Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a 20-month survey of resistance to three aminoglycosides (gentamicin, tobramycin, and amikacin) in Escherichia coli at a university hospital, six tobramycin-, kanamycin-resistant isolates containing a 50 kilobase conjugative R-plasmid which encoded an aminoglycoside phosphotransferase (APH-(3')) were isolated. The APH-(3') conferred resistance to kanamycin (MIC = 100 mg/L) but not to tobramycin (MIC = 20 mg/L). In both the original isolates and transconjugants the six R-plasmids demonstrated an isomeric ladder in the range of 50-112 kb, which was enhanced by exposure of the bacterial cultures to tobramycin. pJFJ2522 is the prototype for this group of plasmids. Bacterial DNA gyrase reversed the isomeric DNA ladder in pJFJ25222 by increasing the supercoiling of the plasmid DNA. Regardless of the level of supercoiling, the plasmids produced indistinguishable restriction endonuclease fragment patterns. The clinical isolates containing these plasmids demonstrated different restriction fragment length polymorphism (RFLP) of their EcoRI digested genomic DNA using E. coli rRNA as a probe. Ladder formation was plasmid specific since other tobramycin R-plasmids did not form a ladder, but it was not host specific. pJFJ25222 formed a ladder in a recA- host and displayed the same restriction pattern in a recA- as in a recA+ environment. In conclusion, pJFJ2522 contains a new tobramycin resistance gene whose mechanism of resistance is not known and whose product probably influences the isomerization of the plasmid.
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PMID:Isomeric DNA ladder formation of a plasmid encoding tobramycin resistance from Escherichia coli. 168 32

Between 1 January 1984 and 31 December 1987, 206 enterococcal blood isolates at the University of Wisconsin Hospital and Clinics were analyzed for high-level aminoglycoside resistance (hereafter high-level aminoglycoside resistance is simply referred to as "resistance") and hemolysin production. Of 190 Enterococcus faecalis isolates, 68 (35.8%) were resistant to gentamicin. Of these 68 strains, 67 (98.5%) contained a gene coding for the bifunctional aminoglycoside-modifying 6'-aminoglycoside acetyltransferase-2"-aminoglycoside phosphotransferase [AAC(6')-APH(2")] enzyme. Of 190 isolates, 85 (44.7%) were hemolytic and contained a gene coding for component A of the enterococcal hemolysin. Sixty-two of 68 (91.2%) gentamicin-resistant isolates but only 23 of 122 (18.8%) gentamicin-susceptible isolates were hemolytic (P less than 0.001). Twelve of the hemolytic, gentamicin-resistant E. faecalis blood isolates, but only 2 of 9 nonhemolytic or gentamicin-susceptible isolates, had identical chromosomal DNA restriction endonuclease digestion patterns, suggesting a common derivation for these strains. A historical cohort study from 1 July 1985 to 31 March 1987 identified by regression analysis postsurgical intensive care unit status (odds ratio [OR], 5.0; 95% confidence interval [CI], 1.1 to 22.8) and prior treatment with an expanded- or broad-spectrum cephalosporin (OR, 3.0; 95% CI, 0.9 to 10.1) as risk factors for gentamicin-resistant E. faecalis bacteremia. Patients with hemolytic, gentamicin-resistant E. faecalis bacteremia had a fivefold-increased risk for death within 3 weeks of their bacteremia compared with patients with nonhemolytic, gentamicin-susceptible strains (95% CI, 1.0 to 25.4).
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PMID:Bacteremia caused by hemolytic, high-level gentamicin-resistant Enterococcus faecalis. 192 36

The sizes of the zones of inhibition around routinely tested antibiotic disks classified gentamicin-resistant isolates of Klebsiella pneumoniae from one hospital into four major antibiotype classes. From each isolate of the prevalent class (A1), two plasmids could be transferred conjugally. One carried genes for resistance to tetracycline, sulfonamides, and chloramphenicol, and for the SHV beta lactamase. The other carried genes for two aminoglycoside-inactivating enzymes, APH (3')-I and AAC (3)-III, for the TEM 1 beta lactamase, and for resistance to sulfonamides. Transconjugants of either plasmid from any A1 isolate yielded the same DNA fragments after restriction endonuclease digestion, but the two plasmids had no fragments in common. Fragments or genes from either plasmid were variously combined or lacking in plasmids from variant isolates (A2, A3, and A4). Plasmids transferable from isolates of classes B and C shared no common DNA restriction fragments with each other or with either plasmid from Class A. Fragments and genes of the plasmids from C isolates, however, were identical with those of a plasmid endemic in a nearby hospital. Routine monitoring by diagnostic microbiology laboratories of distinctive antibiotypes and of the plasmids that produce them would aid infection control and antibiotic usage policy.
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PMID:Diagnostic microbiology laboratory susceptibility test results discriminate distinctive antibiotic resistance plasmids. 609 87

Acinetobacter calcoaceticus strain BM2500 was resistant to ampicillin, aminoglycoside-aminocyclitols, chloramphenicol, sulfonamides, and high levels of trimethoprim. Resistance to ampicillin was due to the presence of a beta-lactamase (TEM-1) and the aminoglycoside-aminocyclitol resistance was mediated by phosphotransferase (APH(3')(5")I) and adenylyltransferase (AAD(3)(9] activities. The resistance genes were carried by a 167 kilobase plasmid, pIP1031, belonging to incompatibility group 6-C; the plasmid was self-transferable, at extremely low frequency, to Escherichia coli by conjugation. Plasmid pIP1031 DNA was analyzed by agarose gel electrophoresis following restriction endonuclease digestion, by nucleic acid hybridization, and by CsCl analytical density gradient ultracentrifugation. The results support the hypothesis that plasmid pIP1031 may have been acquired recently by strain BM2500.
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PMID:Transferable plasmid-mediated antibiotic resistance in Acinetobacter. 635 87