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Two sets of observations suggested that extrachromosomal elements conferring antibiotic resistance might be widespread in streptomycetes. One was the evidence for plasmids affecting various other phenotypic properties in these organisms. Streptomyces coelicolor ~ 3 ( 2 ) contains a plasmid, SCPl, which acts as a conjugal sex factor and also codes for methylenomycin production and resistance (Kirby, Wright & Hopwood, 1975; Wright & Hopwood, 1976); less direct evidence implicates plasmids in the control of antibiotic production in Streptomyces kasugaensis (Okanishi, Ohta & Umezawa, 1970), Streptomyces hygroscopicus (Kahler & Noack, 1974) and Streptomyces venezuelae (Akagawa, Okanishi & Umezawa, 1975), melanin production in Streptomyces scabies (Gregory & Huang, 1964), S. venezuelae (Okanishi et al., 1970) and Streptomyces glaucescens (Baumann & Kocher, 1976), and aerial mycelium production in S. venezuelae, S. kasugaensis, S. scabies (Okanishi et al., 1970) and Streptomyces alboniger (Redshaw et al., 1976); and a plasmid is apparently also involved in resistance to oxytetracycline in a strain of Streptomyces rimosus which produces it (Boronin & Sadovnikova, 1972). Recently a second sex factor, SCP2, has been found in S. coelicolor ~ 3 ( 2 ) (Bibb, Freeman, & Hopwood 1977) and a sex factor, SRPl , has been revealed in a strain of S. rimosus (Friend, Warren & Hopwood, 1978). A second line of evidence was the consideration that antibiotic resistance in clinical isolates of eubacteria is usually due to plasmid-borne genes and it has been suggested (Walker &Walker, 1970; Benveniste & Davies, 1973) that such genes may have originated in the bacteria that produce the antibiotics, notably members of the genus Streptomyces, which synthesize the majority of all known antibiotics (BCrdy, 1974), and may have been transferred to unrelated bacteria. The main argument for this theory is the presence of similar antibiotic-inactivating enzymes in antibiotic-producing streptomycetes and in resistant eubacteria (Benveniste & Davies, 1973; El-Kersch & Plourde, 1976; Shaw & Hopwood, 1976; Nakano et al., 1977). Although this theory does not require the genes to be permanently plasmid-linked in their original streptomycete hosts, their dissemination to other bacteria might have been facilitated if this had been the case. As a preliminary approach to the problem (Freeman, 1976) we determined the level of resistance of about 40 streptomycete strains, chosen essentially at random from various culture collections, to a series of 25 antibiotics and other antimicrobial agents, giving some 1000 tests. Some strains were relatively resistant to the majority of the growth inhibitors while some inhibitors were inactive against all, or nearly all, of the strains. We selected for study four cases in which a particular strain was significantly more resistant to a certain antibiotic than were most of the strains, since such behaviour might be expected if an extrachromosomal element, not uniformly present in the set of cultures, conferred some resistance to an antibiotic.

Unstable Naturally Occurring Resistance to Antibiotics in Streptomyces