Burkholderia vietnamiensis causing infections in noncystic fibrosis patients in a tertiary care hospital in Mexico.

Burkholderia cepacia complex (Bcc) species are opportunistic pathogens widely distributed in the environment and often infect people with cystic fibrosis (CF). This study aims to determine which genomovars of the Bcc can cause infections in non-CF patients from a tertiary care hospital in Mexico and if they carry virulence factors that could increase their pathogenicity. We identified 23 clinical isolates that carry the recA gene. Twenty-two of them belongs to the genomovar V (B. vietnamiensis) and one to the genomovar II (B. multivorans). Thirteen pulsotypes were identified among 22 B. vietnamiensis isolates. All clinical isolates produced biofilm were motile and cytotoxic on murine macrophage-like RAW264.7 and in A549 human lung epithelial cells. In conclusion, B. vietnamiensis causes infections in non-CF patients in a tertiary care hospital in Mexico, rapid identification of this pathogen can help physicians to establish a better antimicrobial treatment.

Bacterial Subversion of Autophagy in Cystic Fibrosis.

Cystic fibrosis (CF) is a genetic disease affecting more than 70,000 people worldwide. It is caused by a mutation in the cftr gene, a chloride ion transporter localized in the plasma membrane of lung epithelial cells and other organs. The loss of CFTR function alters chloride, bicarbonate, and water transport through the plasma membrane, promoting the production of a thick and sticky mucus in which bacteria including Pseudomonas aeruginosa and Burkholderia cenocepacia can produce chronic infections that eventually decrease the lung function and increase the risk of mortality. Autophagy is a well-conserved lysosomal degradation pathway that mediates pathogen clearance and plays an important role in the control of bacterial infections. In this mini-review, we describe the principal strategies used by P. aeruginosa and B. cenocepacia to survive and avoid microbicidal mechanisms within the autophagic pathway leading to the establishment of chronic inflammatory immune responses that gradually compromise the lung function and the life of CF patients.

Pseudomonas Aeruginosa: Genetic Adaptation, A Strategy for its Persistence in Cystic Fibrosis.

Cystic fibrosis (CF) is a progressive autosomal recessive genetic disease that principally affects the respiratory and digestive systems. It is a chronic disease that has no cure. Symptoms often include chronic cough, lung infections, and shortness of breath. Children with cystic fibrosis present failure to thrive as manifested by low weight and height for age. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (cftr) gene that codes for a cell membrane protein of epithelial tissues and affects multiple organ systems in the human body. Mutations on the CFTR causes dysfunctional electrolyte regulation affecting intracellular water content. Defective CFTR function in airways produce a dehydrated and sticky mucus that leads the establishment of bacterial chronic infection that ultimate decrease the lung function. During the first decade of life, affected individuals are colonized principally by non typable Haemophilus influenzae and Staphylococcus aureus. During the second decade, Pseudomonas aeruginosa becomes the most dominant pathogen and persists throughout the remainder of their lives. In this work, we describe the mechanisms used by P. aeruginosa to adapt and persist in lungs of individuals with cystic fibrosis.