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Re: Ms vs Lyme Differential Diagnosis

Posted: Fri 26 Feb 2016 19:39
by lou
I would question the spinal tap. It is invasive and does not often find lyme even when the patient does have it.

Not sure why, with that history and those test results you would still be questioning the diagnosis. Babesia does not always hit hard, can lurk and produce less obvious symptoms. In my case, it was not until the lyme really got bad that the babesia symptoms started showing up and that did not include trouble breathing or major night sweats. There is a lot of variation in patients symptoms and response to treatment.

If you do not want to go back on antibiotics, it is not clear to me why you are still pursuing this. If you get an answer you believe, you will not treat it? No, a month of IV will not cure this if you have had it a long time already.

And BTW, my white blood cell count is low, not high, and that is not unusual for late stage lyme.

If you want truthful answers, don't bother to read Henry's replies. He is a troll.

The thing about the culture is that it is only monitored for a certain period of time. It is not impossible that more time would have given a different result.

If you are told that IGeneX does not provide reliable results, then this is being said by people who will not consider a lyme diagnosis even if you have it.

Re: Ms vs Lyme Differential Diagnosis

Posted: Thu 3 Mar 2016 2:46
by ChronicLyme19
This blog post seems relevant to this thread:
http://www.huffingtonpost.com/dana-pari ... 18660.html

It's an interview with Dr. Steven E. Phillips is a Yale-trained, Lyme specialist who has treated over 20,000 patients in the last two decades.
Another common presentation is MS. When we say that Lyme can mimic MS, it can do so literally 100%. So, we have to ask what percentage of MS is caused by Lyme.

If you look at the epidemiology of Lyme, it overlaps with MS identically. If you look at the diagnostics--whether it's white spots on the brain or spinal cord or optic neuritis, oligoclonal bands in the spinal fluid, or evoked potentials--every single clinical descriptor has been reported with Lyme. There is no clinical, laboratory, or radiologic feature which accurately differentiates the two.

Keep in mind that the majority of symptoms of Lyme are caused by the immune system going after the organism. If you induce immune suppression, you can reduce symptoms in most patients, but at the huge cost of allowing the bacteria go deeper and become more entrenched. So, it's no surprise that steroids given before antibiotics increase the risk of antibiotic treatment failure.

Back in the early MS literature, they found spirochetes in the brains of patients who were autopsied. They called it by a Latin name that meant myelin destroyer.

They knew it was a spirochete that wasn't syphilis but they didn't know what it was, and they did a number of animal studies taking the spinal cord fluid and tissue of those with MS and putting it into baby animals, and the animals got progressive neurologic illness.

But when steroids were discovered, they realized they could suppress symptoms quickly, and this whole concept of autoimmune disease sprang up. So, before steroids, MS was known as an infectious disease.
How many patients come to you with an MS diagnosis who actually get better with antibiotics?
A lot. I have to differentiate the relapse and remitting folks from the primary progressives. I don't know that primary progressives have Lyme--they don't respond the same way--but my relapse and remitting patients respond quite well and the majority have evidence of Lyme if you thoroughly evaluate.
I often have patients come to me on standard MS drugs and I add in some simple tetracycline-based regimens and their symptoms improve and their lesions resolve. I've had doctors tell me they think it's a coincidence when my patients get better, but it doesn't take a rocket scientist to see what's happening.