Studies in Experimental Syphilis

Abstract

The decision in any given case as to whether or not a syphilitic animal, treated and then reinoculated, has acquired a second attack of syphilis, will, of necessity, depend upon the criteria of a successful reinfection. In the older experimental work attention, was directed mainly, if not entirely, to the occurrence of a local lesion (chancre) at the site of reinoculation. If no such lesion developed in the reinoculated animal it was assumed that a second infection had not been established. It is at once apparent that this assumption is justified only if syphilitic infection is always accompanied by the Occurrence of a primary lesion at the portal of entry. That syphilis may occur in human beings without the development of a, chancre is well known (1). The same has been shown to hold true for monkeys (2) and for rabbits (3-5). In view of these now weU established facts it is dear that, in determining in the reinoculated animal whether or not a second infection has been established, one must take into consideration the possibility that second infections may occur without the appearance of any local lesion at the portal of entry. Such second infections might be characterised by dissemination of the treponemata throughout the body and their lodgement in distant organs, with or without the production of lesions at the site of such lodgement. Neisser (2) admitted the possibility of such a result from reinoculation in his discussion of superinfection,

Syphilis reinfections pose problems for syphilis diagnosis in Antwerp, Belgium – 1992 to 2012

“…Stages of syphilis were determined by an infectious disease specialist according to US Centers for Disease Control and Prevention surveillance definitions [19,20]. Latent syphilis was defined as syphilis characterised by RPR/TPPA seroreactivity without other evidence of disease.…”

Current status of syphilis vaccine development: Need, challenges, prospects

“…Complete protection against symptomatic homologous strain challenge develops only after 12 weeks of infection. If rabbits are cured of infection prior to that 12 week milestone, they can be symptomatically re-infected [87–90]. It is now speculated that the slow development of protective immunity to T. pallidum correlates with the unusual protein-poor surface of the bacterium.…”