Knee, Assymptomatic Babesia, Autoimmune neuropathy, Tindamax

Another young woman came into my office with swollen knees. The first doctor she saw, an IDSA doc had no trouble making the diagnosis since Her Lyme ELIZA was positive and she had 13/13 Lyme Western Blot bands present. The ID doctor presented her with 2 options. She could take a 30 day course of Rocephin or she could go on low dose Doxycyline. It was sort of left up to the patient. One has to ponder how these 2 options are interchangeable. Rocephin, a cell wall inhibitor kills only Bb in the spirochete form. Doxy, a protein synthesis inhibitor kills Lyme in the spirochete and the L-form. It always troubles me that the "experts" are unaware of these basic facts. From my perspective it makes more sense to use two antibiotics which can synergistically attack the spirochete and L-form simultaneously. The patient has acute, active synovitis with swollen, inflamed joints. In chronic Lyme arthritis it has been shown that L-forms in the synovial lining are the problem. In acute Lyme arthritis It appears spirochetes are the culprit since such patients typically respond well to only IV Rocephin. In this case IV Rocephin is a reasonable treatment choice. Oral therapy with something like Amoxil and Doxy is also a reasonable option.(There seems to be some controversy about the combination of Amox and Doxy. They are thought to have an adverse interaction. I do not think this is the case. One can use Amox and Biaxin or Ceftin and Doxy if one prefers). The ID docs, as I am oft told, "don't believe in co-infections." This I do not get. I re-tested her. She was positive for Babesia duncani as well. She has no symptoms of Babesiosis.

After 4 weeks of oral combination antibiotic therapy, she came in today about 50% improved. After weighing the options, we decided to go to IV Rocephin for 30 days. Then I looked at the Babesia issue: She is young. She has no symptoms of systemic Lyme disease. She only has knee involvement. Her immune system may be functioning well, at least her CD57 level is normal. In this case I decided to treat Babesia by standard-text book recommendations. I ordered Mepron and Zithromax for only 21 days. Perhaps her immune system could truly eliminate the Babesia but I thought it would be better to treat-prophlactically. After all, chronic Babesiosis when it does occur can be a beast.

I decided to do a little exam of the nervous system. I continue to find that nearly every patient with Lyme disease has some peripheral neuropathy. As with most patients, there was a little stocking/glove loss of pin-prick sensation and a little decrement in vibratory sensation in the feet.

I am now fairly certain that these findings are due to a Lyme induced autoimmune process. Usually the autoimmune process is minor, but it is something that I have learned to keep a close eye one. It can worsen due to Bb infection but it can also worsen as a result of Lyme therapy. I look carefully for symptoms of progressive numbness, tingling and weakness. I examine for a worsening sensory exam. And when I find that previously existent deep tendon reflexes vanish I am particularly concerned.

When I see an increased in autoimmune neuropathy I quickly back off therapy.

I have wondered if some antibiotics have a tendency to cause more autoimmune reactions than others. This is an observation; I cannot back it up with any data.
I have observed that these reactions seem to occur more frequently when Minocin is used early in the course of therapy. I don' think Doxy does it. It seems less common with Amoxil, Rocephin, Biaxin and Zithromax.

So for what it is worth I now avoid Minocin as a first line agent.
On a final note- I am increasingly impressed with the effectiveness of Tindamax.
For example, when a patient responds rapidly to the combination of Amoxil and Biaxin, adding Tindamax a month or two later frequently makes a huge difference.