Klebsiella pneumoniae, an encapsulated gram-negative bacterium, is known to cause infections at multiple sites including the lungs, urinary system, bloodstream, brain, wounds, and surgical sites [2,5]. K. pneumonia infections are prone to develop in patients with underlying disorders commonly found in paediatric and elderly age groups, as well as immunocompromised individuals in hospital settings [2,6]. Multiple studies have reported a 9% to 28% proportion of coinfection of K. pneumonia with pulmonary TB [2,7,8].

To our knowledge, there are no reported cases with a concomitant association of miliary TB and K. pneumonia featuring multiple drug resistance. In our case report, the therapeutic challenge arose from the antimicrobial resistance posed by the underlying K. pneumonia infection during the administration of standard anti-tubercular management.

A 47-year-old nonsmoking male from a low socioeconomic background presented to our outpatient department with an evening rise in fever for 11 days and a cough producing purulent, red-colored sputum for 10 days. He also reported a grade three Modified Medical Research Council dyspnea that persisted for 2 weeks, not alleviated by rest. This dyspnea was not accompanied by orthopnea or paroxysmal nocturnal dyspnea. Upon examination, his blood pressure was 120/70 mm Hg, heart rate 88 beats per minute, oxygen saturation 88% on room air, and body temperature 38°C. Chest X-ray revealed an obscured left costophrenic angle (Figure 1A), homogeneous opacities in the left lower zone and non-homogeneous opacities in the left middle zone. High-resolution computed tomography (Figure 1B) of the thorax showed multiple small, uniform centrilobular and perilymphatic nodular opacities ranging from 1 to 3 mm across the bilateral lung parenchyma, indicative of miliary mottling. These nodules were merging to form small consolidatory patches and ground glass opacities. Multiple peribronchial ground glass opacities and tiny subpleural nodules were noted diffusely involving the bilateral lung parenchyma. Few linear atelectatic bands involved the posterior basal segments of the right lower lobe. Several centimeters of enlarged necrotic paratracheal, left axillary, left pectoral, lower cervical, bilateral hilar, and subcarinal lymph nodes were observed, the largest measuring 5.0×3.0 cm in the left axillary region, with some showing calcification. These findings suggest an extensive active infective etiology consistent with Koch’s disease.

Sputum analysis using the Cartridge Based Nucleic Acid Amplification Test revealed resistance to rifampicin in MTB. A second-line line probe assay identified resistance to isoniazid. The patient began treatment with a multidrug-resistant (MDR) TB regimen. His oxygen saturation fell to 85% on the 9th day after starting the MDR regimen. Intravenous steroids were administered to improve his oxygenation. On the 11th day, persistent fever following the initiation of anti-tubercular drugs raised concerns about an underlying coexisting disease. Bronchoscopy and bronchoalveolar lavage identified K. pneumonia resistant to third-generation cephalosporins, imipenem, and carbapenem, but sensitive to piperacillin. A fixed-dose combination of piperacillin and tazobactam was added to manage pneumonia alongside the ongoing MDR-TB regimen. By day 18, his symptoms began to subside, and his oxygen saturation improved. He was discharged on day 20, stable and advised to continue the MDR-TB regimen. No relapse of symptoms was observed during an 8-month follow-up.

Klebsiella spp. are widespread opportunistic pathogens found in soil and water, colonizing medical equipment and hospital settings [2]. Resistance to carbapenem in carbapenemase-producing K. pneumoniae has emerged internationally as one of the most therapeutically challenging pathogens due to its broad distribution in healthcare facilities and the limited number of effective treatment options, resulting in increased mortality [2,9]. In our case, it was evident that the organism was resistant not only to carbapenem but also to multiple other drugs. The therapeutic challenge in our case stemmed from the coinfection with highly resistant microbes, which was addressed by obtaining accurate culture sensitivity reports. Widespread misuse of antimicrobials remains the primary cause of the development of bacterial strains with multiple drug resistance. These resistant microbes pose a significant threat and challenge to the implementation of standard therapeutic interventions. Miliary TB often leads to pulmonary abnormalities such as diffusion impairment and mild reduction in flow rates [3]. This was also observed in our case when the initiation of anti-tubercular therapy did not improve the oxygen saturation; however, the underlying K. pneumoniae infection also contributed to complicating the patient’s condition. The role of corticosteroids in miliary TB remains contentious [3]. However, in our report, the administration of systemic steroids was found to improve the vital and symptomatic status of our patient.

The concomitant association of TB and K. pneumoniae is likely to occur, and the challenge intensifies when extensive microbial resistance develops. Therapeutic failure is probable, even with standard management, due to underlying coinfection. Guidance based on culture-sensitive reports and the use of corticosteroids under antibiotic cover proves beneficial in such cases.