Nocardia Infection in Patients With Anti-Granulocyte-Macrophage Colony-Stimulating Factor Autoantibodies: A Prospective Multicenter French Study
- PMID: 38915339
- PMCID: PMC11194753
- DOI: 10.1093/ofid/ofae269
Nocardia Infection in Patients With Anti-Granulocyte-Macrophage Colony-Stimulating Factor Autoantibodies: A Prospective Multicenter French Study
Abstract
Background: Nocardiosis, a bacterial opportunistic infection caused by Nocardia spp, has recently been reported in patients with anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibodies, but insufficient data are available about disease presentation, outcomes, and occurrence of autoimmune pulmonary alveolar proteinosis (aPAP) in this population.
Methods: We performed a prospective, multicenter, nationwide study in France and included patients with a Nocardia infection who had anti-GM-CSF autoantibodies. We describe their clinical, microbiological, and radiological characteristics, and their outcome at 1 year of follow-up.
Results: Twenty patients (18 [90%] male) were included, with a median age of 69 (interquartile range, 44-75) years. The organs most frequently involved were the brain (14/20 [70%]) and the lung (12/20 [60%]). Half of the infections were disseminated (10/20 [50%]). Nocardia identification was predominantly made in abscess fluid (17/20 [85%]), among which 10 (59%) were brain abscesses. The 1-year all-cause mortality was 5% (1/20), and only 1 case of aPAP (1/20 [5%]) occurred during the follow-up period.
Conclusions: Nocardiosis with anti-GM-CSF autoantibodies is associated with a low mortality rate despite a high incidence of brain involvement. Although the occurrence of aPAP was infrequent during the 1-year follow-up period, long-term clinical data are needed to fully understand the potential relationship between nocardiosis, anti-GM-CSF autoantibodies, and aPAP.
Keywords: Nocardia; anti-GM-CSF autoantibodies; autoimmune pulmonary alveolar proteinosis; central nervous system infection; nocardiosis.
© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America.
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