Pseudomonas aeruginosa
Pseudomonas aeruginosa doesn't attack immediately.
Pseudomonas aeruginosa doesn't attack immediately. At low population density in a wound or lung, it stays silent - producing no toxins, revealing no presence. Triggering the immune system early would get the bacteria cleared before they could establish a foothold. Instead, P. aeruginosa waits, using chemical quorum sensing to count its neighbors. Only when population density reaches critical mass do two signaling systems (las and rhl) simultaneously activate genes for elastase, exotoxin A, pyocyanin, and rhamnolipids. The coordinated assault overwhelms immune defenses that would have easily contained a small population.
This strategic timing has a second layer: hypermutation. In the chronic infections of cystic fibrosis lungs, 20-40% of P. aeruginosa strains are hypermutators with broken DNA repair genes, generating new mutations 100-1,000× faster than normal bacteria. This mutator phenotype enables rapid evolution of antibiotic resistance under constant selective pressure. The organism demonstrates two business principles: strategic timing of resource-intensive activities (attack only when you have critical mass), and adaptive mutation rates (increase variation when environment shifts rapidly, like antibiotics cycling through a hospital).
Notable Traits of Pseudomonas aeruginosa
- Coordinated virulence factor production
- Biofilm formation
- Antibiotic resistance through coordination
- 20-40% of strains in CF lungs are hypermutators
- Defective mutS/mutL DNA repair genes increase mutation rates 100-1000x
- Rapidly evolves multi-drug antibiotic resistance
- Forms biofilms that protect against immune response and antibiotics
- Uses two quorum-sensing systems (las and rhl) with distinct autoinducers
- Delays virulence factor production until quorum reached
- Major cause of hospital-acquired infections and cystic fibrosis complications
- Biofilm formation regulated by quorum sensing
- Human blood serum contains paraoxonases that degrade its autoinducers
Pseudomonas aeruginosa Appears in 3 Chapters
P. aeruginosa uses quorum sensing to coordinate virulence. At high density, bacteria produce toxins en masse, overwhelming immune defenses. They also form biofilms 100-1,000× more antibiotic-resistant than individual cells.
Learn about quorum sensing coordination →In CF patients' lungs, 20-40% of P. aeruginosa strains are hypermutators with defective DNA repair, generating mutations 100-1000x faster - demonstrating how high mutation rates are favored under constant selective pressure.
Explore adaptive mutation rates →P. aeruginosa delays virulence factor production until population density is high enough to overwhelm host defenses. Two quorum-sensing systems (las and rhl) coordinately activate elastase, exotoxin A, pyocyanin, and rhamnolipids.
Discover strategic timing through quorum sensing →