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February 1985, Vol 139, No. 2 >
Article | February 1985

Necrotizing Enterocolitis, Hemolysis, and Clostridium perfringens-Reply

SHAW WARREN, MD; JOHN R. SCHREIBER, MD; MICHAEL F. EPSTEIN, MD
Am J Dis Child. 1985;139(2):115. doi:10.1001/archpedi.1985.02140040012011.
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In Reply.—The letter by Novak et al has raised an interesting possibility as to the pathogenesis of hemolysis in the two patients with NEC and C perfringens infection whom we have described.1

It seems that there are at least two mechanisms by which C perfringens can induce hemolysis. It is well established that C perfringens elaborates a potent hemolysin called α-toxin, which is capable of lysing RBCs in the absence of serum or antibody.2,3 This toxin functions as a lecithinase, interacting directly with the cell membrane.4,5 In the second mechanism, as recently described by Seger et al6,7 and Novak,8 a neuraminidase produced by C perfringens results in the exposure of a cryptogenic antigen on the surface of RBCs. The RBCs are then agglutinated in the presence of naturally occurring antibody directed towards this antigen. It is unclear which of the mechanisms is quantitatively more

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AAM 2010;304:1493-1495.
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