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Syphilis, a sexually transmitted
disease, caused by the spirochete Treponema pallidum, was
first recognized in Europe in 1490s, and has been related to the
return of Christopher Columbus. Mass movements of peoples caused by
war and urbanization contributed to its rapid spread. At that time,
syphilis was an acute disease that caused destructive skin lesions and
early death, but since then it has become milder, with a more
protracted and insidious clinical course.
The disease is divided into
three stages:
Primary
(the chancre), secondary (disseminated), and tertiary (with lesions of
deep organs<<Selection in Document>> following a latent period of 2 to
20 years or more).
Congenital Syphilis
acquired in utero, may have
any of the secondary or tertiary lesions.
T. pallidum is a helical bacterium, 5
to 20 micrometer long and 0.1 to 0.2 micrometer wide, with 8 to 14 evenly
distributed coils.
The silver impregnation technique precipitates
metallic silver on the wall of the spirochete, enlarging its outline
and making it opaque, features that make it visible in tissue
sections.
When smears from chancres or other syphilitic lesions are
examined by darkfield microscopy, the spirochetes have the appearance
of floating silver-white corkscrews on a black background, spinning on
their long axes and flexing in the middle.
Various direct and indirect immunoflourescent and immunoperoxidase staining procedures are also
available for demonstrating spirochetes in tissue sections and smears.
Several serologic and immunoflourescent
tests detect organisms, and the host’s antibodies to them.
One is the
Treponema pallidum immobilization test, in which the live spirochetes
of T. pallidum are immobilized by antibody in the patient’s serum. The
standard method for demonstrating antibody in the serum is the
indirect fluorescent treponemal antibody test, in which the antigen is
lyophilized T. pallidum. To increase specificity, nonspecific
antibodies in the patients serum are first absorbed by nonpathogenic
treponemes.
A nontreponemal antigen, cardiolipin
from beef heart, is used for diagnostic screening and to assess
treatment. Antigenically, it resembles a lipoid released by T.
pallidum when it invades human tissues. The Veneral Disease Research
Laboratory (VDRL) test and the rapid plasma reagin (RPR) test detect
antibodies to cardiolipin. Although
useful, these tests are not specific, because lipoidal antigen is
released in patients with infectious mononucleosis, viral hepatitis,
leprosy and autoimmune diseases.
Spirochetes are very fragile and are
killed by soap, antiseptics, drying, and cold.
Person-to-person
transmission requires direct contact between a rich source of
spirochetes, for example the chancre, and mucous membranes or abraded
skin of the genital organs, rectum, mouth fingers, or nipples.
Spirochetes enter the skin or mucous membrane, invade blood and lymph
and disseminate almost immediately.
Primary Syphilis:Image1
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The chancre develops at the site of
inoculation in 10 to 90 days (average 21 days).
It begins as a small
papule and may remain a papule.
However, when the lesion is large,
the chancre develops into a shallow, painless ulcer with indurated
margins.
The base is covered by fibrin and cellular debris.
Spirochetes may be anywhere in the chancre, but they concentrate in
the walls of vessels and in the epidermis around the ulcer.
Neutrophils migrate into the epithelium
around the ulcer, drawn there by spirochetes.
The upper dermis is congested and
infiltrated with many lymphocytes and plasma cells.
Chancres, as well as lesions of
secondary, tertiary, and congenital syphilis, have a characteristic “luetic
vasculitis”, in which endothelial cells proliferate and swell, and the
walls of the vessels become thickened by lymphocytes and fibrous
tissue.
Early in the vasculitis, lymphocytes are seen in the wall and
there may be cuff of plasma cells around the adventitia.
Gradually,
the inflammatory cells diminish and fibrous tissue replaces the smooth
muscle of the media.
As the vasculitis continues the lumen
narrows, and by the tertiary stage the lumen is reduced to a minute
caliber.
Spirochetes are visualized in the walls
of the vessels in the primary and secondary stages, but not in the
tertiary stage.
Regional lymph nodes draining the
chancre are enlarged and firm, but painless. The chancre disappears in
3 to 12 weeks, and the patient is asymptomatic and immune to
reinfection.
Secondary
Syphilis:
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Secondary syphilis is characterized by
dissemination and lesions in a variety of organs, most strikingly
skin, mucous membranes, lymph nodes, stomach, and liver.
At first
there is a rash that appears 2 weeks to 6 months after the chancre
heals. The rash is diffuse, macular, bilateral, and symmetrical and
often includes the palms and soles.
Next, the mucous membranes of the
mouth and the moist genital surfaces display “mucous patches”, which
develop into shallow ulcers.
There are a variety of secondary lesions,
including condylomata lata (exudative plaques in the perineum, vulva,
or scrotum) ; follicular syphilids (small papular lesions around hair
follicles that cause loss of hair) ; and nummular syphilids (coinlike
lesions involving the face and perineum). Condylomata lata are
characterized by epithelial hyperplasia, acanthosis, infiltrates of
plasma cells in the dermis, and a luetic vasculitis. These dermal and
mucosal lesions teem with spirochetes.
Characteristic changes in lymphnodes
include a thickened capsule, follicular hyperplasia, increased numbers
of plasma cells, areas of fibrohistiocytic proliferation, clusters of
histiocyte encroaching on the germinal centers, and luetic vasculitis.
Focal abscesses and scattered granulomas containing giant cells are
less common. Numerous spirochetes are present in the walls of vessels,
the areas of fibrohistiocytic proliferation, and abscesses.
In the secondary syphilis of the
stomach, a diffuse infiltrate of the wall by lymphocytes and plasma
cells resembles lymphoma. Usually there are numerous spirochetes in
the vessel walls and the loose connective tissue.
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In secondary
syphilis of the liver, plasma cells, lymphocytes, and neutrophils
infiltrate the portal tracts, in which there is a luetic vasculitis.
The serum alkaline phosphatase activity is unusually high.
Infections of the meninges begins
during the secondary stage and typically persists for life.
There may
also be optic neuritis during secondary syphilis.
The cerebral spinal
fluid is abnormal: the lymphocyte count is about 500 per cubic mm (pleocytosis),
protein levels are increased, glucose levels are normal, and VDRL
tests register positive. The serum likewise is VDRL-positive.
Latent Syphilis
When the lesions of secondary syphilis
subside, there is a silent period of “well-being” that lasts for years
or decades.
However, during this latent period spirochetes continue to
multiply, and the deep-seated lesions of tertiary syphilis gradually
develop and expand.
A few meningeal infections heal spontaneously, but
most remain asymptomatic (latent) for years before some are
reactivated during tertiary meningeal syphilis.
The cerebral spinal
fluid shows reduced pleocytosis (about 5 lymphocytes per cubic mm.),
and both cerebral spinal fluid and serum are VDRL -positive.
During this latent period
spirochetes may be passed in blood transfusions or across the placenta
to the faetus.
Tertiary Syphilis
About 30% of
untreated patients develop tertiary lesions.
Luetic aortitis, a common
tertiary lesion, is characterized by gradual weakening and stretching
of the wall of the aorta to form an aneurysm.
Grossly, the intima of
the aorta appears rough and pitted; it has been described as having
the appearance of tree bark. This rough appearance is caused by
degeneration of the media, and this in turn is caused by luetic
vasculitis of the vasa vasorum.
Over the years lumens are gradually
narrowed to the point of obliteration, causing ischemia of the wall of
the aorta and degeneration of the media.
The specialized arrangement
of the aortic media, which includes a delicate and intimate weave of elastica, smooth muscle, and collagen, is gradually replaced by scar
tissue.
It is the specialized tissue of the media that give the aorta
its strength and resiliency, and when these are replaced by scar, the
aorta gradually stretches, becoming progressively thinner to the point
of rupture, massive hemorrhage and sudden death.
Damage to and
scarring of the first part of the aorta commonly lead to stretching of
the aortic ring, separation of the aortic cusps and regurgitation
through the aortic valve ; so-called aortic insufficiency.
Luetic vasculitis of the coronary vasculitis may narrow
or occlude the vessels and cause
myocardial infarction.
NEUROSYPHILIS:
GUMMA OF
TERTIARY SYPHILIS:
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