1. The document discusses several genera of the families Spirochaetaceae and Leptospiraceae, including Treponema, Borrelia, and Leptospira. 2. Treponema pallidum causes syphilis and has various stages from primary to secondary to latent to tertiary syphilis. Borrelia causes relapsing fevers that are transmitted by ticks or lice. 3. Leptospira interrogans causes leptospirosis, a zoonotic disease transmitted via contact with infected animal urine, and causes symptoms from mild flu-like illness to meningitis, liver damage, and kidney failure.

1. Family
Spirochaetaceae
and
Leptospiraceae
1

2. Family Spirochaetaceae
• Elongated, motile,
–Speira meaning coil
–Chaite meaning hair
• number of endo-flagella or internal flagella
• Sensitive to penicillin and metronidazol
• two genera of major human pathogen;
Treponema and Borrelia
2

3. Genus Treponema
General characteristics
- Motile,
- Gram negative, but stain poorly
- Multiply by binary transverse fission
- Not yet been cultured
3

4. Virulence factors
– Outer Membrane Protein,
– enzymes (hyaluronidase)
– Perivascular inflammation
– Granulomatous changes: tertiary syphilis
4

5. Antigenic structure
1. Non – specific antigen
– A non-specific (reagin) appear in blood of
syphilitic patients that reacts with a lipid hapten
extracted from beef heart.
5

6. 2. Specific Antigen
– Group specific antigen
• a protein Ag present in T. pallidum and non –
pathogenic treponems,
– Species – Specific treponemal antigen
• appears to be polysaccharide in nature
• T. pallidium is used as antigen for detection of
species – specific antibody
6

7. Pathogenicity and Clinical features
 T. pallidum causes:
 Sexually acquired syphilis which has
 Early stage: Includes primary syphilis,
secondary syphilis and early latent syphilis.
 Late stage: Includes late latent syphilis, benign late
syphilis, cardiovascular syphilis, and neurosyphilis.
7

8. 8
Primary Syphilis (9 days to 3months)
 hard chancre, a superficial non painful ulcer
with a firm base, penis, labia, cervix, anorectal
region, mouth: highly infectious
 Regional lymphadenopathy
 After 2-6 weeks , heals without treatment

9. secondary syphilis
3 weeks to 6 months : low grade fever, depression and
mucocutaneous rash
Superficial sores on mouth, vagina, or anus
Highly infectious lesions
After 2-6 weeks healing occur
25% untreated experience recurrence
9

10. Latent syphilis
– Between secondary and tertiary
– When secondary relapse occur
– Cardiovascular syphilis (80%)
– Neurosyphilis (20%)
– In many cases, this is followed by natural cure but
in others, after several years’, manifestation of
tertiary syphilis appear
10

11. Tertiary Syphilis
 It is a slowly progressive disease
 lead to benign ulcerating lesions
 the skin, mucous membranes or bones, or the internal
organs
 The lesion contain ,very few organisms
Congenital syphilis
 occurs when infection is transmitted from mother to
offspring transparently.
 lead to abortions or still birth.
11

12. • Route of transmission – Mother to child during
pregnancy
• Outcome:
– Abortion
– Early neonatal death
– Fetal death
– Organ damage
– Still birth
– Deafness
12

13. Laboratory diagnosis
• Specimen collection
– Tissue exudates, secretions for 10, 20, early congenital syphilis
– Blood, CSF, plasma for 20, latent, 30 and late congenital syphilis
• Microscopic examination
– Dark field, phase contrast
• T. pallidum is slender spiral structure and slow movement
• Culture: can not be cultivated
• Serologic tests
 Non specific treponemal tests
 VDRL, RPR
13

14. Treatment
 Penicillin is the drug of choice
Prevention and control
 Treatment of cases
 Follow up of cases and contact
 use of condom
14

15. Genus Borrelia
• Large, motile,
• Transmitted to vertebrate hosts by
haematophagous arthropode lice or tick
•In some ticks (but not in lice), spirochetes are passed from
generation to generation.
15

16. Antigenic Structure
•The antigenic structure ,changes in the course of a single
infection.
•The relapsing course of the disease appears to be due to
the multiplication of such antigenic variants, against
which the host must then develop new antibodies.
•Ultimate recovery (after three to ten relapses) is
associated with the presence of antibodies against several
antigenic variants.
16

17. – Medically important species include
• , Borrelia recurrentis, Borrelia Vincenti
• Borrelia burgdorferi, Borrelia duttoni
17

18. Pathogenicity and clinical manifestation of Relapsing Fever
• The incubation period is 3–10 days.
• The onset is sudden, with chills and rise of temperature.
• The fever persists for 3–5 days and declines, pts weak
but not ill.
• The afebrile period lasts 4–10 days and is followed by a
second attack of chills, fever, intense headache, and
depression.
• During the febrile stages, mos in the blood; afebrile
periods, are absent. 18

19. • Antibodies against the spirochetes appear during
the febrile stage,.
• These antibodies may select out antigenically
distinct variants that multiply and cause a relapse.
• Several distinct antigenic varieties of borreliae may
be isolated from a single patient's.
19

20. – There are two forms of relapsing fever:
• Louse-borne relapsing fever
• Tick-borne relapsing fever
– Borreliae may also infect the central nervous
system
20

21. Louse-borne relapsing fever
– caused by Borrelia recurrentis,
– is transmitted from person to person
by the body and head louse, Pediculus humanus.
– Relapsing fever is characterized by recurring
periods of high fever with severe headache, body
pains, vomiting and often a cough and dyspnoea.
21

22. Tick-borne relapsing fever
caused by Borrelia duttoni
is transmitted by soft ticks of the genus Ornithodorus.
Clinical manifestation similar to louse-borne
relapsing fever except tick-borne relapsing fever is
usually a less severe illness.
Borrelia vincenti
association with Fusobacterium species and other Gram negative
anaerobes causes:
acute ulcerative gingivitis (Vincent’s angina)
– topical ulcer
22

23. Lyme disease
• The transmission of B. burgdorferi to humans is by injection
of the organism in tick saliva
• After injection by the tick, the organism migrates out from
the site, producing the characteristic skin lesion.
• Lyme disease, occurs in stages with early and late
manifestations.
• . 23

24. • initial stage
• A unique skin lesion that begins 3 days to 4 weeks
after a tick bite often marks the initial stage
• The lesion, near the tick bite and slowly expands,
• With the skin lesion there is often a flu-like illness
with fever, chills, myalgia, and headache
24

25. • The second stage
• occurs weeks to months later and
• includes
• arthralgia and arthritis;
• neurologic manifestations and
• cardiac disease
• . 25

26. • The third stage begins months to years later
with
• chronic skin, nervous system, or joint
involvement.
26

27. 27

28. Laboratory diagnosis
Specimens:
 Blood,cerebrospinal fluid
Microscopic examination
 Borrelia, with uneven size coils.
Culture
Culture is not used routinely as a method
of diagnosing relapsing fever.
 Kelly’s medium – grow 28

29. Treatment
Erythromicin, tetracyclin, penicillin
Prevention and control
avoidance of exposure to ticks and lice
29

30. Genus Leptospira
– It is a single genus of family Leptospiraceae
– It contains the pathogenic species, Leptospira
interrogans, and the free-living nonpathogenic
species, Leptospira biflexa.
– The species are further broken down to more than
200 serovars of L interrogans and more than 60
serovars of L biflexa.
– Leptospirae are tightly coiled, thin, flexible
spirochetes, with very fine spirals 0.1–0.2 m wide;
one end is often bent, forming a hook.
30

31. Pathogenesis and clinical manifestation
– L. interrogans causes leptospirosis, a zoonotic disease with
humans becoming infected following direct or indirect
contact with urine from infected animals.
– The mild form of leptospirosis is often misdiagnosed as a
viral illness or influenza.
– The more serious form of the disease is characterized by
high fever, headache, hypotension, pains in the muscles and
legs, abdominal pain, weakness, and often redness of the
eyes and a rash.
31

32. •Some patients develop meningitis (lymphocytic), jaundice
following liver cell damage, thrombocytopenia with
haemorrhagic symptoms, and renal failure.
Weil’s disease, or syndrome:
This term is occasionally used to describe the severe
form of leptospirosis in which there is liver damage with
jaundice and renal failure.
32

33. Laboratory diagnosis
– Specimens:
• Mainly blood for culture (First week)
• Urine (second and third week)
• Serum (second and third week)
• CSF
Culture
– In Reference Laboratories, specimens can be
cultured for L. interrogans.
– The organism can be grown aerobically at 28–30 ºC
in a semi-solid serum culture medium or a Tween-
albumin (TA) medium. Or Fletcher
– Cultures are examined weekly for leptospires by dark-
field microscopy.
• Cultures are examined weekly for leptospires by
dark-field microscopy.
33

34. Treatment
 Penicillin is the drug of choice
 Doxycyclin, piperacillin, and cefotaxime are also
effective
Prevention and control
 preventing exposure to potentially contaminated water
and reducing contamination by rodent control.
 Doxycycline, 200 mg orally once weekly during heavy
exposure, is effective prophylaxis.
 Dogs can receive distemper-hepatitis-leptospirosis
vaccinations.
34