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Friday, June 19, 2009

Lyme disease and female hysteria

I offer this piece after reading only the abstract of a recently published article. There may be inaccuracies because I have not read the entire piece. Feel free to post corrections.

A syllogism is a form of logical thinking which I learned about in college. Syllogisms are frequently twisted into false logic causing spurious or misleading conclusions. To say( 1) more women have Lyme disease(which is vague) then (2)more women also have depression(which is also vague) THEREFORE women who have Lyme disease likely have depression- is like saying: fire hydrants are red: you are red: therefore you are likely a fire hydrant. This is the sort of logic evinced in a recent article published by prominent anti-Lyme IDSA figures in the Journal of Women's Health. I can understand why women take umbrage with these remarks.

Not only is the logic false, but the implications are insulting to many health care professionals and professional health care organizations. If "Chronic Lyme disease" is a vaguely defined term that has been applied to patients with prolonged subjective symptoms..." The same cannot be said for fibromyalgia, chronic fatigue or depression.

Fibromyalgia is not vague. It is a syndrome which has been clearly described by the American Association of Rheumatology. It is defined by very specific symptoms combined with very specific physical findings. Chronic fatigue syndrome is not vague. It has been very clearly defined. This definition can be viewed in CDC published literature. Depression is certainly not vague. The psychiatric community has meticulously defined this disorder, and its subtypes, in a book called the DMS4.

There are clear cultural differences between men and women. Men are infrequent users of the health care system. Men are less likely to complain of symptoms. Culturally men are taught to be stoic, to not complain and ignore symptoms until they are very advanced.

Their are indeed biological differences between men and women as well. Women are twice as like to suffer with autoimmune diseases as men. Most physicians who treat chronic Lyme disease are well aware of the strong autoimmune component of Lyme disease. Women also live longer than men and are less likely to succumb to severe infectious illnesses. These differences are real.

Are diseases like depression really more common amongst women? We know that women are more likely to seek professional help for depression. MEN ARE FOUR TIMES MORE LIKELY TO SUCCESSFULLY COMMIT SUICIDE. Which gender is more depressed? Men are more likely to suffer with alcoholism, drug addiction and commit acts of violence. These are well known surrogates of depression and other mental illnesses.

The word "hysteria" is derived from an ancient Greek medical concept. It was a female disease related to a disturbance of the uterus. Hysteria has become synonymous with the terms "psychosomatic" and "psychogenic." Sadly, many physicians today are still influenced by this ancient, unwarranted prejudice.

One might conclude that the authors have lumped together these so called female predominant disorders because the underlying beliefs of the authors, like many others in the medical community, is that these "new age" illness are a phony-psychosomatic- manifestation of hysteria- as described by the ancient Greeks.

Why conclude that so called chronic Lyme patients have been misdiagnosed and really have these other syndromes? What evidence is there to back up this conclusion? Perhaps it is the other way around. Typically, chronic Lyme patients do not neatly fit into the syndromes of fibromyalgia or chronic fatigue syndrome. Unfortunately may cynical physicians, who fail to accept the reality of these illness, have used these clinical disorders as a "waste basket" for Lyme patients when in fact no clear diagnosis has been established--at least according to their paradigm.

This sort of thinking seems dismissive and anachronistic with regard to the suffering of so many chronic Lyme sufferers. And as stated at the outset, the logical argument marshaled here is questionable at the very least.

One has to question the motives of the authors: Are they trying to promote a scientific understanding of a disease or are they publishing pabulum in an effort to promote their pre-existing, crumbling paradigm?

I think its time for a change. Don't you?

Monday, June 15, 2009

The accidental patient

I just saw a 32 year old female. This is the patient that I dread to see. She saw my associate for a routine physical. My associate does not treat Lyme disease. The patient complained of severe brain fog, memory loss, inattention and confusion. These alarming symptoms had been increasing over a period of several years. She even told my associate that she felt like she was developing Alzheimer's disease--at age 32. My associate ordered a few lab tests; she threw in a Lyme WB. The results: IgG 41 and 39 bands present. This meets the IgeneX criteria for a positive Lyme test. According to IgeneX the presence of these two bands indicates Lyme exposure with specificity of 96%. Of course IgeneX is looking at their own assay; there is no real basis for transposing this data to WBs obtained elsewhere, even though his may seem logical.The patient researched her symptoms on the Internet. Lyme disease frequently popped up on her browser. She is confused. Does she have Lyme disease? If so, how is it treated. Internet sources inform her that treatment ranges from 28 days to lifelong. How is a medical consumer to make sense of this and other contradiction? Throw more in the mix: She is trying to get pregnant, now what? Can Lyme be passed to the fetus? She has read this on line. On the other hand, aren't antibiotics dangerous to a developing fetus and just dangerous in general.

My exam showed peripheral neuropathy: nothing else concrete.

Cognitive problems are difficult to prove. For the most part the patient's subjective report of symptoms is all you really have to go on. Neuro-psychological testing can be ordered but these tests are nearly impossible to interpret without a before and after. By the time patients present we only have the "after." The tests are expensive, time consuming and rarely covered by insurance companies. What then?

A brain MRI and brain SPECT scan are good starting point. They may be normal or abnormal.
If the brain MRI shows white matter changes a neurologist might to chalk it up to migraine , early MS or vasculitis. A rheumatologist will likely concur: vasculitis. A psychiatrist might suggest depression.

Further Lyme WBs may be positive or negative. Co-infection testing may be positive or negative. From the perspective of other physicians I have found that little credence is given to these results even when they are positive.

This young woman with very troubling symptoms showed up on my schedule for 15 minutes to review "lab results." If not for the 39 band on a WB she probably would never have seen me.
It became my job to introduce her to a medical parallel universe, within the allotted time.

Being an "LLMD," if that is what I am- can sometimes feel like a curse. Ignorance is bliss. But I became a doctor to help people- that is who I am- that is what I do.

How do this tell this young woman that she is lucky she came to see me on this day?- it sounds arrogant, even to me. She may see countless other physicians who will conclude that she definitely does not have Lyme disease. As an "erstwhile" neurologists friend once quipped: "Why is it that you know something that no one else knows?" Why indeed.

I am amongst the very few that believe in chronic Lyme or for that matter the existence of neuroborreliosis it seems. I get no support from local colleagues or local medical institutions held in high esteem who believe my views are incorrect and misguided. Furthermore, they point to the dangers of long term antibiotic therapy for a non-existent illness.

I have but 15 minutes to inform and instruct her. All I can do is order the tests outlined below and give her a lot of reading material. I can ask her to watch Under Our Skin--which my patients tell me is now difficult to find. I direct her to "Cure Unknown" and the ILADS website.
My blog is not a good starting point. It is generally only helpful for those already steeped in the Lyme debacle.

I do not know if she will follow through with any of my recommendations. Lyme patient's with cognitive deficits have trouble reading and processing to start with.

And then there is the problem with family members. They dismiss the diagnosis of Lyme disease and frequently ridicule it. It doesn't exist. They disparage the treating doctor(s) and offer no validation of the patient's suffering or pain. This may lead to depression and feelings of alienation and hopelessness. The high fees charged by many physicians further reduces their credibility in the minds of many.

No this is not the patient I want to see. Not today. Perhaps selfishly I would rather see the patient who has already seen 40 other doctors, those who know more about the nuances of Lyme than I do. If I charged high fees the uninitiated would be weeded out: life would be so much easier.

Treating such patients(the one described here) is a risky business. It is not insurance companies who have "turned me in," contrary to public belief. No, it is my colleagues, members of the IDSA, who have been anxious to report me to the Medical Board.

The anger which I once had is gone. It is pointless and emotionally draining. As the smoke has cleared I am overcome with a new found sense of humility. After all- who I am really- a lone voice shouting into an empty wind only to hear the echo of my own voice.

I put myself into the patient's shoes. How can this one doctor have special knowledge about my illness? It admittedly does not meet the sniff test. She may ultimately see an assortment of specialist who may politely or not so politely tell her that I am a quack- or just wrong at best. Although it is not Lyme disease, no diagnosis will be found. Perhaps years later she will come back with a progressive, mustisystem illness- perhaps with an infected child. Or maybe, after looking into the matter she will decide to return for me to treat her. Time will tell. I cannot control the decisions of others. I can only control my own decisions.

I have no confidence that the IDSA "review" of its guidelines will bring us any closer to the truth.
The public debate in DC is set to occur this July. ILADS is armed with great speakers and a plethora of facts and published scientific studies. But ultimately the IDSA will be passing judgment on itself. How can the accused party fairly judge itself? This runs contrary to human nature.

The light of truth will eventually shine on this national disgrace known as Lyme disease. How long this will take? Nobody knows. We do our best and sail on through the still stormy seas.

I love being a doctor, I always have. Still--some days I wish I were a fisherman, sailing into challenging whimsical ,unpredictable seas-seeking elusive tuna or other prizes.

Perhaps this is what I do after all.

My basic panel of tests ordered for the evaluation of suspected tick borne disease

The diagnosis of Lyme disease is made on clinical grounds. Nonetheless, these are routine test- I suppose standard tests, ordered for many of my patients suspected of having tick borne illness-
Chem panel-CMP
Sed rate
C3a and C4a
B12 and folic acid
Vitamin D: hydroxy 25 and didroxy 1,25
CD57- if covered by insurance
Rheumatoid factor
Bartonella antibody panel
RPR- HIV and hepatitis screen where appropriate
Babesia antibody panel: microti and WA1- although the name has been changed to duncani, Labcorp and Quest only know it by this name
Ehrilchia antibody panel plus Anaplasmosis
Lyme ELIZA C6 peptide index
Lyme Western Blot: 14IgM and 14 IgG bands- if the patient cannot afford the test I will first obtain the 13 blot test- I still get many positives
Wet mount examination of patient's blood
Only the expanded Lyme Western Blot and the Wet mount need to be performed by specialty labs

If further co-infection testing is required then Babesia species and Bartonella species by PCR may be obtained. A FISH test exists for Babesia- I have not generally ordered this test

Mycoplasm fermentans is a tick borne organism. It can only be demonstrated by PCR. An antibiotic active against Mycoplasm species should be given first to increase yield. Alternatively, a Mycoplasma species PCR may be ordered- this has a higher yield. It may demonstrate the presence of non-tick borne tissue organisms. I do not generally order this test

Another other non tick borne organism which I sometimes test for is Chlamydia pneumonia. This is an antibody test. PCR is also available- but is rarely positive

Fluids such as synovial fluid are tested for Lyme antibodies, C6 peptide index and Lyme PCR

Testing for viruses, such as EBV does not change my therapy- these tests only cause confusion- so I do not order them

Patients with fatigue- nearly everyone, gets a sleep study- sleep disorders are incredibly common in this group of patients

Patients with cognitve issues get brain MRI and SPECT scan

This is my basic set of tests for many patients

Localized Herx: knee

A patient presented to me with an acute swollen knee. She had been healthy until another physician prescribed a course of Cipro for a urinary tract infection.
She had typical mono-articular arthritis: arthritis of a single joint. The knee was swollen, red an hot with a large effusion. The patient tested positive for Lyme disease and was successfully treated.

This- I think may demonstrate the concept which I alluded to in the response to my last entry. First of all many ostensibly healthy persons are infected with sub-clinical Lyme. Something- many things, can set off the disease. Second, Herxes can be very localized, presenting in a specific area.

Many thinking in this case was that the Lyme organisms were present in the synovial tissues of this patent's knees. Cipro, a quinolone, was able to have exceptional penetration in to these tissues. As a result, this localized Herx occurred in the patient's knee. Post-quinolone treatment relied on less potent antibiotic, which have less penetration into synovial tissues. These tissues are minimally penetrated by most other antibiotics.Therapy with Amoxil and Biaxin, over time, was successful:swelling and arthritis gradually improved.

It is pure conjecture. I simply ask the question: could tendon rupture seen with quinolones represent a similar reaction?

Wednesday, June 10, 2009

Cipro for Lyme: Back to the future

A 60 year old female came to my office over one year ago. She had been struggling with fibromyalgia, ulcerative colitis and depression for decades. She provided a multi-page list of symptoms. The highlights were: fatigue, pain, loss of sensations, symptoms related to special senses--hearing-vision, AND rather profound cognitive deficits. She was on a list of nutritional supplements which filled a full page. She had been a highly functional professional in the past. She suspected she might have chronic Lyme disease; this diagnosis had never been made.

She brought sheaves of lab work which was unhelpful. I found her to have an elevated rheumatoid factor-(174)-normal less then 14. Her white blood cell count was minimally depressed, 3.7. Her CD57 was slightly depressed, 50. Special Clongen labs showed positive 39 and 23 Western Blot bands. A wet mount exam showed round extracellular bacteria.

The initial physical exam revealed a fairly profound peripheral neuropathy.

Her treatment was complex; she was prescribed a number of antibiotic combinations.
I will not discuss all the antibiotics she has taken over time, except to say that she was aggressively treated for the known co-infections.

One drug which has been particularly efficacious is Cipro. When this was discontinued she has back-pedaled everytime: symptoms which had improved return.

When I started treating chronic Lyme in a serious way, several years ago, I was sent a paper written by Dr. Jemsek. He described a Lyme regimen in which he used Cipro with Doxycyline. He stated that the two drugs worked via an intracellular mechanism and were synergistic.

After reading this I jumped on the Cipro train. Old data on MICs(minimal inhibitory concentrations), showed that Cipro was reasonably active against Bb.

I used Doxy and Cipro and then began switching to Cipro and Amoxicillin.

Doxycyline works by inhibiting protein synthesis within bacteria. Cipro works by inhibiting DNA gyrase necessary for DNA synthesis. Rather than using two intracellular antibiotics I combined a cell wall inhibitor with an intracellular antibiotic with the belief that this might be more effective. This sort of thinking was espoused by many LLMDS if not this particular combination.

In those days I wasn't giving Bartonella much thought, but it is well known that Cipro has activity against Bartonella.

I had years of experience with Cipro prior to launching into the the waters of Lyme. The tendon rupture issue is much exaggerated in my experience. What I know about Cipro is that it is a very powerful antibiotic. It has been claimed that oral Cipro can provide tissue antibiotic levels rivaling that of IV antibiotics. Cipro is one of the few antibiotics able to cross the prostate/blood barrier. Very high tissue concentrations--in many organs, are achieved with oral doses.

As I look back at charts of patients treated with Cipro I find that many had excellent responses. Then I stopped using Cipro for the most part: it was not an LLMD recommended drug.

As of late I am using the drug more. It provides high tissue concentrations, is active against Bb- and also works for Bartonella-or Bartonella syndrome.

I start low: 250 mg daily-- and then increase to 250mg twice daily. This relatively low dose is frequently effective. Patients are warned about tendon/muscle pain. I generally institute it when these pains have already been controlled by other antibiotics. I have never seen a tendon rupture.

As aside, Cipro is also active against Mycoplasmas and Chlamydia pneumonia.

It works.

Friday, June 5, 2009

The murky world of Western Blots

Lyme Western Blots can be quite different.
Some labs make their own kits while other labs buy commercially prepared kits.
The "mill labs" Labcorp and Quest simply report whether or not bands are present or not. Other labs grade Blot/band responses.

Specialty labs typically grade bands on a scale of 1 to 4 and may also use the indeterminate designation. These results are manually read by the person performing the test.

The dark line or blot seen on the patient strip (blot) are visually compared to the control strip. The ratings are subjective and may very from one observer to the next.
The human eye unfortunately is not all that reliable.

I recently looked at some blot results with Dr. K. He has used both manual blot and computerized blot technologies.

He offers state of the art computerized WB results.
Here the computer digitizes the the images seen on the Western Blot strip. The computer counts the pixels and compares the intensity of the patient test reaction with that of the control. To my eye, patient bands may appear equal to the control reaction but may be read negative by the computer.

He uses the "Mayo Clinic" methods. Bands are reported as positive only if the pixelated blot/band is 90% of the control. The report indicates a percent reading as it relates to images present on the control strip. For example, an IgG 41 band might be reported as 300%, this means it has 3X as many pixels as the control band as read by the computer software.

This technology which should be more accurate in fact tends to show less positive bands than manual WB results. This is because the human eye tends to see bands as being more intense than perhaps they actually are. We are biased to see positive bands. However-- since WB have always been performed manually one could question the validity of the computer generated reports.

A strip for one of my patient's recently showed a 34 band with a reading of 85%. Although this is 5% less than the Mayo Clinic criteria, it is pretty clear to me that this is a positive band.

When I look at strips I frequently see weak bands at key locations which are reported as negative. This is based on the set-point of the software. Truly "negative" bands(in my opinion) show no reactivity at all- the strip is blank. Any bands which are visible, even if they are a low percent of the control need to be considered, especially when they are present at critical locations. When physicians are presented with the actual strips it provides more information. Information is always a good thing.

IgeneX makes it own kits and interprets the results manually.
Clongen uses commercial kits, which are CDC approved( I don't know if this is good or bad) and offers both manual and computerized interpretations if requested.

The mill labs only report if bands are present. They do not indicate their cut-off points or methodology.

When WBs are sent to three labs at the same time different results are obtained quite frequently.

As you can see the world of Lyme Western Blots is murky like everything else Lyme; so--what else is new?

Wednesday, June 3, 2009

Interstital Cystitis and Lyme- preliminay report

I would like to comment briefly about this disorder and its potential relationship to Lyme disease. I have been treating at least one patient who has reported an excellent response to treatment. Willie burdorferf, the microbiologist who discovered the Lyme spirochete reported in 1988 that Borrelia burdorferi, the bacteria which bears his name was found consistently in the urinary bladders of mice.
A great deal of research has supported the notion that Bb widely disseminates into many organs. The co-existence of urinary tract disorders in patients with Lyme disease is well documented. There is evidence that Lyme has been found in stomach, colon and gallbladder biopsy samples. To the best of My knowledge no studies have been undertaken to examine bladder tissue samples for the presence of Lyme. At least one study has demonstrated positive Lyme PCR in genital secretions. This may represent contamination from the urinary tract. PCR tests for genitourinary STDs, Chlamydia and gonorrhea, from urine samples have existed for years(this demonstrates that urine contamination from other sources is frequently present). Positive Lyme PCRs have been obtained from urine specimens. Overall, a body of evidence suggests that Lyme can- may reside in the urinary bladder.

Interstitial cystitis is a fairly common disorder. It occurs more commonly in women. It's name is derived from the minimal pathological changes seen in bladder biopsies.
It is associated with symptoms which at times are crippling. Such symptoms may include: pain in various locations, frequency, pelvic pain, bloating and other related symptoms. IC(interstitial cystitis) patients are thought to have a higher incidence of fibromyalgia and chronic fatigue syndrome.
The standard thinking is that the cause is unknown; although it is said not be due to infection and not respond to antibiotics.

These symptoms overlap with several other disorders: chronic pelvic pain of unknown cause, chronic prostatis or prostatosis in men and chronic urethral or para-urethral syndrome seen in women.

Standard urinary tract infections are caused by bacteria that normally live in the colon. Examples include: E. coli and enterococcus. These are classic gram negative and gram positive bacteria. They can be easily grown in standard culture medium. standard antibiotics only treat gram negative bacteria- such as Bactrim.

Lyme is very difficult to grow in culture media, even by expert hands. And- if it is found only in the bladder wall, such cultures will be useless.
Other L-form bacteria have also been implicated in these syndromes, including: Chlamydia and Mycoplasm species. These too are very difficult to culture.

Physicians typically prescribe antibiotics for 7 to 14 days for urinary tract infections. Experience with Lyme disease shows that short courses of antibiotics are not effective. Only in prostate infections have longer courses of antibiotics been used. Physicians are aware of the prostate-blood barrier and bacterial sequestration within the gland. Antibiotic courses up to 90 days have been used- with some success and frequent relapse.

My patient has established IC. She also tests positive for LD by Western Blot and has a variety of other symptom commonly associated with Lyme disease. She had been miserable for two years with a horrendous quality of life. Experts in IC had been unable to help her.

She has been treated with the usual Lyme antibiotic combinations. The combination of Biaxin with Plaquenil was incredibly effective for the IC symptoms and life altering.

My thoughts are that IC and related conditions are caused by L-form infection of perhaps Bb and other L-form bacteria. Biaxin is not an antibiotic used for urinary tract infections in the typical sense. Minocin has also shown some promise. Cipro has been used for both Lyme and urinary tract infections, but I have noticed a very significant "bladder herx" when patients have been treated with it. Perhaps it can be tolerated later in the course of therapy.

I have seen evidence that IC and related syndromes respond to antibiotics. Long term antibiotics are required- patients need to realized that symptoms will not improve over-night.

Lyme disease should be considered in these patients. This is a work in progress. I cannot claim a lot of experience here. However- my patient has reported that other IC patients, with whom she communicates, have also experienced improvement with the combination of Biaxin and Plaquenil.

Tuesday, June 2, 2009

Life after Rocephin

What happens after you stop Rocephin? From the Fallon study we know that all cognitive gains achieved after a 10 week course of Rocephin are quickly lost.
Many patients find themselves in the post-Rocephin boat. I will briefly describe the clinical course of one of those patients whom I saw today for a follow up visit. This 57 year old female in many ways is a typical patient with neuroborreliosis. After an acute illness with Lyme disease 3 years ago she subsequently developed progressive cognitive deficits. She experienced memory loss- both short term and long term, difficulty with concentration, poor attention and slow processing. Along with this she had bouts of confusion and disorientation. I picked her up as a new patient 3 months ago. She had been on 4 months of Rocephin and experienced a terrific clinical response. She was afraid of stopping the Rocephin. She had regained at least 70% of lost cognitive functioning. I told her that she could not stay on Rocephin forever and that in my experience Rocephin gains can be sustained with oral antibiotics once the plug is pulled. To reassure her I also let her know that Rocephin could always be restarted.

Here is my thinking. The primary antibiotic which was so effective, Rocephin or ceftriaxone is a third generation cephalosporin. The oral Lyme medicine which most closely resembles Rocephin- a third generation cephalosporin is Omnicef; so I chose this drug. In my experience Amoxicillin would probably have been equally effective.
To boost the blood concentration, and hopefully the effects of Omnicef, I added Benemid or probenicid. This drugs inhibits renal excretion of penicillins and cephalosporins- increasing the blood/brain concentration. In addition I thought that adding additional-synergistic antibiotics, known to pass the blood brain barrier and improve cognition made sense. So I added Minocin and then Tindamax to the regimen.

Now three months off Rocephin she has continued to improve each month. Her level of cognitive functioning is up to 80 to 90 percent of normal.

There have been no published scientific studies to support these findings. However, my impression at this time is that 1) It may be necessary to use Rocephin for significant cognitive dysfunction and that 2) those improvements can be sustained- if not augmented with the use of appropriate oral antibiotics. The duration of therapy cannot be predicted ahead of time; but an open ended approach makes sense as the patient improves. And beyond this some sort of maintenance therapy may be required.

Monday, June 1, 2009

The Lyme Western Blot revisited

I get a lot of questions about Western Blot test results: Do I have Lyme?
The disease cannot be diagnosed by a blood test. The Western Blot test is one tool used to demonstrate that a patient has been exposed to Borrelia burdorferi. Period.
Testing for Lyme antibodies is much more complicated than testing for most other germs. Antibodies directed against most bacteria and viruses are determined by ELISA or IFA technology, and that it all that is generally required. The Western Blot was supposed to be a confirmation test used to validate a positive ELISA in the case of Lyme disease. Many of us who treat Lyme have found this to be inaccurate. The only other disease that I am aware of that uses this two tier approach is HIV. Some patients who test positive for HIV by the ELISA method are negative by the Western Blot method. These patients are false positive; they do not have HIV. Some patients who test positive by the WB method are ELISA negative and also do not have HIV. For the HIV test to provide accurate result the ELISA must be done first before the WB.

What is true for HIV testing is not true for Lyme testing. Nonetheless, many physicians cling steadfastly to this incorrect line of thinking.

A test is considered sensitive when it picks up all, or nearly all positive cases. Frequently, tests with high sensitivity also include some false positives. When this occurs the test is considered sensitive but not specific. A test is considered specific when a positive result is very accurate and can be relied upon for a diagnosis.

For many reasons, which have been discussed elsewhere, it has been shown that the current Lyme ELISA test is not sensitive. In other words it has many false negatives. This is why most physicians who treat a lot of Lyme disease skip the ELISA test and go right to the WB test.

It has been well established that seronegative(no antibodies) Lyme disease exists. One could debate how frequently this occurs, but in my experience it is quite frequent. This knowledge influences the interpretation of WB bands as will be discussed.

The spirochete has a lot of targets for antibody production. Areas on a germ which elicit the production of antibodies are called antigens. Antigenic regions on the bacteria are associated with the production of unique antibodies which target that specific antigenic region of the bacteria. In the WB test these are seen as bands which appear on the blot.

What is CDC positive? People are very confused about this. The CDC criteria for evaluating Lyme WB bands was created in 1994. Its purpose was epidemiological surveillance. It was never intended for use as or validated for use as a diagnostic tool. Those of us who look at Western Blots do our best to interpret the results based on our knowledge of what the bands represent. Since many patients are seronegative, the diagnosis of Lyme may be suggested when very few bands appear.

What is the IgeneX criteria? IgeneX has developed internal criteria which it reports as evidence of exposure to Bb. Basically if a patient shows two specific bands(in the same antibody class) the test is reported as positive.

The most commonly seen band is the 41 band. Most consider it sensitive but feel that it lacks specificity. I think the jury is still out on this one. It is not yet clear to me whether or not the presence of only this band can be used as supporting evidence of exposure to Bb. I don't think there are as many false positives as has been suggested by other authors. Both the CDC and IgeneX consider this band to be quite specific.

There are no standardized criteria for a positive Lyme Western Blot. This means that your doctor many interpret the results quite differently from other doctors. This includes LLMDS.

What we do know is that some of the bands are not very specific for Bb. I, like IgeneX tend to discount non-specific bands when viewing a report. When highly specific bands appear it is unlikely that their presence represents anything other than Bb exposure. Based on this thinking, many doctors may feel comfortable concluding that the test for Lyme is positive if few of these specific markers are identified on the WB test.

The very specific bands include: 93(region) 41,39,34,31 and 23. Some authors include the 18 band.

Whereas IgeneX will only call the test positive if the two specific WB bands are found in the same subclass of antibodies, IgG or IgM, this designation seems arbitrary and is of less importance to me. For example, If a patient has an IgG 93 band and IgM 23 band I feel comfortable that the patient result shows evidence of Lyme exposure.

In fact, the presence of a single, highly specific band(with the exception of the 41 band) may be taken as evidence that the patient has been exposed to Bb - a positive result. Again, it must be emphasized that there are no universally agreed upon criteria for the assessment of a positive or negative WB. Doctors who treat Lyme may all interpret these results through the lens of their own beliefs and experience and report differing conclusions.

The question then(at least regarding WB tests) is not doctor, do I have Lyme?
The question is, doctor is my Lyme test positive. First off, patients frequently ask: am I CDC positive. I then have to go through the process of explaining why this is not important. Ultimately I can only present patients with my interpretation of the results. This can end up being a bit unsatisfactory for the patient. Unfortunately, as is the case with most things "Lyme," answers to questions are frequently fuzzy. In the example given above, the 93 IgG and the 23 IgM are present. I would interpret this as positive result. There is no text or standard resource which patients can use to validate my interpretation. Ultimately it may come down to the doctor - patient relationship, and a patients comfort level with their doctor's interpretation. Patients should be aware of these complexities when requesting results from their doctor.

This is where the art of medicine trumps the science of medicine once more.