Why doesn't my doctor believe in Lyme disease?

Scientists do research. They work in labs, at Universities. They work with bugs and test tubes; develop hypotheses, and design experiments to prove or disprove their theories. Sometimes they do basic science research-- to discover the basic structure and function of things. They publish their findings in prestigious, peer reviewed journals like Science and Nature. Such scientists have discovered much about the spirochete, Borrelia burdorferi, the causative agent of Lyme disease. This data is called "in vitro." Many doctors will claim that such results may not apply to the "in vivo" processes inside the body.

Physicians do not read these journals. They operate in parallel. They also have hypotheses. They evaluate their hypotheses with controlled clinical trials. Frequently medical trials provide confusing and contradictory data. In such cases the investigators can draw varying conclusions, sometimes informed by pre-existing biases.

Physicians(practitioners) are not scientists, although some may disagree. There are a few exceptions to this rule. Physicians work within the box of their trade. In medical school they are busy learning basic rules: structure and function of the body, types of disease--causes and treatments. Much of this is complex and ever changing. Evidence based medicine has helped physicians develop protocols and algorithms. The evidence is based on an analysis of the published studies in prestigious journals such as The New England Journal of Medicine and others. At times there is no or little data to support diagnoses and therapies. In such cases a body of "experts" informs the public of physicians regarding the best diagnoses and therapies. Even where no "science" exists, these opinions are surrogates for "science" and become-- "evidence based medicine." The waters are muddied. The distinctions between fact and opinion can become blurred.

The field of medicine is vast. It is broken down into various boxes. Some of these would include disciplines such as: internal medicine, orthopedics, rheumatology, neurology and infectious disease. (Of course this is a tiny selection of medical specialties for purposes of this discussion).
Perhaps readers do not know that all infectious disease specialists start out as generalists--internist or pediatricians, followed by a 2 year fellowship in infectious disease medicine. An infectious disease doctor has done: 4 years of college, 4 years of medical school, 3 years of residency and two years of training in infectious diseases. Note: for the first 11 years, the internists or family practitioner has had basically the same training as an "ID" doctor. Infectious disease doctors see sick hospital patients. They familiarize themselves with a wide range of esoteric infections: bacterial, viral, fungal, parasitic and others. They learn by reading text books, rounding with mentors and performing consults on sick patients, generally in hospitals. They spend very little time in an office setting. They become experts. They do not treat patients with chronic, "low grade" illnesses. They do not treat patients with fibromyalgia, depression, chronic fatigue syndrome and a whole other array of syndromes which they sometimes like to diagnose (in lieu of Lyme disease). Of course, they were generalists before they became specialists.

Each specialty has its own box. It works from a list of common diagnoses. Keep in mind--if you are a hammer, everything looks like a nail.

For example, a patient has joint pain. The orthopedist considers: tendinitis, a torn cartilage, a ligament injury, a mechanical injury--or something--not in his specialty, requiring referral to another specialists. The patient may be referred to a rheumatologist who considers: rheumatoid arthritis, lupus, Reiter's syndrome, post-infectious arthritis, gout and Lyme disease and others. He may conclude it is not in his field. He may refer on to an infectious disease specialist where considerations may include: an infected joint with something like gonorrhea, viral synovitis and perhaps Lyme disease. The Lyme results are negative for Lyme by the IDSA /CDC screening test. No answer is found. The patient is referred back to his primary care doctor. Physical therapy and pain medicines are recommended. If the patient asks about Lyme disease he is told this has already been excluded.

Lyme disease--LLMD style-- is outside the normal boxes. It is rejected by practitioners of the traditional boxes. It is foreign and rejected. After all, the true experts have spoken. These new practitioners outside the box, are easily labeled quacks. Paradigms do not change easily.

And in a nutshell, that is why your doctor does not believe in Lyme disease.

Cystic forms and relapse

It happens all the time. A patient has finally done great. No symptoms. Remission at last.
Symptom free with a "maintenance" med or regimen-- Doxycycline alone or Amoxicillin and Biaxin. Meds are stopped. Lyme symptoms return almost instantly, within days or weeks.

Why?

I have given this some thought. Lyme spirochetes grow slowly. They replicate every 24 hours give or take. The Lyme "load" hasn't suddenly grown exponentially. Is it autoimmune? Antibiotics do have anti-inflammatory properties; have they been suppressing a smoldering autoimmune response lying in wait? No--autoimmune processes generally progress gradually.

This leaves only one possibility. What happens quickly? Cyst forms of Lyme quickly convert to spirochetes, within hours. Ah-ha--the ready source of spirochetes!

As a patient recently told me: "The other antibiotics just cause everything (spirochetes and L-forms) to convert to cysts. Do they?

Cysts are metabolically inactive and generally don't make us sick; the brain seems to be the exception.

In the brain, cyst forms are associated with inflammation. There is experimental evidence supporting this. Tindamax-- the magic drug - sharpens the brain - eliminates vestiges of brain fog.

With the relapse, cognitive functions frequently remain intact while other Lyme symptoms explode. If brain cysts cause more damage than spirochestes there-- I quess this makes sense.

Questions: few answers. Do cyst busters lower relapse rates? Early or late?

Are dreaded L-forms in fact more docile than cysts? Not in the brain.

Perhaps a regimen of a cell wall inhibitor-cyst buster might work better in (in patients lacking cognitive dysfunction), assuming the germs have not passed the blood brain barrier.

Just a thought.

How it is supposed to work

I tend to write about unusual cases. Here is a more typical case--a successful one.

A 68 year old female visited me in January 2009. In 2005 she was sero-positive for Lyme disease. Treating was aggressive by standards of the day. She was treated with Doxycyline for 4 months. She recalls that her chief complaints then were rash, fatigue and joint pain associated. After treatment she felt better.

Over the past year she had not felt up to snuff. Pains in the large and small joints had returned. She had neck pains and muscle pains. She had numbness and tingling of her extremities. Her energy level was lower, she had fatigue, headaches, night-sweats, shortness of breath, an unsteady gait, poor sleep and a decline in cognition. She had trouble finding words and focusing.
She had brain-fog. Her sleep was disturbed.

Her exam was abnormal (neurological findings):her Igenex was positive IgG --34, 41: her Igenx B. duncani test IgM, 1:20 was borderline: a Clongen wet mount showed motile bacteria, presumed to be a species of Bartonella. Her SPECT scan showed poor perfusion to the left anterior temporal lobe: her MRI showed multiple white matter lesions consistent with Lyme disease or MS.

After treatment with courses of: Omnicef, Biaxin, Plaquenil, Tindamax, Zithromax, Mepron, Amoxicillin, Tindamax and Rifamin (in various combinations) She feels essentially normal. The treatment to date has lasted about 11 months. She is still on antibiotics and weaning will be done gradually. I suspect she will be on maintenance medications for a long time to come.

Lyme kills

February 2007. A 46 year old female walked into my office for a "Lyme consult." I did not know at of our meeting-- she had recently been found in the middle of a road trying to end her life. Luckily, she was picked up by a police cruiser and subsequently admitted to a psychiatric facility. I did not know, until today, that a past treating physician, a rheumatologist, had called her an "f...ing moron." This patient/human being, has had a long and bumpy ride, but no longer entertains thoughts of suicide. She was sick of being sick. She had been sick for one half of her life, since age 24. She had suffered with total body pain. She had been diagnosed with "seronegative" rheumatoid arthritis. Gold shots, prednisone and other "remedies" offered no respite from her misery. She had swollen lymph node. Her joints and muscles hurt--really hurt. She was told she had "a weak immune system." She had numerous neurological complaints. There was progressive loss of memory and global cognitive function for over 15 years. Most troubling of all was severe, unrelenting abdominal pain. This was her worst symptom. Numerous specialist had been unable to identify the source of the trouble.

Prioritising, the first thing I did was examine her belly. She had right upper quadrant tenderness and a positive Murphy's sign. Gastroenterologists and surgeons insisted there was nothing wrong with her gallbladder. Sonograms and HIDA scans had been abnormal. I sent her for another HIDA CCK test: normal. I told her she had a bad gallbladder--I didn't care what the tests said. Two surgeons refused to operate. A third ( a close friend) reluctantly agreed. Her gallbladder was bad--chronically infected. Her pain was gone! Now she thought I was a genius. No. I have just seen chronic cholecystitis in many Lyme patients. And her physical exam was classic for cholecystitis. I followed a rule one of mentors taught me back in medical school: treat the patient not the lab. I quess most doctors today had a different mentor.

She was seropositive for Babesia at the outset. The Labcorp Western Blot showed no bands. Her Igenex test negative although IgM bands were "inderterminate" at the 39, 41 and 93 positions.
Treat the patient. Rocephin. She Herxed. We went around the block--numerous times. Gradually, after much Mepron, a mix of oral antibiotics and two courses of Rocephin she was significantly better.

We(she) struggled with serious nicotine addiction: 3 packs per day. She ended up with a severe lung infection. I prescribed Levaquin and Cleocin. The Herx brought her to the hospital. It looked like a cavitary mass or abscess. This was February 2009. The surgeons were sure she had a tumor. The biopsies showed no cancer and no microbes would grow in the lab. Faint colonies were seen only to disappear. The surgeons still wanted to operate. Two PET scans later-- no cancer. She had a miracle response to Ivanz. I have written about this before. The pulmonologist gave her months to live(she tells me), severe COPD. I don't think so. She is not short of breath even with moderate excertion. Maybe he is just trying to scare her.

Today I saw her. She is depressed because she retired from her job (voluntarily). She cleans houses part-time! Her pain is mangaged with modest help from "our friends". Good days and bad days. The bad ones aren't that bad. She is nervous: another PET scan. She wants to quit smoking--just can't do it.

I never knew about the suicide attempt--until today.

What do those lab tests mean?

The CD57 test (only from Labcorp) measures a subset of NKT cells. These are Natural Killer T Cells. These T cells are actors in the innate immune response. In other words, these cells automatically attack what our immune system sees as foreign invaders. Our immune systems are naturally smart (anthropomorphically). They have pattern recognition cells which can determine tissues/cells that belong in our bodies from things (like bacteria) that do not belong in our bodies. The second part of the immune system, the acquired immune system relates to a complex set of reactions by which the immune system learns to make specific antibodies to attack the foreign invader. In some situations only the innate immune system is in play. Primarily this occurs when the "invaders" are intracellular. The acquired responses just don't work here. In the case of Lyme disease it is the intracellula- L-forms which are attacked by the NKT cells. When the CD57 count is low it would appear these cells are busy combating the L-forms of Lyme. Unfortunately, the innate immune system is never 100% effective in eliminating the bacteria. This is one of the mechanisms by which Lyme is able to persist in the face of antibiotics and immune responses.

C3a and C4a (Labcorp) are products of the complement system, cleaved from C3 and C4. These proteins are mobilized by the immune system as part of its acquired and to a lesser extent innate immune responses. These proteins can attach to unwanted bacteria and target them for destruction. These tests are sensitive indicators of a busy immune system attacking unwanted proteins or germs. These markers can provide a general sense of immune activation in the face of infection or inflammation.

C3d (Quest only) is a test for circulating immune complexes (CIC). These antibody/antigen complexes are not supposed to be present in our blood. The presence of these CICs indicates infection or inflammation and can be used as another indicator of disease activity.

C-reactive protein (CRP) is a naturally occurring protein found in blood circulation. It is one of two proteins which activate the complement system associated with immune activation. This is another marker which can help assess disease activity. This marker is elevated in many diseases and is not specific for Lyme disease. When used here, the clincially useful cut-off points may be much lower than the "normal" reported by the lab.

There are many other labs/markers of infection/inflammation. But here a few that seem to confuse many patients (and doctors).

Musings with a patient today

Biaxin and Plaquenil? We have been taught that Plaquenil makes the intracellular environment more alkaline so Biaxin works better. Is this true? I don't know. I have also read that Plaquenil is anti-cyst. Sapi has now shown that Plaquenil induces cysts. You are on so many meds: let's drop the Plaquenil for now. The Malarone seems to be making the sweats go away. You are not sure, could the the sweats are hormonally induced? Possibly. My guess is that we are fighting Babesia: you tested positive. The low dose anti-malarial drug seems to work. Other patients require much higher doses.Biaxin decreases the Atovaquone by up to 40%. Many doctors switch to Zithromax for Babesia; Biaxin is a much better Lyme drug. We are covering more territory. The Bactrim you are taking for Bartonella also has some anti-Babesia effects; perhaps that is why you are doing so well. Patients seem to do better in the long run when anti-cyst drugs are added. Tindamax is the best--but that is for later.

How long do we treat Babesia for? Good question. Until the symptoms go away. There is no magic number. It has been said treat for 5 months because red blood cells have a 4 month life span. The only problem is that Babesia can also hide in the bone marrow, liver and spleen. The IDSA claims that it only resides in red blood cells--not true.

You followed all of that? You are doing better than you think!

Bartonella: brief report

A patient with documented chronic Lyme disease had further testing for Bartonella.
A test performed at Fry labs reported abnormally shaped red blood cells without bacteria.

A wet mount at Clongen showed scarce round motile bacteria.
A PCR at Clongen for "Bartonella species," was positive.

In general, PCR testing for Bartonella is not performed because of a low yield.
These results, albeit in a single patient, suggest that: 1) wet mount exams may be more accurate than stained whole blood samples for the identification of these bacteria and 2) these small round organisms seen in patient's blood do in fact suggest ongoing infection with Bartonella species.