMARY SYPHILIS :
Typical lesion of primary syphilis is chancre which appears on
genitals or at extra - genital sites in 2 - 4 weeks after exposure to
infection. Initially, the lesion is a painless papule which ulcerates in the
centre so that the fully - developed chancre is an indurated lesion with
central ulceration accompanied by regional lymphadenitis. The chancre
heals without scarring, even in the absence of treatment.
Histologically - The chancre has following features:
i) Dense infiltrate of mainly plasma cells, some lymphocytes and
a few macrophages.
ii) Perivascular aggregation of mononuclear cells, particularly
plasma cells (periarteritis and endarteritis).
iii) Proliferation of vascular endothelium.
Antibody tests are positive in 1 - 3 weeks after the appearance of
chancre. Spirochaetes can be demonstrated in the exudates by DGI.
Organ involvement in various stages of acquired syphilis : A. Primary syphilis : Primary
lesion is ‘chancre’ on glans penis. B. Secondary syphilis : Mucocutaneous lesions - mucous
patches on oral and vaginal mucosa and generalised skin eruptions. C. Tertiary syphilis :
Localised lesion as gumma of liver with scarring (hepar lobatum), diffuse lesions (right) in
aorta (aneurysm, narrowing of mouths of coronary ostia and incompetence of aortic valve
ring) and nervous system :
2. SECONDARY SYPHILIS :
Inadequately treated patientsof primary syphilis develop
mucocutaneous lesions and painless lymphadenopathy in 2-3 months
after the exposure. Mucocutaneous lesions may be in the form of the
mucous patches on mouth, pharynx and vagina; and generalised skin
eruptions and condyloma lata in anogenital region. Antibody tests are
always positive at this stage. Secondary syphilis is highly infective stage
and spirochaetes can be easily demonstrated in the mucocutaneous
lesions.
3. TERTIARY SYPHILIS :
After a latent period of appearance of secondary lesions and
about 2-3 years following first exposure, tertiary lesions of syphilis
appear.
Lesions of tertiary syphilis are much less infective than the other
two stages and spirochaetes can be demonstrated with great difficulty.
These lesions are of 2 main types :
i) Syphilitic gumma :
It is a solitary, localised, rubbery lesion with central necrosis,
seen in organs like liver, testis, bone and brain. In liver, the gumma is
associated with scarring of hepatic parenchyma (hepar lobatum).
Histologically - The structure of gumma shows the
following features :
a) Central coagulative necrosis resembling caseation but is less
destructive so that outlines of necrosed cells can still be faintly seen.
Typical microscopic appearance in the case of syphilitic gumma of
the liver. Central coagulative necrosis is surrounded by palisades of
macrophages and plasma cells marginated peripherally by
fibroblasts :
b) Surrounding zone of palisaded macrophages with many
plasma cells, some lymphocytes, giant cells and fibroblasts.
ii) Diffuse lesions of tertiary syphilis :
The lesions appearfollowing widespread dissemination of
spirochaetes in the body. These lesions are as under :
a) Cardiovascular syphilis mainly involves thoracic aorta
- The wall of aorta is weakened and dilated due to syphilitic aortitis and
results in aortic aneurysm, incompetence of aortic valve and narrowing
of mouths of coronary ostia.
b) Neurosyphilis may manifest as - Meningovascular
syphilis affecting chiefly the meninges; tabes dorsalis affecting the spinal
cord; and general paresis affecting the brain.
CONGENITAL SYPHILIS :
Congenital syphilis may develop in a foetus of more than 16
weeks gestation who is exposed to maternal spirochaetaemia. The major
morphologic features as under :
i) Saddle - shaped nose deformity due to destruction of bridge of
the nose.
ii) The characteristic ‘Hutchinson’s teeth’ which are small,
widely spaced, peg - shaped permanent teeth.
iii) Mucocutaneous lesions of acquired secondary syphilis.
iv) Bony lesions like epiphysitis and periostitis.
v) Interstitial keratitis with corneal opacity.
vi) Diffuse fibrosis in the liver.
vii)Interstitial fibrosis of lungs.
viii) If the foetus with congenital syphilis is born dead, it is
premature, with macerated skin, enlarged spleen and liver, and with
syphilitic epiphysitis.
Histologically - The basic morphology of lesions in syphilis is
seen in all the affected organs: perivascular plasma cell rich
inflammatory infiltrate and endothelial cell proliferation. Many
spirochaetes can be demonstrated in involved tissues.
