A 40-year-old male presented to the outpatient clinic of the tertiary care hospital with complaints of cough, expectoration, hemoptysis, and fever off and on particularly in the evenings. He had been treated for pulmonary tuberculosis previously in the year 2009 and subsequently in the year 2012 following its remission. He was on oral and inhalational steroids for several years for wheeze-like symptoms. He had sought consultation and had been admitted in other hospitals several times for similar complaints. The patient did not have any other comorbid conditions. He was a welder by occupation and so exposure to fumes and fine metallic dust particles was noted as a significant factor in the clinical history. Physical examination of the respiratory system revealed bilateral coarse crepitations. Examination of other systems did not reveal any contributory findings. Chest radiograph and routine blood workup were undertaken. Chest X-ray revealed bilateral midzone and lower zone consolidation (Figure 1). With a diagnosis of bilateral bronchiectasis, he was admitted to the hospital for further evaluation and to investigate the status of pulmonary tuberculosis in the light of hemoptysis.
The patient was initially started on intravenous piperacillin/tazobactam for empiric treatment of community-acquired secondary pulmonary infection. Despite the antibiotic, the patient had sustained decrease in oxygen saturation leading to deterioration in pulmonary function over the next few days. With impending respiratory failure, he was shifted to the Intensive Care Unit (ICU). The antibiotic was escalated to meropenem due to his deteriorating clinical condition. Blood and urine cultures were sterile, and 20% acid-fast staining of sputum and respiratory secretion was also negative. Sputum was sent for bacterial culture. The culture plates initially had scanty growth of normal flora, but on Gram stain there were few branching Gram-positive bacilli observed which was suggestive of Nocardia (Figure 2). In view of this, modified acid-fast staining with 1% acid was performed on the smear, and it revealed plenty of weakly acid-fast branching slender and filamentous bacilli characteristic of Nocardia (Figure 3). The culture media on further incubation of 72 hours yielded dry chalky white colonies (Figure 4). Gram's stain and acid-fast stain of these colonies confirmed them as Nocardia. For species identification, 16S rRNA gene sequencing was undertaken. BLAST search of the sequence was done using the taxonomy browser of the National Center for Biotechnology Information (NCBI). The 662 bp of the sequence revealed a 100% match with Nocardia cyriacigeorgica. The sequence has been submitted to GenBank with accession number MK641487.
 Nocardia cyriacigeorgica belongs to Nocardia asteroides complex (vi). This species was first described in 2001, and strains of N. cyriacigeorgica have since been recovered as the etiologic agent of human infection in Western Europe, Greece, Turkey, Japan, Thailand, and Canada. Most cases of infection have occurred in the context of HIV-related or iatrogenic immune suppression. Pulmonary nocardiosis caused by Nocardia cyriacigeorgica in patients with Mycobacterium avium complex lung disease has been described before. It has also been identified as the causative agent of an anterior mediastinal abscess in a patient with preexisting lung disease and the aetiological agent of native valve endocarditis in a patient with chronic obstructive pulmonary disease (COPD).
In addition to sulfonamide susceptibility, they are generally susceptible to broad-spectrum cephalosporins, amikacin, imipenem, and linezolid but resistant to penicillin, clarithromycin, and ciprofloxacin. It has been reported in the literature that serious life-threatening infections caused by Nocardia cyriacigeorgica are controlled well with dual therapy. In view of the species identification, the patient was started on injection imipenem and oral trimethoprim sulphamethoxazole. The patient began to improve clinically with this therapy. Oxygen saturation levels improved, fever declined, and the patient was shifted out of the Intensive Care Unit. Subsequently, with sustained improvement, he was discharged from the hospital in good health with the advice to continue oral cotrimoxazole for six months. The patient continues to remain relapse free.