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08 infectious disease spirochetes
1. Sum 07
Spirochetes
⢠Gram negative bacteria that are long, thin,
helical and motile.
⢠Divided in to three genera:
â Treponema
â Borrelia and
â Leptospira
2. Sum 07
Syphilis
⢠A sexually transmitted disease caused by
the bacterium Treponema pallidum.
⢠Transmission:
â Primarily by sexual contact
â Transplacental to fetus.
⢠Main pathology:
â Organism produces a vasculitis k/a
endarteritis obliterans
â This produces localized ischemic necrosis
of tissues.
5. Sum 07
Primary Syphilis
⢠Occurs 3 weeks after contact.
⢠Characterized by
â Chancre: a solitary, indurated, painless ulcer
(hard chancre).
⢠Location: at the site of treponemal inoculation
â Penis, cervix, vagina or anus.
⢠Spirochetes plentiful in the lesion: seen with
dark field microscopy.
⢠Chancre spontaneously resolves after 1-5 weeks.
15. Sum 07
Secondary syphilis
⢠Most contagious stage.
⢠Due to spread and proliferation of organisms in
skin and mucocutaneous tissue.
⢠Characteristic findings include:
â Diffuse maculopapular rash
⢠most characteristically on Palms and soles
â Condyloma latum: raised white lesions
⢠around moist areas of the anogenital region.
â Generalized lymphadenopathy
⢠Lesions Contain Spirochetes.
20. Sum 07
Latent Syphilis
⢠Usually asymptomatic but with positive
serology
⢠Considered noninfectious when duration is >
4 years
â Except in pregnancy (can be transmitted
to fetus)
⢠Can last from 2 to 20 years
⢠30% of untreated patients will develop
clinical features of tertiary syphilis
21. Sum 07
Tertiary syphilis
⢠Occurs after a latent period of 5 years.
⢠Three main manifestations:
1. Cardiovascular disease = Cardiovascular
syphilis
2. CNS disease = Neurosyphilis
3. Locally destructive disease due to formation
of Gummas = Benign tertiary syphilis
22. Sum 07
Cardiovascular syphilis
⢠Characterized by: oblitrative endarteritis of
vasa vasorum ď necrosis and scarring of tunica
media ď aneurysmal dialatation of aorta
⢠Also k/a Syphilitic Aortitis
â Aortic regurgitation because of altered
aortic valve function
â lining of the aorta, âtree-barkingâ
27. Sum 07
⢠Meningovascular syphilis:
â Characterized by chronic low grade meningitis
with vasculitis.
⢠General paresis :
â Occurs because of generalized atrophy
(neuronal loss) of frontal cortex.
â Patients show:
⢠Dementia, Delusions of grandeur ,psychosis
and an Argyll Robertson pupil.
28. Sum 07
Tabes dorsalis
⢠Due to demyelination of posterior columns,
dorsal roots and dorsal root ganglia.
⢠Results in:
1. Impaired joint position sense
2. Loss of pain and vibration sensation
3. Neuropathic joint (Charcotâs joint)
4. Argyll Robertson pupil : pupil accommodates
but fails to react to light.
29. Sum 07
Benign tertiary syphilis
⢠Characterized by formation of GUMMAS.
â Destructive
â White/grey, rubbery,tumor-like masses.
â Sites:
⢠Testis and liver , Bone (pain),
Nose(saddle nose deformity)
⢠Microscopy:
â Granulomatous lesions with gummatous
necrosis (coagulative necrosis) surrounded
by plasma cells & macrophages.
32. Sum 07
Diagnosis
⢠Screening tests:
â Blood: RPR
â CSF: VDRL
⢠Sensitive but not specific
⢠Most specific test:
â Dark field microscopy
⢠Most specific blood test:
â TPI test
33. Sum 07
Congenital Syphilis
⢠Is one of the âOthersâ in TORCH syndrome
⢠Acquired after maternal bacteremia and
passage of the spirochetes across the placenta.
â Transplacental transmission in 3rd trimester
â 1st five months, anatomic barriers of
placenta prevent access to fetal circulation
⢠1/3 fetuses are stillborn remaining reach term.
⢠Clinical disease :
1. Early congenital syphilis
2. Late congenital syphilis
34. Sum 07
Early congenital Syphilis
⢠Occurs within 2 years
⢠Manifestations:
â Nasal discharge (snuffles)
â Widespread rash and condyloma latum
â Sloughing of skin (of hand and feet)
â Hepatomegaly +/- gummas
â Osteochondritis (inflammation of bone)
â Destruction of nose ď collapse of nasal bridge
âsaddle nose deformityâ
35. Sum 07
Late Congenital Syphilis
⢠Manifestations: Hutchinsonâs triad:
1. Interstitial keratitis with blindness
2. Hutchinson teeth
⢠Upper central incisors ď Widely spaced
and with central notch
3. Eighth cranial nerve deafness
⢠Other findings:
â Mulberry / Moons molars
⢠Too many cusps
â Saber shin
⢠anterior bowing of tibia
38. Sum 07
Congenital
Syphilis
Abortion or still birth
Infantile
Child hood
Rash
Periostitis
Osteochondritis
Liver and lung fibrosis
Interstitial keratitis
Hutchinsonâs teeth
Eighth nerve deafness
39. Sum 07
Lyme Disease
⢠Caused by the spirochete Borrelia
burgdorferi
⢠Transmitted by bite of Deer tick (Ixodes
dammini)
⢠Reservoirs are white footed mouse and
white tailed deer
⢠Common disease in USA, Europe and Japan.
41. Sum 07
Lyme disease: divided into three stages
⢠Stage I : multiplication and spread of
spirochetes in the dermis
⢠Causing expanding area of redness with a central
pallor
⢠Lesion is k/a Erytema chronicum migrans
⢠May be accompanied by fever and
lymphadenopathy
⢠Disappears in 4-14 weeks.
43. Sum 07
Lyme disease
⢠Stage II: early dissemination stage
⢠Dissemination via blood to different tissue
causing
â Cardiac abnormalities: heart block,
myocarditis, arrhythmias
â CNS disease : cranial nerve palsies,
particularly bilateral Bellâs palsy;
encephalitis
â Other findings: Lymphadenopathy,
migratory joint and muscle pain,
44. Sum 07
Lyme disease
⢠Stage III : late disseminated stage
â 2-3 years after initial bite
â Disabling joint disease:
⢠Chronic arthritis with damage to large
joints (MC knee joint).
⢠Treatment:
â Early stages: tetracycline
â Late stages : Ceftriaxone
45. Sum 07
Relapsing fever
⢠Characterized by recurrent fever ( once a
week) with spirochetemia.
⢠Two types:
1. Epidemic relapsing fever:
â Caused by Borrelia recurrentis.
â Trasnmitted by: body louse
2. Endemic relapsing fever:
â Caused by several Borrelia species.
â Transmitted by Ornithodorous (soft
bodied) ticks
46. Sum 07
Clinical features
⢠Chills, fever, headache, fatigue and is
â Followed by DIC and multiple organ failure.
⢠Organisms cleared by antibodies against surface
protein
⢠Emergence of bacteria with different surface ag
causes recurrence of symptoms.
⢠The organisms can be visualized in PB smears
during relapses