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Buster

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Everything posted by Buster

  1. Typically zith is way easier on the stomach than Augmentin XR. Certainly possible. When you say Strep Antibodies were elevated did you have a baseline? Usually GABHS isn't accompanied with a cough. I'd recommend being careful about putting too much stock in ASO or Anti-DNAseB unless you have a prior reading 2 weeks earlier. ASO and AntiDNAseB are measured from a rise in titer, not from stable values. That is exactly the point. The immune system is now primed. Think of it like someone with an allergy. Now that the body has learned an abnormal recipe for response, it's primed.
  2. Hi Cristo, Azithromycin is a macrolide that works by preventing replication by inhibiting an enzyme used in bacterial division. Azithromycin does have anti-inflammatory effect and has some immunomodulating effect. Immunomodulating means that it affects the way that T-cells respond to an invading antigen. There are two ways T-cells respond to antigens - they respond to extracellular bacteria and to intracellular threats. Azithromycin shifts the balance so a bit more intracellular Thelpers are created. In some countries certain strains of bacteria have become resistant to macrolides (of which azithromycin is one). What basically this means is that the bacteria is not slowed down by azithromycin. So the advantage of azithromycin (only have to take it once per day, has a long half-life, ...) is great but some strains are resistant to it -- penicillin still works on most strains of GABHS but can't reach intracellular strains and some people are allergic to penicillin. Buster
  3. Hi Cristo, Azithromycin is a broader spectrum antibiotic than penicillin. Penicillin pretty much only goes after extracellular GABHS as long as it is replicating rapidly. It does this by disrupting the cell wall of the GABHS. With respect to viruses (i.e., flu or cold), azithromycin (or any antibiotic) won't be effective against those. The typical "bad side effects" are that long term use of azithromycin will likely enable replication of azithromycin resistant strains. This happens because bacteria basically wants to grow and if you clear out a bunch of gram positive bacteria -- anything left grows in its place. Usually this isn't a problem but occassionally not so nice stuff is lurking around and can grow instead of what was there. This is why a probiotic is usually recommended so you put back non-harmful stuff. Regards, Buster
  4. Depends in what context it is used. On this forum, we usually talk about the immunomodulating effect of azithromycin. Azithromycin has been found to shift the Thelper cell maturation from Th1 to Th2. This means that it changes the cytokine generation and targets intracellular antigens. EDITED to fix Th1 to Th2
  5. Sounds right. The dimple is the telltale sign. Typically eraser size. In people with immune issues they can get size of dime.
  6. Super strange question, but are you sure they are molluscum and not subcutaneous nodules or hives? Are they itchy? How was molluscum determined? How big are they and how many? Where are they located? Buster
  7. Hi Priscilla, There are five main theories why antibiotics might be effective (despite negative throat culture for GABHS): Antiinflammatory properties Intracellular strep Immunomodulating properties non-strep based infection someone else in house is a carrier Azithromycin in particular is antiinflammatory and so you might be seeing that effect. Certain M-strains of GABHS have been shown to go intra-cellular. This means the bacteria is acting more like a virus. As the cell bursts (or is destroyed by a macrophage) the bacteria can reenter the blood stream and the immune system responds again. This is one possible explanation of a chronically elevated titer. It also could help explain why Augmentin XR is being effective. Azithromycin is immunomodulating (shifting Th2 to Th1). Th1 tends to target intracellular infections. There may be another infection (such as mycoplasma pneumonia) that is being contained by the abx. When the abx stop, the infection returns. Finally, what you might be seeing is recolonization from an active carrier in the house (i.e., that when you stop abx you are essentially getting recolonization or a ping-pong effect). This is why we tend to recommend checking all in the house if you are seeing a canary effect. Best regards, Buster
  8. Hi Priscilla, Abx do not remove the antibodies so the ASO or AntiDNAseB will still rise. Abx can limit the # of antibodies by helping the immune system by slowing the advancement of bacterial infection. Those who have ASO rise will have the rise 1-4 weeks after the initial infection and have a rise in AntiDNAseB 6-8 weeks post infection. The rate of fall is not known (literally no studies). Please recall that ASO and Anti-DNAseB are responses exotoxins of the strep, not to the strep itself. Regards Buster
  9. 1 gm/kg/day x 2 days ==> 2 gm/kg total dose in our case.
  10. Probably the most important item in Kurlan's 2008 study is that over a 2 year period, none of the children in his study had more than a 1.6 point variance in OCD symptoms (as measured by CYBOCS). This means these children had no OCD exacerbations with or without streptococcal infection. Pretty unheard of for most PANDAS kids. Kurlan tries to assert that these kids met the PANDAS criteria, but they sure weren't like any of the kids talked about on this forum or in Swedo's studies. Buster
  11. Hi Wilma, I've been trying to think about how to answer this question. To put this in perspective, most of the controversy in PANDAS comes from a specific group of non-pediatric neurologists at Johns Hopkins who have seen fit to run experiments on children and adults diagnosed with Tourettes (i.e., vocal and motor tics for > 3 years without remission for > 3 months) rather than children with sudden onset and episodic course. In my opinion, the researchers didn't have a PANDAS kid in their study. My reason is looking at the CYBOCs scores of their patients. In their study, they had < 2 point variance in CYBOC scores over a 2 year period (i.e., no change in OCD) -- that is just unheard of in most PANDAS kids. Swedo had variances of 26 pts (mild to severe) during an exacerbation. So now you take that they are running tests where they have no PANDAS kids and they get negative results. Rather than recognize a flaw in their experiment, they publish their negative results and publish inflammatory editorials in the same issue calling into question the whole hypothesis of PANDAS. This is, quite frankly, bad science. A negative result is just a failure to confirm, it is not refutation. So irritating. Issue #1 is therefore a failure to properly screen subjects and correctly apply the PANDAS criteria Issue #2 is that PANDAS is both a description of symptoms and a statement about cause. There is little doubt kids have the symptoms (many many videotapes and writing samples and tests done to verify the symptoms), what is questioned is whether GABHS is the cause of the symptoms. Remember to show causality you have to show the result always follows the trigger and can't happen without the trigger. It is a high bar and unfortunately PANDAS is trying to get recognition for symptoms while trying to prove causality (rather than co-occurence) Issue #3 is that GABHS is thought to be a minor infection today. Almost no pediatrician has any experience with Acute Rheumatic Fever or Sydenham Chorea. Most do not know that 30% of ARF patients have SC and 70% of SC patients have OCD. Somehow the medical community has forgotten that many died of GABHS only 50 years ago. Issue #4 is that researchers confuse treated GABHS infection with untreated GABHS infection. PANDAS and SC are thought to be sequela to untreated GABHS infections (hence why you put kids with SC on prophylaxic antibiotic to minimize reinfection). But if you look at research studies, almost all of those studying non-sudden-onset break the blind and "treat" GABHS infections. Uhhh, duh, they ruined the experiment. Sure that was the only way to get through an IRB, but guys, you wouldn't have found SC if you ran an experiment that way. Issue #5 is that researchers think Sydenham Chorea is self-limiting (i.e., clears in 6 months). What most haven't studied is that only the movement disorder last 6 months, the OCD symptoms can last a lifetime without intervention. It is this exact item that Sue Swedo was studying -- the resolution of OCD symptoms due to intervention was the new discovery in SC and subsequently in PANDAS. I am terribly tempted to write a rant here, but will stop and say that I think those who are writing such entertaining titles as "PANDAS: Horses or Zebras" should stop feeling so damn clever with their provocotive title and be aware that their stupid little editorials are inhibiting some really sick kids from getting help. Buster I think there is scientific evidence- maybe proof is too strong a word. More and more, it seems to me, doctors are turning to "standard of care" and protocol checklists to treat patients and avoid personal responsibility for decisions. PANDAS treatment does not yet have a "standard of care" or standardized protocol for treatment, so docs who do treat it are kind of sticking their necks out professionally. God bless them for trying to help our suffering children.
  12. Folks, The halflife of augmentin is 1.3 hours. For a 400mg dose, this means you are down to 9.5 mg remaining at 8 hours. By 12 hours there's only 1.1mg remaining. Essentially if you are not dosing every 12 hours, you are unprotected on Augmentin. If you want to go to low dose, then do 200mg twice a day. Remember every hour the dose is half the prior hour. So to reset the coverage, you have to dose twice a day. Buster
  13. Yes, that's a great paper. Even more interesting is this paper by Cleary and Wang: http://www.pnas.org/content/107/13/5937.full.pdf+html For those who don't love reading about TNF-Beta and T-Helper cell type 17 and Interleukin 17.... What Wang and Cleary found was that (in at least mice), if they sprayed GABHS into the noses of the mice (i.e., just nasal colonization -- not infection), the mice produced abnormal amounts of Th17. Th17 is highly implicated in auto-immune diseases. Curiously, if they innoculated the mice with GABHS in the blood stream, the mice produced Th1 (i.e., non-auto-immune response). The significance of this is not known and whether the result also happens in people is not known -- but awfully interesting. Buster
  14. Steroids do not do anything to GABHS. Steroids suppress the immune response preventing further creation of the antibody that in PANDAS patients cross-reacts with neuronal tissue. So Steroids are an anti-antibody (i.e., stop the formation of the antibody). Short answer is yes. time. a burst is typically 5 days. A tapered course is usually 20-30 days. Usually when someone has a burst/taper it is often the same initial amount/day, but on a taper you are kept on longer and tapered off. well, steroids are really nothing to mess around with, but most doctors feel comfortable with steroids for cases of poison ivy or other immune responses. 5 days is really intended as more a diagnostic technique -- was there improvement. This tends to indicate an auto-immune response. 30 days is more like a treatment dose because it may break a cycle. The half life of one of the antibodies in PANDAS is thought to be 28 days. Generally dosing < 30 days is not thought to create a lot of issues with the immune system -- i.e., shut down the body's own ability to produce anti-inflammatories -- but otherwise you need to taper. Buster
  15. Hi, Yes you can get strep while on antibiotics. Please remember that antibiotics just slow down GABHS, they don't kill it. Strep has four stages: adhesion colonization invasion infection Antibiotics are effective at addressing infection because they slow the growth rate of bacteria. T-cells/macrophages are really the army needed to attack bacteria. During invasion, antibodies do rise and so invasion can absolutely cause symptoms. Invasion can occur even if on antibiotics because most often the macrophages can't get to the invading colony before a T-cell/B-cell response. If the party is particularly sensitive, then you'll get high antibody response. Colonization also seems to cause some antibody rise. It is not clear if this is because the T-cells get across and reach the colony or because members of the colony are invading the connective tissue and reach T-cells. Both are possible. In either case, your IgA is usually the most effective at clearing colonies and breaking adhesion. If someone is IgA deficient, they will often have difficulty clearing colonization and breaking adhesion. One other interesting finding by Cleary in 2009 was that only nasal colonization with GABHS was needed to induce Th17 response in mice (as opposed to the normal Th1 response that comes from invasion). Th17 is implicated in the elevated IL17 associated with auto-immune diseases. Bottom line, you absolutely can have antibody response while on antibiotics and have repeated invasions/colonizations -- antibiotics help the body fight infections. Antibiotics do not in and of themselves clear colonization or adhesion. Regards, Buster
  16. Steph, When was she treated for Babesia and Lyme and what was the treatment? Is the current prescription of Flagyl part of the Lyme treatment or are you treating something else? Was she primarily hospitalized for the ED? I realize she's not really eating -- does she express interest in food (like want to cook it?) Does she like its smell? Does she talk about it a lot? or do you see sort of a disinterest in food or her talking about what happens when she eats? Does she seem fixated on any topic? What dosage are you giving for the azith and clindimycin? What prompted the use of clindimycin? How long has she been on it? If you take the symptoms since August 2nd -- how would you describe the symptoms - relatively constant? Aside from the restrictive eating, what else are you observing? I realize this is a ton of questions but I'm just looking for any hints of anything that might offer a clue about what's going on. Regards, Buster
  17. Wow. I'd like to check a couple things.... Your DD7 has just had 3rd IVIG -- and last one was at 1.5mg/kg (?). You indicate child might be still positive for Lyme and Babesia -- has a recent babesia test been run? Have you tried an anti-reflux medicine like pepcid? Sometimes kids can't tell the difference between acid reflux and a sore throat. Has at least a throat culture been run? Were tonsils red or inflammed? It sounds like your dd7 has been on a lot of different meds -- did you see any real benefit from any of them or has symptom of food refusal been present throughout? DD7 exhibits significant OCD symptoms -- however, at this point mostly choking fear is present. Attempt was made to use SSRI, but this did not seem to improve choking fear (is this still true)? DD7 is still on azith/clindimycin -- clindimycin has some nasty side effects if used for too long -- how long on clindimycin? Is DD7 still having bowel movements? Any thought about whether stomach pain could be an ulcer -- any test done? I realize that not eating could be causing the stomach pain, but wondering what other tests were run there? Buster
  18. Okay, I just had to add to this thread... I recently was following up on an assertion by a bunch of well-known neurologists that Sydenham Chorea was a self-limiting disease. I wanted to know the source for that assertion. What I found was quite the opposite. Sure the chorea seemed to be self limiting, but for those who got Sydenham Chorea who also got OCD, this seemed to be non-self-limiting and would go on for years if not treated. In 1965, Freeman wrote that while the outright chorea tends to resolve, the psychological disabilities of Sydenham Chorea are long lasting. "The major findings in this study are the high incidence of psychological difficulty prior to the onset of chorea, and the startlingly high current incidence of psychiatric disability, an average of twenty-nine years after the original choreic episode.... The 75% incidence of psychiatric disturbance in chorea patients stands in marked contrast [to the control population of 5-33%]." What caught my attention was that neurologists were treating Sydenham Chorea as self-limiting because the chorea tended to go away within 6 months (in many cases). How on earth can a disease that has long term psychiatric symptoms if not treated be called "self-limiting" just because one of the symptoms goes away. If you have found an article indicating the OCD symptoms are self-limiting (i.e., without intervention), I'd be interested in the reference. Buster
  19. In our case, we did the following: We selected 4 handwriting samples: one pre-illness (February) one during exacerbation (March) one pre-treatment (June) one post-treatment (August) This was incredibly effective at conveying the effect treatment had on legibility and fine motor skills. We then had a cover letter that said: ______ has a dysfunction in her basal ganglia specifically around fine motor and orthographic memory. This is a medical condition and not a lack of trying or lack of desire to do better. Like someone who has had a stroke, it is incredibly frustrating for ________ to do simple tasks everyone else can do. Even copying a word is a chore. Orthographic memory is pattern matching that affects both how we recognize words/numbers (sight reading) and how we know how to spell words. ______ struggles to produce words in the right shape. You may be surprised to see that ______ is misspelling a word that is written in the question above her answer. This is because copying is more difficult for her than guessing at the word shape. As such, please provide ways that she doesn't have to copy material particularly far-point copying. ______ is recovering from this illness and it will take some time for her brain to relearn prior skills. In our case, handwriting deterioration is the most noticable sign that something is wrong. We will likely notice symptoms before you will -- but if you do see significant deterioration in legibility please let us know. We would also appreciate being informed if a child in the class is out with a contagious bacterial infection such as strep throat. _______ is particularly sensitive to strep throat and early awareness will help us help her. --------------- In our case our daughter is post treatment but we still had a tough time with the school. It really is tough for them to see her skilled in all sorts of other ways and still not able to spell certain words. Buster
  20. We also had escalations after dental treatment -- we thought it likely that GABHS in throat was getting into blood, but Nitrous Oxide also affect BBB. Buster
  21. So does this mean that you treated your children with an antibiotic when they first tested positive? Was the "lab test positive" a statement about running a agar culture or something else? The behavior you describe certainly matches the OCD symptoms on this forum. Have you tested kids 3 weeks after treatment to ensure they are clear? Were they clear in the summer (easiest time to clear kids typically)? Regards, Buster
  22. In post http://www.latitudes.org/forums/index.php?showtopic=9948&view=findpost&p=83817 , Fixit asked One of the better references on mycoplasma assays is http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1153783/pdf/1937-04.pdf where they compared 10 methods for analyzing Igg and Igm for mycoplasma pneumonia. These assays were from AniLabsystems Biotest CFT Diagnosys ImmunoCard ImmunoWell Novum Platelia Ridascreen Serion classic 4 SerodiaMycoII SeroMP Virotech Of these tests, most had an agreement between the Igg test and the Igm test of ~80% (meaning the two tests the same on the sample 80% of the time). Notably the Novum test only agreed between Igg and Igm tests 54% of the time. In terms of positive predictive value (how often a positive is a real positive) these are all over the map. Novum and Immunocard has a positive predictive value of ~30%, whereas others were around 80%. This means that a lot of the tests had a lot of false positives. The negative predictive value (i.e., how often is a negative a real negative) was more around 80-90%. So you should read this that negatives are more informative than positives. A very nice part of the paper deals with when to run the Igg and Igm tests. figure 2 shows the sensitivity of the test was best at >=16 days after onset. If tested within first week, most did not have results. I do not follow mycoplasma enough to know the significance of rises in test results, but it looks like the tests are exquisitely sensitive to running the same test twice and given the low specificity and low positive predictive value, you should find out which assay was run and look at the negatives more than the positives. Buster
  23. Okay, for the way more than you wanted to know camp see http://jcm.asm.org/cgi/content/abstract/35/4/839 for the different types of measurement procedures for ASO The basic approaches are: Toraysphere Rantz-Randall NA-Latex-ASL method Each of these methods has a variety of false positives (FP) and false negatives (FN) even for a perfect sample. The most useful measures compare True Positives (TP) to false positives(FN): positive predictive value -- how likely a positive is a true positive (TP/(TP+FP)) negative predictive value -- how likely a negative is a true negative (TN/(FN + TN)) In terms of the above tests, the tests have: Toraysphere - 81% PPV, 79% NPV Rantz-Randall - 67% PPV, 62% NPV NA-Latex-ASL method - 76% PPV, 69% NPV However, the most important factor is that if the blood sample is taken at the wrong time then there isn't any ASO in the blood to test for. Undoubtely more than you wanted to know -- but the importance is that > 30% of cases will have false negatives even on very good samples. Buster
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