2. Spirochetes with their diseases
1)Treponema pallidum- Syphilis
Non veneral treponemotoses
2)Borellia recurrentis- Relapsing fever
Borellia burgdorferi- Lyme disease
3)Leptospira- Leptospirosis
3. Treponema pallidum
• Pathogenesis•
•
•
•
•
Agent- Treponema pallidum
Host-Human
Disease- Syphilis
Reservoir- Patient of syphilis
Source of infection-
Primary syphilis- Exudate of ulcer containing bacteria
Secondary syphilis- Muco cutaneous rash
Blood- for both primary & secondary.
4. • Mode of transmission1)Acquired syphilis Sexual contact
Blood
2)Congenital syphilis From mother- fetus
5. Primary syphilis
• T.pallidum can not penetrate intact skin. They
enter into the body through abraded skin
invade locally into blood vessels & lymphatics
multiply within 3-4 weeks they produce local
lesion.
Papule macule vesicle (fluid accumulates) vesicle
rupture painless ulcer Hard chancre (Hallmark)
This is highly contagious stage. Within next 24weeks, ulcer heals spontaneously.
6. Secondary syphilis
• It is the disseminated stage of the disease.
• 4-8 weeks after healing ulcer, patient develop
maculopapular rash involving all over the body
including palm & sole
( characteristics)
• When the lesion occurs in the moist area, peri
anal region condylomata lata
( Hallmark)
8. Latent Syphilis
• Here the patient is infected with the
bacteria but he/she is asymptomatic. The
serological test is positive.
• Types-2
Latent syphilis
Early latent (within 2yrs)
Late latent (3-4yrs after)
May progress to tertiary syphilis
9. • Clinical significance1)In early latent patient ,patient remains
infectious but in late latent patient
becomes non- infectious.
2)It is very dangerous condition.
• Confirmation1) Patient have no S/S
2)Serological test positive
10. Congenital syphilis
• Definition- Syphilis that are transmitted
from mother to fetus when mother is
attacked byprimary & secondary syphilis
rarely in latent syphilis
• Transmission occurs after16th weeks of
pregnancy b/c of atrophy of
syncytiotrophoblast layer.
12. Diagnosis
• Just after delivery,if mother is untreated with
penicillin, both VDRL & TPHA of baby & mother
will be done.
Mother
VDRL- 1:4
TPHA- 1:4
Baby
1:16
1:4
• So 1 month afterVDRL- 1:4
1:4
Comment
Baby is infected
May be it comes from
mother /produced by the baby.
1:8
1:2
Form within the baby
Comes from mother.
13. Diagnosis
• SampleA)Exudate- from primary chancre
B)Serum
• Lab procedureA) Exudate1)Dark field microscopyBright ,slender, spiral bacteria with crock-screw &
flexion-extension motility
2) Immunofluroscence microscopy
19. Histopathology
Primary syphilis• Surface of the ulcer- Treponema are visible in
warthin starry and Immunofluroscence staining.
• Chancre contains infiltration of plasma cells
with scattered macrophages & lymphocytes and
a proliferative endarteritis.
20. Secondary syphilis
• Mucocutaneous lesion shows infiltration of
plasma cell & obliterative endarteritis.
Tertiary syphilis• GummaCenter- Coagulative necrosis
Margin- palisading macrophages & fibroblasts
surrounded by mononuclear leukocytes chiefly
plasma cells. Treponema are scanty in gumma .
21. VDRL
• Advantage1)Very simple
2)Can be done in field level
3)The result may be
quantitive & qualitative.
4)The test is sensitive 70%
in primary syphilis & 98%
in secondary syphilis.
5)Neurosyphilis can be
diagnosed.
• Disadvantage
1)The Ab against Tp takes
about 3-5 weeks times to
become appear. So
before 3-5 weeks it will
show false negative.
2)May give false positive.
22. TPHA
• Advantage1)Very simple
2)Can be done in field level
3)The result may be
quantitive & qualitative.
4)TPHA is very sensitive
5) It detects specific Ab.
5)Can detect neurosyphilis
& latent syphilis.
• Disadvantage
Once become positive,
remains positive for long
time even in cured
patient.
23. Neurosyphilis
• Lab DiagnosisSpecimen- 1)Serum 2)CSF
Lab test1)Serum• TPHA- must be positive
• VDRL-Reactive/ Non reactive
2)CSF• TPHA- positive
• Cell count-lymphocytosis
• Protein-Increase.
24. Serological problem in syphilis
positive HIV
1)Confusing clinical s/s
2)Lack of serological response
3)VDRL,TPHA- non reactive
4)Due to CD4 & CD4:CD8Tp Ab takes long
time to disappear.
5) May be high Ab titer due to B cell
activation.