Azithromycin is an antibiotic that also has antiinflammatory properties. It is these antiinflammatory properties that are thought to account for the improvement in clinical outcome observed when patients with chronic lung diseases such as cystic fibrosis are treated long-term with azithromycin. However, a recent study indicated that azithromycin treatment in patients with cystic fibrosis is associated with increased infection with nontuberculous mycobacteria, a serious complication in such individuals. Now, a team of researchers - led by Andres Floto and David Rubinsztein, at the University of Cambridge, United Kingdom; and Diane Ordway, at Colorado State University, Fort Collins - has confirmed that long-term use of azithromycin by adults with cystic fibrosis is associated with infection with nontuberculous mycobacteria and identified an underlying mechanism.
A study published on bmj.com indicates, that even though improvements have been made in the last half century for the survival of cystic fibrosis sufferers, females and individuals from socio-economically disadvantaged backgrounds continue to die younger than males and those more privileged in society. Findings indicate, that since the first report in 1989, the socio-economic and sex differences of the death age from cystic fibrosis continues to this day. Mainly because of better health care provision, survival in individuals with cystic fibrosis has improved dramatically over the last 50 years, with the average death age rising from 6 months in 1959 to 27 years in 2008. Approximately 20 years ago a discovery was made that males and individuals from advantaged socio-economical backgrounds had a higher age at death.
Case Western Reserve University School of Medicine has received a $2.1 million grant from the National Center for Research Resources, part of the National Institutes of Health (NIH), to expand basic research models for the study of cystic fibrosis (CF). CF is an inherited disease that causes thick, sticky mucus to build up in the lungs and digestive tract. The four-year NIH grant was awarded to Mitchell Drumm, PhD, and Craig Hodges, PhD, co-investigators of the research supported by the grant. Drumm is professor of Pediatrics and Genetics at the Case Western Reserve School of Medicine, and vice chair for research in Pediatrics. He co-discovered the gene that causes CF, CFTR, along with Francis Collins, MD, PhD, the noted physician-geneticist and current director of the NIH. Hodges is an assistant professor of Pediatrics and Genetics at the Case Western Reserve School of Medicine as well.
Microbiologists have uncovered a sneaky trick by the bacterium Pseudomonas aeruginosa to oust rivals. It deploys a toxin delivery machine to breach cell walls of competitors without hurting itself. Its means of attack helps it survive in the outside environment and may even help it cause infection. P. aeruginosa is a common bacterium that lives in soil, and also an opportunistic pathogen best known for infecting the lungs of cystic fibrosis patients. The scientists discovered that /i>P. aeruginosa injects toxins into rival bacteria with a needle-like puncturing device called the type VI secretion system (T6SS). The toxins degrade competitors' protective barricades - their cell walls. The research report also delineates the complex defensive mechanisms by which P. aeruginosa protects itself from its own artillery.
Bacteria use various appendages to move across surfaces prior to forming multicellular bacterial biofilms. Some species display a particularly jerky form of movement known as "twitching" motility, which is made possible by hairlike structures on their surface called type IV pili, or TFP. "TFP act like Batman's grappling hooks, " said Gerard Wong, a professor of bioengineering and of chemistry and biochemistry at the UCLA Henry Samueli School of Engineering and Applied Science and the California NanoSystems Institute (CNSI) at UCLA. "These grappling hooks can extend and bind to a surface and retract and pull the cell along." In a study to be published online this week in Proceedings of the National Academy of Sciences, Wong and his colleagues at UCLA Engineering identify the complex sequence of movements that make up this twitching motility in Pseudomonas aeruginosa, a biofilm-forming pathogen partly responsible for the deadly infections seen in cystic fibrosis.