On 2017 Aug 20, Daniel Weiss commented:

The central problem with current standards of Lyme disease diagnosis and treatment is the absence of a highly sensitive and specific test, a gold standard, that can prove the presence of disease and/or demonstrate cure. When a patient complains of unremitting neurological and/or musculo-skeletal symptoms after completing a treatment, persistent infection is the most logical interpretation. Recent microbiological research has uncovered persistence mechanisms in virtually every prokaryotic organism(Conlon, Rowe, & Lewis, 2015 Advances in experimental medicine and biology; Harms, Maisonneuve, & Gerdes, 2016 Science,; Lewis & Shan, 2016 Molecular cell). It is not surprising that a bacterial species adapted to survive in multiple vertebrate hosts, and through multiple stages of the three-year cycle of its invertebrate host, might persist after antibiotic treatment(Feng, Shi, Zhang, & Zhang, 2015 Emerging microbes & infections). Borrelia species are characterized by immense plasticity in their expression of morphology, antigens, and genes.

In the laboratory, and in infected humans, antibiotics predictably induce the persister phenotype(Bijaya Sharma, Autumn V Brown, Nicole E Matluck, Linden T Hu, & Kim Lewis, 2015 Emerging microbes & infections).

Exposed to antibiotics, Borrelia burgdorferi rapidly loses the morphology of “active” motile, dividing spirochetes(Sapi et al., 2016 Int J Med Sci; Timmaraju et al., 2015 FEMS Microbiol Lett). The organism settles into dormancy in biofilm or as round bodies(Merilainen, Herranen, Schwarzbach, & Gilbert, 2015). Yet, it retains antigenicity and the genetic capacity to return to the spirochete form(Merilainen, Brander, Herranen, Schwarzbach, & Gilbert, 2016 Microbiology).

The failure to respond to a particular antibiotic regimen does not equate with "there is no infection present". The more appropriate conclusion may be that the antibiotic is ineffective for this infection. It is completely unclear whether these patients with presumed autoimmune disorders have persistent infection with B. burgdorferi.

On 2017 Aug 20, Daniel Weiss commented:

The central problem with current standards of Lyme disease diagnosis and treatment is the absence of a highly sensitive and specific test, a gold standard, that can prove the presence of disease and/or demonstrate cure. When a patient complains of unremitting neurological and/or musculo-skeletal symptoms after completing a treatment, persistent infection is the most logical interpretation. Recent microbiological research has uncovered persistence mechanisms in virtually every prokaryotic organism(Conlon, Rowe, & Lewis, 2015 Advances in experimental medicine and biology; Harms, Maisonneuve, & Gerdes, 2016 Science,; Lewis & Shan, 2016 Molecular cell). It is not surprising that a bacterial species adapted to survive in multiple vertebrate hosts, and through multiple stages of the three-year cycle of its invertebrate host, might persist after antibiotic treatment(Feng, Shi, Zhang, & Zhang, 2015 Emerging microbes & infections). Borrelia species are characterized by immense plasticity in their expression of morphology, antigens, and genes.

In the laboratory, and in infected humans, antibiotics predictably induce the persister phenotype(Bijaya Sharma, Autumn V Brown, Nicole E Matluck, Linden T Hu, & Kim Lewis, 2015 Emerging microbes & infections).

Exposed to antibiotics, Borrelia burgdorferi rapidly loses the morphology of “active” motile, dividing spirochetes(Sapi et al., 2016 Int J Med Sci; Timmaraju et al., 2015 FEMS Microbiol Lett). The organism settles into dormancy in biofilm or as round bodies(Merilainen, Herranen, Schwarzbach, & Gilbert, 2015). Yet, it retains antigenicity and the genetic capacity to return to the spirochete form(Merilainen, Brander, Herranen, Schwarzbach, & Gilbert, 2016 Microbiology).

The failure to respond to a particular antibiotic regimen does not equate with "there is no infection present". The more appropriate conclusion may be that the antibiotic is ineffective for this infection. It is completely unclear whether these patients with presumed autoimmune disorders have persistent infection with B. burgdorferi.