Abstract
In patients with cystic fibrosis (CF), the lung is a remarkable ecological niche in which the microbiome is subjected to important selective pressures. An inexorable colonization by bacteria of both endogenous and environmental origin is observed in most patients, leading to a vicious cycle of infection–inflammation. In this context, long-term colonization together with competitive interactions among bacteria can lead to over-inflammation. While Pseudomonas aeruginosa and Staphylococcus aureus, the two pathogens most frequently identified in CF, have been largely studied for adaptation to the CF lung, in the last few years, there has been a growing interest in emerging pathogens of environmental origin, namely Achromobacter xylosoxidans and Stenotrophomonas maltophilia. The aim of this review is to gather all the current knowledge on the major pathophysiological traits, their supporting mechanisms, regulation and evolutionary modifications involved in colonization, virulence, and competitive interactions with other members of the lung microbiota for these emerging pathogens, with all these mechanisms being major drivers of persistence in the CF lung. Currently available research on A. xylosoxidans complex and S. maltophilia shows that these emerging pathogens share important pathophysiological features with well-known CF pathogens, making them important members of the complex bacterial community living in the CF lung.
Highlights
Cystic fibrosis (CF) is the most commonly, still fatal, inherited genetic disease in Caucasian populations, caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene coding for a transmembrane channel allowing the transport of chloride ions
Available research on A. xylosoxidans complex and S. maltophilia shows that these emerging pathogens share important pathophysiological features with well-known CF pathogens, making them important members of the complex bacterial community living in the CF lung
Antimicrobial resistance makes the antibiotic treatment of Achromobacter xylosoxidans complex (Axc) and Stenotrophomonas maltophilia (Sm) infections challenging in CF patients, if we consider that both pathogens may be protected from antimicrobial drugs in the biofilm formed in the CF lung, where higher antibiotic minimal inhibitory concentrations are usually observed compared with the planktonic forms [105,106]
Summary
Cystic fibrosis (CF) is the most commonly, still fatal, inherited genetic disease in Caucasian populations, caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene coding for a transmembrane channel allowing the transport of chloride ions. Different organs are affected, including the respiratory tract, where thick mucus, mucociliary clearance defects, and a decrease in anti-microbial defenses favoring bacterial colonization are observed [1]. The main causes of morbidity and mortality in CF patients are recurrent respiratory infections. Colonization is often initiated by Staphylococcus aureus or Haemophilus influenzae. The microbiology of the lung becomes more complex, as Pseudomonas aeruginosa becomes dominant, and the lung may be colonized by other microorganisms such as nontuberculous mycobacteria (NTM), Burkholderia cepacia complex, Achromobacter xylosoxidans, and Stenotrophomonas maltophilia [2,3]
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