I have been treated a 30 something year old female for disseminated Lyme and neuroborreliosis for over a year. Most symptoms cleared up with oral meds. The cognitive issues stubbornly refused to budge. This patient interestingly also developed a tremor with features of Parkinson's disease. The Rocephin took a while, but after 8 weeks started showing some very positive effects. Memory, brain fog, word retrieval, cognitive processing speed and tremor all improved. Antibiotic therapy was interrupted because of an unrelated medical problem. She did OK for two weeks; during week 3 off Rocephin she experienced a precipitous decline. All the target symptoms mentioned above rapidly returned. She even developed joint pain which had been absent for months. What happened? I am sure this patient is tired of me thinking out loud every time I see her. Where there is no science, I have to logically figure out the process and make therapy decisions based on working hypotheses.
Obviously we restarted the Rocephin right away- but what else, and why?
I had tried Zithro with the Rocephin earlier in the course but after 6 days it was stopped because of side effects (nausea and vomiting- I think).
Why does the disease reactivate so quickly and so aggressively. It is like I whacked a hornet's nest with a baseball bat. As long as I was batting away the hornets stayed in their nest. As soon as I stopped whacking, they came out madder than Hell.
It can't be a Herx reaction. The meds were removed. A reverse Herx? Of course not.
The spriochetes couldn't have grown and spread that quickly. They are very slow replicators- it takes a long time for them to reproduce and invade new tissues.
Is it due to an inflammatory or autoimmune response? Maybe. It is known that Rocephin has some anti-inflammatory neuroprotective effects. Could removing it quickly cause rebound inflammation and/or autoimmunity? Interesting- doesn't pass the sniff test.
Let me put this phenomenon together with something I recently read. Intracellular bacteria cause minimal pathological effects. That's interesting. Perhaps when the Lyme bacteria convert into L-forms and disappear into the cellular cytoplasm they cause less overt disease/symptoms. This is the opposite of what many Lyme experts have claimed, but maybe they are wrong. Many antibiotics like Biaxin and Zithromax can kill Lyme in both the L-forms and the spirochete forms. One thing we know about Rocephin is that it only kills spirochetes forms, leaving L-forms (intracellular) unscathed.
A picture appeared in my mind. I could imagine Rocephin molecules zipping down the blood stream like speeding cars on the Autobahn. Any Lyme (spirochetes) in the way would be wiped off the road instantly. The Lyme germs would have to respond quickly if they were to survive. Quickly they converted into cysts and L-forms and slipped into cells. The Rocephin would clear the blood stream and its surrounding watershed of cell wall possessing spirochete forms. Lyme in its other forms was safe.
Where does this leave us? Autoimmunity? Rocephin doesn't destroy auto-antibodies. Could there be increased inflammation with cytokines and cellular destruction? This could only occur if Rocephin has a very potent immune suppressing effect like a steroid or immunomodulator like an anti TNF drug. There is nothing in the literature to suggest that Rocephin has such properties. If it had a potent immunomodulating effect then benefits after treatment should occur quickly. Usually, the benefits of Rocephin are not seen for several weeks.
Maybe the signs and symptoms associated with Lyme neroborreliosis are mediated almost entirely by intact- motile spirochetes. Rocephin is strictly clearing these forms from body fluids and tissues.
When you take away the Rocephin what happens? The L-forms and cyst forms (metaphorically) duck there heads out from their hiding places. They put a toe in the water to check the temperature. All clear. Party time for spirochetes. It is the rapid release of spirochetes into tissues and fluids which causes the immune response and clinical disease. That is my best hypothesis. Hopefully you followed the logical chain which got me there.
Wasn't there a study showing that Amoxicillin alone controlled symptoms in chronic Lyme? Yes. Perhaps it has always been about the spirochetes after all. The cysts and L-forms were just put there to make it impossible to kill the bastards (pardon my French).
Getting back to the patient. Not having the luxury of time as I put my thought together in this piece I made an executive decision: I started Rocephin and IV Flagyl. The Flagyl should help one mechanism of escape. Before I take her off Rocephin I will have to close the other door as well. If she couldn't take Zithromax, another anti-L-form therapy will be needed. The possibilites include Biaxin, Doxycyline, Minocycline and Cipro.