- Tertiary Syphilis describes the final stage of syphilitic disease which is characterized by progressive dysfunction of a number of organ systems. The clinical consequences of this stage emerge slowly, over years, from a background of Latent Syphilis. The pathogenesis of Tertiary Syphilis is due to long-term inflammation of affected organs due to the chronic presence of T. pallidum. Importantly, only 30% of untreated individuals with Latent Syphilis ever develop signs and symptoms of Tertiary Syphilis.
- Neurosyphilis refers to a constellation of possible neurological disease which include meningitis, meningovascular disease, and general paresis. Syphilitic meningitis is unique among bacterial meningitis in that the CSF Pleocytosis is composed of lymphocytes rather than neutrophils. Meningovascular Disease refers to slow, progressive occlusion of arteries of the meninges resulting in gradual onset of focal neurological impairments typical of stroke. General Paresis is a description of end-stage neurosyphilis and is characterized by a wide variety of neurological abnormalities and deficits. Only highlights are listed below. Paresis is characterized by pupils that accommodate but do not React, termed "Argylle-Robertson Pupils". Tabes Dorsalis may also be a feature of paresis and arises due to demyelination of posterior columns, dorsal roots, and dorsal root ganglia of the spinal cord resulting in disturbances of gait, reflexes, and sensation loss. A wide variety of personality and intellectual deficits also occur in general paresis.
- Cardiovascular Syphilis
- Gummatous Syphilis
- Gummas are largely harmless, solitary, variably-sized nodular lesions which can occur in the skin, bone, or nasopharynx. Gummas display a granulomatous inflammation with a central area of caseous necrosis surrounded by lymphocytes, plasma cells, and macrophages.
|FYI: Syphilis and Philosophy of Science|
- The development of Tertiary Syphilis has been used as a central example in understanding the nature of Scientific Explanations in discussions of Philosophy of Science. The example was first described by Michael Scriven in 1959 where he asked whether citing an individual's previous infection with T. pallidum was sufficient to explain his later development of paresis, given the fact that only a minority of infected individuals ever develop paresis. The example is significant because a number of leading philosophers believed that scientific explanations were only valid if the phenomenon being explained was guaranteed to occur given the events cited in the explanation. However, it is clear that not all individuals with T. pallidum infection develop paresis; therefore, on this model of scientific explanation, citing previous infection with T. pallidum is clearly insufficient to explain the later development of paresis. Yet, as can be seen in any medical text, doctors at the very least would consider citation of an individual's previous infection with T. pallidum to be a fairly good explanation of later development of paresis. A number of notable Philosophers of Science have worked on this question including Carl G. Hempel and Wesley Salmon to name a few.