Abstract

BackgroundDrug resistance in tuberculosis is a major public health challenge in developing countries. The limited data available on drug resistance in extra pulmonary tuberculosis stimulated us to design our study on anti-tuberculosis drug resistance pattern in cases of extra pulmonary tuberculosis in a tertiary referral hospital of North India. We performed Geno Type MTBDRplus assay in comparison with conventional drug susceptibility testing by proportion method to study the mutation patterns in rpoB, katG and inhA genes.MethodsA total of 510 extra pulmonary samples were included in this study. After the smear microscopy, all the specimens were subjected for culture on Lowenstein Jensen (LJ) media. Phenotypic drug susceptibility testing (DST) was performed on LJ media for all the MTB isolates and compared with the results of Geno Type MTBDRplus assay which was performed with the DNA isolated from the culture by conventional method.ResultsOf 510 specimens cultured, the total culture positivity obtained was 11.8% (60) encompassing 54 (10.6%) Mycobacterium tuberculosis and 6 (1.2%) non-tubercular mycobacteria (NTM). DST results by Geno Type MTBDRplus assay and solid culture methods were compared in 51 MTB isolates excluding the two Rif indeterminate and one invalid test. Geno Type MTBDRplus accurately identified 13 of 14 rifampicin-resistant strains, 14 of 15 isoniazid-resistant strains and 13 of 14 as multi drug resistant tuberculosis (MDR-TB) in comparison with conventional method. Sensitivity and specificity were 92.86% and 97.30% respectively for detection of RIF resistance, 93.33% and 94.44% respectively for detection of INH resistance, 92.86% and 97.30% respectively for detection of MDR-TB, while the overall concordance of Geno Type MTBDRplus assay with conventional DST was 94.11%. The turn-around time for performing Geno Type MTBDRplus assay test was 48 hours.ConclusionThe problem of MDR in extra pulmonary tuberculosis (EPTB) cannot be overlooked and due attention on patients should be given. Routine use of Geno Type MTBDRplus assay for the diagnosis of MDR-EPTB can substantially reduce the time between diagnosis and drug therapy. Culture along with Geno Type MTBDRplus assay could be a solution for rapid and accurate diagnosis of MDR-TB in low bacillary non sputum specimens.

Highlights

  • Tuberculosis (TB), a major cause of morbidity and mortality, is the greatest killer worldwide alongside HIV due to a single infectious agent [1]

  • drug susceptibility testing (DST) results by Geno Type MTBDRplus assay and solid culture methods were compared in 51 MTB isolates excluding the two Rif indeterminate and one invalid test

  • Sensitivity and specificity were 92.86% and 97.30% respectively for detection of RIF resistance, 93.33% and 94.44% respectively for detection of INH resistance, 92.86% and 97.30% respectively for detection of multi drug resistant tuberculosis (MDR-TB), while the overall concordance of Geno Type MTBDRplus assay with conventional DST was 94.11%

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Summary

Introduction

Tuberculosis (TB), a major cause of morbidity and mortality, is the greatest killer worldwide alongside HIV due to a single infectious agent [1]. Though Pulmonary TB is the most common presentation of the disease, extra pulmonary TB (EPTB) is emerging as a serious clinical problem, accounting for 15– 20 per cent of all the cases of tuberculosis and the percentage is much higher in HIV-positive patients, where it accounts for more than 50 per cent of all cases [2]. Drug resistance in tuberculosis is the major public health challenge globally. Though drug resistance in EPTB is not as common as in pulmonary tuberculosis yet the transmission of resistant strains is increasing the burden of multi drug resistant tuberculosis (MDR TB) even in extra pulmonary tuberculosis (EPTB). Drug resistance in tuberculosis is a major public health challenge in developing countries. We performed Geno Type MTBDRplus assay in comparison with conventional drug susceptibility testing by proportion method to study the mutation patterns in rpoB, katG and inhA genes

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