Tuesday, March 31, 2009

Fibromyalgia remission with Malarone

I have been treating a 46 year old woman with chronic Lyme syndrome for about 18 months. She resides in Montgomery County Maryland and her favorite hobby is(was) gardening. Her presenting complaints were muscle pain, muscle weakness, fatigue, joint pain, neck pain, headaches- with an exacerbation of pre-existing migraines, night sweats, brain fog with forgetfulness- word recall difficulties- short term memory loss- slow cognitive processing and severe depression. She in fact had no idea that she might be suffering with chronic Lyme disease when I suggested the diagnosis. She had been a regular patient for several years treated only for migraine headaches. She had not shared her other symptoms with me because she was worried that I would think she was a hypochondriac. The muscle pain it turns out, was a prominent symptom. She had incapacitating pains in her muscles, especially around her neck and upper back area. Her muscles were knotted and stringy and exquisitely tender. She saw a pain management specialist who diagnosed "fibromyalgia," and treated her with trigger point injections as well as a mix of pain meds. This occurred during the 6 months prior to the Lyme diagnosis. Looking back, it is now clear that she had suffered with fibromyalgia for 20 years. She did not share her symptoms with others in her life. She blamed herself. Somehow, she believed her symptoms represented a personal failing- as she struggled to keep up with other well functioning people around her. Only by sheer will and determination was she able to create the illusion that she was well, when in fact she was getting sicker and sicker.

Finally, almost inadvertently, she shared her story with me.

Her exam had classic Lyme neurological abnormalities. Her labs were fairly unremarkable. Her IgeneX WB for Lyme showed only a positive IgM 31 band with several other IND bands. She wanted a positive test to be convinced she really had Lyme disease. I explained that the 31 band was highly specific. It took some coaxing, but she agreed to start treatment for Lyme. She took Amoxil and Biaxin for about one year. She was nervous about changing medications so we kept to this one regimen. Most of her symptoms improved. Overall, she was 60% better. Persisting symptoms included sweats- which thought were due to menopause AND there had been no change in the fibromyalgia piece of her syndrome. I convinced her to try Mepron, believing that she had sero-negative Babesia. Her insurance turned down Mepron so I substituted Malarone, perhaps fortuitously. Follow up labs continued to be seronegative for Lyme disease by IgeneX standards and Babesia. I also ordered a blood wet mount performed at Clongen. Extracellular motile organisms were present.

After 3 months on Malarone she noted that the muscle pain was almost completely gone. After five months on Malarone all signs and symptoms of fibromyalgia were 100% gone. Her knotty,lumpy muscles were replaced with smooth, normal tissues. This is one very happy patient! Her "menopausal" sweats were also gone.

This is conjecture: She never had Babesia. The motile parasites seen in blood wet mounts may have been responsible for her muscle disorder. We known that these parasites do not live in blood or blood cells- they are extracellular. This means they primarily reside in other tissues. Their numbers must be so numerous that they egress into the blood. A likely place for parasites to live is muscle tissue. One must wonder: could fibromyalgia be caused by muscle parasites, at least in some patients?

This case shows remission of longstanding fibromyalgia with Malarone- used in conjucntion with Biaxin and Amoxicillin.

Friday, March 27, 2009

A note on Babesia and parasite

The health officials say that B. microti is the most common strain on the East coast.
B. duncani is only supposed to exist on the West coast. Not true. I get positive results for B. duncani with the same frequency as positive results for B. microti. Serology tests exist for these two strains. I finally got Labcorp to find the right code; they now do the test for B. duncani. Labcorp and Quest are a little mixed up. The old name was B.WA1- the new name is B. duncani. Labcorp and Quest still call it B. WA1. If you order serology for B. duncani they have no idea what you are talking about.

Clongen has a "species" PCR test for Babesia. It includes around 15 known species but does not include B. duncani. For some reason this PCR has to be ordered separately. This can get a bit expensive. I have found many patients who have negative antibodies for both B. microti and B. duncani test positive on the Clongen Babesia "species" test. The theory that many otherwise unspecified strains of Babesia exist in Lyme patients is held up by this data.

On a separate note- we have not yet identified the parasites which are seen in many patient's blood. One organism has been described as tear dropped in shape and has a tumbling motion. It appears to respond to Malarone not Mepron! If Mepron doesn't work for parasite- Babesia like symptoms, it may be worthwhile switching to Malarone.
A positive response is easy to determine- the Herx can be quite dramatic.

Wednesday, March 25, 2009

Suspected Bartonella Psychiatric Herx

A 32 year old woman came to see me one month ago. She was diagnosed with LD in 2003.
At that time she presented with EM rash, stiff neck, and flu like symptoms. She tested positive by ELISA and WB criteria. She was treated with 29 days of Doxycyline.
Over the last 6 years she has experienced a progressive illness. At presentation she complained of: joint pains, muscle pains, head and neck pain, memory loss, anxiety, depression, light sensitivity, and sound sensitivity. Additional symptoms included: intermittent facial rash, dizzy spells, loss of balance, profound fatigue, and irritable bowel symptoms. There was also a history of an elevated rheumatoid factor. The neurological exam was normal save sensory loss of sensation of the lower extremities. Initial Labcorp testing, done at this time showed Lyme WB positive IgM 39 and 41 bands. Her rheumatoid factor and other autoimmune parameters were normal.

She was started on therapy with Omnicef, Mincin and Plaquenil.

Four weeks later she was unexpectedly profoundly depressed. She had increased irritability with mood swings and personality changes. All antibiotics were stopped and she began psychotherapy. She deferred the use of psychotropic medications.

One month later she was feeling much better. Not exactly following my instructions, she had stopped the Minocin and Plaquenil and resumed the Omnicef as solo therapy.
Pains and fatigue were essentially gone. Her mood improved. She still had some mood swings, but the major depression was gone. Her prominent complaints were: persistent dizzy spells, night sweats, neck pain and only right hip pain. Other joint pains had vanished. She noted that bowel changes- constipation and diarrhea had abated but she had increased heartburn.

What had happened?

The patient thought the psychiatric exacerbation was due to Plaquenil. I thought not.

Brain Herx: But- she was fine on Omnicef.

Based on her symptoms it seemed likely that she had Babesia. I had not prescribed any medications that would be active against this parasite- so this shouldn't be the issue.

The question then became: Why the Minocin pych herx but no reaction to Omnicef? Omnicef attacks cell wall synthesis of spirochetes, in this case Lyme. It is relatively ineffective against Bartonella and it has no affect on intracellular L-form disease. Bartonella, according to Psych/LLMD literature is frequently associated with pyschiatric disturbances.

My hypothesis then became: Minocin killed Bartonella, perhaps in the brain leading to this peculiar reaction.

With this in mind, I decided to give all drugs with known activity against Bartonella a wide berth for the time being. These drugs do include- Minocin, Doxycyline, Zithromax, Biaxin, Cipro, Levaquin and perhaps a few others including Bactrim.

Given the night sweats and neck pain I decided to approach the suspected Babesia. My inclination was to start with low doses Artemesin while continuing the Omnicef.
The patient told me should could not afford medications that would not be covered by her insurance drug plan-

With a little more trepidation, I decided to test the waters of Babesia and prescribed a low doses of Malarone.

Another option would have been to continue Omnicef alone. My experience tells me to treat Lyme first.

Side bar: The bowel symptoms were worse but there was increased GERD- heartburn symptoms. The most likely explanation is drug induced gastric irritation of the stomach, although this is not common with Omnicef. I am becoming more convinced that Lyme frequently inhabits the GI tract and can cause symptoms there. Perhaps acid blockers which decrease stomach acidity may help kill gastric Lyme; and, regarding a somewhat related issue, it certainly appears that Asacol, a bowel anti-inflammatory, helps colon related symptoms. I prescribed Prevacid- a proton pump inhibitor which decreases stomach acidity. This should improve symptoms and perhaps aid in killing Lyme in her stomach.

Bartonella psychiatric Herx? Perhaps. We shall see.

Monday, March 23, 2009

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.

Friday, March 20, 2009

Lyme symptoms: Smell the coffee- before it is too late

A 43 year old female came in to see me within the last several weeks. She is extremely ill. She became ill about 18 months ago. It started with joint pains and cognitive deficits including confusion. She was initially found to have Lyme and Ehrlichia. She was treated with 30 days of Rocephin followed by two months of Doxycyline (Klempner protocol). She was just starting to improve when the treatment was stopped. All of the initial symptoms and more returned. With further testing she showed antibodies to Bartonella. She was treated with Bicillin and Levaquin. The Bicillin, once weekly was continued for 3 months and the Levaquin given for 3 weeks. Treatment was stopped. Again, she was improving some when therapy was stopped. More symptoms came and she kept getting worse. She has two daughters who also developed Lyme disease from the same field trip. She reports that between the three of them they have seen 40 doctors prior to seeing me.

She works for cardiologists. She developed severe hypertension with wild uncontrolled swings in blood pressure. The heart specialists were at a loss.

She has seen numerous infectious disease specialists, neurologists and others. Mostly she was told that she did not have Lyme or tick borne disease. One told her he didn't know how to treat Bartonella. She told me that it appeared that all the physicians were reading off the same script!

Here are a few test results: Lyme IgM positive (CDC-old criteria), Ehrlichia IgG titer 1:1024, Bartonella henselae IgG 1:320.

Several doctors told her the infections were cured because she had IgG titers, not IgM (Ehrilichi and Bartonella).

This lady is very sick. She has profound fatigue, confusion and pain. She has a boat load of other neurological symptoms. I should report that many psychiatric symptoms became much worse with recent re-treatment with Rocephin and Doxycyline.

She presented with a highly abnormal neurological exam. She had diffuse myoclonus- muscle twitching, absent vibratory sensations of the extremities, poor finger to nose testing and a positive Romberg sign.

She has the core constellation of symptoms and findings upon which I base my diagnosis of chronic, systemic LD and neuroborreliosis. With this in mind, I will list the entirety of her current symptoms:

joint pain
random sharp shooting pains
Pain soles of feet
blood pressure dysregulated
Random muscle twitches
off balance
ringing in ears
sensitivity to sound and light
global cognitive problems- too numerous to list
"intestines slow"
increased headaches
sleep disorders
menstrual irregularities: no periods for years, start with antibiotics
psychosis- started after antibiotics were given- visual and auditory hallucinations

Lyme symptoms reflect a multisystem infection and are extremely varied-

For those who misinterpreted my post about Lyme symptoms I wish to clarify: Patients with Lyme disease may and do have all the symptoms listed by Dr. B in his guidelines. This patient even has the psychosis which I largely dismissed. I have seen all of these symptoms and many more in my Lyme patients.

My concern is that symptom check lists used in self diagnosis should not be displayed on the internet, especially when connected to ILADS. All patient varied symptoms need to be seen within a context of the whole clinical picture. Patients may have many isolated symptoms on the check list, which may occur over a period of time. Only a trained physician can decide if these symptoms fit into the overall clinical pattern of Lyme and tick borne illness.

The IDSA is writing letters and giving lectures claiming that self proclaimed LLMDS are essentially quacks and that symptoms attributed to chronic Lyme are vague and non specific. The IDSA claims such symptoms lists have many other causes- not Lyme disease. They are also making the strange claim that antibiotics just make people feel good for some unknown reason.

I spoke with a University scientist yesterday. His lab does research on Lyme. The IDSA got there before we did. He just heard a lecture which specifically debunked the notion that chronic Lyme disease exists. These guys are busy launching a full frontal propaganda war. We (the Lyme community) are busy quibbling about minutia while the walls are falling down around us.


Lyme patients have: 1) core symptoms which are reproducible in a large population
2) abnormal neurological examinations which are reproducible in a large population
3) abnormal laboratory parameters which are reproducible in a large population and
4) clinical responses to treatment which are reproducible in large populations.

Credible, science oriented physicians, need to go on the lecture circuit and present the other side of the story to these large groups of clinicians and scientists.

We have to win over the hearts and minds of these folks if were are to have any politic success with the legislators.

I unfortunately cannot do this until specific "political" issues which relate to my own situation are resolved.

Wednesday, March 18, 2009

Long term antimicrobials for non-Lyme disease

Long term antibiotics are and have been used to treat a wide range of medical disorders. It seems the use of long term antibiotic therapy is acceptable for other conditions, except Lyme disease.

Rheumatoid arthritis: Doxycyline and Minocycline have been shown to be effective and used as maintenance drugs. Plaquenil, an anti-malarial antimicrobial drug which is frequently used for the treatment of Lyme disease, is also used long term in the treatment of rheumatoid arthritis and systemic lupus erythematosis.

Periodontal disease: Periostat- a formulation of Doxyclyine has been approved for long term use.

Acne: Doxycycline and Minocycline are frequently used for months and years. Acne, unlike Lyme disease, is a cosmetic disease, not a disabling or life threatening disease. Other antibiotics like Bactrim have also been used.

Chronic prostatitis: Cipro and similar antibiotics are frequently prescribed for 90 days and longer.

Urinary tract prophylaxis: Women with recurrent urinary tract infections have been treated with long term antibiotics to prevent recurrences.

Chronic otitis media- ear infections: Long term antibiotics have frequently been prescribed in children to prevent recurrent ear infections. Although this practice has been discouraged in recent years, current peer reviewed studies have again supported the benefits of this therapy.

Chrohn's disease: Antibiotic therapy, at times long term with Cipro and at time Flagyl, have proved to be beneficial, and safer than other recommended therapies.

Rheumatic fever: For patient with recurrent Rheumatic fever related to Steptoccocal infection, the use of Penicillin orally or by injection, on an indefinite basis has been recommended.

PANDAS: Pediatric Autoimmune Neurological Disorder: This disorder associated with OCD disorder and tics, especially in children, has been treated with long term antibiotics such as Penicillin. Although there may be controversy regarding this therapy, no psychiatrist has had medical board sanctions for prescribing this therapy.

Chronic osteomyelitis- bone infection and diabetic ulcers: Frequently treated with long term or indefinite antibiotic therapy.

Chronic constipation: Gastroenterologists frequently prescribe indefinite Erythromycin for the management of refractory constipation.

Herpes simplex: Valtrex, an anti-viral medicine is frequently prescribed indefinitely for this benign condition.

Toe nail fungus: Lamisil, a potent and potentially toxic antifungal, is routinely prescribed for 90 days for this cosmetic condition.

Q fever: May be a chronic bacterial infection requiring 4 years of antibiotic therapy.

Whipple's disease: Another chronic bacterial infection which routinely requires years of antibiotics and may be fatal.

TB: 6 months of a potent antibiotic, toxic to the liver, is frequently prescribed to prevent TB after exposure.

Active TB: 6 to 9 months of triple antibiotic therapy is required. In the recent past therapy was frequently extended for 2 years.

Coronary heart disease: Associated with elevated C-reactive protein. This is a circulating protein associated with activation of the complement cascade. This is an effector mechanism of the innate and acquired immune system responses. Chlamydia pneumonia, a chronic intracellular bacteria has been found in blood vessel plaques. Long term antibiotics have been studied for this disease.

Malaria: For persons in endemic areas long term antimalarials is frequently employed.

MS and other autoimmune neurodegerative disoders: The use of long term Minocycline and other antibiotics is an area of active research.

This list is by no means comprehensive. But is sure demonstrates the existence of a double standard.

Treating Lyme causes super-germs- In a pig's eye (or cow)

A frequent criticism leveled against the use of long term antibiotics for Lyme disease is that it contributes to the rise of super-bugs. Is this true?

LLMDS treating chronic Lyme disease typically use older generation antibiotics such as Amoxicillin or Minocycline. The dreaded MRSA- Methicillin resistant Staphylococcus aureus is resistant to Methicillin. Methicillin is an advanced generation penicillin. It inactivates penicillinase, an enzyme elaborated by evolved, resistant strains of Staph. All Staph aureus have been resistant to Amoxicillin for decades! The use of first generation antibiotics play no role in the development of sophisticated- antibiotic resistant bacteria. This argument holds no water. This overstated theory is not supported by decades of clinical practice or published scientific research. Super-bugs grow in an environment oozing with the latest- "super-antibiotics." Where does this occur?

It has been long established that super-bugs have emerged from the hospital environment. Hospitals have been on the cutting edge of using the latest and greatest antibiotics. In general, the newest, hi-tech antibiotics have been prescribed by infectious disease specialists, who have brandished these new drugs like a kid showing off a new shiny toy. To be fair, in recent years, ID specialists have become increasingly aware of this problem and made efforts to reign in the use of such super-antibiotics. MRSA emerged in hospitals and then spread to nursing homes and long term care facilities. It is only after its genesis in these venues that MRSA egressed into the general population. It has long been known that "nosocomial" infections- hospital acquired infections, are different and much more dangerous and antibiotic resistant than infections acquired in the "community."

Are hospitals the main problem then? No.
70% of antibiotics used in the US are used in agriculture. Farmers have access to latest hi-tech antibiotics and use them with impunity, without any oversight by the IDSA of physicians who are rightfully concerned with the advent of highly resistant germs. For the most part this information has remained outside the purview of public awareness and kept on the back pages of print media. The inappropriate use of antibiotics in agriculture is the invisible 800 pound gorilla sitting in the room when it comes to the issue of emerging super-bugs.

When you get down to brass tacks, the use of long term antibiotics in Lyme patients is criticized because the critics believe that a non-existent disease is being treated. If the disease does not exist off course no drugs, let alone antibiotics should be prescribed.

The problem is that Lyme disease is real. It is a multi-system, frequently life threatening disease. Do Lyme drugs cause Superbugs? NO. It is phony issue.
If the IDSA has issue with the existence of chronic Lyme, then lets have a debate about the real issue and the real science.

Friday, March 13, 2009

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.

Thursday, March 12, 2009

Lyme disease symptoms, or not?

A young man came into my office with a hodgepodge of odd symptoms. He wanted to know if he had chronic Lyme disease. In fact, there was nothing to suggest this diagnosis.
His presentation was consistent with what we used to call "the worried well."

Please note that what follows are my opinions. This is my Blog after all.
I have the utmost respect for the accomplishments of Dr. Burrascano. Nonetheless, I have concerns about some Lyme disease symptoms included in his guidelines.

The ILADS guidelines are quite circumspect and are the product of a committee of interested physicians and scientist. I feel that these guidelines are excellent. The ILADS web page links to Dr. Burrascano's guidelines. Dr. B's guidelines represent his opinions only, but I am not sure that this is made clear to the public.

Here is my concern: Medical Boards, the IDSA and members of the lay public read these guidelines. I am concerned that such entities may interpret small parts of the guidelines in ways which could have a deleterious effect.

A large menu of expanded symptoms is said to be associated with Lyme disease. A point system based on the presence of symptoms is suggested. While I agree that many listed symptoms suggest Lyme disease in its various manifestations, there are many symptoms on the list which I find questionable. I address these below. Again, let me make this clear. I think that the majority of Dr. B's symptoms are right on target. I am only addressing the small number of symptoms on the list which concern me.

Dental Pain: There are numerous reasons for this, I personally do not believe it correlates with Lyme disease. It certainly lacks specificity.

Neck stiffness: This is a common symptom. It is usually due to muscle spasms, cervical arthritis and other common orthopedic disorders. It is thought by many to be a symptom of Babesiosis. However, by itself, it lacks specificity for Lyme and related disorders. I am here not discussing neck pain in the context of pain/complex disorders including fibromyalgia. I am only discussing it as an isolated symptom.

Weight loss or weight gain: Well, which one is it? Appetite and weight changes are commonly seen. I again feel this symptoms is very non-specific.

Irregular menses: Their are numerous reasons for this. Dysfunctional uterine bleeding can be benign but it can also be linked to serious disorders like cervical cancer. This is not a typical symptom of Lyme disease. I understand that abnormal bleeding can be seen in the context of endocrine dysfunction related to Lyme disease. In and of itself this symptom is not specific for Lyme disease.

Bladder dysfunction: This is common and has many causes. Certainly it can be seen in patients with systemic Lyme disease, but it lacks specificity. I do see many patients with bladder issues but I would be hesitant to include this with a list of common Lyme symptoms.

Erectile dysfunction and loss of libido: These are common complaints. When I hear them from my patients I do not think of Lyme. There are many other causes.

Nausea and Heart burn: H. pylori is common. Lyme is fairly far down on the list of possible diagnoses. Patients may have ulcers, Barretts disease or even cancer. I have now seen evidence of Lyme infection of the stomach, as I recently reported. It has not been my experience that this is a common symptom in patients with Lyme disease.

Constipation and Diarrhea: This is a common complaint. It is usually associated with irritable bowel syndrome. It may be associated with celiac disease or even occasionally colorectal cancer. Lyme colitis is probably relatively common. Nonetheless, I would be hesitant to list this symptom.

Heart murmur and valve prolapse: Lyme typically causes arrhythmia, heart block and pericarditis. I have not seen it cause the mentioned syndromes/symptoms.

Head congestion, cough, sore throat: These are common complaints and usually due to upper respiratory infection, GERD or asthma. Air hunger may be seen in Babesia infection. Lyme may cause pleurisy. These symptoms seem to lack specificity for Lyme disease.

Hair loss: Male pattern balding is normal. Hypothyroidism may be considered. Not specific for Lyme disease. Alopecia areata is an autoimmune disease. It may be associated with Lyme disease. This symptom is non-specific.

Swollen glands: This is non-specific. I have seen Lyme present with this finding. Certainly it may be associated with Bartonella. Doctors must first exclude serious disorders like malignancy. It is a fairly non-specific symptom.

Back pain: This is generally due to a variety of common orthopedic disorders. Lyme is typically associated with large and small joint pain. It is rarely associated with back pain unless the sacroiliac joints are inflamed. Non-specific.

Headaches: Non-specific. Most common causes are migraines and tension headache. Headaches are commonly seen in patients with Lyme disease. However, the vast majority of patients with headaches do not have Lyme disease. This is a non-specific symptom.

Seizures and psychosis: Lyme is unlikely. Doctors must exclude brain tumors. Recently we have heard about Lyme rage and associated psychotic behavior. More frequently Lyme is associated with anxiety, depression, mood swings, ADD like symptoms and combinations of the above. Lyme as a cause of psychosis would seem to be quite rare.

Milk production: This may be due to a pituitary growth called a prolactinoma. Not
specific for Lyme disease. It may been seen in disorders of the hypothalmic pituitary axis which have been described in Lyme disease, but its association with Lyme disease is still low on the list of possible causes.

These symptom lists are published on the world wide web and linked to the ILADS web site.

Lyme disease is frequently a multisystem disease. It can be associated with a surprising list of symptoms. Patients cannot self diagnose. Only a physician, after carefully weighing all the clinical data can make the diagnosis. Patients may look at expanded symptom lists and reach unwarranted conclusion, as is the case with the patient I alluded to at the beginning of this Blog.

Such all inclusive symptom lists may create the erroneous impression that LLMDS think that everything is caused by Lyme disease. And this is simply not true.
I am a member of ILADS. My comments here should not be construed as an effort to disparage ILADS or Dr. Burrascano. Lyme disease and associated guidelines are in a state of flux and refinement. To the extent that my comments may seen as critical, my intent is to provide only constructive criticism.

Wednesday, March 11, 2009

Results: Rejected: Not approved

The 12 year old female with massive joint effusions of both knees had samples sent to Labcorp shows the following results:

White blood cells: 10,000- Normal less than 400.

Western Blot Bands: IgG 10/10 reactive- IgM bands 2/3 reactive

This test is still reported as investigational- It has no validity in the eyes of the "authorities" listed in the title.

The rigid IDSA guidelines exclude the use of this data in making the diagnosis.

Physicians who diagnose Lyme arthritis based on these findings run the risk of censure by state medical boards.

I think its time for a change in the rules.

Physicians should be allowed to practice their art to the best of their ability.
If physicians are required to practice medicine according to inflexible- cookbook formulas, the future is bleak. If organized medicine demands mediocrity- they should be careful what they wish for.

Tuesday, March 10, 2009

Documented gastric Lyme

An 18 year old female with an 11 year history of complex multisystem Lyme disease recently had an upper endoscopy for the evaluation of persistent unexplained gastrointestinal symptoms.

Biopsy samples taken from the stomach and duodenum were sent to Clongen labs for PCR analysis. The samples were tested for Mycoplasma fermentans, Borrelia burdorferi, Babesia microti and Bartonella henselae. These specific tests were chosen by Dr. Ray Jones. This patient is new to me and has recently requested that I contribute to her case.


Looking for Lyme by PCR has been difficult because it has not been clear which tissue should be biopsied. Here is a case demonstrating the persistence of the Lyme bacteria in gastric mucosal tissues after 5 years of continuous antibiotic therapy.

This begs the question: Should gastric Lyme be treated differently. Perhaps the acid environment enhances survival of the organism. Drawing from the H. pylori experience, it may be helpful to treat with high dose proton pump inhibitor therapy in addition to combination antibiotics.

Here we are sailing on uncharted waters.

Viral meningitis

A 19 year old male came into my office yesterday for follow up for meningitis diagnosed at his college campus. One month prior to our visit he experienced acute onset of fever, chills, sweats, weakness, headache and stiff neck. He was admitted to the local hospital with a presumptive diagnosis of meningitis. A spinal tap was performed and he was give a single dose of Vancomycin. The results of the CSF (spinal fluid) were reported negative and no further antibiotics were given. He was noted to have a low white blood cell count which subsequently improved. He was diagnosed with viral meningitis and sent home on no treatment. A week after his discharge from the hospital he received a call from the hospital. A blood test showed antibodies to Ehrlichia. He was treated with Doxycyline, 100 mg twice daily for 10 days. He complained that symptoms persisted and the Doxy was renewed for an additional 14 days.

When he came to see me he was still not feeling well. He had persistent low grade headaches, severe fatigue and generalized malaise.

Over the last several years I have seen many patients who have been diagnosed with viral meningitis who have in fact suffered with acute Lyme meningitis.

Although Ehrlichia infection can exist without concomitant Lyme I felt that this was unlikely. Ehrlichia meningitis is extremely rare although a few cases have been reported. In this case the positive serology for Ehrlichia tipped my hand that the "viral meningitis" was actually caused by Lyme disease.

Ehrlichia can be difficult to eradicate since it resides in white blood cells.
For this patient I prescribed Doxycyline 400 mg per day and Rifampin 600 mg per day. This is the most effective combination for Ehrlichia and also covers Lyme disease.

Based on the clinical response future treatments may need to focus more on Borrelia.
I await initial lab studies and will see this patient back in one month.

Monday, March 9, 2009

As the IDSA reviews it 2006 guidelines.....

As the IDSA reviews its 2006 Lyme disease guidelines, it should be reminded of its own statements regarding disease guidelines: "Guidelines are...developed...to assist practitioners and patients in making decisions about appropriate health care for specific clinical circumstances. "Attributes of good guidelines include validity, reliability, reproducibility...clinical flexibility, multidisciplinary process, review of evidence..." The IDSA states that: "It is important to realize that guidelines cannot always account for individual variations among patients. They are not intended to supplant physician judgment...adherence to the guidelines...(is) voluntary..."

Unfortunately, the 2006 Lyme disease guidelines have morphed into something which they are not- a template for the determination of the standard of care regarding the diagnosis and treatment of Lyme disease and tick borne disease. Standards of care are known to vary within different medical communities. Clearly two standards exists. Both ILADS and the IDSA have evidence based guidelines for Lyme disease, which have been vetted be the United States Department of Health and Human Resources and are listed with the National Clearing House of Guidelines.

Lyme is frequently seen as the most controversial and perhaps the most important disease of our times. The IDSA guidelines must be seen in their proper context: they represent the opinions of panel members who were assigned the task of creating said guidelines. Although the guidelines may be based on evidence, ultimately they reflect opinion. It should have been noted that not all panel members were unanimous in their support of the conclusions drawn therein. The existence of strident rejections of guideline conclusions by at least one prominent panel member deserves mention. After all, what is being contested here is the validity of one particular paradigm, supported by the IDSA. In essence, this discussion can be characterized as a war between two diametrically opposed, competing paradigms. To that extent, I believe it is disingenuous when the IDSA either wittingly or unwittingly, promotes the notion that panel members were all in agreement. When a subject is this important, and when the disagreements are so vitriolic, minority opinions become important and should be reported. Similarly, the current requirement that of a quorum of 75% amongst new panel is required to consider revision of the 2006 guidelines is problematic. The IDSA is obligated to report that Lyme disease and the IDSA guidelines remain very controversial. History tells us that paradigms in science and medicine do not easily shift. Not terribly long ago, two scientist were ridiculed by their colleagues for suggesting that peptic ulcer disease was connected to a small bacterium seen in the gastric lining of patients. History later proved that these two pioneers were correct and they were awarded a Nobel prize in 2005.

With this in mind, let us review some of the evidence. The two tier diagnostic test for Lyme disease is simply not valid for the diagnosis of Lyme disease. This test was developed as a surveillance test by the CDC in 1994, not a diagnostic test. It is well known that specific bands 31 and 34 were omitted from the surveillance Western Blot. The United States Congress admonished the CDC to correct the misuse of this test. To date this has not happened. Under oath, CDC representatives, in the Connecticut hearings, reiterated that the test was a surveillance tool and that the diagnosis of Lyme disease was largely clinical. It is an outright embarrassment that the IDSA clings to the incorrect use of the test, stubbornly holding that it is an accurate, evidence based tool for the diagnosis of Lyme disease.

The three NIH sponsored studies looked at a narrow population of Lyme patients: Those who had been previously treated but had persistent symptoms. There are many other groups of patients suffering with Lyme disease who are not included in the cohort which was studied. For example, Some patients have had the disease for years or even decades and yet never sought treatment prior to their initial request for medical care. Many patients are co-infected with Babesia, Ehrlichia and/or Bartonella which may interact with Lyme disease as a syndrome or complex, in ways which have not been studied or established. Some patients are diagnosed with neuroborreliosis showing significant mental status changes with abnormal MRI scans and PET or SPECT scans. Other patients have refractory arthritis as their primary syndrome. These patient types represent the tip of the iceberg. Lyme disease is a multisystem disease associated with protean clinical manifestations. Even if the results of the three NIH studies were in accordance, which they arguably are not, it would be bad science to generalize such results to have wide ranging clinical applicability for many different clinical presentations and patient types suffering with Lyme disease.

The studies were small pilot studies and do not reach the same conclusions. The Klempner study has been widely criticism for a plethora of procedural deficiencies.
Patients with evidence of active Lyme disease- PCR positive were excluded. Test subjects included those who were seropositive as well as those who were seronegative. This is confusing since a key IDSA point is that the standard serological test is accurate. How then was the serogneative-PCR negative test group validated? Assuming the seronegative group did indeed have Lyme disease, how can the two subgroups be combined as a single cohort? The number of study subjects was smaller than the requisite number required by the study design. There is no agreed upon the definition of what constitutes long term therapy. For that matter, the correct choice of antimicrobial therapy has not been agreed upon or has the manner in which it should be administered. For example, perhaps the treatment group would have responded more favorably if the 2 months of oral doxycyline preceded the 30 days of IV Rocephin? The study was vary narrow in its design and outcome measurements. The use of these results to support far reaching conclusions, as has been frequently done, would seem to be bad science at best.

The Krupp study was a rehash of the Klempner trial. In this case patients were treated for 28 days with Rocephin. The results were not entirely negative. Patients with severe fatigue were shown to experience improvement. It was not known what outcomes may have been found if the study was extended to 8 or 12 weeks.

The results of the Fallon study were not available at the time the 2006 guidelines were developed. Here a group of individuals with severe neuroborreliois where shown to have cognitive improvements after 10 weeks of Rocephin. That fact that the improvements were not sustained is not evidence that the therapy did not work. It could be easily construed as evidence that the therapy was inadequate. For example, it is not know whether the cognitive improvements would have been sustained if the IV therapy had been continued- or if Rocephin therapy had been followed by continued oral antibiotic treatment for some period of time.

The guidelines are supposed to include multidisciplinary inputs. Where are the contributions of molecular biologists, microbiologists, immunologists and many others? Borrelia burdorferi has been demonstrated to persist in human and animal hosts in the face of extensive exposure to antimicrobials. Borrelia burdorferi has more plasmids than any other known bacteria. It has numerous mechanisms for evading eradication by the immune system and antibiotics. It has the ability to shift its antigens as has been amply demonstrated. It has the ability to live and proliferate in various protected niches. It has the ability to change its morphology and shift into intracellular L-forms and cystic forms. It is known that intracellular bacteria are not amenable to acquired humoral responses and that immunological defenses are mediated by innate immune responses. These innate responses, as has been shown with numerous other intracellular bacteria, frequently fail to completely eradicate the offending bacteria. Bb has the demonstrated ability to readily cross the blood brain barrier causing persistent infection and inflammation. The immune privileged brain allows a protective niche for long term survival. A large repertoire of well documented basic science, published in respected, peer reviewed journals describing the morphology and complex biological activity of Bb, both in vitro and in vivo, lends a great deal of support for the ILADS paradigm suggesting that long term antibiotics are frequently required for the treatment of established chronic Lyme disease.

In addition, there are published clinical studies supportive of the use of long term antibiotics for chronic, persistent Lyme disease. Studies such as those published by Dr. Donta and Dr. Cameron, are not addressed in the arguments marshaled to support the IDSA guidelines.

The guidelines for Lyme and other diseases should have: reproducibility, flexibility and multidisciplinary input. These are the IDSA's words, not mine. The NIH sponsored studies cited, fail to demonstrate reproducibility. The IDSA guidelines are rigid and fail the flexibility requirement. Certainly, as seen above, the input from other disciplines is clearly lacking.

Moreover, the purpose of the guidelines is to assist patients and practitioners as they make decisions regarding appropriate health care. Again, these are IDSA statements. Patients and physicians who opt to treat Lyme disease outside the IDSA guidelines are well apprised of the IDSA guidelines. In the final analysis, individual decisions regarding treatment should be left to the judgments of the patients and their treating physicians, especially when said patients are fully aware of the differing theories and treatment approaches. This acknowledgment fully comports with the IDSA's own claim that adherence to its guidelines is voluntary.

The science is still uncertain. Only today we learn of a new virulence factor in Lyme bacteria reported by the University of Texas.There is much yet to be learned about this vexing microbe and its associated disease. At this time no Lyme disease guidelines should be considered the final word. For the foreseeable future these guidelines should remain in a constant state of flux and reevaluation.

As the panel is asked to evaluate the current Lyme disease guidelines it will likely be flooded with personal stories and anecdotes. Such stories, although personally moving and emotive, should not confound the important work which needs to be done here. The panel is asked to consider the facts, the science. The panel must remain impartial and assiduously avoid the appearance of partisanship or "rubber stamping" the current guidelines. The findings of this panel may have a tremendous impact on many suffering patients and the dedicated physicians who treat them. And I am sure that panel members in all sincerity desire, that at some future time, as they look back on their work, it will be shown that at this critical juncture, that they were indeed on the right side of history.

Friday, March 6, 2009

IDSA and bad science

The IDSA is accepting comments and letters as they prepare for their open hearing on Lyme disease and the IDSA guidelines this April in Washington D.C. I am sure many are aware of this. At this time I am preparing a model letter which I plan to publish on this BLOG.

One glaring, critical flaw in the IDSA logic is staring me in the face, so in advance of my letter, I have decided to share this one point with my readers.

The IDSA claims that the controlled trials have shown that patients with chronic Lyme or post Lyme do not benefit from prolonged use of antibiotics. They are of course referring to the 3 NIH sponsored studies: Klempner, Krupp and Fallon.

All three studies were designed to look at patients with an established diagnosis of LD who were first treated with IDSA approved courses of antibiotics and yet still complained of various symptoms.

Most of the patients I see with chronic Lyme developed symptoms over a period of years and have never been treated with the IDSA approved Lyme disease regimens or any antibiotics for that matter. These patients are not the subset studied in the 3 NIH sponsored trials.

These studies consider only a small subset of patients identified as having chronic Lyme or post Lyme. The generalization of the findings to all groups of patients with Lyme disease is bad science at the very least.

If one were to study patients who had been previously treated for primary syphilis and then apply the results to heretofore untreated patients with disseminated tertiary syphilis, all would agree that this would be preposterous. In the case of Lyme disease the rules of logic and science apparently do not apply. Not only is the illogical non-science accepted by many well known physicians, but the New England Journal of Medicine agreed to publish an editorial predicated on such nonsensical thinking. One can only conclude that a determined group of individuals, having decided a priori what a particular study would show, twisted, massaged and manipulated the limited data to fit into the "Procrustean bed" of their forgone conclusions. This is not science. Whatever it may be- I have no name for it.

Unfortunately as absurd as this all may seen, the consequences of these machinations has had, and continues to have, a devastating impact on so many suffering patients and the physicians who treat them.

This is not just bad science- it is outside the pale.

Tuesday, March 3, 2009

Chest pain in a young woman- should be an easy one

It looked like an easy one for a change. I picked up the chart of my new patient- a 36 year old woman complaining of chest pain. She appeared to be a fit healthy woman in no obvious stress. Immediately, I began considering the differential diagnosis of chest pain in a young woman. The usual suspects quickly came to mind: chest wall strain, costochondritis- inflammation of the cartilage where the ribs join the sternum, a trapped gas bubble, stress/anxiety, lung infection- especially pleurisy, possible mitral valve prolapse, acid reflux disease and a few others. Coronary heart disease seemed quite unlikely. Pericarditis was near the bottom of my list.

I then took the patient's history. The pain had been present for two months, but recently- over the past one week, it had become more severe. It was constant and was located in the left chest area. It was not pleuritic (it did not increase with respiration). It did not radiate. It was not associated with sweating or shortness of breath. She did not have heartburn. The pain was not reproducible with pressure applied to the chest wall or with movements of her body. There was no history of trauma. These are standard doctor questions in the evaluation of chest pain.

What made the pain better or worse? The pain improved with aspirin and with leaning over. Interesting.

Oddly enough she complained of severe fatigue. She denied a history of a recent respiratory infection or viral syndrome.

And then oddly enough she complained of occasional night sweats over a period of two months corresponding to the time frame of the chest pain. I filed this away in my head.

Her history and exam were unremarkable. She had a mild systolic heart murmur but I thought it was within the normal range.

To be complete I performed an EKG: normal. I considered the fact that the pain decreased when she bent over. I recalled that pericarditis associated chest pain can improve with a change in position. Frequently bending forward makes it worse rather than better.

I have on site cardiac echo. To be thorough, I performed an echocardiogram.

The findings were surprising. There was fluid around the heart in the pericardial sack. This is compatible with the diagnosis of pericarditis. Frequently preicarditis in an otherwise healthy young woman is due to a viral infection and is self limiting. Of course there is a long list of disorders which may cause pericarditis, including: lupus and other autoimmune syndromes, tuberculosis, HIV, fungal infections, parasitic infections, bacterial infections, kidney disease, and unusual cardiac disorders. I also know that pericarditis can be a manifestation of Lyme disease. I ordered an anti inflammatory drug, Indocin assuming she had viral pericarditis.

As we were finishing up the visit I asked another question, as an after thought: Have you had any tick bites?

She answered: Yes, three years ago, it was a tiny tick and I could barely see it. I think there was a rash as well.

Pericarditis, fatigue, night sweats and a tick bite: I had to connect the dots- It looks like Lyme yet again.

Chronic Lyme disease- The debate- Rephrased

Lyme disease symptoms can persist after IDSA recommended antibiotic therapy.
The argument that this represents a post-infection syndrome rather than a continuing infection has become the crux of the debate as framed by the IDSA.
This disagreement is really a sidebar. Let us put this particular discussion aside for the moment and look at things from a different perspective.

Across the board, physicians agree that late disseminated Lyme disease is a real entity. The IDSA argument claims that MOST Lyme patients present with an acute easily discernible syndrome. The IDSA would agree that some patients with well documented Lyme disease present differently.

Let's look at a comparison with syphilis once more. Syphilis starts with a painless lesion in the genitalia, called a chancre- the acute syndrome. Many patients with syphilis can recall no history of such an exposure. For decades syphilis has been called the great imitator. It has the ability to disseminate widely after a quiescent stage and mimic many other medical disorders. We know that syphilis has 3 stages. In the second stage, years or decades may pass without the appearance of symptoms. When syphilis finally shows itself, stage 3, we can see a devastating, multi-system disease. We know that late syphilis of the brain and central nervous is frequently associated with dementia and death and that no satisfactory therapy is reported in current medical literature/guidelines.

Lyme is now referred to as the new great imitator. Does initial Lyme infection always cause features consistent with an acute case? Clearly the answer is no. The most common vector is the nymph forms of the hard body Ixodes ticks. These tiny arthropods are the size of a poppy seed. They are stealthy vectors, and more often than not are unobserved by their victims. Many patient do not develop the tell tale rash. There is some disagreement about the frequency of EM rashes, but there is no dispute that they are absent in some or many patients. Bites frequently occur in areas which are hidden, for example,the back of the neck. If the classic rash does occur it can easily be missed by the patient. Some patient, newly infected with Bb develop acute flu like symptoms; but as we have seen, such symptoms are frequently dismissed as viral.

Lyme may enter into a prolonged asymptomatic phase, just like syphilis. These latent spirochetes can quietly disseminate. Symptomatic disease may not appear for many months or even years. A great imitator like Lyme disease can cause a protean array of symptoms and syndromes. This may be a point of disagreement between ILADS and the IDSA. This dispute can also be put aside for the moment. There is no debate that Bb is very neurotropic: It has a known proclivity for infecting both the brain and nervous system.

Penicillin treatments for neurosyphilis are known to be unsatisfactory. The treatment of established spirochete infection in the brain is known to be very difficult.

Many late stage patients with Lyme disease present with neuroborreliosis. This is clearly established and accepted by all groups familiar with the disease, irrespective of their IDSA/ILADS bias. Neuroborreliosis patients have concrete, object findings: Alterations of mental status, abnormal MRIs and abnormal SPECT scan. Forgive my verbiage- It is "no brainer".

Fallon has shown: patients with neuroborreliosis improve with IV Rocephin. The improvements regress with cessation of therapy. The improvements return when therapy is started again. What does this tell us??

I don't think you have to be a physician (or a rocket scientist) to imagine what might be occurring here. The antibiotics temporarily keep the infection at bay- patients improve; antibiotics are stopped- patients worsen- because the offending germs have not been eradicated. Fallon did not continue patients on oral antibiotics when the IV Rocephin was stopped. Many LLMDS, myself included have found that this approach frequently maintains the improvements gained from Rocephin. This begs the question: Why is there a controversy- at least regarding documented neuroborreliosis.

If something is working why stop therapy ? Why is this considered good medicine?

Monday, March 2, 2009

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.

The amazing Lyme WB 100 Kd band???

Clongen labs reports the whole spectrum of Lyme WB bands. The Bands as seen on a Western Blot strip are shown heaviest to lightness. Other labs that I am familiar with report the heaviest band as 83-93. Lyme WB strips from Clongen show "all the bands"; there are more than 14. The Clongen strips frequently show reactivity at 100 Kd band which exceeds the control response. I asked Dr. K what this 100 Kd band was. He did not know. He just presents the data. Intrigued, I did a little research. I have found nothing in human literature. But I did find something.

Of particular interest is a paper called: Lyme-Disease- "a consensus statement"
This paper is talking about canine, not human Lyme disease.

The piece was written in 2005. It comes from a German lab- LABOKLIN.
The bands discussed in the paper are for the most part quite familiar. They include:
the 24Kd band (23-25), the 31Kd band, the 39Kd band and the 41Kd band.
The article notes that the 41 band is associated with flagellin protein and that the 31 band is associated with OSPA. Sound familiar?

They paper claims that the best Lyme WB band is the 100 Kd band. Although it is seen only in late disease, the authors state "...there is not known cross reaction and (it) is therefore pathognomonic." The means that reactivity at the 100 Kd WB bands confirms Lyme exposure with 100% accuracy. If the same holds true in humans this may be incredibly significant!

Comments please!