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585000.9986Gram-positive merA gene in gram-negative oral and urine bacteria. Clinical mercury resistant (Hg(r)) Gram-negative bacteria carrying Gram-positive mercury reductase (merA)-like genes were characterized using DNA-DNA hybridization, PCR and sequencing. A PCR assay was developed which discriminated between the merA genes related to Staphylococcus and those related to the Bacillus/Streptococcus merA genes by the difference in size of the PCR product. DNA sequence analysis correlated with the PCR assay. The merA genes from Acinetobacter junii, Enterobacter cloacae and Escherichia coli were sequenced and shared 98-99% identical nucleotide (nt) and 99.6-100% amino acid identity with the Staphylococcus aureus MerA protein. A fourth merA gene, from Pantoeae agglomerans, was partially sequenced (60%) and had 99% identical nt and 100% amino acid identity with the Streptococcus oralis MerA protein. All the Hg(r) Gram-negative bacteria transferred their Gram-positive merA genes to a Gram-positive Enterococcus faecalis recipient with the resulting transconjugants expressing mercury resistance. These Gram-positive merA genes join Gram-positive tetracycline resistance and Gram-positive macrolide resistance genes in their association with mobile elements which are able to transfer and express in Gram-negative bacteria.200415358427
596310.9985Expression of the mphB gene for macrolide 2'-phosphotransferase II from Escherichia coli in Staphylococcus aureus. The genes mphA and mphB encode macrolide 2'-phosphotransferases I and II, respectively, and they confer resistance to macrolide antibiotics in Escherichia coli. To study the expression of these genes in Gram-positive bacteria, we constructed recombinant plasmids that consisted of an mph gene and the pUB110 vector in Bacillus subtilis. When these plasmids were introduced into Staphylococcus aureus, the mphB gene was active and macrolide 2'-phosphotransferase II was produced. The gene endowed S. aureus with high-level resistance to spiramycin, a macrolide antibiotic with a 16-membered ring. Moreover, transcription of the mphB gene in S. aureus began at the promoter that was active in E. coli.19989503630
200920.9984Aminoglycoside resistance genes aph(2")-Ib and aac(6')-Im detected together in strains of both Escherichia coli and Enterococcus faecium. Escherichia coli SCH92111602 expresses an aminoglycoside resistance profile similar to that conferred by the aac(6')-Ie-aph(2")-Ia gene found in gram-positive cocci and was found to contain the aminoglycoside resistance genes aph(2")-Ib and aac(6')-Im (only 44 nucleotides apart). aph(2")-Ib had been reported previously in Enterococcus faecium SF11770. aac(6')-Im had not been detected previously in enterococci and was found to be present also 44 nucleotides downstream from aph(2")-Ib in E. faecium SF11770. aph(2")-Ib and aac(6')-Im are separate open reading frames, each with its own putative ribosome binding site, whereas aac(6')-Ie-aph(2")-Ia appears to be a fusion of two genes with just one start and one stop codon. The deduced AAC(6')-Im protein exhibits 56% identity and 80% similarity to the AAC(6')-Ie domain of the bifunctional enzyme AAC(6')-APH(2"). Our results document the existence of a member of the aph(2") family of genes in gram-negative bacteria and provide evidence suggesting the horizontal transfer of aph(2")-Ib and aac(6')-Im as a unit between gram-positive and gram-negative bacteria.200111557456
305230.9984Expression of antibiotic resistance genes from Escherichia coli in Bacillus subtilis. Bifunctional recombinant plasmids were constructed, comprised of the E. coli vectors pBR322, pBR325 and pACYC184 and different plasmids from Gram-positive bacteria, e.g. pBSU161-1 of B. subtilis and pUB110 and pC221 of S. aureus. The beta-lactamase (bla) gene and the chloramphenicol acetyltransferase (cat) gene from the E. coli plasmids were not transcribed and therefore not expressed in B. subtilis. However, tetracycline resistance from the E. coli plasmids was expressed in B. subtilis. Transcription of the tetracycline resistance gene(s) started in B. subtilis at or near the original E. coli promoter, the sequence of which is almost identical with the sequence recognized by sigma 55 of B. subtilis RNA polymerase.19836410152
450340.9984Evolution and transfer of aminoglycoside resistance genes under natural conditions. 3'-Aminoglycoside phosphotransferases [APH(3')] were chosen as a model to study the evolution and the transfer of aminoglycoside resistance genes under natural conditions. Comparison of the amino acid sequences of APH(3') enzymes from transposons Tn903 (type I) and Tn5 (type II) detected in Gram-negative bacteria, from the Gram-positive Staphylococcus and Streptococcus (type III), from the butirosin-producing Bacillus circulans (type IV) and from a neomycin-producing Streptomyces fradiae (type V) indicate that they have diverged from a common ancestor. These structural data support the hypothesis that the antibiotic-producing strains were the source of certain resistance determinants. We have shown that kanamycin resistance in Campylobacter coli BM2509 was due to the synthesis of an APH(3')-III, an enzyme not detected previously in a Gram-negative bacterium. The genes encoding APH(3')-III in Streptococcus and Campylobacter are identical. These findings constitute evidence for a recent in-vivo transfer of DNA between Gram-positive and Gram-negative bacteria.19863027020
304350.9984The role of insertions, deletions, and substitutions in the evolution of R6 related plasmids encoding aminoglycoside transferase ANT-(2"). In 7% of gram-negative bacteria resistance to gentamicin is mainly mediated by plasmid-encoded aminoglycoside transferase ANT-(2"). The genome organization of 15 aadB plasmids (42-110 kb) was analyzed by restriction and hybridization techniques. They appeared to be IncFII-like replicons but were distinct from R6 by virtue of small substitutions in the transfer region. Aminoglycoside resistance genes aadB and aadA were located on Tn21 related elements. Only one of them was able to transpose its resistance genes mer sul aadA and aadB ( Tn4000 ), the other elements were naturally occurring defective transposons. In some of these structures deletions were identified at the termini, at sul, aadA , mer or transposition function--insertions adjacent to aadA or mer. The mode of these rearrangements and their site-specificity were considered with respect to the evolution of the Tn21 transposon family.19846328217
305460.9983Acquisition by a Campylobacter-like strain of aphA-1, a kanamycin resistance determinant from members of the family Enterobacteriaceae. A Campylobacter-like organism, BM2196, resistant to kanamycin and streptomycin-spectinomycin was isolated from the feces of a patient with acute enteritis. The kanamycin and streptomycin-spectinomycin resistances were not transferable to Camplylobacter sp. or to Escherichia coli, and no plasmid DNA was detected in this strain. The resistance genes were therefore tentatively assigned to a chromosomal locality. Analysis by the phosphocellulose paper-binding assay of extracts from BM2196 indicated that resistance to kanamycin and structurally related antibiotics was due to the synthesis of 3'-aminoglycoside phosphotransferase type I [APH(3')-I], an enzyme specific for gram-negative bacteria, and that resistance to streptomycin-spectinomycin was secondary to the presence of a 3",9-aminoglycoside adenylyltransferase. Homology between BM2196 and an APH(3')-I probe was detected by DNA-DNA hybridization. A 2.2-kilobase BM2196 DNA fragment conferring resistance to kanamycin was cloned in E. coli and was sequenced partially. The resistance gene appeared nearly identical to that of Tn903 from E. coli and was adjacent to IS15-delta, an insertion sequence widespread in gram-negative bacteria, thus indicating that Campylobacter species can act as a recipient for genes originating in members of the family Enterobacteriaceae.19872821885
584970.9983Characterisation and molecular cloning of the novel macrolide-streptogramin B resistance determinant from Staphylococcus epidermidis. A total of 110 staphylococcal isolates from human skin were found to express a novel type of erythromycin resistance. The bacteria were resistant to 14-membered ring macrolides (MIC 32-128 mg/l) but were sensitive to 16-membered ring macrolides and lincosamides. Resistance to type B streptogramins was inducible by erythromycin. A similar phenotype, designated MS resistance, was previously described in clinical isolates of coagulase-negative staphylococci from the USA. In the UK, MS resistance is widely distributed in coagulase-negative staphylococci but was not detected in 100 erythromycin resistant clinical isolates of Staphylococcus aureus. Tests for susceptibility to a further 16 antibiotics failed to reveal any other selectable marker associated with the MS phenotype. Plasmid pattern analysis of 48 MS isolates showed considerable variability between strains and no common locus for the resistance determinant. In one strain of S. epidermidis co-resistance to tetracycline, penicillin and erythromycin (MS) was associated with a 31.5 kb plasmid, pUL5050 which replicated and expressed all three resistances when transformed into S. aureus RN4220. The MS resistance determinant was localised to a 1.9 kb fragment which was cloned on to the high-copy-number vector, pSK265. A constitutive mutant of S. aureus RN4220 containing the 1.9 kb fragment remained sensitive to clindamycin. This observation, together with the concentration-dependent induction (optimum 5 mg/l of erythromycin) of virginiamycin S resistance suggests that the MS phenotype is not due to altered expression of MLS resistance determinants (erm genes) but probably occurs via a different mechanism.19892559912
541180.9983Detection of the aminoglycosidestreptothricin resistance gene cluster ant(6)-sat4-aph(3 ')-III in commensal viridans group streptococci. High-level aminoglycoside resistance was assessed in 190 commensal erythromycin-resistant alpha-hemolytic streptococcal strains. Of these, seven were also aminoglycoside-resistant: one Streptococcus mitis strain was resistant to high levels of kanamycin and carried the aph(3 ')-III gene, four S. mitis strains were resistant to high levels of streptomycin and lacked aminoglycoside-modifying enzymes, and two S. oralis strains that were resistant to high levels of kanamycin and streptomycin harbored both the aph(3 ')-III and the ant(6) genes. The two S. oralis strains also carried the ant(6)-sat4- aph(3 ' ')-III aminoglycoside-streptothricin resistance gene cluster, but it was not contained in a Tn5405-like structure. The presence of this resistance gene cluster in commensal streptococci suggests an exchange of resistance genes between these bacteria and enterococci or staphylococci.200717407061
584890.9983Plasmid and chromosomal basis of tolerance to cadmium and resistance to antibiotics in normal bovine duodenal bacterial flora. Cadmium (Cd) tolerance and antibiotic resistance was studied in duodenal flora of 20 normal bovine samples. Twelve bacterial isolates (5 Staphylococcus spp, 4 Enterococcus faecalis, 2 Bacillus spp, and a Pseudomonas sp) were grown in Luria broth containing 0.05 to 0.8 mM of cadmium chloride (CdCl). All isolates displayed multiple antibiotic resistance, with 2 Enterococcus strains and Pseudomonas pickettii demonstrating resistance to 12/17 antibiotics tested. With the exception of Staphylococcus sp, all contained plasmid DNA. Curing to remove plasmid DNA determined if Cd tolerance and/or antibiotic resistance was plasmid or chromosomally mediated. None of the bacteria became sensitive to CdCl after curing, suggesting that tolerance was not plasmid-mediated. Six bacteria became sensitive to antibiotics after curing indicating that antibiotic2 resistance was plasmid mediated. Two of these bacteria became sensitive to multiple antibiotics; a Staphylococcus sp became sensitive to ampicillin, ceftiofur and cephalothin, and a Enterococcus strain became sensitive to neomycin, oxacillin, and tiamulin. All of the isolates were probed for the presence of known Cd-resistance genes (cadA, cadC, and cadD). DNA-DNA hybridization revealed cadA- and cadC-related sequences in chromosomal DNA of a Staphylococcus sp, an Enterococcus strain, and in plasmid DNA of another Staphylococcus sp. No cadD-related sequences were detected in any of the 12 isolates even under reduced stringency of hybridization.200111383651
3044100.9983RSF1010 and a conjugative plasmid contain sulII, one of two known genes for plasmid-borne sulfonamide resistance dihydropteroate synthase. The nucleotide sequence of the type II sulfonamide resistance dihydropteroate synthase (sulII) gene was determined. The molecular weight determined by maxicells was 30,000, and the predicted molecular weight for the polypeptide was 28,469. Comparison with the sulI gene encoded by Tn21 showed 57% DNA similarity. The sulII-encoded polypeptide has 138 of 271 amino acids in common with the polypeptide encoded by sulI. The sulII gene is located on various IncQ (broad-host-range) plasmids and other small nonconjugative resistance plasmids. Detailed restriction maps were constructed to compare the different plasmids in which sulII is found. The large conjugative plasmid pGS05 and the IncQ plasmid RSF1010 contained identical nucleotide sequences for the sulII gene. This type of sulfonamide resistance is very frequently found among gram-negative bacteria because of its efficient spread to various plasmids.19883075438
5965110.9983Virulence and the presence of aminoglycoside resistance genes of Staphylococcus haemolyticus strains isolated from clinical specimens. We examined thirty methicillin-resistant Staphylococcus haemolyticus isolates cultured from clinical specimens for antibiotic resistance, various important interactions of the bacteria with epithelial cells and putative virulence determinants. All strains were resistant to oxacillin and carried the mecA gene. Aminocyclitol-3'-phosphotransferase (aph(3')-IIIa) gene encoding nucleotidyltransferases was detected in 43 %, aminocyclitol-6'-acetyltransferase-aminocyclitol-2″-phosphotransferase (aac(6')/aph(2″)) gene encoding bifunctional acetyltransferases/phosphotransferases in 33 %, aminocyclitol-4'-adenylyltransferase (ant(4')-Ia) gene encoding phosphotransferases in 20 %. The coexistence of resistance to methicillin and aminoglycosides was investigated in multi-resistant strains. Coexisting (aac(6')/aph(2″)) and (aph(3')-IIIa) genes were detected in 33 % of isolates, whereas 63 % of isolates had at least one of these genes. All strains revealed adherence ability and most of them (63 %) were invasive to epithelial cells. Electron microscopy revealed that the bacteria were found in vacuoles inside the cells. We observed that the contact of the bacteria with host epithelial cells is a prerequisite to their cytotoxicity at 5 h-incubation. Culture supernatant of the strains induced a low effect of cytotoxicity at the same time of incubation. Cell-free supernatant of all isolates expressed cytotoxic activity which caused destruction of HEp-2 cells at 24 h. None of the strains was cytotonic towards CHO cells. Among thirty strains, 27 % revealed lipolytic activity, 43 % produced lecithinase and 20 % were positive for proteinase activity. Analyses of cellular morphology and DNA fragmentation exhibited typical characteristic features of those undergoing apoptosis. The Pearson linear test revealed positive correlations between the apoptotic index at 24 h and percentage of cytotoxicity. Our results provided new insights into the mechanisms contributing to the development of S. haemolyticus-associated infections. The bacteria adhered and invaded to non-professional phagocytes. The invasion of epithelial cells by S. haemolyticus could be similar to phagocytosis that requires polymerization of the actin cytoskeleton. The process is inhibited by cytochalasin D. Moreover, they survived within the cells by residing in membrane bound compartments and induced apoptotic cell death.201525586730
5225120.9983Two genes involved in clindamycin resistance of Bacillus licheniformis and Bacillus paralicheniformis identified by comparative genomic analysis. We evaluated the minimum inhibitory concentrations of clindamycin and erythromycin toward 98 Bacillus licheniformis strains isolated from several types of fermented soybean foods manufactured in several districts of Korea. First, based on recent taxonomic standards for bacteria, the 98 strains were separated into 74 B. licheniformis strains and 24 B. paralicheniformis strains. Both species exhibited profiles of erythromycin resistance as an acquired characteristic. B. licheniformis strains exhibited acquired clindamycin resistance, while B. paralicheniformis strains showed unimodal clindamycin resistance, indicating an intrinsic characteristic. Comparative genomic analysis of five strains showing three different patterns of clindamycin and erythromycin resistance identified 23S rRNA (adenine 2058-N6)-dimethyltransferase gene ermC and spermidine acetyltransferase gene speG as candidates potentially involved in clindamycin resistance. Functional analysis of these genes using B. subtilis as a host showed that ermC contributes to cross-resistance to clindamycin and erythromycin, and speG confers resistance to clindamycin. ermC is located in the chromosomes of strains showing clindamycin and erythromycin resistance and no transposable element was identified in its flanking regions. The acquisition of ermC might be attributable to a homologous recombination. speG was identified in not only the five genome-analyzed strains but also eight strains randomly selected from the 98 test strains, and deletions in the structural gene or putative promoter region caused clindamycin sensitivity, which supports the finding that the clindamycin resistance of Bacillus species is an intrinsic property.202032271828
418130.9983Plasmid-mediated mechanisms of resistance to aminoglycoside-aminocyclitol antibiotics and to chloramphenicol in group D streptococci. Genes conferring resistance to aminoglycoside-aminocyclitol antibiotics in three group D streptococcal strains, Streptococcus faecalis JH1 and JH6 and S. faecium JH7, and to chloramphenicol in JH6 are carried by plasmids that can transfer to other S. faecalis cells. The aminoglycoside resistance is mediated by constitutively synthesized phosphotransferase enzymes that have substrate profiles very similar to those of aminoglycoside phosphotransferases found in gram-negative bacteria. Phosphorylation probably occurs at the aminoglycoside 3'-hydroxyl group. Plasmid-borne streptomycin resistance is due to production of the enzyme streptomycin adenylyltransferase, which, as in staphylococci and in contrast to that detected in gram-negative bacteria, is less effective against spectinomycin as substrate. Resistance to chloramphenicol is by enzymatic acetylation. The chloramphenicol acetyltransferase is inducible and bears a close resemblance to the type D chloramphenicol acetyltransferase variant from staphylococci.197896732
433140.9983Expression of the strA-strB streptomycin resistance genes in Pseudomonas syringae and Xanthomonas campestris and characterization of IS6100 in X. campestris. Expression of the strA-strB streptomycin resistance (SMr) genes was examined in Pseudomonas syringae pv. syringae and Xanthomonas campestris pv. vesicatoria. The strA-strB genes in P. syringae and X. campestris were encoded on elements closely related to Tn5393 from Erwinia amylovora and designated Tn5393a and Tn5393b, respectively. The putative recombination site (res) and resolvase-repressor (tnpR) genes of Tn5393 from E. amylovora, P syringae, and X. campestris were identical; however, IS6100 mapped within tnpR in X. campestris, and IS1133 was previously located downstream of tnpR in E. amylovora (C.-S Chiou and A. L. Jones, J. Bacteriol. 175:732-740, 1993). Transcriptional fusions (strA-strB::uidA) indicated that a strong promoter sequence was located within res in Tn5393a. Expression from this promoter sequence was reduced when the tnpR gene was present in cis position relative to the promoter. In X. campestris pv. vesicatoria, analysis of promoter activity with transcriptional fusions indicated that IS6100 increased the expression of strA-strB. Analysis of codon usage patterns and percent G+C in the third codon position indicated that IS6100 could have originated in a gram-negative bacterium. The data obtained in the present study help explain differences observed in the levels of SMr expressed by three genera which share common genes for resistance. Furthermore, the widespread dissemination of Tn5393 and derivatives in phytopathogenic prokaryotes confirms the importance of these bacteria as reservoirs of antibiotic resistance in the environment.19957487022
1759150.9983Macrolides mediate transcriptional activation of the msr(E)-mph(E) operon through histone-like nucleoid-structuring protein (HNS) and cAMP receptor protein (CRP). OBJECTIVES: The msr(E)-mph(E) operon exists widely in diverse species of bacteria and msr(E) and mph(E) genes confer high resistance to macrolides. We aimed to explore whether macrolides regulate the transcription of the operon. METHODS: Antibiotic resistance genes in clinical isolates of Klebsiella pneumoniae were analysed by WGS. The transcription of the msr(E)-mph(E) operon was investigated by quantitative PCR. Construction of enhanced green fluorescent protein (eGFP) reporter plasmids, gene knockout and complementation experiments were used to further explore the induction mechanism of macrolides for the operon. Sequence analysis was finally used to investigate whether the operon exists widely in diverse species of bacteria. RESULTS: We originally found that the treatment of a pandrug-resistant isolate of K. pneumoniae (KP1517) with macrolides obviously up-regulated the msr(E)-mph(E) operon, which was further confirmed in another nine clinical isolates of K. pneumoniae. The induction mechanism of macrolides for the operon was partly elucidated. Macrolides could activate the operon promoter, and the J10/J35 regions (J10: 5'-AGTTATCAT-3'; J35: 5'-TTGTCT-3') of the promoter were determined. Histone-like nucleoid-structuring protein (HNS) and cAMP receptor protein (CRP) were involved in the erythromycin-mediated activation of the operon promoter. The 476 strains of bacteria carrying the msr(E)-mph(E) operon currently in the NCBI database are mainly Acinetobacter baumannii (158; 33%), K. pneumoniae (95; 20%), Escherichia coli (26; 5%) and Proteus mirabilis (25; 5%). They were mainly isolated from human clinical samples (287; 60%) and had a wide geographical distribution. CONCLUSIONS: Macrolides could activate transcription of the msr(E)-mph(E) operon through HNS and CRP in K. pneumoniae and E. coli, and this might occur in diverse species of bacteria.202234747464
3572160.9983Comparative analysis of sequences flanking tet(W) resistance genes in multiple species of gut bacteria. tet(W) is one of the most abundant tetracycline resistance genes found in bacteria from the mammalian gut and was first identified in the rumen anaerobe Butyrivibrio fibrisolvens 1.230, where it is highly mobile and its transfer is associated with the transposable chromosomal element TnB1230. In order to compare the genetic basis for tet(W) carriage in different bacteria, we studied sequences flanking tet(W) in representatives of seven bacterial genera originating in diverse gut environments. The sequences 657 bp upstream and 43 bp downstream of tet(W) were 96 to 100% similar in all strains examined. A common open reading frame (ORF) was identified downstream of tet(W) in five different bacteria, while another conserved ORF that flanked tet(W) in B. fibrisolvens 1.230 was also present upstream of tet(W) in a human colonic Roseburia isolate and in another rumen B. fibrisolvens isolate. In one species, Bifidobacterium longum (strain F8), a novel transposase was located within the conserved 657-bp region upstream of tet(W) and was flanked by imperfect direct repeats. Additional direct repeats 6 bp long were identified on each end of a chromosomal ORF interrupted by the insertion of the putative transposase and the tet(W) gene. This tet(W) gene was transferable at low frequencies between Bifidobacterium strains. A putative minielement carrying a copy of tet(W) was identified in B. fibrisolvens transconjugants that had acquired the tet(W) gene on TnB1230. Several different mechanisms, including mechanisms involving plasmids and conjugative transposons, appear to be involved in the horizontal transfer of tet(W) genes, but small core regions that may function as minielements are conserved.200616870752
5950170.9982Epidemiological study of sulfonamide and trimethoprim resistance genes in Enterobacteriaceae. Sulfonamide (Su) and trimethoprim (Tp) resistance are known to caused by the production of drug resistant dihydropteroate synthase (DHPS) and dihydrofolate reductase (DHFR), respectively. Sulfonamide and trimethoprim are often used in combination under the name cotrimoxazole. Cotrimoxazole resistance in various enteric bacteria isolated at Ramathibodi Hospital was studied. The rate of resistance from 1984-1989 of many genera was rather constant at 40%-60% except in Shigella spp in which the rate increased rapidly in 1987 till 1989. Seventy-five percent of Su-Tp resistant (Sur-Tpr) bacteria were also found to be resistant to other drugs such as ampicillin, aminoglycosides, tetracycline and chloramphenicol in addition to cotrimoxazole. Two hundred and forty Su-Tp resistant strains were analysed for the presence of type I and II dihydropteroate synthase as well as type I and V dihydrofolate reductase genes by hybridization with the corresponding gene probes. Type I DHPS gene predominated in Su-Tp resistant bacteria at 60.8% whereas type II DHPS was found in only 25%. Some strains (11.7%) had both genotypes but 2.5% did not have any. In the trimethoprim resistance study, the DHFR type I gene was also found more frequently (30%) whereas type V DHFR was only 19%. The remaining of Tp resistance (51%) was unclassified. The coexistence of Su and Tp resistance genes of each type was investigated among 118 Su and Tp resistant strains. It was found that type I DHPS gene was found together with either type I or V DHFR gene and type II DHPS was found with type I DHFR gene at about the same rate (28.9%, 27.1% and 26.3%, respectively). However, the presence of type II DHPS together with type V DHFR was rather low, only 5.9% of isolates were found to have both types of genes.19902237584
5846180.9982Distribution of tetracycline resistance genes and transposons among phylloplane bacteria in Michigan apple orchards. The extent and nature of tetracycline resistance in bacterial populations of two apple orchards with no or a limited history of oxytetracycline usage were assessed. Tetracycline-resistant (Tc(r)) bacteria were mostly gram negative and represented from 0 to 47% of the total bacterial population on blossoms and leaves (versus 26 to 84% for streptomycin-resistant bacteria). A total of 87 isolates were screened for the presence of specific Tc(r) determinants. Tc(r) was determined to be due to the presence of Tet B in Pantoea agglomerans and other members of the family Enterobacteriacae and Tet A, Tet C, or Tet G in most Pseudomonas isolates. The cause of Tc(r) was not identified in 16% of the isolates studied. The Tc(r) genes were almost always found on large plasmids which also carried the streptomycin resistance transposon Tn5393. Transposable elements with Tc(r) determinants were detected by entrapment following introduction into Escherichia coli. Tet B was found within Tn10. Two of eighteen Tet B-containing isolates had an insertion sequence within Tn10; one had IS911 located within IS10-R and one had Tn1000 located upstream of Tet B. Tet A was found within a novel variant of Tn1721, named Tn1720, which lacks the left-end orfI of Tn1721. Tet C was located within a 19-kb transposon, Tn1404, with transposition genes similar to those of Tn501, streptomycin (aadA2) and sulfonamide (sulI) resistance genes within an integron, Tet C flanked by direct repeats of IS26, and four open reading frames, one of which may encode a sulfate permease. Two variants of Tet G with 92% sequence identity were detected.199910543801
5851190.9982Arsenic resistance determinants from environmental bacteria. Arsenic resistance determinants from 42 environmental bacterial isolates (32 Gram negative) were analyzed by DNA: DNA hybridization using probes derived from Escherichia coli and Staphylococcus plasmid or chromosomal arsenic resistance (ars) genes. In colony hybridization assays, 11 and 1 Gram negative strains hybridized with the E. coli chromosome and plasmid probes, respectively. No hybridization was detected using a probe containing only the arsA (ATPase) gene from E. coli plasmid or with a Staphylococcus plasmid ars probe. From Southern hybridization tests of some of the positive strains it was concluded that homology to ars chromosomal genes occurred within chromosome regions, except in an E. coli isolate where hybridization occurred in both the chromosome and a 130-kb plasmid. Our results show that DNA sequences homologous to E. coli ars chromosomal genes are commonly present in the chromosomes of environmental arsenic-resistant Gram negative isolates.199810932734