Comments on: Disease by coincidence – why we’re caught in the crossfire of a hidden war http://blogs.discovermagazine.com/notrocketscience/2010/08/16/disease-by-coincidence-why-were-caught-in-the-crossfire-of-a-hidden-war/ Mon, 26 Nov 2012 12:00:51 +0000 hourly 1 http://wordpress.org/?v=3.4.2 By: gillt http://blogs.discovermagazine.com/notrocketscience/2010/08/16/disease-by-coincidence-why-were-caught-in-the-crossfire-of-a-hidden-war/#comment-8854 gillt Fri, 20 Aug 2010 21:36:25 +0000 http://blogs.discovermagazine.com/notrocketscience/?p=2380#comment-8854 Ed: "When Salmonella enterica, another food poisoning germ, is threatened by amoebas, it ends up with more genetic variation at a part of its genome that affects how virulent it is." Do you mean to say "Salmonella in close proximity to amoebas have more genetic variation [...] than ones that aren't threatened by amoebas"? Because it sounds like you're saying amoebas give off some signal that directly affects the genome of nearby Salmonella, which would be weird. Ed: “When Salmonella enterica, another food poisoning germ, is threatened by amoebas, it ends up with more genetic variation at a part of its genome that affects how virulent it is.”

Do you mean to say “Salmonella in close proximity to amoebas have more genetic variation [...] than ones that aren’t threatened by amoebas”?

Because it sounds like you’re saying amoebas give off some signal that directly affects the genome of nearby Salmonella, which would be weird.

]]> By: sittingoverhere http://blogs.discovermagazine.com/notrocketscience/2010/08/16/disease-by-coincidence-why-were-caught-in-the-crossfire-of-a-hidden-war/#comment-8853 sittingoverhere Tue, 17 Aug 2010 03:00:54 +0000 http://blogs.discovermagazine.com/notrocketscience/?p=2380#comment-8853 Apparently there is a suggestion that the S. aureus Vs. S epidermidis battle is also (that you have written about here earlier) may have induced virulence in S. aureus as it searches for a new niche to occupy. Also pneumo has another trick. Whilst producing a thicker coat it can also upregulate surface proteins that bind host factor H. Host factor H is one of the molecule the host uses to distinguish self from non-self. The bacteria essentially put on a host cell 'suit' and say "don't look at me! You're looking for that guy" and the Haemophilius' trick can backfire. Apparently there is a suggestion that the S. aureus Vs. S epidermidis battle is also (that you have written about here earlier) may have induced virulence in S. aureus as it searches for a new niche to occupy.
Also pneumo has another trick. Whilst producing a thicker coat it can also upregulate surface proteins that bind host factor H. Host factor H is one of the molecule the host uses to distinguish self from non-self. The bacteria essentially put on a host cell ‘suit’ and say “don’t look at me! You’re looking for that guy” and the Haemophilius’ trick can backfire.

]]> By: lucas http://blogs.discovermagazine.com/notrocketscience/2010/08/16/disease-by-coincidence-why-were-caught-in-the-crossfire-of-a-hidden-war/#comment-8852 lucas Mon, 16 Aug 2010 21:54:19 +0000 http://blogs.discovermagazine.com/notrocketscience/?p=2380#comment-8852 Wow, I find the hypothesis that virulent strains are pathogenic as a necessary consequence of other adaptations really intriguing. It makes sense, the more I think of it. With all the bacteria and other microscopic lifeforms out there, there's bound to be some of them that 'interact' with us in unforeseen (and unintentional, from their perspective) ways. My only minor point of critique is that the team used a strain was known to be pathogenic to test their hypothesis. It would've been way more cool and convincing if they had artificially selected E. coli cells from a non-pathogenic strain that were able to resist the attacks of <i>Dictyostelium</i>, and show that this strain is more harmful for mice or capable to better resist macrophages. Wow, I find the hypothesis that virulent strains are pathogenic as a necessary consequence of other adaptations really intriguing. It makes sense, the more I think of it. With all the bacteria and other microscopic lifeforms out there, there’s bound to be some of them that ‘interact’ with us in unforeseen (and unintentional, from their perspective) ways.
My only minor point of critique is that the team used a strain was known to be pathogenic to test their hypothesis. It would’ve been way more cool and convincing if they had artificially selected E. coli cells from a non-pathogenic strain that were able to resist the attacks of Dictyostelium, and show that this strain is more harmful for mice or capable to better resist macrophages.

]]>