Postonchospheral stages of Taenia taeniaeformis liberated from rat livers by enzymatic digestion at 1 to 10 days postinfection (DPI) and metacestodes dissected from infected livers at 22, 34, and 69 DPI were exposed in vitro to immune rat serum (IRS) and to normal serum from rats (NRS), human beings (NHS), or guinea pigs (NGS). The onset of rapid and destructive tegumental changes in all organisms exposed to any of the sera was demonstrated to be complement-dependent because the reaction was: (a) inhibited by treatment of serum at 56 C for 30 min; (b) inhibited by prior incubation of serum with zymosan or with complement-fixing, soluble products derived from larvae of T. taeniaeformis maintained in vitro (IVP); and (c) abolished by the addition of EDTA. Lytic effects occurred on exposure to agammaglobulinemic sheep serum, and lysis in the presence of IRS and NRS was shown to result in consumption of available hemolytic complement. Surface changes consisted of vesiculation in the microvillar or microthrix layers followed by sloughing of the tegument, eventually leading to collapse of the cystic bladder and cessation of flame cell activity, or, in the case of early postonchospheral forms, complete disintegration of the organism. When IVP was added to NHS, reduction of hemolytic complement activity was associated with the electrophoretic conversion of C3, and Factor B, but there was little or no consumption of C1. The observations support the hypothesis that complement-mediated effector mechanisms must be counteracted to ensure survival of parasites in vivo, and that the capacity for release of soluble nonspecific complement-fixing factors by taeniid larvae may have an important role to play in this process.