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PRIMARY CHANCRE
SECONDARY SYPHILIS
LATE LATENT
TERTIARY SYPHILIS
WHEN CALLED AS LATE SYPHILIS: AFTER 2 YEARS OF THE DISEASE.
CHARACTERISTICS OF TERTIARY SYPHILIS:
• NON CONTAGIOUS : ORGANISMS CANNOT BE DEMONSTRATED
EXCEPT BY ANIMAL INOCULATION.
• THIS STAGE COMMENCES WITH A PERIOD OF LATENCY.
• Approximately ONE THIRD of the patients with untreated latent syphilis
DEVELOP TERTIARY SYPHILIS, while the other TWO- THIRD remain in
PERPETUAL LATENCY.
• THE MORTALITY AND MORBIDITY OF SYPHILIS ARE MAINLY DUE TO
THE OCCURRENCE OF ITS LATE MANIFESTATIONS IN SKIN, BONES,
CNS OR VISCERA, PARTICULARLY HEART AND GREAT VESSELS.
• LATE LESIONS ARE CHRONIC AND DESTRUCTIVE
• CHARACTERISTIC LESION IS GUMMA ( localised/ diffuse). IT
REPRESENTS A MAXIMAL INFLAMMATORY RESPONSE (ALLERGIC) TO
A FEW ORGANISMS.
• THE MOST TYPICAL FEATURE OF A LOCALISED GUMMA IS CENTRAL
NECROSIS, WITH THE FORMATION OF A STRINGY MASS ( or
‘gum’,hence the name gummata) SARROUNDED BY A ZONE OF
GRANULATION TISSUE WITH A PERIPHERAL NARROW ZONE OF
TOUGH FIBROUS TISSUE. Microscopically the zone of granulation consists
of lymphocytic and plasma cell infiltration around small blood vessels, giving
an appearance of perivascular cuffing. The blood vessels show changes of
ENDARTERITIS OBLITERANS. Epitheloid cells and gaint cells are also
present. Fibroblasts are seen in the periphery of the lesion.
(C) BONES: Although gumma is a destructive pocess, it may be hidden in the bones
by the OSSEUS OR PERIOSTEAL REACTION. They usually occur 5-20 years
after the original infection. Slightly more common in males. Bones most
commonly involved are :
TIBIA, CRANIAL BONES, SHOULDER GIRDLE, FEMUR, FIBULA,
HUMERUS, BONES OF FOREARM.
Lesions usually commence in the fibrous layer of the periosteum
where chonic inflammatory cells infiltrate alongwith endarteritis obliterans of
the vessels ---- this stimulates the adjacent ‘osteogenic layer’ with new bone
formation that lacks the orderly cortical pattern. This leads to thickening of
the cortex and roughening and irregularity of the surface. This process
extends into the cortex via Haversian canals causing erosion and destruction
followed by laying down of new bone. THE NEW BONE IS MORE SCLEROTIC
THAN NORMAL AND THERE IS ABRUPT TRANSITION OF THE NORMAL
AND SCLEROTIC BONE. Due to this, the long bones affected by the
gummatous process are thickened. There is no tendency to bending and
pathological fracture. Occasionally the gummatous process starts in the
medullary canal and erodes the bone from within ----- SYPHILITIC
OSTEOMYELITIS. In the bones of the vault of the skull, nasal septum and
hard palate, destruction outspaces the new bone formation and the periosteal
reaction is slight. There are rounded areas of bone loss . in the skull, known as
‘WORM EATEN SKULL”.
The main symptom is deep seated boring pain at the site of
involvement, usually worse at night. If the bone is subcutaneous, the patient
may become aware of the swelling which may be tender at first. Sometimes
gummatous ulcer may lead from the bone to the skin.
(D) CARTILAGE: perichondritis of the costal cartilage, external ear and the
cartilagenous nasal septum.
(E) MUSCLE: gumma is rare but may occur from extension of the bone and
subcutaneous tissue and later lead to contracture and joint fixity.
(F) JOINTS, BURSA AND TENDON SHEATHS: the sites most exposed to stress
and strain such as the knee joint and prepatellar bursa are affected leading to
SWELLING, JUXTA ARTICULAR NODES ALONG TENDON SHEATHS.
(G) STOMACH: Rare. X-Ray examination shows a filling defect or distortion of the
cardiac end of the stomach. The symptoms are of chronic indigestion..
Elsewhere in the GIT, it can involve the parotid gland ( parotitis, gumma),
esophagus , intestine.
(H) LIVER AND SPLEEN: GUMMATOUS INVOLVEMENT OF THE LIVER IS THE
MOST FREQUENT TYPE OF ABDOMINAL SYPHILIS. It can occur as
DIFFUSE INTERSTITIAL CIRRHOSIS( a form of portal cirrhosis) or LOCAL
GUMMATOUS CONDITION progressing to an irregular fibrosis the so called
‘hepar lobatum’ ( localization--- capsule, parenchyma). Secondary amyloidosis can
occur later on. S/S include----
Jaundice, weight loss , remittent or intermittent fever.
Pain in the right hypochondrium. Palpable liver. ( LEFT LOBE IS
AFFECTED MORE THAN RIGHT)
S/S of portal hypertension.
Abnormal liver function test.
CARDIOVASCULAR SYPHILIS:
The incidence of cardiovascular syphilis in the case of late, untreated
syphilis is probably 10%.
Manifestations usually develop 15-30 years after the initial infection.
Most patients are 40-55 years.
Men: female = 3:1
Reported incidence in India = 0.1 – 2.6 %.
In 40% cases, it is accompanied by neurosyphilis.
The MOST COMMON LESON IS AORTITIS . THE CHANGES ARE MOST
MARKED IN THE ASCENDING AORTA AND AORTIC ARCH.
Pathogenesis: T.pallidum presumely reaches the heart during early stages of blood
borne dissemination --- then invade the vasa vasorum of the aortic wall and cause a
chronic low grade inflammation that eventuates in endarteritis and periarteritis.
This results in necrosis of the muscular and elastic tissues and scarring. This leads
to ----
• Atheromatous plaques in the intima with calcification of the intima.
• Aneurysmal dilatation.
Involvement of the CNS occurs in all stages of syphilis. The very early and
frequent invasion of the meninges by T.pallidum during systemic
dissemination of infection has been confirmed by the isolation of t.pallidum
in the CSF and by CSF abnormalities in 4-24 % of patients with early
syphilis.
Both treponemal isolation and CSF abnormalities appear to be more common
in PATIENTS WITH EARLY SYPHILIS THAN LATE SYPHILIS suggesting
that in some patients CSF ABNORMALITIES MAY RESOLVE WITHOUT
TREATMENT.
Although the true incidence of neurosyphilis is not known , the successful
treatment of early syphilis in the antibiotic era has made this an uncommon
disorder in many parts of world.
The incidence of neurosyphilis in STD patients in INDIA has been reported
to vary from 0.1% to 5.8%.
After resolution of the secondary stage, THE SPIROCHAETES PRESUMELY
REMAIN DORMANT IN THE CNS OF UNTREATED OR INADEQUATELY
TREATED PATIENTS.
In absence of treatment , approximately one third of those with early
invasion will develop signs of neurosyphilis.
Symptoms occur from 5-35 years after the initial infection.
Neurosyphilis is less common in women than in men and in negroes and Asians
than whites.
CLASSIFICATION:
ASYMPTOMATIC NEUROSYPHILIS: C/B
------ no S/S
------- CSF changes like
Elevated cell count ( > 4 lymphocytes per cu.mm ) : FIRST
INDICATION OF CNS INVOLVEMENT.
Elevated protein in the CSF ( > 40 mg%) . the level of IgG and IgM in
CSF may be increased and quantitative determination of these may
help in assessing the activity of the disease.
ABNORMALITIES OF CELL COUNT AND PROTEIN ARE THE MOST
SENSITIVE INDICES OF ACTIVITY OF DISEASE PROCESS. AFTER
SUCCESSFUL TREATMENT, THEY ARE THE FIRST TO RETURN TO NORMAL.
TESTS FOR REAGIN AND COLLOIDAL GOLD CURVE REMAIN
ABNORMAL FOR LONG PERIODS.
POSITIVE REAGIN TESTS GIVE A FIRM INDICATION OF THE
PRESENCE OF SYPHILIS OF THE NERVOUS SYSTEM. FALSE
POSITIVE RESULTS ARE VERY RARE IN CSF ( this sometimes may
occur in meningitis due to other causes due to passage of reagin from
the blood stream through the choroid plexus.
POSITIVE SPECIFIC TESTS OF SYPHILIS IN THE SERUM except
in very long standing burnt out cases of tabes syphilis. If this test is
negative in serum, it is unlikely to give a positive result in CSF.
Specific tests are positive in the CSF.
COLLOIDAL GOLD TEST : It is reported in the form of
• Graph into 3 zones : first zone ( paretic) , midzone ( leutic) and end zone
( meningitic)
• By a series of numericals: 0-1 : normal ; 2-5 : abnormal
This test is not diagnostic since it reflects the proportion of albumin
and globulin. Thus , paretic or leutic curve may be found in disseminated
sclerosis. Therefore always confirm by serological tests, cell count and protein.
Asymptomatic neurosyphilis is classified as:
TYPE 1 : minimal change of cell and protein, negative reagin and normal Lange
curve.
TYPE II: Raised cells and proteins, weakly positive reagin and mid zone Lange
curve.
TYPE III: raised cell and protein, strongly positive reagin, first zone Lange
curve. It is significant since it warrants that without treatment , patient is likely to
develop GPI.
SYPHILIS OF THE BRAIN:
(1) MENINGEAL SYPHILIS:
Meningeal involvement can occur in the secondary stage of the
disease or at any time in the later stages. Manifestations include:
Headache, Nausea, vomiting and stiffness of the neck :
MANIFESTATIONS OF ASEPTIC MENINGITIS.
It may be associated with COMMUNICATING HYDROCEPHALUS
( one third). There may be papilloedema.
The underlying CORTEX may be involved causing ----- convulsions,
aphasia and mental confusion. Monoplegia and hemiplegia can occur.
BASAL MENINGITIS can affect the cranial nerves MOSTLY
OCULOMOTOR, ABDUCENS AUDITORY AND FACIAL NERVES.
ARGYL- ROBERTSON PUPIL -------- where the light redlex is lost
but accomodation reflex is retained. The pupils are irregular and
unequal in size.
The DIAGNOSIS is based on ---- POSITIVE SEROLOGICAL TESTS,
CHANGES IN CSF, PRESENCE OF PUPILLARY ABNORMALITIES
AND IN SOME CASES, THE RESPONSE TO TREATMENT.
Diagnosis is based on C/F, Serum and CSF serologic tests, type iii CSF CHANGES,
good response to antibiotics ( HALTS PROGRESSION IN 80% CASES).
Optic atrophy can occur as an isolated finding. Penicillin does not restore
vision but prevents further progression.
• Gradual onset
• Headache
• Bulbar cranial nerve lesions.
• Redicular Pain in the neck shoulder and upper limb
• Lower motor neuron lesions of the shoulder girdle and arms with lost
reflexes, flaccidity and wasting. Sensory loss from posterior nerve root
compression can occur.
• Upper motor neuron palsy and sensory loss below the level of lesion may
occur due to compression and ischaemia of spinal cord.