Molly Kenner had suffered from persistent respiratory symptoms since she was a young child. Her family physician originally diagnosed her with asthma, complicated by bronchitis and pneumonia, and prescribed anti-allergy medicines, antibiotics, and steroid inhalers. This therapy worked for a few months, but eventually her symptoms of coughing, chest pain, and congestion would return. On many occasions she was ill enough to require hospitalization and a breathing machine. This cycle went on for several years. By the time she was in her twenties, her lungs showed signs of permanent damage and she often struggled to breathe. As her quality of life continued to decline, her family and friends urged her to seek more expert medical intervention with a lung specialist at a university teaching hospital. Based on her history, a physician at the clinic ordered a lung biopsy and chest X-rays. Samples of her lung tissues grew a pure culture of Pseudomonas aeruginosa, described as gram-negative bacillus with a single flagellum and noticeable blue-green pigment. The species is extremely flexible in its environmental and nutritional requirements. Although its usual habitat is soil, water, and plant matter, it is frequently isolated from skin and other regions of the human body. It occasionally causes infections, especially in those with weakened host defenses, but it is not generally pathogenic to healthy individuals.

Molly’s doctor immediately understood the significance of this finding, because the lungs are ordinarily supposed to be sterile and do not harbor a resident microbial population. Yet here was direct evidence of a massive infection developing as large nodules and patches throughout the lungs. The combination of her history and the isolation of this particular species were powerful clues in understanding the real basis of Molly’s medical condition. The specialist immediately ordered a genetic test that came back as positive for a disease called cystic fibrosis (CF). Cystic fibrosis is a recessive disorder caused by a mutation in a gene called the CFTR or cystic fibrosis transmembrane receptor gene. The normal, nonmutated gene codes for a protein that controls the active transport of chloride across epithelial cells. Chloride helps to maintain the liquid content of the mucous coating of lung membranes needed eudnmnnas by the natural host defenses to maintain lung health. Because Molly inherited a defective CFTR gene from each parent, her cells cannot secrete a sufficient amount of chloride into the lung tissues. As a result, the mucus becomes thick and tenacious and creates a specialized habitat that supports the long-term establishment of P. aeruginosa.

Required:
a. What terms from the chapter would you use to describe the natural habitat, biochemical characteristics, and ecological niche of Pseudomonas aeruginosa?
b. What sorts of adjustments would P aeruginosa have to make in adapting successfully to the human lung?