SUMMARY: A high proportion of strains of (599 of 716 strains), (15 of 18), (32 of 33) and (42 of 61), but not of (15 of 209), were resistant to sodium arsenite; the incidence of arsenite resistance was higher in animal than in human strains of . Transmissible arsenite resistance, which was mainly plasmid-borne, was common in resistant strains of (22 of 34 tested) and (11 of 12), but not in resistant strains of (10 of 98), (0 of 32) or (0 of 6). In three strains from which the arsenite resistance genes could not be transferred by direct methods, they were mobilized by implanting the conjugative plasmids F or I intothem. In two strains with transmissible arsenite resistance, the resistance genes were located in the genome of the phage with which they were lysogenized. In several of the enterobacterial strains the plasmid-borne arsenite resistance was not associated with antibiotic resistance or any other character known to be transmissible. In many of the strains, though, it was often associated with transmissible antibiotic, mercury and tellurite resistance and especially with transmissible lactose utilization. The available evidence strongly suggested that the arsenite resistance genes were located on the Lac plasmid. The conjugative plasmids in several of the strains were temperature-sensitive. Many of the arsenite-sensitive strains grew on culture media containing mixtures of sodium arsenite and sodium nalidixate at concentrations of each which by itself would not permit their growth. Arsenite-resistant cultures did not grow under such conditions but any arsenite-sensitive mutants they contained did.


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