You should know that antibiotic resistance is not evolution, but due to loss
of genetic variation in a population. It is basically killing off everything that
is not resistant. The genes were there already, just not in the majority.
The genes weren't already there. In an experiment done by the Lederbergs' back in the 1950's they tested your theory. They started with a single bacterium. If that single bug was resistant the more than 99% of it's descendants should be resistant. They weren't. In fact, only one in billions of bacteria turned out to be resistant, and that resistance developed in the absence of any antibiotic. You should really read the paper. It is one of the classic genetics papers that first established the randomness of mutations:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC169282/pdf/jbacter00003-0114.pdf
Here's a little snippet from the paper:
They saw just 2 or 3 resistant colonies per 3 billion bacteria. That completely falsifies your claims that they start out resistant.
With modern technology, we can now find the exact mutations that lead to spectinomycin resistance.
"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 × 10−6."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1366916/
Not that you probably really care because you will completely ignore all of the facts that prove your wrong, go to another thread, and repeat the same falsehoods. Am I wrong?