Frontiers in medicine · 2026
Case Report: Sequencing-supported probable osteoarticular Mycobacterium avium complex infection in rheumatoid arthritis.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Zhang Jing, Zhang Lina, Li Sheng-Guang, Li Ji, Zou Yadan, Long Ting, Yu Ruohan, Zhang Yanfeng
Аннотация
BACKGROUND: Osteoarticular Mycobacterium avium complex (MAC) infection is uncommon and can resemble inflammatory arthritis during immunosuppression.
CASE DESCRIPTION: A 52-year-old woman with an erosive seronegative rheumatoid arthritis phenotype and overlap autoimmune features developed progressive polyarticular swelling, wrist tenosynovitis, hip effusions, and low-back pain after cumulative immunosuppression. Investigations showed macrocytic anemia, lymphopenia, pan-hypogammaglobulinemia, marked B-cell depletion without anti-CD20 exposure, and cytomegalovirus DNAemia. Pre-treatment mNGS reported MAC-spectrum signals in hip, wrist, and elbow aspirates, including 355 right-hip reads. A separate pathogen-targeted joint-fluid sequencing report, with no anatomical site stated, detected MAC complex (116,330 normalized sequences; assay-estimated 10⁵ copies/mL). Neither result was interpreted as organism burden. No tissue histopathology, dedicated mycobacterial culture, or phenotypic susceptibility testing was performed. The working diagnosis was multisite sequencing-supported probable multifocal osteoarticular MAC infection without culture confirmation. Several interventions began concurrently. Selected follow-up MR images showed persistent destructive wrist disease and residual joint or periarticular fluid, but no standardized imaging or microbiological response endpoint was available.
CONCLUSION: In atypical arthritis progressing during immunosuppression, infection-focused sampling should precede further escalation. mNGS can provide an etiologic clue, but culture, histopathology, targeted testing, and longitudinal reassessment remain essential.
CASE DESCRIPTION: A 52-year-old woman with an erosive seronegative rheumatoid arthritis phenotype and overlap autoimmune features developed progressive polyarticular swelling, wrist tenosynovitis, hip effusions, and low-back pain after cumulative immunosuppression. Investigations showed macrocytic anemia, lymphopenia, pan-hypogammaglobulinemia, marked B-cell depletion without anti-CD20 exposure, and cytomegalovirus DNAemia. Pre-treatment mNGS reported MAC-spectrum signals in hip, wrist, and elbow aspirates, including 355 right-hip reads. A separate pathogen-targeted joint-fluid sequencing report, with no anatomical site stated, detected MAC complex (116,330 normalized sequences; assay-estimated 10⁵ copies/mL). Neither result was interpreted as organism burden. No tissue histopathology, dedicated mycobacterial culture, or phenotypic susceptibility testing was performed. The working diagnosis was multisite sequencing-supported probable multifocal osteoarticular MAC infection without culture confirmation. Several interventions began concurrently. Selected follow-up MR images showed persistent destructive wrist disease and residual joint or periarticular fluid, but no standardized imaging or microbiological response endpoint was available.
CONCLUSION: In atypical arthritis progressing during immunosuppression, infection-focused sampling should precede further escalation. mNGS can provide an etiologic clue, but culture, histopathology, targeted testing, and longitudinal reassessment remain essential.