I was hoping to write this during the conference, but every talk I went to was really interesting and I ended up not using that time for blogging. However, there is at least one talk that I wanted to mention before I forgot to much.
I thought the most interesting talk was from Kim Lewis, who describes "persistor cells" as those bacteria that lay dormant in a population. These persistors are resistant to antibiotics because they are essentially shut down and passivly allow antibiotics to simply wash over them as opposed to normal bacteria cells that actively block or pump out antibiotics. Lewis also showed that late samples taken from cystic fibrosis patients had high levels of persistor cells. Kim then discussed unculturable bacteria (of which 99% of bacteria are) and suggested that when plated on media that these are actually dormant and not dead. To support this Kim showed that by innoculating an unculturable sample with E.coli caused growth of an unculturable strain around the E.coli spot. He later found a mutant that did not cause the effect and identified the key gene to be a sideophore. Lewis ends with this little tidbit, "Dormancy is the default mode of bacterial life". I find this really interesting because it suggests that most bacteria depend on a few bacteria to signal when their surrondings are optimal for growth.
There are a couple of more talks that I hope to blog about in the next day or two.
Thats really interesting.. My friend Satish was just explaining to me how one of the main problems in combatting HIV is viral dormancy. How to find it and destroy it if is just sitting in some tissue somewhere waiting quietly to come out ? Are there medical implications of bacterial dormancy as well ?
obviously there are .. let me rephrase.. Did the talk give any ideas about how to deal with the problem in medical scenarios ?
No, there wasn't any questions about possible ways to combat dormant bacteria, but I'm sure most people were thinking about it. I think one of the big questions is if all bacteria use a common or similar pathway to cause dormancy? If so, then we could possibly start targeting this pathway for drug development to eliminate these persister cells which in combination with antibiotics would be more effective.
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