Cystic Fibrosis (CF) is a disease that includes a collection of clinical conditions which result from mutations in the Cystic Fibrosis Transmembrane co-regulator Receptor (CFTR) gene, leading to altered gene products, irregulation of sodium and chlorine ion channels, and a change in the consistency of mucus lining the digestive, respiratory, and reproductive tracts. Mucus contains anti-microbial compounds and immunoglobulins that prevent bacterial invasion to these places. Altered mucus consistency provides a gateway to opportunistic pathogens to colonize and form biofilms, leading to severe consequences.
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CF is a progressive disease with the most common consequence being pulmonary infection with multidrug-resistant Pseudomonas aeruginosa, to which 90 – 95% of the patients succumb. The condition starts with an acute phase of infection followed by a persistent chronic state. However, a recent study published in the March issue of PLOS One states that the bacteria within chronic cystic fibrosis patients actually become more inactive over time. Dr. Ashleigh Griffin of the University of Oxford and her team have studied bacterial behavioral and co-operative patterns in both laboratory grown and sputum sample derived (from chronic CF sufferers) species, which has led them to conclude that bacteria become ‘selfish’ after a point of time in chronically affected patients.
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According to Dr. Griffin, “This infection is fairly specialized because it’s very long-lived. While doctors can normally cure a bacterial infection in a week, people with cystic fibrosis can suffer with a lung infection can persist for years. During chronic infections, bacteria will change their behavior towards each other. It’s interesting, because we can watch the change over time in patients.”
The key aspects studied in this regard were the production of elastase, protease, and similar degrading enzymes, intensity of the quorum-sensing signal molecules (autoinducers), siderophore (pyoverdine) production, and the ability to form biofilms. Laboratory isolates were compared against those derived from sputum samples of patients living with the disease for more than 6 months.
The study showed a considerable decrease in the amount of degrading enzymes produced, as well as a decrease in the intensity of quorum sensing indicated by low amounts of autoinducers. The intensity of pyoverdine, a green colored pigment responsible for iron-binding, was also lower in patients with the chronic infection. The intensity of biofilms was not much affected by this. These conclusions led to the assumption that bacteria might actually become inactive in case of chronic infection.
It is also worth noting that the lung provides a selective environment for the bacteria to survive, which is why even though “inactive” they still retain the quality to make the infection persist. “If bacteria don’t need iron because the lung is an iron-rich environment, then they won’t need to make this pyoverdin, or something else may be happening that means they don’t need to signal to one another as much,” Griffin explains.
Further research needs to be done in order to determine the pathophysiology and fate of Pseudomonas aeruginosa in the chronic CF sufferer’s lungs. Whether it is the adaptability of the bacteria in the lungs or a result of competition against neighboring bacterial cells of their own species remains to be seen.
A therapeutic key to this condition can also be found out if the mutations of the global regulation factors in the bacterial genome are studied.