Lyme disease symptoms can persist after IDSA recommended antibiotic therapy.
The argument that this represents a post-infection syndrome rather than a continuing infection has become the crux of the debate as framed by the IDSA.
This disagreement is really a sidebar. Let us put this particular discussion aside for the moment and look at things from a different perspective.
Across the board, physicians agree that late disseminated Lyme disease is a real entity. The IDSA argument claims that MOST Lyme patients present with an acute easily discernible syndrome. The IDSA would agree that some patients with well documented Lyme disease present differently.
Let's look at a comparison with syphilis once more. Syphilis starts with a painless lesion in the genitalia, called a chancre- the acute syndrome. Many patients with syphilis can recall no history of such an exposure. For decades syphilis has been called the great imitator. It has the ability to disseminate widely after a quiescent stage and mimic many other medical disorders. We know that syphilis has 3 stages. In the second stage, years or decades may pass without the appearance of symptoms. When syphilis finally shows itself, stage 3, we can see a devastating, multi-system disease. We know that late syphilis of the brain and central nervous is frequently associated with dementia and death and that no satisfactory therapy is reported in current medical literature/guidelines.
Lyme is now referred to as the new great imitator. Does initial Lyme infection always cause features consistent with an acute case? Clearly the answer is no. The most common vector is the nymph forms of the hard body Ixodes ticks. These tiny arthropods are the size of a poppy seed. They are stealthy vectors, and more often than not are unobserved by their victims. Many patient do not develop the tell tale rash. There is some disagreement about the frequency of EM rashes, but there is no dispute that they are absent in some or many patients. Bites frequently occur in areas which are hidden, for example,the back of the neck. If the classic rash does occur it can easily be missed by the patient. Some patient, newly infected with Bb develop acute flu like symptoms; but as we have seen, such symptoms are frequently dismissed as viral.
Lyme may enter into a prolonged asymptomatic phase, just like syphilis. These latent spirochetes can quietly disseminate. Symptomatic disease may not appear for many months or even years. A great imitator like Lyme disease can cause a protean array of symptoms and syndromes. This may be a point of disagreement between ILADS and the IDSA. This dispute can also be put aside for the moment. There is no debate that Bb is very neurotropic: It has a known proclivity for infecting both the brain and nervous system.
Penicillin treatments for neurosyphilis are known to be unsatisfactory. The treatment of established spirochete infection in the brain is known to be very difficult.
Many late stage patients with Lyme disease present with neuroborreliosis. This is clearly established and accepted by all groups familiar with the disease, irrespective of their IDSA/ILADS bias. Neuroborreliosis patients have concrete, object findings: Alterations of mental status, abnormal MRIs and abnormal SPECT scan. Forgive my verbiage- It is "no brainer".
Fallon has shown: patients with neuroborreliosis improve with IV Rocephin. The improvements regress with cessation of therapy. The improvements return when therapy is started again. What does this tell us??
I don't think you have to be a physician (or a rocket scientist) to imagine what might be occurring here. The antibiotics temporarily keep the infection at bay- patients improve; antibiotics are stopped- patients worsen- because the offending germs have not been eradicated. Fallon did not continue patients on oral antibiotics when the IV Rocephin was stopped. Many LLMDS, myself included have found that this approach frequently maintains the improvements gained from Rocephin. This begs the question: Why is there a controversy- at least regarding documented neuroborreliosis.
If something is working why stop therapy ? Why is this considered good medicine?