Preeti S Ajapuje, Shiv Gupta, Geeta Chitre, Samvveda Samel
This case highlights three clinically relevant lessons: first, post-PCI M. abscesses stent-associated mediastinitis demands aggressive source control; second, tedizolid can serve as a viable salvage therapy after linezolid intolerance; third, serial cardiac PET-CT can assist treatment monitoring when repeat deep tissue sampling is impractical; and fourth, advanced multimodal imaging plays a critical role in diagnosis, surgical planning, and monitoring of complex post-cardiac surgical infections.
BACKGROUND: Mycobacterium abscessus infection involving coronary stent material and mediastinal tissues after percutaneous coronary intervention is exceptionally uncommon, difficult to diagnose, and challenging to treat because of biofilm formation, multidrug resistance, and the need for prolonged multidrug therapy.
CASE SUMMARY: A 65-year-old man with diabetes, hypertension, and coronary artery disease developed persistent fever after PCI to the left anterior descending and right coronary arteries. Serial cardiac PET-CT and contrast-enhanced CT demonstrated a hypermetabolic middle mediastinal mass encasing the left main coronary artery and proximal branches, with a pseudoaneurysm arising from the proximal LAD. He underwent removal of the infected coronary stent, coronary artery bypass grafting, pericardiectomy, and biopsy/debridement of the mediastinal lesion. Tissue culture grew M. abscessus subsp. abscessus, identified by MALDI-TOF, with susceptibility to amikacin and linezolid and resistance to macrolides and fluoroquinolones.
INTERVENTION AND OUTCOME: The patient received a multidrug regimen anchored by amikacin and an oxazolidinone. Serum creatinine and audiometry were monitored for IV amikacin. Because of early hematologic intolerance to linezolid, therapy was transitioned to tedizolid 200 mg once daily, with clofazimine later used as the companion oral agent after intolerance to minocycline. The patient completed a total of 6 months of anti-NTM therapy, including approximately 5 months of tedizolid-based therapy. The follow-up monitoring sheets document stable hematological parameters and no peripheral neuropathy observed during the tedizolid phase. Serial imaging showed substantial regression of the mediastinal lesion without clinically significant FDG uptake at end of therapy.
CONCLUSION: This case highlights three clinically relevant lessons: first, post-PCI M. abscesses stent-associated mediastinitis demands aggressive source control; second, tedizolid can serve as a viable salvage therapy after linezolid intolerance; third, serial cardiac PET-CT can assist treatment monitoring when repeat deep tissue sampling is impractical; and fourth, advanced multimodal imaging plays a critical role in diagnosis, surgical planning, and monitoring of complex post-cardiac surgical infections.