Lyme disease tests: New and Old

Diagnostic testing

Testing may be difficult when the standard diagnostic test fails. The gold standard, the identification of the organism by DNA or culture is frequently not feasible or available. Several antibody tests have been developed which may be helpful, but these tests have a low sensitivity, missing many cases. As an adjunct, a newer technology involves lymphocyte stimulation.  When cells (T lymphocytes) are exposed to proteins derived from the pathogen, cell mediated responses such as the release of gamma interferon can be measured indicating prior exposure to the pathogen. This test may have limitations and likely should only be used adjunctively.

Of course, we are talking about diagnostic procedures for Mycobacterium (tuberculosis).

Let’s talk about Lyme.

Testing for Lyme remains problematic.  Tests have been inaccurate, unreliable and at times and prohibitively expensive. 

We depend on clinical diagnosis. But sometimes we are not sure.

All currently available tests have pros and cons.

A lot of labs are suddenly getting into the Lyme testing business.  Many tests are in development.

The Western Blot remains the first line test.  It is important that a Western Blot be ordered, not just an ELISA with reflex to Western Blot. The ELISA is not dependable. An alternative ELISA, the C6 peptide may be ordered. Usually negative, sometimes it is positive when other tests are not.   A C6 from LabCorp/Quest is not adequate, a numerical value, available from various reference laboratories is needed. (MDL, IgeneX, many others).  In my experience, values under the lab recommended positive cutoff may indicate exposure to Lyme.

PCR (polymerase chain reaction) is a test which measures the presence of specific DNA.  Most consider this the gold standard.  DNA testing for Lyme also has a low sensitivity and misses most cases. The only specimen available to test is usually blood. Lyme is a tissue pathogen and may be present in the blood in very small numbers. This is different from viral illnesses such as HIV and Hepatitis C where large numbers of viral particles are present in the blood.  Many clinical labs are working on ways to improve the sensitivity of the test.  Urine may be a better place to look.  Lyme lives in the bladder and is shed in urine. One such test is offered by Quest. So far I have not found any positives. Other clinical labs may have better results.

This is not to be confused with the antigen capture test or the nanotechnology test, which also looks at urine samples.

The Nanotrap captures tiny amounts of proteins found on the surface of the Lyme bacteria. The test so far only measures outer surface protein A, or OspA.  This protein corresponds with the 31 band of the Western Blot.  Remember, Lyme is a clever “shape shifter.” This protein is expressed when the spirochete is attached to the gut of the tick. After infection, this protein disappears (downregulated) and Osp C (upregulated) takes its place. So, the current test is really only helpful for acute Lyme and -- maybe late-stage Lyme. After many months of infection, this protein (OspA) may reappear. The test as it sits is not clinically useful for most patients.

The scientists at the Center for Applied Proteonomics and Molecular Medicine, George Mason University, new to the field, were shocked that the so-called experts in the field insisted that chronic Lyme is not real.  To get "proof of concept" and the blessing of the IDSA, ILADS and the CDC, the new test was designed to detect only acute Lyme. The CDC admits that current testing (two tier test) for acute Lyme is flawed, and THERE IS AN X-PRIZE award for the first lab to develop an accurate acute Lyme test!  

Now there is general proof of concept. An improved test, said to come out soon, will look for many proteins, including OspC.   The improved test may be extremely helpful for the diagnosis of all stages of Lyme disease.  

A culture test from ALS is available. After being slammed by the CDC, the lab is actively engaged in studies to achieve FDA clearance.  The blood culture test has two drawbacks: cost and the patient must be off antibiotics for 2 months before the test is performed. Otherwise, it may be a very good test. At first I was concerned that the test found Borrelia species rather than B. burgdorferi. This may be an advantage rather than a disadvantage because Lyme disease is a borreliosis comprised of an expanding menu of species and strains.

Another test, Lymphocyte transformation test, is available from Pharmasan and others. This test measures a different kind of immune response.  It is based on FDA approved, commercially available TB tests.  The test measures the innate immune response. An initial response which predates acquired immune responses which lead to antibody production. Immune cells patrolling our blood and tissues have the ability to recognize patterns which shouldn't be there (Pattern Recognition Receptors). Killer T cell lymphocytes are the first line of defense. Killer T cells attack offending antigen (Lyme) and turn on other immune responses including the production of cytokines, modulators of immune regulation.  When this reaction occurs it leaves behind permanent T memory cells. These memory cells, when exposed to Lyme antigens react by releasing gamma interferon, a potent cytokine.  This reaction can be measured.  This test may be considered a complement to other tests, such as the Western Blot test. It is somewhat costly.

From a cost perspective, in my experience, it is best to start with a Western Blot (MDL) which provides images and alternative diagnostic criteria.

A fair question might be: since the Western Blot only shows exposure to Lyme, not the presence of actual infection, shouldn’t a test that directly measures Lyme infection be done, to prove that Lyme is there?

Here is my answer:  Since Lyme persists in mice, dogs and monkeys and test tubes and the test subject has symptoms compatible with Lyme disease, it is reasonable to conclude active infection is present. Further testing is not needed.  Additional tests may have false negative results only adding a layer of unneeded confusion. The goal of therapy is remission of symptoms, not eradication of organisms.

At the end of the day, in many cases, the diagnosis of Lyme disease is clinical and the role of lab testing adjunctive only.

Lyme - ALS and the practice of medicine

This 54-year-old female is happy. Rightfully so.  She has been pulled from the grave.

5 months ago she was handed a death sentence, ALS (Lou Gehrig’s disease), the worst kind at that.  She found she suddenly had trouble speaking, becoming hoarse then losing the ability to talk. Shortly thereafter she found it hard to swallow. She lost weight. She developed weakness of the right upper and left lower extremities. She went to a neurology clinic at a famous tertiary care center.  She was diagnosed with bulbar ALS, a most severe and deadly form. The expectation was that she would need a feeding tube followed by ventilator. The doctors at the clinic continued to follow her downhill course over a three-month period. An EMG test showed the expected motor neuron denervation.  The patient reported an ultrasound exam of superficial nerves showed nerve swelling rather than atrophy as expected.   Scratching collective heads, the neurology team decided to do a lumbar puncture. Lyme was considered. The endorsed DNA/PCR test was negative.  One of her doctors ordered a non-sanctioned test:  Lyme Western Blot antibodies in the CSF. The result was positive. A blood test for Lyme (ELISA first) was negative.  Nonetheless, she was referred to an ID doctor who was sufficiently impressed to prescribed IV Rocephin. After 2 weeks routine monitoring showed an elevation of the kidney function tests, BUN and creatinine and antibiotics were discontinued, despite the fact that she had already responded favorably to the 2-week course of treatment.  She told me her neurologists, expecting rapid deterioration, were recently surprised to see her walk into their office under her own power.
This was the point at which I met her.

When I first met her (6 weeks ago) she could barely eke out a few unintelligible vocalizations.    She coughed constantly (due to aspiration secondary to inability to swallow I suspected).  She had other limb weakness and joint pain and swelling.

She had lost 15 pounds and was clinically dehydrated, not in renal failure. Patients with neurological dysphagia (impaired swallowing) have trouble swallowing “thin” water.  Per my recommendation, with the addition of thickener to fluids, she was able to hydrate well and the kidney tests normalized.

After 6 weeks of IV antibiotics, our second visit, she spoke with me with a very hoarse, gravelly but also very intelligible voice. She was no longer coughing. She was getting stronger and becoming more active day by day.

During examinations she evinced typical neurological signs associated with ALS, including:  hyperreflexia, weakness and abnormal reflexes (Hoffman and Babinsky).

Her illness also encompassed my other typical Lyme features:   Brain fog, joint pain, night sweats and air hunger.  These symptoms were in various stages of getting better.

Lab results: Positive Lyme Western Blot IgG, 8/10 bands MDL, Giemsa blood smear positive for parasites (presumptive Babesia).

More of the story unraveled.  She lives in the country near Frederick Maryland.  She loves to garden.  She also is an avid camper in Southern Maryland.  She recalls finding a red patch on her right forearm 2 years which went away with the application of cortisone, given the diagnosis eczema.

She went back to the original neurology clinic and was told that she should only get 28 days of Rocephin based on CDC guidelines.  She also patient sought the opinion of another University based neurologist who said keep treating for Lyme.

Motor neuron disease or ALS is a known, albeit extremely rare manifestation of neurological Lyme disease.

Of course there are no guidelines for the management of Lyme induced ALS.  I suspect the tertiary care specialists (recommending antibiotics be stopped) were extrapolating from obsolete IDSA guidelines, predicated on the belief that Borrelia spirochetes do not persist after antibiotic therapy, a thesis that has been thoroughly discredited and longer the dogma of mainstream thinking.

This must stop.  Lives are at stake.

Health care professionals need to know what Lyme is and what the practice of medicine is.

Lyme is a new and emerging disease, an epidemic of epic proportion with the potential to kill and maim.  The clinical manifestations of the disease are protean.  The extent and severity of the disease has not been recognized by the medical profession and public health officials.  Progress towards a better understanding of the illness has been mired in war of ideas (driven by egos of certain individuals in the academic medical community). Very little research has been done and we sadly know very little about this new disease which reared its ugly head 40 years ago. In a general sense we do not know the optimal therapies for the management of the illness. We know even less about specific variations of therapy which may be optimally effective for the widely divergent clinical presentations of illness.

The practice of medicine is the application of the current iteration of the healing arts as they have evolved over hundreds of years. Today's doctors are better informed (much more is known) than their forbearers of years gone by. By the same token, doctors must be cognizant of the certainty that their future replacements will see them in the same light. The practice of medicine is based on a complex synthesis of science, fact, experience, educated guesses, empiricism, judgement and perhaps philosophy, prescribed by a thoughtful (hopefully intelligent) physician who is committed to his  creed and solemn responsibility. My dad (a surgeon) always said medicine is a calling, not a job. A bit preachy, but true.

Lyme patients frequently suffer a slow, smoldering sort of death with a quality of life comparable to that of terminal cancer patients.

Contemporary notions of medicine, created by institutions and corporations demand tangible metrics by which physicians be judged.  This may or may not work.  Currently the wrong metric is being applied, i.e. following guidelines.  This is bean counting.  What is important? the patients - of course. This may not be obvious to the institutions that oversee medicine.  The primary metric that should be followed is patient outcomes. This is the only useful measure, when the disease, as is the case with Lyme, is complex and poorly understood.

The "system" should learn from doctors who make their patients better, not condemn them, as is frequently the case.

Lyme antibiotics revisited

There are a surprising number of drugs, many of which are not antibiotics, which have anti-lyme/anti-persister effects. An additional 113 agents are presented by Zhang in the latest article published in “antibiotics” September, 2015. Some of these drugs are in common use, amongst Lyme patients – but to treat something else. The list includes antibiotics, antivirals, antifungals, anthelminthics and antiparasitics. Other, unexpected agents are in the list include an arcane antidepressant. Of course daptomycin heads the list. Drugs already in common use include: artemisinin (very effective), Diflucan-fluconazole (very effective) and rifamycin related agents. The latter two from this list are referred to as active hits. Other less active hits include some quinolones (not in clinical use) and a limited list of cell wall agents, available, but also not generally used. Rifampin (rifamycin) is of greater interest to me. My grasp of this drug has evolved. ALS (Advanced Laboratory Services) adds rifampin to culture medium to cultivate Borrelia. This might lead one to conclude that rifampin does not kill Lyme. Studies show that Rifampin kills persister forms of Lyme, not spirochetes: makes sense. Lyme is rarely found in blood. The few free swimmers are referred to as planktonic. These are motile spirochete forms. Spirochete forms are not killed by Rifampin and therefore can be cultured in a medium containing rifampin.  The antipersister properties of rifampin are well known for the treatment of tuberculosis which requires the use of 4 antibiotics over a period of many months.

A new study published in “Nature” Lehar et al, discuses a novel approach for the treatment of Staph aureus. The study states that Staph bacteria hide inside cells, a protected milieu. (Mouse model). Staph aureus survive within phagocytic macrophages (the cells which “eat” and eliminate offending pathogens). The S. aureus were found to spread via a Trojan horse mechanism, a mechanism also employed by Lyme. The most potent anti-Staph aureus, MRSA antibiotics, vancomycin and daptomycin were unable to eradicate intracellular MRSA staph. In the mouse, intracellular infection allowed widespread invasion into many organs, including the brain. Not good.

These researchers took a fresh approach to killing S. aureus. The idea was to clone antibodies against S. aueus, find the best antibody and link it to an antibiotic creating a new molecule, an “antibody-antibiotic conjugate.

The antibiotic chosen for the project was neither vancomycin nor daptomycin. The drug was from the rifamycin class of antibiotics. Compared with vancomycin and daptomycin the minimal inhibitory concentration of the rifampin-like drug, intracellular and extracellular, was infinitely (slight exaggeration) better than the other two drugs. The second best drug studied was a forth agent, linezolid by the way. The rifamycin class of antibiotics were praised for: high potency, unaltered bactericidal activity in low phagosomal pH and an ability to withstand intracellular insults.

This new “AAC” compound was more effective than all other agents and able to clear the S. aureus in the mouse, including organisms hiding inside the intracellular niche. This new class of drug will not be available for human use, if it pans out, for a good 10 years or more.

I will not say exactly how I treat patients (which varies quite a bit), but...

The news about rifampin and related drugs is good. Perhaps with antibodies already present in our system we can hope for a similar result. The new compound is made of a rifampin-liked drug linked to a specific antibody.  

I have long thought that rifampin was essential for treating Bartonella. Maybe this is wrong. Maybe the extra Herx that occurs with the addition of Rifampin because is due to killing a variety of pathogens living within cells, perhaps including Lyme and Staph for all we know.

The paradigm of treating Lyme is expanding and becoming more complex. An understanding of the pharmacology of individual drugs, synergistic properties, tissue penetration and many other factors must be understood by an experienced clinician in the formulation of effective drug cocktails. Individual responses to drugs are quite variable. There is not a one size fits all approach that is consistently effective.

Lyme in a test tube and ILADS' Guidelines validation

Recent test tube studies demonstrate that Lyme is hard to kill. A lab in Johns Hopkins found that over 1500 different antibiotics could not kill Lyme. Viable persisters were found in each case. (1500 different drugs). These persisters were comprised of round body, pleomorphic forms and biofilm-like colonies, as previously described by Sapi.  The study informs us that Lyme does not persist because of antibiotic resistance as it is generally known. For example, bacteria can produce penicillinase, an enzyme witch inactivates the drug. Other bacteria develop pumps wish recognize the antibiotics as toxic and expel the drugs.  Lyme resistance is different, resistance is based on its ability to change its appearance and secure a foot hold within protected colonies. Some antibiotics were found to be more effective against persisters while others were more effective against rapidly dividing spirochete forms. The Hopkins’ lab tried combination therapy and found a single 3 drug combination (cocktail) that completely eradicated the spirochetes (test tube only). The first drug is daptomycin: expensive with limited access; one month of therapy, 30, 0000 dollars. The second drug, cefoperazone, is currently unavailable from the manufacturer. The third drug is doxycycline. Many other combinations of antibiotics using 2 or 3 agents were tested and found to be inadequate. The ingredients of the cocktail are 2 bactericidal drugs and one bacteriostatic drug. In theory these two types of antibiotics can cancel one another out. In clinical practice this is completely untrue.

A newer test tube study shows that the Lyme bacteria may be eradicated with pulsed therapy with a single agent, Rocephin.

Test tube studies cannot be used as a basis for clinical use. But, there is proof of principal. Lyme spirochetes are hard to kill; three drug cocktails and pulsed therapy -- already in clinical use, are vindicated in contradistinction to IDSA recommendations. (Easy to kill, 2 weeks of doxycycline).

What else do we learn? Flagyl is not a “cyst buster.” In the studies it was no more active against persisters than amoxicillin of doxycycline.  Rifampin may convert non-cyst busting drugs, like doxycycline or amoxicillin and confer some anti-cyst capability. By itself Rifampin has no activity against Lyme. Rifampin is added to Lyme culture growth media (ALS new Lyme culture test) to kill non-lyme bacteria.

A major dogma, long bandied about in Lyme circles, a sacred cow, may be incorrect. Flagyl is not a “cyst buster.” Other drugs in cocktails, for example Ceftin, may be doing the cyst-busting, based on published data.

There are other interesting odds and ends. Antifungal drugs, including amphotericin B are active against Lyme. Quinine kills Lyme.  In context, we do not know if these drugs kill Lyme in living systems and this info should not be used as a sole basis for any therapy. 

Claritn and Minocycline - a dark side: odds and ends.

I have been excessively preoccupied with matters discussed below. I do not want to neglect my BLOG entirely. Here are a few odds and ends I have been thinking about lately.

CLARITIN FOR LYME

You cannot take Claritin to kill Lyme.  It has been shown that desloradine, a metabolite of Claritin inhibits the absorption of manganese through the cell membrane of the spirochete. Manganese is used by Lyme bacteria to generate energy in lieu of the iron used by most organisms.  In a test tube it works! We have what is called “proof of concept.” Unfortunately the minimum dose of Claritin needed to accomplish this goal is 40 tablets which no one is recommending. Still, it provides a direction for further work. 

MAST CELLS

Why do I recommend Claritin? Although Claritin is a weak antihistamine, it helps inhibit mast cell activation. Whereas Dr. Afrin recommends a slow process of therapy to treat MCAD, mast cell activation disorder, I favor more of a shotgun approach, beginning with numerous agents. My patients are too sick to wait for the slow approach. My patients seem to have something different: a hybrid of chronic infection and excessive mast cell activation  These drugs are nontoxic and can always be reduced one at a time when patients improve.  The more I have used the therapy the more I have been impressed by its efficacy.  (Lists of agents are available elsewhere: also consider doxepin for sleep in lieu of trazodone; very potent antihistaminic effects and possible mast cell effects as well). I do prescribe a lot of Claritin but not to kill Lyme per se. 

Mast cells may be the overlooked step child of the immune system. They are everywhere and in close proximity to blood vessels. There are omnipresent and heterogeneous. They serve many functions. For example, the glial-mast cell connection or dialogue. The naturally occurring agent palmitoethylanolamide may be helpful based on recent studies. 

ABOUT MINOCYCLINE

More about neuroinflammation. Inflammation is a catch all term. Lyme is a disease of inflammation which translates into some sort of activity of the immune system. Inflammation is not a bad thing in and of itself. Inflammation is needed to fight off infection and for normal “housekeeping” functions of the immune system. It is when inflammation is out of control, like a runaway train that we get into trouble. As a general rule, inflammation can be chronic or acute. Chronic is never good. 

The brain is not quite the immune privileged area I have referenced in the past. Glial cells in the brain comprise the resident immune system and they are quite active. Drugs that reduce neuroinflammation and suppress glial cells should be good, right. Not necessarily.  Minocycline is touted as having anti-inflammatory effects in the brain. It is an active glial cell inhibitor. Minocycline was studied in patients with ALS. Surprise: patients got worse, significantly so. Glial cell activation is a normal, necessary function. In this case, perhaps changing only one side of the equation caused harm, not good. Care should likely be taken when minocycline is prescribed for long periods of time.

Doxycycline may be different. It may reduce brain inflammation also by a reduction of MMP-3 reducing apoptotic effects. (Cell death) and also have an effect on glial cell activation. As with my experience, the effects of two drugs can be quite different. Although minocycline crosses the BBB better than doxycycycline, I have always found that doxy is the more effective drug. Molecular mechanisms are being worked at by scientist as we speak (and also over my head). As clinicians we need to be mindful or potential distinctions amongst drugs of the same class. 

Treatment of excitotoxicity on the other hand appears to always be a good thing, with drugs such as Lamactal and Namenda.  Rocephin treats excitotocity so it should not make neuroinflammatory disease worse. 

Unnecessary neck surgery

After 3 years of therapy my 60 year old patient feels well enough for a trial off antibiotics. During this recent visit I explored the topic:  when do you think you started having symptoms of Lyme disease?

She thinks it started 5 years ago with neck pain and a "pinched nerve."

Twenty percent of patients visiting their primary care physicians have chief complaints considered orthopedic.  One of the more common complaints is neck pain or shoulder pain.  Many of these patients also complain of symptoms which radiate into an arm. This is typically diagnosed as cervical radiculitis or cervical radiculopathy, also known as a pinched nerve in the neck. Large nerve branches called radicals, exit at intervals from the spinal cord between the cervical vertebral bodies. Vertebrae are numbered based on location. If a nerve root exists between the second and third vertebrae in the neck, called C2 and C3 the the corresponding nerve root would be C3. Almost all pinched nerves in the neck occur at the space between C5 and C6, causing C6 nerve root symptoms or between C6-7 leading to C7 nerve root problems. When these nerves are "pinched" symptoms referable to the sensory and motor functions of the particular nerve will typically be seen:  weakness, decreased sensation and loss of the relevant deep tendon reflexes. This is a diagnosis that any 3rd year medical student can easily make.

Doctors today rely more heavily on tests to make or confirm diagnoses. An MRI of the neck is typically ordered. A bulging or herniated disc or a bone spur will be seen in the corresponded area and the diagnosis is made. Simple. In some cases if more information is desired an EMG/NCV will be ordered.

Busy doctors frequently make a quick jump: neck pain to MRI. A diagnosis is made.

My patient with severe neck pain had been followed by her neurosurgeon for over a year.  The patient had been treated with a year of physical therapy and 3 epidural steroid injections all of which only intensified the pain. Her doctor said the finding on the MRI could not support surgical intervention and she should continue conservative measures.  On a subsequent follow-up visit her usual doctor was away and she saw a stand-in. He quickly proclaimed he could fix her pain with an operation. Desperate for relief she agreed to an operation. One surgery led to another. She's got the scars to prove it but her pain did not improve one iota.

Google cervical radiculitis or radiculopathy.  You will find the cause is a disc problem or a bone spur.  You will see that various therapies are available including surgical ones.

Lets go back to the test. MRI of the spine. Studies have been done in asymptomatic folks in the general population. At age 20 15% of folks have disc disease. By age 60 a striking 85-90% of asymptomatic individuals have disc disease in their neck according to MRI findings.

Lets go back to google. Now search Lyme radiculitis or radiculopathy and the connection will clearly appear.  If you had used the search word radiculo-neuropathy to start with Lyme would have immediately popped up.

These conditions looks like the same problem. With Lyme (and other infections) pain does not occur because the nerve is pinched but because the nerve is inflamed by the infection. In many cases there is a combination of the two. The nerve, a little pinched, asymptomatic, becomes very symptomatic when the nerve is inflamed by infection.

In the case of this particular patient she also had a "pinced nerve" in her back as well causing sciatica which worsened with a year of physical therapy and cortisone shots.

In her case both the neck and back pain completely went away with a course of antibiotics.

Radiculoneuropathy is a well known complication of Lyme disease described early on with Bell's Palsy and considered a form of neuroborreliosis in the literature.

An IDSA thinking neurologist recently published a paper which stated there are only three neurological manifestations of Lyme disease: meningitis, cranial neuritis like Bell's Palsy and radiculoneuritis.  His main point was discredit the notion that Lyme is associated with other neurological diseases like MS and ALS as frequently discussed by ILADS types.

My patient's warning:  Think twice before you undergo the knife for a pinched nerve in your neck. 

Neuroprotection: Let the doctor speak!

Last night I heard a doctor try to tell Diane Rehm about neuroprotection. She cut him off. I think we should have heard him out.

Again we hear that there is no "evidence" to support chronic Lyme. There is no evidence to support the use of prolonged antibiotic therapy in patients with persistent Lyme related symptoms. Such are the proclamations made by "experts" who have evaluated the results of 3 NIH sponsored studies. These clinical studies sponsored by the NIH have been woefully misinterpreted. At any rate, none of these studies claim that the Lyme organisms have been eradicated or provide any scientific evidence to support this contention.

Then, when naysayers admit that such therapies seem to help patients, they claim it is due to other, non-specific effects of antibiotics.(Let the doctor speak) After all there are no germs to be killed. Based on what science have such experts concluded that there are no germs to be killed? Sounds like a bait and switch tactic to me.

How can the deniers have it both ways? Do the drugs help or don't they?

Beta-Lactam antibiotics may indeed offer neuroprotection. Included here are drugs in the penicillin family and the cephalosporin family. Animal studies have shown that Rocephin has neuroprotective properties in animal models. These drugs upregulate a molecule called GLT1 which in turn inhibits gluatamate. Glutamate is the principal "excitatory" neurotransmitter in the nervous system. Inflammation of the nervous system, both acute and chronic is associated with "glutamine toxicity." It is thought that drugs such as Rocephin may provide clinical benefits for a wide array of neurological disorders. For example,Rocephin has been shown to improve the clinical course of ALS in the mouse model.

Minocyline is reported to have neuroprotective effects due to inhibition of 5-lipoxygenases, a pro-inflammatory enzyme associated with the aging brain.

Antibiotics are reported to have anti-inflammatory properties independent of their germ killing effects. Some medical literature suggests that tetracycalines are inti-inflammatory because they inhibit nitric oxide. Cipro decreases inflammatory cytokines including: TNF-alpha, IL-6 and others. Erythromycins are said to inhibit cytokine production. And so on.

Naysayers, who deny chronic Lyme say patients improve because of these non-specific effects. Does this argument hold any water? NO!

Let us consider the use of Rocephin in a "neuroborreliosis" patient. This individual has an encephalopathy characterized by significant mental status changes. The brain MRI may be normal or abnormal. The SPECT/PET scan may be normal or abnormal. Something has caused a severe acquired brain disorder. If it is not Lyme disease they what else is it pray tell? After treatment with Rocephin the patients improves, perhaps to the point of baseline health. Here is a fantastic medical success story. Why would any physician be unhappy with the result for this patient regardless of one's beliefs?

My suspicion is that the neuroprotective effects may be playing a significant role. The primary effect of the drug however is to combat spirochetes in the brain.

The same arguments can be made down the line. If antibiotics have additional effects which benefit our patients great, what a plus!

None of this information "proves" that chronic Lyme is not real. The points are interesting but are not scientific evidence that chronic Lyme is not real. In fact they are irrelevant distractions from the debate at hand.

We know that chronic, persistent Lyme disease is real. Lyme hides in niches which cannot be accessed by the immune system. Bb binds to proteins in the intracellular matrix such as decorin. Bb can acquire antigen markers from host endothelial cells to camouflage itself. Bb can enter fibroblasts, an intracellular protected niche. Bb can enter immune privileged areas such as the brain where the immune responses are limited. It can morph into intracellular forms which cannot be accessed by the acquired immune responses. In this arena only primitive, innate immune responses are active; it has been established that such responses are unable to sterilize the cells of such organisms. Lyme spirochetes can morph into a cystic form not destroyed by immune responses. Bb can rearrange the structure of surface antigens by recombination with plasmids. All of these assertions are very well documented in peer reviewed literature and texts.

Animal models and human models have both demonstrated the persistence of the organism after large courses of antibiotic therapy in various tissues. This too is well documented in peer reviewed literature.

Patients with chronic Lyme have been shown to have consistent, reproducible clinical syndromes associated with characteristic physical and laboratory findings.

I treat these patient in my office every day, and for the most part they all get better.

Some of sickest patients I have encountered in my now lengthy medical career seem to be caught between the cracks of a dysfunctional medical system, the byproduct of misguided politics, and a stubborn refusal to really consider all the evidence.

Please let the doctor speak.

Tear of joy

I graduated from medical school 26 years ago. There were 36 hour shifts of on call duty, first as a 3rd and 4th year medical student and then as an intern and resident. I was dedicated. I was totally immersed in a parallel world- the medical world, oblivious to the reality outside the hallowed halls of my hospital. During rare undisturbed moments in the on call room I studied medical texts and current journal articles with inimitable intensity. Shoes were left on in anticipation of the beeper's call to put out the next unknown fire. Those were heady days. Much has happened since. And yet- much is the same. To date medicine has been a satisfying avocation- "Its more than a job," my father, The Physician, would frequently quip. As was usually the case, he was right. Some days, some moments are just better than others and leave an indelible mark. Today I had one those moments.

My ALS lady came back today. Call in motor neuron disease or Lyme imitating ALS, whichever pleases you. When I saw her a month ago for the first time, I cried as I previously posted. I thought the the horse was long out of the barn and that I was hopelessly trying to close the gate. It has never ceased to amaze me the extent to which patients can thwart our prognostications.

I walked into the room. Her head was held up high and she beamed at me brightly.
30 days of Rocephin. She WAS strong enough to hold her head up. She was able to eat and to swallow. She had gained some weight. Ever so slightly, she had begun to move her previously useless right hand.

Unbelievable- She's going to get better! I walked out of the room- with the slightest of tear- this time, a tear of joy. Yes- this was a good day.

Lyme symptoms revisited

First of all, it should be clear, that my post yesterday, like many other posts, was prompted by a visit from a patient who had misconstrued published symptom lists. This patient clearly did not have Lyme disease.

The vast majority of patients who think they have chronic Lyme disease turn out to be correct in their assessments.
I would like to clarify yesterday's post. The TYPICAL patient I see complains of: fatigue, usually severe, pains which come and go of muscles, joints, tendons or ligaments, sensations of numbness and tingling and cognitive dysfunction. I believe that Dr. B's guidelines do a fabulous job covering the most common neuro-cognitive complaints typically seen in chronic Lyme patients. A history of tick bite and rash is important, but not as common as one might think. Established Lyme disease is a multi-system disease. Patients have a plethora of symptoms involving nearly every organ system. The take home point is that Lyme related symptoms occur within a cluster. Patients lacking the core symptoms described above are unlikely to be suffering with clinically significant Lyme disease, based on my clinical experience. The patient that prompted the post had: no fatigue, no cognitive dysfunction and no neurological dysfunction. He had knee pain after running, as well as various short lived symptoms which he found trolling the internet. Chronic Lyme patients are quite ill and have a multi-system illness. Admittedly, may chronic Lyme patients look quite healthy at first blush, but they are in fact quite ill- and this should not be trivialized. Although I think that over diagnosis of Lyme disease is rare, at least in my practice, the potential for this exists. It is clear that the IDSA believes that Lyme disease is grossly over diagnosed by LLMDS; sometimes I write with the specific intent of taking bullets out of their guns.

Neurological symptoms associated with Lyme disease are all over the map. They do include tremors, fasciculations, weakness, myoclonus, Parkinsonian features, MS features, ALS features, vertigo, dizziness, alterations in hearing- vision- sense of smell or taste, neurologically mediated stiffness, sleep disorders including sleep apnea, loss of balance, all manner of speech disturbances and psychiatric disorders as listed elsewhere, stiff neck of the meningitis variety, neurologically mediated changes in bowel and bladder function, pinched nerve syndromes, neurologically mediated pain syndromes of all sorts, trouble swallowing mediated by changes in the brain, stroke like symptoms, a wide variety of neuropathic symptoms not listed here, changes in heat and cold perception, HEADACHES, exacerbations of preexisting migraine or tension headache, ADD syndromes, personality changes, neuromuscular syndromes causing muscle atrophy and weakness--AND these are just a few of the symptoms that come to mind as I sit at my desk on my lunch break. My point is that any one symptoms can be taken out of context. There is a gestalt in diagnosing Lyme disease. Patients have multiple and varied symptoms which come together a whole.

Perhaps sometimes I write Blogs to encourage my readers to think- and to some extent, I am sharing my thoughts, as I think out loud. I hope that readers will understand my comment in this light.

Neck pain is extremely common in Lyme patients. AND it does suggest co-infection with Babesia. I have a general medical practice. One half the patients I see do not have Lyme disease. The vast majority of patients who complain of neck pain as their chief complaint do not have Lyme disease. Please understand this distinction.

If all horses are brown and you are brown it doesn't make you a horse.
This sound silly, but I think it was this sort of logic that brought the above described patients to my office for a consultation.

Alan G. Barbour, M.D: In his own words

Dr. Barbour wrote a wonderful little book intended for the lay public in 1996.
The Book is titled: Lyme Disease, The Cause, the Cure, the Controversy.

The book is full of interesting and sometimes quite detailed information. Dr. Barbour does a wonderful job of explaining the ELISA test, its methodology and "Pitfalls."

The sensitivity and specificity of the test is claimed to be 94 to 98%. But the predictive value of the test is consider "much lower," when the history and physical show that the chance of having Lyme disease is low. This is a critical point. First of all, why would someone perform the test if the likelihood of Lyme disease was low?
The sensitivity and specificity numbers are based on what LLMDS would call a narrow notion of the symptoms and signs associated with Lyme disease. The thinking at that time, which has persisted to this day in IDSA quarters, is that Lyme disease presents with certain well defined syndromes. These include the EM rash,inflammatory arthritis- typically a large joint, Bell's Palsy, acute meningitis and typical cardiac disease such as atrioventricular block. In this "old" thinking, symptoms such as fatigue, generalized pains and brain fog are not part of the equation. These are the classic symptoms that most LLMDS consider typical of Lyme disease.

The ELISA test gives a reaction on a scale. He admits (pages 96,97) that the positive cutoff point is set by "someone, or more likely a committee." This means that a group of experts picked a cutoff point for a positive reaction based on the best information available to the group at the time.

Here are his important words: "How is the cutoff point set? Selecting a cutoff point would be simple if people without Lyme disease showed no reactivity in the assay...But this is not what has been found. On the contrary, a substantial number of healthy people or 'negative controls,' as they are known, have had detectable antibodies that bound to spirochete parts." ...These people seldom had titers or color values which were as high as those of Lyme disease patients, but the two groups did overlap. There was no value below which all control sera fell and which all Lyme disease sera fell."

What he is clearly saying is that patients without Lyme disease and those with Lyme disease could react similarly on the ELISA assay. The people without "Lyme disease" were a healthy control group. Remember, his definition of Lyme disease was quite narrow. Control subjects with fatigue and brain fog could have been included in the "healthy" control group.

He cites 3 reasons for what he considers false positive results: Infection with something that causes cross reactivity, like syphilis; someone could have "sticky" antibodies, as seen in autoimmune disorders; or test subjects may have actually been exposed to Lyme disease in the past. Question: How can previous exposure to Lyme disease be considered a false positive? The science now informs us that Lyme is a persistent infection once it becomes established in the host.

It seems to me that it is relatively easy to rule out the first two items. therefore, a positive ELISA test should indicate exposure to Lyme disease.
As explained above, the cutoff for a positive ELISA was set high based on prevailing beliefs. If a patient has a positive ELISA it would seem to prove Bb exposure.

According to CDC/IDSA rules the positive ELISA must be followed by a Western Blot. Based on what is described above this does not seem reasonable. The WB bands reported are based on the CDC surveillance case definition and have not been validated as a diagnostic test. We know that critical bands such as the 31 and 34 bands have been omitted AND that only 3 IgM bands are reported.
Based on what logic can this test be used to confirm a positive ELISA test? The ELISA tests we are told have many false positives. Dr. Barbour, who was there when the ELISA test for Lyme disease was developed seems to be saying, that in the main, false positive ELISA results indicate previous exposure to Lyme disease.
To make matters worse, labs no longer report the value of the ELISA index. If a physician were to reasonably infer that the cut off for a positive test was set to high, the physician is no longer afforded the ability to apply his clinical judgment to assess the significance of a particular ELISA value.


On page 170, Dr. Barbour discusses the controversy of post-Lyme disease versus chronic Lyme disease. He does not deny that chronic Lyme disease exists. He relates this to "late infection." He states: "The difference between the two disorders is that most patients with late infection, still respond, at least partially, to antibiotic therapy, while patients with the post-infection syndrome usually do not."

Dr. Barbour's writing here would appear to support the ILADS approach: "If a patient improves with continued antibiotic therapy, the patient has chronic Lyme disease."

After all, is this not the basic issue upon which ILADS and IDSA disagree? He states that studies sponsored by the NIH should further clarify the issue. Three studies have now been done, yet, the waters remain muddy.

To be fair to Dr. Barbour, he discounts the correlation of "atypical symptoms": fatigue, generalized aches and pains, sleep problems, brain fog and others with Lyme disease. The paradigm described in the book states that such symptoms are likely not due to chronic Lyme disease. Although, he leaves open the door for post-Lyme correlating with such symptoms.

He wrote that other infections such as HIV should be considered. He wrote that patients may have chronic fatigue syndrome, fibromyalgia or a psychiatric disorder.

He does have an interesting chart in which he compares the features of Post-Lyme disease with Fibromyalgia and Chronic fatigue syndrome. He considers that the following symptoms may be found in all three disorders: Fatigue unrelieved by rest, activity less than 50% normal, unrefreshing sleep, difficulty concentrating, musculoskeletal pain and headache. If current science shows that Lyme persists in the host then would it not be reasonable to at least consider the possibility that post-Lyme really is chronic Lyme?

He further posits the main IDSA argument: Symptoms are subjective- there are no objective measurements which prove that Lyme is the cause for chronic symptoms. At any rate it is assumed that persistent symptoms are largely the product of a post-infection syndrome.

He posits that Lyme is not the cause of neurological disorder such as MS and ALS.

He says that Lyme is not a cause of autoimmune disease such as RA and SLE. He does admit that it has been postulated that infections may trigger such disorders but states there is no objective evidence that treatment is effective.

I believe that Dr. Barbour's statements reflect the ongoing position posited by the CDC and ILADS. Perhaps some updating of these views should be considered.

We certainly know that Lyme disease, if not the cause of MS and ALS, can mimic these disease states.

We know that patients with "autoimmune," inflammatory arthritis have shown positive PCR tests of synovial fluid and tissues for Lyme and Mycoplasms. We know that the same patients have improved with antibiotic therapies. Some patients show positive tests for RA and SLE which improve with antibiotic therapy.

Patients DO GET BETTER WITH CONTINUED ANTIBIOTICS. Shouldn't chronic Lyme rather than post-Lyme be considered based on Dr. Barbour's own comments?
There IS objective evidence in chronic Lyme patients. They have fevers and chills. They have Herxheimer reactions with antibiotic therapy and then seroconvert on ELISA and Western Blot tests. They test positive for co-infections. They have abnormal physical exams which revert to normal after therapy. They have abnormal lab studies, outside of Lyme per say. They have organisms in the blood which have yet to be identified. They have low CD57 counts. They have changes in vitamin D levels. They have changes in vitamin B12 and folic acid. They have abnormalities seen in the- CBC, sed rate, CRP, comlement levels and other lab parameters. They have abnormal MRI and SPECT brain scans.

There is at least one NIH sponsored clinical study which supports the existence of chronic Lyme disease. The two other studies are controversial and can be interpreted in different ways.

This book is full of interesting facts and contradictions. It reflects a mainstream medical position which remains unchanged for years, and which continues to ignore information which undercuts its primary tenants.

The ELISA and Western Blot tests are clearly flawed, as evinced in this book, yet the CDC's has solidified its position regarding the two tiered Lyme test. On what basis?

An oft quoted adage in medicine is: "You only diagnose that which you know."
One must always keep an open mind because in a field like medicine, there will always be much that one does not know.

Today- I cried

It is a busy morning. Running behind- a grabbed the next chart and headed for the exam room. The encounter sheet noted- new patient, "LYME." I entered the room and immediately noticed three people. There was a healthy appearing middle aged man, a healthy looking somewhat younger woman and a very elderly and sick appearing woman in a wheel chair.

"So who is the patient?" I inquired, secretly hoping it was not the lady in the wheel chair; but I knew otherwise.

I looked at my new patient. She looked ancient, weary and barely alive. She was incredibly thin, skin hanging on bones with a few strands of muscle. She couldn't speak or move. Her head fell to her chest; she was only able to keep her head in an upright position with help from the other woman, her caregiver. And yet, she managed a smile. I looked again at her virgin chart. She was 51 years only; the youthful gentleman was her husband.

"Well, I stammered, let me hear your story."
Her husband had only a thin folder with a few sheaves of paper. There was a clear history of tick bites. Her hair dresser once found a small tick embedded in her scalp. She had been an active outdoor person with dogs and horses.
And she had been perfectly well until some time in 2005.

They were country people. Her husband, a blue collar worker, was not the greatest historian; He told me what he could remember. It started with weakness in the right leg. A foot drop developed. The weakness spread to the other lower extremity associated with severe stiffness. Her condition gradually worsened, the weakness and stiffness spread and now affected her entire body. She had incapacitating anxiety and profound fatigue. Her speech became garbled, progressively, over the past year and one half. She was wheel chair bound for the last year and a half. Severe dysphagia- trouble swallowing, led to her dramatic weight loss. She was continent and maintained mental clarity, I was told.

In April 2006 she went to the Hershey Medical Center. She was told she had ALS. Nothing more was offered.

In July 2006, a friend suggested a Lyme test. It was positive. Her husband showed me an IgeneX IgM report, the IgG was missing. It showed positive bands in the 23,31,34,40 and 93 positions. It was noted to be CDC positive.

They live in rural Pennsylvania. No LLMDS there. They found a local doctor who tried to help. He ordered IV Rocephin for 3 months. She improved! Her strength steadily improved. Then, the Rocephin was stopped and she resumed the inexorable down hill slide. She was on oral Doxy and getting worse.

I examined her in her chair. I could not weigh her. She appeared moribund. She was unable to speak. I noted fasiculations in her arms. Her extremities were weak although she could move her arms some. The arms were loose with normal tone. Her legs were extremely stiff with lead pipe immobility. Her reflexes were normal. Sensation was hard to test.

ALS was high on the list of differential diagnoses. The textbooks list Lyme disease as a cause motor neuron disease- ALS; no one was paying any attention. why? If she got better with Rocephin why wasn't it continued? This seems like common sense. No?

Other diagnoses crossed my mind: Anxiety and stiffness.It could be an autoimmune disorder called Stiff Person's syndrome. Then I wondered if she had a primary muscle disorder. I ordered some tests and a consultation with a neurologists expert in muscle disorders. ALS was likely. But damn it- Lyme is known to cause it! And- she had started to respond to treatment; then the rug was yanked from under her.

The woman looked deathly ill. There was not much left to work with. I wished she had seen me or someone else a year ago.

I was afraid. I was afraid to treat her, but even more afraid to not treat her.
I ordered a PIC and Rocephin, with much trepidation, knowing that treatment can at times accelerate the progression of Lyme/ALS.

A profound wave of sadness came over me. I quietly shed a tear for this poor woman.

Then I became angry, as I considered the absurd politics of this disease.

But there were more patients to see; I went into the next exam room.

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.

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.

Patient with Lyme and Guillan Barre

Guianne Barre syndrome acquired notoriety in 1976 when it was associated with the Swine flu vaccine that year. It is a rare neurological syndrome. It is a scary disorder. Patients have a progressive paralysis of the lower extremities and it "ascends" up the trunk. At times it can involve the respiratory muscles requiring the use of a ventilator. Usually it is a post infectious disease and improves spontaneously over time. It is due to an acute demylinating peripheral neuropathy which is acute and sever. It is probably autoimmune in nature. Circulating antibodies or antibody/antigen complexes attack the nervous system causing a rapid loss of the protective myelin sheath of peripheral nerves. Patients have a flaccid paralysis with a loss of deep tendon reflexes. This distinguishes the disease from a motor neuron disease such as ALS or MS. A large number of viral infections as well as bacterial infections have been associated with the disease. Normal treatment is intravenous Ig (immunoglobulin g) derived from a large pool of patient sera, or plasmapherisis, a filtering of the blood which removes immune complexes triggering the disease. The disease is self limited and improves over time. In this case a middle aged gentleman in good health presented with an acute flu like illness associated with fever. Over a period of a week he developed progressive weakness and was diagnosed with Guillan Barre. The spinal fluid showed inflammation and was positive by PCR for Lyme. Note here that it is unusual to get a positive Lyme PCR of any fluid. Lyme antibodies, either C6 peptide or Western Blots are more likely to be positive. Non Lyme literate doctors will not order these tests. This patient was brought to my office after hospital discharge because the family found that the other treating physicians were mystified by the case. Lyme is a factor here but I wonder if there was not another inciting viral infection as well. Currently the patient is being treated. Unfortunately a culture of the spinal fluid revealed an unusual fungus. I am sure this is a red herring, a false positive contaminant. His physicians have placed him on a powerfull and toxic antifungal drug which worries me. I have spoken with a neurologist who is bright and familiar with the causes of this disorder. The patient had an allergic reaction to IV Ig (herx?) and will be treated with plasmapherisis as well as with antibiotics. This case is interesting because it shows one of the myriad and unpredictable Lyme associated neurological syndromes. I all neurological syndromes of the peripheral nerves, brain or motor nerves, Lyme needs always be considered as a possible cause.

ALS: A patient

I have a wide variety of patients in my practice who come with fascinating stories. Some of these patients have been around the block and recieved treatment by some of the top Lyme specialist in the country. One such patient suffers with Lyme complicated by an ALS like syndrome. The primary manifestations of this disease are muscle weakness and atrophy which without treatment have in the past usually been progressive and fatal. This patient was formerly treated by Dr. Martz, the physician who himself was cured of Lyme induced ALS and had created a clinic to specialize in this disorder. Unfortunately, Dr. Martz closed his clinic for health reasons unrelated to Lyme. His patients have been scattered to the four winds seeking out physicians willing to continue their care.

This patient had been stabilized on a combination of IV Rocephin and Zithromax, both used at a low dose. Higher doses in the past had caused brain Herx reactions which exacerbated her symptoms. She also was on Tindamax and Cleocin. The Cleocin had been prescribed by Dr. Jemsek. Dr. Jemsek may be the only Lyme doc in the country who routinely uses Cleocin. He has found this drug to be effective for many patients.

I have made some minor adjustments in her medication regiment and she seems to be improving somewhat. Options may include: Adding Rifampin, gradually increasing the IV meds and a trial of Lithium. A recent publication suggests that Lithium may be helpful in ALS. Interestingly, other sources have suggested that Lithium is helpful with other forms of neurological Lyme disease.

What is Chamydia pneumonia, CPN, and what does it have to do with Lyme disease?

What I have not yet discussed is the controversial notion that Lyme causes "everything." Well, not everything, that's a slight exaggeration. This version of the Lyme paradigm suggests that chronic fatigue syndrome is really Lyme disease. Fibromyalgia is really Lyme disease. Lyme infection triggers autoimmune disease in persons who are genetically inclined such as MS, Lupus, and Rheumatoid arthritis. And many are convinced that Lyme is the key to Alzheimer's disease. Their are a group of physicians who are doing parallel research. They believe that Chlamydia pneumonia, or CPN, is the cause of everything. This group of devotees believes CPN causes fibromylagia, chronic fatigue syndrome, Alzheimer's disease and a host of autoimmune and chronic inflammatory disorders. These two infections intersect at the word L-form. Both exist as intracellular organisms called L-forms. CPN has a 3 phase life cycle which is somewhat reminiscent of Lyme. CPN is very hard to kill. Studies show that it takes months or years of combination antibiotic therapy to eliminate this organism. CPN is ubiquitous. It is common respiratory pathogen, not to be confused with its cousin Chlamydia trachomatis, a sexually transmitted pathogen. Most of the research on CPN has been done at The Vanderbuilt School of Medicine. The chief expert in this area is Dr. Charles Stratton. Dr. David Weldon, a researcher and clinician in England has provided compelling evidence showing a link between CPN and MS. He reports anecdotal evidence of his success in treating MS patients. More startling is the work of Dr. Martz, a victim of ALS, Lou Gehrig's disease. He was shown to be infected with Lyme. Intravenous treatment with Rocephin caused a remission of his otherwise fatal illness. He has treated both ALS and MS patients for Lyme and met with some success. However, his findings have not yet been published. Protocols for treating CPN include Amoxicillin, Docycyline, Zithromax and Flagyl. Interesting. These are all Lyme drugs. Dr. Stratton has also recommended Rifampin, which at times is very effective as a Lyme therapy. He also recommends INH, an anti-Tuberculosis drug, which most physicians avoid because the risk of liver toxicity is substantial. Many patients evaluated for Lyme have high antibody titers to CPN. Since it is an intracellular germ it is difficult, like Borrelia, to prove it is causing active infection. However laboratory experiments attest to its hardyness and its uncanny ability to defeat both the immune system as well as antibiotics. These two areas of research and treatment have been sparate from one another. Again the commonality is the idea of chronic L-form infection leading to a host of consequences. Patients with a high L-form burden may be more likely to have vitamin D dysfunction with reversal of normal levels, as described by Marshall. The importance of CPN may be that simultaneous infection with Borrelia makes treatment more challenging. It may help direct the choices of antibiotics as well as the likely duration of treatment. CPN is not a Lyme co-infection because it is not tick borne. It may ultimately be of much greater importance than the usual co-infections that are stressed by most "Lyme" doctors. Most "Lyme literate MDs" do not discus CPN. Doctors who specialize in CPN, there are not many of them at this time, seem to be unaware of Lyme literature. I believe the integration of these two areas will eventually lead to newer thinking and treatment for what is becoming rather than just Lyme disease, but the Lyme complex syndrome.