Friday, January 30, 2009

Lyme and a knock to the head

A 31 year old female aquatic animal trainer presented to me 6 months ago. She had been referred by another patient. She complained of headache, dizziness, fatigue, muscle weakness, a loss of balance, tingling and numbness, blurred vision, decreased coordination, episodes of confusion, brain fog, anxiety, irritability, palpitations and episodes of random sweats and chills. The headaches were particularly bad. They were daily, felt like pressure in the front of her head and interfered with sleep.
All the symptoms were new. The symptoms were getting worse. About 2 months before she suffered a closed head injury and a concussion. She had been butted in the head by a dolphin. Initially, I filed this part of the history away and focused on the Lyme evaluation.

Let me insert that she had previously seen numerous physicians including a neurologist. A Brain MRI was negative. No diagnosis or therapy had been suggested.

She tested positive for Lyme disease and seemed to be a fairly typical case. She had a lot of muscle weakness and poor endurance with a loss of strength. The sweating pattern suggested a typical Babesia co-infection syndrome. Treatment with antibiotics produced slow and steady improvement. Antimicrobial therapy included Amoxicillin, Biaxin, Flagyl and Mepron. After several months the improvement was incremental but slow. She was unable to work and was concerned that she might be disabled for an extended period of time. I felt that she was doing fairly well. It would take time; she would eventually be able to return to work. It is impossible to predict how long it will take for a particular patient to get better. Nonetheless, every time I see a patient for follow up I review the initial, presenting symptoms: which symptoms have improved and which have not. About 6 weeks ago I noted that the headaches were quite disabling and had not improved to any significant extent. The headaches had a migraine like quality. Empirically, I prescribed a migraine preventing medicine, Topomax.

When I was her last week I was surprised by her dramatic improvement. The Topamax made a huge difference. The headaches resolved, her sleep improved and virtually all the other symptoms disappeared as well. It was a rather amazing transformation. She had scheduled her return to work- full time.

In retrospect her case looks a bit different. I still believe she suffers with chronic Lyme disease, but this may not have been her main problem. Her illness was triggered by a closed head injury and a concussion. Patients can suffer with a post-concussion syndrome which can persist for many months.

Headaches which resemble migraines and all the other presenting neurological symptoms can be seen in post-concussion syndromes. I have seen many such patients over the years. They frequently experience dizziness, balance issues, visual changes, mood swings, memory loss, brain fog and even bouts of frank confusion or disorientation. All of these symptoms dovetail nicely with many of those associated with typical neuro-Lyme- and this patient's initial list of symptoms.

The connection between fibromyalgia and sleep problems has been well known for decades. Patients deprived of deep sleep, stage 4 delta sleep, all develop a fibromyalgia like syndrome after a period of several weeks, as has been experimentally shown.

The improvement in muscle symptoms could be related to the improvement in sleep that she was experiencing. Perhaps the restoration of brain function caused the marked improvement in muscle symptoms by some other mechanism.

Asymptomatic, persistent Lyme infection be transformed into an active process by another illness, usually an infectious illness. I have seen this many times. In this case I suspect that the neurological injury triggered by the concussion and the associated sleep deprivation, created an environment permitting activation of Lyme- and perhaps Babesia.

Wednesday, January 28, 2009

Thinking about thinking

After two years of oral antibiotic therapy this 55 year old female with chronic Lyme disease is doing great- or is she? Her stamina is now great. The annoying numbness and tingling is a thing of the past. She is free from joint pains- after many long years. The sweats the chills, the low grade fevers are all gone. The brain "fog" is gone. She is functioning well as a teacher, well, sort of. She used to be a lot sharper. She used to be organized. Now she is scattered brained. She looses things and she looses her train of thought. The word retrieval issue still drives her mad. When she finally pulls up the word she was searching for it is hours later. She is not herself. The cognitive symptoms were clearly worse at the start. Things steadily improved but they have reached a plateau and not budged for over 6 months. The Lyme diagnosis seems pretty clear, she has been seropositive several times at IgeneX and at Labcorp. She has been empirically treated for Babesia and other co-infections. To look at her- one might envision a picture of restored health and vitality.

Ia she the best she can be? Is there a next step? If so, what is the next step?

Many LLMDS would be happpy with her progress, rightly so, and tell her to give it time. Perhaps in another year or two things will get back to normal. Or perhaps she would be told- as long as things stay the same and don't get any worse then it is best to leave things alone.

Per the title of the post, I find myself thinking about (her) thinking. Objective measurements may be hard to come by. I ordered a SPECT scan and an MRI. For the sake of this excercize, we will assume that they will both be normal. She would easily pass any pen and paper neurocognitive assessment. What is at stake is her subjective sense of her global cognitive functioning- pre-Lyme, her memory of her memory as it were.

This is a very gray area within another very gray area.

I think that a course of Rocephin should be tried. I have seen it work.

Tuesday, January 27, 2009

Hard to catch?

Many have characterized the IDSA and ILADS dispute with the simple dichotomy: Hard to catch easy to cure, versus easy to catch hard to cure. A snappy little sound bite.
I saw one of my delightful patients today. He is a 23 year old male with cerebral palsy. He has been quadriplegic since birth. He has minimal use of his left hand and motors around the house with an electric wheel chair. He suffers with severe cognitive impairments. He rarely leaves the house and never goes anywhere without his elderly grandmother. He lives in an apartment complex. One year ago he had several tick bites. His grandmother thought it was from the mulching of the trees around the entrance to his apartment complex. He is difficult to communicate with because of his handicaps.
Nonetheless, his care giver could easily see a change in his demeanor. He became sullen, less mobile and in general, appeared uncomfortable. His lab tests were positive for Lyme disease by CDC surveillance criteria. He was treated with two months of antibiotics and got better. Two months later he was ill again. He had malaise, low grade fevers, decreased mobility and a change once more, in his normally cheerful demeanor. After 3 additional months of antibiotic therapy he became well and he remains well to this day.

This young man lives in an apartment with his elderly grandmother. He is permanently confined to a wheel chair. For all intents and purposes, he virtually never leaves his home and he certainly never goes outside to enjoy bucolic scenery. He developed classic Lyme disease with positive CDC serology.

The disease is hard to catch???
We can deal with easy to cure another day.

MS? Take another look

This 40 year old woman saw a neurologist only once. She did have tingling on the right side of her face. At that point the neurologist stopped asking questions. He ordered am MRI. But she also had headache, joint pains (multiple and diffuse), cognitive issues and floaters. She spent a lot of time outdoors. The neurologist had no interest in this litany. Her neurological exam showed a typical pattern of sensory peripheral neuropathy, not the central nervous system findings one would expect to see in MS. I do not know what he found when he examined the patient.

The neurologist diagnosed MS. A brain MRI showed periventricular and subcortical white mattter disease. The radiology reports reads "While these are nonspecific these lesions are suspicious for demylinating plaques. Clinical correlation is needed to exclude......Lyme disease......"

These findings MRI findings are fairly classic as seen with MS. The neurologist informed the patient that she had MS. Not quite convinced, the patient sought my attention, seeking another opinion.

Again- MS cannot be diagnosed by MRI findings. There are diagnostic criteria listed in many text books. Per Harrison's Textbook of Medicine, 16th edition, page 2464:
There are 5 specific criteria listed. MRI findings are not a prominent aspect of the criteria. The fifth criteria is clear: "The patient's neurological condition could not better be attributed to another disease."

My history and exam pointed to Lyme disease- not MS: See criteria #5.

During a 6 month process of treatment, other symptoms became manifest. The patient had soaking sweats. She had profound fatigue, which increased with antibiotic therapy- a Herx response. She had muscle pains, diffuse numbness and tingling of the extremities, muscle twitching, tinnitus, floaters and sleep difficulties.

The cognitive difficulties were typical of what I have seen in numerous chronic Lyme patients. The patient had "brain fog," word retrieval difficulties, short term memory loss, slow cognitive processing and new ADD like symptoms- difficulty concentrating.

After 5 months of treatment which has focused on Lyme and Babesia she is feeling 80% better.

She never agreed to have labs run through a specialty lab. A limited Lyme WB showed a 23 IgM band. She has had alterations in vitamin D and high complement levels. Her CRP has remained very elevated. Let me comment on the Western Blot. There is much literature demonstrating the existence of sero-negative Lyme disease. This is denied by the IDSA- even though many of their physicians have authored and published papers in the past refuting their current stance. The 23 band is specific for Osp C. This is a specific antigen, outer surface protein C, which many consider diagnostic Bb- the Lyme bacteria, even in the absence of other bands. In truth, there are no universally accepted Western Blot criteria for the diagnosis of Lyme exposure. What exists is an assortment of surveillance criteria and individual guidelines espoused by a variety of physicians and laboratories familiar with the disease. The diagnosis is not cut and dried or black and white; and the treatment is murkier yet by many orders of magnitude. Perhaps as someone said in reference to Lyme and its controversies: "It is an exercise of nailing jello to the wall." This is true, but we still have to deal with the jello!

I ask physicians to try to do a better job, to keep an open mind- and to consider the fact that those of us who see patients in the northeast US and mid-atlantic region are operating in a Lyme endemic region. I also ask physicians to keep in mind that Lyme has aptly earned the title: "The great imitator." Patients with complex, multi-system complaints cannot be diagnosed with a single imaging study. The basic tools of history and examination are as essential now as they were 100 years ago. Something was ingrained into my mind by one of my mentors early in my medical training, something which has held me in good stead for all these years: Rule one- treat the patient, not the lab.

Friday, January 23, 2009

Lyme and the CDC: A tangled web

A 50 year old male came into my office in March 2007 to inquire about Lyme disease. He had been referred by anther patient. He had previously been diagnosed with fibromyalgia, depression and other ailments. He is an outdoors man and recalls many tick bites over a period of many years. His illness became pronounced in 1994, but in retrospect had been ongoing for at least 20 years.

He complained of arthritis, sleep problems, severe cognitive impairments, weakness, a loss of coordination, a loss of balance and diffuse muscle pains and restless leg syndrome.

His previous physician had treated him with the antidepressants Wellbutrin and Elavil. His examination showed evidence of sensory peripheral neuropathy. Initial screening blood work was normal. His "Western Blot" for Lyme with a "mill" lab showed a single IgG band in the 58 position.

A brain MRI showed white matter disease. Based on my experience with many similar patients, I felt he had chronic Lyme disease and presumptive neuroborreliosis. The medical literature is replete with information regarding many well documented cases of seronegative Lyme disease. Today's IDSA/CDC crowd makes that claim that not only is seronegative Lyme virtually non-existent, but seropositivity is narrowly defined by the two step ELIZA/Western Blot test. History has been re-written. The CDC has repeatedly stated that this test is for surveillance/epidemiological purposes, not diagnostic.

This patient had a good clinical response to oral antibiotics. Virtually all of his presenting symptoms improved- except the cognitive impairments. These were marked and threatening his professional and personal life. He had short term memory loss, word finding difficulties, episodes of confusion and disorientation and an inability to concentrate. His depression and mood swings were marked.

By February 2008 he was about 50% better overall. Cognitive symptoms had not improved. A Lyme Western Blot performed at IgeneX showed positivity at bands: 18,34,39,41. He was CDC and IgeneX positive. I have found no literature which discusses the issue of Lyme seroconversion. This phenomenon is well known to physicians who treat Lyme disease. It is not discussed by the CDC or in IDSA guidelines. The CDC still maintains that a positive test is based on the two tier test or now- a Western blot showing 5/10 IgG WB bands. Those of us who treat chronic Lyme know three things: The two tier test is inaccurate, A direct Western Blot which incorporates IgG is unhelpful since the vast majority of seropositive patients have IgM responses only and many patients who test positive for Lyme only do so after Herx responses folowing antibiotic therapy. The IDSA does not address the existence of Lyme related Herx responses. IDSA physicians I have spoken with claim that seroconversion has no meaning; they believe it represents a false positive response. It is also trying(to say the least) that the CDC has failed to inform laboratories and physicians what a positive Lyme CDC test means- despite congressional instruction to do so in 2002- signed into law by President Bush. At the present time, every mainstream infectious disease specialist, neurologist and rheumatologist I interact with has mistaken beliefs about the meaning and use of this test. Furthermore, they believe that my interpretations of Lyme tests are tantamount to quackery.

A SPECT scan from June 2008 showed decrease perfusion to the frontal and parietal lobes in the brain. The Lyme denialist camp has claimed that SPECT scans have no validity. This denial is made in the face of evidence based data from Columbia University. This patient received a 5 month course of intravenous antibiotics, ultimately including Zithromax and Flagyl added to Rocephin.

His response was nothing short of spectacular. All of his symptoms, virtually 100% are gone. His mentation is perfect. He has not functioned physically or mentally this well in over 20 years. He is weaning of his antidepressants. His mood is normal.
His remission is maintained with oral antibiotics.

Thursday, January 22, 2009

Lyme and CIDP

I have been treating a 45 year old male for several months. He has been sick for a very long time. He is seropositive for Lyme disease and Babesia. He has complained of searing total body pain, joint pain and cognitive difficulties for several years. he had become disabled. I tried treating him with a variety of oral and IV medications, with poor results. It has been a frustrating case and I have tried many different strategies. Finally he called me telling me that he had sudden weakness affecting his lower limbs and he was unable to stand. He went to the Hospital and was diagnosed with Guillan Barre syndrome. He was treated with plasmamapharesis. He had a reasonably positive response. He was able to walk but he was still in severe pain and had total body weakness. He was discharged to a rehabilitation facility before returning to see me in the office. I took another look at him. The diffuse, searing neuropathic pain had been ongoing for years. He had weakness of his legs- but there was also weakness of his arms. He had a diffuse loss of sensation to sharp touch in a diffuse pattern. His pain was also very diffuse. His deep tendon reflexes were diminished. He had evidence of mild muscle atrophy diffusely. The neurologist at the hospital had been dismissive. It was Guillan Barre syndrome. Both his intense pain and Lyme disease were dismissed. Unfortunately, my patients frequently get substandard care when they are admitted to the hospital: " Oh no- not another one of so and so's patients."

Guillan Barre is an acute syndrome. It is associated with an ascending neuropathy. This patient had a chronic neuropathy with an acute exacerbation. The plasmapheresis had bought him a little relief, but not much. I am a family doctor- not a neurologist. But it became clear to me what was going on with this patient. He has CIDP- chronic inflammatory demyelinating poly-neuropathy. The disease is a cousin of Guillan Barre, but it is different. It is a chronic disease. It is an autoimmune disease of the peripheral nervous system. Auto-antibodies attack the lipoprotein coat of peripheral neurons, causing diffuse demyelination of the motor and sensory peripheral nerves. In this case, I believe it was Lyme mediated- at least in part. Every time I had prescribed antibiotics for Lyme I only made matters worse. killing Lyme led to increased antigen presentation- feeding a malfunctioning immune response- cranking out noxious auto-antibodies. This is consistent with my model of how Lyme and other germs provide fuel for an autoimmune process. While many believe that autoimmunity is self perpetuating once it begins; it has been my experience that a reduction in germ load can frequently help quiet down the process.

A diffuse loss of myelin of sensory nerves could easily explain his uncontrollable pain. Similarly, the loss of myelin of motor nerves could easily explain the diminished reflexes, weakness and atrophy.

I temporized his therapy with intramuscular injections of steroids while introducing heomeopathic doses of Minocycline. I referred him to a neurologist- whom I believe will do a more thorough evaluation. EMG and NCV studies should confirm the diagnosis.

I also referred him to a hematologist whom I believe will soon start IViG therapy.

Physicians who treat Lyme disease you must be well versed in all of the autoimmune syndromes of the nervous system; It is clear that Lyme can be associated with any one of them.

The widely held injunction prohibiting the use of steroids is not necessarily the case with severe autoimmune disease. Plasmapheresis and IViG are not always practical. The main problem in this patient is not Lyme infection- it is autoimmune disease. A focus only on Lyme wold be a disservice to my patient. I also believe that a focus which excludes Lyme disease would also be a disservice. In my mind, it makes sense to temper steroid therapy with low doses of antibiotics. But of course this is theoretical and speculative. At least I now think we are headed in the right direction.

Wednesday, January 21, 2009

History lessons

I appreciate the comments of my readers. No, I am not suffering like Semmelweis. And I am not fighting the struggle alone.

In 1847 Viennese Physician Semmelweis was ridiculed for suggesting that attending OB physicians wash their hands between patients. He was subsequently called the "Savior of mothers," when deaths from "childbed fever" plummeted.

In 1862 Pasteur suggested the germ theory of disease. His ideas were met with ridicule for years to come.

In 1979 and 1981 Warren and Marshall discovered a bacteria in the stomach. They suggested that the bacteria (Helicobacter pylori) was pathogenic- and that it was associated with peptic ulcers amongst other things. Colleagues, who knew better, dismissed these ideas as nonsense.

Of course, all of these paradigm shattering physicians and scientists, who advanced our knowledge and medical practice in quantum leaps, are now highly revered heroes of history.

After years of rebuke, Warren and Marshall were given long overdue credit; they were awarded the Nobel Prize for Medicine in 2005.

The question is: Are the "Lyme Wars" just another iteration of the paradigm wars described by Thomas Kuhn in his famous essay "The Structure of Scientific Revolutions?" Or, is this particular process different, in some fundamental- perhaps Orwellian way? This is a debate I will not enter.

Many others have vivisected the Klempner study and other purported pillars of the IDSA view point. The notion that this single- highly flawed study should be allowed to discredit the work of hundreds of scientists and physicians is mind boggling, to say the least. As I have noted in the past, it is difficult to wed medicine and science. The practice of medicine has always given equal weight to the art and the science of medicine. Bench top, basic science research is clear. The basic scientific facts as they have been uncovered, offer unwavering support for our contentions. Clinical science is murky at best and is always open to criticism.
This blog is not science. It is a collection of fact, theory and clinical vignettes sent out into the ether of cyberspace, perhaps the equivalent of a modern day message in a bottle. I suppose my motive is similar to that of any other author who scribbles a note on a piece of paper and then sends it out adrift in the sea; perhaps by chance, It will be found, read by the right person- and make a difference.

It seems clear to me that documentaries, books and scientific assemblies offering compelling, and at times horrifying information, have thus far failed to scratch the armor coat of the other side.

I do believe that history is critical. We must never forget its lessons, as we move forward each day, with the knowledge that we are doing the best that we can.

I will veer off the subject of my blog for a moment. I am awestruck and brought to tears of joy at this incomprehensible moment in history. I could never imagined that I would live to see the prophetic vision of one of my personal heroes, Martin Luther King, become reality, as I now watch a black American take the highest office in the land, perhaps the world.

As always, the people can make a difference. The medical community will not accept the truths of Lyme disease until it is forced down their throats by a grass roots movement coming not from doctors like myself, but from ordinary people- like you.

Tuesday, January 20, 2009

Doctor, Do I have Lyme or MS

Many patients are diagnosed with multiple sclerosis because they present to a neurologist with a variety of neurological symptoms and an abnormal MRI of the brain showing white matter lesions. A diagnosis cannot be made on the basis of an abnormal MRI. The findings in Lyme disease and MS can be identical. Medical diagnoses, including MS must be based on a history and clinical examination of the patient.

Most of the "MS" patients I see have a collection of symptoms which are not typically associated with MS. For example, MS patients do not have generalized muscle and joint pains. The two groups of patients usually have different histories and different physical.

MS is a disease of the brain, central nervous system and optic nerve. Neurological disease found in other areas is not compatible with MS. Many of the symptoms of MS and Lyme are the same: Optic neuritis, motor and sensory loss, vertigo, weakness, cognitive changes and many others. The history tends to be different however. Classically, MS is associated with discrete neurological events which tend to improve over time which is/are followed by additional discrete events involving different aspects of the central nervous system. Traditionally, MS is considered a relapsing and remitting disorder. Lyme tends to be a progressive disorder associated with a bewildering array of symptoms which tend to evolve in a progressive manner over time, without the relapsing and remitting feature.

With MS the neurological abnormalities are specifically associated with disease of the central nervous system. Lyme disease, on the other hand, tends to attack a wide spectrum of the nervous system. These diffuse, seemingly unrelated lesions are bewildering to neurologists, but par for the course for physicians accustomed to treating Lyme disease.

Lyme patients frequently have cranial nerve abnormalities of the type not seen in MS.
Lyme patients have upper motor neuron disease- as seen in MS, but may also have lower motor neuron disease, as seen with nerve entrapment syndromes or less frequently ALS. Lyme patients almost invariably have findings of sensory peripheral neuropathy, as seen with diabetes, hypothyroidism, Lyme disease and others. Sometimes neurologists perform EMG/NCV electrical studies to exclude the presence of peripheral neuropathy. These tests are relatively insensitive and are only revealing when the neuropathy is profound.

Despite proclamations made on the TV show House, there is no definitive diagnostic test for MS. It is a clinical diagnosis.

MS is an autoimmune disease. The neurological manifestations of Lyme disease are also for the most part mediated by autoimmune effects. The cause of MS is felt to be unknown. There are clear geographical differences in its prevalence. Many have felt that infections may be the root cause of the autoimmune process causing MS.

Dr. David Weldon in England, building on the work of Dr. Charles Stratton at Vanderbilt, has promoted the hypothesis that MS is causally related to infection with Chlamydia pneumonia. He has reported that his experimental therapy with antimicrobial therapy has shown benefits to patients with early MS.

The patient I refer to has had a protracted disabling illness. She has suffered with a progressive illness. She has had optic neuritis, vertigo, numbness and tingling, weakness, speech difficulties and progressive cognitive effects. She also lives in a wooded, Lyme endemic area and has suffered with severe muscle and joint pain. Her pain has required the use of narcotic pain killers. She had been treated for MS for several years, without much benefit. Her physical exam was not characteristic of MS. She has multiple neurological abnormalities which do not occur in MS. Recently, lab tests for Lyme and Babesia were positive. After several months of intensive antibiotic therapy she is now showing a great deal of improvement.

When I saw her last she was quite confused: "What do I have- is it Lyme or MS- I don't know what to tell my family?"

I stammered- and gave her a convoluted answer. I was soon clear that the technical details were contributing nothing to her understanding. Finally I said: "Just tell them that you have both."

Both Lyme and MS are associated with autoreactive T cells and autoantibodies directed against the lipoprotein coat of neurons called myelin. Both are Th1 mediated processes. Both are exacerbated by inter-current infections. MS therapies, like beta interferons, have anti-viral effects. They also may down regulate MHC molecules on antigen presenting cells and inhibit pro-inflammatory cytokines and T cell proliferation. These effects should benefit neuroborrelios patients. If a neurologists prescribes such drugs for MS they should dovetail nicely with antibiotic therapy prescribed by LLMDS.

Of course, LLMDS are concerned about the routine use of high dose intravenous steroids prescribed by many neurologists for MS exacerbations when "MS" co-exists with Lyme and neuroborreliosis.

Monday, January 19, 2009

Neurosyphilis in Alabama

Syphilis, like Lyme disease can have a long, asymptomatic latency period. Frequently infected persons are unaware of the illness until horrible manifestations occur. Syphilis is a relatively rare condition in non HIV infected individuals today. It was once a common and devastating disease affecting all tiers of society. Neurosyphilis, a form of tertiary, disseminated disease could be associated with a condition called "general paresis." This is a term familiar to every third year medical student. Syphilis in the brain could lead to insanity and dementia. The famous gangster, Al Copone became demented in Alcatraz due to this ailment. Many famous and infamous figures from the pages of history have been reported to suffer with the ravages of syphilis in its various forms. Today syphilis is still treated with only one drug- penicillin. The results with stage one and stage 2 syphilis are good. Once the spirochete has infected the brain the prognosis is still grim- patients do not generally improve.

Most of our knowledge about the natural history of syphilis comes from the Tuskegee experiment. Black males, without their knowledge, were followed for untreated syphilis for 40 years, from 1932 until 1972. The study was only stopped when its gruesome details were uncovered in a news story in the Washington Star. The physicians involved in the study felt no remorse. Comparison with Dr. Mengele of Nazi fame seems quite appropriate. The study was conducted by the US PUBLIC HEALTH SERVICE- a predecessor to today's CDC. The important data was collected from autopsies of the victims. A doctor involved in the study said: "We have no further interest in these patients until they die."

There were no Nuremberg trials. The physicians claimed they were only following orders. No responsible parties were ever punished.

This heinous, despicable, racist "study" was conducted by OUR GOVERNMENT, in the name of "science". And it was bad science! There was no treated control group. We don't know how often treated syphilis patients go on to develop tertiary disease. The same of course can be said for Lyme. Some cynical Lymies believe that the experiment is happening all over again. These historical precedents justifiably create a sense of distrust of our government.

We do know that spirochetes in the brain are deadly, as is clearly known in the case of syphilis. Neuroborrelios exists. This is not disputed by IDSA types. LLMDS believe that this condition is common. Many of our patients have dramatic mental status changes, abnormal brain MRIs and abnormal SPECT scans.

How can mainstream medicine be so cavalier? How can they be so sure that their patients are not suffering with devastating spirochetal infection of the brain?
How indeed?

Saturday, January 17, 2009

Lyme dieases for dummies: Part two

Lyme disease is so named because the current epidemic was first noticed in the town of Lyme Connecticut in the mid 1970's. A group of children developed an unusual form of arthritis which resembled rheumatoid arthritis. Researchers discovered that it seemed to be a vector(tick borne) illness. It is a zoonosis because it is known to be transferred from infected animals to humans with the aid of a vector. The famous microbiologist, Willie Burdorfer examined the Ixodes ticks which were the suspected vector. He identified small spirochetes- spiral shaped bacteria. These were found to be the cause of the illness. All living organisms in the world are identified by a term which describes features shared by a particular cohort of organisms, and a second term, which designates the species. A species is consider a distinct subset of life which reproduces and maintains its own unique features. Species may mutate-change to some degree, but basic unique features do not change. This spirochete was of the genus- Borrelia. There were other well known spirochetes of this genus. This specific Borrelia was a new species. It should be noted that in biology new species are identified on a regular basis. This species was named after the scientist who discovered it. The new spirochete associated with Lyme disease was named Borrelia(genus) burdoferi(species). The nomenclature has changed over the years, but this remains the primary microbe responsible for Lyme disease. It is likely that the germ has existed for hundreds, if not thousands of years. In the past it probably only rarely caused human disease. Microbes can mutate and become more pathogenic- develop a greater potential to cause a severe disease state. Certainly this can be seen with certain strains of influenza. (Differing strains can exist within a given species- with different biological properties). The standard Influenza A is nasty but not deadly. There are mutated strains which are extremely deadly- this is why there has much concern about "bird flu."

There are perhaps many reasons why the disease spread quickly into the human environment. There has been a loss of habitat for a major host of the adult ticks, the deer. Deer have moved into closer proximity to human habitation. The ticks have rapidly proliferated. Changes in the environment, including global warming, have been considered factors. At any rate, the disease has spread rapidly over the past 30 years. Cases have now been reported in 49/50 states. The disease has also jumped the Atlantic Ocean and is rapidly spreading throughout Europe and many other areas in the world.

Early on scientist performed tests to see which antibiotics worked well against the germ. Test tube tests showed that many antibiotics were active against the germ. Rocephin, Doxycycline, Amoxicillin and others were found to be effective. Treatment recommendations were developed which were based on this early work. It was a new disease. Physicians turned to their experience with other tick borne illnesses when they made initial recommendations about the duration of treatment. For example, experience with diseases such as Rocky Mountain Spotted Fever was drawn upon. Other information about the treatment of spirochetes was drawn from the well known therapy for syphilis. My sense is that the early researchers were thinking about early, stage I syphilis when treatment guidelines were drawn up. It was certainly known that the treatment for stage 2 and stage 3 syphilis is more complex.

Initially it was thought that Lyme was primarily transmitted by the bite of the adult deer tick (Ixodes scapularis). It was thought that the tick bites could generally be observed. It was felt that the ticks needed to be attached to the
host- humans for a prolonged period of time, perhaps 48 hours or more, for the spirochetes to be transmitted. It was also believed that early Lyme infection would be evident because infected individuals would developed the tell tale rash- Erythem chronicum migrams, or just erythema migrans, frequently referred to as EM. The public knows this as the bulls eye rash. It was believed that early treatment would prevent significant complications such as arthritis. Even when these secondary complications occurred, it was still believed that short courses of antibiotics would kill the spirochetes.

Early on it became clear that testing for the illness was problematic. Initially an ELISA test was used. This is a commonly used technology which detects human antibodies to a particular microbe. The test results were surprising. Many blood samples from the control group, not infected with Lyme, also developed antibody reactions in the test. These were considered false positives. The test did not work, it picked up patients who were not Lyme infected. Because of this a second tier test of greater accuracy, the Western Blot was added. The issues surrounding the use of these tests remains the focus of heated controversy.

In 1994 the CDC developed a standard test for surveillance of Lyme cases. The test was not developed as a diagnostic assay. Unfortunately this research tool morphed into something which it was never intended to be: a diagnostic test. This too remains an area of heated controversy.

Since the 1980s and 1990s much has been learned about Lyme disease. I am of the opinion that much of this information has not filtered down to practicing physicians. I am also bewildered as to why the IDSA seems to be ignoring most of this information as well.

It is known that most infections are conferred by the nymph form of the tick, not the adult form. Deer ticks have a two year life cycle and go through three stages: larvae, nymph and adult. The nymphs are about the size of a poppy seed. They are rarely observed when they are attached to human victims. It is not really known how long the ticks need to be attached before the disease is transmitted. The nymph Ixodes ticks are frequently called stealth vectors. It is known that many persons infected with Lyme do not develop the bulls eye rash. It also known that a wide array of rashes can occur which bare little resemblance to the classic EM rash.
These factors make it clear that early detection and treatment if usually not an option.

It is well known that Lyme disease is not just a rash and joint pain illness. The spirochetes can widely disseminate throughout the body causing protean manifestations. For example, their is no dispute that it can cause brain disease and heart disease.

The heated fight over the duration of treatment and the sorts of antibiotics has been protracted. On one side it is argued that the germ is relatively easy to kill and that short courses of antibiotics are all that is needed. The proponents of this approach claim that residual symptoms are due to "Post-Lyme" syndrome. The germs have been eliminated, but an inflammatory or autoimmune response continues. This is the basis of the guidelines which have been promulgated by the Infectious Disease
Society of America.

The other group of physicians with whom I am affiliated, advocate an entirely different position. The term Post-Lyme is not used. Rather the term chronic Lyme is used. This implies that ongoing symptoms are due to persistent infection.

Scientists have demonstrated numerous mechanisms by which the Lyme organism can resist both the immune system and antibiotics. This discussion is beyond the scope of this entry, but some information can be found in other places in this blog.
Perhaps the most important reason for the persistence of Lyme in the body is that it has the ability to become intracellular, live inside our cells. Recent research with regard to Lyme and other intracellular germs like Mycoplasmas and Chlamydia pneumonia, as well as a better understanding of how the immune system responds to these infections, has established that it is impossible to completely eradicate these organisms from our bodies. I do not believe this is conjecture on my part. I believe this assertion is completely supported by current science.

Academic physicians are frequently out of touch with "bench top" science, which characterizes aspects of micro-organisms in the lab setting not in humans.

However, there is a body of clinical evidence, studies on infected humans, which demonstrate the benefits of extended antibiotic therapy, well beyond that recommended by the Infectious Disease Society.

Doctors who treat chronic Lyme patients and their patient are astounded by the lack of acceptance of the existence of chronic Lyme disease by "mainstream" medicine. It is even more astounding that medical boards have systematically attacked the treatments proffered by such physicians and in many cases suspended their licenses to practice medicine.

This is a brief overview which I hope will provide some basic information about terms and concepts frequently seen in Lyme. It also briefly touches upon the professional disputes which have termed a paradigm war or the "Lyme Wars."
This topic is worthy of further discussion.
Future entries will continue to explain Lyme issues in an easy to understand format.

Note: Many of us have forgotten high school biology. All living things are organized in orders/classes, which go from general(more shared features) to specific(more unique features). The categories are: Domain- Kingdom- Phylum- Class- Family-
Genus- Species- and subspecies or strains. Many factors are used in categorizing living things. Frequently, scientists change their minds and re-categorize various organisms. Bacteria species are particularly difficult to classify for various reasons. The Genus is Capitalized and the species is lower case.

Friday, January 16, 2009

Brain fog and memory loss: Not Lyme

Let me say at the outset: this entry is primarily defensive. But I also think it is necessary that my readers understand that I not just a "Lyme MD." Unlike a specialist,(Lyme medicine is not a speciality) I was trained as a generalist. For me that has meant that I have the ability to look at the whole person: all the various systems in the body and their inter-relations. I recently spoke with an opthomologist who jokingly said: "I only specialize on cataract surgery of the left eye." As a generalists, I view my patients through a broader, more integrative model. I think this also creates an open mind set, more adaptive to paradigm changes such as those created with new ways of thinking about Lyme disease. It is interesting to note that LLMDs from the most part come from primary care disciplines, family medicine and internal medicine. Physicians who have specialized, infectious disease and rheumatology are much less open minded. I suspect it is their DNA- so to speak.

Every symptom seen in chronic Lyme patients can also be seen in a wide array of other medical syndromes. It is when multi-system symptoms converge in a single individual that Lyme becomes the primary suspect. Brain fog and memory loss are perhaps one of the most common symptoms seen in chronic Lyme patients. One should always consider that it is not always the case that Lyme is the imitator; sometimes the table is turned- it is another illness which is masquerading as Lyme.

In what follows, I will provide a brief over view of some of the causes of brain fog and cognitve changes in patients which are not due to Lyme disease.

Cognitive deficits are frequently seen with alcohol and substance abuse. A chronic, late stage alcoholic may have a dementia called Korsakofs syndrome, associated with "confabulation." Psychiatric disorders including: depression, anxiety, bipolar disorder and attention deficit disorder may cause the same symptoms. These symptoms can be caused by sleep apnea- which is extremely common- both central and obstructive. Other sleep disorders may include restless leg syndrome and narcolepsy. Non-Lyme autoimmune causes may include: gluten sensitivity, lupus(cerebritis),vasculiltis, MS and others.

Non-Lyme neurodegenerative causes may include: early onset Alzheimer's disease, Parkinson's disease with Lewy body dementia, fronto-temporal dementia and others. Prions, mutated proteins may cause severe cognitive problems, the best known example is mad cow disease(BSE). Brain tumors- either primary or metastatic need to be considered. Neurological disease can also be the result of "paraneoplastic" syndromes. For example, a patient might have lung cancer and the cancer might provoke the development of peculiar auto-antibodies such as anti-Hu or anti-Ro, which cause inflammation of brain tissue. Other infections need to be considered. These include: syphilis, chronic fungal meningitis, viral encephalitis such as Herpes and many others, brain abscess with a variety of microbes including parasites.

Injury needs to be considered. Patients may have a slow bleed around the brain- a subdural hematoma. Patients may have a post-concussion syndrome. The injury may be psycho-physiologic as in PTSD. Low grade atypical seizures can cause these symptoms and need to be considered. Metabolic causes of change in mental status are always a concern. Patients can have fluctuations in blood sugar. My first medicine patient when I was a 3rd year medical student had an insulinoma, an unusual tumor of the pancreas which would secrete insulin at unexpected times. The low blood sugars would have significant brain/cognitive effects. This syndrome(hypoglycemia) is more likely in diabetics, especially those on insulin and certain oral medicines. Vitamin B12 deficiency is a notorious cause of mental status changes as is hypothyroidism.
Systemic infections, especially in the elderly, like pneumonia or a urinary tract infection can cause significant changes in mentation. Low oxygen levels seen in patients with chronic lung disease, congestive heart failure, blood clots to the lungs and others disorders can cause dramatic mental status change. Toxic exposure to a wide range of brain toxins can precipitate cognitive changes. Belladonna like drugs- anti-cholinergics, are a good example. Heavy metals like lead and mercury are very toxic to the central nervous system. Multiple medications from a wide range of classes as well as toxic drug interactions can cause these problems.

Many patients with changes in mental status suffer with the most common disease in America, atherosclerosis. Both clogged arteries and high blood pressure can cause tiny strokes in multiple regions of the brain ultimately leading to memory changes.
This syndrome is much more common in diabetics.

Genetic factors have been identified which are associated with various forms of dementia and neurodegenerative disorders. This of course includes Alheimer's disease.

Perhaps there is a phenomenon of mild forgetfulness associated with aging. I was taught this in medical training. Perhaps it is because I am of that certain age that I am dubious of this explanation unless all other causes have been ruled out.

There is evidence that persons with active minds, those who are engaged in work, problem solving or do puzzles, may preserve cognitive abilities.

This list is not meant to be exhaustive but illustrative. Lyme docs have been criticized as being hammers who see everything as nails-(Lyme).
Those of us who treat Lyme spent many years learning general medicine before we ever became involved in Lyme diagnosis and treatment. We have not abandoned that foundation of knowledge.

I have written this piece, like most of my others, off the top of my head, so please excuse any spelling errors.

A similar list could be constructed for every other symptoms commonly seen in Lyme patients,including: fatigue, muscle pain, joint pain, numbness and tingling, sweats- fevers and chills, headache, dizziness and many more. I would be happy to do this if there is an interest.

I am a family doctor. I see a wide range of patients in my office everyday with a multitude of medical diagnoses. I do not diagnose everyone with Lyme disease as some have suggested. However, I do believe that the Lyme pandemic/epidemic is real. I do find many patients with symptoms, signs and ancillary diagnostic tests which point in that direction.

When I was a medical intern, almost 30 years ago, at DC General Hospital, I remember something a very bright senior medical resident once said. "Every time I get an interesting, exciting case- it always turns out to be tainted by alcoholism."
I will admit, to some extent, that statement reflects my current view of Lyme disease. Nonetheless, my first priority is to practice solid, standard medicine and then put the pieces of the puzzle together to the best of my abilities.

Muscle disease/neurologist/CDC

I am always thrilled to see patients walk into my office with classic signs and symptoms of chronic Lyme disease. I am not always that lucky. More patients have been presenting with atypical syndromes. A 40ish year old man has complained of muscle pain and fatigue after limited physical activity. This has increased over the past one year. He has been a life long athlete. Every time he exercises his muscle enzymes(CPK) become very elevated. After some rest the enzyme levels return to normal. Recently, he has experienced low grade, persistent pain in his muscles without weakness. He has also experienced some fatigue and numbness and tingling.
There are well documented cases of Lyme disease causing myositis (muscle disease).
His Lyme WB shows 4 IgG bands and meets the IgeneX criteria for Lyme exposure. His excellent neurologist has done a thorough job of working him up. He has been unable to establish a diagnosis. He has referred the patient to Johns Hopkins for a muscle biopsy. He asked the neurologist if his symptoms might be due to Lyme disease. He showed the WB report to the neurologist.

The neurologist with whom I have been friends for over 20 years said "Dr (me) is a nice guy, but I don't what is wrong with him. Over the past several years he thinks that everyone has Lyme disease." The neurologist informed the patient that he has only 4 positive bands and that the CDC required 5 bands for a positive diagnosis- case closed- he does not have Lyme disease.

In 2001 the "Lyme Disease Initiative of 2001" was introduced in the House of Representatives. H.R. 1254 was passed. The stated goal was "To establish a program to provide for a reduction in the incidence and prevalence of Lyme disease." The Bill called for the creation of a LYME DISEASE TASKFORCE (sec. 4). Based on this bill a task force was created. Public Law 107-116 was passed by the senate(11/06/01) and was signed into law by president George Bush on January 10, 2002. I quote a portion of that bill:

The Committee is distressed in hearing of the widespread misuse of the current Lyme disease surveillance case definition. While the CDC does state that 'this surveillance case definition was developed for national reporting of Lyme disease: it is NOT appropriate for the clinical diagnosis,' the definition is reportedly misused as a standard of care for healthcare reimbursement, product(test) development, medical licensing hearings and other legal cases. The CDC is encouraged to aggressively pursue and correct the misuse of this definition. This includes issuing an alert to the public and physicians, as well as actively issuing letters to places misusing the definition.

Not only have these recommendations been ignored, but the misuse of the CDC test has become more ingrained in medical institutions and academic medical practice.

Neurologists may point to the new guidelines developed by the American Academy of Neurology. These guidelines are a repackaged version of the disputed IDSA guidelines. Three coauthors, including the lead author were also authors of the IDSA guidelines!

I do not know if this patients signs and symptoms are related to ongoing infection with Lyme disease- but it is a distinct possibility. Unfortunately suffering patients frequently find themselves caught in the cross fire between the two waring factions. I am afraid it is ultimately the patients who suffer in this situation. I will request that the muscle biopsy specimen have a good Lyme PCR and sensitive culture on special media. Unfortunately, such requests from me have always been ignored.

Tuesday, January 13, 2009

Night sweats: Not always Babesia (or Bartonella)

A 22 year old woman likes to camp in the wooded mountains of Pennsylvania and New York. She has had numerous tick bites. Several months ago she consulted with her primary care physician when she complained of fevers, headaches, chills, sweats and strange electrical sensations in her legs. She was diagnosed with a virus- no treatment. Some months later she was treated for a sinus infection with Augmentin. She noted that fatigue improved for a few days. Looking back, perhaps she had not been 100% well for several for a few years. She had experienced migratory joint pains, headache, stiff neck, cycles of chills and sweats, speech problems- speaking gibberish at times, palpitations, mood swings and a plethora of other cognitive problems.

A SPECT scan was normal. Labcorp: Lyme WB IgG 41 band- Ehrlichia chaffeensis IgG 1:512 (normal less than 1:64)- folic acid 11- vitamin D 29/55- reversed ratio.

Clongen: Lyme WB- IgG positive- 60,41 and 23; IgM positive 39

Fairfax Medical Laboratory: Lyme ELISA index 0.86- equivocal range. No WB was performed.

Treatment: Amoxil for 3 weeks, awaiting lab results. No significant change. Doxycyline 400mg per day started- Herx. At 6 weeks she was mostly better. Night sweats were gone. Tindamax was added. At 10 weeks- today, she is 80% better. Fatigue, sweats, joint pains, multiple cognitive and speech problems, palpitations and neck pain are all gone. The only remaining symptom- strange intermittent electrical shocks to the upper extremities- some subtle cognitive issues do persist after careful questioning.

What caused the night sweats and why are they better? Take your pick: Lyme, Babesia or Ehrlychia? I would bet on Ehrlichia. Bacteria which reside in white blood cells are difficult to eradicate. Ehrlichia has been described as a mild Rocky Mountain Spotted fever like disease.

Doxycycline is the best drug. If needed, Rifampin, the second tier drug can be added.
There are no clear(credible) guidelines on how long to treat this infection. I have seen it persist for many months. Eight weeks is not adequate for many patients. Her dramatic response is gratifying. I think it is important not to drop the ball and to continue Doxycyline for several months- it works on Lyme too.

Monday, January 12, 2009

Doctors know about the Lyme controversy- they just are not up to date

The lay public is clueless about how doctors are educated and how they stay up to date. The above statement reflects the beliefs of most patients I encounter on a daily basis. They are wrong. Dead wrong.

Doctors do turn to trusted sources when researching a disease and/or looking for topical updates. Practicing doctors are completely unaware of the raging controversy which has been going on for many years now. Major players on the two sides of the dispute are listed below. It is unlikely that a diligent physician looking for information about Lyme disease would encounter any information suggesting that the IDSA guidelines are in dispute. The current maneuvering of the IDSA is designed to ensure that the status-quo remains unperturbed.

Group number one:
Chronic Lyme is real:
ILADS: marginalized- a fringe group.
Dr Burrascano- Medical board issues- discredited.
Dr. Jones- Medical board issues- discredited.
Dr. Jemsek- license to practice in North Carolina suspended- thoroughly discredited
Dr. Horowitz- ILADS president- emphasis on CAM- ridiculed by mainstream- evidence based medicine
Dr. Stricker- discredited in various and sordid ways- none credible
Other ILADs physicians- off the radar- no academic credentials- irrelevant
Dr. Donta- Good credentials- Professor of infectious disease medicine at Boston University- No publications in highly esteemed journals like New England Journal of Medicine- marginalized- a single voice- an outlier.

Group number two:
Legitimate- dependable sources of Medical information:
There is no chronic Lyme:
Mayo Clinic
Johns Hopkins
All other prestigious medical universities ? Columbia: "Fallon is not a real doctor- he is a psychiatrist- his work doesn't count"
All major textbooks including Harrison's textbook of medicine- all current textbooks of infectious disease medicine
"Up to date"
Quack Watch
Neurologists and their professional organization
Rheumatologists- rheumatology literature and texts
The New England Journal of Medicine
99.999% of practicing infectious disease specialists in the US
Dr. Wormser
Dr. Steere
Local community specialists
US University specialists and medical school professors
Primary care physicians who defer to the above mentioned sources for judgments and recommendations

State Medical Boards and governing authorities

No, doctors are not lazy or poorly informed about new developments in the field of chronic Lyme disease and tick borne illness. They are entirely up to date.
When well informed physicians encounter the treatments of LLMDs along the way they will know one thing for sure. If it looks like a duck- Quack.

PS: Let there be no confusion about what I believe. The so called discredited physicians mentioned above, have been unfairly persecuted. They are all heroes- who have advanced the understanding and treatment of Lyme and related illness at great personal cost and to the benefit of thousands of patients afflicted with this horrific illness.

Two patients: CDC positive

Two new patients this morning.
1) 24 year old male diagnosed with Post-Lyme syndrome. He is CDC positive for Lyme. He suffers with headache, stiff neck, chest discomfort, TMJ, anxiety, depression, floaters, joint pains- knees, hands, feet, facial tics, sleep disorder, trouble concentrating, muscle pains, urinary symptoms, numbness and tingling, poor balance and disorientation. He is barely holding together. He has a history of "spider bites" and rash. His neurological exam is highly abnormal. He has already seen a dozen doctors, including the best. He has been told that there is nothing to be done. Sorry. Only the internet led him to my door.

2) The second patient is a 30 year old female. She is also CDC positive for Lyme. She has disabling symptoms. Headaches and generalized pains are unbearable, even on narcotics. She can't walk. She can't work or care for her children. She suffers with swollen glands, night sweats, weakness of the left side of her body, numbness and tingling and progressing memory loss and global cognitive dysfunction. She has had numerous spinal taps, ER visits and has seen more doctors than she can keep track of. Her neurological exam is extremely abnormal. There is severe weakness of the left side of her body- upper and lower extremities. Her diagnosis: Post-Lyme. She did receive of month of doxycycline and was beginning to feel better. After it was stopped the rug was pulled out from under her. Everything returned- with a vengeance. Diagnosis: Post-Lyme. Again: there is nothing we can do. "More antibiotics just don't work"- her neurologist.

The IDSA is stacking the new Lyme panel, per the agreement with the Connecticut Attorney General: It has excluded doctors who have any experience treating Lyme patients.

The state of New York is questioning Clongen. "Why was an ELISA not done first?" We don't accept the results- send the blood to the CDC for confirmation.

Another documentary is in the works. Another celebrity has Lyme disease.

The more things change- the more they remain the same.

Sunday, January 11, 2009

Vitamins and Supplements

I have indicated in the past that I try to approach Lyme and associated infections from a conservative "allopathic" perspective. I am skeptical of supplements. I have treated many hundreds of patients and had much success without using supplements. So when I read: "Most LLMDs follow Dr. Burrascano's recommendations," because he is the "Man," I feel compelled to respond. My comments here should not be considered an attempt to disparage Dr. Burrascano or his beliefs. Rather, I am simply putting forth an alternative point of view.

I am concerned when the section on supplements recommends that patients buy a pill organizer just for Lyme related supplements. The implication that our bodies cannot heal without a plethora of artificial supplements runs counter to my clinical instincts. I believe that the body, given a reasonably balanced diet, is normally able to extract all the micro-nutrients it requires. Let me explain the distinction between micro-nutrients and macro-nutrients. Micro-nutrients, like vitamins, are molecules our body requires in trace amounts. They are co-factors, required by enzymes, which promote critical metabolic processes in our bodies. Macro-nutrients, on the other hand, are the major fuels and building blocks that our bodies require, including carbohydrates, proteins and fats. Plant derived vitamins are also called phytochemicals. It has been found that vitamins do not act alone. Our bodies have evolved so that a symphony of phytochemicals act in concert, to promote the metabolic processes required in our bodies. Several well documented studies with individual vitamins, such as vitamin C, vitamin E and beta-carotene have shown unexpected negative results, rather than beneficial ones. For example, for decades cardiologists promoted vitamin E as an anti-oxidant which was expected to block the deposit of oxidized cholesterol in arteries. When the study was done, no benefits were seen. Cardiologists no longer recommend this supplement. Two theories have been proposed for these findings: 1)Isolated vitamins, ingested outside the panoply of associated phytochemicals, are ineffective or harmful and 2) artificial vitamins do not act in the same way as natural, food derived vitamins.

Dr. Burrascano introduces the section on recommended vitamins and supplements by indicating that the benefits of some of the vitamins/supplements has been verified by controlled evidence based studies. What studies- which vitamins? If such data exists, its basis should be put forth, allowing readers the opportunity to make their own critical appraisals. The author's conclusions cannot be accepted blindly, especially when the issues are controversial, not to mention potentially very expensive. (I have not foot noted my references- but I am not making firm recommendations- I am only sharing my opinions). The reader should keep in mind that it is not necessary to prove a negative assertion, only a positive one.

Dr. Burrascano puts his reputation on a limb when the supplements are not suggested but rather "required."

Probiotics: Most physicians treating Lyme disease with long term antibiotics would strongly recommend these supplements. Many of us would not recommend specific brands. Many practicing physicians, including myself, would recommend that a brand of Sacchromyces be included, since this yeast based probiotic is not killed by the antibiotics.

Multivitamin: There is no evidence that this is helpful. I do not recommend it, neither do I discourage it.

Co-enzyme Q10: I do not routinely recommend this. It has been shown to be helpful for patients with disease of the heart muscle. It does help the mitochondria increase energy output in some cases. If there is a human study regarding this supplement and its benefits in cardiac Lyme, as suggested, then this information should be brought out. Q10 has been shown to be useful for diseased heart muscle from other medical illnesses. This does not prove that it is beneficial when the heart muscle is not diseased. For example, vitamin C is an essential supplement if someone has a deficiency disease called scurvy. This does not prove that a person without scurvy will accrue any benefits from taking extra vitamin C. Some patients feel that Q10 gives them extra energy. I do not discourage patients from experimenting with this on a case by case basis. It is not required.
My research shows that there is no basis for restricting the supplement while taking Mepron or Malarone.

Alpha Lippoic acid: I don't recommend. What evidence?

B vitamins: I only recommend if there is evidence of deficiency. Again, what are the clinical studies referred to.

Magnesium: It is documented to help with muscle cramps. It is depleted by diuretics.
In general I dot recommend it. There is no evidence to support its use.

Essential fatty acids: I recommend a diet high in fish, whole grains, nuts and seeds. If a proper diet cannot be followed there may be a scientific basis for these supplements. I do not consider their use routine or mandatory.

NT factor, Carnitine, SAM-e: No evidence- not recommended. SAM-e may help with depression. In Lyme patients depression may be modulated by poor frontal lobe function (SPECT scans), sensitivity to glutamine, fatigue and other specific neuro-chemical dysfunctions. Specific drugs may be recommended based on these known or suspected abnormalities.

Green tea? What is the evidence? The "hot topic" is coffee. It is reported to have beneficial effects in the brain and liver. There is some scientific evidence to promote these claims. This issue is of interest. It is not recommended or required.

Cordy Max and other herbal therapies: I confess complete ignorance- but I have helped patients without such things. Herbalists are specialists who have spent many years perfecting their art. I don't think that allopathic doctors should not casually recommend such things based on the unsupported recommendations of one practitioner. Patients who wish to pursue such alternative options should consult with a practitioner fully conversant with this discipline.

Glucosamine: Yes. It has been shown to work as an anti-inflammatory and reduce joint pain. In my experience, pharmaceutical anti-inflammatory medicines like Celebrex are much more effective. Other natural anti-inflammatories, such as Limbrel and Wobenzym may also have benefits. These supplements are only helpful for controlling symptoms.

Vitamin C: No. No evidence that it helps. It has been suggested by some (Donta) that it might interfere with Plaquenil, if this drug is being used.

Creatine: This is another mitochondria energy component. It may be helpful if weakness or muscle dysfunction is present. The comment about its benefits in ALS patients is evidence based. There is no evidence to support its routine use.

Milk thistle: I don't recommend. It has been thought by some to have beneficial effects in the liver. Coffee may work better.

Methyl B12: Very expensive. If vitamin B12 deficiency is present there are much more cost effective supplements. I do not use or recommend. Where is the evidence?

Vitamin D: Very controversial. I do not recommend it. Most Lyme patients, in my experience, have high levels of vitamin D dihydroxy 1,25, the active form. Vitamin D is not actually a vitamin, it is a hormone. It has active immunological effects. The issue is very complex and has been discussed elsewhere in this blog. My thoughts about it are in a state of flux. I plan on re-visiting this topic in the near future.

Let me re-iterate. I am not making this post to discredit, or belittle the recommendations of this well known pioneer in the field of Lyme medicine. I am raising questions and sharing my experiences and beliefs. I do feel that patients should be well informed about treatment options and make decisions based on knowledge rather than ignorance. Doctors are not "God." They do their best to make recommendations based on their evaluation of an unbelievably complex soup of information. I am concerned about many patients I have seen, who have left the offices of other physicians, having spent a fortune on a shopping bag full of supplements, without experiencing any clinical improvements. They have also not received the benefits of treatments which are steeped in the available scientific evidence and theory regarding this complex and frequently baffling syndrome of infection and illness.

Friday, January 9, 2009

Flagyl: On the fence

Why do you need Flagyl or Tindamax? The conventional wisdom is that treatment needs to address all three forms of the bacteria. After all, the spirochete morphs into L-forms and cyst forms; if these different morphologies are not targeted the disease cannot be "cured." Otherwise, the bacteria cannot be eradicated. The cysts after all, become be a reservoir of disease waiting for the right conditions, to become active spirochetes. The science, the bacteriology, the immunology tells us something different. The body cannot be sterilized of Lyme or Bb bacteria. The intracellular niche is too protected. The immune response to intracellular bacteria is not far reaching enough. Despite clinical remission, Bb will forever persist within our cells and tissues. Many patients who are in a clinically remission relapse significantly when "cyts busting" drugs are added. The immune system becomes activated; inflammatory cytokines are produced and the symptoms return. The patient "Herxes" all over again. Frequently cognitive dysfunction worsens, joint pain and fatigue return as well as other symptoms. And to what end?

Yes- Cystic and granular forms of Bb have been demonstrated in the brain. In some cases the addition of Flagyl can lead to cognitive improvement. I don't think this is usually the case. Many cyst and granular forms have found under biofilms. My suspicion is that biofilms are not a cause for alarm. At any rate, there is no way to reach or kill such germs. By far, the biggest source of foreign bacteria is found in our oral cavities. These bacteria contained within biofilms generally cause us no adverse health consequences. It is only when the biolfims become broken down by active infection that these previously walled of colonies of bacteria become problematic. Sometimes- anti-cyst therapy seems to improve mental clarity. If cognitive issues persist, then the drugs can be tried. The mechanism by which this occurs in unclear to me. For the most part treating Bb cysts may be a lot like swatting a stick at an otherwise quiet hornet's nest.

The goal of successful Lyme therapy is to eliminate symptoms and restore health.

These would be parasites(Lyme Bb) have the nasty habit of stimulating our immune responses in ways which are deleterious. The infection- but perhaps to a greater extent, our immune responses makes us sick. If we lower the spirochete load, minimize the ability of the germs to replicate and reduce or eliminate the harmful immune responses, then hopefully a clinical remission can be established.

In order to achieve this balance it may be necessary to keep most patients on persistent low dose antibiotic therapy. This maintains a perpetually hostile environment for cystic forms. No- Minocin for example won't kill the cysts, but if any cysts convert into spirochetes, antimicrobial will be on board and nip the conversion in the bud. Disease reactivation will not occur.

Thursday, January 8, 2009

C6 peptide

I have noticed a change in C6 antibody results. They are generally much lower than they were a year ago. The test measures an ELISA reaction to ViSE, a surface protein unique to Bb. The ability of the Lyme bacteria to alter this surface antigen has been well described. It is not surprising that reactivity would be variable. I would expect this to occur in individual patients; instead the change in reactivity covers a wide swath of patients, many of whom have not been treated. On the other hand, a subset of patients who have been treated extensively with antibiotics "seroconvert" with regard to this parameter. I have noted that the test measures an IgG antibody to a synthetic version of this antigen. Perhaps the test is failing because it fails to measure IgM responses which are more prominent in Lyme patients. Typically, in the past Western Blot positive Lyme patients had C6 peptide index levels, on average of 0.2 to 0.4. Recently I have seen WB positve patients with C6 indices approaching zero.

Tuesday, January 6, 2009

Pneumonia, leg swelling and one sided paralysis

Two years ago a 32 year old female was admitted to the hospital for atypical pneumonia- pulmonary infiltrates and a high fever. Her illness was preceded by a rash on her legs, fever, cough and severe diffuse joint pains. In the hospital she was treated with two weeks of IV Rocephin and Zithromax, to "cover" her for various causes of pneumonia. When I saw her in the office for a follow up visit I noted a significant circular red rash on both lower limbs. Labs at that time showed an elevated CRP of 12, a borderline ANA antibody and a single 41 IgG WB Lyme band out of the standard 13 bands. I continued oral antibiotics. The rash improved within a couple of weeks. She complained only of fatigue and nausea. The physicians who saw her initially could not explain her findings. It was suggested that she had an autoimmune disease. The rash was biopsied. The findings were: non-specific lymphocytic dermatitis. She continued antibiotics for several months and generally did well. Additional symptoms included: persistent fatigue, strange visual changes and bouts of numbness and tingling. She developed right upper quadrant abdominal pain, suggesting gall bladder disease; this improved without intervention. After 6 months of antibiotics, she stopped them without consulting with me. I saw her about 2 months later. She had been hospitalized again. She had experienced acute weakness of her extremities and a loss of sensation in both legs. She also experienced transient double vision. The neurologists who evaluated her listed various differential causes: MS, stroke, Guillain-Barre syndrome and vasculitis. Her work up was negative. She was sent home without a diagnosis. In the medical history provided by the neurologist,"Lyme disease" was mentioned parenthetically. The verbiage in the consultation notes essentially mocked the diagnosis, treatment and physician.

Repeat lab testing showed that a C6 peptide antibody test sero-converted from 0.29 to 1.2. This information was not considered relevant.

The patient improved and her symptoms were stable when she came to see me after this adventure in the local hospital.

I explained to the patient that I felt her symptoms and findings were consistent with chronic Lyme infection. My exam revealed numerous neurological abnormalities- not noted by the neurologists. I don't think she fully believed me. She works in a doctor's office and was hearing many conflicting points of view. Despite this, she continued antibiotics for an additional 4 months.

Two months after stopping antibiotics (again!) she came into my office. She had marked numbness and weakness of the left side, upper and lower extremity. She had nearly absent pinprick and vibratory sensations of both legs. This time she was really sick. Her presentation was typical of MS or an acute stroke. I thought it was all Lyme related. She decided to follow my recommendations. An MRI of brain and spine were normal. She was immediately started on IV Rocephin along with a short course of IV steroids.

She experienced a brief episode of confusion. Within 4 days the weakness was improving. Withing a month she was 80% better. Within 8 weeks she was almost normal.

She has stayed on antibiotics and done well since this episode. She continues to have only minor symptoms. Her markers of inflammation have improved. Her CRP is less than one. Her ANA is negative. She continues to have abnormal physical findings which are slowly improving. Needless to say, she is no longer anxious to stop antibiotics. I think she agrees with my approach and has become a reader of this blog.

She came to me by accident. I was/am her primary care physician. I can imagine how things might have turned out if she had been treated by standard paradigms. Her primary care physician would have said: "I don't know what it is." A rheumatologist would have diagnosed a non-specific autoimmune disorder and treated her with immune modulating therapy. A neurologist would have diagnosed an atypical form of MS and suggested other therapy. She might be disabled with paralysis on one side of her body. She would likely suffer with profound cognitive deficits and diffuse pains.
Perhaps fibromyalgia would be added to the list of symptoms. It seems unlikely that she would be working full time and taking care of her young child. But she is.

These other physicians who encountered my patient on this journey are unaware of her story. She was a consult, an undiagnosed case- lost to follow up. They are busy- seeing new patients and are not looking back.


Patients suffering with "chronic fatigue syndrome," evidence of immune dysfunction- alterations in CD8/CD4 cells and elevated antibodies to a variety of viruses have shown marked improvement in symptoms after taking the anti-viral drug, Valcyte. Valcyte is only FDA approved for CMV retinitis seen in HIV patients; but it is active against other viruses as well. The recommended course of therapy is six months. The best evidence comes from a pilot study from Stanford University. The symptoms of fatigue and cognitive dysfunction closely parallel those seen in my "chronic Lyme" patients. Specifically, patients with evidence of EBV and HHV6/7 have been studied. Other reports include CMV virus, another potential cause of chronic fatigue, in the subset of responders.

Lyme patients have immune dysregulation. High titers of antibodies directed at these viruses are routinely seen. My working hypothesis has been that Lyme- the gatekeeper germ suppresses the immune system which allows these chronic, generally contained, viruses to flourish. Perhaps a sort of vicious cycle betters describes the process. As the viruses replicate, a increasing burden to the immune system makes elimination of Lyme and other opportunistic pathogens more difficult. The various germs in a sense, conspire to weaken one's defenses to all the problematic germs. Lyme treatment failures may occur because the immune defenses never heal adequately to a level which allows control of Lyme. The same arguments have been marshaled regarding other typical, Lyme associated, co-infections.

This drug is toxic to the bone marrow and requires close supervision. The study at Standford is now providing an evidence based justification for trying this drug.
Of course it is used widely in California where medical boards are prohibited from censuring physicians who treat diseases based on alternate hypotheses. Not here.

The early evidence is favorable.

The paradigm, as always, is in a constant state of flux.


What do these letters and numbers mean? The study of immunology is complex and confusing. I will try to simplify this, but it still may be hard to follow. Don't worry- most doctors don't get it either. Lymphocytes are the major white blood cells involved in the body's immune responses to infection- and other conditions, including cancer. They have been subdivided based on receptors located on their surface. The "expression" of these receptors is the basis for categorizing the various types of lymphocytes. The various types of lymphocytes have been shown to have specific functions. Lymphocytes express multiple receptors. The CD8 cells are generally referred to as killer T cells, not to be confused with natural killer T cells. The CD4 cells are referred to as helper T cells.

The initial response, the innate response, is directed by lymphocytes. The natural killer T cells, defined by receptors found on their surface, constitute a very tiny percentage of the T cell population. Nonetheless, they have an important role in fighting infection. Laboratory scientists have developed specialized technology which allows for the separation of these various subsets of lymphocytes.(Flow cytometry).

Most natural killer T cells (NKT cells) are associated with a surface receptor referred to as CD56. The CD57 marker is associated with a smaller subset of NKT cells. Interestingly, these surface receptors (CD57) have been found on both CD8 cells and CD4 cells. Normally, one would expect these markers to be found on CD8 cells- the population of killer T cells.

A powerful CD57 response is associated with Lyme infection and with other bacteria as well. Other spirochetes do not invoke this response because the structure of their cell wall is different. The unique thing about Lyme (Bb) is that it has lipo-polysacharides on its cell wall. This is antigenic(antibody producing) material, which is devoid of protein. CD57 cells respond to this type of antigen whereas other NKT cells do not.

The initial immune reaction- the innate response, involves the mobilization of CD57 cells and other T cells as well as cytokines and other chemicals. Normally, a secondary acquired immune response should follow the innate response. This is mediated by B cells aided by helper T cells. Ultimately, the acquired immune response fails. Lyme (Bb) is driven inside the cells as L-forms. B cell responses do not work here. It then falls on T cell responses to become the body's major immune response needed to keep Lyme and other intracellular germs at bay.

CD57 responses involve the same pro-inflammatory cytokines as seen in Th1 helper T cell responses.

If CD57 responses are low, it may mean that these cells are being consumed by the immune system in the fight against Lyme. If they are high, it may mean that the body is busy cranking out the T cells to assist in the fight against Lyme.

There is little published regarding the clinical usefulness of this test. Dr. Stricker has reported that this measurement "May" be helpful in assessing the degree of illness seen in chronic Lyme patients.

So I have been ordering this test for years. Thousands. Unfortunately, I am left with the conclusion that it has been of very little help to my patients. I have seen no correlation between CD57 and disease activity. Patients in clinical remission may have very low levels and patients with end stage tertiary Lyme disease may have very high levels. Individual immune responses are difficult to predict. Dr. Burrascano has suggested that the CD57 test might be an inexpensive way to screen for Lyme disease. I do not agree. Physicians may order CD57 levels because they are looking for evidence to support the diagnosis. I do not think this approach will not hold up to careful scrutiny. Many patients unfortunately are getting the awful 13 band test performed at "mill labs." Patients don't want to spend the money to get a decent Lyme test. I do throw out a wide net looking for a variety of markers associated with Lyme disease. I could argue that the vitamin D reversal pattern, a possible marker of the Th1 response, is a much better screen for patients with Lyme disease and other chronic intracellular infections.

I have seen recent published statements claiming that it is not known how CD57 and Lyme are associated. My research shows otherwise. (If you could follow any of what I said about it). However, in my opinion and experience, this marker has not been clinically useful.

Friday, January 2, 2009

What I believe: 2009- A brief overview

We are no closer to any acceptance by the medical community of the existence of chronic Lyme disease. Patients and their physicians alike are dismissed.

Lyme is difficult to treat. IV antibiotics are frequently required. In my experience, the disease is frequently under-treated. Excessive concerns about severe Herxheimer reactions are frequently associated with inadequate therapy.

The goal of therapy is clinical remission. The persistence of the organism in cells makes it virtually impossible to eradicate. Despite this, some patients may experience a sustained remission off antibiotics. Other patients may have a remission maintained with low doses of antibiotics.

We still know very little about the disease. I would be concerned about claims that a physician is a "Lyme expert." No such experts exist at this time. The term LLMD has no specific meaning.

Patients frequently harbor a parasite that may or may not be a species of Babesia. The existence of this parasite may be impossible to prove based on current diagnostic standards. Treatment of this entity is critical for recovery of many- not all patients.

Ehrlichia is a fairly common co-infection. It resides in white blood cells. It too can be somewhat difficult to treat, but it usually responds to antibiotics well.

Bartonella appears to be a rare coinfection based on objective measurements. The optimal treatment for this bacteria is a matter of debate.

Bartonella like organism- "BLO" does not exist.(My opinion)

There are major, yet unidentified, co-infections- at least one of which is very difficult to treat. This is the small, highly motile, gram negative bacteria seen in the blood of most Lyme patients. This bacteria is highly resistant to most antibiotics. At this time it is not clear how to treat it. An unidentified small protozoan has also been seen in the blood of Lyme patients. This too is unidentified, but may account for some the clinical responses seen with Flagyl and anti-malaria drugs.

Rickettsia species may be frequently transmitted as a co-infection, but are probably eliminated with anti-Lyme therapy. Atypical Rickettsia have been identified in 20% of Ixodes ticks.

Mycoplasma species and Chlamydia pneumonia are frequently present in Lyme patients. They are intracellular and are also difficult to eliminate. Their role in the pathogenesis of the syndrome is not well known.

Standard allopathic treatments are very effective. I believe the role of CAM in managing this disease has been over emphasized in most quarters.

Therapy must be individualized. It remains difficult to predict how individual patients will respond to any given regimen.

Chronic Lyme disease is associated with objective measurements and findings.

The role of vitamin D remains unanswered. For now, I see it as a marker which relates to an immunological response to infection.

CD57 counts appear to be of little clinical benefit.

Many, if not most of the symptoms associated with chronic Lyme disease, reflect the bodies immunological reactions to infection, rather than infection per say. Auto-immune responses play a large role in the pathogenesis of the disease syndrome.

Proven antibiotics (classes) include: beta-lactams. macrolides, quinolones, rifampin, Flagyl/Tindamax, anti-malarials- Plaquenil, Malarone, Mepron, clindamycin- related to macrolides, tetracycalines and artemesin. I see no significant role for sulfa drugs like Bactrim.

Complementary medicines which appear helpful include: Bile binders- Welchol and Questran. I remain unconvinced about any others. I am cautious about recommending things which have no proven clinical benefits.

Information about Lyme and tick borne illness remains very confusing and contradictory. Lyme patients need to become well informed about their illness so that they can partner with their physician. Patients must also be informed so that can decide whether or not a physician's approach makes sense to them.

Patients and doctors should not be wed to a particular paradigm. If a therapy isn't working then something else should be tried.

I do not believe it is ethical for physicians to sell supplements and books to patients from there office. It may be legal, but I see it as a conflict of interest.

The vast majority, yes 90% or more of patients, experience significant improvement when the correct therapy has been established. There remains a small minority of patients who are resistant to treatment. Even these patients generally improve to a variable extent, if the physician is both creative and persistent.

Multi-specialty Lyme clinics must be developed in the coming years.