Treating Lyme with antibiotics
Somehow I reverted again to a traditional approach to treating disease: Lyme is a spirochete bacteria, therefore we must treat it by killing it with antibiotics. I knew though there were challenges ahead of us, because the spirochete exists in three different stages (Spirochete, cyst, and spirochete colonies), is intracellular, evade the immune system, has the ability to mutate, and can affect essentially any organ. For a microscopic view of this pathogen in human brain samples of Lyme neuroborreliosis and in vitro culture of chicken and rat neurons as well as rat and human astrocytes, please check this paper from Miklossy et al. 2008 (see illustrative figures 1-4). The different forms which this pathogen can adopt require the use of several antibiotics simultaneously. The Cyst form in particular is most resistant. Ninety-five percent of Lyme spirochete can encyst within one minute and remain viable for up to 10 months, survive several cycles of freezing and thawing. Reconversion to motile can occur rapidly within one hour given the right conditions. The cysts survive quite happily in the digestive system from which they can spread throughout the body.
Figure: 1: Characteristic morphology of Borrelia burgdorferi (Dark field microscopy images of Borrelia burgdorferi strain B31 showing the usual spiral form of spirochetes (A) and their agglomeration into colony-like masses (B)
Figure 2: Rolled and cystic forms of Borrelia burgdoferi spirochetes observed after one week of culture in medium to which Thioflavin S had been added.
F-H: Atomic force microscopy (AFM) images of Borrelia cysts. Rolled spirochetes are clearly visible in F (strain B31) and G (strain ADB1). Arrow in G shows that the cyst is formed by two spirochetes rolled together. H: The cystic form is entirely covered by a thickened external membrane masking the content of the cyst (strain B31).
Figure 3: Atypical and cystic Borrelia forms following 1 week exposure of primary neuronal and astrocytic cultures to Borrelia burgdorferi. C: OspA positive Borrelia spirochetes closely surrounding neurons (strain B31). D: Atypical filamentous and ring-shaped cystic, apparently intra-cellular spirochetes in a neuron (strain B31).
Figure 4: Chronic neuroinflammation in the frontal cortex of a patient with Lyme neuroborreliosis. First column (A, D and G): Accumulation of HLA-DR (A) and CD68 (D) immunoreactive microglia forming clumps, and GFAP (G) positive large reactive astrocytes in the frontal cortex of a patient with Lyme neuroborreliosis.
A further complexity related to the fact that my son’s health is extremely fragile and that he is very prone to seizure, especially following an immune challenge. Treating Lyme with antibiotics is known to cause a Heirxheimer reaction, which is essentially equivalent to an increased release of bacterial toxins, with inflammatory consequences. This is very similar to the Lipopolysaccharide (LPS) model of rheumatoid arthritis caused by injection of collagen molecules followed by LPS injection. LPS are molecules found in the outer membrane of Gramm negative bacteria. They acts as potent endotoxins leading to the secretion of pro-inflammatory cytokines and Nitric Oxide. They will cause an endotoxic shock, increasing the auto-immune response to collagen. What happens during antibiotic use is very similar. There is an acute release of a wide range of bacterial endotoxins which drain the immune system, pushing it towards inflammatory stress and potentially auto-immune response. Causing such reaction is a challenge to affected individuals. The reaction is notoriously severe with people describing all the symptoms returning all together concentrated during the reaction. The problem is in the case of my son, that it causes him an increase in epilepsy. Each time his symptoms are clear unwellness, epilepsy, raised lymphocyte count and fever. I have not yet managed to control this reaction (see separate section on Heirxheimer).
We have tried many antibiotics, azythromycin, doxycyclin, Zinnate, Ciflox, Flagyl, Bactrim, Rifampicin, Bactrim, minocyclin and ceftriaxone i.v. Ceftriaxone is the antibiotic that appears to lead to immediate benefits, however, within 10 days of treatment, my son was too unwell with epilepsy to continue. Ceftriaxone is thought to have the best penetrance in the Central Nervous System (CNS), however, it does not work on all the Lyme stages. It has also anti-inflammatory function, which was making this antibiotic a prime candidate. The second best choice was minocycline, again because of CNS penetrance and anti-inflammatory properties.
I am not sure if it makes a great deal of sense to detail the treatments proposed, but for the sake of illustration, I will show what has been suggested to us. However, as I said, we have not managed to do this for more than a few weeks in total and not for any longer than 2 weeks without interruption.
An alternative protocol (oral antibiotics only) was proposed:
I might consider these treatments again, but for now, I feel a much more gentle approach is required. This is where I started to investigate the potential use of plants. The information compiled below come from reading Healing Lyme and also looking at some protocols written by Dr. Klinghadt.