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)

Streptomycin resistance was detected in 17 of 20 multiply-resistant Staphylococcus aureus isolates from a hospital in a southeastern Nigerian town. The isolates were uniformly sensitive to methicillin, erythromycin, gentamicin, mupirocin, ciprofloxacin and vancomycin but produced beta-lactamase and were resistant to other antimicrobial agents and harbored different plasmids which ranged in size and number from 1.0 to c, 40 kb and one to six respectively. Curing and transfer experiments demonstrated that streptomycin resistance (Smr) was located on plasmids in 15 of the 17 isolates. 16 Smr plasmids were isolated and characterized. They belonged to three distinct groups based on size and resistance phenotypes. Eight 4.4 kb plasmids encoded Smr only, three 4.7 kb plasmids encoded resistance to streptomycin and chloramphenicol (SmCm) and five 23.8 kb plasmids encoded resistance to streptomycin, kanamycin, neomycin, cadmium and beta-lactamase production (CPKNS). Restriction endonuclease analysis demonstrated that the 4.4 kb Smr plasmids were similar to one another and indistinguishable from pUB109, an incompatibility group 5 Smr plasmid, suggesting that they may also belong to incompatibility group 5. The SmCm and the CPKNS plasmid groups also gave identical restriction patterns with single and double enzyme digests. Further transfer experiments with one of the SmCm plasmids led to the isolation of a 4.4 kb Smr plasmid which was indistinguishable from the other 4.4 kb plasmids, suggesting that the SmCm plasmids are natural recombinants between a streptomycin and chloramphenicol resistance plasmid. The results demonstrate a multiple origin of streptomycin resistance in the S. aureus population studied.
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PMID:Genetics of streptomycin resistance in methicillin-sensitive multiply-resistant Staphylococcus aureus. 762 50

Development of streptomycin resistance in Mycobacterium tuberculosis is usually associated with mutations in rpsL and rrs genes, although up to 50% of clinical streptomycin-resistant isolates may present no mutation in either of these genes. In the present report we investigate the role of gidB gene mutations in streptomycin resistance. We have analyzed 52 streptomycin-resistant and 30 streptomycin-susceptible Mycobacterium tuberculosis clinical isolates by sequencing and endonuclease analysis of the gidB and rpsL genes. All clinical isolates were genotyped by 12-loci MIRU-VNTR. The gidB gene of 18 streptomycin-resistant isolates was sequenced and four missense mutations were found: F12L (1/18), L16R (18/18), A80P (4/18) and S100F (18/18). The remaining isolates were screened by endonuclease analysis for mutations A80P in the gidB gene and K43R in the rpsL gene. Overall, mutation A80P in the gidB gene was found in eight streptomycin-resistant isolates and 11 streptomycin-susceptible multidrug-resistant isolates. Also noteworthy, is the fact that gidB mutations were only present in isolates without rpsL and rrs mutations, all from genetic cluster Q1. Streptomycin quantitative drug susceptibility testing showed that isolates carrying the gidB A80P mutation were streptomycin intermediate-level resistant and that standard drug susceptibility testing yielded inconsistent results, probably due to borderline resistance. We conclude that gidB mutations may explain the high number of streptomycin-resistant strains with no mutation in rpsL or rrs. These mutations might occasionally confer low-level streptomycin resistance that will go undetected in standard susceptibility testing.
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PMID:GidB mutation as a phylogenetic marker for Q1 cluster Mycobacterium tuberculosis isolates and intermediate-level streptomycin resistance determinant in Lisbon, Portugal. 2410 32