Groups of 10 young male guinea pigs of inbred strains 2 and 13 and outbred strains Hartley A, Hartley B, and one deficient in the fourth component of complement (C4D) were infected intradermally with 80 X 10(6) Treponema pallidum (Nichols). The course of infection and production of antitreponemal antibody were examined. Strain C4D guinea pigs were the most susceptible to infection (100%); inbred strains 2 and 13 and outbred strain Hartley B showed 80-90% symptomatic infection; and the Hartley A strain was the least susceptible to infection (10%). Strain 13 animals responded with the highest antitreponemal antibody activity, and the Hartley A strain with the lowest. The results suggest that genetic factors or complement, or both, may influence the degree of susceptibility to infection with T pallidum in guinea pigs.
Although congenital syphilis has been recognized for several centuries and an efficient treatment with penicillin became available more than a half-century ago, the disease is still with us. Inability to culture in vitro the causative agent, Treponema pallidum, and the lack of an adequate animal model have prevented exploration of the various immunopathological events affecting the natural course of congenital infection. The purpose of this review is to analyze the disease in the context of recent knowledge acquired from human and experimental animals, particularly from the guinea pig model of congenital and neonatal syphilis, and to describe how the infection interacts with the maternal-fetal unit and how it is further modulated by the conceptus' ontogenic development. We also attempt to elucidate several old immunologic concepts and misconceptions that have remained unchallenged for too long.
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