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SYPHILIS
INTRODUCTION
 Syphilis is a venereal (sexually transmitted) disease caused
by spirochetes treponema pallidium , characterised by
periods of latency.
 The word syphilis is derived from the name of
mythological handsome boy,syphilus who was cursed by
greek god apollo with the disease.
CAUSATIVE ORGANISM
• Palladium is a coiled spiral filament.the organism
cannotreponema t be stained by usual methods and can be
demonstrated in the exudates and tissues by:
• Dark ground illumination (DGI) in fresh preparation
• Fluorescent antibody technique
• Silver impregnation techniques
• Nucleic acid amplification techniques by PCR
INCIDENCE
 Since the advent of penicillin therapy in 1843 , syphilis has
shown a decline in incidence.
 Syphilis in pregnant women and adverse outcome of
pregnancy (eg stillbirths neonatal and early fetal death and
baby born with syphilis )are significant health problems in
some countries such as china.
MODE OF TRANSMISSION
 Sexual transmission –most common route of infection .
 Intimate person –to-person contact with lesions on
lips,tongue or fingers.
 Transfusion of infected blood.
 Materno-foetal transmission in congenital syphilis if the
mother is infected.
STAGES OF SYPHILIS
PRIMARY SYPHILIS
 Typical lesion of primary syphilis is chancre which appears on
genital or at extragenital sites in 2-4 weeks after exposure to
infection initially the lesion is painless papule which ulcer rates in
the centre.
 The fully developed chancre is indurated lesion with central
ulceration accompanied by regional lymphadenitis heals without
scarring even in the absence of treatment.
 Antibody test are positive in 1to 3 weeks after the the appearance
of chancre spirochetes can be demonstrated in the exudates
DGI.
HISTOLOGICALLY
THE CHANCRE HAS THE FOLLOWING FEATURES:
Dense infiltrate of mainly plasma cells ,some lymphocytes
and few macrophages .
Perivascular aggregation of mononuclear cells, particularly
plasma cells (periarteritis and endarteritis ).
Proliferation of vascular endothelium.
SECONDARY SYPHILIS
Inadequately treated patients of primary syphilis develop
mucocutaneous lesions and painless lymphadenopathy in 2 to 3
months after the exposure.
 Mucocutaneous lespions maybe in the form of mucous patches on
mouth ,pharynx and vagina and generalized skin eruptions and
condyloma lata in ano- genital region.
Antibody test are always positive at this stage secondary syphilis is
highly infective state and spirochetes can be easily demonstrated in
mucocutaneous lesions.
TERTIARY SYPHILIS
After a latent period of appearance of secondary lesions
and 2-3 years following the first exposure tertiary lesions
of syphilis appear. lesions of tertiary syphilis are much
less effective than the other two stages and spirochaetes
can be Demonstrated with great difficulty .
These lesions are of two main types:
 Syphilitic gumma
 Diffuse lesions
SYPHILITIC GUMMA:
 It is solitary, localised
rubbery lesion with central
necrosis seen ine organs like
liver, testis ,bone and brain.
In the liver the gumma is
associated with scarring of
hepatic parenchyma
(heparlobatum)
DIFFUSE LESIONS OF
TERTIARY SYPHILIS:
Cardiovascular syphilis :
it mainly involves thoracic
aorta .the wall of aorta is
weakened and dilated due to
syphilitic aortitis and result
in aorticaneurysm.
Incompetence of aortic
valve and narrowing of
mouths of coronary ostia.
TERTIARY SYPHILIS
HEPAR LOBATUM AORTICANEURYSM
NEUROSYPHILIS
IT MAY MANIFEST AS;
 Meningovascular syphilis affecting
chiefly the meninges.
 Tabes dorsalis (slow degeneration if
nerve cells and nerve fibers)
affecting the spinal cord .
 General paresis(muscular weakness
caused by nerve damage) affecting
the brain.
NEUROSYPHILIS
CONGENITAL SYPHILIS:
Congenital syphilis may develop in a foetus of more than 16 weeks gestation who
is exposed to maternal spirochetamia . following major morphological features of
seen other at birth or develop subsequently:
Saddle-shaped nose deformity due to destruction of bridge of nose
characterisic hutchinson’s teeth which are small,widely spaced,peg-shaped
permanent teeth.
Mucocutaneous lesions of acquired secondary syphilis
bony lesions like epiphysitis and periostitis
Interstitial keratitis and corneal opacity
Diffuse fibrosis in the liver and interstitial fibrosis of lungs .
HISTOLOGICALLY
The basic morphology of lesions in syphilis is seen in all
the affected organs
Perivascular plasma cells rich in inflammatory infiltrate
and endothelial cell proliferation.
Many spirochetes can be demonstrated in involved
tissues.
IMMUNOLOGY AND TESTS:
Treponema pallidum does not produce any endotoxin and exotoxin the pathogenesis of lesion
appears to be due to host immune response
There of two types of serological test for syphilis:
Treponemal .
Non –treponemal.
A.Treponemal serological tests:
This tests measure antibody to t.palladium antigen and are most useful and sensitive for the
diagnosis of syphilis :
Fluorescent treponema antibody _absorbed(FTA_ABS) test.
Agglutinin assays e.g.microhaemagluttination assay for t.pallidum (MHA-TP) and serious tp-pa.
T.pallidum passive hemagglutinin(TPHA) test.
B.NON-TREPONEMAL SERILLOGICAL TESTS:
These tests measure non –specific reaginic antibodies IgG and IgM immunoglobulins
directed against cardiolipin –lecithin-cholesterol complex are commonly ,the tests
are as under:
Reiter protein complement fixation (RPCF) test: test of choice for rapid diagnosis.
Venereal disease research laboratory(VDRL) or rapid plasma reagin (RPG)test .
Wasserman described a complement fixing antibody against antigen of human
syphilitic tissue .
This antigen is used in standard test for syphilis (STS) in
Wassermann complement fixing test and VDRL test
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Syphilis

  • 2. INTRODUCTION  Syphilis is a venereal (sexually transmitted) disease caused by spirochetes treponema pallidium , characterised by periods of latency.  The word syphilis is derived from the name of mythological handsome boy,syphilus who was cursed by greek god apollo with the disease.
  • 3. CAUSATIVE ORGANISM • Palladium is a coiled spiral filament.the organism cannotreponema t be stained by usual methods and can be demonstrated in the exudates and tissues by: • Dark ground illumination (DGI) in fresh preparation • Fluorescent antibody technique • Silver impregnation techniques • Nucleic acid amplification techniques by PCR
  • 4.
  • 5. INCIDENCE  Since the advent of penicillin therapy in 1843 , syphilis has shown a decline in incidence.  Syphilis in pregnant women and adverse outcome of pregnancy (eg stillbirths neonatal and early fetal death and baby born with syphilis )are significant health problems in some countries such as china.
  • 6. MODE OF TRANSMISSION  Sexual transmission –most common route of infection .  Intimate person –to-person contact with lesions on lips,tongue or fingers.  Transfusion of infected blood.  Materno-foetal transmission in congenital syphilis if the mother is infected.
  • 8.
  • 9. PRIMARY SYPHILIS  Typical lesion of primary syphilis is chancre which appears on genital or at extragenital sites in 2-4 weeks after exposure to infection initially the lesion is painless papule which ulcer rates in the centre.  The fully developed chancre is indurated lesion with central ulceration accompanied by regional lymphadenitis heals without scarring even in the absence of treatment.  Antibody test are positive in 1to 3 weeks after the the appearance of chancre spirochetes can be demonstrated in the exudates DGI.
  • 10.
  • 11. HISTOLOGICALLY THE CHANCRE HAS THE FOLLOWING FEATURES: Dense infiltrate of mainly plasma cells ,some lymphocytes and few macrophages . Perivascular aggregation of mononuclear cells, particularly plasma cells (periarteritis and endarteritis ). Proliferation of vascular endothelium.
  • 12. SECONDARY SYPHILIS Inadequately treated patients of primary syphilis develop mucocutaneous lesions and painless lymphadenopathy in 2 to 3 months after the exposure.  Mucocutaneous lespions maybe in the form of mucous patches on mouth ,pharynx and vagina and generalized skin eruptions and condyloma lata in ano- genital region. Antibody test are always positive at this stage secondary syphilis is highly infective state and spirochetes can be easily demonstrated in mucocutaneous lesions.
  • 13.
  • 14. TERTIARY SYPHILIS After a latent period of appearance of secondary lesions and 2-3 years following the first exposure tertiary lesions of syphilis appear. lesions of tertiary syphilis are much less effective than the other two stages and spirochaetes can be Demonstrated with great difficulty . These lesions are of two main types:  Syphilitic gumma  Diffuse lesions
  • 15.
  • 16. SYPHILITIC GUMMA:  It is solitary, localised rubbery lesion with central necrosis seen ine organs like liver, testis ,bone and brain. In the liver the gumma is associated with scarring of hepatic parenchyma (heparlobatum) DIFFUSE LESIONS OF TERTIARY SYPHILIS: Cardiovascular syphilis : it mainly involves thoracic aorta .the wall of aorta is weakened and dilated due to syphilitic aortitis and result in aorticaneurysm. Incompetence of aortic valve and narrowing of mouths of coronary ostia.
  • 18. NEUROSYPHILIS IT MAY MANIFEST AS;  Meningovascular syphilis affecting chiefly the meninges.  Tabes dorsalis (slow degeneration if nerve cells and nerve fibers) affecting the spinal cord .  General paresis(muscular weakness caused by nerve damage) affecting the brain.
  • 20. CONGENITAL SYPHILIS: Congenital syphilis may develop in a foetus of more than 16 weeks gestation who is exposed to maternal spirochetamia . following major morphological features of seen other at birth or develop subsequently: Saddle-shaped nose deformity due to destruction of bridge of nose characterisic hutchinson’s teeth which are small,widely spaced,peg-shaped permanent teeth. Mucocutaneous lesions of acquired secondary syphilis bony lesions like epiphysitis and periostitis Interstitial keratitis and corneal opacity Diffuse fibrosis in the liver and interstitial fibrosis of lungs .
  • 21. HISTOLOGICALLY The basic morphology of lesions in syphilis is seen in all the affected organs Perivascular plasma cells rich in inflammatory infiltrate and endothelial cell proliferation. Many spirochetes can be demonstrated in involved tissues.
  • 22. IMMUNOLOGY AND TESTS: Treponema pallidum does not produce any endotoxin and exotoxin the pathogenesis of lesion appears to be due to host immune response There of two types of serological test for syphilis: Treponemal . Non –treponemal. A.Treponemal serological tests: This tests measure antibody to t.palladium antigen and are most useful and sensitive for the diagnosis of syphilis : Fluorescent treponema antibody _absorbed(FTA_ABS) test. Agglutinin assays e.g.microhaemagluttination assay for t.pallidum (MHA-TP) and serious tp-pa. T.pallidum passive hemagglutinin(TPHA) test.
  • 23. B.NON-TREPONEMAL SERILLOGICAL TESTS: These tests measure non –specific reaginic antibodies IgG and IgM immunoglobulins directed against cardiolipin –lecithin-cholesterol complex are commonly ,the tests are as under: Reiter protein complement fixation (RPCF) test: test of choice for rapid diagnosis. Venereal disease research laboratory(VDRL) or rapid plasma reagin (RPG)test . Wasserman described a complement fixing antibody against antigen of human syphilitic tissue . This antigen is used in standard test for syphilis (STS) in Wassermann complement fixing test and VDRL test