A total of 199 streptococci isolated from feces of healthy chickens, pigs, and beef cattle and 26 human clinical isolates were tested for resistance to kanamycin, streptomycin, tetracycline, erythromycin, and lincomycin. Of 66 isolates resistant to these antibiotics, 12 transferred one or more resistance traits by conjugation in broth. Erythromycin resistance (Emr) was transferred from 10 of the 12 successful donors. AvaI digests of plasmids isolated from Emr transconjugants derived from two human, two chicken, and one pig isolate contained three fragments similar in size to those produced from Tn3871, an Emr transposon. The three fragments from each of the five digests on Southern blots hybridized to radiolabeled Tn3871. Plasmid DNA from a transconjugant derived from a second pig isolate contained two of the three Tn3871-associated AvaI fragments. One of the AvaI fragments from each of the six plasmids hybridized with a radiolabeled probe containing a cloned AvaI fragment from Tn3871 that contained the Emr determinant. Transposition of the Emr trait was demonstrated for the plasmids derived from one human and one pig isolate. We concluded that extensive DNA homology existed between plasmids from streptococcal strains obtained from two human patients, two chickens, and two pigs and the Emr transposon Tn3871, which is very similar or identical to the well-characterized Emr transposon Tn917. The detection of Tn3871-like sequences in streptococcal isolates from Arkansas, Illinois, North Carolina, and Washington, D.C. indicates wide dissemination of Emr mediated by the same or closely related transposons.

The Emr, Km', and The conjugative R plasmid pJH1 comes from a human clinical isolate of Streptococcus faecalis JH1 (16). This 80-kilobase-pair (kbp) plasmid encodes resistance to erythromycin, kanamycin, streptomycin, and tetracycline. These phenotypes are the most common antibiotic resistance traits found among group D streptococci isolated from human and animal sources (5,7,8,12,22,29,34,36). The genetic basis for Emr in many S. faecalis strains from humans, as well as from healthy pigs and chickens, appears to be the dissemination of a Tn3871-like element (29); the Emr determinant of pJH1 resides on Tn3871 (4), a transposon that is very similar if not identical to Tn917 (33). In this study we expanded our molecular analyses to include the Kmr and Smr determinants of pJH1. We present evidence that the Emr, Kmr, and Smr determinants of pJH1 and those of the majority of multiply resistant group D streptococci from human and animal sources share a common evolutionary origin. We also provide evidence that all three resistance determinants were inherited as a unit within a 9-to 11-kbp DNA fragment on three plasmids from human group D streptococcal isolates (including pJH1) and two plasmids from pig isolates. MATERIALS AND METHODSBacterial strains. The S. faecalis strains used in this study are described in Table 1. Ninety-one group D streptococcal isolates were the sources of plasmid-enriched cell lysates used in the preparation of dot blots. The origins of the 46 chicken and 21 pig isolates and the 2 human clinical isolates from the Walter Reed Army Medical Center, Washington, D.C., were described previously (29). The remaining 22 strains from human clinical sources (6 from a hospital in Houston, Tex., 7 from Chile, and nine from Bangkok, Thailand) were kindly provided by B. Mederski-Samoraj,