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Lecture Treponematosis 1
Lecture Treponematosis 1
Lecture Treponematosis 1
Violeta Melinte
Objectives
To learn which are the endemic treponematosis and
their etiology
To have an idea about their distribution and
prevalence
To recognize the diseases by their symptoms
To be able to treat the patients and contacts
Introduction
Treponematoses
Caused by treponemes (“trepo”= turn;
“nema”= thread)
Belong to the Spirochetaceae
Cause 4 different, chronic, exclusively human
diseases
There is no animal reservoir
Introduction
Treponemes
Cannot be cultivated in vitro (exc. T. pallidum)
Morphologically they cannot be distinguished one from
Conditionally (bejel)
T.pallidum pertenue (yaws)
pathogenic
T.carateum (pinta)
T. vincentii
Endemic treponematosis
1. Non-venereal syphilis or Bejel. (T.p. endemicum)
2. Framboesia or Yaws or Pian (T.p. pertenue)
3. Pinta (T. carateum)
Non-venereal Syphilis, Bejel, Njovera
or Treponarid
Caused by T. endemicum
Occurs in foci (dry, hot climates) in sub-Saharan
Africa, in the Middle East, Australia and in Asia
At present the disease has become rare
Turkey
Syria
Iran
Iraq
Saudi Arabia
Niger
Mali
Senegal Burkina
Transmission
NOT via sexual intercourse, but through human-
to-human contact or contaminated objects
As a rule: non-venereal or
endemic syphilis occurs in
childhood
The oral mucosa = the most
important source of infection
Children probably acquire immunity against T.
pallidum before puberty and are protected
against later venereal syphilis
Pathogenesis
We know little about it!
Chronic bacterial infection
Early in the course of infection – spread
hematogenously – w/o Rx → secondary and late
manifestations (rare)
Regional lymphadenopathy occurs
Little if any evidence of cardiovascular
involvement in late infection, neurologic
sequelae or transmission to children born to
infected, untreated mothers!
Symptoms
Early stage = 5 years
Incubation period = 9-50 days
Oral mucosal lesions (primary white ulcers)
Skin lesions (intermittently)
Osteitis/ periosteitis
Symptoms
Delayed lesions (rare cases)
“Gangosa”= destruction of the nose, lip and palate, and
lead to severe mutilation
Framboesia or Yaws or Pian
Caused by T. pallidum pertenue
Occurs in (warm, humid, tropical areas) Africa,
Central and South America, some islands in
Southeast Asia, in poor isolated rural communities
Indonesia
Papua New
Solomon
Guinea
Islands
Congo
Framboesia or Yaws or Pian
Yaws is believed to have originated in
tropical areas of Africa, and spread to other
tropical areas of the world via immigration
and the slave trade.
The latter is likely the way it was introduced
to Europe from Africa in the 15th century.
The first unambiguous description of yaws
was made by the Dutch physician Willem
Piso (1611-1678).
Yaws was clearly described in 1679 among
African slaves by Thomas Sydenham (1624-
1689) in his epistle on venereal diseases,
although he thought that it was the same
disease as syphilis.
The causative agent of yaws was discovered
in 1905 by Aldo Castellani in ulcers of
patients from Ceylon.
(wikipedia)
Symptoms – primary lesion
Skin and skeleton affected
Wart-like skin lesions with the appearance of
strawberries (yaw = strawberry)
Primary lesion – extragenital
An initial “parent” lesion with various satellite lesions
If the hypertrophic epidermis is removed, an exudate
with a crust forms
Heal w/o scars
Residual skin discoloration
There is no deep ulceration
Swollen lymph nodes
Symptoms – secondary lesions
w/o Rx secondary widespread
lesions (macular/
papillomatous) form
Flare-ups which last wk/mo or 3-
5 years (w/o Rx)
Malaise
Joint pain
Fever
On the palmes and soles –
hyperkeratotic and itchy skin →
painful fissures → “crab gait”
Secondary lesions
Nodules – mainly around the joints
Hard, loose from the skin and the deep
tissue
Elbow, wrists, ankles, sacrum
DD: onchocerciasis
Gumma ~ subcutaneous cold abscess
Gangosa
Caused by gumma
DD: mucocutaneous leishmaniasis;
deep mycosis; leprosy
Secondary lesions
• Sometimes – involvement of the skeleton
• Chronic inflammation of the bones of the fingers ≠
acute dactylitis in sickle cell anaemia
Direct methods
Dark-field microscopy on
a wet preparation of
material obtained from
early lesions
Fluorescent antibody tests
– distinguish pathogenic
from saprophyte
treponemes
Low sensitivity
Diagnosis
Biopsy specimen – skin pathology using silver
impregnation technique
Cannot differentiate them by their shape
Early Bejel: granulomas may be present
Yaws: epidermal hyperplasia, with collection of
neutrophils and typical plasmocytic dermal infiltrate
Pinta: no ulcer formation;
Early lesion – loss of melanin in basal cells;
late – stage – epidermal atrophy and melanophages in dermis
Diagnosis
Molecular methods (PCR)
Distinguish nonvenereal T. pallidum
subspecies
Indirect methods
Serological tests
Cannot distinguish between
endemic treponematoses and
syphilis
The antibody response is often
detectable after one – 3 wk of
infection
Clinical identification of ET has important implications
regarding diagnostic approach, case management and
prevention strategies.
Differential diagnosis
Treatment
Benzathine penicilin
Single IM adm of 1.2 or 2.4 million units
Three weekly adm – better in the late stage
Cure rates = 97%
Tetracyclines, doxycycline,
erythromycin for 14 days = alternatives