His wife, a 36-year-old Vietnamese woman without underlying co-morbidities, underwent TB contact investigation. She reported no respiratory or constitutional symptoms. Physical examination revealed no abnormality, and previous medical history was unremarkable. The IGRA test was positive, and chest radiography was normal (Figure 2A), thus she was diagnosed with LTBI. She was prescribed nine months' isoniazid monotherapy 300mg once daily, directly observed by trained public health personnel. On the fourth month of treatment, she reported numbness and pain in her fingertips, which improved with vitamin B6 supplementation.
A progressive cough developed in the ninth month of treatment. She reported no fever, chills, hemoptysis, or night sweating. Chest auscultation was unremarkable, with a smooth breathing pattern and no lymphadenopathy. Physical examination was otherwise normal. Laboratory data on haemoglobin, blood count, liver and kidney function and laboratory tests were within normal results. Chest radiography revealed an opacity in the left upper lung (Figure 2B). Three consecutive sputum smear examinations were negative for AFB. The sputum GeneXpert test (Cepheid, California, United States) was positive for rifampicin-resistant Mtb. The phenotypic drug susceptibility testing and GenoType MTBDRplus assay later confirmed resistance to isoniazid (katG deletion) and rifampicin (rpoB gene H526D mutation). Based on these findings, the patient was diagnosed as having active pulmonary TB with resistance to isoniazid and rifampicin. Further sequencing revealed susceptibility to fluoroquinolones, aminoglycosides, and pyrazinamide.
The wife was treated with an individualized anti-TB regimen comprising of moxifloxacin, kanamycin, prothionamide, ethambutol, and pyrazinamide, based on the results of the drug-susceptibility test. Following treatment, the sputum culture converted to negative after two weeks. Early on in the treatment course, she reported vertigo, blurred vision, pain on injection site, and gastrointestinal discomfort, thus ethambutol was later replaced with cycloserine. Following 20 months of anti-TB treatment, follow-up revealed no radiological or clinical evidence of recurrence up to a year later. Genotyping of the causative Mtb by the spacer oligonucleotide typing (spoligotyping) and Mycobacterial Interspersed Repetitive Units-Variable Number Tandem Repeats revealed that the Mtb strains from the two cases had identical genotypes.