I spent a little time trying to figure out what todays announcement means and why it is significant. So here are some comments and the sections of articles that I pulled some of the info from.
Please feel free to correct me if I get any of this wrong. Admittedly, I am a science challenged lawyer. <g>
ITMN and Pseudomonas aeruginosa (Pa)
Here is what I think they are after. People with Cystic fibrosis (the most common genetic disease) are at a much higher risk of infection by Pa. Apparently, Pa needs compromised tissue and immune system to thrive and CF provides that. Pa is around us in the soil and at times is airborne. In someone with CF - Pa can be fatal and is very difficult to treat.
So todays announcement suggests that treating Pa in CF is possible. Still too early to be compelling.
Here is a few quotes that help:
Table 2. Disease caused by Pseudomonas aeruginosa
Respiratory infections. Respiratory infections caused by Pseudomonas aeruginosa occur almost exclusively in individuals with a compromised lower respiratory tract or a compromised systemic defense mechanism. Primary pneumonia occurs in patients with chronic lung disease and congestive heart failure. Bacteremic pneumonia commonly occurs in neutropenic cancer patients undergoing chemotherapy. Lower respiratory tract colonization of cystic fibrosis patients by mucoid strains of Pseudomonas aeruginosa is common and difficult, if not impossible, to treat.
Cystic Fibrosis
This disease, the most common genetic disease in America, affects many infants, children and young adults across the country.
The number of Americans living with this lung disorder grows larger each year thanks to recent progress in diagnosis and treatment.
Cystic Fibrosis is the most common genetic disease in the United States affecting one in every two thousand, five hundred births.
ITMN has a big potential in CF treatment of PA
- 90% of CF's die of respratory failure with Pa being one of the primary causes.
NE MacDonald. Pseudomonas aeruginosa and cystic fibrosis: Antibiotic therapy and the science behind the magic. Can J Infect Dis 1997;8(6):335-342.
Respiratory failure secondary to chronic bronchiectasis is the cause of death in more than 90% of patients with cystic fibrosis (CF). The predominant microbes involved in CF lung disease are unusual: Pseudomonas aeruginosa, Staphylococcus aureus and Burkolderia cepacia. While antimicrobial therapy has been a component of CF care programs for decades, randomized controlled studies in the 1980s and early 1990s failed to show consistent measurable benefit. Research that stemmed from the discovery of the CF gene has shed new light on the inter-relationship of these microbes and the respiratory epithelial lung changes secondary to the CF gene. Five mechanisms have been proposed to explain the increased P aeruginosa colonization of the lower airway in CF. Recent research has also shown that antimicrobial therapy in CF may be effective not through eradication of the organism but by decreasing bacterial density and exoproduct production in the lung and thus decreasing inflammatory stimulus; by protecting against the consequences of an overexhuberant host response and in patients with stop mutations, potentially by correcting the gene defect. This tale of misunderstanding of the role and value of antimicrobial therapy in CF care illustrates the importance of ensuring close communiation between clinicians and researchers. The randomized controlled studies of the 1980s were not designed to answer the ‘right’ questions. The clinicians’ observations that the CF patients did improve with antimicrobial therapy have been validated by recent studies using different endpoints.
ITMN - Most patients with CF suffer from recurrent and chronic Pa infections.
Pseudomonas in cystic fibrosis: past, present, future
Niels Høiby MD, Dr. Med. Sci.
Professor & Chairman
Department of Clinical Microbiology 9301 & Danish Cystic Fibrosis Center,
Rigshospitalet,
University of Copenhagen, Juliane MariesVej 22
DK-2100 Copenhagen, Denmark
Phone: +4535457788, Fax: +4535456412
Summary
Most patients with cystic fibrosis (CF) suffer from recurrent and chronic endobronchial P aeruginosa infections. The accumulated knowledge shows that it is possible to prevent or delay the onset of these chronic infections in most CF patients by eliminating cross-infection and by early aggressive antibiotic treatment of intermittent colonization. The lung tissue damage is caused by activation of the immunologically specific inflammatory defense mechanisms of the lungs initiated by the antibody response and dominated by polymorphonuclear neutrophil leukocytes and their proteolytic and oxidative products. This inflammation induces a phenotypic shift from non-mucoid to mucoid, alginate producing phenotypes of P aeruginosa which then grow as a biofilm endobronchially. Such biofilms are impossible to eradicate by antibiotics. By using chronic suppressive antibiotic maintenance therapy and anti-inflammatory drugs it is, however, possible to maintain the lung function of the patients for years. Further improvement of the prophylaxis and therapy may include methods used by environmental microbiologists to prevent and remove biofilm e.g. antibacterial drugs combined with low current electricity, and use of alginate hydrolysis |
