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2. Spirochetes
Are bacteria with a spiral morphology ranging from loose
coils to a rigid corkscrew shape.
The order Spirochaetales is subdivided into two families:
Spirochaetaceae and Leptospiraceae. The family
Spirochaetaceae consists of four genera: Spirochete,
Cristispira, Treponema, and Borrelia. The genera
Treponema and Borrelia include pathogenic species, which
cause diseases in humans. Members of the genus
Cristispira are found in molluscs, while Spirochetes are
saprophytes found in sewage and water. Family
Leptospiraceae contains only one genus Leptospira, which
consists of species pathogenic to humans.

3. Morphology
Spirally coiled and hair like extremely thin
•Cannot be visualized by light microscope
•Visualized by dark field, fluorescent microscope or
silver staining methods (to increase the thickness)
•Pathogenic spirochetes- Treponema, Borrelia,
Leptospira
•Motile but possess endoflagella
•Motility – cork screw, lashing, flexion- extension,
rotatory

5. Treponema pallidum
Was discovered by Schaudinn and Hoffmann
(1905) in the chancres and inguinal lymph
nodes of syphilitic patients.
The generic name Treponema is derived from
Greek word «Trepos», meaning to turn and
«nema» meaning thread.

6. A Brief History of Syphilis
• Syphilis was first recognized in Europe near the end of the fifteenth century. During this
time, the disease reached epidemic proportions in the Mediterranean areas. According to
one hypothesis, syphilis is of New World origin and Christopher Columbus (1451-1506)
and his crew acquired it in the West Indies and introduced it into Spain after returning from
their historic voyage. Another hypothesis is that syphilis had been endemic for centuries in
Africa and may have been transported to Europe at the same time that vast migrations of
the civilian population were occurring (1500). Others believe that the Vikings, who reached
the New World well before Columbus, were the original carriers. Syphilis was initially
called the Italian disease, the French disease, and the great pox as distinguished from
smallpox. In 1530 the Italian physician and poet Girolamo Fracastoro wrote "Syphilis sive
Morbus Gallicus" ("Syphilis or the French Disease"). In this poem, a Spanish shepherd
named Syphilis is punished for being disrespectful to the gods by being cursed with the
disease. Several years later, Fracastoro published a series of papers in which he described
the possible mode of transmission of the "seeds" of syphilis through sexual contact. Its
venereal transmission was not definitely shown until the eighteenth century. Recognition of
the different stages of syphilis was demonstrated in 1838 by Philippe Ricord, who reported
his observations on more than 2,500 human inoculations. In 1905 Fritz Schaudinn and
Erich Hoffmann discovered the causative bacterium, and in 1906 August von Wassermann
introduced the diagnostic test that bears his name. In 1909 Paul Ehrlich introduced an
arsenic derivative, arsphenamine or salvarsan, as therapy.

8. Culture characteristics
The sluggish growth (mean generation time more than 30 hours) of T.pallidum
is felt to be due to lack of enzymes that detoxify reactive oxygen species
(catalase, oxidase) and the absence of efficient energy (ATP)-producing
pathways such as the tricarboxylic acid cycle and electron transport chain.
Treponema pallidum shares the Gram-negative structural style of other
spirochetes, but its outer membrane lacks lipopolysaccaride (LPS) and contains
few proteins.
• T.pallidum doesn’t grow in artificial media.
• Maintained in rabbit testes (Nichol’s strain)
• Non pathogenic spp (Reiter Treponema) culture tried on Smith Noguch
medium

9. Sensitivity to physical and chemical agents:
Treponema pallidum is extremely susceptible to any
deviation from physiologic conditions. It dies rapidly on
drying and is readily killed by a wide range of
detergents and disinfectants. The lethal effect of even
modest elevations of temperature (41-42°C) was the
basis for the technique of fever therapy for syphilis
introduced in Vienna a century ago

10. Pathogenicity factors
• Cardiolipin antigen is a hapten and is chemically a
diphosphatidyl glycerol. The hapten elicits the production of an
antibody, known as reagin antibody.
• Group- specific antigen is protein in nature
• Species- specific antigen is probably polysaccharide
• Outer membrane proteins- promote adherence
• Hyaluronidase – facilitates perivascular infiltration
• Fibronectin – prevents phagocytosis

11. Reservoir – human
genital tract
Transmission-
transmitted sexually
or across the
placenta

12. EPIDEMIOLOGY
• Geographical distribution Syphilis occurs worldwide, mostly
in large cities. The disease is extremely common in areas of
dry, hot climates. Also, it is common in areas of poor
economic status, education, and personal hygiene. The
condition is prevalent in parts of Africa (e.g., Sudan, Southern
Rhodesia, South Africa), parts of the Middle East (e.g.,
Nomadic/Bedouin tribes of Saudi Arabia, Iraq, and Syria),
and parts of Asia (e.g., Turkey, Southeast Asia, the Western
Pacific) and India.

13. PATHOGENESIS
•The spirochete reaches the subepithelial tissues through
unapparent breaks in the skin or possibly by passage
between the epithelial cells of mucous membranes aided by
at least one adhesin that binds to fibronectin and elements of
the extracellular matrix. In the submucosa, it multiplies
slowly stimulating little initial tissue reaction. This is
probably due to the relative paucity of antigens in the T
pallidum outer membrane that would be exposed to the
immune system. As lesions develop, the basic pathologic
finding is an endarteritis.

14. PATHOGENESIS
The small arterioles show swelling and proliferation of their
endothelial cells. This reduces or obstructs local blood supply,
probably accounting for the necrotic ulceration of the primary
lesion and subsequent destruction at other sites. Dense,
granulomatous cuffs of lymphocytes, monocytes, and plasma
cells surround the vessels. There is no evidence that this
injury is due to any toxins or other classic virulence factors
produced by T. pallidum. Although the primary lesion heals
spontaneously, the bacteria have already disseminated to other
organs by way of local lymph nodes and the bloodstream.

15. CLINICAL ASPECTS MANIFESTATIONS
Primary Syphilis
• The primary syphilitic lesion is a papule that evolves to an ulcer at
the site of infection. This is usually the external genitalia or cervix,
but could be in the anal or oral area depending on the nature of
sexual contact. The lesion becomes indurated and ulcerates but
remains painless, though slightly sensitive to touch. The fully
developed ulcer with a firm base and raised margins is called the
chancre. Firm, nonsuppurative, painless enlargement of the regional
lymph nodes usually develops within 1 week of the primary lesion
and may persist for months. The median incubation period from
contact until appearance of the primary lesion is about 3 weeks
(range 3-90 days). It heals spontaneously after 4 to 6 weeks

16. • Secondary (or disseminated) syphilis develops 2 to 8 weeks after
the appearance of the chancre. The primary lesion has usually
healed but may still be present. This most florid form of syphilis is
characterized by a symmetric mucocutaneous maculopapular rash
and generalized nontender lymph node enlargement with fever,
malaise, and other manifestations of systemic infection. Skin
lesions are distributed on the trunk and extremities, often
including the palms, soles, and face, and can mimic a variety of
infectious and noninfectious skin eruptions.

17. Secondary syphilis
About one-third of patients develop painless mucosal
warty erosions called condylomata lata. These erosions
usually develop in warm, moist sites such as the
genitals and perineum. All the lesions of secondary
syphilis are teeming with spirochetes and are highly
infectious. They resolve spontaneously after a few days
to many weeks, but the infection itself has resolved in
only one-third of patients. In the remaining two-thirds,
the illness enters the latent state

18. Latent Syphilis
Latent syphilis is by definition a stage in which no clinical
manifestations are present, but continuing infection is evidenced
by serologic tests. In the first few years, latency may be
interrupted by progressively less severe relapses of secondary
syphilis. In late latent syphilis (>4 years), relapses cease, and
patients become resistant to reinfection. Transmission to others
is possible from relapsing secondary lesions and by transfusion
or other contact with blood products. Mothers may transmit
T.pallidum to their fetus throughout latency. About one-third of
untreated cases do not progress beyond this stage.

19. Tertiary Syphilis
One-third of patients with untreated syphilis develop tertiary syphilis.
The manifestations may appear as early as 5 years after infection but
characteristically occur after 15 to 20 years. The manifestations depend on
the body sites involved, the most important of which are the nervous and
cardiovascular systems.
Neurosyphilis is due to the damage produced by a mixture of
meningovasculitis and degenerative parenchymal changes in virtually any
part of the nervous system. The most common entity is a chronic meningitis
with fever, headache, focal neurologic findings, and increased cells and
protein in the cerebrospinal fluid (CSF).

20. Tertiary Syphilis
Cortical degeneration of the brain causes mental changes
ranging from decreased memory to hallucinations or frank
psychosis. In the spinal cord, demyelination of the posterior
columns, dorsal roots, and dorsal root ganglia produces a
syndrome called tabes dorsalis, which includes ataxia, wide-
based gait, foot slap, and loss of the sensation. The most
advanced central nervous system (CNS) findings include a
combination of neurologic deficits and behavioral
disturbances called paresis, which is also a mnemonic
(personality, affect, reflexes, eyes, sensorium, intellect,
speech) for the myriad of changes seen.

21. Tertiary Syphilis
• Cardiovascular syphilis is due to arteritis involving the vasa
vasorum of the aorta and causing a medial necrosis and loss
of elastic fibers. The usual result is dilatation of the aorta and
aortic valve ring. This in turn leads to aneurysms of the
ascending and transverse segments of the aorta and/or
aortic valve incompetence. The expanding aneurysm can
produce pressure necrosis of adjacent structures or even
rupture. A localized, granulomatous reaction to T.pallidum
infection called a gumma may be found in skin, bones, joints,
or other organ. Any clinical manifestations are related to the
local destruction as with other mass-producing lesions, such
as tumors.

22. Congenital Syphilis
• Fetuses are susceptible to syphilis only after the fourth month of
gestation and adequate treatment of infected mothers before
that time prevents fetal damage. Because active syphilitic
infection is devastating to infants, routine serologic testing is
performed in early pregnancy and should be repeated in the last
trimester in women at high risk for acquiring syphilis. Untreated
maternal infection may result in fetal loss or congenital syphilis,
which is analogous to secondary syphilis in the adult. Although
there may be no physical finding at all, the most common are
rhinitis and a maculopapular rash. Bone involvement produces
characteristic changes in the architecture of the entire skeletal
system (saddle nose, saber shins). Anemia, thrombocytopenia,
and liver failure are terminal events.

23. • The disease is clinically silent until the disseminated secondary
stage develops and then is silent again with entry into latency.
Although evasion of host defenses is clearly taking place, the
mechanisms involved are unknown. Treponema pallidum strains
found in secondary lesions have not been demonstrated to differ
antigenically from those in the primary chancre It may be that the
combination of the low antigen content of its outer membrane
combined with the extremely slow multiplication rate allows the
organism to stay below whatever critical antigenic mass is
required to trigger an effective immune response. Without
virulence factors to explain the tissue destruction, we are left
with injury due to a prolonged delayed-type hypersensitivity
(DTH) response to the persistent bacteria.

26. Laboratory diagnosis

27. Treatment and prevention

28. Prevention
• Safe sex
• Contact tracing
• Benzathine penicillin to contacts