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Neuropsychiatric manifestations of Lyme disease - Part II


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How do I know if I have Lyme disease? Could it be something else? Or am I just crazy?

Is Lyme disease the “disease du jour”, as some have termed it? “I don’t know what is wrong with me, therefore I must have Lyme disease, because I have seen it in the news recently?”

Or is Lyme disease an epidemic new to the 21st century? Was it released from a secret laboratory on Plum Island, as some have claimed?

The disease was first described in the 20th century when a cluster of patients in Lyme, Connecticut developed inflammatory arthritis. The original paper was published in 1977.[1] Even at that time, the diagnosis was controversial, and doctors were already losing their licenses in the 1980s and 1990s for being willing to treat patients with the disease.

It’s not a new disease. Ticks with spirochetes inside them have been found embedded in amber dating from 15 million years ago[2] – and in the Ice Man about 5300 years ago.[3] In 1982 the pathogen known as Borrelia burgdorferi was described by Dr. Willy Burgdorfer. Other tick-borne pathogens causing similar symptoms have been discovered and named since that time.

What makes this particular disease so virulent in the 21st century?

Even more important, why doesn’t everyone who is bitten by a tick develop Lyme disease?

The “natural course” of the disease is as follows:

  • Tick bite occurs – the tick is a carrier for Borrelia or other co-infections
  • Incubation period of 3-32 days – a slowly expending skin rash appears – the typical “bull’s eye” rash, AKA erythema migrans
  • Flu-like symptoms are frequent at this stage – fever, malaise, fatigue, muscle aches, headaches, joint pains. In about 20% of cases, this is the ONLY manifestation of disease – no rash is ever identified.
  • The immune system kicks in. Macrophages engulf (eat) the organisms and kill them. The macrophages also produce inflammatory messengers – especially IFN-Υ(interferon gamma).
  • Within a few days, most patients developed antibody to the OspC flagellar protein of the spirochete. This protein is found at the 41 kDa band of the Western blot test.
  • Within a few days to weeks, the organism travels around our bodies. It has been found in blood, spinal fluid, the heart, the retina of the eye, muscles, bones, the spleen, the liver, the meninges – or coverings of the brain and spinal cord – as well as in the brain.
  • If the immune system recognizes the spirochete bound to proteins on the host cells as foreign, this can explain why sometimes symptoms appear to be auto-immune – our own bodies attack our own tissues, thinking that they are foreign, because spirochetes are now part of the tissue.
  • Antibody production eventually will control a good many of the manifestations of infection, even without antibiotic therapy.
  • However, the intact organisms may survive in protected areas for years. Months after untreated illness, 60% of patient experience intermittent joint pains – especially knee pain. Both CD4 cells and B burgdorferi-specific CD8 cells have been found within infected joints. Attacks mostly seem to decrease in frequency over the years, suggesting that the immune system eventually gets it right.
  • Borrelia afzelii, found more commonly in Europe, may persist in the skin for decades.
  • Borrelia garinii appears to infect the neurologic system, eventually causing diseases diagnosed as encephalomyelitis, multiple sclerosis or amyotrophic lateral sclerosis.

About 10% of patients with Lyme arthritis have persistent joint pain for months or years after infection, even after being treated with antibiotics. The big question is whether these symptoms are due to persistent infection or to infection-induced autoimmunity. [4]

The article quoted above gives an excellent history and description of the clinical course of the disease. Unfortunately, this same article gives mis-information in the “Diagnosis and Treatment” section – reporting that at least 24-72 hours of attachment of a tick is necessary for infection to occur, and that if a tick is found, a single dose of 200 mg of doxycycline is sufficient to prevent the development of disease. For reasons which escape my sense of logic, the same article states that when an IgM response occurs to Borrelia, it must be a false positive, since the patient has already been treated with the inadequate dose of doxycycline mentioned above.

And in those who are treated with antibiotics for a short time, why do at least one third of them still suffer from brain dysfunction, pain and fatigue six months or more later?

We have developed vaccines for other infectious diseases, why not for Lyme?

A vaccine was in fact developed in the 1990s. The cost was high, the patient had to have a booster injection every year, and some patients treated with this vaccine developed what appeared to be an autoimmune arthritis with symptoms identical to those of Lyme arthritis. I have a patient who was never ill until she was given the Lyme vaccine. No wonder the vaccine never became popular.

And now that hardly anyone has received the vaccine, those Borrelia proteins used in the development of the vaccine are no longer considered “positive” response in the theoretically diagnostic Western blot test, even in patients who have not been vaccinated.

How would you suspect that you might have Lyme disease (or one of the co-infections)?

Symptoms of Lyme disease may range from an annoying tick bite without any further symptoms all the way to incapacitating neurologic illness with an ALS-like picture.[5]

History may be of a camping trip, or hiking trip, or outdoor expedition – even a walk in a park. A tick bite may or may not have been noticed.

Typically the progression of disease starts with a tick bite, followed within a few days by a bull’s eye rash (erythema migrans) followed within a week or two by a flu-like illness with fever, muscle aches and fatigue. Because ticks are active in warmer temperatures, this flu-like illness typically occurs during the summer months, when it is unusual to develop influenza.

That’s the typical presentation – which may occur in fewer than 50% of people who are subsequently shown to have Lyme disease.

Atypical symptoms may simply be: “I went hiking or camping, came down with the flu from hell two weeks later, and just never recovered.” The “just never recovered my health” is the most important part of that history.

Even more atypical may be: “I was healthy, and then gradually became not healthy, I cannot identify any specific event. But I was working really hard, exercising to maintain my health, then began to have muscle aches after exercise, and eventually every shopping trip left me in bed for three days because I was so fatigued I could not get up.”

And more atypical yet: “I do not remember ever being healthy. I grew up in the NorthEast (or Mid-West) and was always a sickly child.”

Unless we are suspicious, and do the testing, we will never make the diagnosis.

Symptoms may occur in any organ system.

- a young woman presents with complete heart block[6] and a heart rate of 35 beats per minute, no family history of heart disease and no evidence of any heart disease other than the extremely low rate.

- another young woman gets breast implants, has an infection in the implants, is treated for that infection and then just never recovers her health[7]. She is an avid hiker and exerciser, and has recollection of tick bites in the past.

- another woman spends time outdoors, works very hard, never notices a tick bite, but gradually becomes incapacitated with brain fog, memory loss, inability to function at work. She is terrified that she is developing Alzheimer’s dementia.[8]

- a man presents with generalized arthritis and pain. He is a deer hunter and has taken multiple ticks off his body.[9]

They have all seen multiple physicians and been given various diagnoses, none of which is potentially curable.

We must always consider the possibility of other causes of similar illness. But if the docs in Connecticut had accepted a diagnosis of “Juvenile Rheumatoid Arthritis” in their collection of young patients, we would still be looking for the cause of that cluster of patients with Lyme disease.

We must remain open to the possibility of what the medical establishment calls “co-morbidities” – in other words, it is perfectly possible for an individual to have nutritional depletion, mitochondrial dysfunction, chronic fatigue AND Lyme disease. All these conditions may need to be treated in order for health to be restored.[10]

[1] Steere, A. C., et al. "Lyme arthritis: An epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthrit Rheum., 20: 7- 17 (1977).

[2] Poinar, George, and Alex E. Brown. "A new genus of hard ticks in Cretaceous Burmese amber (Acari: Ixodida: Ixodidae)." Systematic Parasitology 54.3 (2003): 199-205.

[3] Kean, Walter F., et al. "The musculoskeletal abnormalities of the Similaun Iceman (“ÖTZI”): clues to chronic pain and possible treatments." Inflammopharmacology 21.1 (2013): 11-20.

[4] Steere, Allen C., Jenifer Coburn, and Lisa Glickstein. "The emergence of Lyme disease." Journal of Clinical Investigation113.8 (2004): 1093.

[5] AKA Lou Gherig’s disease – Amyotrophic Lateral Sclerosis

[6] Kimball, Suzanne A., Paul A. Janson, and Paul J. LaRaia. "Complete heart block as the sole presentation of Lyme disease." Archives of internal medicine 149.8 (1989): 1897-1898.

[7] Genovese, M. C. "Fever, rash, and arthritis in a woman with silicone gel breast implants." Western journal of medicine 167.3 (1997): 149.

[8] Miklossy J. “Alzheimer’s disease – a neurospirochetosis.” J Nuroinflammation 2011, 890.

[9] Jordan, Robert A., Terry L. Schulze, and Margaret B. Jahn. "Effects of reduced deer density on the abundance of Ixodes scapularis (Acari: Ixodidae) and Lyme disease incidence in a northern New Jersey endemic area." Journal of medical entomology 44.5 (2007): 752-757.

[10] Richard Horowitz, MD. How Can I Get Better? An Action Plan for treating resistant Lyme & Chronic Disease. St. Martin’s Press ©2017 – ISBN978-1-250-07054-8.