The Models of Infection and KD

General discussion regarding Kawasaki disease
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The Models of Infection and KD

Post by bremen » Sat Aug 22, 2009 9:37 pm


I intend this thread to be a discussion for the people that research and are knowledgable about KD. It is long, as I have much to say along with a great deal of research. This post is not really a good starting point for people that have arrived here because their loved-ones have been recently diagnosed (I am sorry you have had to find your way here) and your time would probably be better spent reading the huge amount of fantastic feedback and support throughout the rest of this site.

Basically you catch a bug and get sick from it. This is the model of illness we are all familiar with. It is what the field of medicine diagnoses and treats to great success. It is how we catch the cold and flu, but is this the only model of infection? “It is estimated that 500 to 1000 species of bacteria live in the human gut and a roughly similar number on the skin. The average human body, consisting of about 1013 (10,000,000,000,000 or about ten trillion) cells, has about ten times that number of microorganisms in the gut” Note that this number does not include fungi and archaea which are also a part of the human ‘flora’. There are also many pathogens that infect us and stay with us for life such as Epstein-Barr virus or herpes viruses. What happens when one of these many organisms is allowed to grow to a great abundance due to genetics, favorable conditions, an illness that allows them to proliferate, etc? It seems logical beyond refute that if there are organisms allowed to live in our body then there will be conditions that allow one of them to thrive. The treatment of too much of one type of organism in the body is a part of alternative medicine, with the professional designation being a Naturopathic Doctor. Naturopathy aims to strengthen the body through proper diet, exercise and supplements to control and eliminate these infections beforehand while boosting the immune system and therefore is more of a preventative medicine. In other cultures, it is the first line of defense before seeing a physician. In North American culture, we are conditioned to think of alternative medicine as a bit ‘out there’ even though much of what they propose makes very good sense and nobody can really argue that you should eat good food, get all the right vitamins and exercise.

State of Alternative Medicine
Many practitioners of alternative medicine believe that pathogens naturally found in the body allowed to grow to huge numbers are the reason for many of the illnesses/diseases that we know little about. “The Arthritis Trust of America/Rheumatoid Disease Foundation considers the nearly 100 rheumatoid diseases - including Rheumatoid Arthritis - systemic diseases. Since the disease can affect any organ or system in the body, manifestation of symptoms produced give rise to the various name classifications often misconstrued as totally separate diseases. Breaking physician health specialties into different practices according to parts of the body affected lends even more credence to the illusion that separate and distinct diseases are presented.” Another example is the Hoxsey Clinic – an alternative medicine clinic that has been treating cancer as an infection since 1963. It has been driven out of the states but has a presence in Mexico

These are both somewhat fringe, but I mention them because there does seem to be relationships as many have seen here – you get KD and then have allergies, asthma, sinusitis, arthritis, eczema, etc. even though aneurysms is the only recognized long-term side effect. Most practitioners of Naturopathy present themselves in a much more subdued and non-sensational way. Many believe that Candida infection (a yeast/fungi naturally found in the human body) is at epidemic levels within the population due to high carb/sugar (pasta, bread, flour, alcohol) lifestyles as well as overuse of antibiotics and that this pathogen alone causes a great many illnesses. They believe that bad organisms naturally found in the body feed upon sugars (and what your body converts to sugar) and that Candida, benefits immensely from antibiotics by having all of its natural competition wiped out. They offer many treatments based around diet (eliminating food for bad organisms), supplements and lifestyle changes with a primary goal of strengthening the body and immune system to allow it to fight off infection.

Interestingly, many of the animal models of vasculitis and arteritis (i.e. inflammation) used to study KD are based upon Candida – the yeast/fungi responsible for thrush, diaper rash and female yeast infections. It is recognized in medicine that it will grow to great abundance in immune-compromised people as evidenced in cancer and AIDS but anything more than this lacks experimental proof. Searching for case studies where Candida has been found results in almost every illness imaginable – it is very opportunistic.

I have chosen to discuss this pathogen as a base infection of self because it has the most experimental data available, I have spent over a year researching it, it is used heavily in creating the models of vasculitis/arteritis studied in KD, it can cause aneurysms, it is superantigenic, it is in everyone to some extent, etc. Candida infection experimentally exhibits many of the medical markers of KD such as TNF alpha, V beta, SED rates, response to immunoglobulin and any other aspect I have researched (links to some of my research on this are here: viewtopic.php?f=7&t=1829 ). It has some very interesting properties, which I believe most are unaware of and which I suspect are very important.

Candida is normally found within the digestive system. It is both yeast and fungi depending upon whether it has colonized (called dimorphic). In yeast form it is basically harmless, but in a colonized form it can release up to 79 different toxins. The release of toxins by organisms is one of the research paths of KD as illustrated in this quote from Kawasaki Disease: A Brief History by Jane C. Burns, MD, Howard I. Kushner, PhD, John F. Bastian, MD, et al., “…the idea that bacterial toxins acting as superantigens could trigger the cascade of events that lead to KD has been widely debated. This controversial hypothesis has been supported by some studies and refuted by others ... /2/e27.” Note that it says “bacterial” – fungi are always overlooked but in some respects they are even more potent than other pathogens.

This is a decent write-up on what alternative medicine believes about Candida infections: Read it with a grain of salt if you are medically grounded. Medicine is based on experimental results while alternative medicine is based on observation of improvement with or without experimental proof where many treatments are based on hundreds of years of observations in various cultures. Some things linked to Candida through observation in alternative medicine include allergy, ear infections, sinus infections, eczema, fatigue, headaches, extreme sensitivity to mould and chemicals, etc.

Important Properties of Candida (and likely other pathogens)
Aside from the fact that Candida may exist as yeast or fungi and that a live fungal form in experimentation is essential in understanding it, there are several properties that are extremely important to understand:
1. The Herxheimer Reaction ( When massive quantities of an organism within the body die, the host experiences a Herxheimer or die-off reaction due to the release of a massive quantity of toxins. Basically, a large amount of inflammation is caused and the host experiences flu-like symptoms (fever, nausea, etc). This reaction is medically proven and first noted in the treatment of syphilis. In alternative medicine, it is well noted that patients being treated for Candida experience this and there are numerous cases/evidence. If you search for the Herxheimer Reaction and TNF alpha or sepsis, you will see quite a few cases where the medical markers (TNF alpha, IL6, IL8, etc.) match those in KD.
2. Quorum Sensing ( Candida can communicate and coordinate activities between fungal colonies by emitting and receiving molecules. It is disturbing that something within us can coordinate its own rate of infection, colonization and in all probability, response. This opens the possibility that there are various signals it could receive to make it behave in an unexpected way (i.e. chemicals, enzymes, our immune signals, etc.).
3. Killer-Sensitivity - the most important property. Candida is very sensitive to numerous ‘killer’ toxins. Certain toxins emitted by other organisms may decimate Candida and it cannot prevent its own demise from a small amount of toxin from another pathogen ( ... tid=283789 and ... tid=272739). This is a bit different than ‘Programmed Cell Death’ – the situation where a huge amount of cells/organisms die (like a mass suicide); however, I have read some articles insinuating that programmed cell death could be triggered by something ( ... ;170/3/391 ).

Until this point, everything written is a decent representation of medicine and alternative medicine to the best of my knowledge. I apologize if I have misrepresented or offended anybody with respect to my understanding.

Alternate Ideas of Pathogenesis
Given the experimentally proven properties of Candida, the fact that Candida is commonly used to create the animal models of inflammation studied in KD, and the fact that Candida portrays many of the medical markers of KD, I have to wonder:
• If a person had a large amount of Candida (for example) in their body and they were exposed to another pathogen that it was sensitive to (Killer-Sensitivity), could this cause a massive die-off of the base Candida infection and result in a huge Herxheimer reaction (which would be acute KD)?
• Could there be a relationship between virulence/infestation, quorum sensing and human genetic polymorphisms (i.e. the genetic deviations already found in KD)?
• Could a massive toxic response be generated by exploiting the quorum sensing abilities of this organism? If (as in first bullet) a secondary pathogen were introduced with a killer toxin, could quorum sensing illicit a huge toxic response against a threat?

The question of how to figure out the pathogenesis of KD would then be a matter of pairing base infections to other pathogens or chemicals that they are sensitive to or which triggers a response and there is no shortage of pathogens found in KD. This would mean that acute KD is not one infection, but two – called ‘concomitant infection’ in medical terminology. I have spent countless hours researching this aspect of KD and as far as I can tell, no experiment has ever been performed where a KD animal model is exposed to another pathogen (my top pick is exposing a Candida animal model to active Epstein - Barr virus or pseudomonas). Epstein-Barr virus is heavily implicated in KD with no conclusive findings, it is superantigenic, it is very common in the population and ultimately it has been found to be involved in several types of cancer and other terrible illnesses.

Some Research Paths
Given the ‘important properties of Candida’ and ‘alternate ideas of pathogenesis’ above, the belief in alternative medicine that high amounts of sugar allow proliferation of bad organisms and several other details mentioned throughout this write-up, I hope to offer some research to provoke your thoughts. The animal models of inflammation used to study KD lack a trigger for acute KD. They seem to be more of a model of long-term infection of one type of organism.

Acquiring a base infection:
•For Candida, is there relationship between inositol 1,4,5-triphosphate (ITKPC) as a signal to proliferate and colonize ( to the already found KD genetic relationship to ITKPC (viewtopic.php?f=7&t=1801). “In Japan, experience of treating IVIG resistant KD cases successfully with Cyclosporin A (CsA) is accumulating (unpublished observations). CsA is an immunosuppressant targeting calcineurin that dephosphorylate and lead nuclear translocation of NFAT ... ase.8.aspx .” What does this mean when compared to, “Calcineurin Is Essential for Virulence in Candida albicans” I cannot fully understand all of this but generally these articles seem to state that there are genetic deviations in an area that codes enzymes/CA+/NFAT signaling in KD and that Candida may use these somehow. If the genetically deviant signal is to proliferate and colonize, then this could be a method to grow a large fungal infection.

•In alternative medicine it is believed that bad organisms thrive on sugar (and what your body converts to sugar).
  • o “Kawasaki Disease in Young Adult with Concomitant new Onset of Type 1 Diabetes and Autoimmunethryoiditis.” ... 010P23.htm
    o “Insulin-Dependent Diabetes Mellitus in 2 Male African American Children After Kawasaki Disease” ... /110/2/e27
    o Do these people truly have a new case of diabetes, or does diabetes cause a large amount of sugar, proliferation of a base infection consuming it, death of a huge amount of the base infection from exposure to something else and subsequent recognition of KD followed by recognition of diabetes?
Concomitant Infections:
•“Kawasaki Disease Onset During Concomitant Infections with Varicella Zoster and Epstein-Barr Virus.” ... =pmcentrez. Two herpes viruses.

•Imagine a person has a high level of Candida and is given the BCG vaccination. Candida is a fungus and BCG (vaccination for tuberculosis) seems to have anti-fungal macrophages ( ... tid=348022). This does not seem to be a ‘Killer-Sensitive’ reaction or a trigger, though I suspect if you had the vaccine in your stomach (where most Candida live), it would be. Oddly enough, giving a BCG vaccine to the stomach is the therapy for several cancers of the digestive system. •“Systemic candidiasis with acute Epstein Barr virus infection.” ... 2/abstract . EBV is related to herpes and has been found in cancers. It causes mononucleosis and is implicated many times over in KD without conclusive findings.

•“Hemophagocytosis complicating Kawasaki disease.” . Please search for Hemophagocytosis Syndrome – you will find KD and a few other autoimmune disorders.

•“Hemophagocytic Syndromes and Infection.”

• “Evidence that Amphotericin B Mediates Reactivation of Latent Epstein-Barr Virus in Hodgkin's Lymphoma Allowing Cytotoxicity by Acyclovir.” ... id=2687644 “. They suspect that this person had an EBV infection that went dormant but and was reactivated with amphotericin B (a fungicide given to rid this patient of Candida). This allowed the EBV infection to be destroyed and thereby kill the cancer it caused. This person went into remission within a day because treatment was halted due to a septic (Herxheimer reaction?) condition after initial treatment.

•“Pseudomonas-Candida Interactions: An Ecological Role for Virulence Factors.” ... /5576/2229 •“Detection of Multiple Superantigen Genes in Stools of Patients with Kawasaki Disease.” ... ct?rss=yes

•Ortho Phenylphenol is a relatively common microbiocide (anti-fungal and anti-bacterial) found in carpet cleaners and many other items. What happens if a little person inhales this? Can it induce a reaction if they have large base infection of self? •Infection in KD is relatively common. “Infections and Kawasaki Disease: Implications for Coronary Artery Outcome.” ... 116/6/e760 . “... 33% of children with typical KD had 1 confirmed infection at KD diagnosis…” Likely difficult to nail them down if one or more are in their death throws.

•Candida research link: viewtopic.php?f=7&t=1829

As stated previously, I suspect that acute KD is a case of base infection X meets new infector Y. The list of ‘things’ I have found that should probably be paired (from models and case studies) include Candida, tuberculosis/bcg vaccine, Yersinia pseudotuberculosis, Epstein-Barr virus (EBV), dengue, bocavirus, coronavirus, pneumonia, diabetes, staphylococcus aureus, varicella zoster, streptococcal infection, Aspergillus fumigates, herpesvirus 6, anaplasma species, pseudonomonas and Lactobacillus casei (Sick Kids, TO animal model). I am certain there are many more and I have not spent much time on this list.

Benefits of this Model of Infection in KD
From everything I have read of KD, the model of single infector = KD would need to cover a whole lot of ground to explain adult cases, incomplete and atypical KD, even with the variability in genetics/immunity. I think it more likely that we need a paradigm shift in our thinking of infection and how it applies to rheumatology. Using a model where a person has a base infection exposed to something to induce acute KD could explain all of the variability. I suspect it can explain:
• The space/temporal findings, epicenter and mini-epidemics (i.e. a virus pops up and those with base infection X get acute KD)
• Observation of carpet cleanings (look at orthophenylphenol as an antimicrobial in some cleaners even though KD has been noted in steam-only cleaning which could also stir up a secondary pathogen. This chemical inhibits asexual reproduction of Candida)
• Swamps and vaccines (other pathogens)
• Season correlation (links to the mould/fungi life cycle, flu season, etc)
• Noted BCG vaccine effects
• Atypical cases such as gangrene, diabetes, etc.
• Incomplete cases including lack of fever (only growth of base infection? missing a secondary infection?)
• Acquiring other rheumatologic/autoimmune disorders pre and post
• Pathogenesis
• What is being observed in IVIG and steroid therapy (does the KD patient provide a genetically altered signal that an infection proliferates within and does IVIG and steroid therapy affect signals and states by introducing a normal signal, different pathogens would then determine the differences in therapy observed such as resistance, etc.)
• The usefulness of the KD animal models which has been an ongoing discussion in KD
• The field of rheumatology and everything from allergy to Sjoren’s, Behçets and Coeliacs and anything that causes vasculitis/arteritis
• Unifies alternative medicinal theory with rheumatology which are both at somewhat of a standstill.
• Why your kids crave sugar, get joint pains, get sick more than average and have odd reactions to certain things.
• “Kawasaki disease may be a hyperimmune reaction of genetically susceptible children to variants of normal environmental flora.”

I am not a doctor or naturopath but a professional and academic computer programmer who had KD 27 years ago without IVIG treatment. I never put much thought into KD until a year and a half ago when I found that treating myself for GERD/acid reflux affected the migraines I began having within 2 weeks post KD that have haunted me since. I hope that someday one of the animal models of inflammation with a Candida base infection is exposed to other pathogens and chemicals to see if it could cause acute-KD. I believe that the model of infection I have explained above is the next step in understanding rheumatology and autoimmunity. Ultimately, KD would have two forms. One would be the long and slow growth of a base infection of self causing slowly increasing vasculitis and the other would be an immediate, acute response from exposure to another pathogen causing instant vasculitis. While I am certain I have misunderstood and misrepresented some things in this write-up, I do not think I am incorrect about everything. I have over 350 links to abstracts, cases and experiments I have gathered and each one paints a little bit of the picture. I have searched for proof that this is impossible and came up with nothing. This area is a void in experimentation and taboo to talk about. I suspect that this needs researched by somebody trained with proper/full access to data as I do not think it has never been considered and ultimately, there needs to be controlled experimentation.

Last edited by bremen on Sat Sep 05, 2009 9:33 pm, edited 1 time in total.

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Re: The Models of Infection and KD

Post by liquidambar » Tue Aug 25, 2009 11:14 pm

Acid reflux is probably part of the KD. My daughter also has acid reflux, she is 28. She had KD when she was 2. Kids with autism also have trouble with their gut as well as acid reflux too. I would know this because my son has autism. You sure have worked on all this, so here is another clue: it is also a mitochondria disorder that is not genetic but environmental acquired. Those in the autisic community are coming to realize this. Autism is the same disease as KD only it is in different parts of the body.

The thought is that peroximes (hope I spelled this right) it is an organelle in the cell and is responsible for breaking down the very long chains of fattiy acids or tryglyerides, and getting them ready to be used by the mitochondria. Peroximes have to have a lot of L-Carnitine to break down the long chain triglycerides. All three of my family my daughter, my son, my husband have low L carnitine levels! All had a reaction to a vaccine booster. For my two children it was the DPT shot, and for my husband it was a tetanus shot.

For my son the vaccine reaction which was an inflammatory response caused a stroke. But the inflammation does stick around and - It messes up the mitochondria pathway. But how I do not know nor does the medical or science, or rhuematogilst! Nobody knows, can you believe that in this day and time.

what I do know is that there are two ways that food is processed in the body to make energy. One is carbhydrates turned into glucose, and the other is taking fats and turning them into ketones. As long as there are carbohydrates only the glucose energy pathway runs the body and the fat (ketones) does not operate at all. Only through starvation will the ketones work, that or a diet of fats like the famous ketogenic diet or the atkins diet or the low glycemic diet. Many epileptic, alzeihemers, austistic, and some with mitochondrial disorders use these diets. With epileptics a third of them can be cured if on the ketogenic diet for two years (although they know within days if it is going to work or not). In a recent study this year the Mormons that fast once a month, have fewer heart attacks.. Something about the ketones or fat metabolism does control inflammation! If you are ill, you might consider one of these diet. My son after starting on this diet claims his stomach is much better (he is high functioning autistic - aspergers is what they call him, he is also an epileptic and we hope that in a few years he may no longer needs meds.) My husband was put on oxygen all the time (he was haveing low oxygen issues) he still is on oxygen at night but since he is on this diet he has not needed oxygen during the day! My daughter, I don't think she is following the diet like she should she is still stiff and has acid reflux. (she recently had three shots of the Hib B vaccine because she is a nurse and after becoming very stiff again visited the doctor and found her SED rates were high again). Both my husband and son fast once a week plus follow the low glycemic diet and if we can get her on board she might once again feel better.

I too am long, sorry! Hope this helps!

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Re: The Models of Infection and KD

Post by award » Sun Aug 30, 2009 11:59 am

Well done Jason, very interesting and thought provoking topic.
I have often felt we need to marry traditional, western medicine with naturopathic medicine. I don't think either field has all the answers alone but together, it could be exceptional. I think many physicians and scientists make an enormous mistake when they discount naturopathy as it seems obvious they have some excellent points and equally obvious that there is always a price to be paid when we change the natural order of things.

For instance, when we went from small farms to mechanized, industrialized feedlots which require hords of antibiotics so the animals survive dysentery and other infectious disease by being forced to live in such tiny, cramped quarters........this clearly paved the way for antibiotic resistance, not that the medical profession has helped when they throw these drugs at every person who complains of a sore throat or the sniffles.

Then add in growth hormones so they can grow them bigger and faster and you probably have other issues....precocious puberty in girls? Cancers known to be associated with these drugs?

Vaccines...are they dangerous? I am a firm believer that nothing comes without a price. But does this price include everyone? Probably not. Like anything, some do well having penicillin for strep throat while others have a rash, or develop diarrhea, or even death from allergic reaction, but the medical community becomes complacent to these possibilities since so many people are on these meds and do well. The fact remains that a certain percentage of the population will respond negatively and positively to drugs...vaccines being no exclusion.

I remember the oath physicians take upon graduation and the underlying premise is "physician, do no harm" but this directly opposes the brainwashing they receive for 8 years of med school and residency that they are "healers" that they must treat the patient. This often leads to doing "something" and yes, something can be dangerous.

On the other hand, if naturopathy continues to diagnose in a manner that appears trendy & sometimes, irresponsibly....I cannot tell you how many women are diagnosed with "adrenal fatigue", they will not be accepted as mainstream. But I think that medicine has caught on just a smidge because the Gasteroenterologists are now recognizing candida as the source of some of our problems and have even recommended probiotics...imagine that! I have been telling my patients for years to buy them at the natural health food store whenever we cannot find the "source" of their digestive issues or if I have to give them antibiotics for a kidney infection, strep throat, etc., (I am VERY stingy with the antibiotics, you had better be sick to get them from me!!) and my colleagues have looked at me like I was some sort of kook and here they are.....slowly but surely doing the same. Maybe there is hope afterall.


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Re: The Models of Infection and KD

Post by moitza » Wed Sep 02, 2009 4:04 pm

Dear Jason,
I find your post very interesting and challenging (I guess,I belong to those, who think candida might be a bit overlooked or underestimated as far as the official medicine goes, too). You gave us a lot of homework to do. I admit I'm not quite done with reading yet, there are many links to follow. But since you point out the Epstein-Barr virus quite a bit, I'd like to tell you my son was tested for it in the acute phase. Blood was withdrawn upon the admission to the hospital (third day of symptoms) and then again on day six. Tests came back negative. And I think I remember reading another post here, where mom says Epstein Barr was excluded.

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Re: The Models of Infection and KD

Post by bremen » Wed Sep 02, 2009 6:01 pm


To clarify, I mean a base infection of X meets new infector Y. Candida would seem to be a common X. EBV a common X or Y. The toxins released by Y invoke a huge reaction from the larger quantity of X through Killer-Sensitive properties, Programmed Cell Death, a coordinated response, etc. These pathogens are here as I have researched them more than the rest.

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Re: The Models of Infection and KD

Post by Momcat » Wed Sep 02, 2009 8:23 pm

I'm wondering that if Candida is a yeast like infection and you are implicating it has something to do with KD, then how do steroids really nail KD and the auto-immune response in out of control KD or IVIG resistant cases? I understand that steroids inflame yeast type infections, as it did with my daughters gastro-intestinal tract and in another obvious place. Wouldn't your theory mean that steroids would make the candida worse and thereby make the KD worse? Steroids are typically found treating auto-immune disease, mainly as a last resort, but usually as a way of really getting the immune system to shut down---with rhuematoid arthritis to lupus to bechets disease.....many are treated with steroids. How then can the treatment not cause the condition to worsen if it is related to candida?
I have to admit I haven't read through all of this, so if there is an answer in there that I missed, please forgive me. I really am swamped lately and am not keeping up all on the latest theories and many suspicions that have been posted on this site lately.

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Re: The Models of Infection and KD

Post by bremen » Thu Sep 03, 2009 12:20 am

Great question. Keep in mind that while I implicate Candida, my overall theme is base infection X meets new infector Y and therefore Candida is not the base infection in all cases and I am uncertain it is involved in steroid therapy. The article, "Effects of steroid pulse therapy on immunoglobulin-resistant Kawasaki disease. " sets up the stats for what we are discussing with the most important quote being, "411 patients with KD were treated with a single dose of IVIG. Of the 63 IVIG-resistant patients, 44 were then given IVMP and 19 were given additional IVIG. Treatment was successful in 34 (77%) of the patients who received IVMP and 12 (63%) who received additional IVIG. Five of the 10 patients who did not respond to IVMP and two of the seven who did not respond to additional IVIG developed coronary artery aneurysms" (IVMP is steroids).

So the question really comes down to IVIG resistance versus additional steroid therapy and whether Candida could be involved in the minority of people that are resistant. I have researched this avenue a great deal as it is very important. My thoughts are:
1. Candida proliferates greatly with steroids (so much evidence, just skim the net)
2. Candida has quorum sensing abilities - it interprets and transmits signals from its environment to systemically coordinate activities/virulence. It reacts to the signals it receives which means that it can be artificially controlled by altering the signals it receives (through IVIG/steroids). Quorum sensing is not unique to Candida in any way, so this point can be applied to numerous infections.
3. Therefore the base infection should have a state - aggressive, growth, etc. In my field of computer science this is called a finite state machine, and basically means that inputs can change the state and therefore affect the outputs (toxicity). This would mean that if it is in an aggressive state (because it got exposed to something) and is releasing toxins and soliciting the host immune response to combat a threat, that you could theoretically provide a new input (i.e. steroids/IVIG) to change its state to something more desirable.

So, if you followed that, I do not think that steroids would make the immediate acute KD response worse but would change the state of the infection to one of growth which would be less aggressive/toxic. There is a huge lack of experimentation in microbial states versus virulence and aggressiveness. The fact that organisms can exist in our body and coordinate through signaling means that their states can be artificially altered through unintended signals. It is why I posted this genetic link on ITPKC: viewtopic.php?f=7&t=1801, which could provide a signal to propagate and colonize and set up the ability to get acute KD when you are exposed to another pathogen that the (now huge amount of) base infection responds (or dies) to. Does IVIG from a genetically 'normal' person provide the signal for an infection to return to a typical state where the genetically different immune system of a KD provides a signal of growth?

"Fluconazole plus adjunct high-dose prednisolone treatment was most effective when administered 9 days after infection. The delayed application of corticosteroids after treatment with antimycotic drugs in cases of fungal keratitis is therefore not contraindicated and may be beneficial in patients ." This is an experiment of a Candida eye infection where results showed that treatment with steroids after day 9 of infection improved the outcome where treatment before 9 days with steroids just grew the Candida infection.

To conclude, I don't have answers on this but a whole bunch of questions where there is a lack of experimentation. The fact that 2 infections could react to each other has barely been looked at. The fact that quorum sensing exists for intra-cellular communication in various infections has barely been touched. The concept that the state of an infection can be altered through what it senses in its environment is not even on the horizon. This is complicated stuff but I hope I explained it decently. It all comes down to signals and states.

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Re: The Models of Infection and KD

Post by moitza » Thu Sep 03, 2009 2:45 am

Dear Jason,
oh, I did get that. I find your idea about the infections colliding quite plausible the way you thoroughly put it all together. But then I speak from a completely amateur point of view. At this point It would be interesting to have a micro biologist with perhaps some experience in a field of medicine to look into it. I'd be definitely excited to learn more. You seem to have acquired quite a bit of a background there and I guess for most of us it's a bit hard to engage in a debate with you at this point (which you deserve after all the input). I just wanted to let you know you've raised my interest and made me think. I hope you get more response.
Thank you.

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Re: The Models of Infection and KD

Post by joshysmom » Thu Sep 03, 2009 12:43 pm

Jason - well though out, I have not read the whole paper, I am not a huge wikipedia fan for references so I have to say I kind of stopped reading but I do have an open mind and will come back to it..

So -infection X meets infection Y and thwarts you into the acute vasculitis?

You may have seen my post ---

My son 5 at Diagnosis - successfully treated with IVIG - echo follow ups to come (no aneurysms so far)
Origin - as we all know - UNKNOWN -
In telling my story about Kawasaki - a friend mentions a friend that was Diagnosed at 25 years old..
I reassure them they must be mistaken - it is a childhood disease..

So -get this - it was Kawasaki She recieved a kidney transplant from a 2 year old and 1 month later diagnosed with Kawasaki
Research and medical journals are forthcoming..

My son - has had inflammed kidneys since birth, this was followed via ultrasound and caused no symptoms and it was a fluke that we even knew they were inflammed..

I didn't think it was related..but it points to an underlying X infection.

And my friend the microbiolgist - based on the similarites
kidney - and - kawasaki has determined it is either blood borne or blood related...
shouldn't be immune triggered as the 25 yr old transplant recipient who got KD was on immuno supressent drugs at the time..

I will keep reading your post and go through the links

Thanks for the research


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Re: The Models of Infection and KD

Post by bremen » Sat Sep 05, 2009 9:42 pm

Hi. I edited the main post to reword a few things and add a few more links with most under the 'concomitant infection' secion. Thanks for the comments.

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Re: The Models of Infection and KD

Post by atwinmomsyrny » Sun Sep 06, 2009 12:30 am

Hi, I may be way off here but....

I have identical twins..If there is a possibility that the x meets the y theory is true, then the reason my one twins did not get KD may be because the other had a base infection going on. And when the one twin with the "cold" (started off as scratchy throat) gave it to the other, then this could have been the y factor? Then that could explain why both didn't get KD.. maybe...... I still wonder why one got it and not the other. They do and go everywhere together.. I don't know. It's a mystery to me.. Sorry if I'm going off somewhere out of the context. thanks for your info..


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Re: The Models of Infection and KD

Post by Momcat » Fri Oct 07, 2011 10:55 am

I'm glad someone brought this thread back up. I have reread most of it and have a question. First of all, thanks for all the work you did putting this presentation together! I studied KD soooo long when my daughter was recovering and read just about anything I could get my hands on within the first couple of years post-KD. I am now finding boxes of articles I printed and stored--unsure whether to keep them or not now!! HA! So I know you have really done a lot of homework.
The question is this (and thank you for your response to the steroid question I had before) I am wondering about the long term effect of Candida you mentioned regarding a slow, chronic vasculitis. I can't seem to find where I read that in what you posted. Is there a link to finding out more about this?

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Re: The Models of Infection and KD

Post by bremen » Tue Oct 11, 2011 11:41 pm

Sorry for the slow response. Here are a few articles and links. While none specifically say it, I think you can safely assume that this would be a slow, chronic vasculitis. A benign infection that slowly grows undiagnosed causing an ever-increasing level of inflammation until it becomes bad enough to get recognized as something...

Vasculitis: Pathogenesis

"Infection may be the most common trigger leading to vasculitis. As a model, vasculitis due to infection is mediated through a type III or immune-complex reaction where the antigens are the infectious agents or antigenic portions of them.[36] After the zone of equivalence is reached, the immune complexes precipitate and become trapped within vessel walls, stimulating an immune response that ultimately leads to vascular injury. Candida polysaccharides and fragments of gram-positive and gram-negative organisms can activate the alternate pathway and also lead to the inflammatory reaction characteristic of vasculitis.[36-38] Alternatively, direct endothelial cell invasion can be the main pathogenic process in infections caused by cytomegalovirus, herpes simplex, rickettsiae, fungi, and bacteria.[37,38] Recent concepts suggest other mechanisms may be at work as well in the development of vasculitis within the context of infection.[39] Cytokines, such as tumor necrosis factor and various interleukins, are produced directly by the stimulation from the infectious agents. Subsequently, recruitment of neutrophils to the small vessels occurs and leads to the development of vasculitis. Vasculitis related to infection due to streptococcus and staphylococcus has been associated with this mechanism of vascular injury. The association between hepatitis B and polyarteritis nodosa (PAN) has been well documented.[28,40,41] One report found 54 percent of patients with PAN having hepatitis B virus (HBV) infection.[42] Hepatitis C (HCV) infection has also been associated with vasculitis mediated through the production of cryoglobulins.[43] A genetic susceptibility was proposed by Lenzi, et al., in 1998, who reported the association between HCV-related cryoglobulinemia and HLA-B8 and DR3 markers.[44]"

Cerebral vasculitis associated with chronic mucocutaneous candidiasis ... 7698700721

[Candida vasculitis].

Models - while not a slow process, they involve injection of a superantigen and therefore imitate a point in time where the infection has reached a large level. Many of the KD models use candida to study the effects of vasculitis and aneurysms.

Effect of Candida albicans septicemia on the cardiovascular function of rabbits ... 6905000135

Murine model of Kawasaki disease induced by mannoprotein-beta-glucan complex, CAWS, obtained from Candida albicans

Superantigenic activity is responsible for induction of coronary arteritis in mice: an animal model of Kawasaki disease. ... 9.abstract

Most of the links I collected are here.
If you look through 'Kawasaki Disease' it contains links to many articles about KD, scientific observations, etc. and lays out what has been observed. If you then go to 'Meeting KD with Candida', it is the same findings about Candida. For example if you look for, TNF alpha, MMP9, T-Cells, SAPS, etc. on the KD page, you will find the corresponding links on the 'Meeting ...' page.

Hope this helps.

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Re: The Models of Infection and KD

Post by liquidambar » Sun Oct 16, 2011 9:12 am

Observations of my husband who has mitochondrial cytopathy that yeast is certainly involved in all of this!

Two weeks ago he cheated a lot on the low carb diet. The beginning of this week he had a yeast infection .
I gave him my AZO tablets -

He now has spent the last three days in bed, sleeping, complaining if he moves his chest hurts, not only his chest but it hurts to put his feet on the floor, and the back of his legs hurt too.

I have to say that I too have experienced what he has for 10 yeasrs but now I am well. I too had constant yeast infections, pain in the bottom of my feet and up the back of my legs and my thyroid getting worse and worse, and very bad migraines. The first yeast infection I every had was at age 21 and wait for it : it was a few weeks after a tetanus shot which might have been, probably was a DPT shot.

My husband suffered a seizure with in hours after receiving a tetanus shot (AKA - DPT shot) at age 28 .
At age 34, trusting the medical profession which I told him not too he recieved antoher tetanus shot. My husband suffered severe pain in his legs, muscle weakness, things that involved the peripheral nervous system - three weeks after receiving a tetanus shot (AKA - DPT shot) -Emory clinic dignoseds it as acquired mitochondrial cytopathy.

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Re: The Models of Infection and KD

Post by liquidambar » Wed Oct 26, 2011 9:18 am

Could oxalates being absorbed into the soft connective tissues be the cause of pain after the die off of yeast?

In my family I now have the fifth member of my family suffering from kidney stones. It has been a two month ordeal that almost took her life, and is still on going. This family member is not on the low carb diet and is a little sugar-holic; and has a devil of a time with yeast infections all her life.

Oxalates are the main cause in the formation of kidney stones as they crystallize with calcium.
Oxalates usually combine with calcium in the gut and pass on out with no problem, but if it does not pass out of the gut, it is then absorbed into the blood and eventually finds it way to the bone, as well as excreted through the kidneys. Oxalate arthritis as well as vasculitis has been noted at the end stages of a type of renal disease were in which renal patients have a metabolic disorder.

Oxalates are found in a lot of foods. It is oxalates that makes the rhubarb leaf poisonous. Yet, even plants high in oxalates is really not that high, nor can the intake of high oxalate foods accountfor what is going on in some with renal disease, or Nephritis inflmmation of the kidneys. After all; lots of people eat dark leaf vegs such as swiss chard and not develop nephritis.

The National Institute of Health has a study out about a common bacteria that normally grows in our gut. It feeds upon oxalates.

Oxalobacter Formigenes is a common bacteria in the gut of humans. It breaks down oxalates in the gut. . O Formigenes was given in a soft pill. AND it significantly broke down oxalates in the gut where it passed out of the body harmlessly. It worked in those patients with continous reoccurring kidney stones of oxalatecalcium cystals. .

It also appears that people that have mitochondrial dysfunction also has trouble getting rid of oxalates too, "double whammie" sort of.

Perioxsomes ( organelle in the cell that is suppose to break down long chain carbs and transfer them to the mitrochondrial by attaching the now medium chain carbs onto a carnitine complex making it more able to be absorbed through the Mitochondrial membrane. (my son and husband labs have come back with low amounts of L-carnitine).

mitrochondrial (organelle in the cell that makes all the energy)

Perioxosomes within the cells; are not doing their job. Intead these long chain carbs by-pass perioxsomes, and go directly to the mitochondria. The mitochondria can break down long chain carbs too - but the mitrochondrial has a tendency to break down these long chains rather sloppily, and there is a lot of oxalates formed in the process. I found this information from looking up inherited renal disease called hyperoxaluria and it is rare. But I am learning that with all these metabolic diseases there is genetic and then there is the word "acquired" .

Also a suprise, Candida Albicans "Yeast" actually MAKES MORE oxalates in gut.
One more thing Yeast does that is bad to us.

Lots of oxalates are also involved with thyroid disease.

But what surprised me, stunned me was; If oxalates is eliminated in the body;

Oxalates will come out of the bone and linger in the connective tissues causing tempory pain and stiffness untill the oxalates are finally flushed out. Is this the cause of the muscle pain in the described die off of yeast? Could this be the toxin?

So it is complex problem.
1.)You have a damaged mitrochondrial (metabolism) that is not breaking up long chain of carbohydrates correctly thus making more oxalates
2.) You have antibotics reducing the numbers of good bacteria in the gut that break down the oxalates, so we are not getting rid of as many oxalates as we normally would.
3.) Not only that but the reduction of good bacteria allows more space for yeast growth and yeast is not bothered by antibiotics.
4.) You have a diet rich in fast release carbs, plus a bad metabolism that can not break down these fast release carbs, and you have Candida - yeast that is thriving on this type of food.
4.) And the yeast to make matters worse is actually producing more oxalates a usless by- product that our bodies have to get rid of.

This soft pill of O Formigenes is not available at this time. But those three bacteria that they sell over the counter for yeast infections - lactobillus, and bacteria found in Yogurt are also good bacteria for breaking down oxalates in the gut. Plus these bacteria crowds out the yeast in our gut as well. Unfortunally all these bacteria are harmed by antibiotics too.
Last edited by liquidambar on Thu Oct 27, 2011 2:59 pm, edited 7 times in total.

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