Editorial

Despite decades of research on the effects of zinc in infectious diarrhea, there is surprisingly little consensus on how zinc works (or even if it works), on whether zinc’s effects are pathogen-specific, and what patient populations are most likely to benefit from zinc supplementation.1,2 Some recent articles focus on the growth-promoting effects of zinc on the pathogen itself, leading the reader to wonder if zinc supplements might make certain kinds of gastroenteritis worse, not better.3 Indeed, zinc is an essential mineral for all known forms of life, including bacteria, archea, fungi, protists, animals, and plants. The article by Medeiros et al. in this issue of Virulence focuses on zinc and enteroaggregative E. coli (EAEC), strain 042.4 In this study, concentrations of zinc salts in the range of 0.05 to 0.2 mM inhibited several measures of EAEC viru-lence, including adherence to cultured host intestinal cells, formation of biofilm on polystyrene plastic, and inhibition of expression of several virulence factors, including aggR, virK, aatA, and so on. Furthermore, zinc-deficient mice chal-lenged with EAEC orogastrically showed weight loss that was reversed by “res-cue ” with supplemental zinc. The study by Medeiros et al. was conducted with a single EAEC strain, and since EAEC are fairly diverse genetically, follow-up experi-ments with a collection of EAEC strains would help expand the generalizability of this study. The article by Medeiros et al. on zinc and EAEC adds to the literature show-ing a beneficial effect of zinc on infection with diarrheagenic E. coli. For strains of enterotoxigenic E. coli (ETEC) producing From ambivalent to divalent Has the “zinc age ” finally arrived