Management of Polydrug-Resistant Tuberculosis.

Background and Objectives: There is a lack of information regarding the effective duration of treatment necessary to prevent the development of acquired resistance when fluoroquinolones (FQ), and/or pyrazinamide (Z) resistance has occurred in patients with polydrug-resistant tuberculosis and isoniazid resistance. The management of these kinds of patients should be carried out in experienced centers according to drug susceptibility test results, clinical status of the patient and the extensity of the disease. Materials and Methods: We evaluated treatment regimens, treatment outcomes, and drug adverse effects in seven patients with polydrug-resistant tuberculosis, including those with Z and/or FQ resistance in a retrospective analysis Results: Regarding the patients with polydrug-resistant tuberculosis in addition to isoniazid (H) resistance, three had Z, two had FQ, and the remaining two had both Z and FQ resistance. In the intensive phase of the treatment, the patients were given at least four drugs according to drug susceptibility tests, and at least three drugs in the continuation phase. The duration of treatment was 9-12 months. Two of the patients were foreign nationals, and could not be followed up with due to returning to their home countries. Regarding the remaining five patients, three of them were terminated as they completed treatment, and two as cured. No recurrence was observed in the first year of the treatment. The most common, and serious drug side effect was seen for amikacin. Conclusions: In patients with polydrug-resistant TB, if Z and/or FQ resistance is detected in addition to H resistance, the treatment of these patients should be conducted on a case-by-case basis, taking into account the patient's resistance pattern, clinical condition, and disease prognosis. Close monitoring of the side effects will increase the success rate of the treatment.

A 34-Year-Old male admitted with pulmonary tuberculosis complicated by hydropneumothorax and mediastinal emphysema.

Spontaneous hydropneumothorax (HP) and mediastinal emphysema (ME) are infrequently presented complications of pulmonary tuberculosis (TB). A-34-year-old Pakistani male presented with dyspnea, productive cough, and right-sided pleuritic chest pain. He had no history of any surgery, TB, comorbid disease, or other serious pulmonary diseases. Chest radiography revealed a right-sided HP and parenchymal infiltration. The laboratory results of pleural effusion showed elevated adenosine deaminase levels with the empyema features. Acid-fast bacilli were detected and Mycobacterium tuberculosis without any drug resistance grew in the culture both in the sputum and pleural fluid. A chest tube was inserted immediately. A prolonged airway leak was detected. Hepatotoxicity protocol has been initialized (due to increased hepatic enzymes in the initial presentation) and followed without observing any complications associated with the treatment. On the 25th day of the standard TB treatment protocol, we observed hepatic enzymes in the normal range. Around 40-days of a hospitalization period, he started developing fever and methicillin-resistant Staphylococcus aureus was detected in the pleural fluid culture. We introduced linezolid to the treatment regimen in addition to the antituberculosis protocol. Although spontaneous ME is a benign disease, it might be life-threatening and difficult to manage when complicated with HP and active TB infection. Active TB should be considered a differential diagnosis once ME or HP was detected, and treatment should be started immediately for both diseases.