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Medical Forum / Diseases and Disorders / Sinusitis / February 2008

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last day on omnicef..

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dolysods@yahoo.com - 16 Feb 2008 21:12 GMT
and i'm still blowing and spitting some green.  Not nearly as
much..but there is still green phlegm. My family doc thought i was
treating it too soon? I don't get it.   Not sure if i spent the money
and went back to urgent care if they would give me another round of
omnicef or not.   I just don't want to get sick again.  I'm still
fatigued.. and until the other day didn't realize that it could
actually becoming from my sinus problems!
Steven L. - 16 Feb 2008 22:49 GMT
> and i'm still blowing and spitting some green.  Not nearly as
> much..but there is still green phlegm. My family doc thought i was
[quoted text clipped - 3 lines]
> fatigued.. and until the other day didn't realize that it could
> actually becoming from my sinus problems!

If you're still having any green phlegm even after completing a full
course of Omnicef, then this bug may be resistant to Omnicef.  It's
possible that another course may do the job, but I doubt it.  Can you
suggest changing to Levaquin or Avelox?  And this time, take those
antibiotics for 3 weeks.

If even that fails, then it may be time to see an ENT.

Signature

Steven L.
Email:  sdlitvin@earthlinkNOSPAM.net
Remove the NOSPAM before replying to me.

dolysods@yahoo.com - 16 Feb 2008 23:28 GMT
> dolys...@yahoo.com wrote:
> > and i'm still blowing and spitting some green.  Not nearly as
[quoted text clipped - 17 lines]
> Email:  sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.

I think i will call my allergist's office on Monday.  My doc retired
but they would be able to refer me to a ENT, or they may even treat
me. I'm just tired of being made to feel... it will run its course.

thanks
truehawk - 16 Feb 2008 23:51 GMT
> dolys...@yahoo.com wrote:
> > and i'm still blowing and spitting some green.  Not nearly as
[quoted text clipped - 17 lines]
> Email:  sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.

The development of resistance has been the reasonable assumption but
the amount of green has greatly diminished, then it is probably not
resistant.
What doctors have not understood is that the bacterial population
produces sleeper cells called persister cells.
These cells suspend respiration and other operations to the point that
antibiotics wash over them, but since they
are not taking up nutrients or dividing, most antibiotics leave them
unscathed.
On the average they remain in stasis about 3 weeks but some are still
in stasis another 10 days longer.
Unless the antibiotic is one that can kill the persister cells, three
weeks is not long enough.

http://www.sciencedaily.com/releases/2004/12/041206213515.htm
http://www.ncbi.nlm.nih.gov/pubmed/14734160
judy.n - 17 Feb 2008 01:24 GMT
> > dolys...@yahoo.com wrote:
> > > and i'm still blowing and spitting some green.  Not nearly as
[quoted text clipped - 33 lines]
>
> http://www.sciencedaily.com/releases/2004/12/041206213515.htmhttp://www.ncbi.nlm
.nih.gov/pubmed/14734160

Elizabeth.
 You are amazing. Your information never ceases to be cutting edge
and completely applicable to the situation.
 My younger daughter is flying to Germany tomorrow--in the midst of
flu season--she had a sinusitis earlier in the month, and our ENT told
her to continue the Augmentin until she gets home, as there was no
point in coming off of it, only partially healed, and provoking her
sinuses with barotrauma/dry air/ evil airplane microbes.
 And now, I understand another reason why sometimes sinusitis feels
like a fire where you never completely get the embers out. It's
biofilms and persister cells. Not a simple situation.
 I always think of tuberculosis and how long we treat new converters:
9 months, because most of the bacteria are in suspended animation.
 I didn't know that other organisms used that trick.
Judy
truehawk - 17 Feb 2008 19:32 GMT
> > > dolys...@yahoo.com wrote:
> > > > and i'm still blowing and spitting some green.  Not nearly as
[quoted text clipped - 49 lines]
>   I didn't know that other organisms used that trick.
>  Judy

Hey Judy:

Admiration back at you.
Presisters documented in staph, e-coli, and psudo, so the gang is all
able to go into suspended animation.
Hope your daughter travels safe and continutes to get better.
judy.n - 18 Feb 2008 12:17 GMT
Elizabeth,
 Unfortunately, she spent the whole day at Logan as the first
connecting flight to DC was cancelled and United couldn't figure out a
way to get them there (even though they were 10 hours early).
Ultimately she ended up in a hotel in DC at midnight. The tour company
doesn't answer their phone, and the professor (chaperone) attempted to
grab a flight to Germany and leave 30 undergraduates behind. What a
nightmare: flying stinks.
 Today, they'll try for the overnight to Germany again.
 She takes azithromycin weekly, and I keep hoping that it's keeping
the bugs at bay, along with the Augmentin.
 She called from the hotel last night, and apologized (like it was
her fault) but said it was essentially a bunch of 19 year olds trying
to figure it out. (I told her to shower and neti....)
 If it was me: I'd have rebooked for the next day and gone home.
 This singing tour company is about as suspect as the "travel abroad"
kick back schemes.
 So, I'm holding my breath/worrying until her return because
yesterday showed just how much support she has from the University/
tour company/airlines. None.
 They were supposed to sing at Dachau tomorrow--a memorial concert.
 I know, if I chill out (impossible) that it's a learning situation,
I just knew that I never liked the whole setup, but she was adamant
about going.
  Sorry to rant, but it's hard to worry about her medical issues
getting triggered by international travel--migraine, sinus, peak flu
season with a worthless flu shot--and then have the airlines be worse
than useless.

 Seriously, Elizabeth, I've been trying to consolidate your posts to
sent to my ENT: he was so intrigued by the tannins. You add
immeasurably to the knowledge base of this group.

Judy
judy.n - 18 Feb 2008 12:22 GMT
Elizabeth:
 Your link to Science daily news brings up an article from 1999 about
biofilms. 1999! Why did I have massive surgery at Mass Eye and Ear in
2000 that left me with pseudomonas osteomyelitis???
 It's almost 10 years later, and biofilms are just addressed.
Judy
Andi - 18 Feb 2008 13:02 GMT
Add another 10 years before that info reaches other countries. I've been
to three ENTs and they had absolutely no clue at all. The guidelines
used here haven't been updated since 1997! So, basically, as insurance
here covers most things, they send everyone to surgery right away
(otherwise I think it's good to have public insurance, but in that
regard you have to be really suspicious about what treatments you get
offered or not).
And little is known about alternative treatments (I've even been to a
university clinic!). So at the moment I have no ENT (again).

I asked the question in another thread but didn't get any replies: do I
have any chance of getting cured by longterm antibiotics? For me, taking
medication indefinitely is not desirable as I can manage my symptoms
without them. It would just be nice to have better sense of smell and no
more discharge from my right nostril.

Andi

P.S.: Taking the Vitamin D3 at the moment, it made a small difference
but no instant cure. I will keep on taking it some more days and will
report back.

> Elizabeth:
>   Your link to Science daily news brings up an article from 1999 about
> biofilms. 1999! Why did I have massive surgery at Mass Eye and Ear in
> 2000 that left me with pseudomonas osteomyelitis???
>   It's almost 10 years later, and biofilms are just addressed.
> Judy
judy.n - 18 Feb 2008 13:14 GMT
> Add another 10 years before that info reaches other countries. I've been
> to three ENTs and they had absolutely no clue at all. The guidelines
[quoted text clipped - 26 lines]
> >   It's almost 10 years later, and biofilms are just addressed.
> > Judy

Andi,
 For me and my family adding low dose, long term macrolides--starting
in 2002, initially based on the work of Anders Cervin and multiple
authors from Japan has made all the difference.
 I've gone from constant infections, to isolated episodes about every
three years. And, I have an immune deficiency (IgG subclass deficiency
of classes 1,3,4) and I work in health care.
 My daughter--22--has gone from constant asthma/sinusits, to no
asthma symptoms and no sinusitis for over a year. (She is IgA
deficient, with celiac)
 Macrolides are anti-inflammatory and disrupt biofilms.
 Common dosages are erythromycin 250mg twice a day, biaxin
(clarithryomcin) 250 mg/ day, azithromycin 250 mg once or twice a
week, and there is a European drug (?) roxithryomycin, that has been
studied extensively and it's a daily dose, but I don't know it off
hand.
 So, long term antibiotics are helpful if they are macrolides (some
thought that the tetracyclines may be helpful as well--long term
doxycyline ) and at low doses.
 Caveat: it takes a few months for the macrolides to really begin to
work.
 They work best on people with low IgE levels.
Judy
blades49456 - 18 Feb 2008 16:17 GMT
I recall an employees nine year old with constant sinusitis.  It took
nine months of antibiotics (don't recall which one) to be rid of the
problem.

Bruce

> Andi,<snip>
>   Caveat: it takes a few months for the macrolides to really begin to
> work.
>   They work best on people with low IgE levels.
> Judy
truehawk - 18 Feb 2008 19:15 GMT
> I recall an employees nine year old with constant sinusitis.  It took
> nine months of antibiotics (don't recall which one) to be rid of the
[quoted text clipped - 7 lines]
> >   They work best on people with low IgE levels.
> > Judy

Bruce:
Sounds about right.

Judy:
Doctor Couch published a paper in 1980 about the link between staph
infections and the flu.
I believe that he lost funding to AIDs research.
Then Montana State began to do work in biofilms,  but even Bill
Costerson, when I talked to him,  did not know that staph uses fibrin
for it's biofilm, or that about the bacteria makeing beta amyloid.
When I talked to ENTs their story was that biofilms were only seen on
implants. That was their story and they were sticking to it.
When I suggested that they take a look at tissue samples surgically
removed from CS sufferers they ask for 100K to write a proposal to the
human experiment committee to get permission to do that. Now remember
that I was not suggesting that they remove samples just to look at
them, but rather use tissue samples already in the archives.
I decided that I had better try to get the word out when I discovered
that the biofilm lab at the CDC had been absorbed into something
else.
I was delighted when Sanderson reported his work at the Naval Hospital
at San Diego. I would have thought that it's results would have been
shouted from the rooftops, but the signal gets lost in the noise.

Thousands of articals talking about inflammation and an allergic
etiology  and only about 30 talking about biofilms. Even over at
Wikipedia the medical students that hold sway in the sinusitis entry
won't let biofilms be posted as the cause of sinusitis because
according to the rules, Wikipedia must reflect the consensus, and the
baby docs are not being taught that biofilms are the root cause behind
most sinusitis, so they quickly edit out the biofilm entries because
do not represent the consensus.
That is what it comes down to, provable reality, with a cure at the
end, against consensus that the disease has no cure but  surgery every
three years.
Meanwhile the Soviets routinely use phages against staph with great
efficacy , and I would love to know their incidence of sinusitis.
The FDA will not let the phages into the country, even though we used
to have our own and they predate antibiotics as a therapy. (Anyone
ever hear of Pastur or read Arrowsmith?)  Nope the American public has
to be protected from antistaph phages so that they can have Trasylol
used on them.

Links
   Bacterial biofilms on the sinus mucosa of human subjects with
chronic rhinosinusitis.
   Sanderson AR, Leid JG, Hunsaker D.

   Department of Otolaryngology, Naval Medical Center San Diego, San
Diego, California 92134-2200, USA. arsanderson@nmcsd.med.navy.mil

   INTRODUCTION: Chronic rhinosinusitis (CRS) is a common disease
poorly controlled by antibiotics. Postulated etiologies of CRS include
allergy, fungi, functional factors, and biofilm. OBJECTIVES: We
presented a preliminary study demonstrating bacterial biofilms'
presence on the sinus mucosa of patients with CRS using fluorescent in
situ hybridization (FISH). The advantage of FISH in biofilm
identification is that it is the only method that identifies the
specific bacteria creating the biofilm matrix. We now present the
results of a larger series of patients. METHODS: Patients with CRS
scheduled for sinus surgery were enrolled in the study. Biopsies of
the sinus mucosa and cultures were taken at the time of surgery.
Control samples were taken from patients undergoing septoplasty.
Specimens underwent FISH testing for Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilus influenza, and Pseudomonas
aeruginosa. RESULTS: Bacterial biofilms were present on 14 of 18
specimens. The predominant species were H. influenzae, S. pneumoniae,
and S. aureus. P. aeruginosa biofilm was not identified on any
specimens. The intraoperative cultures of the planktonic bacteria
present in the sinuses did not correlate with the biofilms identified.
Two of the five control samples were positive for biofilm. CONCLUSION:
The presence of biofilms on the mucosa of patients with CRS offers a
possible cause of antimicrobial therapy failure and could change the
approach to treatment. However, the presence of biofilms on healthy
control samples implies that biofilms may simply be colonizers. The
precise role that biofilms play in CRS still remains to be determined.
Further studies with larger sample sizes are needed.

   PMID: 16826045 [PubMed - indexed for MEDLINE]

That two of the controls had biofilms does not mean that biofilms
don't cause sinusitis, but rather that it take some time for the
biofilm to accumulate, be thick enough and cover enough area for a
patient to become symptomatic. The control biofilms have quite likely
not yet acquired the bacterial strains that more aggressively express
toxins and cause more PND.
Every cc that you breath contains 2000 bacteria that normally can not
attach to the lining of the sinuse, but a biofilm is a welcome mat. A
biofilm makes every breath a gamble as to who is going to come to
dine.
judy.n - 18 Feb 2008 20:36 GMT
> > I recall an employees nine year old with constant sinusitis.  It took
> > nine months of antibiotics (don't recall which one) to be rid of the
[quoted text clipped - 98 lines]
> biofilm makes every breath a gamble as to who is going to come to
> dine.

Elizabeth,
 Doing a pubmed search: "biofilms + sinusitis": I found Anders Cervin
just published again on macrolides:
http://www.ncbi.nlm.nih.gov/pubmed/18085018?ordinalpos=2&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

: Rhinology. 2007 Dec;45(4):259-67.Links
Macrolide therapy of chronic rhinosinusitis.

Cervin A, Wallwork B.
Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Lund
University, Sweden. anders.cervin@med.lu.se
There is growing evidence that several antibiotics exert their
beneficial effect not only by inhibiting or killing bacterial
pathogens but also by down-regulating pro-inflammatory mechanisms.
This review aims to give an overview of the immunomodulatory
properties of macrolide antibiotics in chronic rhinosinusitis and to
present a treatment algorithm for managing the difficult CRS patient
with long-term, low-dose macrolide antibiotics. The most prominent
effect of macrolides noted in vitro is the inhibition of pro-
inflammatory cytokines such as interleukin-8. This effect is probably
secondary to inhibition of the activation of transcription factor NF-
kappaB. As a result an attenuation of neutrophilic inflammation takes
place. Moreover, macrolides inhibit bacterial virulence and biofilm
formation. In vivo, a reduction of pro-inflammatory cytokines is
evident in nasal lavage as well as a reduction in nasal secretions.
The clinical effect is shown in less facial pain, less headache, less
post nasal drip, fewer exacerbations of sinusitis and improved quality
of life. The treatment should be targeted towards the non-atopic
patients with bilateral disease whereas in unilateral disease, surgery
is the first option. Macrolide resistant bacterial strains have to be
monitored, but to date they have not been of clinical importance.
PMID: 18085018 [PubMed - indexed for MEDLINE]

I want to highlight the last line: macrolide resistance has not been
important and inhibition of biofilm formation is important.

Per Wikepedia and concensus statements: here's one. I teach medical
students, and they are the last people to look to for the final word--
not that they aren't great to work with, but experience is important.

http://www.ncbi.nlm.nih.gov/pubmed/17415138?ordinalpos=1&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusDrugs1


Laryngoscope. 2007 Apr;117(4):668-73. Links
Biofilms in ear, nose, and throat infections: how important are they?

Vlastarakos PV, Nikolopoulos TP, Maragoudakis P, Tzagaroulakis A,
Ferekidis E.
ENT Department, Hippokrateion General Hospital of Athens, Athens,
Greece. pevlast@hotmail.com
BACKGROUND: Biofilms present a new challenging concept in sustaining
chronic, common antibiotic-resistant ear, nose, and throat (ENT)
infections. They are communities of sessile bacteria embedded in a
matrix of extracellular polymeric substances of their own synthesis
that adhere to a foreign body or a mucosal surface with impaired host
defense. The aim of this paper is to review the literature on ENT
diseases that can be attributed to biofilm formation and to discuss
options for future treatment. MATERIALS AND METHODS: Literature review
from Medline and database sources. Electronic links and related books
were also included. STUDY SELECTION: Controlled clinical trials,
animal models, ex vivo models, laboratory studies, retrospective
studies, and systematic reviews. DATA SYNTHESIS: Biofilm formation is
a dynamic five-step process guided by interbacterial communicating
systems. Bacteria in biofilms express different genes and have
markedly different phenotypes from their planktonic counterparts.
Detachment of cells, production of endotoxin, increased resistance to
the host immune system, and provision of a niche for the generation of
resistant organisms are biofilm processes that could initiate the
infection process. Effective prevention and management strategies
include interruption of quorum sensing, inhibition of related genes,
disruption of the protective extrapolymer matrix, macrolides
(clarithromycin and erythromycin), and mechanical debridement of the
biofilm-bearing tissues. With regard to medical indwelling devices,
surface treatment of fluoroplastic grommets and redesign of cochlear
implants could minimize initial microbial colonization. CONCLUSION: As
the role of biofilms in human infection becomes better defined, ENT
surgeons should be prepared to deal with their unique and tenacious
nature.
PMID: 17415138 [PubMed - indexed for MEDLINE]

There were lots more articles and systemic reviews.
Now, we just have to figure out an effective and non toxic way of
removing them and keeping them at bay.

Here's a reference for macrolides disrupting biofilms:
http://www.ncbi.nlm.nih.gov/pubmed/17254499?ordinalpos=14&itool=EntrezSystem2.PE
ntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Curr Infect Dis Rep. 2007 Jan;9(1):7-13.Links
Macrolide immunomodulation of chronic respiratory diseases.

Healy DP.
College of Pharmacy, University of Cincinnati Medical Center and
Shriners Hospitals for Children, 3225 Eden Avenue, P.O. Box 670004,
Cincinnati, OH 45267-0004, USA. daniel.healy@uc.edu.
Important immunomodulatory properties of 14- and 15-membered
macrolides may benefit patients with respiratory diseases associated
with chronic inflammation. These properties include decreased
neutrophil chemotaxis and infiltration into the respiratory
epithelium, inhibition of transcription factors leading to decreased
proinflammatory cytokine production, downregulation of adhesion
molecule expression, inhibition of microbial virulence factors
including biofilm formation, reduced generation of oxygen-free
radicals, enhanced neutrophil apoptosis, and decreased mucus
hypersecretion with improved mucociliary clearance. Chronic, low-dose
macrolides have dramatically improved survival in patients with
diffuse panbronchiolitis (DPB). Given the overlap in pathogenesis
between DPB and other chronic respiratory diseases, macrolides are
being investigated for cystic fibrosis, asthma, chronic bronchitis,
chronic sinusitis, and chronic obstructive pulmonary disease.
Preliminary data (largely from open-label trials) are promising, but
conclusive results are needed.
PMID: 17254499 [PubMed - in process]
"inhibition of microbial virulence factors including biofilm
formation"

Tannins, surfactant, macrolides, topical bactroban: these all seem to
be options at this point.

Judy
dolysods@yahoo.com - 18 Feb 2008 21:07 GMT
Went to the allergist today.. not sure why i never went to them when
i've had issues.  My doc retired and i saw a new doctor.  He said
since i had shown improvement on the Omnicef he wanted to continue
that.  I have 14 more days, rx for the diflucan and he gave me a
steroid shot. That in itself should help the swelling in my face.  He
said to continue with the sinus wash

Keeping my fingers crossed!
judy.n - 18 Feb 2008 22:45 GMT
On Feb 18, 4:07 pm, dolys...@yahoo.com wrote:
> Went to the allergist today.. not sure why i never went to them when
> i've had issues.  My doc retired and i saw a new doctor.  He said
[quoted text clipped - 4 lines]
>
> Keeping my fingers crossed!

The steroids make sense: I've used a short course of oral steroids
with a bad infection and it has helped: question--what swelling in
your face? Why the diflucan (candida?)
I've run to my allergist when I'm sick--and he's been great. He's
pulling back from practice, and it's rough not to count on him. A
couple of years ago I got the flu and he refused to treat me over the
phone: good thing--he did a chest xray, rapid flu (negative), blood
serology for flu (positive) and uncovered the IgG deficiencies. He's a
thorough guy. And he put me on antibiotics and steroids.
 I hope you continue to wipe out those persister bacteria.
Judy
truehawk - 18 Feb 2008 22:59 GMT
> On Feb 18, 4:07 pm, dolys...@yahoo.com wrote:
>
[quoted text clipped - 18 lines]
>   I hope you continue to wipe out those persister bacteria.
> Judy

"Per Wikepedia and concensus statements: here's one. I teach medical
students, and they are the last people to look to for the final word--
not that they aren't great to work with, but experience is important.
"

I quite agree, but the little pests keep editing my biofilm references
down to zero, and slamming me for pushing a
POV, Point of View. I would aver that experiment is important.
If the pups would drag themselves and some samples over to the e-scope
lab they could easily see for themselves if they have the skills. I
gather they would rather talk than go through the hassle of arranging
to look.
dolysods@yahoo.com - 20 Feb 2008 13:33 GMT
> On Feb 18, 4:07 pm, dolys...@yahoo.com wrote:
>
[quoted text clipped - 18 lines]
>   I hope you continue to wipe out those persister bacteria.
> Judy

The diflucan is for the impending yeast infection. I had a really bad
one the first 10 days.  I'm eating some yogurt and taking my ultra
flora.  The steroid shot has given me some energy and taken noticeable
swelling down in my face.  It feels like it is still there but others
do not see it. Only bad thing about the shot.. i'm waking up every
1.5-2 hours during the night.  I'm trying to get some rest but it is
getting hard.  Still irrigating

Tracey
truehawk - 20 Feb 2008 20:49 GMT
> > On Feb 18, 4:07 pm, dolys...@yahoo.com wrote:
>
[quoted text clipped - 30 lines]
>
> - Show quoted text -

Fungus never passes up an easy meal.
( actually I have never seen candida, but pleanty of white, black,
green and red fungus.)
The only good thing is that most of them don't seem to do well at
temperatures above about 80 F or so
which confines them to the cooler parts of your nose and sinuses. They
are well and truely a pest none the less.
Some are adapted to higher temperatures though. Hopefully you won't
run into one of those strains.
Murray Grossan - 19 Feb 2008 06:40 GMT
On 2/18/08 11:15 AM, in article
311b1474-8f4d-41c9-9ec5-617a38d36dce@d4g2000prg.googlegroups.com, "truehawk"

> Bill
> Costerson, when I talked to him,  did not know that staph uses fibrin
> for it's biofilm, or that about the bacteria makeing beta amyloid.
Not sure when you spoke to him or perhaps you misunderstood. That was the
subject of his presentation in Jnauary. This year.
truehawk - 20 Feb 2008 03:09 GMT
> On 2/18/08 11:15 AM, in article
> 311b1474-8f4d-41c9-9ec5-617a38d36...@d4g2000prg.googlegroups.com, "truehawk"
[quoted text clipped - 6 lines]
> Not sure when you spoke to him or perhaps you misunderstood. That was the
> subject of his presentation in Jnauary. This year.

That is wonderful!!
I am glad to know that he is well.

I e-mailed Bill Costerson when he was at the Center for Biofilm
Engineering to that effect around Feb of 2002 right after I read Scott
Hutlgren's work.

http://www.sciencedaily.com/releases/2002/02/020201080207.htm.

Hutlgren's full artical was a thing of beauty and was
published in Science Mag.
I had been trying to determine the exact nature of my chokeing snot,
and I was pretty sure that it never saw the inside of a goblet cell.
Looked like egg white, or the stringers of blood where they do a
coagulation test. Engineers do mass and energy balances and the only
place that that protein could be coming from was me, and the likely
source in me would be blood plasma fibrin which contains pretty much
the same number of Daltons as bets amyloid. Why manufacture amyloid to
hold on with if all they had to do was fold a readily available
protein from the wound into a new shape?

JW replied at that time that the biofilm was a polysacride.
I e-mailed back to him that I had perhaps the dubious advantageous of
having readily available
a lot of sample material to work with (my own) and that I found that
part of it readily takes up
congo red and looks apple green under ultraviolet light, and is not
digested by amylese
so I was pretty sure that it was bacterial amyloid protein, much like
that produced by e-coli or cave glow worms,
and that considering the quantity produced in a day, it was likely
derived from plasma fibrin catalyzed to amyloid.
I also wrote that I believed that the soluble beta amyloid in the
sinuses is a probable source of the amyloid in the
brain, since the immune system begins to clear amyloid in the presence
of drugs that shut down the blood/brain barrier, and Alzheimer's is
associated with a leaky blood brain barrier, something  that staph
engineers with Hyaluronidase, only it does not invade, it just sits
there bungeed on the surface where the immune system can't get at it,
and eats what leaks out of the blood vessels that it has caused to
leak.
He did not reply further.
truehawk - 20 Feb 2008 04:31 GMT
> > On 2/18/08 11:15 AM, in article
> > 311b1474-8f4d-41c9-9ec5-617a38d36...@d4g2000prg.googlegroups.com, "truehawk"
[quoted text clipped - 49 lines]
> leak.
> He did not reply further.

I also had an e-mail correspondence with Philip M. Tierno in 2002. He
did not know biofilms existed, much
less that they produced fibin goo. I also e-mailed Hutlgren, who was
doing work on the urinary tract to ask him
to look in the sinuses, and e-mailed back and forth with one of his
grad students, who did not know that quinine's main mode of action it
to shut down pili expression.  And I e-mailed the guy what's his face,
that is privately funded to examine the brains of deceased
schizophrenics looking for signs of bacterial proteins. (he was
finding clymidia antibodies, but I was not that sure that they were
that clymidia specific. I told him while he was in the neighborhood,
he should take a look a what was in their sinuses. (Since then
toxoplasmosis, actually more associated with undercooked meat than
cats, has been shown to cause at least some cases of schizophrenia,
and outright dementia in AIDs patients.) And I wrote to my
congressman, and the wife of my foster brother who is also in
congress, and 60 minutes, and the guy in the Howard Hughes Foundation
that runs the community(of bacteria) genome project where they look
for genes in a community rather than depending on culturing species
when 95-99% refuse to grow in culture. No one has looked at the
community genome of the sinus mucus and biofilm of CS sufferers and
compared it to those without CS.  And others that I can't remember
right now.

If fact I have campaigned long and hard to get them to look at what is
really in the in the sinuses.
You could say that I have been ignored (seemingly) by some of the best
minds in the business.
But then i am just an engineer with a sinus condition, good bone and
no blockage in my sinuses, just stuff stuck there on the CAT scan, and
heart burn and nausa if the sinusitis is not being treated, suddenly
high blood pressure, a perfectly healthy immune system, no allergies
to speak of and a swallowing apparatus with no pathology, and a
constant slightly elevated temperature and no energy compared to what
I used to have.

I am a metallurgist. I already knew what bacterial biofilms that
organize to dine on iron pipes looked like.  It was not much of a
stretch to look for them in my sinuses and then try to get the medical
community to realize what is there. Jeff Goldblum's character in
Jurassic Park says the line "Life will find a way."  The life in my
sinuses has found a way to live there and return as a pest for 8
years. My campaign to effect a paradigm shift to the biofilm model of
sinusitis is my life finding a way of curing this morbid condition, by
directing the tremendous resources and potential intelligence of the
medical community who can do things that I legally can't, toward the
real cause of the problem rather than considering the sinuses sterile,
as they did when I started,  and chasing each symptom  as a separate
entity when  they can all be accounted for by the bacteria. (and fungi
and actinomycetes. (i was watching a discovery channel piece on
Tyrannosauri and the comment was made that the holes in the jaw area
of Sue's skull had likely been made by actinomycetes, sinusitis in
Cretaceous Park)). I am confident that once the puppy docs quit
chasing butterflies, and their tails, and get on the scent, cure
should follow soon and become routine in 4 or 5 years,, gallium,
phages, bromides. Some combination of treatments, there is hope guys,
but you have to push.  I think that Couch at the CDC pretty much had
it figured out in the early 80s but he lost funding to AIDS research
and retired. Soon there will be a cure if we don't let it get
sidetracked.
Till then we have to share knowledge, question bull, and survive as
best we can.
judy.n - 20 Feb 2008 12:43 GMT
Soon there will be a cure if we don't let it get
sidetracked.
Till then we have to share knowledge, question bull, and survive as
best we can.

Elizabeth,
 You share wonderful knowledge, and persevere in the face of
scientific disinterest. It does give me hope when you explain the
biofilm, document it, and share some information about disrupting it.
Judy
truehawk - 21 Feb 2008 06:34 GMT
> Soon there will be a cure if we don't let it get
> sidetracked.
[quoted text clipped - 6 lines]
> biofilm, document it, and share some information about disrupting it.
> Judy

Judy:
Your support helps a lot.
Elizabeth

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