Treponema pallidum is a spirochete bacterium that causes the sexually transmitted disease syphilis. It has four stages: primary, secondary, latent, and tertiary. Primary syphilis presents as a chancre, while secondary syphilis causes a rash and mucous membranes lesions. Without treatment, later stages can involve the cardiovascular system, central nervous system, and other organ systems. Syphilis screening and treatment are important for preventing transmission and progression of disease.

1. OM SAKTHI

2. SYPHILIS

4. CAUSED BY TREPONEMA
PALLIDAM
It is a sexually transmitted disease

5. Caused by Treponema pallidum.
Caused by Treponema pallidum.
Transmission: sexual; maternal-fetal, and rarely by other
means.
Primary and secondary syphilis in the US dropped by ~ 90 %t
from 1990 to 2000, the number of cases have gone up since
then.
A dramatic increase in cases in men from 2000 to 2002
reflected syphilis in MSM.
Syphilis increases the risk of both transmitting and getting
infected with HIV.
Do HIV testing in all patients with syphilis: sexual; maternal-
fetal, and rarely by other means.

6. syphilis
• Treponema pallidam
• Slender ,cork screw shaped
• fragile, can be killed by soap,drying,cold and
antiseptics.

7. Transmission
• Sexual contact ; syphilis is an transmitted by
direct contact between an open lesion full of
spirochetes and genital mucosa or abraded
genital skin causes transmission of the
spirochete.
• Intimate person to person contact ; contact of
an open lesion with nipples,fingers and
rectum,mouth,lips,tongue.

8. Transmission
• Materno-foetal transmission
• Syphilis may spread from an infected
mother to the foetus .called as congenital
syphilis.
• Blood transfusion.

9. Stages of syphilis
• Primary syphilis
• Secondary syphilis
• Tertiary syphilis

10. primarysyphilis
• Characteristic lesion is chancre
• Sites ; penis, vulva, cervix,anus ,mouth
• Gross appearance; papule formation ,red
coloured ,slightly elevated with firm border
makes it a button like mass -hard chancre.
• Ulcer, papule erodes to form ulcer

13. Microcopic appearance
• End arteritis ; The capilllary endothelium
proliferates along with fibrosis of intima
obliterating the lumen. The wall is infiltrated
by lymphocytes.
• Plasma cell infiltration ; dense infiltration of
plasma cells. Lymphocytes and macrophages
also the lesion.
• Spirochetes identified in the ulcer bed

14. Clinical features
• Chancre appears three weeks after contact
• Chancre is painless and often goes
unnoticed
• Chancre heals spontaneously after 3-8
weeks.

15. SECONDARY SYPHILIS
Seen 6 wks to 6 mos after primary chancre
Usually with diffuse non-pruritic, indurated rash,
including palms & soles.
May also cause:
Fever, malaise, headache, sore throat, myalgia,
arthralgia, generalized lymphadenopathy

16. • Hepatitis (10%)
• Renal: an immune complex type of
nephropathy with transient nephrotic
syndrome
• Iritis or an anterior uveitis
• Bone: periostitis
• CSF pleocytosis in 10 - 30% (but, symptomatic
meningitis is seen in <1%)

17. Skin lesions
• Diffuse,
• often with a superficial scale
(papulosquamous).
• May leave residual pigmentation or
depigmentation.

18. Condyloma lata
• Formed by coalescence of large, pale, flat-
topped papules.
• Occur in warm, moist areas such as the
perineum.
• Highly infectious.

19. Mucosal lesions
• 30% of secondary syphilis patients develop
mucous patch (slightly raised, oval area
covered by a grayish white membrane, with a
pink base that does not bleed).
• Highly infectious

20. Secondary syphilis
• Mucocutaneous lesions ,painless
lymphadenopathy, condyloma latum
• Mucocutaneous lesions ; red coloured
maculopapular rash.sometimes they may be
pustular. The sites are
• Palms, soles, trunk, extremities

21. Secondary syphilis
• Painless lymphadenopathy; lymphoid follicles
are enlarged. Numerous spirochetes can be
identified.
• Condyloma latum ; broad elevated
exudative plaques. Highly infective lesions
containing numerous spirochetes. Sites are
• Perineum, vulva, scrotum.

25. ALOPECIA AREATA

31. Microscopically
• Plasma cell infiltration and end arteritis
obliterans.

32. SECONDARY SYPHILIS
Differential diagnosis
• The rash may be confused with
• Pityriasis rosea (usually has a herald patch and lesions seen along
lines of skin cleavage)
• Drug eruptions
• Acute febrile exanthems
• Psoriasis
• Lichen planus
• Scabies
• The mucous patch may be confused with oral thrush.
• Malaise, sore throat, generalized adenopathy, hepatitis, & rash may
be confused with infectious mononucleosis.
• Fortunately, the serologic tests for syphilis are positive in 99% of
secondary syphilis pts.

33. Tertiary syphilis
• Rare due to medical treatment .
• Untreated cases an asymptomatic period
follows after secondary syphilis has
subsided.
• Syphilitic aortitis , neurosyphilis-
meningovascular syphilis ,tabes dorsalis .
General paresis , gumma formation.

34. Syphilitic aortitis
• Syphilitic involvement of the aorta
• Saccular aneurysm ; involves ascending aorta .
• Pathogenesis ; the vascular lesion of the syphilis
‘’endarteritis obliterans ‘ slowly obliterates the
vasa vasorum causes necrosis of the aortic
media leading to weakening of the aortic wall .
• Aortic Wall slowly stretches giving rise to sac
like dilatation called saccular aneurysm.

35. Aortic insufficiency
• Necrosis of the media due to endarteritis
obliterans is replaced by fibrous tissue due to
which the aorta looses its elastic strength and
slowly dilates
• Involves ascending aorta it leads to dilatation
of aortic ring
• Aortic wall fail to close properly causing
regurgitation and aortic insufficiency.
• Aortic intima – appears rough and pitted called
tree bark appearance.

36. SACCULAR ANEURYSM

37. Meningovascular syphilis
• Shows chronic meningitis
• Site of involvement ; base of the brain ,
cerebral complexes, spinal leptomeninges.
• Microscopically shows obliterative
endarteritis. The inflammatory cells consists
mainly of plasma cells.

38. SYPHILITIC MENINGITIS
• ‘Aseptic meningitis’
• Usually within the first year of infection, but may occur at any time after
the primary stage.
• CSF shows:
• Lymphocytic pleocytosis
• Elevated protein and usually normal glucose concentrations

39. • VDRL test is usually reactive.
• It can mimic tuberculous or fungal meningitis
or aseptic meningitis of various causes.
• Often involves the base of the brain and may
result in unilateral or bilateral cranial nerve
palsies.
• Without treatment, syphilitic meningitis
usually resolves, like the other manifestations
of early

40. Tabes dorsalis
• Tabes dorsalis is due to demyelination
damage by the spirochete of the posterior
columns, dorsal roots and dorsal root
ganglia.

41. TABES DORSALIS
• It’s a slowly progressive, degenerative disease involving the
posterior columns and posterior roots of the spinal cord.
• Results in progressive loss of peripheral reflexes, impairment
of vibration and position sense, and progressive ataxia.
• Sudden and severe painful crises are a characteristic:
• Usually involve the lower extremities but may occur at any
site.

42. Tabes dorsalis
• Loss of axon and myelin in the dorsal roots
• Atrophy of dorsal column.

43. • Severe, sharp abdominal pains may lead to
exploratory surgery.
• Attacks may be triggered by exposure to cold or
other stresses or may arise with no obvious
precipitating cause.
• Bladder incontinence & impotence are common.
• Chronic destructive changes of the large joints of
the affected limbs may be seen in advanced cases
(i.e., Charcot's joints).

44. Tabes dorsalis
• Clinical picture ;
• Ataxia –wide based gait due to impaired joint
position sense.
• Loss of position sense
• Loss of deep pain sensation often resulting in
ulceration of feet.
• Loss of temperature sensations.
• Degeneration of joints (charcots joints)
• Argyll robertson pupil. Pupil becomes irregular.

45. TABES DORSALIS
• Optic atrophy is seen in 20% of cases.
• Typical cases present with: lightning pains,
ataxia, Argyll Robertson pupils, absent deep
tendon reflexes, and loss of posterior column
function. Atypical cases are difficult to
diagnose.
• Serum VDRL may be non-reactive in 30 - 40%,
CSF-VDRL may be non-reactive in 10-20%,
serum FTA-ABS is almost always reactive.

46. General paresis
• General paresis occurs because of wide
spread brain parenchymal damage by
spirochete. Clinically it manifests as
• Illusion, delusion of grandeur , hallucinations
,severe dementia.

47. General paresis
• Loss of neurons
• Proliferation of rod cells
• Increase in glial cells called gliosis
• Granular ependymitis – proliferation of
subependymal glial cells.

48. Gumma formation
• Gumma formations are solitary or multiple
localised nodular lesions .
• They are rubbery with central area of
necrosis.
• They commonly occur in bone, skin,brain,
mucous membrane of upper airway.
• Liver –liver gummas cause scarring of liver
parenchyma called hepar lobatum.

51. Other types of syphilis
• Congenital syphilis
• Congenital syphilis occurs due to materno-
foetal transmission.
• If Mother is suffering from primary or
secondary stage of syphilis , the spirochetes
are numerous .
• If pregnancy occurs in these stages,
spirochetes crosses the placenta and enters
the foetus.

52. Congenital syphilis
• Due to antibiotic therapy and routine
serologic testing during pregnancy
congenital syphilis is rare.
• Infantile or early syphilis (within 2 years of
age)
• Tardive or late syphilis (after 2years of age)
• Intra uterine death
• Perinatal death.

53. Infantile syphilis
• Bullous eruptions ; bullous eruptions leads
to sloughing of the skin . The sites are
• Palm, soles, around mouth , anus
• Osteochondritis ; osteochondritis is
inflammation of bone and cartilage mainly
plasmacytic inflammation. It affects all bones
-nasal bone involvement causes destruction
of vomer leading to collapse of the nasal
bridge called ‘‘saddle nose’’ deformity

54. SADDLE NOSE DEFORMITY

55. Infantile syphilis
• Periostitis ; periostitis of tibia leads to
excessive new bone formation on the
anterior surface of tibia leading to anterior
bowing –saber shin deformity
• Nasal discharge.

56. SABER SHIN DEFORMITY

57. Tardive or late syphilis
• Characteristic manifestation is HUTCHINSON
TRIAD
• Central incisors are notched and peg shaped
• Interstitial keratitis wit blindness
• Eighth, cranial nerve injury causing deafness.

58. LATENT SYPHILIS
• Positive syphilis serology without clinical signs of
syphilis (& has normal CSF).
• It begins with the end of secondary syphilis and may
last for a lifetime.
• Pt may or may not have a h/o primary or secondary
syphilis.
• Diseases known to cause occasional false-positive
nontreponemal test reactions for syphilis, such as
systemic lupus erythematosus (SLE), and congenital
syphilis must be excluded before the diagnosis of latent
syphilis can be made.
• Is divided into early and late latency

59. LATE OR LATENT SYPHILIS
• Early latent:
• The first year after the resolution of primary or
secondary lesions, or
• A reactive serologic test for syphilis in an
asymptomatic individual who has had a negative
serologic test within the preceding year.
• Infectious.
• Late latent:
• Usually not infectious, except for the pregnant
woman, who may transmit infection to her fetus

61. Lab diagnosis
• Detection of specific antibodies
• Detection of wassermann antibodies ; this is
a complement fixing antibody against
antigen of syphilis
• Wassermann complement fixing test.
• Venereal disease research laboratory
test(VDRL)

62. Lab diagnosis
• Detection of treponemal antibodies ;
treponemal antibodies bind with treponemal
protein
• Treponemal pallidum immobilisation
test(TPI)
• Fluorescent treponemal antibody test (FTA)
• Treponema pallidum haemagglutination
test(TPHA)
• Reiter protein complement fixation test(RPCF)

63. DARK FIELD EXAMINATION

64. HISTO PATHOLOGY

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