It has been suggested that antibiotic treatment of O157
infection may facilitate HUS development by causing an increase
in toxin production or an enhanced release of preformed toxin. The
mechanisms by which antibiotics increase toxin production and
release are not clear, but may involve increased cell permeability
due to membrane alterations and the induction of phage-encoded
genes encoding 2 Shiga toxins, Stx1 and Stx2. Laboratory studies
have demonstrated that antibiotics can dramatically affect the
production and release of Shiga toxins from O157.17,18,20–25 The
results of these studies vary, however, making it difficult to use
them to draw conclusions concerning the effect of antibiotic usage
on HUS development. What is apparent from these studies, however,
is that the response of O157 to antibiotics can vary markedly
depending on the strain, the class of antibiotic, and the concentration
of antibiotic.