Korean J Lab Med.  2009 Oct;29(5):455-460. 10.3343/kjlm.2009.29.5.455.

Detection of Isoniazid and Rifampicin Resistance by Sequencing of katG, inhA, and rpoB Genes in Korea

• Cho EH
• Bae HK
• Kang SK
• Lee EH

• KMID: 1077422
• DOI: http://doi.org/10.3343/kjlm.2009.29.5.455

Abstract

BACKGROUND
In Korea, tuberculosis is resistant to isoniazid (INH) and/or rifampicin (RIF) in more than 10% of cases. To prevent the spread of resistant Mycobacterium tuberculosis strains, it is crucial to develop more rapid resistance detection methods.
METHODS
To determine the feasibility of using direct sequencing for detecting INH- and RIF-resistant strains, the katG gene, the regulatory region of the inhA gene, and the 81-bp hot-spot region of the rpoB gene from 95 culture isolates and 46 respiratory specimens were sequenced. Total 141 culture isolates were classified by conventional drug susceptibility testing (DST) as INH(R)/RIF(R) (N=30), INH(R)/RIF(S) (N=23), INH(S)/RIF(R) (N=15), and INH(S)/RIF(S) (N=73).
RESULTS
Compared with phenotypic DST, the overall sensitivity and specificity of sequencing were 83.0% (44/53) and 96.6% (85/88), respectively, for INH resistance, and 93.3% (42/45) and 100% (96/96), respectively, for RIF resistance. The rates were similar between culture isolates and respiratory specimens. Interestingly, three specimens with inhA -15C>T mutation were susceptible to INH by conventional DST.
CONCLUSIONS
Detection of mutations in the katG codon 315, the inhA regulatory region, and the hot-spot region of rpoB would be useful for rapid detection of INH and RIF resistance in Korea.

Keyword

Mycobacterium tuberculosis; inhA; katG; rpoB

MeSH Terms

Antitubercular Agents/*pharmacology
Bacterial Proteins/*genetics
Catalase/*genetics
Drug Resistance, Multiple, Bacterial
Genotype
Humans
Isoniazid/*pharmacology
Mutation
Mycobacterium tuberculosis/*genetics/isolation & purification
Oxidoreductases/*genetics
Republic of Korea
Rifampin/*pharmacology
Sensitivity and Specificity
Sequence Analysis, DNA/*methods

Figure

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  Fig. 1. A mixed pattern of the inhA-15C and T mutation.

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