posted
I am pretty much stuck in a horrible position.
I started having more neuro symptoms in January, so in February My LLMD and I decided to step up the treatment. I started doing claforan IM and Lovenox SQ...we were going to add a few orals on top, but then...
My liver enzymes jumped way up and kept climbing even when I stopped all medication. They have now been going down (slowly) and I haven't been on any abx or anticoagulant tx for over 2 months now.
I went for my yearly MRI and it showed 3 new lesions (never had an increase in # of lesions before and this is my 4th MRI), one is the biggest so far at 8mm.
So NOW WHAT??? I guess my biggest fear is that the lyme would trigger an autoimmune disease (MS) that would then take on a life of its own.
IMHO, there is such a thing as an active infection causing lesions and then there is also an autoimmune disease in which the lesions are caused by the antibodies attacking the myelin.
If my liver was healthy, I would start rocephin ASAP....but sadly that is not an option and probably won't be for some time. ALT is still over 200, and my next test is scheduled for the end of May.
I am looking into rife, but I am guessing that my liver enzymes should probably be back to normal before starting that too?
My husband wants me to go see an East Coast Neuro/LLMD that could evaluate me and give me some kind of opinion on if this is only an active infection, or if this is now truly an autoimmune disease.
I go to Dr. C. in Missouri and he told awhile back that he thought it was significant that I did have 1 O-band show up on my LP. He doesn't usually see that. He always throws out comments like' "Your MS could get better...etc." and I have always been quick to say "I was never diagnosed with MS"
I love Dr. C. and am not looking to change LLMD's, but just wanted a consultation about this specific position that I find myself in.
I am wondering if it is really possible to tell the difference?
I think I must have been in denial when I got the news last week, because I called and spoke to the radiologist just to make sure. It really started to hit me yesterday...had a few tears.
Thanks for listening and for any advice that you might have.
SForsgren
Frequent Contributor (1K+ posts)
Member # 7686
posted
In my opinion, MS is infections + toxins. If one adequately treats Lyme, other infections and toxins, many people previously told they had MS improve. I had a practitioner suggest I had MS 12 years ago before I learned I had Lyme and the MS-like symptoms did resolve with treatment.
Looking into the possibility of autoimmunity, however, may be appropriate. It has been said that autoimmunity such as in anti-myelin basic protein antibodies can be seen in Lyme disease and often goes away with appropriate treatment.
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
| IP: Logged |
posted
We've been through this....and a lyme-literate neurologist we saw in NYC said there was no way to tell - except time.
After all, MS is just a descriptive term meaning that the patient has multiple lesions of unknown cause. The O-band is evidence of myelin damage (i.e. an active lesion).
Have you tried oral doxy? My husband had lesions in his spinal cord only, and had a lot of trouble walking - stumbling, off-balance, etc. He had a really good response to 400mg daily of doxy.
Also, we learned with MRIs that there are different generations of machines so make sure your radiology center has the latest generation, and its best to go to the same facility for each repeat study. Finally, don't just accept the radiology report - make sure that you have a neuro or another doc read your MRI films WITH you - we got a radiologist report that was way off and written with much more certainty about location and size than is actually possible to determine.
I recognize your username, but haven't followed your story - so I'm sorry if this information is too basic to be helpful....but thought I'd post it anyway...
Posts: 39 | From wdc | Registered: Aug 2007
| IP: Logged |
Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
Lyme also eats away at the myelin sheath around the nerves.
As the above posters explain, the word, term and "disease" of "MS" is not really anything but a description of the the damage that has occurred.
The underly disease process is what should be addressed.
And, that is mostly likely infection and toxins (and the liver's strength to work with that).
Whatever can help support the myelin sheath is good (but I'm not there yet in my research other than B-vitamins) . . . .
Personally, I believe that 99% of the time "autoimmune disease" is undiagnosed infection. However, the author of the next article does show a difference in lyme and MS with lyme.
Still, when your doctor says "your MS can get better" may be using MS as a term for all the neuro patterns that trouble you. MS really means the lesions, quite technically speaking, multiple lesions. So, maybe he means that the lesions can shrink and therefore, you'd have fewer symptoms.
Engage him in a conversation about this if it perplexes you. It's impossible to second-guess. Find out exactly what his thoughts are and it may put your mind at ease.
-
[ 04-20-2009, 02:21 PM: Message edited by: Keebler ]
Posts: 48021 | From Tree House | Registered: Jul 2007
| IP: Logged |
Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
from BettyG: copying entire article here and breaking it up for neuro lymies like me!
Controversies in Neuroborreliosis **********************************
Audrey Stein Goldings, M.D.
Updated October, 2002
The objectives of this article are to cover issues related to Lyme disease that are not even-handedly addressed in the current literature. It will:
Present a practical approach for making the diagnosis of neuroborreliosis,
Explore the other side of the post-Lyme syndrome (i.e. the likelihood of chronic ongoing infection),
Discuss the relationship between MS and Lyme,
Critique the current regimens published for treating neuroborreliosis, and
Present my own approach which may differ from some leading authorities.
``Anyone who, in discussion, relies upon authority uses not his understanding but rather his memory.'' --Leonardo da Vinci, Notebooks (c. 1500)
It is hoped this data will provide the reader with a broader understanding of neuroborreliosis so that he or she may better use current and evolving knowledge for clinical decision making.
I. NEUROBORRELIOSIS: MAKING THE DIAGNOSIS
Because of difficulties in making the diagnosis of neuroborreliosis, the physician will need a familiarity with the most common forms of presentations, which will be emphasized.
The following points will help evaluate the patient for neuroborreliosis:
For most patients, systemic features of disease coexist with, or predate, neurologic manifestations.
Both central nervous and peripheral nervous system involvement is frequent with Lyme disease and typically occur together.
Laboratory data may or may not confirm the diagnosis, and other disease in the differential diagnosis must be evaluated thoroughly in cases where diagnostic ncertainty exists.
Although history of exposure to B. burgdorferi should be sought, for various reasons, patients may not remember a history of a tick bite, or the pathognomonic rash particularly if the disease is presenting years after the exposure.
Early on, personality changes, psychiatric symptoms, or cognitive manifestations may be the first, and occasionally the only, symptoms that the patient or family is aware of.
CLINICAL DESCRIPTIONS OF NEUROBORRELIOSIS ******************************************
CENTRAL NERVOUS SYSTEM INVOLVEMENT
Meningismus with normal CSF Lymphocytic Meningitis Meningoencephalomyelitis Subacute Encephalopathy (SAE) PERIPHERAL NERVOUS SYSTEM INVOLVEMENT
Patients may present with headache and stiff neck without evidence of CSF inflammation.
Since early CNS seeding has been described, as well as culture positivity during latent disease without concurrent CNS inflammatory changes, these symptoms probably indicate active infection.
Stiff neck might alternatively be due to axonal degenerative changes of the cervical paraspinal musculature, but there should be other evidence of a more widespread neuropathy when this is the case.
LYMPHOCYTIC MENINGITIS
Lymphocytic Meningitis may appear to be indistinguishable from aseptic meningitis during early-disseminated disease (weeks to months after inoculation with B. burgdorferi).
Most patients will have headaches that will fluctuate in intensity. Associated features may include a cranial neuropathy in about one-third.
Low-grade encephalopathy is present in up to one-half, with mild memory concentration deficits, mood changes, and sleep disturbance.
MENINGOENCEPHALOMYELITIS
Rarely, focal parenchymal CNS lesions occur.
The MRI may show punctate white matter lesions best seen on T2-weighted images; larger lesions occur infrequently.
One brain biopsy showed increased numbers of microglia cells, rare spirochetes, and minimal inflammation. Transverse myelitis, movement disorders (extrapyramidal cerebellar, chorea and myoclonus), and hemiparesis can occur.
PSYCHIATRIC DISORDERS
Psychosis, mood swings (mild or bipolar), profound personality changes, depression, anorexia nervosa, obsessive-compulsive disorder, and panic attacks may occur. CSF may be normal.
SUBACUTE ENCEPHALOPATHY (SAE)
The most common chronic CNS manifestation is a SAE, characterized by memory problems and depression.
Many patients (or their families) will complain of their excessive daytime sleepiness and extreme irritability.
These patients generally come to the office disorganized (despite a supreme effort to be organized), unable to give a coherent history.
They will bring copious notes, which are invariably in the wrong order.
Most patients will complain of fatigue, and about one-half have headaches.
Coincident polyneuropathy is very common with spinal or radicular pain, or distal paresthesias.
Quantifiable deficits in memory, learning and retrieval, attention and concentration, perceptual-motor skills, and problem solving are common.
MMPI testing generally shows a stable psychological pattern without significant psychopathology, similar to other medically ill patients.
ADDITIONAL CNS TESTING: **********************
NEGATIVE TEST RESULTS DO NOT RULE OUT THE DIAGNOSIS OF NEUROBORRELIOSIS
Confirmation by CSF CULTURE is seldom practical because the organism is very fastidious, present in small numbers, takes a long time to grow out, and may undergo changes to forms which cannot be cultured easily.
CSF ANTIBODY TITERS may be present but are inconsistent and therefore their absence does not rule out CNS infection. The MRI is seldom abnormal and the findings, when present, are not specific for Lyme.
CSF PCR (test for spirochetal DNA) is a useful tool, but at present, because the capture of DNA is inconsistent, a few questions still need to be addressed.
OLIGLOCLONAL BANDS AND IGG INDEX -- Looking for evidence of an intrathecal immune response may be helpful, but it is not specific.
As a rule, oligoclonal bands and an elevated IgG index are not present in North American Lyme disease and their presence should suggest other diseases.
THE PERIPHERAL NERVOUS SYSTEM
Cranial neuropathy, painful radiculitis, distal neuropathy, and plexopathy are seen and generally reflect different clinical presentations of mononeuritis multiplex (polyneuropathy).
Bell's Palsy occurs in almost 11% of all Lyme patients and is bilateral in up to 1/3.
Therefore, a bilateral Bell's Palsy is very suspicious for Lyme in an endemic area.
Painful radiculitis or cranial neuropathy can be seen with meningitis but also with normal CSF due to axonal neuropathy.
Myositis may occur with Lyme as well as polymyalgia rheumatica.
Symptoms of chronic involvement of the peripheral nervous system in a series of patients with chronic neurologic manifestations of Lyme disease developed a median of 16 months after the onset of infection, while CNS involvement began a median of 26 months after the onset of disease.
PERIPHERAL NERVOUS SYSTEM TESTING
Electrophysiological testing may show evidence of a mild peripheral neuropathy.
Axonal degeneration and perivascular inflammatory infiltrates are noted on pathological specimens.
THE MOST COMMON PRESENTATION IS SAE, POLYNEUROPATHY, AND ARTHRITIS
Most typically, patients present with SAE, most often combined with polyneuropathy.
Brief episodes of arthritis, primarily involving the knees, generally predate the symptoms and may persist after onset of neurological abnormalities.
The TRIAD OF SAE, POLYNEUROPATHY, AND ARTHRITIS IS HIGHLY SUSPICIOUS FOR NEUROBORRELIOSIS.
Since serologies may be contradictory or negative, the physician will have to settle for treating if clinical suspicion is strong enough and assess whether the patient has ``possible'' or ``probable'' neuroborreliosis.
Vigilant attempts to rule out other disorders should be undertaken.
Screening should be done for collagen vascular disease, other infections, cancer, metabolic or endocrinological disturbances, etc. when a definite diagnosis cannot be made.
II. CURRENT MEDICAL MYTHOLOGY *********************************
``YOU HAVE FIBROMYALGIA. YOU MIGHT HAVE HAD LYME DISEASE IN THE FIRST PLACE, AND EVEN IF YOU DID, YOU WERE GIVEN ENOUGH ANTIBIOTICS. RETREATMENT WILL NOT HELP.''
PERSISTENT INFECTION VERSUS POST-LYME SYNDROME ********************************************
Many patients are sent home with antidepressants, muscle relaxers, but no antibiotics from doctors' offices because they have symptoms of fibromyalgia.
Pictures similar, or identical, to fibromyalgia may be part of the constellation of symptoms of Lyme; it may occur more rarely as an isolated symptom, or surface after what would otherwise be considered successful treatment.
Symptoms of fibromyalgia due to Lyme disease have not been cured with short-term oral or intravenous antibiotics, so some argue fibromyalgia is not due to active infection.
I would question whether those particular antibiotic regimens were adequate to eliminate the infection, rather than assume the patient has developed ``Post-Lyme Syndrome'' (some yet to be defined immunologically triggered disorder).
THE SCOPE OF THE PROBLEM
Bujak et al. evaluated patients a mean of almost five years after treatment.
15% of these patients had symptoms of fatigue and arthralgia.
Almost one-half met criteria for fibromyalgia or chronic fatigue syndrome.
Fibromyalgia is thought to be a variant of the chronic fatigue syndrome.
Of note, nearly all patients continued to complain of memory loss or concentration difficulties.
One quarter had objective evidence of cognitive impairment, and 15% manifested depression.
SYMPTOMS OF FIBROMYALGIA AND CHRONIC FATIGUE SYNDROME IN LYME DISEASE MAY BE ATTENUATED FORMS OR CHRONIC MANIFESTATIONS OF THE FLU-LIKE SYMPTOMS ASSOCIATED WITH EARLY DISSEMINATION
All physicians experienced with treating Lyme disease have had patients who present with a recurrence of flu-like symptoms, months to years after they have completed the usual antibiotic course of therapy, oral or intravenous, and re-exposure had not occurred.
These patients describe their flu-like symptoms as identical to their early-disseminated stage of Lyme disease.
The flu-like symptoms may reoccur following what appears to be a trivial stressor, such as an uncomplicated viral URI.
Patients may be able to ``contain'' their symptoms without specific antimicrobial therapy, but many will have to resume antibiotics.
These patients complain of having to go to bed due to excessive fatigue or hypersomnolence.
They cannot think straight, their muscles and joints ache, and they may have a low-grade fever.
Do these symptoms sound like a ``fibromyalgia-like syndrome'' or ``acute fatigue syndrome?''
Prior medical experience suggests reactivation of infection.
Despite what may appear to have been a previous ``cure,'' relapse of symptoms in this context would appear to be due to failure to eradicate the infection and with reactivation after a period of dormancy.
Reoccurrence of symptoms due to immunologically triggered disease, INDEPENDENT of persistent infection seems unlikely.
In reality, DISTINCTIONS BETWEEN FLU-LIKE SYNDROME, FIBROMYALGIA, AND CHRONIC FATIGUE BLUR.
It seems more logical to postulate that fibromyalgia and chronic fatigue syndrome, when seen with Lyme disease, may be attenuated forms of chronic manifestations of earlier flu-like symptoms associated with early dissemination.
[page 2]
III. THE ASSOCIATION BETWEEN MULTIPLE SCLEROSIS AND LYME DISEASE:
THREE DIFFERENT SCENARIOS
1) LYME CAN LOOK LIKE MS BUT SYMPTOMS AND PATHOLOGY RESIDE OUTSIDE THE CENTRAL NERVOUS SYSTEM
Lyme may present as a MS-like illness, but on many occasions the pathology is not actually in the CNS.
Since chronic Lyme symptoms often are predominantly shifting, vague, behavioral-psychological, psychiatric, and, as mentioned, neurological, they are likely to conjure up the diagnosis of MS in patients and physician alike.
However, the existence of pathology outside the CNS should rule out the diagnosis of MS.
Some of the vague symptoms that can be mistaken for MS include those that are better attributed to peripheral nervous system damage, as part of the mononeuritis multiplex that may occur.
This might cause numbness, tingling, facial weakness, diplopia, etc.
The diagnosis of MS cannot be made in the absence of CNS symptoms and signs.
MRI and CSF findings would also help support the diagnosis of MS.
In addition, a significant CSF pleocytosis may occur with Lyme disease, which should not be present with MS.
2) OTHER LYME PATIENTS DO HAVE CNS LESIONS, BUT THESE ARE GENERALLY DISTINCTLY DIFFERENT, CLINICALLY, AND PATHOLOGICALLY FROM MS
Patients can have CNS lesions in the brain or spinal cord with Lyme disease.
The European literature includes many more cases than the American for encephalomyelitis, strokes, etc.
In those cases where there is focal involvement of the brain or spinal cord, it may be more difficult to distinguish neuroborreliosis from MS.
Again, a brisk CSF pleocytosis would help diagnose Lyme and the specific aforementioned test for CNS Lyme antibodies.
Simultaneous appearance of peripheral nervous system abnormalities or arthritis should suggest the diagnosis of Lyme.
3) ANOTHER GROUP OF PATIENTS HAS MULTIPLE SCLEROSIS AND LYME
There are some patients who have a clear-cut preexisting history of MS before the onset of Lyme disease.
The Lyme appears to accelerate their clinical course.
For others, it appears to be the initiating infection that triggers the MS.
These patients are most likely genetically predisposed to MS and the Lyme bacteria exerts its major effect by ``turning on'' immunologically directed CNS injury.
It is not uncommon to get a history of the onset of an exacerbation of MS related to infections, so Lyme exacerbating MS would be expected.
HLA Class II molecules determine the intensity of the immune response to pathogenic foreign or self-antigens.
With MS, the HLA-DR4 DQw8 haplotype has been associated with chronic progressive MS and the HLA-DR2 DQw6 haplotype has been associated with susceptibility to both chronic progressive and relapsing or remitting MS.
It is possible that in genetically predisposed patients of certain HLA types that infection by Lyme bacteria would cause a high production of cytokines that would mediate the demyelination and destruction of oligodendrocytes.
Most recently, researchers are studying positive outcomes when antibiotics that are most useful in treating Lyme disease are used to treat ``MS.''
IV. WHAT'S WRONG WITH ``CURRENT GUIDELINES FOR TREATMENT'' OF NEUROBORRELIOSIS?
First, read the fine print.
It is interesting to note that recommendations for treatment in the medical literature may carry provisos in small print that can easily be overlooked but are instrumental to understanding how important individualization of therapy is at the current time.
For instance, in the past and in small print, Dr. Alan Steere has written, ``treatment failures have occurred in all these regimens, and retreatment may be necessary; the duration of therapy is based on clinical response, and the appropriate duration of therapy with late neurological abnormalities may be longer than two weeks.''
A more recent article written by Rahn and Malawista states ``these guidelines are to be modified by new findings.
It should always be applied with close attention to the clinical course of individual patients.''
Dr. Katzel surveyed several Lyme Borreliosis conferences, including international ones. He finds a trend towards the use of antibiotics for longer periods than previously described and lack of standardization of care worldwide.
50% of physicians responding considered using antibiotics for time periods greater than one year in symptomatic seropositive patients, with almost as many extending therapy up to one and a half years when necessary.
THE CASE FOR PERSISTENT INFECTION
Studies have shown that Lyme bacteria can be an intracellular pathogen and may evade the normal host immune response.
The causative spirochete, B. burgdorferi, for instance, may persist within fibroblasts and survive at least 14 days of exposure to ceftriaxone.
In addition, B. burgdorferi has been cultured from CSF more than a half year after a standard regimen of IV antibiotics, according to Preac-Mursic.
Logigian and Steere looked at patients with chronic neuroborreliosis, evaluating them six months after two weeks of IV ceftriaxone.
Over one-half of the patients had already been treated with therapy that was thought appropriate for their stage of illness, yet the illness progressed.
The majority of patients studied had subacute encephalopathy and polyneuropathy.
Most had persistent fatigue, and almost one-half had headaches.
One-third of these patients had to stop working or had to go part-time, underscoring the disability that may be seen with Lyme disease on an individual and societal level.
After therapy, two-thirds of patients improved markedly, but seldom completely. Twenty-two percent improved but then relapsed, and fifteen percent had no change in their condition.
This study suggests that additional antibiotics greatly helped the majority with neuroborreliosis but they were insufficient to cause long lasting remission in those patients who subsequently relapsed.
Persistent residual or irreversible disease may explain the fifteen percent who had no change in their condition.
For those clinicians who have had extensive experience with chronic neuroborreliosis, more recent recommendations suggesting that a regime of only 20 to 28 days or even 6 weeks of intravenous antibiotics is sufficient for cure proved contrary to clinical experience.
That brief dosing does not appear to prevent relapse or improve long-term outcome dramatically in many cases.
Perhaps, as recent information has instructed, that is because the immune system does not begin to repair itself until the beginning of the fourth month of antibiotic treatment.
A trial of prolonged use of oral antibiotics seems more reasonable in many cases, given these circumstances.
Antibiotics used for chronic neuroborreliosis should be able to penetrate the blood-brain barrier, express activity against intracellular organisms, and assure good intraphagocytic penetration.
It is anticipated that the microbe during late disease has achieved maximal adaptation to its host environment. Also, because of the long generation time of the organism, lengthier therapy is warranted.
V. WE DON'T HAVE ALL THE ANSWERS BUT HERE'S WHAT IS RECOMMENDED
If a patient has meningitis or appears acutely ill, particularly with possible arrhythmia, admit him or her to the hospital for intravenous antibiotics and observation.
Generally, however, in patients with stable late disease, oral antibiotics can be tried first.
The majority of patients will have some improvement or gradual resolution of encephalopathic symptoms with a better energy level.
After a six-week trial of appropriate antibiotics, the patient is re-evaluated.
If there is no Herxheimer response or some clinical improvement during this interval, it is worrisome, and the physician needs to be concerned about:
1) misdiagnosis, 2) noncompliance, and/or 3) permanent end organ damage.
These possibilities should be addressed with the patient before proceeding with intravenous antibiotics since they may not be maximally beneficial either
Over the long haul, whether intravenous antibiotics are used for two weeks or longer, with chronic refractory disease, ultimately other methods are necessary.
A lengthier use of oral antibiotics seems more logical than intravenous antibiotics for some patients.
Unfortunately, there are no current tests that adequately measure disease activity with neuroborreliosis in all patients.
We are sorely in need of a test similar to the CSF VDRL for syphilis that would give us a measure of disease activity.
Culture negativity or disappearance of a specific immune response in the serum or CSF has not been useful at this time to establish cure. CSF antibodies may persist for years after otherwise successful treatment.
Particularly in the CNS, judging response of therapy is problematic because pathological changes may incompletely or, at least, very slowly reverse.
Any clinical improvement would be expected to occur in a delayed fashion after therapy is given.
Likewise, one would expect neuropathy related to axonal degeneration to remit slowly and/or incompletely.
Formal neuropsychiatric testing is of value in documenting pathology and following the patient.
It also helps delineate what the patient can and cannot do.
It also can help to define the disease for the patient, family, insurer, and the employer.
The patient needs to be told that his or her symptoms should remit slowly and incompletely, when on antibiotic treatment.
This is particularly important when the symptoms have been chronic.
VI. IN SUMMARY ****************
The premise of this approach to diagnosing and treating neuroborreliosis needs to be reinforced.
There is no current laboratory test that makes or breaks the diagnosis of neuroborreliosis.
It is a clinical diagnosis substantiated by laboratory data when possible.
Fortunately, the majority of cases are fairly uniform in their lack of uniformity, and other diagnoses are easily ruled out.
In situations where the physician simply cannot achieve diagnostic certainty, he or she should notify the patient that the diagnosis is ``possible'' or ``probable'' neuroborreliosis.
This has been done previously with MS (i.e., possible, probable, and definite MS), another disease where laboratory testing does not make the diagnosis in and of itself.
There is no perfect current laboratory test to monitor success of therapy, and this is critically needed.
Until better testing is available, assessing progress, or lack thereof, will largely be determined with clinical acumen.
The infection is difficult to eradicate and may require long-term treatment.
The spirochete, particularly in later stages, becomes well adapted to survival within its host environment.
There are some patients that we may not be able to cure, but will be able to palliate with currently available antibiotics.
Although immunopathogenic factors may play a crucial role in disease presentation, the presence of chronic infection appears necessary to perpetuate the process and play a causative role in persistence of immunologically triggered symptoms.
There is no Diagnostic and Statistic Psychiatry Manual (DSM IV) category for ``antibiotic seeking behavior.''
It is common for physicians who are unable to explain patients' symptoms or effect their cure to ascribe a psychiatric cause to their malady.
This is easily done with Lyme since objective findings may be subtle or non-existent.
Because neuropsychiatric symptoms may pre-dominate, it is easy in some patients to attribute their symptoms to depression or secondary gain.
These patients do not in any other way seek other medication that would be associated with habituation or addiction (i.e., pain medicine).
Many patients suffer unfairly at the hands of physicians who refuse to make the diagnosis because blood tests are either contradictory or negative.
``Lyme bashing,'' for instance, referring to Lyme disease as ``yuppie flu,'' is demeaning.
The ``just say no'' attitude of certain physicians towards Lyme patients who request retreatment with antibiotics should not be condoned in the face of continuing experience with this potentially chronically disabling infectious disease. -----
Audrey Stein Goldings, MD is a private practice neurologist in Dallas. (She no longer sees lyme patients, though.)
She is member of ILADS and a founding member of the Board of Directors.
In addition to the usual coinfections from ticks (such as babesia, bartonella, ehrlichia, RMSF, etc.), there are some other chronic stealth infections that an excellent LLMD should know about -
such as HHV-6, mycoplasma and Cpn. Links included in this wonderful thread:
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
Printer-friendly view of this topic