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.
Friday, October 30, 2009
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.