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Lyme Disease symptoms vary from person to person. (lymes disease lyme's disease lime disease limes disease)
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Consult a qualified Lyme ( Borreliosis ) Disease literate doctor for medical advice if Lyme Disease is suspect to discuss your Lymes Disease Symptoms.
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Antimicrob Agents Chemother. 2006 Feb;50(2):445-52
Mutations Conferring Aminoglycoside and Spectinomycin Resistance in
Borrelia burgdorferi.
Criswell D, Tobiason VL, Lodmell JS, Samuels DS.
Division of Biological Sciences, The University of Montana, 32
Campus Dr., Missoula, MT 59812-4824. scott.samuels@umontana.edu.
We have isolated and characterized in vitro mutants of the Lyme
disease agent Borrelia burgdorferi that are resistant to
spectinomycin, kanamycin, gentamicin, or streptomycin, antibiotics
that target the small subunit of the ribosome. 16S rRNA mutations
A1185G and C1186U, homologous to Escherichia coli nucleotides A1191
and C1192, conferred >2,200-fold and 1,300-fold resistance to
spectinomycin, respectively. A 16S rRNA A1402G mutation, homologous
to E. coli A1408, conferred >90-fold resistance to kanamycin and
>240-fold resistance to gentamicin.
Two mutations were identified in
the gene for ribosomal protein S12, at a site homologous to E. coli
residue Lys-87, in mutants selected in streptomycin. Substitutions
at codon 88, K88R and K88E, conferred 7-fold resistance and 10-fold
resistance, respectively, to streptomycin on B. burgdorferi.
The 16S
rRNA A1185G and C1186U mutations, associated with spectinomycin
resistance, appeared in a population of B. burgdorferi parental
strain B31 at a high frequency of 6 x 10(-6).
These spectinomycin-
resistant mutants successfully competed with the wild-type strain
during 100 generations of coculture in vitro.
The aminoglycoside-
resistant mutants appeared at a frequency of 3 x 10(-9) to 1 x10(-7)
in a population and were unable to compete with wild-type strain B31
after 100 generations.
This is the first description of mutations in
the B. burgdorferi ribosome that confer resistance to antibiotics.
These results have implications for the evolution of antibiotic
resistance, because the 16S rRNA mutations conferring spectinomycin
resistance have no significant fitness cost in vitro, and for the
development of new selectable markers.
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