A patient comes in to the office. Let's say he or she is 5o years old. Many friends and family members have Lyme disease, he wants to know if he has it too. He is generally well but complains of some aches and pains. His joints hurt occasionally, especially after exercise, but recover quickly. His energy level and sleep are good. When asked about memory and cognitive problems he pauses for a moment: Perhaps his memory is not as good as it used to be. There has been some decline over several years. Word retrieval is a problem at times. His focus is not as good as it used to be. His mathematical abilities are not as good as they once were but they are OK. There are no other neurological symptoms. He functions normally at work and at home. These mild changes in cognition have occurred gradually over a period of years but are not bothersome.His family history reveals than a parent developed Alzheimer's disease at age 86. A recent physical has been done. His exam and routine lab work were fine. Should he be tested for Lyme disease?
No. Many patients have asymptomatic infection. This could be the case; still, I would not test. Positive results would only open a Pandora's box. These symptoms are mild and likely within the range of what might be expected in a 50 year old. The normal brain is sharper at age 25-35: minimal cognitive changes--neuronal fall out, occur in normal people. Alzheimer's disease? His risk may be slightly greater than that of the general population. Perhaps general recommendations would be made: exercise brain and body--eat well--perhaps drink coffee and take extra vitamin D.
The patients would be given a list symptoms to watch for. Treatment: watchful waiting--a term frequently used by doctors.
Tuesday, December 22, 2009
Monday, December 21, 2009
Vitamin D: A retraction--I got it all wrong
Vitamin D is much more complex than I have indicated earlier. The only thing I can say about the reversed pattern (active D higher than inactive D) is that it appears to be a marker for Lyme disease and/or inflammation--perhaps a very good marker.
Much research has been done on vitamin D. All of it is based on measurement of the inactive form, vitamin D hydroxy 25, which correlates with stored vitamin D. Yes, vitamin D has anti-inflammatory properties, but this may not be a bad thing. It affects cytokines andT-cell activation. But contrary to previous comments, it is active vitamin D that increases production of an anti-microbial peptide: cathelicidin. (Past statements that active D tilts the immune system from Th1 to Th2--causing production of anti-microbial peptides is wrong). The binding of active D to receptors modulates the genetic expression of complex proteins. VDRs (vitamin D receptors) are found in many organs in the body, including: brain, heart, skin, gonads, prostate and breast. Vitamin D receptors are found on a variety of immune cells, including: monocytes, B-cells and activated T-cells. It also has effects on dendritic cells. Vitamin D toxicity is very rare, even in patients with very high levels of active vitamin D, the 1,25 dihydroxy form.
Anti-inflammatory effects of D may lower the risk cancers, autoimmune disease, diabetes, heart disease and others. Recent research has shown that vitamin D is required to activate the histocompatibility gene, HLA-DRB 1501. This activation is necessary for the immune system to differentiate between self and non self in a select group of patients.
A link between vitamin D and MS has been shown. Perhaps the lack of MS in tropical climes
is not related to the absence of Bb and other infectious agents, as some have postulated, but due to higher levels of D from birth on.
The main source of D is sun light. Increased melanin decreases UVB penetration through the skin needed for conversion of D. It has been shown the black skin increases the risk of prostate cancer in the US but not in Africa--perhaps evidence of D's cancer fighting effects.
The Canadian Cancer Society has recommended that all it's citizens supplement with 1000 units of D daily.
D supplements are generally in the form called D3. This is the same form obtained from sun exposure. There are many forms of D and it's metabolism is very complex. Clinically, we only measure D in its stored and active forms.
In these numerous studies, only stored vitamin D is measured. Some doctors on the "cutting edge" have suggested that vitamin D hydroxy 25 levels are optimal at 75 (normal
32 to 100). But they are not looking at lab values I see in my practice. The range for normal active vitamin has been expanded, (10 to 75).
Many of my patients typically have stored vit D levels of 12--very low-- and active vit D levels of 100-- still high even though the range has changed.
In some way, the body--the immune system ostensibly, is trying to rectify the problems related to the infection (maybe). After treatment many patients have D levels in the normal ranges. This varies: some patients have D levels which drop across the board.
It now seems to me that judicious supplementation of D may in fact be very useful. Levels need to be monitored. the use of Benicar to inhibit renal conversion of inactive to active D may be a bad idea. Our bodies are pretty smart: let them balance the levels as needed. If active levels are above 100 I am somewhat hesitant to recommend D supplements. I have no basis for this. Again, vitamin D toxicity is difficult to attain. Reported cases have only been reported in individuals taking 40,000 units daily over a period of time.
Much research has been done on vitamin D. All of it is based on measurement of the inactive form, vitamin D hydroxy 25, which correlates with stored vitamin D. Yes, vitamin D has anti-inflammatory properties, but this may not be a bad thing. It affects cytokines andT-cell activation. But contrary to previous comments, it is active vitamin D that increases production of an anti-microbial peptide: cathelicidin. (Past statements that active D tilts the immune system from Th1 to Th2--causing production of anti-microbial peptides is wrong). The binding of active D to receptors modulates the genetic expression of complex proteins. VDRs (vitamin D receptors) are found in many organs in the body, including: brain, heart, skin, gonads, prostate and breast. Vitamin D receptors are found on a variety of immune cells, including: monocytes, B-cells and activated T-cells. It also has effects on dendritic cells. Vitamin D toxicity is very rare, even in patients with very high levels of active vitamin D, the 1,25 dihydroxy form.
Anti-inflammatory effects of D may lower the risk cancers, autoimmune disease, diabetes, heart disease and others. Recent research has shown that vitamin D is required to activate the histocompatibility gene, HLA-DRB 1501. This activation is necessary for the immune system to differentiate between self and non self in a select group of patients.
A link between vitamin D and MS has been shown. Perhaps the lack of MS in tropical climes
is not related to the absence of Bb and other infectious agents, as some have postulated, but due to higher levels of D from birth on.
The main source of D is sun light. Increased melanin decreases UVB penetration through the skin needed for conversion of D. It has been shown the black skin increases the risk of prostate cancer in the US but not in Africa--perhaps evidence of D's cancer fighting effects.
The Canadian Cancer Society has recommended that all it's citizens supplement with 1000 units of D daily.
D supplements are generally in the form called D3. This is the same form obtained from sun exposure. There are many forms of D and it's metabolism is very complex. Clinically, we only measure D in its stored and active forms.
In these numerous studies, only stored vitamin D is measured. Some doctors on the "cutting edge" have suggested that vitamin D hydroxy 25 levels are optimal at 75 (normal
32 to 100). But they are not looking at lab values I see in my practice. The range for normal active vitamin has been expanded, (10 to 75).
Many of my patients typically have stored vit D levels of 12--very low-- and active vit D levels of 100-- still high even though the range has changed.
In some way, the body--the immune system ostensibly, is trying to rectify the problems related to the infection (maybe). After treatment many patients have D levels in the normal ranges. This varies: some patients have D levels which drop across the board.
It now seems to me that judicious supplementation of D may in fact be very useful. Levels need to be monitored. the use of Benicar to inhibit renal conversion of inactive to active D may be a bad idea. Our bodies are pretty smart: let them balance the levels as needed. If active levels are above 100 I am somewhat hesitant to recommend D supplements. I have no basis for this. Again, vitamin D toxicity is difficult to attain. Reported cases have only been reported in individuals taking 40,000 units daily over a period of time.
Monday, November 23, 2009
Why doesn't my doctor believe in Lyme disease?
Scientists do research. They work in labs, at Universities. They work with bugs and test tubes; develop hypotheses, and design experiments to prove or disprove their theories. Sometimes they do basic science research-- to discover the basic structure and function of things. They publish their findings in prestigious, peer reviewed journals like Science and Nature. Such scientists have discovered much about the spirochete, Borrelia burdorferi, the causative agent of Lyme disease. This data is called "in vitro." Many doctors will claim that such results may not apply to the "in vivo" processes inside the body.
Physicians do not read these journals. They operate in parallel. They also have hypotheses. They evaluate their hypotheses with controlled clinical trials. Frequently medical trials provide confusing and contradictory data. In such cases the investigators can draw varying conclusions, sometimes informed by pre-existing biases.
Physicians(practitioners) are not scientists, although some may disagree. There are a few exceptions to this rule. Physicians work within the box of their trade. In medical school they are busy learning basic rules: structure and function of the body, types of disease--causes and treatments. Much of this is complex and ever changing. Evidence based medicine has helped physicians develop protocols and algorithms. The evidence is based on an analysis of the published studies in prestigious journals such as The New England Journal of Medicine and others. At times there is no or little data to support diagnoses and therapies. In such cases a body of "experts" informs the public of physicians regarding the best diagnoses and therapies. Even where no "science" exists, these opinions are surrogates for "science" and become-- "evidence based medicine." The waters are muddied. The distinctions between fact and opinion can become blurred.
The field of medicine is vast. It is broken down into various boxes. Some of these would include disciplines such as: internal medicine, orthopedics, rheumatology, neurology and infectious disease. (Of course this is a tiny selection of medical specialties for purposes of this discussion).
Perhaps readers do not know that all infectious disease specialists start out as generalists--internist or pediatricians, followed by a 2 year fellowship in infectious disease medicine. An infectious disease doctor has done: 4 years of college, 4 years of medical school, 3 years of residency and two years of training in infectious diseases. Note: for the first 11 years, the internists or family practitioner has had basically the same training as an "ID" doctor. Infectious disease doctors see sick hospital patients. They familiarize themselves with a wide range of esoteric infections: bacterial, viral, fungal, parasitic and others. They learn by reading text books, rounding with mentors and performing consults on sick patients, generally in hospitals. They spend very little time in an office setting. They become experts. They do not treat patients with chronic, "low grade" illnesses. They do not treat patients with fibromyalgia, depression, chronic fatigue syndrome and a whole other array of syndromes which they sometimes like to diagnose (in lieu of Lyme disease). Of course, they were generalists before they became specialists.
Each specialty has its own box. It works from a list of common diagnoses. Keep in mind--if you are a hammer, everything looks like a nail.
For example, a patient has joint pain. The orthopedist considers: tendinitis, a torn cartilage, a ligament injury, a mechanical injury--or something--not in his specialty, requiring referral to another specialists. The patient may be referred to a rheumatologist who considers: rheumatoid arthritis, lupus, Reiter's syndrome, post-infectious arthritis, gout and Lyme disease and others. He may conclude it is not in his field. He may refer on to an infectious disease specialist where considerations may include: an infected joint with something like gonorrhea, viral synovitis and perhaps Lyme disease. The Lyme results are negative for Lyme by the IDSA /CDC screening test. No answer is found. The patient is referred back to his primary care doctor. Physical therapy and pain medicines are recommended. If the patient asks about Lyme disease he is told this has already been excluded.
Lyme disease--LLMD style-- is outside the normal boxes. It is rejected by practitioners of the traditional boxes. It is foreign and rejected. After all, the true experts have spoken. These new practitioners outside the box, are easily labeled quacks. Paradigms do not change easily.
And in a nutshell, that is why your doctor does not believe in Lyme disease.
Physicians do not read these journals. They operate in parallel. They also have hypotheses. They evaluate their hypotheses with controlled clinical trials. Frequently medical trials provide confusing and contradictory data. In such cases the investigators can draw varying conclusions, sometimes informed by pre-existing biases.
Physicians(practitioners) are not scientists, although some may disagree. There are a few exceptions to this rule. Physicians work within the box of their trade. In medical school they are busy learning basic rules: structure and function of the body, types of disease--causes and treatments. Much of this is complex and ever changing. Evidence based medicine has helped physicians develop protocols and algorithms. The evidence is based on an analysis of the published studies in prestigious journals such as The New England Journal of Medicine and others. At times there is no or little data to support diagnoses and therapies. In such cases a body of "experts" informs the public of physicians regarding the best diagnoses and therapies. Even where no "science" exists, these opinions are surrogates for "science" and become-- "evidence based medicine." The waters are muddied. The distinctions between fact and opinion can become blurred.
The field of medicine is vast. It is broken down into various boxes. Some of these would include disciplines such as: internal medicine, orthopedics, rheumatology, neurology and infectious disease. (Of course this is a tiny selection of medical specialties for purposes of this discussion).
Perhaps readers do not know that all infectious disease specialists start out as generalists--internist or pediatricians, followed by a 2 year fellowship in infectious disease medicine. An infectious disease doctor has done: 4 years of college, 4 years of medical school, 3 years of residency and two years of training in infectious diseases. Note: for the first 11 years, the internists or family practitioner has had basically the same training as an "ID" doctor. Infectious disease doctors see sick hospital patients. They familiarize themselves with a wide range of esoteric infections: bacterial, viral, fungal, parasitic and others. They learn by reading text books, rounding with mentors and performing consults on sick patients, generally in hospitals. They spend very little time in an office setting. They become experts. They do not treat patients with chronic, "low grade" illnesses. They do not treat patients with fibromyalgia, depression, chronic fatigue syndrome and a whole other array of syndromes which they sometimes like to diagnose (in lieu of Lyme disease). Of course, they were generalists before they became specialists.
Each specialty has its own box. It works from a list of common diagnoses. Keep in mind--if you are a hammer, everything looks like a nail.
For example, a patient has joint pain. The orthopedist considers: tendinitis, a torn cartilage, a ligament injury, a mechanical injury--or something--not in his specialty, requiring referral to another specialists. The patient may be referred to a rheumatologist who considers: rheumatoid arthritis, lupus, Reiter's syndrome, post-infectious arthritis, gout and Lyme disease and others. He may conclude it is not in his field. He may refer on to an infectious disease specialist where considerations may include: an infected joint with something like gonorrhea, viral synovitis and perhaps Lyme disease. The Lyme results are negative for Lyme by the IDSA /CDC screening test. No answer is found. The patient is referred back to his primary care doctor. Physical therapy and pain medicines are recommended. If the patient asks about Lyme disease he is told this has already been excluded.
Lyme disease--LLMD style-- is outside the normal boxes. It is rejected by practitioners of the traditional boxes. It is foreign and rejected. After all, the true experts have spoken. These new practitioners outside the box, are easily labeled quacks. Paradigms do not change easily.
And in a nutshell, that is why your doctor does not believe in Lyme disease.
Cystic forms and relapse
It happens all the time. A patient has finally done great. No symptoms. Remission at last.
Symptom free with a "maintenance" med or regimen-- Doxycycline alone or Amoxicillin and Biaxin. Meds are stopped. Lyme symptoms return almost instantly, within days or weeks.
Why?
I have given this some thought. Lyme spirochetes grow slowly. They replicate every 24 hours give or take. The Lyme "load" hasn't suddenly grown exponentially. Is it autoimmune? Antibiotics do have anti-inflammatory properties; have they been suppressing a smoldering autoimmune response lying in wait? No--autoimmune processes generally progress gradually.
This leaves only one possibility. What happens quickly? Cyst forms of Lyme quickly convert to spirochetes, within hours. Ah-ha--the ready source of spirochetes!
As a patient recently told me: "The other antibiotics just cause everything (spirochetes and L-forms) to convert to cysts. Do they?
Cysts are metabolically inactive and generally don't make us sick; the brain seems to be the exception.
In the brain, cyst forms are associated with inflammation. There is experimental evidence supporting this. Tindamax-- the magic drug - sharpens the brain - eliminates vestiges of brain fog.
With the relapse, cognitive functions frequently remain intact while other Lyme symptoms explode. If brain cysts cause more damage than spirochestes there-- I quess this makes sense.
Questions: few answers. Do cyst busters lower relapse rates? Early or late?
Are dreaded L-forms in fact more docile than cysts? Not in the brain.
Perhaps a regimen of a cell wall inhibitor-cyst buster might work better in (in patients lacking cognitive dysfunction), assuming the germs have not passed the blood brain barrier.
Just a thought.
Symptom free with a "maintenance" med or regimen-- Doxycycline alone or Amoxicillin and Biaxin. Meds are stopped. Lyme symptoms return almost instantly, within days or weeks.
Why?
I have given this some thought. Lyme spirochetes grow slowly. They replicate every 24 hours give or take. The Lyme "load" hasn't suddenly grown exponentially. Is it autoimmune? Antibiotics do have anti-inflammatory properties; have they been suppressing a smoldering autoimmune response lying in wait? No--autoimmune processes generally progress gradually.
This leaves only one possibility. What happens quickly? Cyst forms of Lyme quickly convert to spirochetes, within hours. Ah-ha--the ready source of spirochetes!
As a patient recently told me: "The other antibiotics just cause everything (spirochetes and L-forms) to convert to cysts. Do they?
Cysts are metabolically inactive and generally don't make us sick; the brain seems to be the exception.
In the brain, cyst forms are associated with inflammation. There is experimental evidence supporting this. Tindamax-- the magic drug - sharpens the brain - eliminates vestiges of brain fog.
With the relapse, cognitive functions frequently remain intact while other Lyme symptoms explode. If brain cysts cause more damage than spirochestes there-- I quess this makes sense.
Questions: few answers. Do cyst busters lower relapse rates? Early or late?
Are dreaded L-forms in fact more docile than cysts? Not in the brain.
Perhaps a regimen of a cell wall inhibitor-cyst buster might work better in (in patients lacking cognitive dysfunction), assuming the germs have not passed the blood brain barrier.
Just a thought.
Wednesday, November 11, 2009
How it is supposed to work
I tend to write about unusual cases. Here is a more typical case--a successful one.
A 68 year old female visited me in January 2009. In 2005 she was sero-positive for Lyme disease. Treating was aggressive by standards of the day. She was treated with Doxycyline for 4 months. She recalls that her chief complaints then were rash, fatigue and joint pain associated. After treatment she felt better.
Over the past year she had not felt up to snuff. Pains in the large and small joints had returned. She had neck pains and muscle pains. She had numbness and tingling of her extremities. Her energy level was lower, she had fatigue, headaches, night-sweats, shortness of breath, an unsteady gait, poor sleep and a decline in cognition. She had trouble finding words and focusing.
She had brain-fog. Her sleep was disturbed.
Her exam was abnormal (neurological findings):her Igenex was positive IgG --34, 41: her Igenx B. duncani test IgM, 1:20 was borderline: a Clongen wet mount showed motile bacteria, presumed to be a species of Bartonella. Her SPECT scan showed poor perfusion to the left anterior temporal lobe: her MRI showed multiple white matter lesions consistent with Lyme disease or MS.
After treatment with courses of: Omnicef, Biaxin, Plaquenil, Tindamax, Zithromax, Mepron, Amoxicillin, Tindamax and Rifamin (in various combinations) She feels essentially normal. The treatment to date has lasted about 11 months. She is still on antibiotics and weaning will be done gradually. I suspect she will be on maintenance medications for a long time to come.
A 68 year old female visited me in January 2009. In 2005 she was sero-positive for Lyme disease. Treating was aggressive by standards of the day. She was treated with Doxycyline for 4 months. She recalls that her chief complaints then were rash, fatigue and joint pain associated. After treatment she felt better.
Over the past year she had not felt up to snuff. Pains in the large and small joints had returned. She had neck pains and muscle pains. She had numbness and tingling of her extremities. Her energy level was lower, she had fatigue, headaches, night-sweats, shortness of breath, an unsteady gait, poor sleep and a decline in cognition. She had trouble finding words and focusing.
She had brain-fog. Her sleep was disturbed.
Her exam was abnormal (neurological findings):her Igenex was positive IgG --34, 41: her Igenx B. duncani test IgM, 1:20 was borderline: a Clongen wet mount showed motile bacteria, presumed to be a species of Bartonella. Her SPECT scan showed poor perfusion to the left anterior temporal lobe: her MRI showed multiple white matter lesions consistent with Lyme disease or MS.
After treatment with courses of: Omnicef, Biaxin, Plaquenil, Tindamax, Zithromax, Mepron, Amoxicillin, Tindamax and Rifamin (in various combinations) She feels essentially normal. The treatment to date has lasted about 11 months. She is still on antibiotics and weaning will be done gradually. I suspect she will be on maintenance medications for a long time to come.
Tuesday, November 10, 2009
Lyme kills
February 2007. A 46 year old female walked into my office for a "Lyme consult." I did not know at of our meeting-- she had recently been found in the middle of a road trying to end her life. Luckily, she was picked up by a police cruiser and subsequently admitted to a psychiatric facility. I did not know, until today, that a past treating physician, a rheumatologist, had called her an "f...ing moron." This patient/human being, has had a long and bumpy ride, but no longer entertains thoughts of suicide. She was sick of being sick. She had been sick for one half of her life, since age 24. She had suffered with total body pain. She had been diagnosed with "seronegative" rheumatoid arthritis. Gold shots, prednisone and other "remedies" offered no respite from her misery. She had swollen lymph node. Her joints and muscles hurt--really hurt. She was told she had "a weak immune system." She had numerous neurological complaints. There was progressive loss of memory and global cognitive function for over 15 years. Most troubling of all was severe, unrelenting abdominal pain. This was her worst symptom. Numerous specialist had been unable to identify the source of the trouble.
Prioritising, the first thing I did was examine her belly. She had right upper quadrant tenderness and a positive Murphy's sign. Gastroenterologists and surgeons insisted there was nothing wrong with her gallbladder. Sonograms and HIDA scans had been abnormal. I sent her for another HIDA CCK test: normal. I told her she had a bad gallbladder--I didn't care what the tests said. Two surgeons refused to operate. A third ( a close friend) reluctantly agreed. Her gallbladder was bad--chronically infected. Her pain was gone! Now she thought I was a genius. No. I have just seen chronic cholecystitis in many Lyme patients. And her physical exam was classic for cholecystitis. I followed a rule one of mentors taught me back in medical school: treat the patient not the lab. I quess most doctors today had a different mentor.
She was seropositive for Babesia at the outset. The Labcorp Western Blot showed no bands. Her Igenex test negative although IgM bands were "inderterminate" at the 39, 41 and 93 positions.
Treat the patient. Rocephin. She Herxed. We went around the block--numerous times. Gradually, after much Mepron, a mix of oral antibiotics and two courses of Rocephin she was significantly better.
We(she) struggled with serious nicotine addiction: 3 packs per day. She ended up with a severe lung infection. I prescribed Levaquin and Cleocin. The Herx brought her to the hospital. It looked like a cavitary mass or abscess. This was February 2009. The surgeons were sure she had a tumor. The biopsies showed no cancer and no microbes would grow in the lab. Faint colonies were seen only to disappear. The surgeons still wanted to operate. Two PET scans later-- no cancer. She had a miracle response to Ivanz. I have written about this before. The pulmonologist gave her months to live(she tells me), severe COPD. I don't think so. She is not short of breath even with moderate excertion. Maybe he is just trying to scare her.
Today I saw her. She is depressed because she retired from her job (voluntarily). She cleans houses part-time! Her pain is mangaged with modest help from "our friends". Good days and bad days. The bad ones aren't that bad. She is nervous: another PET scan. She wants to quit smoking--just can't do it.
I never knew about the suicide attempt--until today.
Prioritising, the first thing I did was examine her belly. She had right upper quadrant tenderness and a positive Murphy's sign. Gastroenterologists and surgeons insisted there was nothing wrong with her gallbladder. Sonograms and HIDA scans had been abnormal. I sent her for another HIDA CCK test: normal. I told her she had a bad gallbladder--I didn't care what the tests said. Two surgeons refused to operate. A third ( a close friend) reluctantly agreed. Her gallbladder was bad--chronically infected. Her pain was gone! Now she thought I was a genius. No. I have just seen chronic cholecystitis in many Lyme patients. And her physical exam was classic for cholecystitis. I followed a rule one of mentors taught me back in medical school: treat the patient not the lab. I quess most doctors today had a different mentor.
She was seropositive for Babesia at the outset. The Labcorp Western Blot showed no bands. Her Igenex test negative although IgM bands were "inderterminate" at the 39, 41 and 93 positions.
Treat the patient. Rocephin. She Herxed. We went around the block--numerous times. Gradually, after much Mepron, a mix of oral antibiotics and two courses of Rocephin she was significantly better.
We(she) struggled with serious nicotine addiction: 3 packs per day. She ended up with a severe lung infection. I prescribed Levaquin and Cleocin. The Herx brought her to the hospital. It looked like a cavitary mass or abscess. This was February 2009. The surgeons were sure she had a tumor. The biopsies showed no cancer and no microbes would grow in the lab. Faint colonies were seen only to disappear. The surgeons still wanted to operate. Two PET scans later-- no cancer. She had a miracle response to Ivanz. I have written about this before. The pulmonologist gave her months to live(she tells me), severe COPD. I don't think so. She is not short of breath even with moderate excertion. Maybe he is just trying to scare her.
Today I saw her. She is depressed because she retired from her job (voluntarily). She cleans houses part-time! Her pain is mangaged with modest help from "our friends". Good days and bad days. The bad ones aren't that bad. She is nervous: another PET scan. She wants to quit smoking--just can't do it.
I never knew about the suicide attempt--until today.
Monday, November 9, 2009
What do those lab tests mean?
The CD57 test (only from Labcorp) measures a subset of NKT cells. These are Natural Killer T Cells. These T cells are actors in the innate immune response. In other words, these cells automatically attack what our immune system sees as foreign invaders. Our immune systems are naturally smart (anthropomorphically). They have pattern recognition cells which can determine tissues/cells that belong in our bodies from things (like bacteria) that do not belong in our bodies. The second part of the immune system, the acquired immune system relates to a complex set of reactions by which the immune system learns to make specific antibodies to attack the foreign invader. In some situations only the innate immune system is in play. Primarily this occurs when the "invaders" are intracellular. The acquired responses just don't work here. In the case of Lyme disease it is the intracellula- L-forms which are attacked by the NKT cells. When the CD57 count is low it would appear these cells are busy combating the L-forms of Lyme. Unfortunately, the innate immune system is never 100% effective in eliminating the bacteria. This is one of the mechanisms by which Lyme is able to persist in the face of antibiotics and immune responses.
C3a and C4a (Labcorp) are products of the complement system, cleaved from C3 and C4. These proteins are mobilized by the immune system as part of its acquired and to a lesser extent innate immune responses. These proteins can attach to unwanted bacteria and target them for destruction. These tests are sensitive indicators of a busy immune system attacking unwanted proteins or germs. These markers can provide a general sense of immune activation in the face of infection or inflammation.
C3d (Quest only) is a test for circulating immune complexes (CIC). These antibody/antigen complexes are not supposed to be present in our blood. The presence of these CICs indicates infection or inflammation and can be used as another indicator of disease activity.
C-reactive protein (CRP) is a naturally occurring protein found in blood circulation. It is one of two proteins which activate the complement system associated with immune activation. This is another marker which can help assess disease activity. This marker is elevated in many diseases and is not specific for Lyme disease. When used here, the clincially useful cut-off points may be much lower than the "normal" reported by the lab.
There are many other labs/markers of infection/inflammation. But here a few that seem to confuse many patients (and doctors).
C3a and C4a (Labcorp) are products of the complement system, cleaved from C3 and C4. These proteins are mobilized by the immune system as part of its acquired and to a lesser extent innate immune responses. These proteins can attach to unwanted bacteria and target them for destruction. These tests are sensitive indicators of a busy immune system attacking unwanted proteins or germs. These markers can provide a general sense of immune activation in the face of infection or inflammation.
C3d (Quest only) is a test for circulating immune complexes (CIC). These antibody/antigen complexes are not supposed to be present in our blood. The presence of these CICs indicates infection or inflammation and can be used as another indicator of disease activity.
C-reactive protein (CRP) is a naturally occurring protein found in blood circulation. It is one of two proteins which activate the complement system associated with immune activation. This is another marker which can help assess disease activity. This marker is elevated in many diseases and is not specific for Lyme disease. When used here, the clincially useful cut-off points may be much lower than the "normal" reported by the lab.
There are many other labs/markers of infection/inflammation. But here a few that seem to confuse many patients (and doctors).
Friday, November 6, 2009
Musings with a patient today
Biaxin and Plaquenil? We have been taught that Plaquenil makes the intracellular environment more alkaline so Biaxin works better. Is this true? I don't know. I have also read that Plaquenil is anti-cyst. Sapi has now shown that Plaquenil induces cysts. You are on so many meds: let's drop the Plaquenil for now. The Malarone seems to be making the sweats go away. You are not sure, could the the sweats are hormonally induced? Possibly. My guess is that we are fighting Babesia: you tested positive. The low dose anti-malarial drug seems to work. Other patients require much higher doses.Biaxin decreases the Atovaquone by up to 40%. Many doctors switch to Zithromax for Babesia; Biaxin is a much better Lyme drug. We are covering more territory. The Bactrim you are taking for Bartonella also has some anti-Babesia effects; perhaps that is why you are doing so well. Patients seem to do better in the long run when anti-cyst drugs are added. Tindamax is the best--but that is for later.
How long do we treat Babesia for? Good question. Until the symptoms go away. There is no magic number. It has been said treat for 5 months because red blood cells have a 4 month life span. The only problem is that Babesia can also hide in the bone marrow, liver and spleen. The IDSA claims that it only resides in red blood cells--not true.
You followed all of that? You are doing better than you think!
How long do we treat Babesia for? Good question. Until the symptoms go away. There is no magic number. It has been said treat for 5 months because red blood cells have a 4 month life span. The only problem is that Babesia can also hide in the bone marrow, liver and spleen. The IDSA claims that it only resides in red blood cells--not true.
You followed all of that? You are doing better than you think!
Bartonella: brief report
A patient with documented chronic Lyme disease had further testing for Bartonella.
A test performed at Fry labs reported abnormally shaped red blood cells without bacteria.
A wet mount at Clongen showed scarce round motile bacteria.
A PCR at Clongen for "Bartonella species," was positive.
In general, PCR testing for Bartonella is not performed because of a low yield.
These results, albeit in a single patient, suggest that: 1) wet mount exams may be more accurate than stained whole blood samples for the identification of these bacteria and 2) these small round organisms seen in patient's blood do in fact suggest ongoing infection with Bartonella species.
A test performed at Fry labs reported abnormally shaped red blood cells without bacteria.
A wet mount at Clongen showed scarce round motile bacteria.
A PCR at Clongen for "Bartonella species," was positive.
In general, PCR testing for Bartonella is not performed because of a low yield.
These results, albeit in a single patient, suggest that: 1) wet mount exams may be more accurate than stained whole blood samples for the identification of these bacteria and 2) these small round organisms seen in patient's blood do in fact suggest ongoing infection with Bartonella species.
Friday, October 30, 2009
Odds and ends and ILADS
Patients treated for Bartonella seem to experience of lot of itching which may be associated with rashes, bumps or normal skin. It seems to be some sort of Herx reaction.
Eva Sapi's research: very revealing. Lyme in the test tube quickly convert to cyst form when doxycyline is added to the cultures. Plaquenil also increases cyst formation (some Lyme literature claims that Plaquenil is an anti-cyst drug). Three drugs were shown to reduce the cyst load. In order of increasing potency: albendazole, metronidazole (Flagyl) and tinidazole (Tindamax). Of course this is in a test tube or culture medium. There are no cells. L-form transformation cannot be observed.
The ILADS' conference was great this year. Presentations were scientific and evidenced based.
Sessions discussing therapeutic options were great as well. I started my first patient on tigacyline, a drug much favored by Dr. Burasanno.
I have liked the layering approach for very ill patients. Start with IV Rocephin, add IV Zithromax and then add IV Flagyl. Dr. Martz agrees with my approach. We have both found this to be very effective. Other physicians recommend pulsing antibiotics in very high doses, primarily with Rocephin. Dr. Burasanno and Dr. Horowitz were animated and informative. "There is no one right way to treat Lyme."---Dr. Burascanno.
Eva Sapi's research: very revealing. Lyme in the test tube quickly convert to cyst form when doxycyline is added to the cultures. Plaquenil also increases cyst formation (some Lyme literature claims that Plaquenil is an anti-cyst drug). Three drugs were shown to reduce the cyst load. In order of increasing potency: albendazole, metronidazole (Flagyl) and tinidazole (Tindamax). Of course this is in a test tube or culture medium. There are no cells. L-form transformation cannot be observed.
The ILADS' conference was great this year. Presentations were scientific and evidenced based.
Sessions discussing therapeutic options were great as well. I started my first patient on tigacyline, a drug much favored by Dr. Burasanno.
I have liked the layering approach for very ill patients. Start with IV Rocephin, add IV Zithromax and then add IV Flagyl. Dr. Martz agrees with my approach. We have both found this to be very effective. Other physicians recommend pulsing antibiotics in very high doses, primarily with Rocephin. Dr. Burasanno and Dr. Horowitz were animated and informative. "There is no one right way to treat Lyme."---Dr. Burascanno.
Tuesday, October 27, 2009
A second opinion
A 36 year woman recently requested a second opinion after a recent diagnosis of MS.
She reported a history of tick bite. A Lyme WB from Labcorp revealed positive bands: IgG 41 and IgM 23. She was told her test results excluded Lyme in the differential.
One month prior to our visit she complained of numbness in her left upper and lower extremities. She also reported some stiffness in her neck.
Other symptoms were discounted: flu like symptoms with sweats and low grade fevers, swollen glands, joint swelling and pain and fatigue. Additional history revealed Bell's Palsy 15 years ago, heart palpitations and irritability. She initially denied all cognitive symptoms, only after further questioning she did admit to some progressive memory loss of the preceding two years.
An MRI revealed 4 white matter lesions in the brain and one in the cervical spinal cord.
The radiology report: "....demyelination due to multiple sclerosis or Lyme disease." This report was not from a radiology source which is familiar with my work.
As part of the MS work up the neurologist did an LP (spinal tap). I asked her to send a specimen to Clongen for PCR.
A report came to my desk amongst the usual pile of of daily lab reports and various requests.
This one caught my eye. Her spinal fluid was PCR positive for Lyme.
I called back to the office right away.
Her lab result and her appearance were incongruent. She sat across from me smiling, in no distress, appearing healthy in a casual glance.
This patient had Lyme in her spinal fluid. She had lesions in her brain.
She felt minimally ill and looked remarkably well. Of course I started IV Rocephin immediately.
During our most recent visit she told me she had seen "Under Our Skin."
She asked me: "How comes I am not sick like those people with Lyme?"
She reported a history of tick bite. A Lyme WB from Labcorp revealed positive bands: IgG 41 and IgM 23. She was told her test results excluded Lyme in the differential.
One month prior to our visit she complained of numbness in her left upper and lower extremities. She also reported some stiffness in her neck.
Other symptoms were discounted: flu like symptoms with sweats and low grade fevers, swollen glands, joint swelling and pain and fatigue. Additional history revealed Bell's Palsy 15 years ago, heart palpitations and irritability. She initially denied all cognitive symptoms, only after further questioning she did admit to some progressive memory loss of the preceding two years.
An MRI revealed 4 white matter lesions in the brain and one in the cervical spinal cord.
The radiology report: "....demyelination due to multiple sclerosis or Lyme disease." This report was not from a radiology source which is familiar with my work.
As part of the MS work up the neurologist did an LP (spinal tap). I asked her to send a specimen to Clongen for PCR.
A report came to my desk amongst the usual pile of of daily lab reports and various requests.
This one caught my eye. Her spinal fluid was PCR positive for Lyme.
I called back to the office right away.
Her lab result and her appearance were incongruent. She sat across from me smiling, in no distress, appearing healthy in a casual glance.
This patient had Lyme in her spinal fluid. She had lesions in her brain.
She felt minimally ill and looked remarkably well. Of course I started IV Rocephin immediately.
During our most recent visit she told me she had seen "Under Our Skin."
She asked me: "How comes I am not sick like those people with Lyme?"
Monday, October 19, 2009
Thoughts on psych drugs for Lyme patients
These are my opinions based on my reading and clinical experiences.
Most of the patients I treat with significant chronic Lyme disease suffer with a variety of neuro-psychiatric symptoms. Patients have recently commented to me about the post on Klonopin.
Patients with Lyme-Brain seem to have poor tolerance for SSRIs: drugs which increase serotonin levels in brain synapses. Perhaps the injured brain is sensitive to these drugs. Many patients come to me already taking drugs with a strong affinity for serotonin receptors in the brain such as Lexapro or Cymbalta. These drugs may cause increased brain fog, irritability and a paradoxical increase in depression.
Other anti-depressants act primarily on the brain chemical norepinephrine. Patients seem to tolerate these drugs better. These includes the anti-depressant Wellbutrin and ADD medicines which also effect dopamine. Charts in pharma books show the relative affinity of anti-depressants for serotonin and norepinephrine. If the ratio favors norepinephrine the patients may tolerate this drug better. This includes drugs such as Desipramine, an old TCA antidepressant. These meds are best tolerated in low doses.
Drugs used for ADD can be quite helpful. These drugs target the neuro-transmitter dopamine as
well as norepinephrine. These drugs increase wakefulness and energy and may correct some frontal lobe dysfunction seen in many Lyme patients. My favorite drug here is Ritalin which comes in a variety of doses and can be carefully titrated.
Mood stabilizers can be very helpful as well. These drugs are anti-convulsants which stabilize abnormal chemical/electrical imbalances in the brain. I like Lamictal because it has antidepressant effects and mild glutamate inhibition. This drug has significant toxicity and should only be prescribed by physicians familiar with its side effects. Glutamate toxicity is thought to be a major problem in the injured brain. The best drug for glutamate toxicity may be the anti-Alzheimer's drug Namenda, which frequently improves cognitive dysfunction.(Rocephin also works by this mechanism).
Klonopin binds to the neuro-transmitter GABA, which is a major inhibitory neuro-transmitter.
Lyme patients can suffer with excessive expression of excitatory neurochemical in the brain. Most of this is mediated by serotonin, the "work horse of the brain." This dovetails with my comments about the potential harmful effects of serotonergic drugs.
Other commonly used GABA drugs are Neurontin and Lyrica which may be well tolerated. In my experience, benzodizapines like Klonopin work better. This may be due their increased anti-anxiety effects.
Anti-psychotic medicines, like Seroqel, are certainly helpful for patients experiencing psychotic symptoms such as hallucinations. They may help in other ways. Although they inhibit dopamine, they bind to different receptors, deep in the brain, unlike ADD medications which stimulate dopamine pathways in the cortex of the brain.
Many Lyme patients have sleep disorders. The activating neuro-chemicals, serotonin and norepinephrine are prominent during waking hours. This is counteracted by a predominance of acetlycholine effects which occur during sleep. Restful sleep is important. When a "sleeper" is needed I prefer Restoril which produces a good night's sleep and promotes normal sleep architecture. Lunesta may be a good alternative.
Most of the patients I treat with significant chronic Lyme disease suffer with a variety of neuro-psychiatric symptoms. Patients have recently commented to me about the post on Klonopin.
Patients with Lyme-Brain seem to have poor tolerance for SSRIs: drugs which increase serotonin levels in brain synapses. Perhaps the injured brain is sensitive to these drugs. Many patients come to me already taking drugs with a strong affinity for serotonin receptors in the brain such as Lexapro or Cymbalta. These drugs may cause increased brain fog, irritability and a paradoxical increase in depression.
Other anti-depressants act primarily on the brain chemical norepinephrine. Patients seem to tolerate these drugs better. These includes the anti-depressant Wellbutrin and ADD medicines which also effect dopamine. Charts in pharma books show the relative affinity of anti-depressants for serotonin and norepinephrine. If the ratio favors norepinephrine the patients may tolerate this drug better. This includes drugs such as Desipramine, an old TCA antidepressant. These meds are best tolerated in low doses.
Drugs used for ADD can be quite helpful. These drugs target the neuro-transmitter dopamine as
well as norepinephrine. These drugs increase wakefulness and energy and may correct some frontal lobe dysfunction seen in many Lyme patients. My favorite drug here is Ritalin which comes in a variety of doses and can be carefully titrated.
Mood stabilizers can be very helpful as well. These drugs are anti-convulsants which stabilize abnormal chemical/electrical imbalances in the brain. I like Lamictal because it has antidepressant effects and mild glutamate inhibition. This drug has significant toxicity and should only be prescribed by physicians familiar with its side effects. Glutamate toxicity is thought to be a major problem in the injured brain. The best drug for glutamate toxicity may be the anti-Alzheimer's drug Namenda, which frequently improves cognitive dysfunction.(Rocephin also works by this mechanism).
Klonopin binds to the neuro-transmitter GABA, which is a major inhibitory neuro-transmitter.
Lyme patients can suffer with excessive expression of excitatory neurochemical in the brain. Most of this is mediated by serotonin, the "work horse of the brain." This dovetails with my comments about the potential harmful effects of serotonergic drugs.
Other commonly used GABA drugs are Neurontin and Lyrica which may be well tolerated. In my experience, benzodizapines like Klonopin work better. This may be due their increased anti-anxiety effects.
Anti-psychotic medicines, like Seroqel, are certainly helpful for patients experiencing psychotic symptoms such as hallucinations. They may help in other ways. Although they inhibit dopamine, they bind to different receptors, deep in the brain, unlike ADD medications which stimulate dopamine pathways in the cortex of the brain.
Many Lyme patients have sleep disorders. The activating neuro-chemicals, serotonin and norepinephrine are prominent during waking hours. This is counteracted by a predominance of acetlycholine effects which occur during sleep. Restful sleep is important. When a "sleeper" is needed I prefer Restoril which produces a good night's sleep and promotes normal sleep architecture. Lunesta may be a good alternative.
Tuesday, October 13, 2009
The sick role and Lyme
I saw a patient today who has been treated by another physician. The patient spends nearly his entire day taking supplements along with a complex regime of antimicrobials meticulously scheduled. The medicines are rotated and pulsed within specific protocols. This patient is going broke, in part because of the high cost of supplements which he assiduously takes per his physician's directions. He has stopped working in part because his illness is a full time job. His life centers around being THE PATIENT. Lyme disease has become his life. There is no time for normalcy. The sick role can become integrated into the disease. Perhaps, ironically, some readers of this BLOG focus all of their attention on their illness--scouring discussion forums, constantly perusing the Internet, seeking some new tidbit of esoteric information. The disease becomes a life style.
Many of my patients have told me that they no longer read my BLOG or read about Lyme disease, the politics and the controversies. Of course when I see such patients we discus the course of their disease and the rationale behind prescribed therapies during each visit.
These patients may be free to pursue a life which is as normal as possible. They spend time with family and friends. They function at the highest level possible in a multitude of domains. Suffering with Lyme disease becomes something they live with: It is not the center of their universe.
Such patients get up every morning, despite pain and other symptoms, put on their best faces and face life head on in spite of adversity. Other patients are constrained within a prison, imagined or real, comprised of walls, esmeshed in the fabric of illness and its attendant disabilites.
So I like to keep the regimens simple, and largely devoid of supplements. Changes are made when patients see me at scheduled appointments.
A word about supplements. Some patients certainly report benefits from a variety of add-ons. Some feel energized from Co-enzyme Q10, which I truly think helps many people. Some swear by teasel root. I may recommend one or two additional supplements but not many. I do not recommend multi-vitamins on a routine basis.
I was reared in medicine with a healthy dose of skepticism regarding vitamins.(I have discussed this before). Vitamin E--the "miracle worker," turned to offer no benefits to heart patients in controlled, published studies. Vitamin C turned out to be potentially harmful to heart patients. It was shown to increase plaque in arteries, increasing the risk of heart disease unexpectedly. Simple chemistry may give us the reason. Vitamin C can exist chemically in a reduced or oxidized form. The reduced form is an anti-oxidant; the oxidized form can be a harmful pro-oxidant. Supplements may not be properly balanced. So I perfer to leave nutrients and vitamins in the capable hands of Mother Nature. I stress a healthy diet with fruits, vegetables and whole grains which gives the body vitamins in their proper form along with the potpourri of photochemicals needed for these nutrients to perform optimally.
A folksy argument I frequently share with patients is something like this: A chronically ill patient is likely to be deficient in a variety of nutrients. This is caused by the illness or chronic infection as in the case of Lyme disease. One can think of such a patient as akin to a gas tank with a hole in its bottom. You keep filling up the tank with gas (supplements) but the tank is perpetually empty because the fuel drains through the gaping hole. Close the hole first--by getting the infection under control, and then the metaphorical tank can become full with the needed fuel.
A case of not putting the cart before the horse.
This does not apply to patients with dramatic deficiencies. And of course, this is just my working hypothesis and I know that most other physicians operate from the opposite paradigm.
My experience tell me that it works both medically and psychologically for my patients.
Many of my patients have told me that they no longer read my BLOG or read about Lyme disease, the politics and the controversies. Of course when I see such patients we discus the course of their disease and the rationale behind prescribed therapies during each visit.
These patients may be free to pursue a life which is as normal as possible. They spend time with family and friends. They function at the highest level possible in a multitude of domains. Suffering with Lyme disease becomes something they live with: It is not the center of their universe.
Such patients get up every morning, despite pain and other symptoms, put on their best faces and face life head on in spite of adversity. Other patients are constrained within a prison, imagined or real, comprised of walls, esmeshed in the fabric of illness and its attendant disabilites.
So I like to keep the regimens simple, and largely devoid of supplements. Changes are made when patients see me at scheduled appointments.
A word about supplements. Some patients certainly report benefits from a variety of add-ons. Some feel energized from Co-enzyme Q10, which I truly think helps many people. Some swear by teasel root. I may recommend one or two additional supplements but not many. I do not recommend multi-vitamins on a routine basis.
I was reared in medicine with a healthy dose of skepticism regarding vitamins.(I have discussed this before). Vitamin E--the "miracle worker," turned to offer no benefits to heart patients in controlled, published studies. Vitamin C turned out to be potentially harmful to heart patients. It was shown to increase plaque in arteries, increasing the risk of heart disease unexpectedly. Simple chemistry may give us the reason. Vitamin C can exist chemically in a reduced or oxidized form. The reduced form is an anti-oxidant; the oxidized form can be a harmful pro-oxidant. Supplements may not be properly balanced. So I perfer to leave nutrients and vitamins in the capable hands of Mother Nature. I stress a healthy diet with fruits, vegetables and whole grains which gives the body vitamins in their proper form along with the potpourri of photochemicals needed for these nutrients to perform optimally.
A folksy argument I frequently share with patients is something like this: A chronically ill patient is likely to be deficient in a variety of nutrients. This is caused by the illness or chronic infection as in the case of Lyme disease. One can think of such a patient as akin to a gas tank with a hole in its bottom. You keep filling up the tank with gas (supplements) but the tank is perpetually empty because the fuel drains through the gaping hole. Close the hole first--by getting the infection under control, and then the metaphorical tank can become full with the needed fuel.
A case of not putting the cart before the horse.
This does not apply to patients with dramatic deficiencies. And of course, this is just my working hypothesis and I know that most other physicians operate from the opposite paradigm.
My experience tell me that it works both medically and psychologically for my patients.
Sunday, October 11, 2009
THREE WEEKS OF DOXYCYCLINE
"Childhood friend's daughter in ICU for two weeks with-- Lyme disease---It is one thing after the next."
Keith Olbermann on health care.
THREE WEEKS OF DOXYCYCLINE.
"I just saved your life (diagnosing Lyme disease in friend's wife)." Larry David.
THREE WEEKS OF DOXYCYCLINE.
"I heard you never get over Lyme disease; I have a friend in a wheel chair; so many people are so sick, its a very scary disease." A patient.
THREE WEEKS OF DOXYCYCLINE.
"I used to function at a high level (computer engineer), now I can no longer do my job" A patient.
THREE WEEKS OF DOXYCYCLINE.
"I have been to 40 doctors. No one ever took me seriously--thank God you are listening to me."
THREE WEEKS OF DOXYCYCLINE.
" I would like to help you--but we have a two tier test--you never had a rash--NIH studies--
IDSA recommendations--and CDC--I can't treat you I might get in trouble--those ILADS, LLMDS are--I don't know, out there--you don't want to miss another "real" diagnosis like fibromyalgia or depression."
THREE WEEKS OF DOXYCYCLINE.
Keith Olbermann on health care.
THREE WEEKS OF DOXYCYCLINE.
"I just saved your life (diagnosing Lyme disease in friend's wife)." Larry David.
THREE WEEKS OF DOXYCYCLINE.
"I heard you never get over Lyme disease; I have a friend in a wheel chair; so many people are so sick, its a very scary disease." A patient.
THREE WEEKS OF DOXYCYCLINE.
"I used to function at a high level (computer engineer), now I can no longer do my job" A patient.
THREE WEEKS OF DOXYCYCLINE.
"I have been to 40 doctors. No one ever took me seriously--thank God you are listening to me."
THREE WEEKS OF DOXYCYCLINE.
" I would like to help you--but we have a two tier test--you never had a rash--NIH studies--
IDSA recommendations--and CDC--I can't treat you I might get in trouble--those ILADS, LLMDS are--I don't know, out there--you don't want to miss another "real" diagnosis like fibromyalgia or depression."
THREE WEEKS OF DOXYCYCLINE.
Tuesday, October 6, 2009
Cipro and Klonopin
A 59 year old patient was prescribed Cipro in 1992 for a urinary tract infection. He experienced a variety of progressive symptoms. These included burning sensations, shortness of breath, fatigue, confusion, chills, sleep disturbances, night sweats, a feeling of alternating hot and cold, ocular problems, increasing cognitive dysfunction, a sensation of electric shocks and many other symptoms. After a long evaluation it was decided that he was suffering with a severe quinolone reaction; he was prescribed Klonopin which he has taken every since. The Klonopin has been effective.
He recently visited my office because he was not feeling well. He had been off Klonopin for 5 months and symptoms were returning. Off the Klonopin recently--he developed: severe fatigue, sleep disorders, tinnitus, head pressure, a sensation of electric shocks, numbness and tingling, joint pain, increased anxiety and hot and cold sensations.
Upon further questioning, perhaps he has not felt entirely normal on Klonopin. He has suffered with stiff fingers, anxiety, periodic weakness in his legs. dry mouth with dental carries and progressive brain fog associated with progressive memory loss. He has written these symptoms off to normal aging.
His wife has been successfully treated for chronic Lyme disease.
An exam showed evidence a stocking glove pattern of decreased sensitivity to pin prick, a loss of vibratory sense and absent deep tendon reflexes in his ankles.
A brain MRI showed non specific, periventricular white matter changes compatible with microvascular ischemic changes. He has no risk factors for this disease.
An initial set of lab studies (lLabcorp) showed: CD57 24, Bb Western blot no bands, Bababesia duncani positive, titer 1:256, all other studies negative. He vitamin D levels were properly balanced. There was no evidence of autoimmune dysfunction or inflammation.
He is an outdoors-man. He lives in a wooded area frequented by visiting deer.
I sent off another Lyme Western Blot to Clongen. (pending)
Many questions remain in this case, answered at this point. Is this truly a case of quinolone toxicity? If so, why have symptoms persisted for 17 years. Are quinolone reactions, at least in some cases, really "Herx" reactions in patients with asymptomatic but disseminated Lyme disease? I have documented such a case in a previous post. He does test positive for Babesia; this suggests exposure to tick borne illness. He has many symptoms and signs frequently seen in chronic Lyme disease. Why has Klonopin, a sedative, been so effective in stabilizing many of his symptoms for so many years, and why does he quickly relapse off Klonopin? The persistence of symptoms 5 months after stopping Klonopin makes withdrawal an unlikely explanation for this phenomenon. Does Klonopin. a GABA agonist in the brain have any positive benefits for some Lyme patients? For now, I have questions, not answers.
I hope the second Western Blot will be telling.
He recently visited my office because he was not feeling well. He had been off Klonopin for 5 months and symptoms were returning. Off the Klonopin recently--he developed: severe fatigue, sleep disorders, tinnitus, head pressure, a sensation of electric shocks, numbness and tingling, joint pain, increased anxiety and hot and cold sensations.
Upon further questioning, perhaps he has not felt entirely normal on Klonopin. He has suffered with stiff fingers, anxiety, periodic weakness in his legs. dry mouth with dental carries and progressive brain fog associated with progressive memory loss. He has written these symptoms off to normal aging.
His wife has been successfully treated for chronic Lyme disease.
An exam showed evidence a stocking glove pattern of decreased sensitivity to pin prick, a loss of vibratory sense and absent deep tendon reflexes in his ankles.
A brain MRI showed non specific, periventricular white matter changes compatible with microvascular ischemic changes. He has no risk factors for this disease.
An initial set of lab studies (lLabcorp) showed: CD57 24, Bb Western blot no bands, Bababesia duncani positive, titer 1:256, all other studies negative. He vitamin D levels were properly balanced. There was no evidence of autoimmune dysfunction or inflammation.
He is an outdoors-man. He lives in a wooded area frequented by visiting deer.
I sent off another Lyme Western Blot to Clongen. (pending)
Many questions remain in this case, answered at this point. Is this truly a case of quinolone toxicity? If so, why have symptoms persisted for 17 years. Are quinolone reactions, at least in some cases, really "Herx" reactions in patients with asymptomatic but disseminated Lyme disease? I have documented such a case in a previous post. He does test positive for Babesia; this suggests exposure to tick borne illness. He has many symptoms and signs frequently seen in chronic Lyme disease. Why has Klonopin, a sedative, been so effective in stabilizing many of his symptoms for so many years, and why does he quickly relapse off Klonopin? The persistence of symptoms 5 months after stopping Klonopin makes withdrawal an unlikely explanation for this phenomenon. Does Klonopin. a GABA agonist in the brain have any positive benefits for some Lyme patients? For now, I have questions, not answers.
I hope the second Western Blot will be telling.
Monday, October 5, 2009
Case of Lyme pneumonitis with suspected resistant strain
See recent post about Lyme resistance to antibiotics.
This case is now much more interesting.
This is the patient as you may recall had neuroborrelios which improved when the patient was given Zosyn for pneumonial
The patient received only a short course of Zosyn in the hospital. She was discharged with oral Levaquin. She went on to develop shortness off breath. Follow up radiographic studies showed a pattern of lung nodules and diffuse interstitial disease. Various diagnoses were entertained, including: sarcoidosis, lung cancer and other better known opportunistic infection.
A brochoscopy was performed to obtain a tissue specimen. The biopsy was negative for the usual suspects with non-specific findings. Slides from the specimen were sent to Clongen Labs. A highly sensitive real time PCR test was positive for Borrelia burdorferi--the agent that causes Lyme disease.
I spoke with the pulmonologist today. He is not familiar with any medical literature supporting cases of disseminated Lyme disease in lung tissue. Lyme may have been a factor in her original pneumonia, but this is not my current hypothesis. Her initial pneumonia was due to aspiration. Perhaps the inflamed/damaged post-pneumonia lung tissue created an environment for the dissemination of Lyme bacteria into the lungs.
I offer the hypothesis that this patient has a resistant form of Lyme. This is why courses of Rocephin and Zithromax have failed. I have restarted Zosyn since it is the drug which has proved effective in the past.
There exists some research data which supports the notion that Lyme can become resistant to antibiotics. One would certainly expect this. Bb has an incredibly complex genomic structure.
It has more plasmids than any other know bacteria. Extra-nuclear DNA in plasmids can recombine with native DNA to create resistant strains of bacteria.
This is an exciting case; I hope to keep you posted.
This case is now much more interesting.
This is the patient as you may recall had neuroborrelios which improved when the patient was given Zosyn for pneumonial
The patient received only a short course of Zosyn in the hospital. She was discharged with oral Levaquin. She went on to develop shortness off breath. Follow up radiographic studies showed a pattern of lung nodules and diffuse interstitial disease. Various diagnoses were entertained, including: sarcoidosis, lung cancer and other better known opportunistic infection.
A brochoscopy was performed to obtain a tissue specimen. The biopsy was negative for the usual suspects with non-specific findings. Slides from the specimen were sent to Clongen Labs. A highly sensitive real time PCR test was positive for Borrelia burdorferi--the agent that causes Lyme disease.
I spoke with the pulmonologist today. He is not familiar with any medical literature supporting cases of disseminated Lyme disease in lung tissue. Lyme may have been a factor in her original pneumonia, but this is not my current hypothesis. Her initial pneumonia was due to aspiration. Perhaps the inflamed/damaged post-pneumonia lung tissue created an environment for the dissemination of Lyme bacteria into the lungs.
I offer the hypothesis that this patient has a resistant form of Lyme. This is why courses of Rocephin and Zithromax have failed. I have restarted Zosyn since it is the drug which has proved effective in the past.
There exists some research data which supports the notion that Lyme can become resistant to antibiotics. One would certainly expect this. Bb has an incredibly complex genomic structure.
It has more plasmids than any other know bacteria. Extra-nuclear DNA in plasmids can recombine with native DNA to create resistant strains of bacteria.
This is an exciting case; I hope to keep you posted.
Friday, October 2, 2009
Stranger than fiction: The third rail?
I have avoided the topic. But this story must be told.
My patient described in this post is a fifty something year old woman who has suffered with intractable neuroborreliosis for years. She failed numerous courses of IV Rocephin. Several years ago she presented with diffuse, small circular, open skin lesions particularly on her forearms. She told me fibers were coming out of the lesions. The patient had never heard of Morgellon's disease; still, I was a bit skeptical. When I witnessed fibers extruding through her skin while she was in my office I knew something unusual was afoot. Treating Lyme disease pursuant to ILADS methods is troublesome enough in my state. Thankfully, she was able to see another physician in California who has had success treating this strangest of maladies.In addition to her strange dermatological disorder she experienced chronic weakness, pain and confusion. Psychiatric symptoms included auditory hallucinations and racing manic-like thoughts. Her brain MRI showed diffuse white matter lesions. Her neuro-motor and cognitive disabilities left her disabled and feeling hopeless. She failed numerous courses of intensive treatment for both Lyme and co-infections. Her last fairly-recent course of Rocephin for 6 consecutive months had proved unhelpful. My colleague 3000 miles away treated her aggressively with a unorthodox regimen of Stromectal, Ivermectin and Albendazole in various combinations along with Diflucan and antibiotics.
After a year of these therapies her skin was clearing but the other symptoms remained.
She was seropositive for Babesia and had been treated with Mepron and Zithromax for nearly a year. Still, she continutined to have Babesia-like episodes associated with severe sweating. I decided to head in a new direction.
I started with IV Zithromax and Plaquenil. She had some good days: promising. I added Tindamax--a different anti-parasitic drug. It appeared to offer some further benefits. Then I added Malarone, one three times a day with Artemesin; she was definitely improving but my end point, cessation of sweating, had not occurred. Then I added Cleocin, only 300mg twice daily. The sweats were finally gone. And magically--she was back.
Of course she wasn't 100% better but she was stronger and able to attend to household activities. Her mind was fairly clear. She even helped one her kids with math homework.
None of this would have been conceivable 5 years ago.
So what is Morgellon's disease? Is a parasite? Is it a strange manifestation of a Lyme co-infection? It has been reported that 95% of Morgellon's patients also test positive for Lyme.
Saturday, September 19, 2009
Why BLOG?
As I have said in the past, this BLOG and others are a venue for putting ideas and experiences into the blogosphere for others to consider. My posts have covered many areas of agreement and controvery: mostly controvery. In my mind this is a major the role of this tool. Of course I have meant it to be informative. I learned much from my father. He frequently said outrageous things for the purpose of prodding others into a lively debate: The devil's advocate. If I have "criticized" other LLMDs it must be seen within this context. Please remember that just because something is in writing does not mean it is true.
This war over Lyme disease has been fomenting long before I came into the picture.
A belief in even the possibility of chronic Lyme disease would next exist except for the pioneering work of many who have bravely challenged the establishment, putting their careers and reputations on the line.
I have never intended to impeach the reputations of Burrascano, Jemsek, Jones, Stricker, Singleton, Fry or countless other physicians or scientist involved in this field over a period of 3 decades.
I personally do not know many of the great physicians and scientist involved in this field.
Many of my comments are based on information obtained only indirectly.
I have worked alone in my small corner of the world. By luck alone my office is a stone throw away from Clongen lab: I now have a colleague who helps me contemplate some of the mysteries associated with this illness.
Many clinicians have developed ideas and therapies which have been EFFECTIVE, even though the exact mechanisms were not fully understood by the clinicians at the time. Unable to get attention from mainstream medicine/science many "LLMDs" have functioned independently without the benefit of consultation with others. For example, the small round gram negative bacteria swarming in the blood of so many patients may be the labaoratory equivalent of the BLO described by Dr. Burasccano. The diagnosis was made strictly on clinical grounds. It was Fry labs who first put a face on this organism, giving it a name.
I have tried to the best of my ability to confine many comments to that which I believe has a factual basis supported by evidence of some kind. Much I have written has been editorial: opinion and conjecture; and I hope this has been made clear along the bumpy road.
Lyme disease is now Lyme-Borreliosis-Complex. It is a new and emerging disease. Much remains enigmatic. In essence all I have done is thow my hat into the ring.
I appreciate positive AND negative comments posted here. We are all learning and I suspect we will continue to do so for years to come.
This war over Lyme disease has been fomenting long before I came into the picture.
A belief in even the possibility of chronic Lyme disease would next exist except for the pioneering work of many who have bravely challenged the establishment, putting their careers and reputations on the line.
I have never intended to impeach the reputations of Burrascano, Jemsek, Jones, Stricker, Singleton, Fry or countless other physicians or scientist involved in this field over a period of 3 decades.
I personally do not know many of the great physicians and scientist involved in this field.
Many of my comments are based on information obtained only indirectly.
I have worked alone in my small corner of the world. By luck alone my office is a stone throw away from Clongen lab: I now have a colleague who helps me contemplate some of the mysteries associated with this illness.
Many clinicians have developed ideas and therapies which have been EFFECTIVE, even though the exact mechanisms were not fully understood by the clinicians at the time. Unable to get attention from mainstream medicine/science many "LLMDs" have functioned independently without the benefit of consultation with others. For example, the small round gram negative bacteria swarming in the blood of so many patients may be the labaoratory equivalent of the BLO described by Dr. Burasccano. The diagnosis was made strictly on clinical grounds. It was Fry labs who first put a face on this organism, giving it a name.
I have tried to the best of my ability to confine many comments to that which I believe has a factual basis supported by evidence of some kind. Much I have written has been editorial: opinion and conjecture; and I hope this has been made clear along the bumpy road.
Lyme disease is now Lyme-Borreliosis-Complex. It is a new and emerging disease. Much remains enigmatic. In essence all I have done is thow my hat into the ring.
I appreciate positive AND negative comments posted here. We are all learning and I suspect we will continue to do so for years to come.
Thursday, September 17, 2009
Antibiotic resistance: Wet mounts re-visited: IV Flagyl
The Bb genome has apparently been sequenced at the Craig Ventnor Institute in Rockville, MD.
The project took an extraordinary amount of time. The genetic structure of Bb unexpectedly complex.
Resistance: It is hard to know if Lyme spirochetes are resistant to antibiotics or not. There is no way to culture the bacteria and test for this. It is known that in vitro (in the test tube) a germ may appear resistant to an antibiotic, but when the antibiotic is administered at super high doses it is able to kill the organism. This begs the question: Do some patients only respond to Rocephin when it is administered at high doses for prolonged periods of time?
Recently, a patient of mine who appeared to have intractable Lyme neuroborreliosis--having failed Rocephin and Zithromax was admitted to a local hospital for pneumonia. In the hospital she was given an intravenous antibiotic called Zosyn. Zosyn is a third generation penicillin with an additional ingredient to protect from the effects of penicillin resistance. Within just a few days the patient had a response which was nothing short of miraculous.
Unfortunately, The only IV antibiotic on the IDSA list is Rocephin. The LLMD list of intravenous therapies for Lyme is expanded, but still limited. Perhaps in jurisdictions which give LLMDs more latitude--- (Connecticut, Rhode Island and California), other IV therapies should be tried.
The incredible wet mount exam: Numerous blood wet mounts of tick borne disease patients have now been studied. Four results have been found repeatedly.
1) Small motile gram negative bacteria, outside the cells are seen frequently. These unknowns may be the BLO, Bartonella like organisms described by other physicians. These bacteria respond to treatment with Bactrim, quinolones like Cipro, Rifampin and other similar drugs.
2) Crescent shaped organisms. These organisms do resemble Toxoplasmosis, which they are not. The seem to respond to therapy based on Malarone.
3) Elongated, larger structures are frequently seen. Very strange. These are thought to be parasites, worms--microfilaria like. These entities seem to respond to Tindamax based regimens. It has been suggested that Ivermectin may be effective but I have little experience here.
4) This is the finding which intrigues me the most at this time. White blood cells are observed with swarms of intracellular organisms. This resembles Ehrlichia or related organisms--but no positive ID has been made. It may be that Zithromax and Rifampin are effective here. I have just begun to do before and after analyses.
In many patients with neuroborreliosis syndromes the contribution of the BLO is very significant and must be considered. I apologize for old entries in which I questioned this issue.
One problem is that many non ill patients also show swarming gram negative bacteria in the blood as seen in some healthy controls. Here, clinical judgement rules the day.
Revisiting an old patient. Two years ago a patient with terrible neuroborreliosis was succesfully treated with a combination of first IV Rocephin followed by the addition of IV Zithromax and finally IV Flagyl. According to his recollections it was the IV Flagyl which helped him dramatically improve. Both oral Flagyl and oral Tindamax had not been helpful. This patient stabilized on long term oral antibiotics. After some time he was "lost to follow up." He stopped all antibiotics.
He has now returned with a full relapse of florid neuroborreliosis. He has been treated the same way. Rocephin during the entire course--Zithromax adding for a second phase of the course --and finally IV Flagyl added to the mix. He has improved with the first two drugs but is only 60% better after three and on half months. Today I ordered the Flagyl. He told me: " Doc, now I am going to turn the corner." I hope so. I have seen this result in other patients as well. The Flagyl is administered as a once daily dose of 500mg.
The project took an extraordinary amount of time. The genetic structure of Bb unexpectedly complex.
Resistance: It is hard to know if Lyme spirochetes are resistant to antibiotics or not. There is no way to culture the bacteria and test for this. It is known that in vitro (in the test tube) a germ may appear resistant to an antibiotic, but when the antibiotic is administered at super high doses it is able to kill the organism. This begs the question: Do some patients only respond to Rocephin when it is administered at high doses for prolonged periods of time?
Recently, a patient of mine who appeared to have intractable Lyme neuroborreliosis--having failed Rocephin and Zithromax was admitted to a local hospital for pneumonia. In the hospital she was given an intravenous antibiotic called Zosyn. Zosyn is a third generation penicillin with an additional ingredient to protect from the effects of penicillin resistance. Within just a few days the patient had a response which was nothing short of miraculous.
Unfortunately, The only IV antibiotic on the IDSA list is Rocephin. The LLMD list of intravenous therapies for Lyme is expanded, but still limited. Perhaps in jurisdictions which give LLMDs more latitude--- (Connecticut, Rhode Island and California), other IV therapies should be tried.
The incredible wet mount exam: Numerous blood wet mounts of tick borne disease patients have now been studied. Four results have been found repeatedly.
1) Small motile gram negative bacteria, outside the cells are seen frequently. These unknowns may be the BLO, Bartonella like organisms described by other physicians. These bacteria respond to treatment with Bactrim, quinolones like Cipro, Rifampin and other similar drugs.
2) Crescent shaped organisms. These organisms do resemble Toxoplasmosis, which they are not. The seem to respond to therapy based on Malarone.
3) Elongated, larger structures are frequently seen. Very strange. These are thought to be parasites, worms--microfilaria like. These entities seem to respond to Tindamax based regimens. It has been suggested that Ivermectin may be effective but I have little experience here.
4) This is the finding which intrigues me the most at this time. White blood cells are observed with swarms of intracellular organisms. This resembles Ehrlichia or related organisms--but no positive ID has been made. It may be that Zithromax and Rifampin are effective here. I have just begun to do before and after analyses.
In many patients with neuroborreliosis syndromes the contribution of the BLO is very significant and must be considered. I apologize for old entries in which I questioned this issue.
One problem is that many non ill patients also show swarming gram negative bacteria in the blood as seen in some healthy controls. Here, clinical judgement rules the day.
Revisiting an old patient. Two years ago a patient with terrible neuroborreliosis was succesfully treated with a combination of first IV Rocephin followed by the addition of IV Zithromax and finally IV Flagyl. According to his recollections it was the IV Flagyl which helped him dramatically improve. Both oral Flagyl and oral Tindamax had not been helpful. This patient stabilized on long term oral antibiotics. After some time he was "lost to follow up." He stopped all antibiotics.
He has now returned with a full relapse of florid neuroborreliosis. He has been treated the same way. Rocephin during the entire course--Zithromax adding for a second phase of the course --and finally IV Flagyl added to the mix. He has improved with the first two drugs but is only 60% better after three and on half months. Today I ordered the Flagyl. He told me: " Doc, now I am going to turn the corner." I hope so. I have seen this result in other patients as well. The Flagyl is administered as a once daily dose of 500mg.
Tuesday, July 28, 2009
Lyme-Bartonella-B12-Folic acid and vitamin D
A 35 year old female was seen by my associate one month ago with complaint of fatigue, malaise joint pain and fatigue. The symptoms had been present for about 2 months. My associate ordered a Lyme Western Blot. Bingo. Three of three IgM bands were present: Lyme disease. Here are some additional result:B12 280, folic acid 5.8, C4a 3200, vitamin D 25-Hydroxy 26, vitamin D 1-25 dihydroxy 75. I saw her 3 weeks ago. Today was our second visit. The symptoms had really been present for the past 6 months or longer. She had experienced fever, swollen lymph nodes, muscle weakness--especially of the arms, profound fatigue, pain in knees-feet-shoulders, total body pain, brain fog and forgetfulness as well as episodes of confusion, depression, word salads, tingling and drenching sweats. The exam showed weakness of the arms and evidence of peripheral neuropathy.
Here is what I think I have learned and how I applied it for this patient. Lyme and Bartonella seem to be co-travellers. It is the combination that causes many of these symptoms, especially the cognitive ones. The swollen glands are a tip off-Bartonella. Soaking sweats do not always equate with Babesia. The low B12 and folic acid are a tip-off. These nutrients are essential for the manufacture of red blood cells. Depletion of these vitamins suggest a bacteria or parasite of red blood cells causing rapid turn over and depletion. Bartonella are present in large numbers whereas Babesia are present in relatively small numbers; these vitamin deficiencies would seem to be the calling card of Bartonellosis.
Vitamin D is a useful parameter. The conversion to active vitamin D in the kidneys occurs because the immune system is attempting to regain equilibrium. This push to the Th2 state away from Th1 occurs because the infection is causing excessive inflammation. As an aside, it doesn't matter if the patient is given supplemental D or not. More vitamin D might provide additional fuel to cool off the rambunctious Th1 response: it is OK to give and may help the patient feel better. Vitamin D toxicity is a non-issue. The only potential issue is hypercalcemia--excessively high levels of calcium in the blood. This is highly unlikely and can be monitored.
Forget the whole Marshall distraction.
I placed the patient on Doxycyline and low dose Cipro. Three weeks later she is doing fabulously.
The Herx was bad for 2 weeks. Now: the fog has lifted, her muscles are strong again and even the night sweats are gone.
The old Doxy plus Cipro was not treating Lyme by two different intracellular mechanisms; it was treating Lyme and Bartonella all along. That is why it has worked so well!
The low dose Cipro seems safe and effective. This patient has allergies to Penicillin and Sulfa.
It is all coming together.
Here is what I think I have learned and how I applied it for this patient. Lyme and Bartonella seem to be co-travellers. It is the combination that causes many of these symptoms, especially the cognitive ones. The swollen glands are a tip off-Bartonella. Soaking sweats do not always equate with Babesia. The low B12 and folic acid are a tip-off. These nutrients are essential for the manufacture of red blood cells. Depletion of these vitamins suggest a bacteria or parasite of red blood cells causing rapid turn over and depletion. Bartonella are present in large numbers whereas Babesia are present in relatively small numbers; these vitamin deficiencies would seem to be the calling card of Bartonellosis.
Vitamin D is a useful parameter. The conversion to active vitamin D in the kidneys occurs because the immune system is attempting to regain equilibrium. This push to the Th2 state away from Th1 occurs because the infection is causing excessive inflammation. As an aside, it doesn't matter if the patient is given supplemental D or not. More vitamin D might provide additional fuel to cool off the rambunctious Th1 response: it is OK to give and may help the patient feel better. Vitamin D toxicity is a non-issue. The only potential issue is hypercalcemia--excessively high levels of calcium in the blood. This is highly unlikely and can be monitored.
Forget the whole Marshall distraction.
I placed the patient on Doxycyline and low dose Cipro. Three weeks later she is doing fabulously.
The Herx was bad for 2 weeks. Now: the fog has lifted, her muscles are strong again and even the night sweats are gone.
The old Doxy plus Cipro was not treating Lyme by two different intracellular mechanisms; it was treating Lyme and Bartonella all along. That is why it has worked so well!
The low dose Cipro seems safe and effective. This patient has allergies to Penicillin and Sulfa.
It is all coming together.
Monday, July 27, 2009
The Untouchables
My critically ill patient is back in the office. She is literally disintegrating before my eyes, her encephalopathy worse. Confused, hallucinating and delusional-- she is unable to speak. A week ago she was somewhat mobile. Now she is confined to a wheel chair resembling many unfortunate patients I have cared for in nursing homes with end stage Alzheimer's disease: this patient is 47 years old. Another doctor had cared for her for 7 months. She has been under my care for only one month. She needs hospitalization. I have sent other patients to many hospitals over a period of years with poor outcomes. This different University Hospital is reputed to be a bit more friendly. We shall see.
I send her to the hospital with a stack of studies and a hand written summary. She is sero-positive for both Lyme and Ehrlichia--thank God! I have written down the name of a neurologist who is reputed to be "Lyme friendly."
The only way to be admitted to hospitals these days is through the ER, unless you are an "attending" with direct admitting privileges. And even this occurs rarely these days.
The intern is the first to call me: "We don't see anything acutely wrong with patient"--not wanting to admit her to his service.
She is very ill, please admit her.
I am called back by a supercilious second year resident, his boss. "The patient has been the same for a month--there is nothing acute here--we don't want to admit her. The neurologist whose name you wrote down won't be able to see her unless you call him. You should not have sent the patient to the ER: you have given her the erroneous impression that she will be admitted. I don't see any reason for an admission."
"Please admit this patient. She is getting worse. She has a severe progressive encephalitis. She absolutely must be admitted for a work up; she needs a a lumbar puncture. You cannot send this patient home"-- I implore.
"Humf, I will get neurology to see her." The neurologist you have requested will not see her unless you arrange it--here is his beeper number."
I page the doctor: no response.
The gatekeeper--the man who would keep my critically ill patient from admission to the esteemed University Hospital is a "sagacious" 26 year old doctor with a major "...tude."
The patient is crazy of course, the doctor a wack-job. Tick borne disease causing encephalopathy--"whatever". Reluctantly: "I'll see what neurology has to say."
The untouchables: cursed-- damned-- invisible.
At least that how it seems.
Why take the blue pill if the red one works just as well?
Something about chasing a white rabbit down a hole I think.
"I'm sorry-- which pill do we take?"
I send her to the hospital with a stack of studies and a hand written summary. She is sero-positive for both Lyme and Ehrlichia--thank God! I have written down the name of a neurologist who is reputed to be "Lyme friendly."
The only way to be admitted to hospitals these days is through the ER, unless you are an "attending" with direct admitting privileges. And even this occurs rarely these days.
The intern is the first to call me: "We don't see anything acutely wrong with patient"--not wanting to admit her to his service.
She is very ill, please admit her.
I am called back by a supercilious second year resident, his boss. "The patient has been the same for a month--there is nothing acute here--we don't want to admit her. The neurologist whose name you wrote down won't be able to see her unless you call him. You should not have sent the patient to the ER: you have given her the erroneous impression that she will be admitted. I don't see any reason for an admission."
"Please admit this patient. She is getting worse. She has a severe progressive encephalitis. She absolutely must be admitted for a work up; she needs a a lumbar puncture. You cannot send this patient home"-- I implore.
"Humf, I will get neurology to see her." The neurologist you have requested will not see her unless you arrange it--here is his beeper number."
I page the doctor: no response.
The gatekeeper--the man who would keep my critically ill patient from admission to the esteemed University Hospital is a "sagacious" 26 year old doctor with a major "...tude."
The patient is crazy of course, the doctor a wack-job. Tick borne disease causing encephalopathy--"whatever". Reluctantly: "I'll see what neurology has to say."
The untouchables: cursed-- damned-- invisible.
At least that how it seems.
Why take the blue pill if the red one works just as well?
Something about chasing a white rabbit down a hole I think.
"I'm sorry-- which pill do we take?"
Saturday, July 18, 2009
Bartonella re-visited
Bartonella is a facultative (difficult to culture), gram negative intracellular bacteria. New strains--known to cause human disease are being discovered on a regular basis. Standard serologic (antibody) tests ordered by physicians for Bartonella test only antibodies against B. henselae and B. quintana. A quick survey of medical literature shows a long list of Bartonella species with exotic sounding names: B. clarrideiae, B. koehlerae, B. vinsoni, B. berkhoffi, B. elizabethe, B. bovis, B. rochalimae, B. melophagi, B. facilliformis and others. The "species PCR Bartonella" test could miss other Bartonella species whose DNA is different. A CDC (Lyme-division) representative, recently said that new species of Bartonella in mice are being discovered on a regular basis. The CDC plans to publish a point-counterpoint piece regarding the significance of Bartonella in human disease.
Could the mystery bacteria seen in blood wet mounts and smears of many tick borne disease patients be yet unclassified forms of Bartonella? I think the answer is YES. These small bacteria stain gram negative and do not culture. Although Bartonella are intracellular organisms--live in cells, Bartonella species can exhibit prolonged bacteremia (bacteria in the blood).
Is the treatment of Bartonella different than that for Lyme? Both Lyme-Borrelia burdorferi and Bartonella are gram negative bacteria. The medical literature claims that both bacteria can for the most part be treated with the same antibiotics: Doxycyline, Biaxin, Zithromax, Rocephin, Levaquin and others. These drugs are bacteriostatic. Only two drugs are reputed to be bactericidal: Gentamycin and Rifampin. The standard medical literature also claims that Bartonella can be treated with short courses of antibiotics (similar to claims for Lyme). The literature indicates that Bartonella can cause brain infection but states that there is only one reported mortality. It is recommended that such cases should be treated more aggressively.
Back to the CDC. Most readers of this BLOG are familiar with the concept of tick borne disease. This concept is foreign to the CDC, despite a web-page which is misleading . The groups which study Lyme and co-infections are separated, even geographically(Colorado versus Georgia). Lyme is linked with spirochete diseases. Ehrlichia/Anaplasmosis are in a Rickettsia group. Babesia is in a parasite/protozoa group and Bartonella is in another group. The CDC admits it has never studied how multiple tick borne infections interact in a single host.
But I digress.
We don't really know what the germs (mystery bugs) are, what their role in disease is and how best to treat them.
A new patient, one who is extremely sick, was recently referred to my practice by one of my difficult patients--who is finally getting better--thanks.
This patient has a long history of chronic Lyme disease with pain and severe encephalopathy. She is only 45 years old but has moderate to severe dementia. Her previous physician, a well known Lyme treating doctor had prescribed a prolonged course of Rocephin--without benefit and essentially informed the patient and family that there was nothing else he could do.
I agreed to take the patient on to see if I could help. Based on experience I know that some patients respond to IV Zithromax even when IV Rocephin has failed. Perhaps this is a manifestation of the "Bartonella" syndrome.
There was a response. Within two weeks her pain was 50% better. Her encephalopathy worsened--a Baronella brain Herx?? At least it was something. These results are contemporaneous with this entry; adjustments in therapy are being made.
Clearly, there are patients who respond better to: Bactrim, IV Zithromax, Rifampin, Cipro, Levaquin and other drugs. LLMDS and their patients will attest to this.
Many patients are clinically diagnosed with the triad of: Lyme-Babesia-Bartonella--frequently on clinical grounds.
If there is a method to my madness I have found that patients respond best when the treatment strategy targets: Lyme then Babesia then Bartonella and then back to Lyme. Of course it may be desirable to use drugs which overlap in their ability to address the collection of infections. And so it goes.
Could the mystery bacteria seen in blood wet mounts and smears of many tick borne disease patients be yet unclassified forms of Bartonella? I think the answer is YES. These small bacteria stain gram negative and do not culture. Although Bartonella are intracellular organisms--live in cells, Bartonella species can exhibit prolonged bacteremia (bacteria in the blood).
Is the treatment of Bartonella different than that for Lyme? Both Lyme-Borrelia burdorferi and Bartonella are gram negative bacteria. The medical literature claims that both bacteria can for the most part be treated with the same antibiotics: Doxycyline, Biaxin, Zithromax, Rocephin, Levaquin and others. These drugs are bacteriostatic. Only two drugs are reputed to be bactericidal: Gentamycin and Rifampin. The standard medical literature also claims that Bartonella can be treated with short courses of antibiotics (similar to claims for Lyme). The literature indicates that Bartonella can cause brain infection but states that there is only one reported mortality. It is recommended that such cases should be treated more aggressively.
Back to the CDC. Most readers of this BLOG are familiar with the concept of tick borne disease. This concept is foreign to the CDC, despite a web-page which is misleading . The groups which study Lyme and co-infections are separated, even geographically(Colorado versus Georgia). Lyme is linked with spirochete diseases. Ehrlichia/Anaplasmosis are in a Rickettsia group. Babesia is in a parasite/protozoa group and Bartonella is in another group. The CDC admits it has never studied how multiple tick borne infections interact in a single host.
But I digress.
We don't really know what the germs (mystery bugs) are, what their role in disease is and how best to treat them.
A new patient, one who is extremely sick, was recently referred to my practice by one of my difficult patients--who is finally getting better--thanks.
This patient has a long history of chronic Lyme disease with pain and severe encephalopathy. She is only 45 years old but has moderate to severe dementia. Her previous physician, a well known Lyme treating doctor had prescribed a prolonged course of Rocephin--without benefit and essentially informed the patient and family that there was nothing else he could do.
I agreed to take the patient on to see if I could help. Based on experience I know that some patients respond to IV Zithromax even when IV Rocephin has failed. Perhaps this is a manifestation of the "Bartonella" syndrome.
There was a response. Within two weeks her pain was 50% better. Her encephalopathy worsened--a Baronella brain Herx?? At least it was something. These results are contemporaneous with this entry; adjustments in therapy are being made.
Clearly, there are patients who respond better to: Bactrim, IV Zithromax, Rifampin, Cipro, Levaquin and other drugs. LLMDS and their patients will attest to this.
Many patients are clinically diagnosed with the triad of: Lyme-Babesia-Bartonella--frequently on clinical grounds.
If there is a method to my madness I have found that patients respond best when the treatment strategy targets: Lyme then Babesia then Bartonella and then back to Lyme. Of course it may be desirable to use drugs which overlap in their ability to address the collection of infections. And so it goes.
Tuesday, July 14, 2009
Babesia questions
For convenience we can divide physicians into two camps: those who follow the IDSA and those who follow ILADS. This is an over-simplification. Many physicians fall in between. I am seeing more infectious disease physicians cross over into the chronic Lyme side of things. Many other physicians are becoming more interested in treating Lyme as a chronic disease and treating it as such. The paradigm has broadened for many of us; chronic Lyme has evolved into chronic tick borne disease. Many patients do not improve or recover, at least not fully, unless other co-infections are treated as well. The treatment of co-infections exposes Lyme aware physicians to increased criticisms by IDSA leaning physicians because the presence of these entities is frequently more difficult to demonstrate than Lyme--Borrelia burdorferi.
Readers must be reminded that in the main, laboratory evidence suggesting the presence of Babesia tells the physician only one thing: the patient has been exposed to Babesia. Here I am referring to serological antibody tests. Other, more convincing tests, for the non-believers, include a blood smear which shows the organisms or a FISH test offered by IgeneX. These tests are not particularly sensitive missing most cases. Serologically, we can test for two strains of Babesia through commercial labs: B. microti and B. duncani. There are numerous other strains of Babesia for which no simple test exists. Clongen lab can perform a Babesia "species" PCR test which is very specific but not all that sensitive. It screens for the presence of Babesia DNA for about 15 species of Babesia.
In routine lab panels described elsewhere, anybodies directed against B. microti and B. duncani or WA1 are routinely obtained. It is always nice to have one's clinical suspicions mirrored in a laboratory test. But like most things Lyme: the diagnosis of Babesiosis is a clinical one.
Many clinical signs and symptoms have been ascribed to Babesiosis. In my practice the primary symptom is sweating. Patients have night sweats, sweats after a hot shower, day sweats or chills and flu like symptoms which recur cyclically. A secondary feature is muscle pains in preference to joint pain.
Another helpful test is the evaluation of a wet mount slide. Many patients show a crescent shaped organism which resembles Toxoplasmosis. I do not believe this organism is Toxo: many patients with the organism have negative serology (antibodies) directed against Toxo. I will explain why I mention this finding in connection with Babesiosis in a moment.
The standard treatment for Babesiosis has been Mepron, usually combined with Zithromax.
Mepron is a yellow liquid which is unpleasant tasting and very expensive. It contains a single ingredient: Atovaquone. Malarone, on the other hand, contains two anti-parasite ingredients: Atovaquone and Proguanil. Malarone is a less expensive, convenient tablet.
Malarone seems to address this crescent shaped parasite whereas Mepron does not. It is my suspicion that this other, yet unknown parasite, is responsible for much muscle pain, including that associated with fibromyalgia syndromes.
Even though the dose of Atovaquone in Malarone is only 1/3 of that present in Mepron, I have found it is effective for Babesia symptoms. My experience has informed me that it is the length of therapy, not the dose of Atovaquone which helps ameliorate Babesia related symptoms and presumably infection. Anti-Babesia or parasite therapy can be augmented by adding the herbal medicine, Artemsin, usually 200mg twice daily.
So yes, there are more positive serologies for B. duncani than B. microti here on the east coast which contrasts with the views of local health officials, still, the diagnosis of this syndrome is made strictly on clinical grounds. There exists a subset of patients with antibodies to Babesia who never exhibit symptoms of this infection. Most of these patients improve even though this specific co-infection has not been treated. Presumably, in these cases, the infection was mild and eliminated by a well functioning immune system. Even so, the presence of these antibodies can be used to substantiate the diagnosis of chronic Lyme in patients who are Lyme seronegative: where there is smoke there is usually fire.
A basic rule of thumb which has served me well for over 25 years of medical practice still holds: treat the patient, not the labs.
Another comment: Zithromax is not very is not very effective against Lyme disease; its cousin macrolide Biaxin is. Biaxin is frequently avoided when antibiotics are combined because of its it "sloppy" tendency to cause adverse drug to drug interactions: it doesn't play well with others.
Biaxin may reduce blood levels of Atovaquone by 40%. Still, in patients where the treatment of Lyme is imperative along with the treatment of Babesia, this combination has still been effective in many patients.
Another, quite effective drug can be mixed with Malarone for Lyme disease: Cleocin. But this drug carries its own unique risks, especially C. diff colitis, the nemesis of physicians treating chronic Lyme and related disorders. As always the need for probiotics can not be stressed enough. I prefer the combination of Sacchromyces with an Acidophilus mix.
Readers must be reminded that in the main, laboratory evidence suggesting the presence of Babesia tells the physician only one thing: the patient has been exposed to Babesia. Here I am referring to serological antibody tests. Other, more convincing tests, for the non-believers, include a blood smear which shows the organisms or a FISH test offered by IgeneX. These tests are not particularly sensitive missing most cases. Serologically, we can test for two strains of Babesia through commercial labs: B. microti and B. duncani. There are numerous other strains of Babesia for which no simple test exists. Clongen lab can perform a Babesia "species" PCR test which is very specific but not all that sensitive. It screens for the presence of Babesia DNA for about 15 species of Babesia.
In routine lab panels described elsewhere, anybodies directed against B. microti and B. duncani or WA1 are routinely obtained. It is always nice to have one's clinical suspicions mirrored in a laboratory test. But like most things Lyme: the diagnosis of Babesiosis is a clinical one.
Many clinical signs and symptoms have been ascribed to Babesiosis. In my practice the primary symptom is sweating. Patients have night sweats, sweats after a hot shower, day sweats or chills and flu like symptoms which recur cyclically. A secondary feature is muscle pains in preference to joint pain.
Another helpful test is the evaluation of a wet mount slide. Many patients show a crescent shaped organism which resembles Toxoplasmosis. I do not believe this organism is Toxo: many patients with the organism have negative serology (antibodies) directed against Toxo. I will explain why I mention this finding in connection with Babesiosis in a moment.
The standard treatment for Babesiosis has been Mepron, usually combined with Zithromax.
Mepron is a yellow liquid which is unpleasant tasting and very expensive. It contains a single ingredient: Atovaquone. Malarone, on the other hand, contains two anti-parasite ingredients: Atovaquone and Proguanil. Malarone is a less expensive, convenient tablet.
Malarone seems to address this crescent shaped parasite whereas Mepron does not. It is my suspicion that this other, yet unknown parasite, is responsible for much muscle pain, including that associated with fibromyalgia syndromes.
Even though the dose of Atovaquone in Malarone is only 1/3 of that present in Mepron, I have found it is effective for Babesia symptoms. My experience has informed me that it is the length of therapy, not the dose of Atovaquone which helps ameliorate Babesia related symptoms and presumably infection. Anti-Babesia or parasite therapy can be augmented by adding the herbal medicine, Artemsin, usually 200mg twice daily.
So yes, there are more positive serologies for B. duncani than B. microti here on the east coast which contrasts with the views of local health officials, still, the diagnosis of this syndrome is made strictly on clinical grounds. There exists a subset of patients with antibodies to Babesia who never exhibit symptoms of this infection. Most of these patients improve even though this specific co-infection has not been treated. Presumably, in these cases, the infection was mild and eliminated by a well functioning immune system. Even so, the presence of these antibodies can be used to substantiate the diagnosis of chronic Lyme in patients who are Lyme seronegative: where there is smoke there is usually fire.
A basic rule of thumb which has served me well for over 25 years of medical practice still holds: treat the patient, not the labs.
Another comment: Zithromax is not very is not very effective against Lyme disease; its cousin macrolide Biaxin is. Biaxin is frequently avoided when antibiotics are combined because of its it "sloppy" tendency to cause adverse drug to drug interactions: it doesn't play well with others.
Biaxin may reduce blood levels of Atovaquone by 40%. Still, in patients where the treatment of Lyme is imperative along with the treatment of Babesia, this combination has still been effective in many patients.
Another, quite effective drug can be mixed with Malarone for Lyme disease: Cleocin. But this drug carries its own unique risks, especially C. diff colitis, the nemesis of physicians treating chronic Lyme and related disorders. As always the need for probiotics can not be stressed enough. I prefer the combination of Sacchromyces with an Acidophilus mix.
Wednesday, July 8, 2009
Ambien and a bump to the head with surprising consequences
A 42 year old female was in good health until she took an Ambien one night to help with some insomnia. Apparently she got up during sleep (sleep walking), went into the kitchen, and began to cook a meal. She then proceeded to fall down and bang her head. She presented to my office with a headache, some dizziness and severe pain and swelling in her lower extremities. Her calf muscles were extremely swollen and tender. I was concerned that she might have a subdural hematoma ( a clot in the skull) or rhabdomyolysis, a condition of muscle breakdown after injury which can lead to kidney failure. I sent her to the ER for a work up. The results were negative.
She came back in a day later. Her calf muscles were increasingly tight, swollen and painful. I was worried about a DVT (a blood clot). I sent her for a duplex (ultrasound) study to exclude this. It was negative. The pain was increasing in intensity. Narcotics, at a fairly high dose were needed to control the pain. The Percocet was not working; she returned with tears streaming down her face. She did not have myositis--inflammation of the muscles because the muscle enzyme CPK or CK was normal. Did she has some sort of myopathy? I ran some blood tests for an autoimmune disease. Oddly, her rheumatoid factor was elevated at 285. New symptoms appeared: there was now a tremor of her arms. I started a tapering dose of steroids. It was of no help.
She came back in a day later. Her calf muscles were increasingly tight, swollen and painful. I was worried about a DVT (a blood clot). I sent her for a duplex (ultrasound) study to exclude this. It was negative. The pain was increasing in intensity. Narcotics, at a fairly high dose were needed to control the pain. The Percocet was not working; she returned with tears streaming down her face. She did not have myositis--inflammation of the muscles because the muscle enzyme CPK or CK was normal. Did she has some sort of myopathy? I ran some blood tests for an autoimmune disease. Oddly, her rheumatoid factor was elevated at 285. New symptoms appeared: there was now a tremor of her arms. I started a tapering dose of steroids. It was of no help.
A neurological exam was performed. Deep tendon reflexes were absent across the board. Pin prick sensation was decreased in a stocking/glove pattern affecting all limbs. Vibratory sensation was minimal in the feet. A tick borne disease panel was ordered.
The results: Lyme ELISA IgM 0.91--equivocal range, Lyme WB 41 IgM and IgG bands, Babesia WA1 antibody elevated 1:256, C6 peptide 0.2, CD57 63. Did she in fact have tick borne illness? Had trauma activated a latent tick borne infection leading to an autoimmune syndrome with progressive symptoms in a previously well individual? That was my thinking.
And her symptoms were progressive--rapidly. She developed uncontrolled rhythmic seizure like jerking of her arms. This was associated with uncontrolled vocalizations typical of Tourettes syndrome. The pain and muscle swelling continued to be severe and difficult to manage. She developed night sweats. None of these symptoms existed prior to her traumatic injury.
Treatment for Lyme and Babesia with typical antimicrobials over a 2 month period has been successful. The neuro symptoms--the seizures and Tourettes resolved. The pain and swelling has lessened. She is now returning to work half time, a feat which would have been unimaginable a few weeks ago.
This is the clinical vingette.
These are my thoughts--conjectures.
There are a large number of patients who harbor Lyme (Bb) and its associated co-infections without clinical illness. These parasitic entities are contained by the host and its immune system.
The healthy state can be quite tenuous. Many things can unleash the ticking bomb: intercurrent infection, stress or even physical trauma.
The percent of individuals in endemic areas who are assymptomatic carriers of TBD may be much higher than suspected, given my suspicion that the vast majority of infected individuals exhibit no symptoms of disease.
A positive Lyme ELISA test should not be discounted when the second tier--the Western Blot is negative. Any positive result for Lyme: ELISA, Western Blot or C6 peptide should be considered as potential evidence of the disease.
Positive tests for Babesia WA1 or Babesia duncani have become extremely common, much more so than B. microti. There has to date been no acknowledgement of this change in distribution of this parasite from the west coast to the east coast by health departments.
There are better sleeping medications than Ambien.
And her symptoms were progressive--rapidly. She developed uncontrolled rhythmic seizure like jerking of her arms. This was associated with uncontrolled vocalizations typical of Tourettes syndrome. The pain and muscle swelling continued to be severe and difficult to manage. She developed night sweats. None of these symptoms existed prior to her traumatic injury.
Treatment for Lyme and Babesia with typical antimicrobials over a 2 month period has been successful. The neuro symptoms--the seizures and Tourettes resolved. The pain and swelling has lessened. She is now returning to work half time, a feat which would have been unimaginable a few weeks ago.
This is the clinical vingette.
These are my thoughts--conjectures.
There are a large number of patients who harbor Lyme (Bb) and its associated co-infections without clinical illness. These parasitic entities are contained by the host and its immune system.
The healthy state can be quite tenuous. Many things can unleash the ticking bomb: intercurrent infection, stress or even physical trauma.
The percent of individuals in endemic areas who are assymptomatic carriers of TBD may be much higher than suspected, given my suspicion that the vast majority of infected individuals exhibit no symptoms of disease.
A positive Lyme ELISA test should not be discounted when the second tier--the Western Blot is negative. Any positive result for Lyme: ELISA, Western Blot or C6 peptide should be considered as potential evidence of the disease.
Positive tests for Babesia WA1 or Babesia duncani have become extremely common, much more so than B. microti. There has to date been no acknowledgement of this change in distribution of this parasite from the west coast to the east coast by health departments.
There are better sleeping medications than Ambien.
Friday, June 19, 2009
Lyme disease and female hysteria
I offer this piece after reading only the abstract of a recently published article. There may be inaccuracies because I have not read the entire piece. Feel free to post corrections.
A syllogism is a form of logical thinking which I learned about in college. Syllogisms are frequently twisted into false logic causing spurious or misleading conclusions. To say( 1) more women have Lyme disease(which is vague) then (2)more women also have depression(which is also vague) THEREFORE women who have Lyme disease likely have depression- is like saying: fire hydrants are red: you are red: therefore you are likely a fire hydrant. This is the sort of logic evinced in a recent article published by prominent anti-Lyme IDSA figures in the Journal of Women's Health. I can understand why women take umbrage with these remarks.
Not only is the logic false, but the implications are insulting to many health care professionals and professional health care organizations. If "Chronic Lyme disease" is a vaguely defined term that has been applied to patients with prolonged subjective symptoms..." The same cannot be said for fibromyalgia, chronic fatigue or depression.
Fibromyalgia is not vague. It is a syndrome which has been clearly described by the American Association of Rheumatology. It is defined by very specific symptoms combined with very specific physical findings. Chronic fatigue syndrome is not vague. It has been very clearly defined. This definition can be viewed in CDC published literature. Depression is certainly not vague. The psychiatric community has meticulously defined this disorder, and its subtypes, in a book called the DMS4.
There are clear cultural differences between men and women. Men are infrequent users of the health care system. Men are less likely to complain of symptoms. Culturally men are taught to be stoic, to not complain and ignore symptoms until they are very advanced.
Their are indeed biological differences between men and women as well. Women are twice as like to suffer with autoimmune diseases as men. Most physicians who treat chronic Lyme disease are well aware of the strong autoimmune component of Lyme disease. Women also live longer than men and are less likely to succumb to severe infectious illnesses. These differences are real.
Are diseases like depression really more common amongst women? We know that women are more likely to seek professional help for depression. MEN ARE FOUR TIMES MORE LIKELY TO SUCCESSFULLY COMMIT SUICIDE. Which gender is more depressed? Men are more likely to suffer with alcoholism, drug addiction and commit acts of violence. These are well known surrogates of depression and other mental illnesses.
The word "hysteria" is derived from an ancient Greek medical concept. It was a female disease related to a disturbance of the uterus. Hysteria has become synonymous with the terms "psychosomatic" and "psychogenic." Sadly, many physicians today are still influenced by this ancient, unwarranted prejudice.
One might conclude that the authors have lumped together these so called female predominant disorders because the underlying beliefs of the authors, like many others in the medical community, is that these "new age" illness are a phony-psychosomatic- manifestation of hysteria- as described by the ancient Greeks.
Why conclude that so called chronic Lyme patients have been misdiagnosed and really have these other syndromes? What evidence is there to back up this conclusion? Perhaps it is the other way around. Typically, chronic Lyme patients do not neatly fit into the syndromes of fibromyalgia or chronic fatigue syndrome. Unfortunately may cynical physicians, who fail to accept the reality of these illness, have used these clinical disorders as a "waste basket" for Lyme patients when in fact no clear diagnosis has been established--at least according to their paradigm.
This sort of thinking seems dismissive and anachronistic with regard to the suffering of so many chronic Lyme sufferers. And as stated at the outset, the logical argument marshaled here is questionable at the very least.
One has to question the motives of the authors: Are they trying to promote a scientific understanding of a disease or are they publishing pabulum in an effort to promote their pre-existing, crumbling paradigm?
I think its time for a change. Don't you?
A syllogism is a form of logical thinking which I learned about in college. Syllogisms are frequently twisted into false logic causing spurious or misleading conclusions. To say( 1) more women have Lyme disease(which is vague) then (2)more women also have depression(which is also vague) THEREFORE women who have Lyme disease likely have depression- is like saying: fire hydrants are red: you are red: therefore you are likely a fire hydrant. This is the sort of logic evinced in a recent article published by prominent anti-Lyme IDSA figures in the Journal of Women's Health. I can understand why women take umbrage with these remarks.
Not only is the logic false, but the implications are insulting to many health care professionals and professional health care organizations. If "Chronic Lyme disease" is a vaguely defined term that has been applied to patients with prolonged subjective symptoms..." The same cannot be said for fibromyalgia, chronic fatigue or depression.
Fibromyalgia is not vague. It is a syndrome which has been clearly described by the American Association of Rheumatology. It is defined by very specific symptoms combined with very specific physical findings. Chronic fatigue syndrome is not vague. It has been very clearly defined. This definition can be viewed in CDC published literature. Depression is certainly not vague. The psychiatric community has meticulously defined this disorder, and its subtypes, in a book called the DMS4.
There are clear cultural differences between men and women. Men are infrequent users of the health care system. Men are less likely to complain of symptoms. Culturally men are taught to be stoic, to not complain and ignore symptoms until they are very advanced.
Their are indeed biological differences between men and women as well. Women are twice as like to suffer with autoimmune diseases as men. Most physicians who treat chronic Lyme disease are well aware of the strong autoimmune component of Lyme disease. Women also live longer than men and are less likely to succumb to severe infectious illnesses. These differences are real.
Are diseases like depression really more common amongst women? We know that women are more likely to seek professional help for depression. MEN ARE FOUR TIMES MORE LIKELY TO SUCCESSFULLY COMMIT SUICIDE. Which gender is more depressed? Men are more likely to suffer with alcoholism, drug addiction and commit acts of violence. These are well known surrogates of depression and other mental illnesses.
The word "hysteria" is derived from an ancient Greek medical concept. It was a female disease related to a disturbance of the uterus. Hysteria has become synonymous with the terms "psychosomatic" and "psychogenic." Sadly, many physicians today are still influenced by this ancient, unwarranted prejudice.
One might conclude that the authors have lumped together these so called female predominant disorders because the underlying beliefs of the authors, like many others in the medical community, is that these "new age" illness are a phony-psychosomatic- manifestation of hysteria- as described by the ancient Greeks.
Why conclude that so called chronic Lyme patients have been misdiagnosed and really have these other syndromes? What evidence is there to back up this conclusion? Perhaps it is the other way around. Typically, chronic Lyme patients do not neatly fit into the syndromes of fibromyalgia or chronic fatigue syndrome. Unfortunately may cynical physicians, who fail to accept the reality of these illness, have used these clinical disorders as a "waste basket" for Lyme patients when in fact no clear diagnosis has been established--at least according to their paradigm.
This sort of thinking seems dismissive and anachronistic with regard to the suffering of so many chronic Lyme sufferers. And as stated at the outset, the logical argument marshaled here is questionable at the very least.
One has to question the motives of the authors: Are they trying to promote a scientific understanding of a disease or are they publishing pabulum in an effort to promote their pre-existing, crumbling paradigm?
I think its time for a change. Don't you?
Subscribe to:
Posts (Atom)