smooth muscle. Classic symptoms include pallor and then diffuse erythema, urticaria and itching, subcutaneous edema, edema and spasm of the larynx, wheezing, tachycardia, hypotension, and hypovolemic shock (Kniker, 1988; Pearlman and Bierman, 1989). If death occurs, it is most commonly from airway obstruction caused by laryngeal edema or bronchospasm, or cardiovascular collapse from transudation of fluids from the intravascular space (Pearlman and Bierman, 1989). The tissues at autopsy show primarily widespread edema.
The clinical presentation of anaphylaxis can be produced by intravascular antigen-antibody reactions that activate the complement system. In this case, the antibodies may be of the IgG or IgM class. Peptides that are split from activated complement components act on mast cells and basophils to induce the release of the same mediators (Kniker, 1988). This reaction is recognized most clearly after intravenous administration of antigen; it has been hypothesized to occur rarely after intramuscular or subcutaneous injection through rapid entry (within 1 to 5 minutes) of large amounts of the antigen into the venous circulation. This reaction in an infant presumably could be mediated by IgG antibody received transplacentally from the mother; such antibody would be expected to persist for the first 6 months of life and possibly longer (Benacerraf and Kabat, 1950; Cohen and Scadron, 1946). Anaphylaxis also can occur without an obvious cause (Wiggins et al., 1989).
Shock caused by bacteremia with circulating bacterial endotoxin also appears to involve activation of the complement system (Fearon et al., 1975; Lachmann and Peters, 1982). Endotoxin shock has a clinical presentation different from that of anaphylaxis, however; it develops more slowly and is almost always associated with disseminated intravascular coagulation, with consumption of clotting factors and hemorrhage (Colman, 1989; Suffredini et al., 1989a,b). Endotoxin elicits the release of mediators of inflammation in addition to those from mast cells and basophils, including interleukin-1 and tumor necrosis factor (Michie et al., 1988; Morrison and Ryan, 1987). The Jarisch-Herxheimer reaction, described classically in patients with spirochetal disease within hours after beginning drug therapy, may be a form of endotoxemia or, at least, complement activation caused by circulating bacterial products (Bryceson, 1976).
The Arthus reaction is another immunologic response that can be associated with tissue damage. This reaction is mediated differently from anaphylaxis. The formation of antigen-antibody complexes with deposition in the walls of blood vessels is basic to this reaction. This is not an acute, immediately overwhelming condition. It generally develops over 12 to 24 hours if antibody levels are already high, or it can develop over several days (e.g., in serum sickness) as antibody levels increase and antigen persists. In this reaction, immune complexes in the walls of blood vessels