A 53 year old showed up at my door a little more than 2 years ago. He had been diagnosed with Lyme disease and was looking for help. He had already been ill for more than 3 years. He suffered with severe pain- on serious opiates. He had neuropathic pain- including a relentless trigeminal neuralgia. To date, this has persisted. He had already received 40 days of IV Rocephin and 30 days of oral antibiotics for CDC positive disease- to no avail. I took him on- a challenge. We have been through ups and downs with courses of Rocephin and oral antibiotics. His cognitive issues have been very worrisome and not improved until recently. His mother died of Alzheimer's disease and he sees the same syndrome in himself. Lab testing has shown consistently positive antibody WB bands, both IgM and IgG. He is also ELISA positive, for what that is worth. His C6 peptide has consistently been high as well. This is of some interest since Immunetics- the makers of this assay- claim that one sees a 4 fold decrease in C6 titers after successful treatment of Lyme disease. Perhaps his most interesting finding is his Brain MRI. It shows "deep white matter lesions bilaterally, consistent with the clinical diagnosis of Lyme disease." The radiologist notes that the lesions are not in a distribution typical for demyelinating plaques. (MS).
After trying many therapies, with mediocre results, I decided to try something novel for his dementia. His significant short term memory loss, bouts of mental confusion and aphasia were similar to presentations seen in the early to moderate stages of Alzheimer's disease. This is something quite familiar to me; I spent 15 years as the medical director of a large Nursing Home at one time. Based on the notion that Lyme dementia is related to glutamine sensitivity- as seen in Alzheimer's disease as well, I prescribed Namenda. This made a dramatic difference and has perhaps been one of the most helpful therapies for this most challenging patient.
Recently I sent a blood sample to Clongen for a wet mount. His blood, like that of so many other Lyme patients, has numerous, highly motile, extracellular organisms.
Clongen's attempts to sequence the "bacteria" have failed. It does not amplify with any of the known universal primers for bacteria used in PCR assays. Attempts to culture it in various media have also failed. Perhaps it is not a bacteria, but a tiny parasite of some kind. Clongen plans to test for this possibility as well.
The mystery of the motile organisms for now, remains unsolved.
There is no evidence that it is any known bacteria including a relative of Bartonella or a relative of Pseudomonas.
It is not killed with a plethora of antibiotics and anti parasite drugs.
Today this patient told me that a doctor friend said he should have a spinal tap to rule out MS. As previously discussed, there is no diagnostic test for MS. Myelin basic protein can be measured in the CSF- it is a marker for destruction of myelin- but it does not diagnose MS. Based on his MRI- it would not be unexpected to find MBP in his spinal fluid. Actually, I recommended that he see his neurologists. There is no research regarding the use of typical MS therapy in neuroborreliosis patients. It is possible that interferon therapy might help. Other, less commonly used MS therapies, including plasmapheresis and IVIg have been recommended for Lyme patients.
My final musing here is: "What do radiologists think?"
Infectious disease physicians, rheumatologists and neurologists dismiss the notions that such patients are suffering with neuroborreliosis. Many have proposed a Post-Lyme autoimmune disorder. The radiologists have not been steeped in this dogma. They call MRIs and SPECTs all the time: "Compatible with Lyme disease." They see the evidence in black and white; from my discussions with radiologists, they believe in chronic Lyme disease. They do not diagnose Post-Lyme. Apparently neuroborreliosis has not been censured from their text books. They in fact know that neuroborreliosis exists and that it has been well documented.