Abstract
Chronic lung infection by Pseudomonas aeruginosa is the leading cause of morbidity and mortality in cystic fibrosis (CF) patients. This is associated with the conversion of the non-mucoid to the mucoid phenotype. However, there is little information about the occurrence of alginate-producing P. aeruginosa in CF patients outside Europe and North America. The aim of the present study was to investigate mutations in the algTmucABD operon in mucoid and non-mucoid isolates from Brazilian CF patients. Twenty-seven mucoid and 37 non-mucoid isolates from 40 CF patients chronically infected by P. aeruginosa attending a CF reference center in Brazil were evaluated by sequence analysis. Mutations in mucA were observed in 93% of the mucoid isolates and 54% of the non-mucoid isolates. Among these non-mucoid isolates, 55% were considered revertants, since they also had mutations in algT (algU). Most isolates associated with moderate alginate production presented point mutations in mucB and/or mucD. We identified 30 mutations not previously described in the operon. In conclusion, mutations in mucA were the main mechanism of conversion to mucoidy, and most of the non-mucoid isolates were revertants, but the mechanism of revertance is not fully explained by changes in algT.
Highlights
The onset of chronic airway infection with Pseudomonas aeruginosa in cystic fibrosis (CF) patients is usually preceded by a period of recurrent, intermittent colonization, most often by environmental strains [1]
The aim of the present study was to obtain a better understanding of the adaptation and genomic evolution that occurs in P. aeruginosa during chronic lung infection in CF patients
Sixty-four P. aeruginosa isolates were selected in the period of study, 27 mucoid and 37 nonmucoid
Summary
The onset of chronic airway infection with Pseudomonas aeruginosa in cystic fibrosis (CF) patients is usually preceded by a period of recurrent, intermittent colonization, most often by environmental strains [1]. During the chronic lung infection, P. aeruginosa persists and survives for decades under the challenging selective pressure imposed by an oscillating inflammatory response, continuous exposure to antibiotic therapy, and variable nutrient availability. Adaptation of P. aeruginosa to chronic phenotypes in CF design, data collection and analysis, decision to publish, or preparation of the manuscript
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