Comparison of the microbiological profile of sputum and percutaneous endoscopy gastrostomy fed gastric juice aspirate in Cystic Fibrosis patients : descriptive evidence of a potential aerodigestive microbiome

Abstract

Gastro-Oesophageal Reflux (GOR) occurs in Cystic Fibrosis and is associated with deteriorating lung function. The hypothesis of this project is that the CF gastric and lung microbiome are related suggesting potential bidirectional transmission of pathogens through swallowing and aspiration of gastric contents. Gastric pepsin and bile might impact upon the lung microbiome and potentially exacerbate pulmonary disease. Paired gastric and sputum cultures were obtained from 18 adult CF patients receiving percutaneous endoscopic gastrostomy (PEG) feeding. Non-CF gastric juice samples were obtained from 14 patients without known lung disease through endoscopy. Bacterial and fungal isolates were identified by culture and next generation sequencing (NGS) of the 16S rRNA gene. The impact of pepsin, pH and bile acids on the growth and behaviour of Pseudomonas aeruginosa (PA) were tested. Culture-based and molecular-based approach demonstrated that the bacterial species present in CF gastric juice were different compared to the control group (non-CF patients). A high rate of pathogenic bacteria and organisms such as PA and Non-Tuberculosis Mycobacterium (NTM) were isolated from CF gastric juice samples and PEG tubes. Identical strains of PA and NTM in sputum and gastric juice from the same patient were isolated. Gastric juice samples and the PEG tube of 3 patient were positive for PA or NTM and had no PA or NTM present in the their sputum samples. This suggests that PA can survive acid environments in the presence of pepsin and bile acids. The hostile gastric environment may have a negative effect upon PA growth and induce drug resistant biofilm formation. In conclusion, the stomach is a potential microbiological niche where organisms relevant to CF pathophysiology can survive particularly for biofilm PA and NTM. This may be influenced by CF related gastrointestinal pathophysiology, antibiotic therapy and acid suppression.