Buster
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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
I read a post on this site that said that azithromycin is an immune suppresser. I believe that it what it said. I can't locate it now. I am wondering if giving a child azithromycin will cause immune deficiency.
My ds7 seems to get fevers on and off, and sore throats more regularly than usual. I am wondering if azithromycin could have caused some kind of immune defiency. Some people on this site suggested that I take my child to an immunologist to check his immune system, so now I am wondering about azithromycin.
Also...how do you know when azithromycin stops workng,and the person can no longer use it because of over use? Pharmacists and doctors say that they are fearful that using azithromycin will cause people to not be able to use the medication, because it will no longer work. CAn someone explain this.
Any thoughts on this topic?
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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
I read an old post by EAmom about azithromycin, and have a question. She was talking about the possible bad effects.
Does this mean that azithromycin will help strep and pneumonia, but will make the body stop fighting against ordinary things like the flu or a cold, whereas pen v will still keep the body fighting against things?
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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
What does immune modulating effect mean?
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Sounds right. The dimple is the telltale sign. Typically eraser size. In people with immune issues they can get size of dime.
They are on the inner thigh and she has three on one leg and about 6-8 on the other. They have a little dimple in the middle of the bump. Two are red at the moment. We saw S. Smith in Edison, who looked at them and said they were molluscum because of the dimple.
He also felt that she was a little old for them and that could be a sign of an immune problem.
Thanks for responding.
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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
We are about 6 weeks into our current recurrence. Our dd had a molluscum tag get infected (bad) they thought it may be a staff infection and treated with abx about 6 months ago. She still has them and they off and on get red and irritated if she scratches them. I'm wondering if these could be part of the culprit for this latest recurrance and since this one is the worst ever, whether she is not getting better with the Abx because she her body is dealing with the molluscum virus?
Any input would be helpful.
Also, just to complicate things, she had a deer tick bite 2 years ago and I got bit when I was pregnant with her.
We are just trying to figure out how to get these symptoms to subside and treat the appropriate thing.
Sooooooo Confused.
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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
I understand the abx don't remove antibodies, and may help supress infection progression "if" there is still an infection (may be even property of some abx). I guess it just gets complicated when there hasn't been ANY sign of infection for at least 3-4 months, and antibodies are elevated (our case). Of course as you said, we don't know how long it takes for them to fall, but the severe exacerbation of symptoms was not until 3-4 mos post illness, and it was the ASO that was elevated. Then I get stumped on why abx work so well, symptoms resurge when off abx, then they work again. So as speculated, either the antibody production doesn't shut down (even in the absence of infection), or the infection persists, in our case, with No signs or symptoms of infection. Then a child could be doing ok, and exacerbate without a strep illness. Again, either glitch in antibody production, or a low lying chronic infection resurfacing. (So just thinking outloud online) I am wondering if it is an infection, why has it become so hard to erradicate, even after months of abx- has this strep morphed into a "superbug", and enabled itself to hide from abx, then trigger this immune response again and again. I know we don't have all the answers we want (if we did, we wouldn't be here). Just my PANDAS mom mind spinning again. Thanks
- Antiinflammatory properties
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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
Thanks Buster. I have also noticed some reports of titers rising after abx. I was thinking about how Lyme antibodies can rise after abx due to the changing of the organism (possibly migration???) Got me wondering if an intracellular strain of Strep lurking could cause the same response (increase in titers after abx) Any thoughts??
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what dosage have others been receiving for the IVIg infusions for their children that have had success?
1 gm/kg/day x 2 days ==> 2 gm/kg total dose in our case.
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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
Thanks Phasmid - I was able to read the article. Really just the same stuff we saw before. The article is by kurlan only and the PANDAS section just highlights his prospective study. It says:
The observation that Tourette's syndrome resolves or becomes less severe in a substantial number of patients as they grow into adulthood suggests that the underlying mechanisms involve processes that may correct themselves as the brain matures. On the basis of clinical similarities between Sydenham's chorea and Tourette's syndrome with OCD, the PANDAS syndrome (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) was hypothesized as an autoimmune response to streptococcal infection that might precipitate or exacerbate tics. A recent intensive, prospective, blinded, clinical and laboratory cohort study, however, did not identify any temporal link between streptococcal infection and clinical exacerbations in patients who met the criteria for PANDAS.49 The reference for this quote is:
Kurlan R, Johnson D, Kaplan EL, Tourette Syndrome Study Group. Streptococcal infection and exacerbations of childhood tics and obsessive-compulsive symptoms: a prospective blinded cohort study. Pediatrics 2008;121:1188-1197
CrossRef | Web of Science | Medline
Yes.. it was definitely double blinded. Actually... the study was TRIPLE blinded since no one knows how many of the kids with PANDAS got antibiotics during the course of the study and no one knows if they would have actually had exacerbations linked to strep if they did not have antibiotics and /or if they were not taking psychotropic drugs to reduce their tics and OCD symptoms. Funny... Kurlan does not mention these limitations when he discusses the 2008 study....
... and I was hoping Kurlan was coming around after publishing with Murphy and Leckman! Maybe this article was submitted a long time ago - before the NIMH meeting in July 2010
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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
why don't all doctors believe that PANDAS exists? Isn't there scientific proof that backs the validity of PANDAS? Why such controvery? Thanks
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.
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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
the first 2 months after ivig were great, lots of improvements. then she went downhill a bit with exposure in school. she was taking 400mg of augmentin once a day. i feel terrible, i first thought her complaints were anxiety based because the augmentin would cover her, i should have brought her in right away. so far she is still functioning, but ocd is worse and some other stuff. really though it is not too bad so far. except for taking meds, she is really scared to take them like before. i am wondering why her reaction to strep this time is so mild compared to the others that were debilitating. could it be from the ivig, or the low dose abx?
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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
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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
Hi Buster,the IVIG #3 was 1.5gm/kg.(Sorry typo)I haven't had much sleep lately.It was done the 2 nd week of August.Sept 2 until 9th she was in the hospital.The ped in the hospital refused to do a ENT consult even though she c/o severe sore throat and was red on one side.Also uvula was long and probably swollen.She has a central line in and is getting IV fluids,Azith on Mon,Wed,Fri and Clinda Tue and Thur.Also this week had a few doses of Flagyl.I have asked about prevacid IV but the doc wanted to hold off.(In August when this started she c/o abd pain and sore throat)If anyone reading this has a good ENT or GI doc we will go.We saw a ENT months ago but he didn't even do a culture even though she c/o a scratchy throat.It is frustrating dragging her to a doctor and then just being blown off.She has not taken the zoloft yet.She can swallow-had a few sips of oj this am.(Only thing that she will drink)I don't know if it is all OCD related or if there is also a medical issue.Her aso and anti d nase b was always low.But was higher in the hospital ,so it could have been rising or falling.(The one doc in the ED wouldn't even check it)If I could order the d---stuff myself I would!The one doc did not call me back today and I have called several times.I will ask again about the prevacid.I think you are right. IV antibiotics has been for 2 weeks.She is having a small bm.Dr.Jones said it can take months to treat babesia and we have not had it re-checked.It was done not long ago.She had a tick bite 2 years ago so brewing.She had a bite or two of jello today but that is all.Prior to August she had no problems eating.She c/o mucous and her throat being scratchy.This has been on going.Sometimes the ocd changes and we hope that we can get this turned around.I told Dr.Bransfield about Wendy mentioning that Benadryl is helpful with lyme because of issues with histamines.He was going to order Benadryl or Vistaril IV.I don't know when we will get it.We tried Ativan cream (topical)but no effect.We do see a difference being on antibiotics-ocd s/s and anger decreased.Thanks,Steph
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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
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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
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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.
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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
- one pre-illness (February)
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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
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We rechecked 10 days later rapid strep negative but lab test positive
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
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In post http://www.latitudes.org/forums/index.php?showtopic=9948&view=findpost&p=83817 , Fixit asked
Buster..does the same hold true for myco p..
a reading in mayish was 1.60 another draw 3 weeks ago was 1.79 (above .90 igg could be positive)
dan doc said no worry...margin or error..and these numbers can fluctuate...
however..in last week we have motor tics which were 90% other than times of stress or a specific trigger..
how much time should go by before another draw...??
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
- AniLabsystems
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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
First, to compare results you need to use the same laboratory and test procedure.
- Toraysphere
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My dd9 is in the category of always having normal ASO/D-NASE titers, but her recent blood test shows an increase in ASO (but still normal). Is this just due to exposure, not infection?
ASO= Nov-17, Dec-17, August-48
D-NASE= Nov-60, Dec-120, August-60
The Dnase in December would indicate a potential infection in September/October. The low ASO is pretty meaningless as it is less than one dilution apart. I'll explain below:
First, to compare results you need to use the same laboratory and test procedure. Generally a positive rise is defined as > than a 2 dilution rise. This means that if you measured 1:60 when convalescent and later 1:120 you would be considered to have a positive rise. The dilutions are typically: 1:60, 1:85, 1:120, 1:170, 1:240, 1:340, 1:480, 1:680, 1:960, 1:1,360, 1:1,920, and 1:2,720.
Numbers that fall inbetween can be done by individual labs but aren't standardized. Numbers under 60 are outside the sensitivity of the typical measurement system (although you might want to check your particular lab). Basically, I'm saying they can't tell you very much about your ASO because it is below 60 (the first dilution).
So for what you posted, the anti-DnaseB would be considered a rise indicating that there was a likely infection in late September. It is not surprising that the ASO would not rise.
In terms of what your doctor will say, he/she will likely say both are "normal" despite the rise (because most doctors don't know that rise is more important than absolute value).
The CDC back in 1971 set the upper limit of normal http://www.ncbi.nlm.nih.gov/pmc/articles/PMC377331/ for school-age kids of: school age, ASO = 170; ADNB of 170.
Kaplan from the world health organization did a broader study in 1998 http://pediatrics.aappublications.org/cgi/content/abstract/101/1/86 and found the ULN for their sample to be 240 for ASO and
640 for AntiDNAseB. Many laboratories (including the Mayo clinic) use an ULN of 400 for ASO.
Bottom line is that rise is more important than absolute value. If you don't have a prior reading you are forced to use ULN. To compare for rise, you must use the same laboratory and equipment/test. A rise must be two dilutions apart to avoid experimental error.
Regards,
Buster
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PhillyPA,
Call your doctor. Shooting chest pains and shortness of breath are definitely cause for concern. Both are rare side effects attributable to augmentin. Is the shooting chest pain more gastric reflux or heartburn? He may not know what that feels like.
Also, did your child have other movement disorder or subcutaneous nodules before the diagnosis of PANDAS?
Regards,
Buster
My 6 year old son got PANDAS this summer. It was caught early. He spit out his food for three weeks. Steroids and augmentin took care of it.
He has been complaining of trouble breathing. Tonight he got shooting chest pains about 10 minutes after I gave him his augmentin. I read the side effects and these symptoms seem to from the augmentin. I am stopping it tomorrow.
Has any one else had these side effects?
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Vickie's comment is also correct. There is asymptomatic carriage where there is only colonization, then there is low level invasion ( I.e where there is an immunologic response such as elevated ASO/AntiDNAseB) and then there is all out infection where the bacteria overwhelms the immune system.
Only the first one is referred to as asymptomatic carriage because in the second case there is an immunologic response. I asked Dr Kaplan why he think there isn't an immunologic response in the first (i.e., couldn't it just be ineffective IgA clearance of the colonization). He said they don't know. They just know that antibiotics such as penicillin don't work great if the bacteria is growing slowly.
So for those with colonization only and slow growth, they need a different type of antibiotic to clear that doesn't rely on rate of growth.
Buster
A little bit about ASO Titers
in PANS / PANDAS (Lyme included)
Posted
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.