Varicella-zoster immune globulin (VZIG), an immunoglobulin prepared from normal donor plasma selected for high titer of antibody to varicella-zoster virus (VZV), and zoster immune globulin (ZIG), prepared from the plasma of donors convalescing from herpes zoster, were compared in a double-blind, randomized clinical trial to determine their relative efficacy in protecting immunosuppressed children from severe varicella. VZV infection occurred in 49 (60.4%) of 81 recipients of VZIG and in 57 (68.6%) of 83 recipients of ZIG. These rates and the clinical severity of varicella were not significantly different; however, the subclinical infection rate was significantly higher in ZIG recipients (31.3% vs. 16.0%). This difference was accounted for by a subgroup of patients receiving immunosuppressive therapy for nonneoplastic diseases. Doubling the dose of VZIG administered reduced the rate of subclinical infection. These data indicate that VZIG can be used to protect immunosuppressed children from severe chicken pox.

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We studied the pretreatment of human polymorphonuclear neutrophils (PMN) with purified preparations of the anthrax toxin components--protective antigen (PA), edema factor (EF), and lethal factor (LF)--and their effects on release of superoxide anion (O-2) after stimulation with the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP). PMN isolated in the absence of lipopolysaccharide (LPS) (less than 0.1 ng/ml) released only small amounts of O-2 after FMLP stimulation; pretreatment with anthrax toxin had little effect. The release of O-2 was increased fivefold by prior treatment with 3 ng/ml LPS for 1 h at 37 degrees C, an effect referred to as priming. PMN were primed to an equivalent extent by treatment with 100 ng/ml N-acetyl-muramyl-L-alanyl-D-isoglutamine (muramyl dipeptide [MDP]). Pretreatment of PMN with anthrax toxin components PA plus EF or PA plus LF inhibited priming by LPS or MDP, as shown by the reduction in the release of O-2 up to 90% relative to controls not treated with toxin; single toxin components were inactive. The inhibition was markedly reduced when priming with LPS or MDP was carried out before exposure to toxin. O-2 release after stimulation by phorbol myristate acetate was not increased by priming, and pretreatment with toxin did not inhibit O-2 release after this stimulus. Evidently, anthrax toxin inhibits the priming that is normally induced in PMN by bacterial products and is necessary for the full expression of antimicrobial effects.

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