The total production of HCN in vitro over 30 h was compared with the level in breath of the corresponding patients.Īll S. The strains were isolated from sputum that was collected on the day of breath sampling. aureus-infected patients in whom HCN was detected in breath were capable of producing HCN, we measured the HCN production from these five separately cultured S. Exhaled HCN levels were normalised to respiratory CO 2 concentration and mean values were considered for analysis. Quantification of HCN in breath was performed using laser-based photoacoustic spectroscopy as described earlier. The breath samples were collected 90 s apart and stored for a maximum of 8 h prior to analysis. From the total exhalation, the dead space air (150 mL) was discarded and the remaining part collected in the sampling bag. Briefly, the participants exhaled through a bacterial filter (Air Safety Limited, Morecambe, UK) and a non-rebreathable T-piece (Vacumed, Ventura, CA, USA) which were connected to a CO 2 sensor and a calibrated buffer pipe. s −1 using a breath sampler (Loccioni, Angeli di Rosora, Italy).Each subject provided two single mouth-exhaled breath samples that were collected in separate 3-L Tedlar bags (ProCare B.V., Groningen, the Netherlands) at a constant flow rate of 300 mL Before sampling, all participants rinsed their mouth with water. Sputum samples were obtained as a part of routine clinical care. cepacia in sputum samples (minimum of four samples) over the previous 12 months. cepacia in sputum on the day of breath sampling or in >50% of sputum samples (minimum of four samples) over the previous 12 months. We included nonsmoking, infected and non-infected CF patients and healthy controls. Oral consent was obtained from participants aged ≥12 years and from parents of children aged 6–18 years. This study was approved by the local medical ethics committee (CMO – Nijmegen/Arnhem) which waived written informed consent. The setup used for analysing bacterial headspace (in triplicate) and determination of growth curves has been previously described.ĬF patients (aged ≥6 years old) were recruited from the outpatient clinic of Radboud University Medical Center and Erasmus Medical Center (Nijmegen and Rotterdam, the Netherlands, respectively). aureus from sputum of CF patients were inoculated into 50-mL brain-heart infusion broth in an initial concentration of 5×10 6 CFU aureus strains cultured from patients in whom HCN was detected in breath, were capable of producing HCN.įive clinical isolates of S. Furthermore, we investigated whether the S. aureus-infected CF patients, in comparison with non-infected CF patients, as well as healthy persons as controls.

aureus isolates in vitro, and HCN levels in the exhaled breath of S. We therefore measured the real-time HCN production by clinical S. In a single report, five strains have been shown to produce low values in vitro, and in vivo studies have not been reported. Investigations into the emission of HCN by Staphylococcus aureus, a predominant CF pathogen throughout childhood, have been very limited. To our knowledge, actual proof that HCN is not produced by other pathogens is lacking. Only Burkholderia cepacia is also known to produce HCN in vitro, but HCN is not a biomarker for B. Until now, it has been assumed that hydrogen cyanide (HCN) can be considered as a specific biomarker for P. Early detection of Pseudomonas aeruginosa in cystic fibrosis (CF) patients is crucial, since eradication in a later stage is extremely difficult.

Hydrogen cyanide