Transplant infectious disease : an official journal of the Transplantation Society · 2026
Performance of the BioFire FilmArray Pneumonia Panel Plus Compared to Standard Microbiology in Lung Transplant Donor and Recipient Samples: A Prospective Cohort Study.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Lombardi Andrea, Renisi Giulia, Rosso Lorenzo, Morlacchi Letizia, Fumagalli Jacopo, Cariani Lisa, Righi Ilaria, Rossetti Valeria, Liparoti Arianna, Azzarà Cecilia, Mangioni Davide, Alagna Laura, Saltini Paola, Liporace Maria Francesca, Abbruzzese Chiara, Callegaro Annapaola, Blasi Francesco, Grasselli Giacomo, Nosotti Mario, Bandera Alessandra
Аннотация
BACKGROUND: Lung transplantation (LuTx) is hampered by infectious risks. Perioperative antibiotic prophylaxis (PAP) is widely used; however, real-time adjustment is hindered by the timing of standard microbiology. Syndromic molecular panels offer rapid results, yet their integration into PAP strategies remains unclear.
METHODS: We conducted a prospective cohort study comparing the BioFire FilmArray Pneumonia Panel Plus (PNplus) with standard of care (SOC) on bronchoalveolar lavage (BAL) samples obtained from donors at procurement and from recipients 72 h after LuTx. Concordance between PNplus and SOC was assessed for bacterial species and antimicrobial resistance genes.
RESULTS: Fifty-three donor-recipient pairs were analyzed. In donor BAL, PNplus identified at least one pathogen in 67.9% (36/53) of cases versus 63.5% (33/53) by SOC, with a markedly shorter time to result (221 min vs. 5.3 days). Concordance between PNplus and SOC for bacterial species was substantial (Cohen's κ = 0.654), particularly for Staphylococcus aureus (Cohen's κ = 0.689), Streptococcus pneumoniae (Cohen's κ = 0.658), and Pseudomonas aeruginosa (Cohen's κ = 0.731). In recipient BAL, PNplus detected pathogens in 61.5% (32/53) compared to 47.2% (25/53) with SOC, but overall concordance was only moderate (κ = 0.365). Resistance gene concordance was minimal, with PNplus often identifying additional determinants not confirmed by SOC. Viruses were detected exclusively by PNplus, while fungi were identified only by SOC.
CONCLUSION: PNplus provides rapid, clinically relevant pathogen detection in LuTx, showing substantial agreement with SOC in donor samples and offering potential to support PAP adjustment. In early post-transplant recipient BAL, interpretation requires caution, and SOC remains indispensable, particularly for detecting fungi and confirming phenotypic resistance.
METHODS: We conducted a prospective cohort study comparing the BioFire FilmArray Pneumonia Panel Plus (PNplus) with standard of care (SOC) on bronchoalveolar lavage (BAL) samples obtained from donors at procurement and from recipients 72 h after LuTx. Concordance between PNplus and SOC was assessed for bacterial species and antimicrobial resistance genes.
RESULTS: Fifty-three donor-recipient pairs were analyzed. In donor BAL, PNplus identified at least one pathogen in 67.9% (36/53) of cases versus 63.5% (33/53) by SOC, with a markedly shorter time to result (221 min vs. 5.3 days). Concordance between PNplus and SOC for bacterial species was substantial (Cohen's κ = 0.654), particularly for Staphylococcus aureus (Cohen's κ = 0.689), Streptococcus pneumoniae (Cohen's κ = 0.658), and Pseudomonas aeruginosa (Cohen's κ = 0.731). In recipient BAL, PNplus detected pathogens in 61.5% (32/53) compared to 47.2% (25/53) with SOC, but overall concordance was only moderate (κ = 0.365). Resistance gene concordance was minimal, with PNplus often identifying additional determinants not confirmed by SOC. Viruses were detected exclusively by PNplus, while fungi were identified only by SOC.
CONCLUSION: PNplus provides rapid, clinically relevant pathogen detection in LuTx, showing substantial agreement with SOC in donor samples and offering potential to support PAP adjustment. In early post-transplant recipient BAL, interpretation requires caution, and SOC remains indispensable, particularly for detecting fungi and confirming phenotypic resistance.