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» LymeNet Flash » Questions and Discussion » Medical Questions » Bb REALLY doesn't become resistant? It has the same replication time as TB...

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Author Topic: Bb REALLY doesn't become resistant? It has the same replication time as TB...
adamm
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http://aac.asm.org/cgi/content/full/48/4/1289/T2

Bb's is 24-hours, right?

[ 04. February 2008, 05:23 PM: Message edited by: adamm ]

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Keebler
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Adamm -

for statements such as these, LINKS are vital.

We need to know who said it and have exact quotes posted, not just a catchy news-headline.

The sources of such statements must be included for any reasonable consideration of the question.


Would you please let us know where you read this ?


Thanks so much for posting background. It's very helpful.


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Keebler
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Adamm,

thanks for going back to edit in the link.


I went there and still have many questions about how you came to your question.


All I see is a chart about a tuberculosis. No text interpretation, no evaluation, no comparison.


There is no mention of Bb in the article linked to this chart:

("Effect of rpoB Mutations Conferring Rifampin Resistance on Fitness of Mycobacterium tuberculosis")


So, if you can post the origin of where you found your Bb statement, that would be helpful for others to offer their knowledge. Thanks.


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adamm
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The chart lists the doubling times for the various TB cultures.

They're all around 24 hours, I'd read in the Burrascano

guidelines that Bb

has this replication time as well, I was wondering if populations

of the two organisms would develop resistance similarly.


There's been no statement with regards to resistance

development

made in any literature I've thus

read; it was just something I was wondering about.

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Keebler
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Wow ! that was a fast reply.

I'm too toasted to think right now. Maybe others can address that.

I think that Savely ( http://tinyurl.com/2dmvs2 ) and I know that Goldings ( http://www.ilads.org/goldings.html ) speak to the replication time in their articles.

Replication time and resistance are different topics, with the resistance thing quite involved. Resistance is not ignored and that is why combination therapies - very specific combinations and for certain times &/or different mode of delivery - are used by LLMDs.

The topic of resistance also covers different forms of Bb, different strains, too - various protocols address this, too, in different ways.

Resistance also involves understanding a person's immune system and their liver health, etc., among other things.


I'm done with my "academic" exercise for the day. Rest and diversion call loudly to me right now. Others may have a few sources for you.


Cheers !

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[ 04. February 2008, 06:52 PM: Message edited by: Keebler ]

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bpeck
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The word resistance is sometimes used with 2 difference meanings..

Antibiotic resistance usually means the bacteria morphs in a way to make it self impervious to a specific antibiotic- rendering the antbiotic useless.

There is only one antibiotic that borrelia may be resistant to: see ref 1 & 2

Then there are people who's Lyme is resistant to antibiotic therapy in general- meaning they just don't get better.. this is an entirely differnt thing and suspected to have alot to do with a person's tissue type.
See reference #3

Barb


Reference 1
Int J Antimicrob Agents. 2007 Dec;30(6):496-504. Epub 2007 Oct 1
Evidence of a conjugal erythromycin resistance element in the Lyme disease spirochete Borrelia burgdorferi.Jackson CR, Boylan JA, Frye JG, Gherardini FC.
Antimicrobial Resistance Research Unit, ARS, SAA, USDA, Russell Research Center, Athens, GA 30602, USA.

REFERENCE 2
Antimicrob Agents Chemother. 2002 Nov;46(11):3637-40
Erythromycin resistance in Borrelia burgdorferi.Terekhova D, Sartakova ML, Wormser GP, Schwartz I, Cabello FC.
Departments of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595, USA.

Susceptibility testing of laboratory strains and clinical isolates of Borrelia burgdorferi indicates that resistance to erythromycin is present in them. Evaluation of the MICs, minimal bactericidal concentrations, and kinetics of bacterial killing of erythromycin suggests that this resistance is increased by preexposure to the antibiotic, is dependent on inoculum size, and may be the result of selection of subpopulations of bacterial cells with increased resistance.

PMID: 12384380 [PubMed - indexed for MEDLINE]

REFERENCE 3
J Exp Med. 2006 Apr 17;203(4):961-71. Epub 2006 Apr 3.
Antibiotic-refractory Lyme arthritis is associated with HLA-DR molecules that bind a Borrelia burgdorferi peptide.Steere AC, Klitz W, Drouin EE, Falk BA, Kwok WW, Nepom GT, Baxter-Lowe LA.
Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. [email protected]

An association has previously been shown between antibiotic-refractory Lyme arthritis, the human histocompatibility leukocyte antigen (HLA)-DR4 molecule, and T cell recognition of an epitope of Borrelia burgdorferi outer-surface protein A (OspA163-175). We studied the frequencies of HLA-DRB1-DQA1-DQB1 haplotypes in 121 patients with antibiotic-refractory or antibiotic-responsive Lyme arthritis and correlated these frequencies with in vitro binding of the OspA163-175 peptide to 14 DRB molecules. Among the 121 patients, the frequencies of HLA-DRB1-DQA1-DQB1 haplotypes were similar to those in control subjects. However, when stratified by antibiotic response, the frequencies of DRB1 alleles in the 71 patients with antibiotic-refractory arthritis differed significantly from those in the 50 antibiotic-responsive patients (log likelihood test, P = 0.006; exact test, P = 0.008; effect size, Wn = 0.38). 7 of the 14 DRB molecules (DRB1*0401, 0101, 0404, 0405, DRB5*0101, DRB1*0402, and 0102) showed strong to weak binding of OspA163-175, whereas the other seven showed negligible or no binding of the peptide. Altogether, 79% of the antibiotic-refractory patients had at least one of the seven known OspA peptide-binding DR molecules compared with 46% of the antibiotic-responsive patients (odds ratio = 4.4; P < 0.001). We conclude that binding of a single spirochetal peptide to certain DRB molecules is a marker for antibiotic-refractory Lyme arthritis and might play a role in the pathogenesis of the disease.

PMID: 16585267 [PubMed - indexed for MEDLINE]

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bpeck
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The word resistance is sometimes used with 2 difference meanings..

Antibiotic resistance usually means the bacteria morphs in a way to make it self impervious to a specific antibiotic- rendering the antbiotic useless.

There is only one antibiotic that borrelia may be resistant to: see ref 1 & 2

Then there are people who's Lyme is resistant to antibiotic therapy in general- meaning they just don't get better.. this is an entirely differnt thing and suspected to have alot to do with a person's tissue type.
See reference #3

Barb


Reference 1
Int J Antimicrob Agents. 2007 Dec;30(6):496-504. Epub 2007 Oct 1
Evidence of a conjugal erythromycin resistance element in the Lyme disease spirochete Borrelia burgdorferi.Jackson CR, Boylan JA, Frye JG, Gherardini FC.
Antimicrobial Resistance Research Unit, ARS, SAA, USDA, Russell Research Center, Athens, GA 30602, USA.

REFERENCE 2
Antimicrob Agents Chemother. 2002 Nov;46(11):3637-40
Erythromycin resistance in Borrelia burgdorferi.Terekhova D, Sartakova ML, Wormser GP, Schwartz I, Cabello FC.
Departments of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595, USA.

Susceptibility testing of laboratory strains and clinical isolates of Borrelia burgdorferi indicates that resistance to erythromycin is present in them. Evaluation of the MICs, minimal bactericidal concentrations, and kinetics of bacterial killing of erythromycin suggests that this resistance is increased by preexposure to the antibiotic, is dependent on inoculum size, and may be the result of selection of subpopulations of bacterial cells with increased resistance.

PMID: 12384380 [PubMed - indexed for MEDLINE]

REFERENCE 3
J Exp Med. 2006 Apr 17;203(4):961-71. Epub 2006 Apr 3.
Antibiotic-refractory Lyme arthritis is associated with HLA-DR molecules that bind a Borrelia burgdorferi peptide.Steere AC, Klitz W, Drouin EE, Falk BA, Kwok WW, Nepom GT, Baxter-Lowe LA.
Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. [email protected]

An association has previously been shown between antibiotic-refractory Lyme arthritis, the human histocompatibility leukocyte antigen (HLA)-DR4 molecule, and T cell recognition of an epitope of Borrelia burgdorferi outer-surface protein A (OspA163-175). We studied the frequencies of HLA-DRB1-DQA1-DQB1 haplotypes in 121 patients with antibiotic-refractory or antibiotic-responsive Lyme arthritis and correlated these frequencies with in vitro binding of the OspA163-175 peptide to 14 DRB molecules. Among the 121 patients, the frequencies of HLA-DRB1-DQA1-DQB1 haplotypes were similar to those in control subjects. However, when stratified by antibiotic response, the frequencies of DRB1 alleles in the 71 patients with antibiotic-refractory arthritis differed significantly from those in the 50 antibiotic-responsive patients (log likelihood test, P = 0.006; exact test, P = 0.008; effect size, Wn = 0.38). 7 of the 14 DRB molecules (DRB1*0401, 0101, 0404, 0405, DRB5*0101, DRB1*0402, and 0102) showed strong to weak binding of OspA163-175, whereas the other seven showed negligible or no binding of the peptide. Altogether, 79% of the antibiotic-refractory patients had at least one of the seven known OspA peptide-binding DR molecules compared with 46% of the antibiotic-responsive patients (odds ratio = 4.4; P < 0.001). We conclude that binding of a single spirochetal peptide to certain DRB molecules is a marker for antibiotic-refractory Lyme arthritis and might play a role in the pathogenesis of the disease.

PMID: 16585267 [PubMed - indexed for MEDLINE]

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dguy
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(relative to most bacteria, a 24 hour repro rate is glacially slow)
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charlie
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....seems like we were always taught that Bb replication time is more like 3 weeks. Hence the textbook '21 days of doxy' treatment.

Charlie

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Keebler
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I think this article says it's either 3 months or 4 months (I don't recall which) for the full life cycle range for minimum treatment.

Goldings - http://www.ilads.org/goldings.html


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