Unusual mode of infection of a ubiquitous bacterium
Pseudomona aeruginosa is ubiquitous in nature and is able to thrive on humans, plants, animals, human-made surfaces, and also in water and soil. But how it is able to detect so many types of hosts is a mystery.
A new study conducted by two groups of researchers at Princeton University and Dartmouth College identified the first pathogen to initiate infection by simply attaching itself to host surface, by a sense of touch. This mode of infection is completely different from other pathogens, which depends on “taste,” and triggers a chemical signalling pathway as a response. By their unique sense of touch, P. aeruginosa can equally identify any kind of suitable host and initiate infection in an attempt to kill it. They are lethal and cause organ infections in humans and many hospital-acquired illnesses such as, sepsis. They often become antibiotic resistant too.
The researchers identified only two satisfying conditions for Pseudomonas to start an infection: surface attachment and “quorum sensing,” a common mechanism wherein the organisms detect a large concentration of their kind is present. Recent research revealed a lot about the initiation of infection, particularly via quorum sensing and chemical signals, but the question about how that’s done across a spectrum of unrelated hosts has remained unanswered.
However researchers have identified a protein, PilY1 on Pseudomonas surface. When protein PilY1 was deleted, the bacteria lost virulence and thus were unable to kill the test host, an amoeba. This ecto-protein is a sort of lynchpin for the entire virulence response, opening the door to therapeutic design that specifically disrupts the mechanical cues for activating virulence instead of an attempt to kill the pathogen. Experts think that this idea will become the paradigm in anti-virals and anti-microbials designing in future.
Targeting ecto-proteins offers an avenue for combating the growing problem of antibiotic resistance also. Antibiotic resistance results when a drug kills all of its target organisms, but leaves behind a few, which develops a resistance to the drug. These mutants multiply at a super fast rate and become the dominant strain of the pathogen. Disabling or deleting PilY1obstruct the bacterial infection only. However this do not stop the bacteria to multiply. Thus it would be very unlikely that mutant organisms would be prevalent. Moreover PilY1 is a surface protein and required for virulence, thus it presents a comprehensive and easily accessible target for drug development.
PilY1 is also found in few other bacteria having a wide range of hosts like, Neisseria gonorrhoeae and the genus Burkholderia, which, respectively, cause gonorrhea in humans and are, along with Pseudomonas, a leading cause of lung infection in cystic fibrosis patients. It is quite possible that PilY1 has a similar role in detecting surfaces and initiating infection, and thus could be a treatment target in these cases also.
Surface attachment induces Pseudomonas aeruginosa virulence. A. Siryaporn, S. L. Kuchma, G. A. O’Toole, Z. Gitai. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1415712111
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