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19 Dec 2022
updated 21 Dec 2022

The Etiology of Syphilis

Syphilis was probably introduced to the Old World from the New World in the late 1400's, in return for the smallpox that Europeans introduced to the Americas. It was spread relentlessly by the armies which marched and countermarched across the continent in the endless wars of those days, and also by the colonisation of the Third World by the major European nations.

It became so widespread that I'm not sure whether it would have been described as epidemic or endemic. But the fact remains that you could catch syphilis more or less anywhere you lived or travelled in the known world. Also, in the hot, moist air of tropical areas the possibility of contracting syphilis by non-sexual contact (10% of cases) was increased. Sexual contact (90% of cases) might equally well be heterosexual or otherwise.

Infection of a previously healthy persion from another person is called acquired syphilis, but it is also possible to be born with this disease and this is called congenital syphilis.

In the era before Mendelian genetics became widely publicised, there were two schools of thought as to the mechanism of congenital syphilis. The contagionists attributed it to maternal infection (ie that the mother was already infected, or that the father infected the mother at the time of conception) and the hereditists thought it was transmitted 'germinally' via the father's sperm (they could equally have supposed that it might be transmitted via the mother's ovum).

It is now clear that there is no hereditary (ie genetic) aspect, and that contagionism was essentially correct. Infected maternal body fluids pass their 'contagion' either in utero, or in transit through the birth canal. The former of these is by far the more serious for the poor child.

The acquired disease is often called first-generation syphilis, the congenital case being correspondingly referred to as second-generation syphilis. And evidence for third-generation or even fourth-generation syphilis started to accumulate during the nineteenth century, though it is still a controversial idea. Whereas at least one acquisitively-infected parent is necessary for the second generational case, the third and fourth generational cases arise from intervening generations that were not acquisitively-infected. It all starts to sound rather Biblical.

Wicher & Wicher§ have provided firm evidence for third and fourth generation transmission in research conducted with guinea-pigs, and also note (as far as I can understand) that the effects decline from generation to generation, as would only be expected. So the buck seems to stop with the fourth generation.

The organism responsible for syphilis is a spirochete (spiral bacterium) called treponema pallidum. It was first identified in the tissue of an infected patient under the microscope by Schaudinn and Hoffmann in 1905, and the brain tissue of a neurologically infected patient by Hideyo Naguchi in 1913.

Historically, the principal treatment had been mercuric chloride (HgCl2, corrosive sublimate), with toxic symptoms frequently confused with those of syphilis itself. Indeed, the Mad Hatter in Alice in Wonderland and Through the Looking Glass was symbolic of the occupational insanity characteristic of workers exposed to mercuric nitrate (Hg(NO3)2) in the manufacture of good quality felt for making men's hats.

An extreme treatment for neurologically infected patients was to deliberately infect them with malaria, which caused a recurrent high fever (spiking every 48 hours) killing the syphilis bacterium. The malarial infection was then treated, with a reasonable chance of success, with quinine.

The synthesis of arsphenamine by Sachahiro Hata and Paul Ehrlich in 1909, was a turning point in the clinical treatment of syphilis. Nicknamed 'Compound 606', its molecule can be visualised most simply as a phenylamine group substituted into arsine (arsenic trihydride, AsH3) but in reality it exists as a dimer, trimer or even pentamer of the basic unit. It was marketed in 1910 as Salvarsan.

Originally noticed by a French medical student, Ernest Duchesne, in 1896, penicillin was re-discovered by the Scottish bacteriologist Alexander Fleming in 1928, who spotted its bacteriocidal property. It was not until 1939 that Dr. Howard Florey, a future Nobel Laureate, and three colleagues at Oxford University began intensive research and were able to demonstrate penicillin's ability to kill a wide range of infectious bacteria – including treponema pallidum … The rest of the story is well known to us all.

The effects of syphilis on a victim typically progress in several distinct stages, as tabulated below, principally to identify the medical terminology involved. The actual symptoms are described in the various references at the end.

Primary(affects ~40% of people exposed to infection,
90% of these by sexual contact)
Secondary(2 – 6 months after initial infection, most infective phase)
  • Early (<2 years after I° infection, high possibility of relapse)
  • Late (ongoing, low possibility of relapse)
Tertiary(affects 35% of cases, very much less infectious)
  • Cardiovascular (affects 27% of cases)
  • Neurosyphilis (affects 8% of cases)
    • asymptomatic
    • meningovascular = meningoencephalitis
    • tabes dorsalis 
      = locomotor ataxia
      = syphilitic myelopathy
    • general paresis (paralysis) of the insane (GPI) = dementia paralytica



patient.info/health/syphilis-leaflet (or click here)
www.encyclopedia.com/article-1G2-2584700844/syphilis.html (or click here)

§Victoria Wicher and Konrad Wicher "Pathogenesis of Maternal-Fetal Syphilis Revisited", Clinical Infectious Diseases, Vol 33, Issue 3, pp 354-363