Medical Forum / Diseases and Disorders / Sinusitis / February 2008
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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