SUMMARY: Enterochelin, the iron chelator produced by a number of pathogenic enterobacteria, appears to be an essential metabolite for multiplication within the host, where it transports iron from the host iron-binding proteins to the bacteria. Previous work showed that complexes of enterochelin containing either scandium (Sc) or indium (In) exerted a bacteriostatic effect on in serum, whilst the Sc complex exerted a significant therapeutic effect on mice infected with . These observations have now been extended to a number of pathogenic serotypes of including those carrying either the K1 antigen or the ColV plasmid. The Sc and In complexes each exert a bacteriostatic effect on these organisms growing in either whole serum or media containing an iron-binding protein. Evidence is presented that the Sc complex may act as a competitive inhibitor of the Fe complex. In contrast to their effects on , sideramines other than enterochelin fail to reverse the bacteriostatic effect of the Sc complex of enterochelin in , suggesting that the complex produces a more profound derangement of metabolism in this organism. The Sc complex exerts a significant therapeutic effect on infections in mice although the In complex is less active.


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