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Can strep hide in the body from a throat culture?


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Why is it not being published that Azith has the abilities to penetrate the biofilms defenses and kill the bacteria within? I thought we had a few medical researchers on this site. In my opinion that would be a great article to write and publish. It would also be useful to all the parents out there who are trying to explain this connection to our Dr's that don't seem to get the PANDAS /strep connection because our kids often culture negative from a throat swab. If only that article was out there I believe the treatment of our PANDAS kids would be so much more cut and dry. I pray one day the confusion of this diagnosis will be cleared.

 

The research being done on zith's effects on biofilms is in the area of cystic fibrosis, and there have been papers published on its effectiveness in that area- it just hasn't been applied to other areas. I suspect many doctors would simply say that it doesn't apply because your child doesn't have cystic fibrosis, but, If I was trying to convince a doc to try zith, I'd bring the info on biofilms and the studies done on using zith to destroy biofilms in CF.

 

 

It sure makes sense to me. However what's so confusing is when I google zith vs. augmentin I always get a ton of articles that insist that augmentin is superior to zith in eradicating strep?

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It sure makes sense to me. However what's so confusing is when I google zith vs. augmentin I always get a ton of articles that insist that augmentin is superior to zith in eradicating strep?

 

Augmentin may be better at killing strep (I honestly don't know), but it can't kill it if it can't get to it. Zith can penetrate the biofilm defense system, augmentum can't. The interesting thing in the CF studies is that zith is not supposed to be effective against the bacteria that cause CF- and yet it does break up the films thatcause the problem. What I absolutely know for sure, is my child responds amazingly well to zith, but only minimally to other antibiotics.

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Peglem, Pat, Collen, Natterbus...

 

Peglem...maybe different??? Intracellular strep is strep that's gone into epithelial cells:

 

Intracellular survival of persistent group A streptococci in cultured epithelial cells.Marouni MJ, Barzilai A, Keller N, Rubinstein E, Sela S.

Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.

 

Group A streptococcus (GAS) is the principle etiologic agent of bacterial pharyngotonsillitis and a wide range of other diseases. Failure to eradicate GAS from patients has been documented in 5-30% of patients with pharyngotonsillitis, in spite of the continued sensitivity of GAS to penicillin and other beta-lactams. It was recently proposed that eradication failure might be attributed to the ability of GAS to maintain an intracellular reservoir during antibiotic treatment. We have previously shown that strains derived from patients with bacterial eradication failure, despite antibiotic treatment (persistent strains), adhered to and were internalized by cultured epithelial cells more efficiently than strains that were successfully eradicated. Since, penicillin and other beta-lactams do not penetrate well into mammalian cells, intracellular survival of GAS is crucial in order to persist during prolonged antibiotic treatment. In this study, we compared the survival of GAS strains from cases of eradication failure and eradication success, using an epithelial cell culture model. We found that persistent strains show significantly increased intracellular survival, compared to the 'eradication success' strains. This finding supports the idea that an intracellular reservoir of GAS plays a role in the etiology of antibiotic eradication failure.

 

Colleen...on a similar vein, we've wondered about combining antibiotics...eg using Azithromycin with one that is bactericidal. Although DH read somewhere that Azithromycin is bacteriocidal at higher doses. Someone posted a while ago about seeing an immunologist in SF who put their child on an antibiotic cocktail...when I asked what the drug combo, she didn't respond.

 

Pat...maybe the articles that say Augmentin is better than Az were referring to in vitro studies, not factoring in the intracellular problem (or biofilm?)?

 

Natterbus...oohh. Dh had an article somewhere about culturing post abs...hopefully I'll find it soon.

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Peglem, Pat, Collen, Natterbus...

 

Peglem...maybe different??? Intracellular strep is strep that's gone into epithelial cells:

 

Intracellular survival of persistent group A streptococci in cultured epithelial cells.Marouni MJ, Barzilai A, Keller N, Rubinstein E, Sela S.

Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.

 

Group A streptococcus (GAS) is the principle etiologic agent of bacterial pharyngotonsillitis and a wide range of other diseases. Failure to eradicate GAS from patients has been documented in 5-30% of patients with pharyngotonsillitis, in spite of the continued sensitivity of GAS to penicillin and other beta-lactams. It was recently proposed that eradication failure might be attributed to the ability of GAS to maintain an intracellular reservoir during antibiotic treatment. We have previously shown that strains derived from patients with bacterial eradication failure, despite antibiotic treatment (persistent strains), adhered to and were internalized by cultured epithelial cells more efficiently than strains that were successfully eradicated. Since, penicillin and other beta-lactams do not penetrate well into mammalian cells, intracellular survival of GAS is crucial in order to persist during prolonged antibiotic treatment. In this study, we compared the survival of GAS strains from cases of eradication failure and eradication success, using an epithelial cell culture model. We found that persistent strains show significantly increased intracellular survival, compared to the 'eradication success' strains. This finding supports the idea that an intracellular reservoir of GAS plays a role in the etiology of antibiotic eradication failure.

 

Colleen...on a similar vein, we've wondered about combining antibiotics...eg using Azithromycin with one that is bactericidal. Although DH read somewhere that Azithromycin is bacteriocidal at higher doses. Someone posted a while ago about seeing an immunologist in SF who put their child on an antibiotic cocktail...when I asked what the drug combo, she didn't respond.

 

Pat...maybe the articles that say Augmentin is better than Az were referring to in vitro studies, not factoring in the intracellular problem (or biofilm?)?

 

Natterbus...oohh. Dh had an article somewhere about culturing post abs...hopefully I'll find it soon.

 

 

all very good thoughts. I wonder if a child would have an elevated ASO titer if there is intracellular strep (that is not cultured out in the throat)? Pat

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Pat,

Skin strep doesn't cause a rise in ASO.

That's a really good question about intracellular strep, whether it causes less of a rise than reg. strep throat.

 

I know certain strains of strep are going to cause more of an ASO rise than other strains. And certain strains of strep are more likely to to intracellular. Certain strains of strep are more likely to cause Acute Rheumatic Fever. And I would assume certain strains of strep are more likely to cause PANDAS...that is something that the CDC should tract, if certain strains of strep are triggering PANDAS episodes...

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all very good thoughts. I wonder if a child would have an elevated ASO titer if there is intracellular strep (that is not cultured out in the throat)? Pat

 

 

my daughter did have positive throat cultures, but never had high titers. Her strep always came back between antibiotics, with the only symptoms being behavioral.

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On the subject of different strains of strep, I earlier posted about us recently testing positive for Group B strep in respiratory culture and beta strep, non A,B,C,F, or G. This has also happened in the past where we culture positive for non A strep, but the lab reports they don't know what strain. I have always wondered if we have a certain strain of strep that doesn't register positive in our cultures. Years ago when I took my daughter to meet with Dr. Swedo at NIMH (2001)and she instructed me to always insist on 72 hr. cultures b/c it can take that long to register positive in PANDAS kids, I asked her if she thought it was b/c they got a different type of strep. She smiled and nodded her head, which I took to mean she thought so. This has always made me wonder if my kids are picking up some different strain.

Colleen

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Natterbus...here is the study I was thinking about http://www.journals.uchicago.edu/doi/pdf/10.1086/320745

It was actually comparing Azithromycin (5 day course) vs Clarithromycin (10day course). For Azithromycin, cultures 13-19 days after the final dose showed 91% eradication rate, by 28-38 days the eradication rate had fallen to 79%.

 

The article also cited another study that showed 95% eradication rate 14 days after final dose. The eradication rate fell to 79% by 30 days after final dose...a change of 16%.

 

So it looks like we should be waiting at least 30 days after final dose to say a culture is truly negative! It is interesting to note that these studies didn't go any further out (45-60 days) and what the effect would be there.

 

In any case, taking all this into account, the culturing 3 days after the end of antibiotics seems way too soon to me, even assuming that there is a difference in types of antibiotics (augmentin, amoxcillin, vs macrolides like azithromycin.)

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Natterbus...here is the study I was thinking about http://www.journals.uchicago.edu/doi/pdf/10.1086/320745

It was actually comparing Azithromycin (5 day course) vs Clarithromycin (10day course). For Azithromycin, cultures 13-19 days after the final dose showed 91% eradication rate, by 28-38 days the eradication rate had fallen to 79%.

 

The article also cited another study that showed 95% eradication rate 14 days after final dose. The eradication rate fell to 79% by 30 days after final dose...a change of 16%.

 

So it looks like we should be waiting at least 30 days after final dose to say a culture is truly negative! It is interesting to note that these studies didn't go any further out (45-60 days) and what the effect would be there.

 

In any case, taking all this into account, the culturing 3 days after the end of antibiotics seems way too soon to me, even assuming that there is a difference in types of antibiotics (augmentin, amoxcillin, vs macrolides like azithromycin.)

 

 

I'm not sure I understand this - is it to mean that the abx eradicate the strep within the first 14 days, but after 30 days it comes back which accounts for the drop in the rate of eradication to 79%? Pat

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So Pat, in the 2nd study (for example), if you culture just 2 weeks after the last dose you'll have a small amount of "false negative" (16%) cultures that will actually re-culture positive if you wait another 2 weeks after that. The antibiotic knocks out the strep to a low enough level where you temporarily (for 2-3 weeks) can't grow it on a culture, but it eventually comes back, given enough time.

 

It would be interesting to see how many more "false negatives" if you only waited 3 days after stopping antibiotics?

 

Nice eh? <_<

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So Pat, in the 2nd study (for example), if you culture just 2 weeks after the last dose you'll have a small amount of "false negative" (16%) cultures that will actually re-culture positive if you wait another 2 weeks after that. The antibiotic knocks out the strep to a low enough level where you temporarily (for 2-3 weeks) can't grow it on a culture, but it eventually comes back, given enough time.

 

It would be interesting to see how many more "false negatives" if you only waited 3 days after stopping antibiotics?

 

Nice eh? <_<

 

I wonder if that is residual bacteria that was resistant & not killed the first time - or... if its a new strep infection? Pat

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The assumption would be that the strep was not completely killed off the first time. They did check to see that the strep bacteria which re-grew was of "concordent serotype" which I took to mean the same strain (or something like that) as the original infection.

 

Although, I suppose it is possible that someone could have gotten re-infected with the same strain as before. However, the interesting thing is it looked like the mean age of participants in the Kaplan study were 26 years old and for the vast majority, this was their first infection in a year. In other words, these were not like our younger kids who get many repeated strep infections in a school year (from lots of exposure) and it seems more logical that these adults are presenting with their own strep infections which were not completely killed off.

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