kim

I thought this site had some really good info that others might want to take a look at. Video, test results etc. Sickening to think that this child may have missed out on the healing process if the parents would not have persisted http://www.stopcallingitautism.com/

Many PANDAS threads with idea's for natural remedies here: http://www.ch3nutrigenomics.com/phpBB2/welcome.html Dr. Nancy Mullan treats PANDAS kids based on concepts from this protocol http://conference.autismone.org/abstracts.cfm?a1year=2010 An Overview and Clarification of the Dr. Amy Yasko Protocol This presentation highlights some of the important interventions in the treatment of autism spectrum disorder and other chronic immunologic, neurologic, metabolic, or gastrointestinal dysfunctions that can be made with the help of genetic and biochemical testing. It is not intended to be a comprehensive review of Dr. Yasko's method. Instead, it highlights those areas that are critical for the success of her method and defines points of similarity to and divergence from other ASD treatments. It demonstrates the competence of Yasko's method for promoting the development of function and language, and for inducing the excretion of toxic materials without problematic pharmaceuticals, frequent blood draws, or other even more invasive and stressful treatments. Nancy Mullan, MD received her undergraduate degree from the University of Pennsylvania and an MD from Tufts University. She completed an internship and residency in psychiatry and a fellowship in child psychiatry at the University of Chicago Hospitals and Clinics. While there she studied at the Chicago Institute for Psychoanalysis and taught at the Psychosomatic and Psychiatric Institute for Research and Training at Michael Reese Hospital. In Los Angeles, Dr. Mullan joined the medical staff at Cedars-Sinai Medical Center and taught at both UCLA and USC Schools of Medicine. She earned psychoanalytic certification from the Psychoanalytic Center of California. Currently, Dr. Mullan is practicing nutritional medicine and psychiatry in Burbank, California, treating children on the autism spectrum and adults with neurologic, immunologic, metabolic and/or gastroenterologic dysfunction that might otherwise be thought of as psychiatric illness.

http://www.jlaforums.com/link.php?url=http...ink-autism.html

From article Cheri originally posted from my reply This article seems pretty relevant. Celery and green peppers! http://www.dietaryfiberfood.com/antioxidan...antioxidant.php and I just came across this on the page for the "Presenters/Presentations" for the autism one 2010 conference http://conference.autismone.org/abstracts.cfm?a1year=2010 This is some info on the presenter Theoharis Theoharides, MD, PhD is a professor of pharmacology, Internal Medicine and Biochemistry, and the director of the Laboratory of Molecular Immunopharmacology and Drug Discovery; Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine. He trained in allergy and clinical immunology at Yale and internal medicine at New England Medical Center. Dr. Theoharides was director of medical pharmacology at Tufts (1986-1993), and became full professor in 1995. He has 300 publications and 3 books, including a Textbook of Pharmacology. Dr. Theoharides was the first to show mast cells and acute stress promote inflammation in autism, cancer, interstitial cystitis, migraines and multiple sclerosis. I think there is a lot of info on the page that many would find interesting including Dr. T and Sammy's moms description of their presentations

3boysmom, I have to wonder if there isn't something here, regarding your genetics test. I think I might do some real research on this pathway and see if you can come up with something. http://www.google.com/search?q=+acyl-coenz...amp;startPage=1 acyl-coenzyme A synthetases 16p13.11 http://www.latitudes.org/forums/index.php?...st=0#entry51478 pyruvate kinase, subject of strep antibody attack Acetyl-CoA synthetase http://en.wikipedia.org/wiki/Acetyl-CoA_synthetase be sure to click on Pyruvic acid Pyruvate dehydrogenase complex

From the 2nd link that JMTho provided...I'm remembering a post of Buster's that pointed out how the antibodies crossed the bbb was important in the mouse model. Does anyone think that the "stress" that was being investigated in this study was looking to reinforce this idea? Was epinephrine thought to be the catalyst in relationship to stress?

Peglem. I thought this was interesting and sort of fits in with some of the info in the Megson paper, i think. I didn't reread it, but remember some of what it's about. I was originally looking at this study here. http://www.latitudes.org/forums/index.php?...amp;hl=aluminum I shouldn't have said that the toll like receptors were bypassed (on the other thread) maybe they aren't stimulated ENOUGH to produce the protective effects of vit A when alum is added? Anyway, just wondering if you could make anything of it in regards to CamK etc. http://www.ncbi.nlm.nih.gov/pubmed/19252500 2009 Apr;15(4):401-9. Epub 2009 Mar 1. Toll-like receptor 2-dependent induction of vitamin A-metabolizing enzymes in dendritic cells promotes T regulatory responses and inhibits autoimmunity. Manicassamy S, Ravindran R, Deng J, Oluoch H, Denning TL, Kasturi SP, Rosenthal KM, Evavold BD, Pulendran B. Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. QUOTE Immune sensing of a microbe occurs via multiple receptors. How signals from different receptors are coordinated to yield a specific immune response is poorly understood. We show that two pathogen recognition receptors, Toll-like receptor 2 (TLR2) and dectin-1, recognizing the same microbial stimulus, stimulate distinct innate and adaptive responses. TLR2 signaling induced splenic dendritic cells (DCs) to express the retinoic acid metabolizing enzyme retinaldehyde dehydrogenase type 2 and interleukin-10 (IL-10) and to metabolize vitamin A and stimulate Foxp3(+) T regulatory cells (T(reg) cells).

Isabel, I know you have enough on your mind right now, but when I read posts like this I have to wonder how many kids are being affected by strains of infection that have been kicked up since the introduction PCV7. S pneumoniae causes a lot of ear infections. Do the Dr.s even keep up on this stuff!!!? Would love to see you ask him about this. Maybe ask him if a culture would be in order before your child is placed on yet another anti biotic (determine btwn viral and bacterial and WHAT STRAIN if bacterial). excerpt bolding mine http://www.immunizationinfo.org/vaccines/p...ococcal-disease However, while the PCV7 vaccine has reduced pneumococcal disease caused by the seven most common types causing infection in children, there are other pneumococcal types which can also cause serious infections in children. Surveillance suggests an increase in disease in children aged < 5 years due to these nonvaccine serotypes, especially serotypes 3, 7F, and 19A, some of which are antibiotic resistant. Because children are the reservoir for the serotypes that cause invasive disease in older people, broadening the coverage of serotypes in the vaccine is desirable.

3boysmom, I wonder if this would be helpful to you? What I'm taking away from this is that a DUPLICATION is not as strongly suggestive of anything certain. A deletion seems to be more significant? excerpt from http://www.ncbi.nlm.nih.gov/pubmed/18550696 Not long ago I read an article where they talked about some of the disappointments regarding genetics. They thought it would be easier to nail down certain genetic profiles with specific disease, but as they identified variants of certain genes (commom to patients) they also found these same changes in healthy people. This seems to suggest that in some circumstances the genetic variables are not the whole picture which could lead us right back to environmental triggers/variables. I think the main idea is to support/correct the pathways that are affected by genetic change/error.

Vickie, If we attract some headlines, I want it on record that it's not just bears and cat's, it's hot water heaters too. Boys can't get within 10 feet of it with out symptoms kicking up. Must be something about the exocomponant nanoparticles interacting with the glycosaminoglycan compostion attached to the cellular proteins that are ill constructed in the golgi apparatus. Nancy, Please understand that you are no more science dumb than I am. No science or medical background here, so some (ok probably alot) of what I wrestle with is way over my head too, but I get some tid bid understanding with every hour that I invest (usually). I LONG to sit down with someone who can say "yes," this is plausable, and "no," you've got this part all wrong! Anyway, I think you might be confusing NAC with NAG. I'm assuming you are using NAC because of the possibility that it may help with the OCD (precursor to glutathione, sulfur donor, etc)? In people with autoimmune and allergic disease I have no doubt that there are many antigens (and components of) that can set things off, but I feel at least in our case, the state of the HOST is very important in how we react to the water heater, I mean antigen. I also feel NAG is a big part of that picture, at least initially.

I think we had another report of this or something similar. Was it pixiesmom that posted that her daughter had it, that she mostly noticed when she got out of the bath? Seems I came across this condition when searching "skin stuff," after her post.

That ones goooood!

There once was a cool cat named Buster Analysis he always could muster Did you get his post? He’s smarter than most. No wonder my brain starts to fluster. So I take a step back Reconsider the facts and allergy to cats Where was it that I have seen Cat dander and a relationship to N acetylglucosamine Ok only half joking. 2 boys who IgE test positive to cats.....You don't suppose?????? http://www.sciencedirect.com/science?_ob=A...b04db014cd0c506 Lectin histochemistry of glycoconjugates in the feline hair follicle and hair http://www.wipo.int/pctdb/en/wo.jsp?WO=199...;DISPLAY=CLAIMS 2. Affinity purified human T cell reactive feline protein treated in such a manner as to remove O-linked carbohydrate moieties, thereby producing modified human T cell reactive feline protein which stimulates T cells and which interacts with human immunoglobulin E to a lesser extent than affinity purified human T cell reactive feline protein interacts with human immunoglobulin E.

This gives a little info on what titers looked like at different points in time in 3 adults ACUTE RHEUMATIC FEVER OR POST-STREPTOCOCCAL REACTIVE ARTHRITIS: A CLINICAL PROBLEM REVISITED http://rheumatology.oxfordjournals.org/cgi...nt/37/3/335.pdf

I don't think we've heard the last from this man and personally I think he's a gift straight from heaven http://www.ageofautism.com/2010/04/stateme...-sanctions.html Statement from Dr. Andrew Wakefield Regarding GMC Hearing Sanctions I recieved this in my email. As I was watching the "today," clip, I was waiting for them to get to some of the info that the article talked about regarding the children having been sick and them receiving vaccines. It didn't happen. excerpt from: http://today.msnbc.msn.com/id/36120715/ns/today-today_books/ Facing the trauma of autism diagnosis Former NFLer Rodney Peete writes about his son’s condition Then I remembered reading this a little while back. The paper that started this thread is part of "what the science has shown." Wondering if the media is going to cave just as some real progress was being made in regards to open conversation on the safety of vaccination. bolding mine http://www.ageofautism.com/2010/03/did-kat...ety-voices.html There are groups out there that insist that vaccines are responsible for a variety of problems despite all scientific evidence to the contrary. We have reached out to media outlets to try to get them to not give the views of these people equal weight in their reporting to what science has shown and continues to show about the safety of vaccines,” (HERE) according to HHS Secretary, Kathleen Sebelius, in her interview with Arthur Allen for The Reader’s Digest, on February 5th of this year. Sebelius basically admitted to pressuring media outlets to report disinformation to the public in place of information that does not support the safety of the government’s most heavily promoted drug. As shocking as this statement was the first time I read it, I honestly could have predicted such a scenario.

Johnsmom, Try this link http://circ.ahajournals.org/cgi/content/fu.../742#R41-191906

Anne, My 17 year old son was diagnosed with mild gastroperesis this year after a respiratory illness too (right around same time). His presentation was more of intense crampy, painful gassey feeling shortly after waking. It might go on for 4 or 5 hours and then disappear. In the mornings, I would be SCARED TO DEATH and by early evening he seemed the picture of health. He had 4 or 5 periods of waking up from deep sleep vomiting. It seems to be slowly getting better. The gastro's words were, "I think he had a virus that affected the nerves in his stomach. He's young, I think he'll recover just fine." This was after the "down the throat scope," (he has had other tests as well). She poked her head in the room where I was waiting, dropped that little bomb and left. In one way I was shocked, in another, not surprised at all. Does your friends son have any time of the day that is better/worse? I will PRAY this little guy heals quickly and yes, I sure think it's worth while for your friend to investigate the autoimmune aspects of this illness for her son. EAmom, Thank you for that article.

Parents4eyes, Have you read anything on the use of benfotiamine for uveitis? We have a couple of threads with some info that you might want to read thru. Some of the symptoms of Beriberi seem to correlate with some reported PANDAs symptoms. here are the two threads with a couple of excepts from those threads below vision problems http://www.latitudes.org/forums/index.php?...vision+problems PANDAS and floaters http://www.latitudes.org/forums/index.php?...AS,and,floaters Beriberi https://health.google.com/health/ref/Beriberi Overview Beriberi is a disease in which the body does not have enough thiamine (vitamin B1). Symptoms Symptoms of dry beriberi include: Difficulty walking Loss of feeling (sensation) in hands and feet Loss of muscle function or paralysis of the lower legs Mental confusion/speech difficulties Pain Strange eye movements (nystagmus) Tingling Vomiting excerpt http://www.betterhealthresearch.com/news/v...dness-19159004/ QUOTE A form of vitamin B1 could become a new and effective treatment for one of the world’s leading causes of blindness, according to Texas scientists. Researchers from the University of Texas Medical Branch at Galveston have presented promising results achieved with benfotiamene, a fat-soluble form of vitamin B1 which is absorbed rapidly by the body and lacks negative side effects. In their study, they injected laboratory rats with toxins that produce a reaction mimicking uveitis and noticed that when the rats were fed benfotiamene they failed to develop any signs of the inflammatory disorder. about uveitis http://autoimmunedisease.suite101.com/article.cfm/uveitis As an autoimmune disorder, uveitis may occur alone or it may accompany other systemic autoimmune diseases such as rheumatoid arthritis, Bechet syndrome, sarcoidosis, Kawasaki disease, Reiter disease, psoriasis, ulcerative colitis, multiple sclerosis, systemic lupus erythematosus, or ankylosing spondylitis. Uveitis may also occur in AIDS, cytomegalovirus infection, syphilis, tuberculosis, Lyme disease, and in fungal infections. http://www.iherb.com/Source-Naturals-Benfo...blets/7342?at=0 Benfotiamine is a more bioavailable derivative of thiamin (Vitamin B-1). Unlike normal thiamine, benfotiamine is fat-soluble and more physiologically active. It supports normal glucose utilization by stimulating transketolase, the enzyme essential for maintaining normal glucose metabolic pathways. Normal glucose levels are also vital for the promotion of endothelial cell health in the kidneys and retinas.

momto2, Take a look at these. Wondering about this whole pathway and how IVIG may improve if this situation is involved? In regards to above posts, some things I'm wondering...... Galactose-deficient IgG binds to the mannan-binding lectin and thus activates the complement cascade by the lectin pathway It appears the mannose residues in Mycobacterium tuberculosis are important in it's antigenicity. If a state of deficient glactose IgG exists, would a hyperimmune response to TB infection occur? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC96927/ Mannan-binding lectin pathway The Mannan-binding lectin pathway (also known as the Ali/Krueger Pathway) is homologous to the classical complement pathway. This pathway uses a protein similar to C1q of the classical complement pathway, which binds to mannose residues and other sugars in a pattern that allows binding on multiple pathogens. Mannan-binding lectin (MBL; also called mannose-binding lectin) is a protein belonging to the collectin family that is produced by the liver and can initiate the complement cascade by binding to pathogen surfaces. http://en.wikipedia.org/wiki/Mannan-binding_lectin_pathway and fasting may increase the glycosylation status of IgG . I know it's probably very hard to think of any case of AN as being beneficial in any way, but I wonder if it's possible that the body fighting to stabilize in some cases? Maybe a protective mechanism that doesn't reverse properly when it's no longer required? Since your AN was not associated with body image problems, it makes me even more curious. http://rheumatology.oxfordjournals.org/cgi...nt/35/2/117.pdf CHANGES IN GLYCOSYLATION OF IgG DURING FASTING IN PATIENTS WITH RHEUMATOID ARTHRITIS Also, the possible Crohn's connection in this pathway sure seems noteworthy (bolding mine) http://en.wikipedia.org/wiki/Anti-saccharo...siae_antibodies Anti-Saccharomyces cerevisiae antibodies (ASCA), along with perinuclear antineutrophil cytoplasmic antibodies (pANCA), are among the two most useful and often discriminating markers for colitis.[1] ASCA tends to recognize Crohn's disease more frequently, whereas pANCA tend to recognize ulcerative colitis.[2] ASCA antibodies react to the following yeast proteins Mannans[3] edited to remove my edit!

Thanks SFmom and this was a wonderful statement to read!

mom2pandas & all, I was wondering if you would take a look at something I was trying to figure out a while ago. I was specifically seaching for info on "galactose deficiency," (therefore exposing N acetylglucosame ). The first excerpt was an article regarding hep B (these are just excerpts that I saved can't remember the whole article specifically). What struck me, was the "repeated immunization," statement. I was wondering how vaccines along with all of the illness that our children are exposed to in early childhood, plays into the whole scenerio. It seems incredible to me that there ISN"T a dangerous situation that gets set up with the immune system? Apparently, some lose the ability to synthesize galactose as a result of aging, but our little kids (if this is part of the problem)??? http://jvi.asm.org/cgi/reprint/JVI.01600-07v1.pdf A more exciting explanation for our results is that it is the result of immune stimulation. That is, it has been shown that a decrease in galactosylation of IgG is associated with repeated immunization and response to a specific antigen. Surprisingly, this is the same alteration that we have observed and it strongly suggests that there may be clonal expansion of a specific set of B cells, presumable those that secrete alpha-gal antibodies. It is noted that the glycosylation of IgG has shown to be directly associated with immune function(2). That is, it has been recently reported that IgG mediates pro440 and anti-inflammatory activities through the engagement of its Fc domain (Fc) with distinct Fc receptors (FcgRs). One type of interaction generates a pro-inflammatory effect while other interactions generate anti-inflammatory effects. The type of interaction is dependent upon the presence of terminal sialic acid residues on the N-linked glycan present on the IgG molecule(18). IgG molecules containing terminal sialic acid molecules lead to anti-inflammatory responses while IgG molecules lacking terminal sialic acid lead to a pro-inflammatory response. more on same subject http://jdr.sagepub.com/cgi/reprint/84/10/897.pdf In many respects, periodontal disease shares some common features with other chronic inflammatory diseases, particularly with rheumatoid arthritis, including: production of IgM and IgA rheumatoid factor (Hirsch et al., 1989); infiltration of inflamed tissue with mainly IgG-secreting plasma cells (Ogawa et al., 1989); production of auto-antibodies to tissue components (collagen II in rheumatoid arthritis; collagens I and III in periodontal disease; Hirsch et al., 1988); similar cytokine profiles (Fujihashi et al., 1993; Pistoia, 1997); and increased levels of IL-6 (Fujihashi et al., 1993; Pistoia, 1997). Extensive structural studies of IgG molecules produced at the site of chronic inflammation and detectable in the circulation revealed profound alterations in the glycan moieties. Specifically, deficiencies of some monosaccharides, especially galactose on IgG, have been described in human chronic inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease, tuberculosis, and infection with HIV (Mullinax and Mullinax, 1975; Parekh et al., 1985, 1988; Tomana et al., 1988; Bodman et al., 1992; Tsuchiya et al., 1993; Rademacher et al., 1994; Tomana, 1996; Moore et al., 2005). IgG contains one complex-type oligosaccharide (Fig. 1A) per each heavy chain linked to the conserved glycosylation site on asparagine 297 within constant region domain 2, which presumably has a role in maintaining the three-dimensional structure of the Fc portion of IgG. In IgG with galactose-deficient glycans, the terminally exposed sugar molecule is N-acetylglucosamine. Analysis of experimental data has indicated that galactose-deficient IgG is pathogenic (Rademacher et al., 1994): Galactose-deficient IgG binds to the mannan-binding lectin and thus activates the complement cascade by the lectin pathway (Malhotra et al., 1995). Furthermore, glycans on IgG molecules affect binding and internalization by Fc receptors expressed on phagocytic cells (Krapp et al., 2003) and, thus, influence opsonization of antigens by phagocytosis. http://www3.interscience.wiley.com/journal...470730/abstract Abstract Patients with rheumatoid arthritis have a reduced prevalence of immunoglobulin G (IgG) oligosaccharide chains terminating in galactose, thus exposing N-acetylglucosamine. We analyzed IgG glycosylation in patients with rheumatoid arthritis, patients with early synovitis, and in controls by means of isoelectric focusing and lectin-affinoblotting. The ratio of N-terminal N-acetylglucosamine and galactose was determined using specific biotin-labeled lectins. The IgG glycosylation state may well be of clinical value in the differential diagnosis of patients presenting with early synovitis. http://www3.interscience.wiley.com/journal...=1&SRETRY=0 ABSTRACT The relationship between increased levels of IgG oligosaccharide chains lacking galactose (GO) and the development of rheumatoid arthritis is unclear. In order to further our understanding of the observed correlation between raised serum GO and arthritis, we have studied GO levels in arthritis prone and non-susceptible (i.e., non-arthritis-prone) mice and the effects on GO of mycobacterial antigens, which have been postulated to play a role in the early events leading to the development of arthritis. We have shown that different age-matched mouse strains have characteristic "resting" levels of GO which (in six out of seven strains of mice) increase with age. We have also shown that these increases can be enhanced by immunization of arthritis-prone strains of mice with an adjuvant containing mycobacteria (Freund's complete adjuvant (FCA)), suggesting that deflects in the ability to regulate these GO changes may be related to susceptibility to arthritis. http://www.ncbi.nlm.nih.gov/pubmed/1146794...ogdbfrom=pubmed Glycoengineering of therapeutic glycoproteins: in vitro galactosylation and sialylation of glycoproteins with terminal N-acetylglucosamine and galactose residues. Raju TS, Briggs JB, Chamow SM, Winkler ME, Jones AJ. Analytical Chemistry, Genentech Inc., One DNA Way, South San Francisco, California 94080, USA. sraju@gene.com Therapeutic glycoproteins produced in different host cells by recombinant DNA technology often contain terminal GlcNAc and Gal residues. Such glycoproteins clear rapidly from the serum as a consequence of binding to the mannose receptor and/or the asialoglycoprotein receptor in the liver. To increase the serum half-life of these glycoproteins, we carried out in vitro glycosylation experiments using TNFR-IgG, an immunoadhesin molecule, as a model therapeutic glycoprotein. TNFR-IgG is a disulfide-linked dimer of a polypeptide composed of the extracellular portion of the human type 1 (p55) tumor necrosis factor receptor (TNFR) fused to the hinge and Fc regions of the human IgG(1) heavy chain. This bivalent antibody-like molecule contains four N-glycosylation sites per polypeptide, three in the receptor portion and one in the Fc. The heterogeneous N-linked oligosaccharides of TNFR-IgG contain sialic acid (Sia), Gal, and GlcNAc as terminal sugar residues. To increase the level of terminal sialylation, we regalactosylated and/or resialylated TNFR-IgG using beta-1,4-galactosyltransferase (beta1,4GT) and/or alpha-2,3-sialyltransferase (alpha2,3ST). Treatment of TNFR-IgG with beta1,4GT and UDP-Gal, in the presence of MnCl(2), followed by MALDI-TOF-MS analysis of PNGase F-released N-glycans showed that the number of oligosaccharides with terminal GlcNAc residues was significantly decreased with a concomitant increase in the number of terminal Gal residues. Similar treatment of TNFR-IgG with alpha2,3ST and CMP-sialic acid (CMP-Sia), in the presence of MnCl(2), produced a molecule with an approximately 11% increase in the level of terminal sialylation but still contained oligosaccharides with terminal GlcNAc residues. When TNFR-IgG was treated with a combination of beta1,4GT and alpha2,3ST (either in a single step or in a stepwise fashion), the level of terminal sialylation was increased by approximately 20-23%. These results suggest that in vitro galactosylation and sialylation of therapeutic glycoproteins with terminal GlcNAc and Gal residues can be achieved in a single step, and the results are similar to those for the stepwise reaction. This type of in vitro glycosylation is applicable to other glycoproteins containing terminal GlcNAc and Gal residues and could prove to be useful in increasing the serum half-life of therapeutic glycoproteins.

SFmom, Could you say what test was used for toxic levels, and what toxins were indicated?

bubbasmom, I will pray that you have good news to report in the days to come. Hugs to you and your son. Tell him that his struggles might very well be helping many others and the willingness of your family to share his experience is SO appreciated. Mommd, I'm assuming that you mean that IVIG will clear lodged immune complexes? Can you give any further info on how IVIG accomplishes this and what the likelyhood is that more won't form?

IMHO, I think there is room for it to go both ways... harmful or helpful. Did anyone notice it was Trevor Marshall who was involved in the report? We have a couple of threads with some info on his theories, if anyone would like to look deeper http://www.latitudes.org/forums/index.php?...rshall+protocol http://www.latitudes.org/forums/index.php?...rshall+protocol

Susan, I was just reading this thread and wanted to say that I'm praying your daughter recovers well too. It's awful when your child is just plain old sick, not to mention the special fears that go along with all of this. I have to keep reminding myself that we have had many illnesses around here where nothing went haywire. Hoping tomorrow brings good news on her recovery