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Late (Tertiary) Syphilis

Clinical Findings

Tertiary disease, usually seen 5-20 years after initial infection, traditionally includes cardiovascular syphilis, late benign (or gummatous) syphilis, and neurosyphilis (see Box 1). Fewer organisms are found in lesions during this stage.

Late syphilis

Cardiovascular Syphilis

The incidence of cardiovascular involvement is probably underestimated, although clinically significant disease eventually develops in ~ 10% of all untreated patients. Lesions include coronary ostial stenosis and coronary artery insufficiency, aortic valvular regurgitation with left ventricular hypertrophy and congestive heart failure, and saccular aortic aneurysms of the ascending and transverse portions of the thoracic aorta. These aneurysms usually do not dissect and rupture but can present as pulsating supraclavicular chest wall masses with associated hoarseness, dysphagia, dyspnea, and cough due to impingement on adjacent vital structures.

Syphilis should always be considered in patients whose chest radiograph reveals ascending aortic calcifications or those with isolated aortic valvular disease and positive treponemal serologies, particularly if other manifestations of late disease are present.

Late Benign Syphilis

The classic lesion of late benign syphilis seen in ~ 15% of untreated patients is the gumma, a granulomatous inflammatory process that usually affects the skin, subcutaneous tissues, and bone but may involve the liver, respiratory tract, stomach, heart, and almost any other organ of the body.

Usually nodular before ulcerating, gummas are noninfectious, indurated, violaceous, and painless. Gummas may heal or become chronic, resulting in destructive local disease. The differential diagnosis includes causes of other granulomatous processes such as mycobacterial and fungal infections, sarcoidosis, and malignancies.

Late syphilis symptoms

Neurosyphilis

Clinically apparent CNS involvement is estimated to occur in ~ 5-10% of all syphilis patients and can be seen at any stage of infection; however, early silent dissemination of T pallidum to the CNS is almost the rule. Asymptomatic neurosyphilis is usually accompanied by CSF cellular or protein abnormalities, the presence of T pallidum in the CSF, or a positive CSF VDRL test.

These CSF abnormalities resolve spontaneously in many patients; the likelihood of developing symptomatic CNS infection is proportional to the degree of these abnormalities. Symptomatic neurosyphilis classically takes the forms of aseptic meningitis (see Secondary Syphilis), meningovascular syphilis, and parenchymatous neurosyphilis (general paresis and tabes dorsalis), in ascending order of frequency.

Meningovascular syphilis usually occurs 4-10 years after infection and presents with stroke-like symptoms in younger patients, a consequence of endarteritis obliterans of the cerebral arteries.

CSF abnormalities characteristically include a lymphocytic pleocytosis, an elevated protein, and a reactive VDRL.

Stages of syphilis

Parenchymatous neurosyphilis, a consequence of neuronal destruction by T pallidum, is divided into two discrete syndromes, tabes dorsalis (more common) and general paresis. It is not uncommon, however, to see patients exhibiting neurologic features of both syndromes.

Tabes dorsalis results from progressive demyelination of the posterior columns and dorsal roots. It is manifested by sharp pains of the lower extremities, dysuria, and ataxia; physical findings may include areflexia and loss of pain, temperature, and position sense. Patients with general paresis present with a slowly progressive dementia. Neuropsychiatric manifestations include tremors, dysarthria, ataxia, delusions, and personality changes. The irregular Argyll-Robertson pupil of parenchymatous syphilis results from pupillary constriction to accommodation but not to light.

The clinical diagnosis is supported by CSF abnormalities in patients with positive treponemal serologies. Unlike the other forms of late syphilis, the lesions of general paresis contain a significant number of spirochetes. The effect of concomitant HIV infection on the clinical course of syphilis, including neurosyphilis, is discussed in a later section (see Syphilis and HIV, below).

Useful links

https://en.wikipedia.org/wiki/Syphilis http://goaskalice.columbia.edu/answered-questions/late-stage-syphilis http://www.nytimes.com/health/guides/disease/syphilis-tertiary/overview.html http://www.healthcommunities.com/syphilis/syphilis-diagnosis-stages-treatment.shtml

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