0 Failure of Topical Antibiotics to Prevent Disseminated Borrelia burgdorferi Infection

Last week, I posted an article on how topical azithromycin could help prevent Lyme disease infection. And now, this new abstract has turned up on PubMed...

Failure of Topical Antibiotics to Prevent Disseminated Borrelia burgdorferi Infection Following a Tick Bite in C3H/HeJ Mice. Wormser GP, Daniels TJ, Bittker S, Cooper D, Wang G, Pavia CS. J Infect Dis. 2011 Sep 19. [Epub ahead of print]

Abstract

A prior study in mice has shown that the timely application of topical antibiotics to the skin at the tick bite site could eradicate Borrelia burgdorferi infection. That study, however, did not evaluate antibiotic preparations that are considered suitable for use in humans. In this murine study, topical application of 2% erythromycin and 3% tetracycline preparations that are acceptable for use in humans was found to be ineffective in eliminating B. burgdorferi from the tick bite site or in preventing dissemination to other tissues. Reasons for the discrepant findings are discussed.

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I find it very odd that they would choose erythromycin as a topical antibiotic for Borrelia burgdorferi - there is research that shows that Borrelia burgdorferi is resistant to erythromycin. I would have never thought to make that a choice for treatment. Tetracycline makes more sense.

How many previous studies of topical antibiotics for treating early Lyme disease have there been, and what have the outcomes been? How many have been done using suitable human antibiotic preparations versus ones only effective in animal subjects?

It seems to me that the researchers who filed this patent might already have a good idea of what might work - is this the same formulation that was used in the study I posted last week?

Composition C
Composition [mg]
Component per unit [1 g]
Azithromycin 150
Dermacryl 79 50
Klucel MF 25
Miglyol 812 50
Ethanol 94% (w/w) ad 1 g

Or is it different?

Results: There is no infection of Lyme disease detectable when composition C is applied to the area where the ticks were allowed to feed. The topical application of Formulation C results in antibody titers, which are not different from naïve mice (KELA values between 10 and 40), whereas the infected mice show KELA values of 160 to 400.

Especially, the tissue and serum samples taken from different parts of the mice 56 days after the tick bite show no Borrelia burgdorferi organisms when cultivated and no specific antigenes are detectable. Tissue probes are taken from heart tissue, bladder, joint and ear. The group of mice topically treated with Formulation C show complete absence of B. burgdorferi , whereas B. burgdorferi is detected in untreated mice, which are exposed to tick-feed.

The recultivation conditions of B. burgdorferi are suitable to detect B. burgdorferi in any morphological form known to date. Surprisingly, Formulation C was able to eradicate B. burgdorferi in a way, that no infectious agents of B. burgdorferi are detected in the target tissues of B. burgdorferi.

How were these tissue probes completed and could they have missed any bacteria? What about the parenchyma of the brain, since this is low passage N40 they're talking about? (Problematic in rodent studies - should be studied in other animals.) I wonder about the methodology...

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