Molecular study of antibiotic resistance Mycobacteriumtuberculosis isolated from clinical samples in Baghdad city
DOI:
https://doi.org/10.37506/ijfmt.v14i4.12717Keywords:
Antibiotic resistance; Mycobacteriumtuberculosis: clinical samplesAbstract
Background: Drug-resistant TB is the most important issue that threatens to interrupt the improvements
achieved in tuberculosis control. Multidrug-resistant (MDR) tuberculosis is defined as resistance to both
rifampicin and isoniazid.
Objectives: To find molecular feature via DNA extraction for genes in charge of drug resistance in pulmonary
tuberculosis patients with hyperglycemia and role of the Xpert MTB/RIF Ultra molecular test efficacy in
DR-TB cases detection.
Method: 106 pulmonary TB patient sputum and blood samples were collected in the Institute of Chest and
Respiratory diseases in Baghdad and Medical City Hospital from December 2018 - July 2019, 52 were drug
resistances TB patients. All patients were examined by conventional method such as direct examination
(AFB test), Gene-Xpert test, FBS and HbA1c test were carried out for all cases.
Results: GeneXpert/ultra results revealed 43 cases were Rif resistance in which it was highly significant.
The GeneXpert/ultra quantity was mostly medium in the bacillary load. The Rif’s resistance cases were
mostly registered in the age group (20-59) and in male population. The most frequent patient’s type was New
MDR. The GeneXpert/ultra quantity and HbA1c levels results showed that most elevated HbA1c cases had
a medium to high bacillary load. The DST results were significant in which 95.3% were Rif’s resistance and
62.8% were STR’s resistance. The LPA on 23 DR cases showed the following; 13 patients were MDR cases
in which a deletion in the band WT8 and mutation in the MUT3 band of the gene rpoB and deletion in the
inhA WT1 band of the inhA gene were the most notice.
Conclusions: Molecular method had showed that mutations in the rpoB gene especially 530 and S531L
codon are responsible for majority of RMP resistance in MTB while mutations at the -15/-16 InhA codon
and 315 of KatG codon responsible for most INH-resistance cases.
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