Our patient is a 68-year-old woman who had undergone a splenectomy for Felty's syndrome and who presented with one month of worsening lower back pain and fever. Her back pain was chronic and previously managed with intra-articular steroid injections over the course of several years but had recently worsened significantly. Spinal CT imaging revealed a stable compression deformity at the L1-L2 level and new L1-L2 discitis (Fig. 1). MRI showed L1-L2 discitis, vertebral body enhancement, and a contrast-enhancing anterior paraspinal soft tissue prominence (Fig. 2). An aerobic bacterial culture of the affected disc obtained via CT-guided aspiration was sterile, and she was treated empirically with intravenous (IV) vancomycin and ceftriaxone. Fever and back pain persisted while on antibacterial therapy, and repeat CT 4 weeks into treatment showed progression of the L1-L2 compression fracture without significant change in discitis.
She was transferred to our tertiary hospital and underwent an anterior L1 and L2 corpectomy with anterior T12 through L3 interbody fusion. The empiric antibiotics were held for three days preoperatively to improve the diagnostic yield of specimens obtained during surgery. Erythrocyte sedimentation rate (ESR) and C-reactive peptide (CRP) were elevated at > 120 mm/hr (normal range 0-40 mm/hr) and 99.6 mg/L (normal range 0-4.9 mg/L), respectively.
Surgical pathology revealed acute and chronic osteomyelitis and osteonecrosis with necrotizing granulomas. Acid-fast bacilli (AFB) smear showed 10-99 AFB per field ("1+" designation), and aerobic and anaerobic bacterial tissue, bone, and blood cultures were negative for growth. Risk factors for exposure to MTB were absent. Induced sputum for AFB was smear and culture negative, and the patient had no respiratory symptoms. M. tuberculosis (MTB) interferon-gamma release assay (Quantiferon-TB ) was indeterminate due to low mitogen reactivity.
The patient was diagnosed with non-tuberculous mycobacterial (NTM) osteomyelitis/discitis and started on rifampin, ethambutol, moxifloxacin, and clarithromycin to cover broadly for the most common causes of NTM infection. The isolate was sent to the Maryland State Department of Health laboratory, where probes for MTB, M. avium/intracellulare complex (MAC), M. kansasii and M. gordonae were negative. It was then sent to a commercial laboratory for definitive identification and susceptibility testing. At approximately four weeks, growth was seen on the mycobacterial growth indicator tube (MGIT), presumptively identified as M.fortuitum/chelonae complex, though this species is a rapid grower, typically growing in 7-10 days. The regimen was switched to clarithromycin, moxifloxacin, and IV imipenem and amikacin. Subsequently 16 S sequencing was performed, and M. xenopi was identified. The isolate was reported as susceptible to amikacin, ciprofloxacin, clarithromycin, linezolid, moxifloxacin, and trimethoprim/sulfamethoxazole, and resistant to ethambutol, rifampin, and streptomycin (Table 1). Her regimen was changed to clarithromycin, moxifloxacin and linezolid based on susceptibility results, but severe nausea necessitated a switch from clarithromycin to azithromycin. The patient's back pain eventually subsided, and at a follow-up visit one month after beginning M. xenopi treatment, she was free of fever and other symptoms of infection. Objective data revealed a down-trending ESR and CRP with values of 52 mm/hr and 10.4 mg/L two months into treatment. Overall, she received approximately 4 months of appropriate treatment for M. xenopi, before dying of non-infectious causes related to her underlying illness.