Outbreak of Invasive Aspergillosis After Major Heart Surgery Caused by Spores in the Air of the Intensive Care Unit

• Published in: Clinical infectious diseases Vol. 54; no. 3; pp. e24 - e31
• Main Authors: Peláez, T., Muñoz, P., Guinea, J., Valerio, M., Giannella, M., Klaassen, C. H. W., Bouza, E.
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.02.2012
• Subjects: Aged, 80 and over; Air Microbiology; Antifungal Agents - therapeutic use; Aspergillosis - drug therapy; Aspergillosis - epidemiology; Aspergillosis - etiology; Aspergillus - isolation & purification; Cardiac Surgical Procedures - adverse effects; Coronary Care Units; Disease Outbreaks; Echinocandins - therapeutic use; Epidemics; Female; Fungi; Genotype & phenotype; Heart surgery; Humans; Incidence; Intensive care; Lipopeptides; Male; Middle Aged; Nonnative species; Pyrimidines - therapeutic use; Spores, Fungal - isolation & purification; Triazoles - therapeutic use; Voriconazole
• DOI: 10.1093/cid/cir771
• ISSN: 1058-4838

We report on an outbreak of invasive aspergillosis in a major heart surgery unit related to peaks of high counts of genotypically related Aspergillus conidia in the environment. Background.  Outbreaks of invasive aspergillosis (IA) are believed to be caused by airborne Aspergillus conidia. Few studies have established a correlation between high levels of Aspergillus fumigatus conidia and the appearance of new cases of IA or have demonstrated matching genotypes between clinical isolates and those from the environment. Methods.  We detected an outbreak of IA (December 2006 through April 2008) in the major heart surgery intensive care unit (MHS-ICU) of our institution. Our local surveillance program consists of monthly environmental air sampling in operating rooms and ICUs for quantitative and qualitative identification of filamentous fungi. During the study period, we obtained 508 environmental samples from 3 different periods: 6 months before the outbreak, during it, and 6 months after it. Available environmental and clinical strains were genotyped according to the short tandem repeats assay. Results.  Seven patients developed proven or probable IA (5 with lung infection, 1 with mediastinitis, and 1 with lung infection and mediastinitis). A. fumigatus was involved in 6 cases. The underlying conditions of the patients were heart transplantation (n = 3), corticosteroid-dependent conditions (n = 2), and diabetes mellitus (n = 2). The mortality rate was 85.7%. Before and after the outbreak (±6 months), the median airborne A. fumigatus conidia levels were 0 colony-forming units (CFUs) per cubic meter, and no cases of IA occurred during these periods. However, during the outbreak period, the occurrence of the 6 cases of IA caused by A. fumigatus was linked to peaks of abnormally high A. fumigatus airborne conidia levels (175, 50, 25, 20, 160, and 400 CFUs/m3) in the MHS-ICU, whereas counts in the air of both operating rooms remained negative. Matches between A. fumigatus genotypes collected from the air of the MHS-ICU and from representative clinical samples were found in 3 of the 6 patients. The outbreak abated when high-efficiency particulate air filters were installed in the affected areas. Conclusions.  Our study revealed that abnormally high levels of airborne A. fumigatus conidia correlated with new cases of IA, even in patients who were not severely immunocompromised. The demonstration of matches between air and clinical genotypes reinforces the role of environmental air in the acquisition of IA during the period following MHS. Environmental monitoring of Aspergillus spores in the air of postoperative units is mandatory, even when these units receive nonimmunocompromised patients undergoing major surgery.