Abstract

The role of complement in humoral-mediated resistance to frambesial infection (yaws) needs to be defined. The level of serum C3 was reduced shortly after infection of hamsters with Treponema pallidum subspecies pertenue. Five weeks after frambesial infection, the serum C3 level began to increase and by week 7 no difference was detected between infected and uninfected hamsters. When C3 was depleted in hamsters by injection of 20 units of cobra venom factor (CoVF), two alterations in host resistance to frambesial infection occurred. Depletion of C3 abrogated the ability of immune serum to confer complete protection on normal hamsters against infection with the yaws spirochete. In all hamsters receiving immune serum but not CoVF, lesions failed to develop and lymph nodes weighed significantly less (P less than or equal to 0.1) than those of controls. Furthermore, no treponemes were detected in the lymph nodes of passively immunized animals. Second, depletion of C3 increased the susceptibility of hamsters to frambesial infection. The onset and progression of frambesial lesions were enhanced as compared with frambesial-infected hamsters not treated with CoVF. Finally, CoVF treatment did not reduce the ability of frambesia-immune hamsters cured of disease with penicillin to resist reinfection. These results demonstrate that complement influences the pathogenesis of yaws.

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