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Re: bacteria like a villainous shape-shifter

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Penny,

You're welcome.I'm not sure if that URL will remain active, so I'll

just post the article:

Reported June 18, 2007

Bacteria Sneaks and Hides in Cells

(Ivanhoe Newswire) -- Researchers have found Staphylococcus aureus

bacteria may elude the immune system by sneaking into cells and

hiding out to avoid detection.

Researchers from University Hospital of Geneva in Switzerland and the

Institute of Food Research in Norwich, UK, embarked on a study to

find out just what S. aureus does in human lung epithelial cells. S.

aureus is a major cause of human and animal infections.

Just like a villainous shape-shifter, shortly after S. aureus entered

the lung cells, researchers found the bacteria's gene expression

profile changed dramatically. They found the gene expression for

bacterial metabolic functions and transport actually shut down,

leaving the infectious bug in a dormant state. At the same time,

researchers discovered the production of toxins that can kill

epithelial cells became strictly controlled to limit cell damage.

Then, the mechanisms that help the bacteria survive resumed.

Results of the study could pave the way to a better understanding of

these types of infections as well as help researchers come up with

better antibacterial drugs to fight them. It could also help them

better understand what goes on at the molecular level that makes S.

aureus so persistent. Researchers say the bacteria can re-surface and

cause another infection years after the initial episode was " cured. "

Patrice Francois, from University Hospital in Geneva, was quoted as

saying, " S. aureus intracellular survival appears related to its

capability to adopt a discrete behavior instead of actively

duplicating. S. aureus then benefits from natural or programmed cell

death to re-emerge and trigger another episode of infection, leading

to chronicity. "

This article was reported by Ivanhoe.com, which offers Medical Alerts

by e-mail every day of the week. To subscribe, click on:

http://www.ivanhoe.com/newsalert/.

SOURCE: BMC Genomics, June 14, 2007

> http://tinyurl.com/3c9c8u

>

> Roy

>

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Weird thing about this paper is that they mention in the intro how

staph can either escape from the endosome of a non-pro-phagocytic cell,

or remain inside it, or escape after a delay. But I don't see any

methods used here (ie, electron microscopy) to find out which one(s) of

those possibilities were occuring in their system - although the

transcriptome does " look " distinctly more like most of the varmints are

endosomal, considering the extreme upregulation of transporters.

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Yeah, that's what I was thinking...;-) penny <usenethod@...> wrote: Weird thing about this paper is that they mention in the intro how staph can either escape from the endosome of a non-pro-phagocytic cell, or remain inside it, or escape after a delay. But I don't see any methods used here (ie, electron microscopy) to find out which one(s) of those possibilities were occuring in their system - although the transcriptome does "look" distinctly more

like most of the varmints are endosomal, considering the extreme upregulation of transporters.

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Yeah, the nutritional status of bacteria inside cells is kind of a

tough thing to study. There's a lot that isn't known and a lot of

details to cover. But generally speaking the endosome/phagosome is

nutrient-poor, and the cytosol nutrient-rich. When the bacterium starts

sythesizing tons of transporters, it looks like it is having a hard

time getting itself fed. Most bacterial transporters are for uptake of

nutrients, though a few may be for excretion of wastes, etc.

> Yeah, that's what I was thinking...;-)

> Weird thing about this paper is that they mention in the

intro how

> staph can either escape from the endosome of a non-pro-phagocytic

cell,

> or remain inside it, or escape after a delay. But I don't see any

> methods used here (ie, electron microscopy) to find out which one(s)

of

> those possibilities were occuring in their system - although the

> transcriptome does " look " distinctly more like most of the varmints

are

> endosomal, considering the extreme upregulation of transporters.

>

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this isn't only for me and penny, everyone on this forum has staphs,

and they also have some form of inflammation regardless of the term

used, rhinosinusitis, or whatever.

Also if you did more than a few swabs you'd definately have a

pseudomonal component to boot.So anything describing why we can benefit

from antimicrobials, yet have an infection persist, is important to us

all.

I tend to feel that if we can buy powdered forms of bacteria, just add

water and gain five billion organisms. we should accept that we can

have infections that persist..

tony

>

>

> The corresponding paper is free and the preprint PDF is at:

>

> http://www.biomedcentral.com/content/pdf/1471-2164-8-171.pdf

>

> Penny and Tony, you might be interested as they mention something

about

> staph and refractory chronic rhinosinusitis.

>

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something else for you to ponder.If people with strep throat (a

nasty bacterium -streptococcus pyogenes) don't normally have a

problem day to day until an inflammation cycle starts.What's going on

in these cases?

tony

>

>

> The corresponding paper is free and the preprint PDF is at:

>

> http://www.biomedcentral.com/content/pdf/1471-2164-8-171.pdf

>

> Penny and Tony, you might be interested as they mention something

about

> staph and refractory chronic rhinosinusitis.

>

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I'm not sure exactly what you mean? What's an inflammation cycle?

I don't know much about S py or strep throat, but I was told in my

Intro Micro lecture (lo these many years ago) that S py can be

isolated from the throats of ~10% of normal people walking around, at

any given time. Why they don't always behave virulently, I don't know.

Whether anyone is permanently colonized, I also don't know. With Staph

aureus, some asymptomatic people are colonized permanently and some

transiently.

> something else for you to ponder.If people with strep throat (a

> nasty bacterium -streptococcus pyogenes) don't normally have a

> problem day to day until an inflammation cycle starts.What's going on

> in these cases?

> tony

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What I'm noticing is that bad bacteria are calm until a set of

circumstances arises to bring out the worst in them.People with bad

strep bacteria do fine until something throws the switch in the

bacteria to make it angry.It's this switchability that's possably

more a problem and by adding more resistant genes to a bacterium your

increasiing it's ability to be switched.

Another way of looking at this is that some bacteria are only found

on there own, possably due to being able to switch on and take out a

competitor. A healthy person wityh no sinus inflammation can have a

harmony of bacteria and fungus's and the cfs people have

pseudonomas , staph areus and staph epi..

Yet another way of looking at this switching is steven johnson

syndrome. Something will annoy the bacterium and they'll throw out a

shit load of toxins that will exfoliate you like a third degree burns

patient.

>

>

> I'm not sure exactly what you mean? What's an inflammation cycle?

>

> I don't know much about S py or strep throat, but I was told in my

> Intro Micro lecture (lo these many years ago) that S py can be

> isolated from the throats of ~10% of normal people walking around,

at

> any given time. Why they don't always behave virulently, I don't

know.

> Whether anyone is permanently colonized, I also don't know. With

Staph

> aureus, some asymptomatic people are colonized permanently and some

> transiently.

>

>

> > something else for you to ponder.If people with strep throat

(a

> > nasty bacterium -streptococcus pyogenes) don't normally have a

> > problem day to day until an inflammation cycle starts.What's

going on

> > in these cases?

> > tony

>

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