A patient I saw today:
This was one of my early cases. I was just learning. The daughter saw me first. She was diagnosed with some form of reactive arthritis by a rheumatologist. She had a borderline rheumatoid factor, borderline ANA and a high CRP and sed rate. She was placed on Methotrexate, a commonly used immune/disease modifying drug. Around that time she began seeing me. I demonstrated evidence of chronic infection, either old or active, with Lyme as well as other bacteria. Ongoing infection could be an explanation for her problems. This could imply an alternative approach to her problems might be helpful. The rheumatologist became aware of this. A cough led to a chest X-ray. Surprise. It showed enlargement of hilar lymph nodes in her thorax. The rheumatologist was alarmed. He knew that Methotrexate(MTX) could be associated with Lymphoma- a type of cancer. He also knew that MTX induced lymphoma could regress when the MTX was stopped. The MTX was stopped. A repeat Chest film was normal. He was relieved: another one pulled out of the fire. The ball was in my court. I treated her for Lyme and chronic Salmonella- something I considered more important at that time. She responded poorly. Antibiotics didn't help. I sent her to another LLMD/rheumatologist. The other physician tried her on everything under the sun, including many alternative medical therapies. She also struck out. The new rheumatologist, as a last resort, suggested the patient try Enbrel, another immune modulating drug. After the close call with MTX my patient said no thank you and returned to me.
The father is another story. The same (first rheumatologist) diagnosed him with rheumatoid arthritis. It was atypical. He was in his 60s and it occurred after an acute viral infection. He had high titers against EBV and a dramatic positive WB for Lyme. He was upset when he realized the rheumatologist made the "wrong" diagnosis. Unlike his daughter, he responded beautifully to anti-Lyme treatment and went into a complete remission. He too had a positive rheumatoid factor test and other markers for autoimmune disease.
My impression is that both father and daughter have the same genetic profile. They share an HLA genetic type which put them at risk for infection-activated autoimmune disease. One had responded well to anti-microbial treatment, the other had not.
Let's get back to the daughter. She has a very high CRP, about 45. Her sed rate is in the same range, about 45. She has persistent joint pain and fatigue. She also has radicular pain of the left upper extremity (pinched nerve pain in the neck), but this could be due to a mechanical problem such as a disc, not Lyme disease.
She has no other neurological symptoms or cognitive symptoms, and no other symptoms of note. She had been on three years of antibiotics and other therapies, with no change in her complaints. She has some other low grade, nagging lab abnormalities: low carnitine, low B12. low folate and vitamin D dysregulation. Her RA factor and ANA remain modestly elevated. If I were not a "Lyme doctor" I would say she has a variant of rheumatoid arthritis. The Enbrel seems appropriate- except that it might give her cancer, and she wasn't willing to risk it.
So what to do? I dazzled her with fancy foot work. I explained the molecular mechanisms of autoimmune disease- various theoretical constructs- Th1 and Th2- I was stalling. It was the end of the day.
Sometimes I just don't have a great answer. So I ended up prescribing a novel combination of antibiotics- maybe I'll (she'll) get lucky. Perhaps not. One out of two isn't bad, is it?
I don't get everyone better. But I never quit trying.
What do the immune modulating drugs do and do you think they could be helpful in the treatment of Lymes? I've been seeing articles recently comparing Lyme with HIV as they are both immnusuppresent illnesses. Do you see any hope there?
Did she have initially cognitive dysfunction and other neuro signs? Did Dad? Did she worsen with Methotrexate- ie was she active at that time?
I would think the autoimmune subset of patients would present a difficult challenge in that our typical immune modifications would reactivate the underlying disease. Assuming the antimicrobials with immune modifying capacity (plaq, mino, ect ect) have no effect, where can you safely go with these patients? If they are in remission for the underlying disease that set off the autoimmune issues, how can you keep them that way and address autoimmune disease? It is a clinical catch-22, calm one down and stop what is holding the other at bay.
As an aside, what is your opinion of lose dose nalaxone therapy used by some in these situations?
That is courageous of you to post your failures as well as your successes. I am another of the readers that loves case reports, and there is as much to learn from all of them, regardless of the outcome.
I also enjoy your candid thinking-out-loud posts about the puzzling nature of the disease -- one of the things that holds some morbid appeal to me, even as a Lyme patient, is the challenge of understanding it with all its marvelous complexity and unknowns (although I would probably enjoy the view better from an OUTSIDE perspective).
You are doing a really excellent job with the blog and I encourage you to continue.
Would insurance cover IVIG for the daughter--considering she was prescribed methotrexate and it endangered her life? How about a gluten free diet, as you've noticed gluten seems connected for a lot of us.
Thanks--nice story--hope we can revisit it later.
Follow up on this very case. Surprising find. I sent the daughter's blood for a look-see to find any bacteremia. The sample was taken on 12/03/08. Yesterday the results were not in the chart, I asked Clongen to forward them to me.
The original wet mount and smears had been done when Dr. K was out of town, by an associate. He didn't like the quality and repeated a wet mount yesterday. The first result was entirely negative. When he looked at the wet mount of three weeks "incubation" in the refrigerator he saw bacteria in the white blood cells- suggesting Ehrlichia. This could not be a contaminant. These bacteria were not seen in the extracellular compartment, they were only seen in WBCs. She had negative Ehrlichia serology in the past. I asked him to run PCR for Ehrlichia and Anaplasmosis. These are the only two known forms of the organism. If these tests are negative we will have another DNA sequencing challenge. The Zithromax, Rifampin and Minocin I had prescribed for her may have some benefits after all.
This begs the question: Are we missing a lot of occult Ehrilichia infections? From what I have learned, intracellular bacteria which reside in white blood cells may be impossible to eradicate. The standard two months of Doxycycline may only temporarily suppress the organism. Even adding Rifampin, which is done for difficult cases, would only suppress the infection as well. Since it is intracellular, chronic forms may stay sero-negative. Remember- antibodies are only produced when germs present in an extracellular form. They should shake out with a good PCR test.
Incidentally, a blood wet mount on another patient with negative Ehrlichia serology had the same results.
Cool. I wonder if Dad had erlichia too? Every case history is fascinating. Clongen sounds very good.
I have always heard that PCR testing for Lyme produces many false negatives. That in fact the odds of a positive are only around 6%.
Any idea how accurate PCR tests are for the coinfections? I asked Dr K this question and he had no data on false negative rates.
Just further wondering. Were other family members perfectly healthy? Would Kilani be interested in seeing if father's wbc's grow out the same organism--and yet it might not be affecting him? Or could he have cleared it, or never been exposed? These are the kind of questions that plague me and feel urgent to me...the yard where I got "slymed"--in retrospect she and her husband had symptoms. She had bad migraines, bipolar symptoms, inexplicable hip pain that would put her in bed with percoset for a day or two, a spring bronchitis out of nowhere etc...he had knee problems...*but* neither of them got anywhere as sick as I did. They led active lives. Did I get the 0.4% of ticks (per Eva Sapi) that had four or six bad bugs? Or am I genetically primed with an already "tilted" immune system (rarely get "sick" but allergies, autoimmune, and celiac show up in various places on my family tree and in me too of course).
It seems if Kilani's work is this meticulous maybe he can start helping us find some answers. I do remember reading that bugs/ticks/mice and even deer have their own little ecosystems. You will find different strains/common bugs in the ticks in different parts of town even. That's why I wonder about testing all family members just to see what they're carrying.
Beyond that, sometimes I just wonder how one little vector can carry so many stealth bugs, hiding in various cells and tissues. It seems truly creepy.
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