March 20th, 2008 ecoli
Helicobacter pylori is a fascinating bacteria with an interesting historical timeline. The Microbiology Blog ran a little segment on it, to announce an upcoming book, and I thought I’d add to the story.
Back in the days before 1979, stomach ulcers were blamed entirely on spicy food and stress. People that came down with ulcers or gastritis were put on a bland diet of oatmeal and soft foods like that.
Enter Australian pathologists, Robin Warren and Barry Marshall. They successfully isolated and cultured H. pylori from mucosal linings of the stomach specimens. They suggested that it was H. pylori in fact, and not diet, that was the direct agent of stomach ulcers and gastritis.
Initially, the response of the scientific community was skepticism. The consensus was that no organism could survive the high acidity of the stomach (pH 2). However, in an astonishing experiment, they proved the entire scientific community wrong.
Dr. Marshall drank H. pylori cultures, subsequently developing gastritis and the organism was recovered from his stomach lining. After ten days, an endoscopy was taken proving his symptoms were, in fact, gastritis and that H. pylori was present. He then treated himself with bismuth salts and Metronidazole, antibiotics to anaerobic organisms. They went on to show antibiotics as an effective treatment for many clinical cases of stomach ulcers.
To make the case even more interesting, in turned out, from later DNA sequencing data, this organism represented an entirely new genus of bacteria. Of which, several other species were discovered in other mammals and birds.
For their work and obvious dedication to ‘hands on’ experimentation, Warren and Barry received the 2005 Nobel Prize in medicine.
*disclaimer: drinking bacterial cultures will not necessarily garauntee a Noble Prize, though if you’re really desperate, it might be worth a try*
Posted in medicine, microbiology | 1 Comment »
March 18th, 2008 ecoli
Original ideas that categorized filamentous bacteria as the stressed and dying members of a population are apparently wrong. This is not a terribly unusual finding since scientists are always correcting ideas; assigning roles to presumably defunct systems and finding mechanisms for what were thought to be random processes.
Filamentation in bacteria occur when the cell continues to grow after its chromosomes have been copied, but the cell doesn’t divide. Filamentous cells are characterized by their elongated shape, which can be 10-50 times longer than normal. Certain bacteria have genes that encode proteins which can make alterations to cell length for the purpose of becoming filamentous, but random mutations can cause deletions in components controlling cell division with a similar affect.
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Posted in evolution, microbiology | No Comments »
February 6th, 2008 ecoli
Enterotoxigenic E. coli is a scary bug that makes people sick. Immuno-naive people, tourists, children and the elderly in third would countries mostly.
I am working with the ‘alternate’ chaperone usher pathway of CS1 pili in ETEC. It’s known as the alternate pathway because its functionally similar but genetically distinct from the ‘classic’ PAP pathway that we all know and love.
The original thinking is that this is an example of convergent evolution, since there is no homology, as far as we can tell between the two systems. And, until now, it was thought that the subunit interactions ran on slightly different mechanisms.
My project is trying to show that the chaperone-usher interaction is like that of the PAP pathway, showing that this actually a case of ancient divergence rather than convergence.
If I can do that, it could help elucidate a new model of infection for ETEC. w00t.
I don’t have any significant results yet, but I’m presenting my proposal and preliminary work to my lab group on Friday, and am currently working on my presentation. I’ll probably upload it to this blog upon it’s completion. Expect to be kept updated on my project and its results.
ecoli out.
Posted in microbiology, my research | 2 Comments »
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