Much of the morbidity and mortality of cystic fibrosis (CF), an inherited mucus condition of the lungs, is due to infections by the bacterial pathogen Pseudomonas aeruginosa. Some data indicate that between 60-80% of CF patients are positive for P. aeruginosa. The incidence may be declining, being replaced by more Staphylococcus aureus infections. Metagenomic analysis of the entire CF microbiome may be more accurate to predict long-term clinical outcomes than screening for pathogens individually, yet little is known about the microbiome diversity in CF patients.
Michael D. Parkins from the University of Calgary, Canada, and colleagues, hypothesized that the clinical course of patients in Prairie-based Canadian CF centers may be due in part to fundamental differences in the bacterial composition of their lower airways microbiota. Samples from a longitudinal sputum biobank containing whole sputum samples from patients collected since 1998 and a comprehensive strain biobank starting in 1978, located at the Calgary Adult CF Clinic, were deployed for the study. The results were published in the journal frontiers in Cellular and Infection Microbiology.
In combined controls and Prairie Epidemic Strain (PES) samples, Pseudomonas (42.6%), followed by Streptococcus (35%), Haemophilus (7.8%), Staphylococcus (4%), Prevotella (3.5%), Rothia (1.2%), Granulicatella (0.8%), Neisseria (0.8%), Burkholderia (0.5%), Veillonella (0.4%), Fusobacterium (0.2%), and Actinobacillus (0.2%) were the most common.
Epidemic P. aeruginosa had significantly more Pseudomonas compared to the unique (u)PA strains (54.3 vs. 19.18%, P = 0.0005). Interestingly, differences in mucoid phenotype (biofilm glyco-layers) were also significantly correlated with CF bacterial community structure.
No individual phenotype or genetic marker has been consistently associated with epidemic PA status, and the present study did not identify any molecular targets. On the supramolecular level polysaccharide content possibly indicating structural biofilm differences were inferred.
The study was limited by a small size and also the extrapolation to “epidemic” PA, which only included the Prairie Epidemic Strains. The area of research is still nascent and could benefit from more studies. Low resolution metagenomics was accomplished by sequencing the V3-V4 region of the 16S rRNA gene. Higher resolution metagenomics could provide more granularity to the data.
“We observed that patients infected with PES, an ePA associated with worse CF clinical outcomes, have different bacterial community structures than those infected with uPA. While ePA may still be disproportionally more virulent than other PA strains as it has been previously reported, they may also function to modify the CF microbiome to one that is more harmful to the host by which patients infected with ePA experience worse lung clinical outcomes. Further study is required on the mechanism by which ePA might contribute to adverse outcomes,” concluded the authors.