This is a one time response.
One of my loyal patients brought in dialogue from a forum called LymeNet. I do not read forums. He was concerned about people disparaging my writing. I told him I was happy that folks were reading my stuff and discussing it. I certainly do not expect people to agree with everything I write. If they disagree with everything it is OK. As a friend of mind is fond of saying: "This is America." I welcome reasonable criticism and am not offended by it in any way. A Blog, unlike a book, is a fluid process. It reveals my thinking in real time. I have changed my mind about many things and I expect this will continue in my ongoing quest for knowledge. I perceive this to be a good thing. Lyme/TBD is a very gray area of medicine. Whereas most physicians prefer dealing with the black and white; I, for some reason, have always been attracted to the gray areas of medicine and other disciplines.
The term "pure culture" Lyme refers to patients thought to have only Lyme. It does not mean that Lyme has been cultured from a patient. I have never cultured Bb from any patient. The best I have accomplished is positive PCRs from synovial fluid and blood.
Please read dog doc's comments. I am not black and white in thinking. The point is that we treat empirically without knowing for sure what we are treating. It is very difficult, if not impossible, to prove that "Bart" patients have Bartonellosis. What we know is that there is a subset of patients who respond better to certain antibiotics. Several co-infections: Bacteria in white blood cells, motile organisms in the blood and a small tumbling organism- resembling a small parasite, have now been seen in TBD patients but remain unknowns. These organisms have been seen through a microscope at 1000 power in whole blood wet mounts by Dr. K., who has extensive experience and training in molecular biology, parasitology and microbiology.
Batonella has, and can be seen in the brain; in a couple of case reports it has proved fatal. But- there are only a few case reports. It is widespread, perhaps the most common tick and vector borne infection found in humans, and it is not generally considered to be highly pathogenic. It is far more likely, in my opinion, that most CNS syndromes in Lyme/TBD patients are do to Bb. AND- most Lyme patients with CNS symptoms respond better to Rocephin than any other drug.
This is not to say that other pathogens or coinfections do not contribute to CNS symptoms. For example, we know that HHV 6 is the most neurotrophic virus in existence. Stratton and Weldon have clearly demonstrated that CPN is a major player in MS. How then does one know with certainty that so called Bart drugs are not really targeting CPN. The point is that there is much we do not know. I think the gate theory may have validity. Lyme may be the gateway germ. It may damage the immune system in such a way that other, heretofore, benign germs, become opportunistically pathogenic. If this is the case, then the treatment of Lyme alone may frequently put these other germs back in their box.
LymeMD is just a blog. If I say controversial things it is to get people thinking; obviously that is the case. Tons of microorganisms can cross the blood brain barrier: bacteria, viruses, protozoa, fungi and who knows what else. For the most part, these are infrequent occurrences (I think). In patients with Lyme disease/neuroborrelis, Bb is generally assumed to be the culprit until proven otherwise. Admittedly, in patients with profound sweating I consider Babesia or a Babesia like organism to be a major factor. I prefer to treat for this after some Lyme therapy; I have found this approach to be more effective.
I do not rely entirely on lab tests despite rumors to the contrary. Many patients treated even with IV antibiotics are seronegative. That includes Babesia as well.
Biofilms are of unknown significance. This is not a specific feature of infection with Bb. Nearly all bacteria can form biofilms. The formation of biofilms has been best described with regards to oral cavity bacteria. These bacteria usually do not cause clinical disease unless the biofilms are disrupted by active inflammation.
The successful treatment of patients with TBD frequently requires patience and trial and error. There is no one "miracle" drug that works for everyone. I wish there was.
Some patients respond best to: Rocephin, Biaxin, Plaquenil, Doxycyline, Minocycline, Cipro/Levaquin, Rifampin, Zithromax, Cleocin, Mepron, Malarone, Amoicillin, Amoxicillin at a high dose with or without Benemid, Omnicef with or without Benemid, Ceftin, Flagyl, Tindamax and others, this is just off the top of my head. At least one patient had a spectacular response to Ivanz.
Experience? I have treated an average of 50 patients with tick borne illness per week for the past 3 years. I schedule face time with patients, 60 hours per week. As of late, I typically see 75 Lyme patients per week. Patients are referred to me on a regular basis by other well known LLMDS, especially the sickest ones. I treat several physicians and their families.
I do not claim to have the experience of Jones or Burrascano. But I am constantly in a learning and thinking mode.
Politically the focus should be on Lyme. This is where the best scientific evidence exists. People in "Lyme land" should not loose sight of this. If the politics do not change LLMDS will become a threatened species.
I am saying that LLMDS should not work within a rigid box. The correct paradigm is far from established. As noted, Dr. Burrascano has frequently changed his opinion and emphasis.
My words should never be construed as authoritative. That has never been my intent or claim. But at least I am putting food for thought on the table.
I starting writing this Blog for personal reasons. I am not computer or internet savvy. I hope this has helped straighten out some confusion generated by my comments.
Many voices on the forum sound very angry, perhaps rightfully so. However I would suggest that a more sanguine, and perhaps unified approach, would be more helpful in effecting the political change that we all desperately need.
PS: I never suggested that Rocephin kills Bartonella. Rather, I suggested that many patients diagnosed with Bartonella based strictly on clinical grounds get better with Rocephin. The implication here is that the described syndrome was the result of Bb infection, not Bart. One can conjure up many other explanations. Sometimes my comments are misunderstood and/or taken out of context.
Friday, February 27, 2009
Thursday, February 26, 2009
Ignorance is no excuse!
A troubled 43 year old woman sat across from me yesterday. She told me I was her last hope. I hate it when patients say that. She had obvious memory problems and struggled to get out her words. Sitting across from me she evinced strange, periodic jerking spasms and movements of her four limbs in a random fashion. She told me her story.
She had been well until October 2007. She lived in Southern Maryland and has spent a lot of time outdoors. It started with pains involving multiple joints, especially from the waist down. Then came the brain symptoms, hard and fast. In short order she became forgetful and confused. She continues to have trouble speaking and loosing things as her memory deteriorates. A local physician found positive tests for Lyme and Ehrlichia. She was treated with 30 days of Rocephin followed by two months of Doxycyline. She started to get better on the Rocephin but all the symptoms quickly returned when the meds were discontinued.
By August 2008 she was sicker than ever. Repeat blood work showed that the IgG Ehrlichia titer was higher. And now she tested positive for Bartonella.
Her physician prescribed Levaquin for 3 weeks and 3 months of Bicillin. Once again, she was just starting to feel better when the treatment was stopped and her symptoms returned.
Over the past 5 weeks things have taken a turn for the worst. Withing the past two weeks she has seen two infectious disease physicians. One said the patient does not have Lyme and the other said he did not know how to treat Bartonella. In the meantime she has been referred to a neurologist. She has developed progressive myoclonus- muscle jerking and increased generalized pain. Her blood pressure became dangerously high with erratic swings both up and down. She has had episodes of SVT- rapid heart beat. Her sense of balance has become diminished and she has fallen several time.
Specifically, she has had no skin nodules, stretch marks, depression, anxiety, foot pain or "depersonalization." These are signs and symptoms in LLMD literature associated with Bartonella.
She has recently lost her job, working for a group of cardiologists.
She is totally disabled.
She does admit to episodes of chills and sweats.
Her exam shows an elevated blood pressure. Her mental status is abnormal. She is forgetful with some aphasia. She had the jerking myoclonic movements as described. Sensations are abnormal, notably she has absent vibratory sense in the left foot. There is poor finger to nose accuracy or speed. The Romberg test shows her falling to the right.
Current labs: Lyme WB IgM positive 23 and 41 bands, Ehrichia chaffeenis IgG 1:1024,
Bartonella henselae IgG 1:320.
This woman clearly has three tick borne infections: Lyme, Ehrlichia and Bartonella.
Clinically, she may also have Babesia. She is very ill- an understatement.
The classic signs and symptoms attributed to Bartonella and/or BLO are absent. Bartonella is a small intracellular bacteria which may at times cause brain and central nervous system disorders. How often this occurs is unknown. Bartonella is commonly seen in the homeless, HIV- immunsuppresed patients and younger patients. Classically B. henselae has been associated with cat scratch fever, enlarged lymph nodes and "occuloglandular syndrome." There are isolated reports of meningitis and encephalitis in the medical literature.
My assumption is that the majority of her symptoms are due to Lyme rather than Bartonella. Her previous response to Rocephin and Pencillin seems to support this hypothesis. She was just started on Doxycyline, 100mg twice daily before seeing me. I recommended that she increase the dose to two capsules twice daily,
The first order of business is placing a PIC and restarting Rocephin.
Ehrlichia can be a tricky business. In is also intracellular and resides in white blood cells. Such bacteria can be notoriously difficult to eradicate.
After the initial expected "herx" the next step would be to add Rifampin. The combination of Doxy and Rifampin seems to be quite effective against Ehrlicia.
Many proponents have suggested that Rifampin is also effective against Bartonella.
It is not clear which antibiotics are most effective against Bartonella. Different drugs may be more effective depending on the particular species being treated.
Standard literature claims that Zithromax and Doxy are effective.
LLMD literature claims that Levaquin, Bactrim and Rifampin are effective. I have not seen any scientific evidence to support the efficacy of these particular agents. Based on my knowledge of microbiology, I would expect Levaquin and perhaps Rifampin to be effective.
The use of Bactrim by many LLMDS has confused me. Anecdotally, LLMDS report that it is effective against BLO. I am not sure what BLO is.
After a little research I considered the following possibility. Sulfa drugs like Bactrim have been shown to have some activity against Malaria. Rather than treating Bartonella or Lyme, I wonder if these drugs have activity against Babesia species.
Perhaps in cases where the response to Mepron or Malarone is poor or sluggish, the addition of Bactrim may provide some additional benefits.
The chills and sweats certainly suggest the possibility of a Babesia species. Alternatively, Ehrlichia can cause similar symptoms. We shall see.
This patient has been kicked around by a system which can offer her no help. To make matters worse, the system denies the existence of here illness.
For some reason, this patient in particular, has hardened my resolve to continue treating patients with Lyme and TBD. I am confident that with proper treatment she will have a full recovery. Many such patients are critically ill with a disease which remains unknown to all but a few practicing physicians. Without correct treatment, she and numerous others like her would certainly face progressive disability and/or death.
She had been well until October 2007. She lived in Southern Maryland and has spent a lot of time outdoors. It started with pains involving multiple joints, especially from the waist down. Then came the brain symptoms, hard and fast. In short order she became forgetful and confused. She continues to have trouble speaking and loosing things as her memory deteriorates. A local physician found positive tests for Lyme and Ehrlichia. She was treated with 30 days of Rocephin followed by two months of Doxycyline. She started to get better on the Rocephin but all the symptoms quickly returned when the meds were discontinued.
By August 2008 she was sicker than ever. Repeat blood work showed that the IgG Ehrlichia titer was higher. And now she tested positive for Bartonella.
Her physician prescribed Levaquin for 3 weeks and 3 months of Bicillin. Once again, she was just starting to feel better when the treatment was stopped and her symptoms returned.
Over the past 5 weeks things have taken a turn for the worst. Withing the past two weeks she has seen two infectious disease physicians. One said the patient does not have Lyme and the other said he did not know how to treat Bartonella. In the meantime she has been referred to a neurologist. She has developed progressive myoclonus- muscle jerking and increased generalized pain. Her blood pressure became dangerously high with erratic swings both up and down. She has had episodes of SVT- rapid heart beat. Her sense of balance has become diminished and she has fallen several time.
Specifically, she has had no skin nodules, stretch marks, depression, anxiety, foot pain or "depersonalization." These are signs and symptoms in LLMD literature associated with Bartonella.
She has recently lost her job, working for a group of cardiologists.
She is totally disabled.
She does admit to episodes of chills and sweats.
Her exam shows an elevated blood pressure. Her mental status is abnormal. She is forgetful with some aphasia. She had the jerking myoclonic movements as described. Sensations are abnormal, notably she has absent vibratory sense in the left foot. There is poor finger to nose accuracy or speed. The Romberg test shows her falling to the right.
Current labs: Lyme WB IgM positive 23 and 41 bands, Ehrichia chaffeenis IgG 1:1024,
Bartonella henselae IgG 1:320.
This woman clearly has three tick borne infections: Lyme, Ehrlichia and Bartonella.
Clinically, she may also have Babesia. She is very ill- an understatement.
The classic signs and symptoms attributed to Bartonella and/or BLO are absent. Bartonella is a small intracellular bacteria which may at times cause brain and central nervous system disorders. How often this occurs is unknown. Bartonella is commonly seen in the homeless, HIV- immunsuppresed patients and younger patients. Classically B. henselae has been associated with cat scratch fever, enlarged lymph nodes and "occuloglandular syndrome." There are isolated reports of meningitis and encephalitis in the medical literature.
My assumption is that the majority of her symptoms are due to Lyme rather than Bartonella. Her previous response to Rocephin and Pencillin seems to support this hypothesis. She was just started on Doxycyline, 100mg twice daily before seeing me. I recommended that she increase the dose to two capsules twice daily,
The first order of business is placing a PIC and restarting Rocephin.
Ehrlichia can be a tricky business. In is also intracellular and resides in white blood cells. Such bacteria can be notoriously difficult to eradicate.
After the initial expected "herx" the next step would be to add Rifampin. The combination of Doxy and Rifampin seems to be quite effective against Ehrlicia.
Many proponents have suggested that Rifampin is also effective against Bartonella.
It is not clear which antibiotics are most effective against Bartonella. Different drugs may be more effective depending on the particular species being treated.
Standard literature claims that Zithromax and Doxy are effective.
LLMD literature claims that Levaquin, Bactrim and Rifampin are effective. I have not seen any scientific evidence to support the efficacy of these particular agents. Based on my knowledge of microbiology, I would expect Levaquin and perhaps Rifampin to be effective.
The use of Bactrim by many LLMDS has confused me. Anecdotally, LLMDS report that it is effective against BLO. I am not sure what BLO is.
After a little research I considered the following possibility. Sulfa drugs like Bactrim have been shown to have some activity against Malaria. Rather than treating Bartonella or Lyme, I wonder if these drugs have activity against Babesia species.
Perhaps in cases where the response to Mepron or Malarone is poor or sluggish, the addition of Bactrim may provide some additional benefits.
The chills and sweats certainly suggest the possibility of a Babesia species. Alternatively, Ehrlichia can cause similar symptoms. We shall see.
This patient has been kicked around by a system which can offer her no help. To make matters worse, the system denies the existence of here illness.
For some reason, this patient in particular, has hardened my resolve to continue treating patients with Lyme and TBD. I am confident that with proper treatment she will have a full recovery. Many such patients are critically ill with a disease which remains unknown to all but a few practicing physicians. Without correct treatment, she and numerous others like her would certainly face progressive disability and/or death.
Tuesday, February 24, 2009
Guerrilla antibiotics
A 35 year old Vietnamese gentleman was well until September, 2008. At that time he developed burning sensations in his upper extremities. He developed a chronic sore throat. Muscle and joint pains started coming and going in a diffuse distribution. He developed fatigue with some brain fog, then intermittent night sweats. Additionally he has experienced dyspnea- shortness of breath at night and occasional palpitations. There has been progressive weakness affecting both arms and the left leg. The pains, especially around his shoulders and neck have been disabling at times.
He went to his primary care physician who ran a plethora of tests. Finally a Lyme test was done. It was positive. He was referred to ID.
He saw the Nurse Practitioner. She prescribed Doxycyline for 3 weeks. After two weeks he developed a rash on his face. The Doxy was stopped and he was given Amoxil for an additional 3 weeks. Even though symptoms persisted the NP would prescribe no further antibiotics.
He went to a neurologist who found nothing amiss.
I saw him today for the first time. I examined him.
He had obvious weakness of the left arm. His deep tendon reflexes were asymmetrical, increased in the left versus right upper extremity. An obvious decrease of sensation to pin prick in a stocking/glove pattern was present.
He has lived in this country for 25 years but his accent is a bit thick.
I wanted to get a clear history about his use of antibiotics. He told me the Amoxil had been prescribed at a dose of 500 mg 3X daily. I asked if he only took it for the three weeks? He was quiet for a moment as if he were trying to size me up. Quietly, sheepishly, he confided: He had been taking Amoxil from Vietnam- continuously.
Not trusting or believing in his health care providers, this patient like many others went underground to acquire antibiotics. These are the guerrilla warfare tactics of Lyme disease I allude to in the title of the post.
He recently visited the ID again. He showed me those labs. The ELISA was positive at 1.3. The IgM was positive with 23 and 41 bands. The IgG showed 23 and 66 bands. This of course is "CDC positive" and according to the CDC model indicates acute infection. The possibility of another bite, a new infection and co-infection was apparently not considered.
The Lyme disease is gone quipped the nurse practitioner. The patient was sent on his way.
He was worried that the self prescribed Amoxil had caused harm, that perhaps it had made his germs resistant.
I told him that this was unlikely. Rather, he had been under treated.
I thought: "Underground for antibiotics: A sad state of affairs."
He went to his primary care physician who ran a plethora of tests. Finally a Lyme test was done. It was positive. He was referred to ID.
He saw the Nurse Practitioner. She prescribed Doxycyline for 3 weeks. After two weeks he developed a rash on his face. The Doxy was stopped and he was given Amoxil for an additional 3 weeks. Even though symptoms persisted the NP would prescribe no further antibiotics.
He went to a neurologist who found nothing amiss.
I saw him today for the first time. I examined him.
He had obvious weakness of the left arm. His deep tendon reflexes were asymmetrical, increased in the left versus right upper extremity. An obvious decrease of sensation to pin prick in a stocking/glove pattern was present.
He has lived in this country for 25 years but his accent is a bit thick.
I wanted to get a clear history about his use of antibiotics. He told me the Amoxil had been prescribed at a dose of 500 mg 3X daily. I asked if he only took it for the three weeks? He was quiet for a moment as if he were trying to size me up. Quietly, sheepishly, he confided: He had been taking Amoxil from Vietnam- continuously.
Not trusting or believing in his health care providers, this patient like many others went underground to acquire antibiotics. These are the guerrilla warfare tactics of Lyme disease I allude to in the title of the post.
He recently visited the ID again. He showed me those labs. The ELISA was positive at 1.3. The IgM was positive with 23 and 41 bands. The IgG showed 23 and 66 bands. This of course is "CDC positive" and according to the CDC model indicates acute infection. The possibility of another bite, a new infection and co-infection was apparently not considered.
The Lyme disease is gone quipped the nurse practitioner. The patient was sent on his way.
He was worried that the self prescribed Amoxil had caused harm, that perhaps it had made his germs resistant.
I told him that this was unlikely. Rather, he had been under treated.
I thought: "Underground for antibiotics: A sad state of affairs."
Monday, February 23, 2009
Today- I cried
It is a busy morning. Running behind- a grabbed the next chart and headed for the exam room. The encounter sheet noted- new patient, "LYME." I entered the room and immediately noticed three people. There was a healthy appearing middle aged man, a healthy looking somewhat younger woman and a very elderly and sick appearing woman in a wheel chair.
"So who is the patient?" I inquired, secretly hoping it was not the lady in the wheel chair; but I knew otherwise.
I looked at my new patient. She looked ancient, weary and barely alive. She was incredibly thin, skin hanging on bones with a few strands of muscle. She couldn't speak or move. Her head fell to her chest; she was only able to keep her head in an upright position with help from the other woman, her caregiver. And yet, she managed a smile. I looked again at her virgin chart. She was 51 years only; the youthful gentleman was her husband.
"Well, I stammered, let me hear your story."
Her husband had only a thin folder with a few sheaves of paper. There was a clear history of tick bites. Her hair dresser once found a small tick embedded in her scalp. She had been an active outdoor person with dogs and horses.
And she had been perfectly well until some time in 2005.
They were country people. Her husband, a blue collar worker, was not the greatest historian; He told me what he could remember. It started with weakness in the right leg. A foot drop developed. The weakness spread to the other lower extremity associated with severe stiffness. Her condition gradually worsened, the weakness and stiffness spread and now affected her entire body. She had incapacitating anxiety and profound fatigue. Her speech became garbled, progressively, over the past year and one half. She was wheel chair bound for the last year and a half. Severe dysphagia- trouble swallowing, led to her dramatic weight loss. She was continent and maintained mental clarity, I was told.
In April 2006 she went to the Hershey Medical Center. She was told she had ALS. Nothing more was offered.
In July 2006, a friend suggested a Lyme test. It was positive. Her husband showed me an IgeneX IgM report, the IgG was missing. It showed positive bands in the 23,31,34,40 and 93 positions. It was noted to be CDC positive.
They live in rural Pennsylvania. No LLMDS there. They found a local doctor who tried to help. He ordered IV Rocephin for 3 months. She improved! Her strength steadily improved. Then, the Rocephin was stopped and she resumed the inexorable down hill slide. She was on oral Doxy and getting worse.
I examined her in her chair. I could not weigh her. She appeared moribund. She was unable to speak. I noted fasiculations in her arms. Her extremities were weak although she could move her arms some. The arms were loose with normal tone. Her legs were extremely stiff with lead pipe immobility. Her reflexes were normal. Sensation was hard to test.
ALS was high on the list of differential diagnoses. The textbooks list Lyme disease as a cause motor neuron disease- ALS; no one was paying any attention. why? If she got better with Rocephin why wasn't it continued? This seems like common sense. No?
Other diagnoses crossed my mind: Anxiety and stiffness.It could be an autoimmune disorder called Stiff Person's syndrome. Then I wondered if she had a primary muscle disorder. I ordered some tests and a consultation with a neurologists expert in muscle disorders. ALS was likely. But damn it- Lyme is known to cause it! And- she had started to respond to treatment; then the rug was yanked from under her.
The woman looked deathly ill. There was not much left to work with. I wished she had seen me or someone else a year ago.
I was afraid. I was afraid to treat her, but even more afraid to not treat her.
I ordered a PIC and Rocephin, with much trepidation, knowing that treatment can at times accelerate the progression of Lyme/ALS.
A profound wave of sadness came over me. I quietly shed a tear for this poor woman.
Then I became angry, as I considered the absurd politics of this disease.
But there were more patients to see; I went into the next exam room.
"So who is the patient?" I inquired, secretly hoping it was not the lady in the wheel chair; but I knew otherwise.
I looked at my new patient. She looked ancient, weary and barely alive. She was incredibly thin, skin hanging on bones with a few strands of muscle. She couldn't speak or move. Her head fell to her chest; she was only able to keep her head in an upright position with help from the other woman, her caregiver. And yet, she managed a smile. I looked again at her virgin chart. She was 51 years only; the youthful gentleman was her husband.
"Well, I stammered, let me hear your story."
Her husband had only a thin folder with a few sheaves of paper. There was a clear history of tick bites. Her hair dresser once found a small tick embedded in her scalp. She had been an active outdoor person with dogs and horses.
And she had been perfectly well until some time in 2005.
They were country people. Her husband, a blue collar worker, was not the greatest historian; He told me what he could remember. It started with weakness in the right leg. A foot drop developed. The weakness spread to the other lower extremity associated with severe stiffness. Her condition gradually worsened, the weakness and stiffness spread and now affected her entire body. She had incapacitating anxiety and profound fatigue. Her speech became garbled, progressively, over the past year and one half. She was wheel chair bound for the last year and a half. Severe dysphagia- trouble swallowing, led to her dramatic weight loss. She was continent and maintained mental clarity, I was told.
In April 2006 she went to the Hershey Medical Center. She was told she had ALS. Nothing more was offered.
In July 2006, a friend suggested a Lyme test. It was positive. Her husband showed me an IgeneX IgM report, the IgG was missing. It showed positive bands in the 23,31,34,40 and 93 positions. It was noted to be CDC positive.
They live in rural Pennsylvania. No LLMDS there. They found a local doctor who tried to help. He ordered IV Rocephin for 3 months. She improved! Her strength steadily improved. Then, the Rocephin was stopped and she resumed the inexorable down hill slide. She was on oral Doxy and getting worse.
I examined her in her chair. I could not weigh her. She appeared moribund. She was unable to speak. I noted fasiculations in her arms. Her extremities were weak although she could move her arms some. The arms were loose with normal tone. Her legs were extremely stiff with lead pipe immobility. Her reflexes were normal. Sensation was hard to test.
ALS was high on the list of differential diagnoses. The textbooks list Lyme disease as a cause motor neuron disease- ALS; no one was paying any attention. why? If she got better with Rocephin why wasn't it continued? This seems like common sense. No?
Other diagnoses crossed my mind: Anxiety and stiffness.It could be an autoimmune disorder called Stiff Person's syndrome. Then I wondered if she had a primary muscle disorder. I ordered some tests and a consultation with a neurologists expert in muscle disorders. ALS was likely. But damn it- Lyme is known to cause it! And- she had started to respond to treatment; then the rug was yanked from under her.
The woman looked deathly ill. There was not much left to work with. I wished she had seen me or someone else a year ago.
I was afraid. I was afraid to treat her, but even more afraid to not treat her.
I ordered a PIC and Rocephin, with much trepidation, knowing that treatment can at times accelerate the progression of Lyme/ALS.
A profound wave of sadness came over me. I quietly shed a tear for this poor woman.
Then I became angry, as I considered the absurd politics of this disease.
But there were more patients to see; I went into the next exam room.
Thursday, February 19, 2009
Under the train
The post entitled "Routine Physical," is the essence of my quandary. I have been clearly instructed from legal quarters: DON'T DO LYME- JUST DO REGULAR FAMILY MEDICINE. How do I do that? To paraphrase Plato: Once you have seen the light it is impossible to return to the cave. The old me, the pre-Lyme me, would have thought: "Of course he has brain fog, he abuses alcohol and marijuana, what does he expect." "Depression- sure- common, connected to substance abuse." Aches and pains- It is just a somatic manifestation of his depression and other issues." He would have been treated with Prozac and Motrin; and sent for extensive substance abuse counseling and rehab, for which he would have likely been non compliant. He would likely have never returned to my office and been "lost to follow up." This is the world I am told I must to go back to. For God's sake, this patient had 12 of 13 standard bands positive on a Lyme Western Blot WHICH I OTHERWISE WOULD NOT HAVE ORDERED. NOW HIS ENTIRE LIFE HAS BEEN TURNED AROUND BECAUSE HE HAS BEEN TREATED FOR THIS NON EXISTENT LYME DISEASE!
The Lyme community is busy spitting hairs while the system prepares to throw yet another LLMD under the train- AND then how many more?. Folks if this is important, and of course it is, PLEASE unite over the big issues. News Flash: A single payer system utilizing "Evidence Based Medicine" will be a disaster for the Lyme community if the ILASDS guidelines are not put into the mainstream. This will only happen through political change.
I started this blog for personal reasons. It was a therapeutic way of venting my frustrations. I began writing about odds and ends, patient stories and my understanding of the science as it has evolved. Perhaps the Blog took on a life I had not considered. Often I say things that challenge the status quo and force people to think. That is the point. We are all learning. It is a work in progress.
The debated about CAM must come to an end- at least here. That is another battle for another day which should be fought somewhere else. Yesterday, a patient with neuro- degenerative disease asked me if IV glutathione would be of help. I told him I didn't know but that perhaps he should explore this avenue. I certainly had nothing to offer from my bag of tricks.
I personally am not CAM. I was trained as an allopathic physician and that is the model within which I practice. Unfortunately or not, depending upon your point of view, a mainstream acceptance of chronic Lyme can only come from an allopathic perspective. In terms of the pecking order of "the system," CAM physicians are at the lowest rung on the totem pole.
I DO NOT DISPARAGE CAM PRACTITIONERS. They frequently are very valuable. I think it would be an insult to well trained CAM doctors if a physician like myself were to casually enter into the fray. These physicians, many of whom are quite accomplished, have spent many years honing their trade. Patients should make informed choices and discover what works for them.
Medicine sometimes seem like a religion. Perhaps in many ways it is. To the extent it is possible, Lyme medicine must be fact driven if we are to win this war. The discussion should not be: "So you don't believe in Bartonella." Rather the discussion should be" "The Bartonella hypothesis is interesting, what evidence do we have to support it?"
Having given this a great deal of thought, if I were to be told by a governing body of physicians, as may happen in the near future, that I have to follow the IDSA guidelines, then I could no longer in good faith be able to practice the medicine that I love. I couldn't live with myself if I were compelled to throw this young man described in the vignette above "under the train." I already have enough trouble sleeping some nights.
The Lyme community is busy spitting hairs while the system prepares to throw yet another LLMD under the train- AND then how many more?. Folks if this is important, and of course it is, PLEASE unite over the big issues. News Flash: A single payer system utilizing "Evidence Based Medicine" will be a disaster for the Lyme community if the ILASDS guidelines are not put into the mainstream. This will only happen through political change.
I started this blog for personal reasons. It was a therapeutic way of venting my frustrations. I began writing about odds and ends, patient stories and my understanding of the science as it has evolved. Perhaps the Blog took on a life I had not considered. Often I say things that challenge the status quo and force people to think. That is the point. We are all learning. It is a work in progress.
The debated about CAM must come to an end- at least here. That is another battle for another day which should be fought somewhere else. Yesterday, a patient with neuro- degenerative disease asked me if IV glutathione would be of help. I told him I didn't know but that perhaps he should explore this avenue. I certainly had nothing to offer from my bag of tricks.
I personally am not CAM. I was trained as an allopathic physician and that is the model within which I practice. Unfortunately or not, depending upon your point of view, a mainstream acceptance of chronic Lyme can only come from an allopathic perspective. In terms of the pecking order of "the system," CAM physicians are at the lowest rung on the totem pole.
I DO NOT DISPARAGE CAM PRACTITIONERS. They frequently are very valuable. I think it would be an insult to well trained CAM doctors if a physician like myself were to casually enter into the fray. These physicians, many of whom are quite accomplished, have spent many years honing their trade. Patients should make informed choices and discover what works for them.
Medicine sometimes seem like a religion. Perhaps in many ways it is. To the extent it is possible, Lyme medicine must be fact driven if we are to win this war. The discussion should not be: "So you don't believe in Bartonella." Rather the discussion should be" "The Bartonella hypothesis is interesting, what evidence do we have to support it?"
Having given this a great deal of thought, if I were to be told by a governing body of physicians, as may happen in the near future, that I have to follow the IDSA guidelines, then I could no longer in good faith be able to practice the medicine that I love. I couldn't live with myself if I were compelled to throw this young man described in the vignette above "under the train." I already have enough trouble sleeping some nights.
Wednesday, February 18, 2009
Another case: A somewhat different description of what transpired
A 30 year old female was first seen about 15 months ago. She believed she had been exposed to Lyme disease on a Maryland farm. She had a year of progressive symptoms before our first visit. She developed: joint pain, muscle pain, memory loss, numbness and tingling and sweats. She had been a patient at Kaiser and had previously tested negative for Lyme twice. Labcorp found 41 bands in the IgM and IgG positions. She was treated with: Amoxicillin, Biaxin and Plaquenil. After three months low dose Flagyl was added. An IgeneX test showed the dramatic IgM response with 11/14 bands positive after three months of treatment. Over time, her antibiotics were modified. Amoxicillin and Biaxin were changed to Ceftin and Doxycyline. She had a quick positive response to treatment, but her symptoms waxed an waned over a period of months despite continuous antibiotic therapy. After one year she reported about a 70% overall improvement. At that point Zithromax and Rifampin were used in place of the Doxyclyine. The Ceftin was continued. She showed some incremental improvement. About three months ago it was decided to target the Babesia syndrome. She was placed on Malarone and a low dose of Clindamycin.
Things quickly turned around. At our last visit, one week ago she was almost 100% improved. This is a very grateful patient who feel she might have become disabled without the help I provided for her.
Points: I think the Rifampin was of some help. I don't know why. The current model would suggest it was more active against a Bartonella organism. I would not make this claim.
The Malarone and Clindamyin was effective. The current model would suggest this treatment was active against a persistent form of Babesia. This is theory. There is no laboratory evidence to confirm this. It has been pointed out that Malaron and Mepron may also have activity against cystic forms of Lyme. There are other potential explanations for the efficacy of this therapy. Of course, she may indeed have had chronic Babesiosis. I have found, in my practice, that Malarone works just as well as Mepron. It is more palatable and much more cost effective. I do not push the dose beyond two tablets per day. I have found that the timing of its application is the critical factor. It is more effective after a prolonged course of more typical Lyme therapy. The addition of Artemesin may have some additional benefits, but I not yet convinced of this.
I believe the presence of a WB 31 band is good evidence that the disease was longstanding. It does not matter if it presents as an IgM or IgG band.
Things quickly turned around. At our last visit, one week ago she was almost 100% improved. This is a very grateful patient who feel she might have become disabled without the help I provided for her.
Points: I think the Rifampin was of some help. I don't know why. The current model would suggest it was more active against a Bartonella organism. I would not make this claim.
The Malarone and Clindamyin was effective. The current model would suggest this treatment was active against a persistent form of Babesia. This is theory. There is no laboratory evidence to confirm this. It has been pointed out that Malaron and Mepron may also have activity against cystic forms of Lyme. There are other potential explanations for the efficacy of this therapy. Of course, she may indeed have had chronic Babesiosis. I have found, in my practice, that Malarone works just as well as Mepron. It is more palatable and much more cost effective. I do not push the dose beyond two tablets per day. I have found that the timing of its application is the critical factor. It is more effective after a prolonged course of more typical Lyme therapy. The addition of Artemesin may have some additional benefits, but I not yet convinced of this.
I believe the presence of a WB 31 band is good evidence that the disease was longstanding. It does not matter if it presents as an IgM or IgG band.
Routine physical
A 22 year old man, a new patient, scheduled an appointment for a physical, a general check up. This was supposed to be a health maintenance exam. I asked a series of questions and kept uncovering positive responses. He had suffered with fatigue, depression and anxiety for several years. He also complained of memory loss which he attributed to marijuana use. I further elicited complaints of joint pain and night sweats. Then it was uncovered that he in fact had a history of tick bite and rash 6 years previous to our encounter which had been treated with Doxycyline.(He didn't complete the course). He admittedly abused alcohol and tobacco, in addition to marijuana. There was a positive family history of anxiety and depression.
His physical exam showed multiple neurological abnormalities, including a positive Babinsky sign in addition to the usual changes in sensation.
His labs were impressive. All 10 IgG Lyme WB bands were present. Two IgM bands, 23 and 41 were present.
After only 2 weeks of therapy with Minocin and Biaxin his improvement has been astounding. The joint pain is better- almost gone. His energy is better, the fatigue almost gone. His memory has improved and the sweats are gone. His depression and anxiety are also markedly improved. He has stopped drinking and cut down his use of marijuana to a minimum. He continues to smoke cigarettes.
Perhaps, he has responded so quickly because of his youth. There is another possibility. Perhaps his dramatic IgG response is a marker for an improved immune response.
One thing is clear. The presence of IgG antibodies does not mean that he is clear of Lyme, as has been suggested by some. The diagnosis rests of an assessment of symptoms and signs.
Furthermore, the same would be said in the event that IgM bands were completely absent as well.
His physical exam showed multiple neurological abnormalities, including a positive Babinsky sign in addition to the usual changes in sensation.
His labs were impressive. All 10 IgG Lyme WB bands were present. Two IgM bands, 23 and 41 were present.
After only 2 weeks of therapy with Minocin and Biaxin his improvement has been astounding. The joint pain is better- almost gone. His energy is better, the fatigue almost gone. His memory has improved and the sweats are gone. His depression and anxiety are also markedly improved. He has stopped drinking and cut down his use of marijuana to a minimum. He continues to smoke cigarettes.
Perhaps, he has responded so quickly because of his youth. There is another possibility. Perhaps his dramatic IgG response is a marker for an improved immune response.
One thing is clear. The presence of IgG antibodies does not mean that he is clear of Lyme, as has been suggested by some. The diagnosis rests of an assessment of symptoms and signs.
Furthermore, the same would be said in the event that IgM bands were completely absent as well.
Tuesday, February 17, 2009
Lyme disease, coinfections and its discontents
We are having a hard enough time convincing the mainstream of medicine that persistent Lyme infection exists. I am concerned that some ILADS physicians have adopted questionable and unsubstantiated approaches regarding the diagnosis and treatment of purported co-infections. There are a lot of test for Lyme. There is well documented seronegative disease. OK- we are on fairly solid footing here. I am afraid some LLMDS sometimes conjure up diagnoses out of whole cloth- based on my observations. For example, a patient may report neuropsychiatric symptoms; AND without further ado, the physician may then proclaim the patient has "Bart." (Bartonella). These patients usually have negative serology, negative blood smears and negative PCRs for all the known strains of Bartonella; yet, the physician will make the diagnosis with a sense of absolute certainty. The facts do not support this conclusion. There is no evidence that BLO- Bartonella like organisms exists. Therapy then, is directed against these clinically diagnosed "Bartonella." Perhaps drugs like Levaquin- Rifampin- Zithromax and Minocin work for these patients because of their excellent penetration into the central nervous system, past the blood brain barrier. They are all effective against Borrelia burdorferi- Lyme. More often than not we don't REALLY know what we are treating. Patients with established Lyme disease respond differently to different antibiotics and different antibiotic combinations.
Chronic Lyme disease, or Lyme Borreliosis Complex if you prefer, is a complex multi-system disease with protean manifestations. The illness may frequently be associated with a polymicrobial mix of other pathogens. But much of this is very speculative at this time. For example, patients with severe episodes of sweating- considered the sin qua non of Babesiosis by many Lyme experts, frequently get better with only Lyme antibiotics. And- patients with positive Babesia antibodies may show no signs of the illness and get better without specific therapy.
Frequently the treatment of Lyme and its associated co-infections is based on empirical grounds, trial and error. Patients may respond to a wide range of therapeutic options, frequently in unexpected ways. Patients may indeed have a mix of pathogens contributing to the disease state. These may include: Mycoplasmas, Chlamydia pneumonia, Ehrlichia, Babesia, viral infections and many as of yet, unidentified pathogens, in addition to the known co-infections. For example, Clongen labs has identified an organism frequently found in the blood stream of patients afflicted with tick borne illness. It looks like a small bacteria but no DNA match can be found. Research into the nature of this organism is still ongoing. Clongen has twice reported bacteria inside white blood cells which resemble Ehrlichia. However, all standard tests, serological and PCR for known variants of Ehrlichia and Anaplasmosis have been negative. I don't know what this bug is. An unusual species of Rickettsia has been found in a high percentage of Maryland Ixodes ticks. The significance of this microbe has not been determined.
Rather than labeling patients with: Lyme- Babesia and Bartonella, perhaps it would be best to describe the individual clinical responses seen in each patient. For example, patient A has a syndrome which is responsive to Rifampin.
Why is this important. It is beyond important: It is critical.
A narrow ILADS paradigm or box, can ironically begin to resemble more and more the sort of narrow paradigm or box utilized by the IDSA, of which we are so critical. The IDSA box in my opinion is wrong, but it is fact based. If ILADS is to successfully spar against the IDSA it needs to marshal arguments which are clear, cogent and fact based. LLMDS are for the most part community primary care physicians. The opponents have all the resources of medical academia at their disposal. The fight is lopsided at the outset.
And I am very concerned that the LLMD box may have already disenfranchised some of the most critical players in the Lyme versus IDSA debate. The academic support for the chronic Lyme cause has come from Fallon and Donta. If they don't buy into the significance of the co-infection hypothesis, this should not be seen as a negative. Rather, it is a positive. They are academic in their approach. If they are going to give their stamp of approval on something there has to exist a significant body of evidence to support that thing.
As the two sides of the debate hunker down and prepare for battle, with medical licenses on the line and the future ability of Lyme patients to have access to any LLMDS, the lines must be clearly drawn. It must be a fight about whether or not Lyme organisms persist in the body and cause chronic illness in patients necessitating the use of long term antibiotics.
PERIOD.
Additional point: It has come to my attention that some advocacy groups within the Lyme community have been over zealous. Changes need to be incremental. If groups insist that every thing change at once this will continue to have disastrous effects on efforts for political reform. Sometimes well meaning individuals can become their own worst enemies.
Chronic Lyme disease, or Lyme Borreliosis Complex if you prefer, is a complex multi-system disease with protean manifestations. The illness may frequently be associated with a polymicrobial mix of other pathogens. But much of this is very speculative at this time. For example, patients with severe episodes of sweating- considered the sin qua non of Babesiosis by many Lyme experts, frequently get better with only Lyme antibiotics. And- patients with positive Babesia antibodies may show no signs of the illness and get better without specific therapy.
Frequently the treatment of Lyme and its associated co-infections is based on empirical grounds, trial and error. Patients may respond to a wide range of therapeutic options, frequently in unexpected ways. Patients may indeed have a mix of pathogens contributing to the disease state. These may include: Mycoplasmas, Chlamydia pneumonia, Ehrlichia, Babesia, viral infections and many as of yet, unidentified pathogens, in addition to the known co-infections. For example, Clongen labs has identified an organism frequently found in the blood stream of patients afflicted with tick borne illness. It looks like a small bacteria but no DNA match can be found. Research into the nature of this organism is still ongoing. Clongen has twice reported bacteria inside white blood cells which resemble Ehrlichia. However, all standard tests, serological and PCR for known variants of Ehrlichia and Anaplasmosis have been negative. I don't know what this bug is. An unusual species of Rickettsia has been found in a high percentage of Maryland Ixodes ticks. The significance of this microbe has not been determined.
Rather than labeling patients with: Lyme- Babesia and Bartonella, perhaps it would be best to describe the individual clinical responses seen in each patient. For example, patient A has a syndrome which is responsive to Rifampin.
Why is this important. It is beyond important: It is critical.
A narrow ILADS paradigm or box, can ironically begin to resemble more and more the sort of narrow paradigm or box utilized by the IDSA, of which we are so critical. The IDSA box in my opinion is wrong, but it is fact based. If ILADS is to successfully spar against the IDSA it needs to marshal arguments which are clear, cogent and fact based. LLMDS are for the most part community primary care physicians. The opponents have all the resources of medical academia at their disposal. The fight is lopsided at the outset.
And I am very concerned that the LLMD box may have already disenfranchised some of the most critical players in the Lyme versus IDSA debate. The academic support for the chronic Lyme cause has come from Fallon and Donta. If they don't buy into the significance of the co-infection hypothesis, this should not be seen as a negative. Rather, it is a positive. They are academic in their approach. If they are going to give their stamp of approval on something there has to exist a significant body of evidence to support that thing.
As the two sides of the debate hunker down and prepare for battle, with medical licenses on the line and the future ability of Lyme patients to have access to any LLMDS, the lines must be clearly drawn. It must be a fight about whether or not Lyme organisms persist in the body and cause chronic illness in patients necessitating the use of long term antibiotics.
PERIOD.
Additional point: It has come to my attention that some advocacy groups within the Lyme community have been over zealous. Changes need to be incremental. If groups insist that every thing change at once this will continue to have disastrous effects on efforts for political reform. Sometimes well meaning individuals can become their own worst enemies.
Monday, February 16, 2009
Understanding the Western Blot
Many patients ask me questions about the meaning of the Lyme Western Blot test. I will try to clear up the mystery. Admittedly, it is a bit complicated.
First of all, one must understand that the Western Blot test is used to detect antibody responses made by a host- in this case humans, exposed to the Lyme bacteria, Borrelia burdorferi. Antibodies are produced when special specialized circulating immune cells encounter proteins or other molecules- called antigens, on the surface of a foreign invader. This information is transmitted through a complex process to specialized cell which produce antibodies. Antibodies are tiny proteins- immunoglobulins, which attach to target areas found on the surface of the germ, Lyme in this case. Finding antibodies directed at a particular pathogen is like finding footprints in the sand. It says "Lyme was here," like a name etched on an old oak tree. It in no way proves that Lyme is still present in the body. This is key to understanding the divergent views held by the IDSA and ILADS.
Our immune system can produce several classes of immunoglobulins. For the purpose of evaluating exposure to Lyme only two are relevant: IgM and IgG.
If one looks at the the areas of the Lyme bacteria which are antigenic- the areas associated with antibody formation, one generally finds 14 different regions or molecules. If these proteins are allowed to diffuse on a specially prepared strip or Blot, one finds that these tiny antigentic areas separate out based on their respective weights. These Lyme related antigens have molecular weights which progress from 18 Kilodaltons (Kd) to 93 Kd. The unit of measurement is frequently omitted- frequently the bands are referred to only be a number, 41 for instance.
To perform a Western Blot test a patient's serum is incubated with a specially prepared Blots or strips containing the Lyme antigenic proteins. If antibodies are present in the blood/serum they cause a reaction on the strip. Anyone who has looked at a home pregnancy test or a rapid strep test is familiar with the appearance of such a reaction on a test strip. The reactions show up as linear streaks called bands. Individual bands can be identified by their position on the strip. When the lab performs a Western Blot test four strips are prepared. There is a Blot which detects IgM antibodies and a Blot which detects IgG antibodies. Both are matched against control strips.
It should be noted that the significance of IgM versus IgG antibodies may be very different regarding Lyme compared with many other infections. This topic will not be addressed here, but it is extensively discussed elsewhere.
Frequently results are referred to as CDC positive or negative. These designations are misleading. In 1994 the CDC established a national surveillance criteria for Lyme disease. A national standard for reporting a positive DIAGNOSTIC result has never been developed. Most labs erroneously only report results based on these CDC criteria. The CDC criteria was developed concurrently with the Lyme vaccine. Certain key bands were omitted in the CDC test because these bands would react in persons who had received the Lyme vaccine. For a variety or reasons, the vaccine was removed from the market. Unfortunately, some key bands were never added back to the most commonly used Lyme Western Blot tests.
Of 28 possible bands, the standard CDC test, which is not a diagnostic test, reports only 13 out of a possible 28 bands. Only 3 IgM bands are reported and only 10 IgG bands are reported. The test is called positive if 2/3 IgM bands react or if 5/10 IgG bands react. Unfortunately, the CDC has recently made the test even more restrictive. If a patient has a positive IgM response it must be followed by a positive IgG response after 4 weeks to be considered a positive result.
Again, it must be emphasized that this is a surveillance test- a research tool- it cannot be claimed to be a accurate test for proving exposure to Lyme disease.
Other laboratories have developed alternate Western Blot criteria. For example, IgeneX labs will report a test positive if a patient has 2 critical bands in the IgM or IgG subset.
There has been a longstanding concern that cross reactivity may occur with some bands. In other words, a prior infection with a non-Lyme germ may cause a reaction to occur at some of the bands. Because of this, the bands have been analyzed to determine which are very specific for Lyme infection. If a patient shows reactivity with these very specific bands, the likelihood of a false positive reaction is low.
Doctors vary in their interpretation of Western Blot bands.. For example, if a patient has a reaction at even a single key band, some physicians will consider this a positive result. There is even some disagreement about which bands are very specific. Bands 23,31,34,39, and 93 are considered very specific by most. The significance of the 18 and 41 bands is open to more controversy.
Most laboratories will only report a positive band if it reacts with an intensity very close to the control band. Bands with an intensity which exceeds the control may be designated by a series of pluses or a percentage greater than the control.
Only IgeneX reports bands as indeterminate. This indicates that the reaction is not zero but is does not meet the strict criteria to be called a positive reaction.
It should be kept in mind that many patients who have Lyme disease may have minimal or even no reaction on a Western Blot. Many Lyme patients are known to be "seronegative." Western Blot reports are always interpreted along side a physician's overall clinical assessment of a patient.
The Western Blot is a tool used by physicians who diagnose and treat Lyme disease. The results from this test do not provide answers to questions relating to: the persistence of Lyme infection, a particular course of therapy or a patient's prognosis. Western Blot results, whether they are positive, negative, equivocal or controversial, must always be interpreted along side other clinical information. Typically, IDSA doctors and ILADS doctors are likely to judge results differently based on individual biases.
I discourage patients from obtaining Lyme Western Blots without first consulting with a physician. These results need to be analyzed based on a physician's clinical assessment of a patient. A positive result does not guarantee that a patient has Lyme disease and a negative result does not guarantee that a patient does not have Lyme disease.
First of all, one must understand that the Western Blot test is used to detect antibody responses made by a host- in this case humans, exposed to the Lyme bacteria, Borrelia burdorferi. Antibodies are produced when special specialized circulating immune cells encounter proteins or other molecules- called antigens, on the surface of a foreign invader. This information is transmitted through a complex process to specialized cell which produce antibodies. Antibodies are tiny proteins- immunoglobulins, which attach to target areas found on the surface of the germ, Lyme in this case. Finding antibodies directed at a particular pathogen is like finding footprints in the sand. It says "Lyme was here," like a name etched on an old oak tree. It in no way proves that Lyme is still present in the body. This is key to understanding the divergent views held by the IDSA and ILADS.
Our immune system can produce several classes of immunoglobulins. For the purpose of evaluating exposure to Lyme only two are relevant: IgM and IgG.
If one looks at the the areas of the Lyme bacteria which are antigenic- the areas associated with antibody formation, one generally finds 14 different regions or molecules. If these proteins are allowed to diffuse on a specially prepared strip or Blot, one finds that these tiny antigentic areas separate out based on their respective weights. These Lyme related antigens have molecular weights which progress from 18 Kilodaltons (Kd) to 93 Kd. The unit of measurement is frequently omitted- frequently the bands are referred to only be a number, 41 for instance.
To perform a Western Blot test a patient's serum is incubated with a specially prepared Blots or strips containing the Lyme antigenic proteins. If antibodies are present in the blood/serum they cause a reaction on the strip. Anyone who has looked at a home pregnancy test or a rapid strep test is familiar with the appearance of such a reaction on a test strip. The reactions show up as linear streaks called bands. Individual bands can be identified by their position on the strip. When the lab performs a Western Blot test four strips are prepared. There is a Blot which detects IgM antibodies and a Blot which detects IgG antibodies. Both are matched against control strips.
It should be noted that the significance of IgM versus IgG antibodies may be very different regarding Lyme compared with many other infections. This topic will not be addressed here, but it is extensively discussed elsewhere.
Frequently results are referred to as CDC positive or negative. These designations are misleading. In 1994 the CDC established a national surveillance criteria for Lyme disease. A national standard for reporting a positive DIAGNOSTIC result has never been developed. Most labs erroneously only report results based on these CDC criteria. The CDC criteria was developed concurrently with the Lyme vaccine. Certain key bands were omitted in the CDC test because these bands would react in persons who had received the Lyme vaccine. For a variety or reasons, the vaccine was removed from the market. Unfortunately, some key bands were never added back to the most commonly used Lyme Western Blot tests.
Of 28 possible bands, the standard CDC test, which is not a diagnostic test, reports only 13 out of a possible 28 bands. Only 3 IgM bands are reported and only 10 IgG bands are reported. The test is called positive if 2/3 IgM bands react or if 5/10 IgG bands react. Unfortunately, the CDC has recently made the test even more restrictive. If a patient has a positive IgM response it must be followed by a positive IgG response after 4 weeks to be considered a positive result.
Again, it must be emphasized that this is a surveillance test- a research tool- it cannot be claimed to be a accurate test for proving exposure to Lyme disease.
Other laboratories have developed alternate Western Blot criteria. For example, IgeneX labs will report a test positive if a patient has 2 critical bands in the IgM or IgG subset.
There has been a longstanding concern that cross reactivity may occur with some bands. In other words, a prior infection with a non-Lyme germ may cause a reaction to occur at some of the bands. Because of this, the bands have been analyzed to determine which are very specific for Lyme infection. If a patient shows reactivity with these very specific bands, the likelihood of a false positive reaction is low.
Doctors vary in their interpretation of Western Blot bands.. For example, if a patient has a reaction at even a single key band, some physicians will consider this a positive result. There is even some disagreement about which bands are very specific. Bands 23,31,34,39, and 93 are considered very specific by most. The significance of the 18 and 41 bands is open to more controversy.
Most laboratories will only report a positive band if it reacts with an intensity very close to the control band. Bands with an intensity which exceeds the control may be designated by a series of pluses or a percentage greater than the control.
Only IgeneX reports bands as indeterminate. This indicates that the reaction is not zero but is does not meet the strict criteria to be called a positive reaction.
It should be kept in mind that many patients who have Lyme disease may have minimal or even no reaction on a Western Blot. Many Lyme patients are known to be "seronegative." Western Blot reports are always interpreted along side a physician's overall clinical assessment of a patient.
The Western Blot is a tool used by physicians who diagnose and treat Lyme disease. The results from this test do not provide answers to questions relating to: the persistence of Lyme infection, a particular course of therapy or a patient's prognosis. Western Blot results, whether they are positive, negative, equivocal or controversial, must always be interpreted along side other clinical information. Typically, IDSA doctors and ILADS doctors are likely to judge results differently based on individual biases.
I discourage patients from obtaining Lyme Western Blots without first consulting with a physician. These results need to be analyzed based on a physician's clinical assessment of a patient. A positive result does not guarantee that a patient has Lyme disease and a negative result does not guarantee that a patient does not have Lyme disease.
Thursday, February 12, 2009
Seronegative Lyme
A Lyme patient was treated on clinical grounds. She was seronegative. An initial Western Blot from Labcorp showed only 41 IgM and IgG bands.
After 4 months of antibiotics a Western Blot was sent to IgeneX. These are the results:
IgM- 18 3+, 23 2+, 30 2+, 31 3+, 34 2+, 39 2+, 41 3+, 45 +, 58 2+, 66 +, 93 2+.
IgG- 41 2+.
According to the CDC web pages, regarding Lyme diagnosis she is seronegative.
If an initial positive IgM is not followed by a positive IgG response then the initial IgM response was a false negative.
Makes sense to me.
After 4 months of antibiotics a Western Blot was sent to IgeneX. These are the results:
IgM- 18 3+, 23 2+, 30 2+, 31 3+, 34 2+, 39 2+, 41 3+, 45 +, 58 2+, 66 +, 93 2+.
IgG- 41 2+.
According to the CDC web pages, regarding Lyme diagnosis she is seronegative.
If an initial positive IgM is not followed by a positive IgG response then the initial IgM response was a false negative.
Makes sense to me.
Tuesday, February 10, 2009
OK- It is not Lyme disease- does it matter?
A 58 year old woman came for a Lyme consult 10 months ago. She had been diagnosed with psoriasis and rheumatoid arthritis. She suffered with joint pains affecting her knees, ankles, hands and elbows. In addition she suffered with chronic fatigue headaches visual changes, neuropathy, forgetfulness, impaired cognitive processing and night sweats. She was interested in exploring an alternative explanation of her symptoms because her daughter had been diagnosed with Lyme disease. Her rheumatologist had prescribed Methotrexate, Suflasalazine and Celebrex. Baseline laboratory studies showed a very borderline ANA 125, a normal rheumatoid factor and an elevated CRP of 11.5. She has consistently tested negative for Lyme disease. She has had positive IgG and IgM 41 bands and IND 31 and 39 IgG bands per Igenex.
She has been treated for Lyme disease and Babesia based on clinical symptoms. In November her CRP was 3.8. Another set of labs was ordered today.
Today, 10 months later- she has no joint pain. Her memory is back to normal. The sweats are gone. Minimal neuropathy remains. Her psoriasis has resolved. She takes Plaquenil and is off Methrotrexate and Sulfasalzine. Incidentally, I have observed clearing of psoriasis in several other patients treated for Lyme disease.
What has she been on? Biaxin, Zithromax, Plaquenil, Mepron and now Minocin. She is allergic to penicillin.
For the sake of argument, let us posit the standard rheumatology opinion. She never had Lyme disease. Antibiotics helped her because of non specific anti-inflammatory properties and modification of cytokine responses.
The patient came to me on a powerful immune suppressing drug, Methotrexate, which is known to have serious complications, including cancer. And besides, the drug wasn't helping her. She improved with antibiotics. Rheumatologists have argued with me, claiming that long term antibiotic therapy is dangerous. Millions of teenagers take chronic antibiotic therapy for acne. I fail to see any merit to these arguments.
OK- LLMDS are wrong. It is not Lyme disease. It is something else. It doesn't matter what you call it. It works and it is much safer than "standard" therapy.
Apparently ego trumps the best interest of the patient.
She has been treated for Lyme disease and Babesia based on clinical symptoms. In November her CRP was 3.8. Another set of labs was ordered today.
Today, 10 months later- she has no joint pain. Her memory is back to normal. The sweats are gone. Minimal neuropathy remains. Her psoriasis has resolved. She takes Plaquenil and is off Methrotrexate and Sulfasalzine. Incidentally, I have observed clearing of psoriasis in several other patients treated for Lyme disease.
What has she been on? Biaxin, Zithromax, Plaquenil, Mepron and now Minocin. She is allergic to penicillin.
For the sake of argument, let us posit the standard rheumatology opinion. She never had Lyme disease. Antibiotics helped her because of non specific anti-inflammatory properties and modification of cytokine responses.
The patient came to me on a powerful immune suppressing drug, Methotrexate, which is known to have serious complications, including cancer. And besides, the drug wasn't helping her. She improved with antibiotics. Rheumatologists have argued with me, claiming that long term antibiotic therapy is dangerous. Millions of teenagers take chronic antibiotic therapy for acne. I fail to see any merit to these arguments.
OK- LLMDS are wrong. It is not Lyme disease. It is something else. It doesn't matter what you call it. It works and it is much safer than "standard" therapy.
Apparently ego trumps the best interest of the patient.
Monday, February 9, 2009
Lyme Dementia, Namenda, MS, A bug, and Radiologists
A 53 year old showed up at my door a little more than 2 years ago. He had been diagnosed with Lyme disease and was looking for help. He had already been ill for more than 3 years. He suffered with severe pain- on serious opiates. He had neuropathic pain- including a relentless trigeminal neuralgia. To date, this has persisted. He had already received 40 days of IV Rocephin and 30 days of oral antibiotics for CDC positive disease- to no avail. I took him on- a challenge. We have been through ups and downs with courses of Rocephin and oral antibiotics. His cognitive issues have been very worrisome and not improved until recently. His mother died of Alzheimer's disease and he sees the same syndrome in himself. Lab testing has shown consistently positive antibody WB bands, both IgM and IgG. He is also ELISA positive, for what that is worth. His C6 peptide has consistently been high as well. This is of some interest since Immunetics- the makers of this assay- claim that one sees a 4 fold decrease in C6 titers after successful treatment of Lyme disease. Perhaps his most interesting finding is his Brain MRI. It shows "deep white matter lesions bilaterally, consistent with the clinical diagnosis of Lyme disease." The radiologist notes that the lesions are not in a distribution typical for demyelinating plaques. (MS).
After trying many therapies, with mediocre results, I decided to try something novel for his dementia. His significant short term memory loss, bouts of mental confusion and aphasia were similar to presentations seen in the early to moderate stages of Alzheimer's disease. This is something quite familiar to me; I spent 15 years as the medical director of a large Nursing Home at one time. Based on the notion that Lyme dementia is related to glutamine sensitivity- as seen in Alzheimer's disease as well, I prescribed Namenda. This made a dramatic difference and has perhaps been one of the most helpful therapies for this most challenging patient.
Recently I sent a blood sample to Clongen for a wet mount. His blood, like that of so many other Lyme patients, has numerous, highly motile, extracellular organisms.
Clongen's attempts to sequence the "bacteria" have failed. It does not amplify with any of the known universal primers for bacteria used in PCR assays. Attempts to culture it in various media have also failed. Perhaps it is not a bacteria, but a tiny parasite of some kind. Clongen plans to test for this possibility as well.
The mystery of the motile organisms for now, remains unsolved.
There is no evidence that it is any known bacteria including a relative of Bartonella or a relative of Pseudomonas.
It is not killed with a plethora of antibiotics and anti parasite drugs.
Today this patient told me that a doctor friend said he should have a spinal tap to rule out MS. As previously discussed, there is no diagnostic test for MS. Myelin basic protein can be measured in the CSF- it is a marker for destruction of myelin- but it does not diagnose MS. Based on his MRI- it would not be unexpected to find MBP in his spinal fluid. Actually, I recommended that he see his neurologists. There is no research regarding the use of typical MS therapy in neuroborreliosis patients. It is possible that interferon therapy might help. Other, less commonly used MS therapies, including plasmapheresis and IVIg have been recommended for Lyme patients.
My final musing here is: "What do radiologists think?"
Infectious disease physicians, rheumatologists and neurologists dismiss the notions that such patients are suffering with neuroborreliosis. Many have proposed a Post-Lyme autoimmune disorder. The radiologists have not been steeped in this dogma. They call MRIs and SPECTs all the time: "Compatible with Lyme disease." They see the evidence in black and white; from my discussions with radiologists, they believe in chronic Lyme disease. They do not diagnose Post-Lyme. Apparently neuroborreliosis has not been censured from their text books. They in fact know that neuroborreliosis exists and that it has been well documented.
After trying many therapies, with mediocre results, I decided to try something novel for his dementia. His significant short term memory loss, bouts of mental confusion and aphasia were similar to presentations seen in the early to moderate stages of Alzheimer's disease. This is something quite familiar to me; I spent 15 years as the medical director of a large Nursing Home at one time. Based on the notion that Lyme dementia is related to glutamine sensitivity- as seen in Alzheimer's disease as well, I prescribed Namenda. This made a dramatic difference and has perhaps been one of the most helpful therapies for this most challenging patient.
Recently I sent a blood sample to Clongen for a wet mount. His blood, like that of so many other Lyme patients, has numerous, highly motile, extracellular organisms.
Clongen's attempts to sequence the "bacteria" have failed. It does not amplify with any of the known universal primers for bacteria used in PCR assays. Attempts to culture it in various media have also failed. Perhaps it is not a bacteria, but a tiny parasite of some kind. Clongen plans to test for this possibility as well.
The mystery of the motile organisms for now, remains unsolved.
There is no evidence that it is any known bacteria including a relative of Bartonella or a relative of Pseudomonas.
It is not killed with a plethora of antibiotics and anti parasite drugs.
Today this patient told me that a doctor friend said he should have a spinal tap to rule out MS. As previously discussed, there is no diagnostic test for MS. Myelin basic protein can be measured in the CSF- it is a marker for destruction of myelin- but it does not diagnose MS. Based on his MRI- it would not be unexpected to find MBP in his spinal fluid. Actually, I recommended that he see his neurologists. There is no research regarding the use of typical MS therapy in neuroborreliosis patients. It is possible that interferon therapy might help. Other, less commonly used MS therapies, including plasmapheresis and IVIg have been recommended for Lyme patients.
My final musing here is: "What do radiologists think?"
Infectious disease physicians, rheumatologists and neurologists dismiss the notions that such patients are suffering with neuroborreliosis. Many have proposed a Post-Lyme autoimmune disorder. The radiologists have not been steeped in this dogma. They call MRIs and SPECTs all the time: "Compatible with Lyme disease." They see the evidence in black and white; from my discussions with radiologists, they believe in chronic Lyme disease. They do not diagnose Post-Lyme. Apparently neuroborreliosis has not been censured from their text books. They in fact know that neuroborreliosis exists and that it has been well documented.
Lyme tests: Truth and Consequences
The CDC seems to contradict itself quite a lot regarding this issue. One the one hand, it states that the two tier test is very accurate. On the other hand, it states that the two tier test is to be used for surveillance, and is not the basis for diagnosis. The CDC seems quite concerned that Lyme disease is over diagnosed. There are repeated comments that false positive tests are common. It is claimed that a lack of an IgG response following an initial IgM response is associated with false positivity. This is the opposite of what most LLMDS and their patients have found. In fact, the incidence of under diagnosis and seronegativity has been well documented. Dr. Wormser- closely affiliated with the CDC- has expressed concerns that Lyme disease has become a "wastebasket" for many patients. A preoccupation with first ruling out other disease entities like fibromyalgia is asserted.
There are inherent biases in the IDSA and ILADS positiion regarding Lyme diagnosis based on one's initial beliefs about the incidence of the infection. Seronegativity has been extensively documented, as outlined by Dr. Philips of ILADS. Given a bias that Lyme is under diagnosed, rather than over diagnosed, one views the diagnostic conundrums from a different starting point or bias. If one believes that Lyme, for example,may be a frequent underlying cause for the clinical entity called fibromyalgia-considered a clinical syndrome,not a disease, then one approaches testing from a different angle. The bias in making the diagnosis is based on a physician's sense of a "pretest" likelihood that a particular disease is present.
The first diagnostic tools are the history and physical examination. I believe that most papers, scientific and otherwise, which discuss Lyme diagnosis frequently underplay the significance of such data. I believe that historical data must be interpreted in a more narrow way than has been suggested by some authors. Common symptoms like fatigue, brain fog, numbness and tingling and migratory pains should be given a lot of weight. Symptom which are associated with numerous other entities should be given little weight.
To understand diagnostic tests, one must have an appreciation for the biological diversity of the Lyme organism, as it exists in living tissues. Lyme can be an extracellular bacteria, but intracellular and cyst forms of Borrelia burdorferi have clearly been shown to exist.
Antibody responses- acquired immune responses to intracellular bacteria are poor. The primary immune response here is mediated by T cells- the innate immune response. This must be taken into account in the understanding of seronegative disease.
Let us look at TB for example. Tuberculosis is an intracellular bacteria. There is no antibody test for it for the reason discussed above. A PPD skin test looks for a delayed hypersensitivity T cell response. A new FDA approved test is quite unique. Lymphocytes from a patient are incubated with TB antigens. Gamma interferon is measured. If a patient has had previous exposure to TB a Th1 immune response is provoked and the associated cytokine is released.
Newer diagnostic tests for Lyme have focused on its intracellular nature. One test, called a lymphocyte transfer test, measures lymphoctye reactivity after exposure to Lyme antigens. Another test measures cell mediated chemokine responses, as a signature of infection with a specific bacteria such as Lyme. The CDC has criticized such tests claiming that its two tier surveillance test remains the "gold standard," in the diagnosis of Lyme disease.
The CDC hangs much of what follows regarding Lyme disease- diagnosis and treatment based on testing procedures which are at least controversial. The CDC/IDSA cling steadfastly to the same tired positions, despite ample evidence that they may be incorrect. The CDC web pages about Lyme disease do not address the FACT that its positions are controversial and that other viewpoints are considered valid- based on the listing of ILADS guidelines with the National Clearing House of guidelines, held by the department of HHS.
What if even 10% if the ILADS position is correct? Can the IDSA and CDC afford the risk that they might be wrong about such a huge issue? What if there is in fact a raging epidemic of a super germ, with biological characteristics of both TB and syphilis, ravaging the population of the US and much of the world?
Doctors are taught that they must exclude potentially life threatening medical conditions when they evaluate a patient before more benign conditions are considered. Perhaps the CDC has it backwards. Perhaps physicians should be taught to rule out disseminated tertiary Lyme disease and neuroborreliosis, before considering fibromyalgia of benign cause, depression and hypochondriasis.
The issue is too important. There is no room for posturing, spinning, politics and egos.
We are left with two possibilities. Either LLMDS and their patients are suffering with mass delusions and hysteria- per the IDSA position, OR the mainstream of medicine is sitting on the sidelines while an epidemic of plague like proportions is disabling and at times killing many thousands of Americans.
If you don't like the message it can be convenient to kill the messenger. This has happened throughout history. In general, one of the best predictors of the future is the past. Can we really afford to let history repeat itself once more?
There are inherent biases in the IDSA and ILADS positiion regarding Lyme diagnosis based on one's initial beliefs about the incidence of the infection. Seronegativity has been extensively documented, as outlined by Dr. Philips of ILADS. Given a bias that Lyme is under diagnosed, rather than over diagnosed, one views the diagnostic conundrums from a different starting point or bias. If one believes that Lyme, for example,may be a frequent underlying cause for the clinical entity called fibromyalgia-considered a clinical syndrome,not a disease, then one approaches testing from a different angle. The bias in making the diagnosis is based on a physician's sense of a "pretest" likelihood that a particular disease is present.
The first diagnostic tools are the history and physical examination. I believe that most papers, scientific and otherwise, which discuss Lyme diagnosis frequently underplay the significance of such data. I believe that historical data must be interpreted in a more narrow way than has been suggested by some authors. Common symptoms like fatigue, brain fog, numbness and tingling and migratory pains should be given a lot of weight. Symptom which are associated with numerous other entities should be given little weight.
To understand diagnostic tests, one must have an appreciation for the biological diversity of the Lyme organism, as it exists in living tissues. Lyme can be an extracellular bacteria, but intracellular and cyst forms of Borrelia burdorferi have clearly been shown to exist.
Antibody responses- acquired immune responses to intracellular bacteria are poor. The primary immune response here is mediated by T cells- the innate immune response. This must be taken into account in the understanding of seronegative disease.
Let us look at TB for example. Tuberculosis is an intracellular bacteria. There is no antibody test for it for the reason discussed above. A PPD skin test looks for a delayed hypersensitivity T cell response. A new FDA approved test is quite unique. Lymphocytes from a patient are incubated with TB antigens. Gamma interferon is measured. If a patient has had previous exposure to TB a Th1 immune response is provoked and the associated cytokine is released.
Newer diagnostic tests for Lyme have focused on its intracellular nature. One test, called a lymphocyte transfer test, measures lymphoctye reactivity after exposure to Lyme antigens. Another test measures cell mediated chemokine responses, as a signature of infection with a specific bacteria such as Lyme. The CDC has criticized such tests claiming that its two tier surveillance test remains the "gold standard," in the diagnosis of Lyme disease.
The CDC hangs much of what follows regarding Lyme disease- diagnosis and treatment based on testing procedures which are at least controversial. The CDC/IDSA cling steadfastly to the same tired positions, despite ample evidence that they may be incorrect. The CDC web pages about Lyme disease do not address the FACT that its positions are controversial and that other viewpoints are considered valid- based on the listing of ILADS guidelines with the National Clearing House of guidelines, held by the department of HHS.
What if even 10% if the ILADS position is correct? Can the IDSA and CDC afford the risk that they might be wrong about such a huge issue? What if there is in fact a raging epidemic of a super germ, with biological characteristics of both TB and syphilis, ravaging the population of the US and much of the world?
Doctors are taught that they must exclude potentially life threatening medical conditions when they evaluate a patient before more benign conditions are considered. Perhaps the CDC has it backwards. Perhaps physicians should be taught to rule out disseminated tertiary Lyme disease and neuroborreliosis, before considering fibromyalgia of benign cause, depression and hypochondriasis.
The issue is too important. There is no room for posturing, spinning, politics and egos.
We are left with two possibilities. Either LLMDS and their patients are suffering with mass delusions and hysteria- per the IDSA position, OR the mainstream of medicine is sitting on the sidelines while an epidemic of plague like proportions is disabling and at times killing many thousands of Americans.
If you don't like the message it can be convenient to kill the messenger. This has happened throughout history. In general, one of the best predictors of the future is the past. Can we really afford to let history repeat itself once more?
Friday, February 6, 2009
Scientific, peer reviewed evidence supports chronic Lyme: Why the denial?
1999- Annals of Medicine, 31(3):225-32
32 of 165 patients treated with 3 months of antibiotics had culture or PCR evidence of he live spirochetes in 40% of patients who relapsed. The authors concluded:
"We conclude that the treatment of Lyme Borreliosis with appropriate antibiotics for even more than 3 months may not always eradicate the sprirochetes."
1998- Annals of the Rheumatic Diseases, 57(2):118-21
Detection of Borrelia burdorferi by PCR in the synovial membrane, but not the synovial fluid from patients with persiting Lyme arthritis after antibiotic therapy.
1997- American College of Rheurmatology, Voll 40(9) Suppl, Sept,p.S270
PCR evidence for Borrelia burdorferi DNA in synovium in absence of positive serology.
1996- Infection,24(3):218-26 Formation and cultivation of Borrelia spheroblast L-forms variants. "The persistence of Bb even after therapy with antbiotics has been demonstrated in cerebral spinal fluid, in skin, iris, heart and joint biopsies." The authors suggest that atypical forms may allow Borrelia to survive antibiotic treatment.
1993- Arthritis and Rheumatism,36(11):1621-8 Persistence of Borrelia burdorferi in ligamentous tissue from a patient with chronic Lyme borreliosis.
1993- Clinical Orthopedics, 297:238-41 Chronic septic arthritis causes by Bb.
1993- Neurology, 43(12):2705-7 Stroke due to Lyme disease
1989- Survival of Borrelia burdorferi an antibiotically treated patients with Lyme Borreliosis
"...it has become questionalbe if a definite eradication of Bb with antibiotics is possible."
1993- JAMA,(270):1369. SERONEGATIVE LYME DISEASE (Steere AC.)
"THERE IS LITTLE QUESTION THAT SERONEGATIVE LYME CAN EXIST."
LymeMD- Germantown, Maryland 2008- non published. Persistent Lyme in synovial fluid.
A patient with disseminated Lyme disease including neuroborreliosis, who had received more than 2 years of antibiotics, including 2 courses of IV antibiotics, had a positive Lyme PCR of synovial fluid aspirated from knee.
Clinical Immunology- Textbook- 2008- Page 390 "Only a few intracellular bacteria, such as L. monocytogenes, are sterily eradicated once the immune response has reached its height. More often, the intracellular habitat provides a protective niche that promotes persistent infection in the face of an ongoing immune response."
32 of 165 patients treated with 3 months of antibiotics had culture or PCR evidence of he live spirochetes in 40% of patients who relapsed. The authors concluded:
"We conclude that the treatment of Lyme Borreliosis with appropriate antibiotics for even more than 3 months may not always eradicate the sprirochetes."
1998- Annals of the Rheumatic Diseases, 57(2):118-21
Detection of Borrelia burdorferi by PCR in the synovial membrane, but not the synovial fluid from patients with persiting Lyme arthritis after antibiotic therapy.
1997- American College of Rheurmatology, Voll 40(9) Suppl, Sept,p.S270
PCR evidence for Borrelia burdorferi DNA in synovium in absence of positive serology.
1996- Infection,24(3):218-26 Formation and cultivation of Borrelia spheroblast L-forms variants. "The persistence of Bb even after therapy with antbiotics has been demonstrated in cerebral spinal fluid, in skin, iris, heart and joint biopsies." The authors suggest that atypical forms may allow Borrelia to survive antibiotic treatment.
1993- Arthritis and Rheumatism,36(11):1621-8 Persistence of Borrelia burdorferi in ligamentous tissue from a patient with chronic Lyme borreliosis.
1993- Clinical Orthopedics, 297:238-41 Chronic septic arthritis causes by Bb.
1993- Neurology, 43(12):2705-7 Stroke due to Lyme disease
1989- Survival of Borrelia burdorferi an antibiotically treated patients with Lyme Borreliosis
"...it has become questionalbe if a definite eradication of Bb with antibiotics is possible."
1993- JAMA,(270):1369. SERONEGATIVE LYME DISEASE (Steere AC.)
"THERE IS LITTLE QUESTION THAT SERONEGATIVE LYME CAN EXIST."
LymeMD- Germantown, Maryland 2008- non published. Persistent Lyme in synovial fluid.
A patient with disseminated Lyme disease including neuroborreliosis, who had received more than 2 years of antibiotics, including 2 courses of IV antibiotics, had a positive Lyme PCR of synovial fluid aspirated from knee.
Clinical Immunology- Textbook- 2008- Page 390 "Only a few intracellular bacteria, such as L. monocytogenes, are sterily eradicated once the immune response has reached its height. More often, the intracellular habitat provides a protective niche that promotes persistent infection in the face of an ongoing immune response."
Thursday, February 5, 2009
Lyme disease: Can you count by sevens?
A new patient yesterday.
A 50 year old female developed a flu like syndrome last May. She had fever, chills and malaise. She went to her family doctor and was told she had a virus. No therapy was prescribed. Two months later she complained of persistent symptoms. She now had severe fatigue, migratory joint pains, numbness and tingling and a brain fog associated with some memory impairments and difficulty concentrating. Her doctor didn't know what she had. she requested a test for Lyme disease. The two step ELISA/WB was positive for Lyme. She was prescribed Doxycyline for 28 days. Within a week she experienced dramatic improvement and was nearly back to normal. Her physician proudly pronounced her cured. Over the ensuing 3 months all of the original symptoms returned. A second round of Doxycycline was prescribed. When I saw her yesterday she was two weeks into the course and feeling a little better. The physician would not extend the therapy beyond this second course.
Lyme is treated for 14 days, perhaps 21 or even 28 days. That's what the text books say. After all, it is new disease, very mysterious, so confusing. Doctors feel obligated to follow the textbooks- to stay in their safe zone.
I once heard that doctors treat things for 10 days because we have 10 fingers on our hands. They treat for seven days because there are seven days in the week. Is this true???
Suppose a patient came into the same doctors office with sinusitis. Recommendations for the length of therapy vary, in part based on which antibiotic is chosen. Doctors are taught that antibiotics penetrate poorly into the sinus cavities. For the sake of this discussion let us say that the physician prescribed an antibiotic for 10 days. Perhaps the same patient returned after 10 days feeling somewhat better, but complained of persistent sinus pain and bloody green mucous. The physician then prescribed another course of antibiotics, this time for 14 days. Subsequently, the patient was still unimproved. The physician then ordered a CT scan which showed infection of the frontal and ethmoid sinuses. The concerned doctor quickly started IV antibiotics; after all, this sort of infection can spread into the brain and be deadly.
The point here is a clear. A physician will not stop treatment because textbook guidelines say that drug X should be used for Y days, for a particular infection: Y days exactly, not Y+1 or Y-2. No. The treatment stops when the patient is better.
Unless of course you have Lyme disease. Lyme has different rules.
Sinusitis is a common, generally self limited disease. Even without treatment it generally resolves. Lyme is a much more serious disease. Extension into the brain, past the blood brain barrier is the rule, not the exception.
What are these doctors thinking? Even the IDSA says its guidelines or just that, "guidelines." Treatment decisions should be individualized with each patient.
Perhaps they are not (thinking).
A 50 year old female developed a flu like syndrome last May. She had fever, chills and malaise. She went to her family doctor and was told she had a virus. No therapy was prescribed. Two months later she complained of persistent symptoms. She now had severe fatigue, migratory joint pains, numbness and tingling and a brain fog associated with some memory impairments and difficulty concentrating. Her doctor didn't know what she had. she requested a test for Lyme disease. The two step ELISA/WB was positive for Lyme. She was prescribed Doxycyline for 28 days. Within a week she experienced dramatic improvement and was nearly back to normal. Her physician proudly pronounced her cured. Over the ensuing 3 months all of the original symptoms returned. A second round of Doxycycline was prescribed. When I saw her yesterday she was two weeks into the course and feeling a little better. The physician would not extend the therapy beyond this second course.
Lyme is treated for 14 days, perhaps 21 or even 28 days. That's what the text books say. After all, it is new disease, very mysterious, so confusing. Doctors feel obligated to follow the textbooks- to stay in their safe zone.
I once heard that doctors treat things for 10 days because we have 10 fingers on our hands. They treat for seven days because there are seven days in the week. Is this true???
Suppose a patient came into the same doctors office with sinusitis. Recommendations for the length of therapy vary, in part based on which antibiotic is chosen. Doctors are taught that antibiotics penetrate poorly into the sinus cavities. For the sake of this discussion let us say that the physician prescribed an antibiotic for 10 days. Perhaps the same patient returned after 10 days feeling somewhat better, but complained of persistent sinus pain and bloody green mucous. The physician then prescribed another course of antibiotics, this time for 14 days. Subsequently, the patient was still unimproved. The physician then ordered a CT scan which showed infection of the frontal and ethmoid sinuses. The concerned doctor quickly started IV antibiotics; after all, this sort of infection can spread into the brain and be deadly.
The point here is a clear. A physician will not stop treatment because textbook guidelines say that drug X should be used for Y days, for a particular infection: Y days exactly, not Y+1 or Y-2. No. The treatment stops when the patient is better.
Unless of course you have Lyme disease. Lyme has different rules.
Sinusitis is a common, generally self limited disease. Even without treatment it generally resolves. Lyme is a much more serious disease. Extension into the brain, past the blood brain barrier is the rule, not the exception.
What are these doctors thinking? Even the IDSA says its guidelines or just that, "guidelines." Treatment decisions should be individualized with each patient.
Perhaps they are not (thinking).
Tuesday, February 3, 2009
Not Lyme...
I saw one of my better success stories today in the office. I have mentioned her before. She presented with a weird pneumonia, arthritis and rash. She had two stroke like syndromes. The first time she was sent home with a "mystery diagnosis." The second time she saw me. She had severe weakness on the left side of her body. She was treated with IV antibiotics and she is now fully recovered.
She initially had an elevated ANA titer and was told she had a variant of Lupus.
This returned to normal with antibiotics.
Her Labcorp Lyme WB was negative. She couldn't afford the IgeneX test, but- she tested positive by the Lyme C6 peptide test. According to the CDC and the IDSA this doesn't count.
When I tried to explain the political/legal aspects of the illness she was totally befuddled. She is highly insulted. Are THEY trying to say she doesn't have Lyme disease? YES. Are THEY trying to say her doctor is a quack? YES.
She initially had an elevated ANA titer and was told she had a variant of Lupus.
This returned to normal with antibiotics.
Her Labcorp Lyme WB was negative. She couldn't afford the IgeneX test, but- she tested positive by the Lyme C6 peptide test. According to the CDC and the IDSA this doesn't count.
When I tried to explain the political/legal aspects of the illness she was totally befuddled. She is highly insulted. Are THEY trying to say she doesn't have Lyme disease? YES. Are THEY trying to say her doctor is a quack? YES.
To not treat Lyme disease means....
A 28 year old female came into my office 18 months ago. She complained of acute left hip pain for 3 days and was unable to walk. My previous training told me that it was something called "toxic synovitis," an acute joint inflammation or a hip joint, possibly do to a virus or a rheumatological disorder. She was in severe pain, I prescribed a Medrol dose pack and Vicodin. Her initial labs showed a sed rate of 32 a CRP of 160- which is off the charts, a Lyme C6 peptide index of 0.3, vitamin D reversal, a Lyme WB 41 band on the 13 band test. She took antibiotics for 2 months for presumptive Lyme disease and got better. She stopped the antibiotics and relapsed 4 months later. This time her hip and knee hurt. She had mild neurological signs of peripheral neuropathy.
"Standard" labs were negative for Lyme. Her sed rate was 47 and her CRP 30.
After one week of resuming antibiotics she was better. Her course was complicated by a yeast infection. Her antibiotics were adjusted. After 4 months, a more careful history elicited- some tingling in the hands, some fatigue and some subtle cognitive issues.
At 7 months her CRP was normal at 1.2 and she felt entirely normal; all the symptoms had resolved. New labs showed that her vitamin D dihydroxy 1,25 had climbed to 98. The vitamin D hydroxy 25 was 12. I was a little nervous about the vitamin D and prescribed 2 months of Benicar. The levels quickly corrected 28 and 20 respectively.
After 3 negative Labcorp WB for Lyme, the last two showing no bands, a Lyme WB was sent to IgeneX. This time she was CDC positive and IgeneX positive by IgM criteria. She had positive bands 23,31,34,41 and 58.
We both felt confident that the diagnosis of Lyme disease had been correct all along.
She has been maintained on low doses of maintenance antibiotics and is symptom free.
To not treat Lyme disease means: To not consider Lyme in the differential diagnosis, to omit neurological examinations of my patients, to not order the labs I am familiar with- stop practicing medicine as I know it- just go through the motions to make a living, and still smile? Not worth it. If that what it comes down to I will leave medicine and find something else to do.
More importantly: God knows what would have happened to the patient?
"Standard" labs were negative for Lyme. Her sed rate was 47 and her CRP 30.
After one week of resuming antibiotics she was better. Her course was complicated by a yeast infection. Her antibiotics were adjusted. After 4 months, a more careful history elicited- some tingling in the hands, some fatigue and some subtle cognitive issues.
At 7 months her CRP was normal at 1.2 and she felt entirely normal; all the symptoms had resolved. New labs showed that her vitamin D dihydroxy 1,25 had climbed to 98. The vitamin D hydroxy 25 was 12. I was a little nervous about the vitamin D and prescribed 2 months of Benicar. The levels quickly corrected 28 and 20 respectively.
After 3 negative Labcorp WB for Lyme, the last two showing no bands, a Lyme WB was sent to IgeneX. This time she was CDC positive and IgeneX positive by IgM criteria. She had positive bands 23,31,34,41 and 58.
We both felt confident that the diagnosis of Lyme disease had been correct all along.
She has been maintained on low doses of maintenance antibiotics and is symptom free.
To not treat Lyme disease means: To not consider Lyme in the differential diagnosis, to omit neurological examinations of my patients, to not order the labs I am familiar with- stop practicing medicine as I know it- just go through the motions to make a living, and still smile? Not worth it. If that what it comes down to I will leave medicine and find something else to do.
More importantly: God knows what would have happened to the patient?
The fight about Lyme
As readers know, many physicians have been targeted by state Medical Boards for treating Lyme disease based on ILADS guidelines. The process generally has occurred because well meaning IDSA doctors have felt that the treatment rendered by such physicians has been incorrect or possibly dangerous to patients. I believe that players on both sides, the IDSA and ILADS, for the most part are sincere in their beliefs. This is a war of ideas.
Unfortunately, it is also a war about patient care. Physicians who treat chronic Lyme disease based on the ILADS paradigm, and their patients, are convinced that such treatments are correct and have been extremely helpful, and at times life saving.
Many ILADS physicians have the sense that Ivory Tower physicians, who follow the IDSA are not experienced in the treatment of patients suffering with the ravages of chronic Lyme disease. Infectious disease physicians are a relatively small group and are for the most part hospital based. They don't see the flow of patients with vague complaints such as fatigue, joint pain and brain fog that frequent primary care offices. LLMDS have learned that many such patients and others are suffering with chronic Lyme disease. Infectious disease physicians are charged with the management of hundreds of infectious illnesses. It makes sense that they would follow guidelines created by members of their professional society. Medical Boards are charged with the responsibility of investigating all complaints lodged against physicians. Typically, they defer to peer review- the opinions of experts. These peer reviewers have generally been unaware of the ILADS guidelines and or not given them much credence. It is this cascade of circumstance which leads to Medical Board charges against LLMDS. We have seen this scenario played out in many states with many doctors.
The cost of litigation is extremely high. Because of this, physicians at times have
required financial assistance from the patients they treat and other members of the Lyme community.
I believe that ultimately reform must occur at a fundamental level,t through changes in state laws, to protect ILADS physicians and the patients they care for. These battles must be fought on a state by state basis. I hope this blog has been informative and I thank you for your support.
Unfortunately, it is also a war about patient care. Physicians who treat chronic Lyme disease based on the ILADS paradigm, and their patients, are convinced that such treatments are correct and have been extremely helpful, and at times life saving.
Many ILADS physicians have the sense that Ivory Tower physicians, who follow the IDSA are not experienced in the treatment of patients suffering with the ravages of chronic Lyme disease. Infectious disease physicians are a relatively small group and are for the most part hospital based. They don't see the flow of patients with vague complaints such as fatigue, joint pain and brain fog that frequent primary care offices. LLMDS have learned that many such patients and others are suffering with chronic Lyme disease. Infectious disease physicians are charged with the management of hundreds of infectious illnesses. It makes sense that they would follow guidelines created by members of their professional society. Medical Boards are charged with the responsibility of investigating all complaints lodged against physicians. Typically, they defer to peer review- the opinions of experts. These peer reviewers have generally been unaware of the ILADS guidelines and or not given them much credence. It is this cascade of circumstance which leads to Medical Board charges against LLMDS. We have seen this scenario played out in many states with many doctors.
The cost of litigation is extremely high. Because of this, physicians at times have
required financial assistance from the patients they treat and other members of the Lyme community.
I believe that ultimately reform must occur at a fundamental level,t through changes in state laws, to protect ILADS physicians and the patients they care for. These battles must be fought on a state by state basis. I hope this blog has been informative and I thank you for your support.
Sunday, February 1, 2009
The war: IDSA vs ILADS
Physicians/scientists are a conservative lot. They operate within a paradigm- a construct of ideas the theories which form the basis of the reality or truth from which they operate. Unfortunately, physicians sometimes confuse a working paradigm with absolute truth. A blurring of this distinction makes it easier for physicians to treat patients on a daily basis. A popular metaphor is "the box." People are said to think within the box or outside the box. Physicians who treat chronic Lyme disease are challenging the conventions. They challenge not only the prevailing paradigm, but they challenge the process which creates and massages the paradigms which form the basis of contemporary medical practice. It is also a story of the few taking on the many, a tale of David versus Goliath. Both sides, IDSA and ILADS, can become very determined, arrogant and angry as they posit their points of view. This has the effect of pushing the other side into a defensive posture. The defensive posture does not lend itself to listening or collegiality; instead, it can create a more bellicose tone. I think some readers have a hard time understanding the vitriol found in the IDSA-ILADS paradigm war.
As the war between the IDSA and ILADS has played out, the IDSA has become more dug in. The guidelines have become more rigid, less flexible. The mainstream has clung tenaciously to its Bible. I would argue that the "Bible"- Harrison's textbook of medicine and other iconic sources allows for more lee way than the mainstream opinion would have one believe. History has shown that minority opinions frequently turn out to be correct.
The fight has morphed into a populist movement. Patients and Lyme treating physicians have tried to sway governmental politics. Those who do not know, a prior, that chronic Lyme does not exist, can easily see the "truth" to this side of the argument. Physicians who do not have a dog in the fight, those who don't know enough about the issues to have an opinion, stay mute on the sidelines. The political machine of mainstream medicine, with its certainty and arrogance, sits tight in its opposition, ever convinced that it will prevail. The fate of Lyme patients, many of whom are desperately ill, and their physicians, many of whom are passionate in their mission to heal- hangs in the balance.
Chronic Lyme is a very real medical issue. This is why I push for a mainstream look at the issues, which avoids CAM and other medical practices for which organized medicine has nothing but disdain. Whether or not herbs and accupuncture work is another fight for another day. My fight is about germs, antibiotics, physiology, immunity, molecular biology and medical practice.
As the war between the IDSA and ILADS has played out, the IDSA has become more dug in. The guidelines have become more rigid, less flexible. The mainstream has clung tenaciously to its Bible. I would argue that the "Bible"- Harrison's textbook of medicine and other iconic sources allows for more lee way than the mainstream opinion would have one believe. History has shown that minority opinions frequently turn out to be correct.
The fight has morphed into a populist movement. Patients and Lyme treating physicians have tried to sway governmental politics. Those who do not know, a prior, that chronic Lyme does not exist, can easily see the "truth" to this side of the argument. Physicians who do not have a dog in the fight, those who don't know enough about the issues to have an opinion, stay mute on the sidelines. The political machine of mainstream medicine, with its certainty and arrogance, sits tight in its opposition, ever convinced that it will prevail. The fate of Lyme patients, many of whom are desperately ill, and their physicians, many of whom are passionate in their mission to heal- hangs in the balance.
Chronic Lyme is a very real medical issue. This is why I push for a mainstream look at the issues, which avoids CAM and other medical practices for which organized medicine has nothing but disdain. Whether or not herbs and accupuncture work is another fight for another day. My fight is about germs, antibiotics, physiology, immunity, molecular biology and medical practice.
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