Antimicrobial agent resistance in mycobacteria: molecular genetic insights.

Musser, James M.

doi:10.1128/cmr.8.4.496-514.1995

Cited by 125 publications

(190 citation statements)

References 39 publications

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“…In this sense, the genetic diversity characterising the rpoB mutations does not limit the performance of the method, and it is likely that the GeneChip array is also efficient in detecting minor mutations not represented in the collection of clinical isolates tested. The mutation frequencies found in the present study for the two positions 526 and 531 were similar to those reported previously by other investigators, and confirm that most (88%) of the substitutions occur in codons 526 and 531, which are associated generally with a high level of Rif R [2,15,19]. A deletion of the asparagine residue found at position 519 was identified in a Rif S isolate yielding c. 0.1% of resistant colonies; Fig.…”

Section: Discussionsupporting

confidence: 91%

“…The genetic basis for Rif R in M. tuberculosis comprises mutations in the rpoB gene, which encodes the b-subunit of RNA polymerase [1,2]. The genetic changes leading to Rif R are now wellcharacterised.…”

mentioning

confidence: 99%

“…In > 95% of Rif R isolates, resistance is conferred by mutations within the 81-bp motif of the rpoB gene that corresponds to the 511-533 region of the RNA polymerase b-subunit [1,3,4]. Substitutions affecting amino-acid residues 526 and 531 represent 30% and 50%, respectively, of the rpoB mutations detected in clinical isolates [2]. Most other mutations involved in clinical resistance to rifampicin are scattered throughout positions 513-533, and include a large variety of amino-acid substitutions [5][6][7].…”

mentioning

confidence: 99%

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Use of a high-density DNA probe array for detecting mutations involved in rifampicin resistance in Mycobacterium tuberculosis

Sougakoff

Rodrigue

Truffot-Pernot

et al. 2004

Clinical Microbiology and Infection

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A Mycobacterium high-density DNA probe array designed to detect rpoB mutations conferring rifampicin resistance in Mycobacterium tuberculosis was evaluated. The rpoB hybridisation patterns produced by 41 susceptible (RifS) and 59 rifampicin-resistant (RifR) clinical isolates of M. tuberculosis were compared with the results of conventional dideoxynucleotide sequencing of the rpoB gene. For all the RifR isolates, the rpoB hybridisation patterns correlated with the rpoB sequencing results. Among the 59 isolates, 11 distinct amino-acid changes were detected by the DNA probe array. Of these, 36 (61%) corresponded to replacement of the serine residue found in position 531 (S531L in 34 isolates and S531W in two isolates), 16 (27%) affected histidine 526 (five H526D, five H526Y, four H526L, one H526N and one H526R), four (6.8%) replaced aspartate 516 with a valine, and one (1.7%) replaced glutamine 513 with a leucine. Deletion of the asparagine residue at position 519 was detected in one isolate susceptible to rifampicin, but yielding c. 0.1% resistant colonies on rifampicin-containing medium. No mutation was detected in the rpoB region from one isolate yielding c. 5% of resistant colonies on rifampicin-containing medium. Finally, a D516Y substitution was detected in association with an unexpected mutation, G523W, not tiled on the DNA probe array, but which could be detected by analysing the hybridisation pattern obtained with the wild-type probes covering codon 523. In conclusion, the Mycobacterium probe array is a promising approach to rapid detection of mutations involved in rifampicin resistance in M. tuberculosis.

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Section: Discussionsupporting

confidence: 91%

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confidence: 99%

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confidence: 99%

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Use of a high-density DNA probe array for detecting mutations involved in rifampicin resistance in Mycobacterium tuberculosis

Sougakoff

Rodrigue

Truffot-Pernot

et al. 2004

Clinical Microbiology and Infection

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“…Another topic of interest concerns the evolution of antibiotic resistance in the case of Mycobacterium tuberculosis (Mtb). The sole source of resistance to anti-TB drugs is by mutation of the target genes and no transferable antibiotic resistance plasmids have been found to encode resistance in Mtb: This pathogen seems to take care of antimicrobials quite nicely without participating in sex (Musser 1995).…”

Section: A Brief Historical Perspectivementioning

confidence: 99%

The Whys and Wherefores of Antibiotic Resistance

Strachan¹,

Davies

2016

Cold Spring Harb Perspect Med

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“…M. tuberculosis resistance to rifampicin is related to the mutations in a region of 81 base pairs of the gene rpoB which codes for the RNA polymerase sub-unit ␤ [39][40][41][42][43]. Isoniazid resistance is partly associated to a mutation of the gene katG which codes for a catalase-peroxidase and partly to a mutation of the regulator gene inhA [41,42].…”

Section: Tuberculosismentioning

confidence: 99%

DNA microarrays for the diagnosis of infectious diseases

Donatin

Drancourt

2012

Médecine et Maladies Infectieuses

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The diagnosis of bacterial infections relies on isolation of the bacterium, which is rarely achieved when needed for patient management. Furthermore, culture is poorly suited to the diagnosis of polymicrobial infections. Finally, a syndromic approach should target both bacteria and viruses causing the same syndrome. The detection of specific DNA sequences in clinical specimen, using DNA microarrays, is an alternative. Microarrays were first used as a diagnostic tool in 1993, to identify a hantavirus associated with an outbreak of acute respiratory diseases. The main advantage of microarrays is multiplexing, enabling exploration of the microbiota and pathogen detection in bacteremia, respiratory infections, and digestive infections: circumstance in which DNA arrays may lack sensitivity and provide false negatives. Enrichment of sampling can increase sensitivity. Furthermore, chips allow typing Streptococcus pneumoniae and detecting resistance in Staphylococcus aureus (MRSA) and Mycobacterium tuberculosis (rifampicin, isoniazid, fluoroquinolones). However, the cost and high technical requirements remain a problem for routine use of this bacterial infection diagnostic technology.

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Antimicrobial agent resistance in mycobacteria: molecular genetic insights.

Abstract: The knowledge acquired about drug resistance, then, will long remain of great practical value, and advances in the field will undoubtedly benefit the fight against tuberculosis considered on a worldwide scale.'' Georges Canetti J. Burns Amberson Lecture, 1965

Cited by 125 publications

References 39 publications

Use of a high-density DNA probe array for detecting mutations involved in rifampicin resistance in Mycobacterium tuberculosis

Use of a high-density DNA probe array for detecting mutations involved in rifampicin resistance in Mycobacterium tuberculosis

The Whys and Wherefores of Antibiotic Resistance

DNA microarrays for the diagnosis of infectious diseases

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