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Effect of tellurite on growth of extensively drug resistant (XDR) Mycobacterium tuberculosis and action on mycobacterial drug efflux pump

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DOI: 10.1016/j.jksus.2023.102629

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Tellurite; XDR-TB; mmpL7 gene; Drug efflux pump

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Genotypic resistance of bacterial strain to anti-tuberculosis drugs was determined using Line probe assay. The toxic effect of tellurite on Mycobacterium tuberculosis growth was observed at different concentrations through SEM and EDX analysis. RT-PCR was used to measure the impact on the efflux pump gene. XDR-TB strain showed sensitivity to tellurite, resulting in delayed growth and morphological changes. The exact mechanism of action needs further investigation.
In the present study genotypic resistance of bacterial strain to first- and second-line anti-tuberculosis drugs was determined by Line probe assay. Toxic effect of tellurite on the growth of Mycobacterium tuberculosis (MTB) was determined by growing cells in different concentrations of tellurite (1 to 5 mM). Morphological effects of tellurite and uptake of metal in bacterial cells were confirmed by Scanning electron microscope (SEM) and energy dispersive X-ray (EDX) analysis. Change in fold expression of the efflux pump gene was measured by RT-PCR. Mycobacterial strain was characterized as XDR-TB based on the genotypic resistance to rifampicin and isoniazid, along with resistance to fluoroquinolones and second line injectable. XDR-TB showed black colonies in tellurite presence and growth was delayed (2-3 weeks) when compared with the control. The reduced cell size, metal accumulation and the characteristic tellurite peaks appeared in metal-treated cells. MTB showed MIC value of 1 mM and had high susceptibility for higher concentrations (2-5 mM). However, no significant metal inhibitory effect on the mmpL7 efflux system was determined. Tellurite shows significant growth reduction potential against XDR-TB strain. However, the exact mechanism of action needs to be elucidated with further research. & COPY; 2023 The Author(s). Published by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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