Treponema pallidum is a spirochete bacterium that causes syphilis and other diseases. It has a thin, helical shape with periplasmic flagella and tightly coiled cells. Syphilis infection progresses through primary, secondary, latent, and tertiary stages and can involve multiple organ systems if left untreated. Diagnosis involves darkfield microscopy, serological tests like VDRL and RPR, and specific treponemal tests since the bacterium cannot be cultured.

1. Treponema pallidum
*

2.  Extremely thin and can be very long
 Tightly coiled helical cells with tapered ends
 Motile by periplasmic flagella (also known as axial
fibrils or endoflagella)
 Outer sheath encloses axial fibrils wrapped around
protoplasmic cylinder
General overview of Spirochaetales
• Axial fibrils originate from
insertion pores at both poles of
cell
• May overlap at center of cell in
Treponema and Borrelia, but not
in Leptospira
• Differering numbers of
endoflagella present according to
genus & species
Figure: Periplasmic flagella diagram
Figure: Treponema pallidum

3. Genus Species Disease
Treponema pallidum ssp. pallidum
pallidum ssp. endemicum
pallidum ssp. pertenue
carateum
Syphilis
Bejel
Yaws
Pinta
Borrelia burgdorferi
recurrentis
Many species
Lyme disease (borreliosis)
Epidemic relapsing fever
Endemic relapsing fever
Leptospira interrogans Leptospirosis
(Weil’s Disease)
Spirochaetales Associated Human
Diseases

4. Bejel (also known as endemic syphilis)
• Caused by Treponema pallidum subsp. endemicum
• Initial lesions: nondescript oral lesions
• Secondary lesions: oral papules and mucosal patches
• Late: gummas (granulomas) of skin, bones & nasopharynx
• Transmitted person-to-person by contaminated eating utensils
Yaws: granulomatous disease
• Caused by Treponema pallidum ssp. pertenue
• Early: skin lesions Late: destructive lesions of skin, lymph nodes & bones
• Transmitted by direct contact with lesions containing abundant spirochetes
Figure: Papillomatous Lesions of Yaws
(painless nodules widely distributed over
body with abundant contagious
spirochetes)

5. Pinta: (primarily restricted to skin)
• Caused by Treponema carateum
•1-3 week incubation period
• Initial lesions: small pruritic papules
• Secondary: enlarged plaques persist for
months to years
• Late: disseminated, recurrent
hypopigmentation or depigmentation of
skin lesions; scarring & disfigurement
Transmitted by direct contact with skin
lesions
Figure: Hypopigmented Skin
Lesions of Pinta
Syphilis: (Venereal Treponemal Disease)
• Primarily sexually transmitted disease (STD)
caused by T. pallidum subsp. pallidum
• May be transmitted congenitally (from mother to
fetus)

6.  Too thin to be seen with light microscopy in specimens stained with Gram
stain or Giemsa stain
• Motile spirochetes can be seen with darkfield micoscopy
• Staining with anti-treponemal antibodies labeled with fluorescent dyes
 Intracellular pathogen
 Cannot be grown in cell-free cultures in vitro
• Koch’s Postulates have not been met
 Do not survive well outside of host
• Care must be taken with clinical specimens for laboratory culture or testing
General Characteristics of Treponema pallidum

7. 1. Primary
2. Secondary
3. Latent
4. Late or tertiary
* May involve any organ, but main parts are:
* Neurosyphilis
* Cardiovascular syphilis
* Late benign (gumma)
Stages of Acquired veneral Syphilis

8. * Primary disease process involves invasion of mucus membranes, rapid
multiplication & wide dissemination through perivascular lymphatics
and systemic circulation
* Develops at site of contact/inoculation and incubation period ranges
from 9-90 days, usually ~21 days.
* Classically: single, painless, clean-based, indurated ulcer, with firm,
raised borders. Atypical presentations may occur.
* Mostly anogenital, but may occur at any site (tongue, pharynx, lips,
fingers, nipples, etc...)
* Non-tender regional adenopathy, Very infectious.
* May be darkfield positive but serologically negative.
* Untreated, heals in several weeks, leaving a faint
scar.
Primary Syphilis

9. * Secondary syphilis usually starts to manifest itself 3 to 8 weeks
after healing of primary chancre. Secondary lesions results from
the widespread multiplication of the treponemes and their
dissemination through the blood.
* Clinical signs include low fever, malaise, lymphadenopathy and
alopecia areata.
* On skin, the rash is most often maculopapular and is found on
the palms and soles.
* On mucous membranes, the rash appears in the form of
discolored patches. Condylomata lata (flat plaques) are
characteristic and found on the anal mucosa.
* In most patients, the disease is cured spontaneously due to
sufficient build up of immune response. About 13-15 % of the
untreated cases will progress to a letent stage and finally to the
tertiary stage.
Secondary Syphilis

10. *Condylomata lata
*Condylomata lata

11. Alopecia areata

12. * In latent stage, the infection remains dormant
(latent) for variable period ( usually up to 2
years) without any clinical signs and symptoms
but serological tests are positive during latent
stage.
Latent Syphilis
Tertiary or late stage Syphilis
Tertiary syphilis is characterized by localized granulomatous dermal lesions
(gummas) in which few organisms are present
• Granulomas reflect containment by the immunologic reaction of the host to chronic
infection
Late neurosyphilis develops in about 1/6 untreated cases, usually more than
5 years after initial infection
• Central nervous system and spinal cord involvement
• Dementia, seizures, wasting, etc.
Cardiovascular involvement appears 10-40 years after initial infection with
resulting myocardial insufficiency and death
May also involve deep visceral organs, particularly the respiratory tract,
gastrointestinal tract, bones, larynx, lung, liver,

13. Neurosyphilis - spirochetes in neural tissue Neurosyphilis - spirochetes in neural tissue
Late syphilis - ulcerating gumma
Tertiary or late stage Syphilis
Late syphilis - serpiginous gummata of
forearm

14. *Congenital syphilis is transmitted in utero after the first 16 weeks of pregnancy,
therefore it is usually not a cause of abortion during the first trimester.
*The infected child born later in a family usually has less severe syphilis.
*Again, it has been divided according to the arbitrary dividing line of two years
into early and late types.
*Early Congenital
*The features are similar to secondary syphilis. Usually it occurs 2-8 weeks after
birth, presenting with failure to thrive, muco-cutaneous lesions (condylomata
lata), generalized lymphadenopathy, nasal snuffles and skin rash.
*Late Congenital
*The onset usually occurs at or near puberty. Well-known stigmata include nerve
deafness, interstitial keratitis, Hutchison's teeth (Hutchison's triad), rhagades
around mouth, clutton's joint, osteitis & chondritis (saddle nose, frontal bossing,
sabre tibia) and perforated palate.
Congenital syphilis

15. Congenital syphilis - perforation of palate

16. Diagnostic Tests for Syphilis
NOTE: Treponemal antigen tests indicate experience with a treponemal
infection, but cross-react with antigens other than T. pallidum ssp.
pallidum.
(Original Wasserman Test)

17. Laboratory diagnosis
• Since T. pallidum cannot be cultured in clinical laboratory, the diagnosis of syphilis
consist of direct demonstration of the treponema and serological tests for detection
of antibodies .
A. Direct demonstration of treponema by dark-ground microscopy: Under dark-ground
illumination, T. pallidum appears as a slender, spiral organism exhibiting rotational
as well as flexion and extension movements
B. Stained preparation: for direct demonstration of T. pallidum , acetone fixed smears
are made from exudate and stained either by silver impregnation method
(Fontana’s stain) or by fluorescein labelled anti-treponemal antibody (fluorescein
labelled antibody test). In positive cases, treponemes fluoresce displaying typical
morphology when viewed under fluorescent microscope.

18. C. Tissue Biopsy:
Treponemes can be demonstrated in tissues (skin, visceral lesion) by silver
impregnation method of staining or by Warthin-Starry stain or by
immunofluorescence in tertiary syphilis.
Serological Tests:
In addition to blood, CSF is also examined in relevant cases.
I. Non-treponemal tests: In the standard tests for syphilis (STS), reagin antibodies
in patient serum is detected by cardiolipin antigen. Before performing the
test, the patient’s serum is inactivated by heating in a waterbath at 560C for
30 minutes to destroy the complement. The STS includes flocullation tests
(VDRL, RPR, TRUST, KT) and complement fixation test
a. Flocculation test: VDRL (Venereal Disease Research laboratory) test
It is the most widely used simple and rapid test. The VDRL antigen must be prepared
freshly. In a specially prepared slide with depression of 14 mmdiameter each, 0.05
ml decomplemented serum is taken to which one drop of freshly prepared
cardiolipin antigen is added by a syringe delivering 60 drops in one ml. the slide is
then rotated at 180 revolutions per minute for four minutes either by VDRL rotator
or manually. The antigen-antibody reaction is then studied under low power
objective of microscope. Uniformly distributed crystals indicate negative test while
presence of clumps signifies positive reaction. Quantitative tests with serial
dilutions (1:4, 1:8 and so on ) of positive serum are performed.

19. b. Rapid plasma reagin (RPR) test:
It is almost similar to VDRL test where finely divided carbon (charcoal)
particles and choline are added to stabilized VDRL antigen. The
addition of finely divided carbon particles enable the result to be read
visually instead of microscopically.
C. Toludine red unheated serum test (TRUST):
It is a modification of RPR card test. The antigen is more stable then
RPR antigen and can be stored at room temperature.
 Commonly used specific tests for syphilis are the treponemal
antibody test, FTA-ABS test and the MHA-TP:
These tests use recombinant proteins or treoponemal antigens extracted
from T. pallidum. Tests in common use include:
• Enzyme-linked immunosorbent assays which detect IgM and IgG.
• The Fluorescent treponemal antibody absorption (FTA-ABS) test in which the
patient’s serum is first absorbed with non-pathogenic treponemes to remove
cross-reacting antibodies before reaction with T. pallidum antigens;
• The micro-hemagglutination assay for T. pallidum (MHA-TP)