Lyme builds resistance to Fluroquinolone

[Guest guest]

Hmmmmmmmm.. this is the first time I've ever seen reference that

b.burgdorferi mutates and becomes resistant to abx.

Barb

Antimicrob Agents Chemother. 2005 Oct;49(10):4354-7.

parC Mutations in Fluoroquinolone-Resistant Borrelia burgdorferi.

Galbraith KM, Ng AC, Eggers BJ, Kuchel CR, Eggers CH, s DS.

Division of Biological Sciences, The University of Montana, 32 Campus

Dr. 4824, Missoula, MT 59812-4824. scott.samuels@....

We have isolated in vitro fluoroquinolone-resistant mutants of the

Lyme disease agent, Borrelia burgdorferi. Mutations in parC, which

encodes a subunit of topoisomerase IV, were associated with loss of

susceptibility to sparfloxacin, moxifloxacin, and Bay-Y3118, but not

ciprofloxacin. This is the first description of fluoroquinolone

resistance in the spirochete phylum.

PMID: 16189120 [PubMed - in process]

[Guest guest]

> Hmmmmmmmm.. this is the first time I've ever seen reference that

> b.burgdorferi mutates and becomes resistant to abx.

> Barb

" We have isolated fluoroquinolone-resistant first-step mutants of B.

burgdorferi by selection in increasing doses of three different

fluoroquinolones in vitro. Although B. burgdorferi is not susceptible

to many fluoroquinolones (5, 12, 20, 21, 30), recently developed

fluoroquinolones demonstrate some therapeutic potential (16). This

study provides the first description of fluoroquinolone resistance in

the spirochete phylum and is only the second report, to our

knowledge, in which genomic mutations have been associated with

antibiotic resistance in B. burgdorferi (32). "

[abstract of reference 32 follows]

J. Bacteriol., May 1994, 3072-3075, Vol 176, No. 10

Copyright © 1994, American Society for Microbiology

gyrB mutations in coumermycin A1-resistant Borrelia burgdorferi

DS s, RT Marconi, WM Huang and CF Garon

Laboratory of Vectors and Pathogens, Rocky Mountain Laboratories,

National Institute of Allergy and Infectious Diseases, Hamilton,

Montana 59840.

We have isolated and characterized mutants of Borrelia burgdorferi

that are resistant to the antibiotic coumermycin A1, which targets

the B subunit of DNA gyrase. Mutants had either 100- or 300-fold

higher resistance to coumermycin A1 than wild-type B. burgdorferi. In

each case, a single point mutation in the gyrB gene converted Arg-133

to Gly or Ile. Mutations in the homologous Arg residue of Escherichia

coli DNA gyrase are also associated with resistance to coumarin

antimicrobial agents.

[The mutants in the above 2 investigations were created in glass by

serial selection using increasing drug concentrations. I have 3

papers all from different groups on suceptibilites of Bb isolated

from the same patient before and after standard treatment of acute

lyme disease. Few or no suceptibilities changed in most cases, and

only occasionally did any suceptibility go down as much as 4 fold,

which is considered thresshold-significant.]