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DEPARTMENT OF CLINICAL MEDICINE
MICROBIOLOGY &IMMUNOLOGY
LECTURE 14 : PATHOGENIC BACTERIA (SPIROCHETES, Treponema
pallidum)
MRS N NG’ANDWE ..BSc, BMS
 Gram negative
 long, thin, helical, motile
 Many types e.g Treponema, Borrelia
and Leptospira
 Treponema pallidum is a slim spirochete which causes syphilis
 It is an exclusively human pathogen under natural conditions
 Infection is acquired from direct sexual contact with a person having active primary or
secondary syphilitic lesions
 Less commonly, the disease may be spread through nongenital contact with a lession eg lips,
 Transplacental transmission possible within approximately the first 3 years of maternal
infection
 Late disease is not infectious
 The incidence of new primary and secondary syphilis in developed countries is minimal
 World-wild syphilis remains a major public health problem with an expected 12 million new
cases annually
 Evidence shows that syphilitic lesions are portals for HIV transmission
 genital/genital
 in utero or during birth
 The spirochete reaches subepithelial tissue via unapparent breaks in the skin or
by passage between epithelial cells of mucous membranes
Primary Syphilis
 The primary syphilitic lesion is a papule that evolves into an ulcer at the site of
infection
 This appears on external genitalia or the cervix
 The ulcer becomes indurated and ulcerates but remains painless, though slightly
sensitive to touch
 The fully developed ulcer with a firm is called a chancre
 Firm, painless enlargement of the regional lymph nodes usually develops within a
week of the primary lesion and may persist for a month
 Incubation period until the appearance of chancre is about 3 weeks
 It heals spontaneously after 4-6 weeks
Secondary Syphilis:
 Develops about 2-8 weeks after the appearance of the chancre
 The primary lesion has usually healed, but may still be present Characterized by
symmetrical mucocutaneous macopapulary rash
 Generalized non tender lymph node enlargement
 Fever
 Malaise
 Other manifestations of systemic infection
 Skin lesions are distributed on the trunk and extremities often including palms,
soles, and face
 About 1/3 of pts may develop painless warty erosions called Condylomata lata
 The erosions usually develop in warm moist sites such as perineum and genitals
 All lesions of secondary syphilis have spirochetes and are highly infectious
 They resolve spontaneously after a few days to many weeks
 But infection resolves only in about 1/3. remaining 2/3 go into latency
Latent Syphilis:
 This is the stage in which no clinical manifestations are present
 Continued infection is evidenced by serologic tests
 In the first few years, latency may be interrupted by less severe relapses of
secondary syphilis
 In late latent syphilis (>4yrs), relapses cease and pt becomes resistant to
reinfection
 Transmission to others is only possible from relapses, transfusion or other
contacts with blood products
 Mothers may transmit to fetus in latency
 About1/3 of untreated pts do not progress beyond this stage
Tertiary Syphilis:
 Manifestations may appear as early as 5yrs after infection, but characteristically
occur 15-20 yrs later
 Manifestations depend on the site involved: most important are neural and
cardiovascular
Neurosyphilis:
 Damage is produced by meningovasculitis and degenerative parenchymal changes
in virtually any part of the nervous system
 The most common entity is a chronic meningitis with fever, headache, increased
cells and protein in the CSF
 Cortical degeneration of the brain causes mental changes ranging from decreased
memory to hallucinations
 In the spinal cord, demyelination of posterior columns, dorsal roots and dorsal root
ganglia, produces a syndrome called Tabes dorsalis which includes ataxia and loss
of sensation
 Most advanced CNS findings include combinations of neurologic deficits and
behavioral disturbances called paresis (Personality, Affect, Reflexes, Eyes,
Sensorium, Intellect, Speech
Cardiovascullar syphilis:
 Due to artaritis involving the vasa vasorum of the aorta and causing medial
necrosis and loss of elastic fibres
 The usual result is dilatation of the aorta and aortic valve rings
 This in turn leads to aneurisms of the ascending and transverse segments of the
aorta or aortic valve incompetence
 The expanding aneurism can produce pressure to necrosis of adjuscent structures
or even rapture
 A localised granulomatous reaction called Gumma may be found in skin, joints, or
other organs
Congenital Syphilis:
 Fetuses are susceptible to syphilis only after the 4th month of gestation
 Adequate treatment of the mother before that time prevents fetal damage
 Routine serological testing is done early in pregnancy in high risk groups and
repeated in the last trimester
 Untreated maternal infection may result in fetal loss or congenital syphilis which
is analogous to secondary syphilis in adults
 Child may have rhinitis and papulary rash
 Bone involvement produces characteristic changes in the entire skeletal system
 May have anemia, thrombocytopenia, and liver failure
Microscopy
 T. pallidum can be seen in dark field microscopy in primary and secondary lesions
 Serologic Tests
 Non Treponema & Treponema tests
 They are sensitive to penicillin (benzathin penicillin) in all stages
 Those hypersensitive to penicillin are treated with doxycycline/ er
 Safe sex practices are the most effective preventive measure

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Spirochetes ppt microbiology and immunology

  • 1. DEPARTMENT OF CLINICAL MEDICINE MICROBIOLOGY &IMMUNOLOGY LECTURE 14 : PATHOGENIC BACTERIA (SPIROCHETES, Treponema pallidum) MRS N NG’ANDWE ..BSc, BMS
  • 2.  Gram negative  long, thin, helical, motile  Many types e.g Treponema, Borrelia and Leptospira
  • 3.  Treponema pallidum is a slim spirochete which causes syphilis  It is an exclusively human pathogen under natural conditions  Infection is acquired from direct sexual contact with a person having active primary or secondary syphilitic lesions  Less commonly, the disease may be spread through nongenital contact with a lession eg lips,  Transplacental transmission possible within approximately the first 3 years of maternal infection  Late disease is not infectious  The incidence of new primary and secondary syphilis in developed countries is minimal  World-wild syphilis remains a major public health problem with an expected 12 million new cases annually  Evidence shows that syphilitic lesions are portals for HIV transmission
  • 4.  genital/genital  in utero or during birth  The spirochete reaches subepithelial tissue via unapparent breaks in the skin or by passage between epithelial cells of mucous membranes
  • 5. Primary Syphilis  The primary syphilitic lesion is a papule that evolves into an ulcer at the site of infection  This appears on external genitalia or the cervix  The ulcer becomes indurated and ulcerates but remains painless, though slightly sensitive to touch  The fully developed ulcer with a firm is called a chancre  Firm, painless enlargement of the regional lymph nodes usually develops within a week of the primary lesion and may persist for a month  Incubation period until the appearance of chancre is about 3 weeks  It heals spontaneously after 4-6 weeks
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  • 7. Secondary Syphilis:  Develops about 2-8 weeks after the appearance of the chancre  The primary lesion has usually healed, but may still be present Characterized by symmetrical mucocutaneous macopapulary rash  Generalized non tender lymph node enlargement  Fever  Malaise  Other manifestations of systemic infection
  • 8.  Skin lesions are distributed on the trunk and extremities often including palms, soles, and face  About 1/3 of pts may develop painless warty erosions called Condylomata lata  The erosions usually develop in warm moist sites such as perineum and genitals  All lesions of secondary syphilis have spirochetes and are highly infectious  They resolve spontaneously after a few days to many weeks  But infection resolves only in about 1/3. remaining 2/3 go into latency
  • 9. Latent Syphilis:  This is the stage in which no clinical manifestations are present  Continued infection is evidenced by serologic tests  In the first few years, latency may be interrupted by less severe relapses of secondary syphilis  In late latent syphilis (>4yrs), relapses cease and pt becomes resistant to reinfection  Transmission to others is only possible from relapses, transfusion or other contacts with blood products  Mothers may transmit to fetus in latency  About1/3 of untreated pts do not progress beyond this stage
  • 10. Tertiary Syphilis:  Manifestations may appear as early as 5yrs after infection, but characteristically occur 15-20 yrs later  Manifestations depend on the site involved: most important are neural and cardiovascular
  • 11. Neurosyphilis:  Damage is produced by meningovasculitis and degenerative parenchymal changes in virtually any part of the nervous system  The most common entity is a chronic meningitis with fever, headache, increased cells and protein in the CSF  Cortical degeneration of the brain causes mental changes ranging from decreased memory to hallucinations  In the spinal cord, demyelination of posterior columns, dorsal roots and dorsal root ganglia, produces a syndrome called Tabes dorsalis which includes ataxia and loss of sensation  Most advanced CNS findings include combinations of neurologic deficits and behavioral disturbances called paresis (Personality, Affect, Reflexes, Eyes, Sensorium, Intellect, Speech
  • 12. Cardiovascullar syphilis:  Due to artaritis involving the vasa vasorum of the aorta and causing medial necrosis and loss of elastic fibres  The usual result is dilatation of the aorta and aortic valve rings  This in turn leads to aneurisms of the ascending and transverse segments of the aorta or aortic valve incompetence  The expanding aneurism can produce pressure to necrosis of adjuscent structures or even rapture  A localised granulomatous reaction called Gumma may be found in skin, joints, or other organs
  • 13. Congenital Syphilis:  Fetuses are susceptible to syphilis only after the 4th month of gestation  Adequate treatment of the mother before that time prevents fetal damage  Routine serological testing is done early in pregnancy in high risk groups and repeated in the last trimester  Untreated maternal infection may result in fetal loss or congenital syphilis which is analogous to secondary syphilis in adults  Child may have rhinitis and papulary rash  Bone involvement produces characteristic changes in the entire skeletal system  May have anemia, thrombocytopenia, and liver failure
  • 14. Microscopy  T. pallidum can be seen in dark field microscopy in primary and secondary lesions  Serologic Tests  Non Treponema & Treponema tests
  • 15.  They are sensitive to penicillin (benzathin penicillin) in all stages  Those hypersensitive to penicillin are treated with doxycycline/ er  Safe sex practices are the most effective preventive measure