Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
Revised June 2003
WELCOME TO LYMENET
Are you looking for a doctor to assist you with Lyme or other tick borne infections?
If so, suggestions are posted below to assist you in your search. If you would like to have general information about tick borne diseases, please skip down to the next post.
To find a LLMD (Lyme Literate MD)
Go to the Seeking a Doctor section here at Lyme Net and post a message mentioning your area in the title of the post. If you get no reply, please post another request in the Medical Section and ask for help. OR...
If you are looking for Lyme Literate Medical Doctors you can write to (email) the person who helps find patients a Lyme doctor. She is at the Lyme Disease Association. Her name is Kim Uffleman and her email address is:
Please let Kim know where you are located (town, county, state). She will make every effort to reply with up to 4 LLMD's that are as close as possible. Please put the name of your state in the subject line of the email.
OR....
The Lyme Disease Association has a toll free line (1-888-366-6611) you can use to request a LLMD referral.
GOOD LUCK!
[This message has been edited by Tincup (edited 02 January 2004).]
Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
Welcome to Lyme Net!
NOTE- It is time for an edit and update for this post. Sorry some of the older links are not working. I will re-do the site soon!
When posting at Lyme Net, please break up your post (see this example) with frequent spaces so the folks with neurological problems or eye problems can read them easier.
You will most likely get more replies that way. Thank you!
Below are direct links to basic sites about Lyme and other tick borne infections. We have also posted a few articles that may interest you. Please let us know if you have any questions or if we can help.
Notes:
1. Most members at Lyme Net are not doctors and they are not providing medical advise. They may make suggestions or share their personal experiences on non-emergency topics. If you have an emergency or need the advise of a doctor, please go to the nearest hospital or contact your physician.
2. We only post doctors names on the board if we have their permission. Since Lyme Net does not have people who are paid to respond to posts, all answers come from volunteers who will try to assist you as they are able. It may take a while to get responses so please understand any delays. We hope you will feel free to respond to others while you are on the road to recovery. It would certainly help lighten the load of others here and we would appreciate it. There is bound to be an experience you can share with someone that will help them with their questions, if nothing more than letting someone know they are not alone and you care.
3. If you need a specific person to respond to your questions, please use their name in the title so they have a better chance to see your post.
4. To find information about most, if not all topics previously discussed here, you might try doing a search. Look at the TOP of your screen for a tiny button that says SEARCH. Once you click on that button a new screen will appear. Fill out the information requested and submit the topic. Since most topics have been discussed in the past, you should pull up some very informative posts. If you can?t find the answers you need through a search, please feel free to ask folks on the board by starting a new post.
International Lyme and Associated Diseases Society (ILADS) home page: http://www.ilads.org/
ILADS- DIAGNOSTIC HINTS AND TREATMENT GUIDELINES FOR LYME AND OTHER TICK BORNE ILLNESSES JOSEPH J. BURRASCANO JR., M.D. Fourteenth Edition, November, 2002 http://www.ilads.org/burrascano_1102.htm
Downloadable summaries of peer-reviewed, scientific literature in PDF (Adobe Acrobat Reader) format are available at the following website. The topics covered include: documented symptoms of Lyme disease, persistent infection despite antibiotic treatment, seronegative Lyme disease, and a collection of photographs and quotations on the cystic form of the Lyme disease bacterium. Click below at Cheryl?s site:
Dr. Brian Fallon- Study of Chronic Lyme Disease SPECT Imaging of Chronic Lyme Disease vs Other Disorders Developmental Delay and Lyme Disease in Children-Children with Lyme Disease & Autistic Spectrum disorders age 2-17 http://www.columbia-lyme.org/flatp/resstud.html
Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
Latest report concerning chronic Lyme and treatment:
Med Clin North Am 2002 Mar;86(2):341-9, vii.
LATE AND CHRONIC LYME DISEASE- Sam T. Donta, MD* Prof. of Medicine, Divisions of Infectious Disease and BioMolecular Medicine Director, Lyme Disease Unit Boston University Medical Center, Boston, Massachusetts Corresponding author for proof and reprints: Sam T Donta MD Boston Medical Center 650 Albany Street-8th floor Boston MA 02118 (617) 638-6017 (617) 638-6009 (fax) [email protected] (email)
INTRODUCTION- Following the introduction of Borrelia burgdorferi into the skin by an infected tick, the organisms begin to spread both locally and systemically. Several days typically elapse before the appearance of the first sign of infection, i.e. erythema chronicum migrans (ECM), or other less typical rashes (29). The rash occurs in fewer than 50% of patients with Lyme Disease (8,10), but the true incidence of Lyme Disease in the absence of a rash is unknown. The occurence of multiple rashes is indicative of systemic spread of the organisms. Multiple rashes usually do not occur until 2-4 weeks following the initial tick bite. This is the same time period during which the organisms are being disseminated to their target tissues and cells. The incidence of multiple rashes was initially reported to occur in as many as 50% of cases, but has been much less common in the last two decades, probably because of frequent use of antibiotics. Approximately 4-6 weeks following the tick bite, the first systemic symptoms (other than multiple rashes) occur in some patients, usually in the form of "flu" (15). These symptoms include sore throat, severe headaches and neck aches, and severe fatigue. Rhinitis, sinusitis, and cough are not usually present, distinguishing this "flu" from other influenza-like illnesses. While the Lyme-flu symptoms can spontaneously resolve, patients can experience recurrent "flu". Soon after the onset of Lyme-flu, fatigue, arthralgias and/or myalgias may begin. The arthralgias appear to primarily involve the large joints (i.e. knees, elbows, hips, shoulders), although smaller joints (e.g. wrists, hands, fingers, toes) may be involved (29). Some patients may have actual arthritis, often oligoarticular, more frequently in men than in women. Earlier estimates were that 50-75% of patients who developed late Lyme Disease had arthritis, but more recent analyses suggest that the incidence of actual arthritis in patients with late or chronic disease is closer to 25% (33). Neck stiffness is common. The pains are described as severe, jumping from joint to joint, and may be present for only short periods of time. Pain in the teeth or in the temporal-mandibular joints is not uncommon. Rib and chest pains occur frequently, leading some patients to seek care in emergency rooms and urgent care centers for evaluation of possible cardiac disease. Frequently as well are paresthesias such as burning, numbness and tingling, and itching. Some patients experience crawling sensations, vibrations, or electric shock-like sensations. Rarely is there any actual palsy of the affected areas, making this much more of a neurosensory, rather than a motor, disease. In addition to paresthesias, purely neurological symptoms and signs include headaches, an aseptic meningitis, facial nerve (Bell's) palsy, and encephalitis or encephalopathy that may be manifested by cognitive dysfunction, especially short-term memory loss, and psychiatric symptoms such as panic, anxiety, or depression (14). The aseptic meningitis and Bell's palsy tend to occur within the first few months following the tick bite, but may also occur as part of reactivation disease (9). Other symptoms may include fevers (usually low grade, but may be high), sweats (which may be severe), visual dysfunction (described primarily as blurriness, but can include optic neuritis or uveitis), tinnitus, sensitivity to sounds, or hearing loss. Shortness of breath, palpitations and/or tachycardia, abdominal pains, diarrhea or irritable bowel, testicular or pelvic pain, urinary frequency or urgency, dysequilibrium, and tremors are also common symptoms. Some of the dysautonomia symptoms can be disabling. Rarer symptoms may relate to panniculitis and hepatitis. Rarely as well are congenital and intrautero infection; when this occurs, it appears to be similar to toxoplasmosis and rubella, i.e. a primary infection during the first trimester. The occurrence of optic neuritis or uveitis raises other possibilities such as multiple sclerosis, but can be part of Lyme Disease. The course of the disease can best be described as persistent, but with periods of worsening symptoms, often cyclical every few weeks or monthly. Especially disconcerting are persistent symptoms such as headaches and fatigue that can be exhausting. Some patients are more symptomatic than are others, which may reflect genetically-determined differences in responsiveness or extent of infection. The disease does not appear to be progressive or destructive, as with cancer, nor is it fatal, but can be very debilitating. The incidence of asymptomatic infection has not been adequately delineated. There appear to be substantial numbers of patients who remain asymptomatic, but reactivate their disease a number of months or years later, following trauma, pregnancy, a medical illness for which an antibiotic is prescribed, or other stresses, including psychological stresses (9). The Lyme OspA vaccine has appeared to reactivate Lyme Disease in a number of individuals who knew, but some who did not know, they had prior Lyme Disease (11). The mechanisms responsible for the reactivation of the disease have not been defined, but may include both molecular mimicry and underlying infection.
PATHOGENESIS- The pathogenesis of Lyme Disease remains to be defined. From the available studies, it would appear that the organisms are trophic for either the endothelial cells of the blood vessels that serve the nervous system or for the glial or neural cells themselves (4,24,26,31). Accumulating evidence supports the hypothesis of a persistent infection as the cause of the persisting or relapsing symptoms (26,31). Whether molecular mimicry is involved in the pathogenesis of some of the symptoms remains more speculative (18). Although arthritis can occur in Lyme Disease, the organisms can only rarely be found in synovial tissue. And as many of the arthralgias that occur in the disease do not respond well to antiinflammatory agents, the disease is more of an infectious neuropathy than an actual invasion of synovial or bursal tissues.
DIAGNOSIS- The diagnosis rests heavily on the clinical symptomatology. When there are clinical signs, e.g. rash, aseptic meningitis, optic neuritis, arthritis, an appropriate differential diagnosis must be pursued. On a clinical basis, "chronic fatigue syndrome" or "fibromyalgia" cannot be readily distinguished from chronic Lyme Disease. Indeed, accumulating experience suggests that Lyme Disease may be a frequent cause of fibromyalgia or chronic fatigue (8,12). Other microbes have been proposed as causative agents of multisymptom disorders that are being termed chronic fatigue and fibromyalgia, especially more recently recognized mycoplasma species such as M.fermentans and M.genitalium, but definitive proof of cause and effect has not yet been established (6, 23). There has been an attempt to separate "late" Lyme Disease from "chronic" Lyme Disease, the former being manifested by objective signs of arthritis or neurological disease (32). Some have denied the existence of chronic disease, inferring that these patients suffer from psychiatric disorders; some have used the term "chronic" to mean post-treatment disease ("post-Lyme"), assuming that the infection has been treated, and the remaining symptoms are in the same realm as those patients who have "fibromyalgia" or "chronic fatigue" (27, 30). These assertions are speculative and remain unproven. That chronic Lyme Disease actually exists, and is likely the most common form of the disease, is supported by epidemiologic studies demonstrating that 30-50-% of treated and untreated patients go on to develop a multisymptom disorder typical of, and indistinguishable from, fibromyalgia and chronic fatigue (1, 28). As with other multisymptom disorders, chronic Lyme Disease is a clinical syndrome consisting of fatigue, arthralgias and myalgias, and other nervous system dysfunction (7). Furthermore, the results of treatment studies appear to support the hypothesis that persistent infection is responsible for the chronic symptoms. It is likely that Lyme Disease will serve as a useful model for other chronic multisymptom disorders. Whether the pathogenesis of "late" Lyme Disease differs from that of the chronic form of the disease remains to be established. Routine laboratory tests are usually normal in Lyme Disease. The ESR is most often normal, distinguishing it from some of the inflammatory disorders such as rheumatoid arthritis or lupus. Culture of the borrelia is possible early in the disease, usually from biopsies of the erythema migrans rash; however, most laboratories are not capable of culturing the organisms. The only currently available useful laboratory tests are the immunologically-based ELISA and Western blot assays. The recommendation was made in 1994 to have a two-tiered testing system in which the Western Blot would only be done on ELISA-positive samples (5). The recommendation was based primarily on the results obtained from patients with arthritis (13), did not take into account the chronic form of the disease, and was made despite the lack of consistent reproducibility of results between various laboratories (2, 16). The ELISA has been shown to be an unreliable test in many patients with Lyme Disease, both in early infection and later disease (8, 10). Part of the reason for the lack of sensitivity of the ELISA is the use of whole organisms, resulting in a high amount of background absorbance. After correction for the high background, only a small percentage of positives can be detected. Because Western blots separate the proteins of the borrelia, specific reactions can be visualized, and more accurate interpretations of the results made. Over 75% of patients with chronic Lyme Disease are negative by ELISA, while positive by Western blot (8, 10). Patients with oligoarticular arthritis may be more likely to have robust IgG responses and positive ELISA tests and IgG Western Blots (13). By Western blot analyses, the first immunologic reactions in Lyme Disease are to the 41kd flagellar protein, and the 23kd OspC protein. Typically, at the time of the ECM rash, there will be an IgM reaction against the 23kd and 41kd proteins, and no IgG reactions. Within the next few weeks, the IgM reactions persist, sometimes accompanied by less specific reactions against 60kd and 66kd proteins, and IgG reactions are now visible against the 23kd and 41kd proteins. Thus, in the presence of an appropriate clinical picture, the immunoreactivity against the 23kd and 41kd proteins appear to be diagnostic of Lyme Disease. Whereas the 41kd protein is not unique to B. burgdorferi, the 23kd protein appears to be unique. Also apparently unique proteins of B.burgdorferi are the 31kd (Osp A) and 34kd (Osp B) outer membrane proteins, and the 35kd, 37kd, 39kd, and 83/93kd proteins. Reactions to the 31kd proteins are not usually seen until after a year or more following the onset of disease. Not all patients with symptoms for more than one year, however, display reactions to the outer membrane proteins. Most symptomatic patients have specific reactions on IgM Western blots (8,10). With resolution of the symptoms, the IgM reactions disappear or attenuate. IgG reactivity may continue to be present with resolution of symptoms, but it typically also disappears or attenuates with successful therapy. There are some patients (20%) who have symptoms, but whose Western blots are negative (8,10). If the borrelial organisms remain intracellular, with no extracellular reemergence once established, this could explain the absence of additional or persistent immune responses. PCR (Polymerase Chain Reaction) is a highly sensitive means to detect microbial DNA or RNA, and it was hoped that this technique would find an important role in the diagnosis of Lyme Disease. Thus far, however, despite the specificity of this method, borrelial DNA or RNA has not been reliably detected in the blood, urine, or spinal fluid of patients with early or later forms of Lyme Disease, findings again supportive of an intracellular reservoir for the borrelia. It should be possible to develop a better, highly specific ELISA for Lyme Disease, using recombinant 41kd, 23kd, 31kd and/or 34kd (and perhaps other B.burgdorferi-specific) proteins. Currently, however, the Western blot assay is the most reliable immunologic test.
TREATMENT- In vitro, B. burgdorferi is sensitive to several antibiotics (20,25). This assumption is complicated, however, because of the long incubation times needed to determine minimum inhibitory concentrations (MIC), as the borrelia have doubling times of 20-24 hrs. With these limitations, the results of a few studies show minimum bactericidal concentrations (MBC) to penicillin of 8ug/ml, ampicillin: 2ug/ml, tetracycline: 1-2ug/ml, doxycycline: 2ug/ml, ceftriaxone: 0.5ug/ml, cefotaxime: 0.5ug/ml, cefuroxime: 1-2ug/ml, cefixime: 8ug/ml, erythromycin: 0.5ug/ml, clarithromycin: 0.5ug/ml, azithromycin: 0.5ug/ml, and ciprofloxacin: 4ug/ml. At the time of the first rash, any one of several antibiotics appear to be effective, if given for 2 weeks, according to several published studies. However, a number of patients so treated developed subsequent symptoms of arthralgias, fatigue, and paresthesias, with positive Western blots, who were then successfully treated with longer courses of antibiotics (8, 10). The recommendation at this time, therefore, is that tetracycline, doxycycline, or amoxicillin be used for 1 month if ECM is the only symptom of Lyme Disease. Once any other symptoms appear, the treatment of Lyme Disease for only 2-4 weeks is associated with frequent failures and relapses (8, 10). Our initial experience suggested that a 3 month course of tetracycline was associated with a higher success rate (8). In patients with symptoms present for more than six months, the treatment course may need to be more prolonged, or a retreatment course of varying length may be needed. In patients with symptoms for more than a year, 12-18 months may be needed for complete resolution of symptoms. The rationale for a longer treatment course is based on extensive observations (8,10), plus the analogy to the longer treatment courses required for tuberculosis, leprosy, Q fever, and certain fungal diseases. With Lyme Disease, the slow growth rate and metabolic activity of the borrelia would seem to correlate with the need for longer treatment periods. Once treatment is initiated for patients beyond the earliest signs of infection, their symptoms frequently increase during the first several days, or even for the first several weeks of therapy. For patients with preexisting symptoms of more than a few months, relief of any of their symptoms may not occur until after 4-6 weeks of therapy (8, 10). Typically, there are short periods of relief, followed by relapsing or migrating symptoms; with continued therapy there are longer symptom-free periods. Some arthralgias may require 3 months or more to resolve, and fatigue may be the last symptom to disappear. The preference for tetracycline evolved because of the large number of failures that were noted in patients who had been on ampicillin and doxycycline. Patients generally had some response to doxycycline, but it was uaually not complete, nor long-lasting. Tetracycline may be more effective than doxycycline simply because of the greater dose, i.e., 100mg of doxycycline twice daily is not equivalent to 500mg of tetracycline three times daily; also, doxycycline is highly protein-bound, compared to tetracycline, which could limit the availability of free drug to diffuse into tissues and cells. Some physicians use doxycycline at doses of 300-400mg daily to try to achieve a successful result. A strict comparison between doxycycline and tetracycline has not yet been made. Minocycline has also been used by some physicians, with varying success, but faces the same issues of dosage and protein binding. Of the beta lactams used for the treatment of Lyme Disease, the most efficacious appears to be ceftriaxone. In limited comparitive trials, cefotaxime appears to be equally efficacious, and high-dose IV penicillin may also be effective. In early Lyme Disease, oral amoxicillin is as effective as doxycycline. In later disease, many failures are noted, despite the use of up to 3 grams of amoxicillin daily, with probenicid. Cefixime would also not appear to be effective therapy. Cefuroxime axetil has been evaluated only in the treatment of early Lyme Disease, and appears comparable to doxycycline. Limited reports of its use in later Lyme Disease have not shown it to be efficacious. The role of the newer macrolides in the treatment of Lyme Disease needs further assessment. Erythromycin has been regarded as ineffective, despite its good in vitro sensitivities. Azithromycin has been reported to be less effective in the treatment of early Lyme Disease than amoxicillin (21). Some physicians use clarithromycin and azithromycin in higher dosages and for longer periods of time, but there have been no reports of greater success with these drugs than with the tetracyclines or beta-lactams. In our experience, all macrolides are effective when combined with a lysosomotropic agent, especially hydroxychloroquine (see below) (10). In evaluating the possible factors, it would appear that antibiotics that can achieve intracellular concentrations and activity are the most efficacious drugs. The results of studies in Klempner's laboratory using a tissue culture model of borrelia infection demonstrated that ceftriaxone was incapable of eradicating intracellular organisms (17); similar experiments in Raoult's laboratory using an endothelial cell model demonstrated that tetracycline and erythromycin were effective, but beta lactam antibiotics were not (3). These results are in line with our experience that the tetracyclines and macrolides achieve the greatest success. In contrast to beta lactams, antibiotics of the tetracycline and macrolide classes are capable of good intracellular penetration. Experience with the macrolide antibiotics has been disappointing, however, when compared with its in vitro activities against the Lyme borreliae, and with the established efficacy of macrolides against other intracellular parasites such as chlamydia, legionella, mycobacterium-avium intracellulare, and toxoplasma. If, though, the Lyme borreliae reside in intracellular vesicles that are acidic, the macrolides' activity would be sharply decreased at the lower pH. This is in contrast to the tetracyclines, which are active at acid pH; even so, the activity of doxycycline was shown to be further increased by increasing the pH. In a tissue culture model of ehrlichia infection, the use of lysosomotropic agents such as amantidine, NH4Cl, and chloroquine increased the killing of intracellular organisms by doxycycline (22). Based on those studies, and the hypothesis that late Lyme Disease symptoms are due to persisting intracellular infection, we have been successfully treating patients using the combination of a macrolide and hydroxychloroquine (10). As regards "CNS" disease, there is no evidence that ceftriaxone is more successful than either the tetracyclines or the combination of macrolide and hydroxychloroquine; if our presumption that the pathogenesis of the disease involves the localization of the borrelia to the endothelial cells of the blood vessels serving the nervous system or to glial or neural cells is correct, then one would not need to have a drug that can cross the blood-brain barrier to be effective. Indeed, the tetracyclines can cross the blood-brain barrier to some extent, and were used when initially introduced into clinical medicine for the treatment of meningitis, with some success. Macrolide antibiotics do not cross the blood-brain barrier, but have been effective in treating other CNS infections (eg toxoplasmosis), and in our experience have been effective in reversing the neuropsychiatric symptoms and signs (eg SPECT scans) of Lyme Disease (10). With regard to the issue of bactericidal vs bacteristatic effects, any such effect in vivo has not been demonstrated. Finally, there have been no reports showing any change in antibiotic resistance patterns during the course of treatment. Ultimately, the determination of efficacy of therapy depends on the clinical response.
FUTURE - The diagnosis and treatment of Lyme Disease have been hampered by less than adequate diagnostic tests and inadequate comparisons of antibiotic regimens. Specific antigen-based ELISA tests should result in greater specificity, but sensitivity of any tests based on measurements of the host immune response might still be of limited value if the borrelia remain intracellular. Most useful would be the development of tests that can determine the presence and extent of any residual borreliosis. In the therapy of Lyme Disease, double-blind, placebo-controlled and comparitive trials are needed to answer the questions relating to duration and class of antibiotic therapy. The apparent failure of a regimen of one month of IV ceftriaxone, followed by two months or oral doxycyline, to improve the outcomes of patients with chronic Lyme Disease (19) was not surprising, based on prior observations that neither regimen used for a limited duration was capable of yielding patient improvement (8,10,33). Additional trials are needed to evaluate whether longer durations of treatment, using tetracycline itself, or the novel combination of macrolide and lysosomotropic agent, would be proven effective treatments.
REFERENCES 1. Asch ES, Bujak DI, Weiss M, et al. Lyme Disease: an infectious and postinfectious syndrome. J Rheum 21:454-61, 1994. 2. Bakken LL, Case KL, Callister SM, et al. Performance of 45 laboratories participating in a proficiency testing program for Lyme Disease serology. JAMA 268:891-5, 1992. 3. Brouqui P, Bodiga S, and Raoult D. Eucaryotic cells protect Borrelia burgdorferi from the action of penicillin and ceftriaxone but not from the action of doxycycline and erythromycin. Antimicrob Agents Chemother 40:1552-4, 1996. 4. Cadavid D, O'Neill T, Schaefer H, and Pachner AR. Localization of Borrelia burgdorferi in the nervous system and other organs in a nonhuman primate model of Lyme disease. Lab Investigation 80:1043-54, 2000. 5. Centers for Disease Control. Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR 44:590-1, 1995. 6. Choppa PC, Vojdani A, Tagle C, et al. Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis, and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome. Mol Cell Probes. 12:301-8, 1998. 7. Donta ST. Lyme Disease: A clinical challenge. J Spirochet and Tick Dis 2:50-51, 1995. 8. Donta ST. Tetracycline therapy of chronic Lyme Disease. Clin Infect Dis 25: S52-56, 1997. 9. Donta ST: Reactivation of latent Lyme Disease. X Annual LDF International Conference on Lyme Borreliosis, National Institutes of Health, April 1997. 10.. Donta ST. Treatment of chronic Lyme disease with macrolide antibiotics. In: Program and abstracts of the VIIIth International Conference on Lyme Borreliosis; June 20-24, 1999; Munich, Germany. Abstract P193. 11. Donta ST: Reactivation of Lyme Disease following OspA vaccine. Int J Antimicrob Agents 17:S116-7, 2001. 12. Donta ST: The existence of chronic Lyme Disease. Current Treatment Options in Infectious Diseases 3:261-2, 2001. 13. Dressler F, Whalen JA, Reinhardt BN and Steere AC. Western blotting in the serodiagnosis of Lyme disease. J Infect Dis 167:392-400, 1993. 14. Fallon B and Nields JA. Lyme disease: a neuropsychiatric illness. Am J Psych 141:1571-83, 1994. 15. Feder HM Jr, Gerber M, and Krause PJ. Early Lyme disease: a flu-like illness without erythema migrans. Pediatrics 91:456-9, 1993. 16. Fister RD, Weymouth LA, McLaughlin JC, et al. Comparative evaluation of three products for the detection of Borrelia burgdorferi antibody in human serum. J Clin Microbiol 37:2834-7, 1989. 17. Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme Disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. J Infect Dis166:440-4, 1992. 18. Gross DM, Forsthuber T, Tary-Lehman M, et al. Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis. Science 281:703-6, 1998. 19. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme Disease N Engl J Med. 345: 85-92, 2001. 20. Levin JM, Nelson JA, Segretti J, et al. In vitro susceptibilities of Borrelia burgdorferi to 11 antimicrobial agents. Antimicrob Agents Chemother 37:1444-6, 1993. 21. Luft BJ, Dattwyler RJ, Johnson RC, et al. Azithromycin compared with amoxicillin in the treatment of erythema migrans. A double blind, randomized, controlled trial. Ann Int Med 124:785-91, 1996. 22. Maurin M, Benoliel AM, Bongrand P, and Raoult D. Phagolysosomal alkalinization and the bactericidal effect of antibiotics: the Coxiella burnetii paradigm. J Infect Dis 166:1097-102, 1992. 23. Nicolson GL, and Nicolson NL. Chronic infections as a common etiology for many patients with chronic fatigue syndrome, fibromyalgia, and Gulf War Illness. Intern J Med 1:42-6, 1998. 24. Pachner AR, Delaney E, O'Neill T, and Major E. Inoculation of nonhuman primates with the N40 strain of Borrelia burgdorferi leads to a model of Lyme neuroborreliosis faithful to the human disease. Neurology 45:165-72, 1995. 25. Preac-Mursic V, Wilske B, Schierz G, et al. In vitro and in vivo susceptibility of Borrelia burgdorferi. Eur J Clin Microbiol 6:424-6, 1987. 26. Roberts ED, Bohm RP Jr, Lowrie RC Jr, et al. Pathogenesis of Lyme neuroborreliosis in the Rhesus monkey: the early disseminated and chronic phases of disease in the peripheral nervous system. J Infect Dis 178:722-32, 1998. 27. Seltzer EG, Gerber MA, Carter ML, et al. Long-term outcomes of persons with Lyme disease. JAMA 283:609-616, 2000. 28. Shadick NA, Phillips CB, Logigian EL, et al. The long-term clinical outcomes of Lyme Disease. Ann Intern Med 121:560-7, 1994. 29. Steere AC, Malawista SE, Hardin JA, et al. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med 86:685-98, 1977. 30. Steere AC. Lyme Disease. NEJM 345:115-25, 2001. 31. Straubinger RK. PCR-based quantification of Borrelia burgdorferi organisms in canine tissues over a 500-day postinfection period. J Clin Microbiology 38:2191-9, 2000. 32. Wormser G, Nadelman RB, Dattwyler RJ, et al. Practice guidelines for the treatment of Lyme disease. Clin Infect Dis 31(S1):S1-S14, 2001. 33. Ziska MH, Donta ST, and Demarest FC. Physician preferences in the diagnosis and treatment of Lyme Disease in the U.S. Infection 23:1-5, 1995.
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
Since I keep having to find this.. I am posting it here.
LYME DISEASE QUESTIONS AND ANSWERS
Q: What is Lyme disease?
A: Lyme Disease is caused by a bacteria, specifically known as a spirochete (similar to the one that causes syphilis) and can be found at least 9 different species of ticks, 6 species of mosquitoes, 13 species of mites, 15 species of flies, 2 species of fleas, and numerous wild and domestic mammals including rabbits, rodents, and birds. Once transmitted to humans, the spirochete causes damage by spreading to various parts of the body. It can infect any and all organs and tissues in the body, causing a multitude of symptoms that can make a person very ill, sometimes totally disabled, and it can be fatal.
Q: Can Lyme Disease be transmitted from person to person?
A: The spirochete that causes Lyme disease has been found in semen, urine, blood, breast milk and other body fluids and tissues. Those who have Lyme disease are prohibited from donating blood or organs. Lyme disease has also been shown in a number of cases to be passed from mothers to their unborn children and to babies through breast milk. The spirochete can be found in the blood of deer which poses a threat to hunters and it is recommended that anyone handling raw venison use gloves.
Q: What are some of the signs and symptoms of the disease and its effects?
A: Unless a doctor is very experienced with Lyme disease, (he or she) may not recognize it until it is too late or not at all. Lyme Disease has been misdiagnosed as a variety of other conditions, including but not limited to, multiple sclerosis, chronic fatigue, Alzheimer's, Fibromyalgia, depression, lupus, ADD, and various forms of arthritis. The list of possible symptoms is overwhelming. Anything from hearing loss to panic attacks surfacing in otherwise healthy individuals can be the first indication a person has contracted Lyme. Many patients do not recall a tick bite (thought to be the most common form of transmission) and many never get the typical bulls eye rash or flu-like symptoms that are sometimes associated with early stages of Lyme. Lyme can affect the eyes causing sensitivity to light, floaters, conjunctivitis, unequal pupils, bacterial infections, optic neuritis, blurred or double vision, and even blindness.
The brain and surrounding tissues may become infected and can leave the patient with permanent damage and/or pain. Cranial nerve palsies, encephalopathy, meningitis, dementia, memory deficits, brain hemorrhage, intracranial pressure, and aseptic meningitis can all be caused by Lyme Disease.
A number of people develop problems with their digestive tract and people with Lyme can battle acid reflux, diarrhea, bloating, cramps, partial to full blockages, and pain. The bladder and reproductive organs are not spared and menstrual problems may surface in woman, while swollen testicles and pelvic pain may cause problems for men. There is often brain "fog," memory problems, confusion, difficulty thinking, and speech difficulties. Extreme fatigue may be a constant problem, along with muscle spasms and joint pain. The heart and lung problems found in Lyme patients can range from palpitations and shortness of breath, to heart block and respiratory failure.
Depression, severe anxiety, insomnia, and mood swings are common. The list goes on and on. The most important thing to remember is to consider Lyme even though a tick was not seen, or as rash did not appear, or a blood test comes back negative, especially if someone seems to have ``bizarre'' or seemingly unrelated symptoms, ``atypical'' diseases of any kind, or a disease that does not respond to ``standard'' treatment. The standard blood tests often used to detect Lyme antibodies are missing approximately half of the cases of Lyme Disease. Lyme, according to the Center for Disease Control, is a ``clinical diagnosis'' and negative tests should NOT rule out the disease. A lab specializing in Lyme Disease and co-infections should be used for the best chances of aiding the clinical diagnosis.
Q: Can Lyme cause other diseases?
A: Lyme can mimic many diseases and can force the patient to require treatment for a variety of other problems. The thyroid responses can be off and require adjunct therapy.
Other infections (such as bladder, sinus, eye, and kidney infections) often develop and are hard to fight off once the immune system is compromised. As the spirochetes inhabit and die off in the human body, toxins develop, which can cause a multitude of chronic problems unless treated properly. A VCS test should be done to detect toxins.
Q: If caught early, can the effects be minimized?
A: Outdated information indicates a tick must be attached for at least 24 to 48 hours to infect a person. This is NOT the case. If you are bitten by a tick, the old wait-and-see approach can be devastating. Once in contact with an infected source, the earlier the treatment the better. You should NOT wait for blood tests, rashes, or symptoms to appear before being treated if you have a tick bite.
Q: What type of treatment is available and how long does it run?
A: Treatment protocols vary depending on the amount of time between the infection and when treatment begins. Current guidelines indicate newly discovered tick bites and early cases should be treated with antibiotics for a minimum of four to six weeks, and late stages usually require a minimum of four to six months of treatment, either IV or oral medications, or both. If treatments are discontinued before all symptoms of Lyme disease have ended, the person can remain ill and relapse. Many patients who were not treated properly in the past have developed chronic cases of lyme and may need ongoing treatment to be able to keep from deteriorating.
Q: What are the long-term effects of Lyme disease?
A: Patients can relapse with any and all of the original symptoms, develop new ones and progressively deteriorate as time goes by. Lyme disease can cause pain and may affect the ability to walk and may limit the range of motion. Speech, writing skills, or communication problems may worsen. Many patients become bedridden or house bound. Damage to the brain and other organs can result. The financial burden of Lyme can be devastating. In addition, some insurance companies continue to deny necessary treatments, which further stresses individuals and worsens their condition.
Q: What is the risk of contracting Lyme disease?
A: In some areas of the country where winters are not severe, it is possible to have nearly year-round exposure to ticks and other insects carrying Lyme disease. One female tick can produce 2,000 to 5,000 babies. Once an area has a small tick population, the numbers increase rapidly. Ticks are carried into new areas by birds, pets, wildlife and people.
Q: What is the best way to prevent getting Lyme disease?
A: Often it is difficult to wear long pants, long sleeve shirts, shoes and socks and a hat outdoors in the summer without suffering from heat related problems. I recommend wearing light colored clothing, doing regular tick checks while outdoors and again after returning home. Showering using a stiff wash cloth may help to dislodge ticks before they become fully attached. I also recommend Repel Permanone be applied to outdoor clothing, hats, outdoor duffel bags and equipment. This unscented product kills ticks as they crawl across treated surfaces instead of trying to simply deter them as most repellents try to do. Yards can be treated with Sevin which is available locally in the garden department of many stores in a dust or concentrated liquid form. It won't kill all of the ticks but it will reduce the numbers to a safer level. I do NOT recommend the current Lyme vaccine that was recently pulled from the market.
Q: What other tick borne diseases can affect humans?
A: There are increasing numbers of Babesia, Bartonella (cat scratch fever), Rocky Mountain Spotted Fever, and Ehrlichiosis being found as in patients originally diagnosed with Lyme disease or in patients who are exposed to ticks. These diseases may appear with or without typical symptoms and are often being overlooked, causing patients to suffer. These co-infections may become chronic if left untreated and all have been found to be responsible as a cause of death in some individuals.
It is well known that co-infections may occur with Lyme Disease relatively frequently. Patients with a history of Lyme Disease who have incomplete resolution of symptoms should be evaluated for Bartonella infections. Bartonella is an intracellular, gram-negative bacteria that can become chronic. Certain lab tests may not detect the infection due to a variety of strains and the lack of sensitivity of the tests. It is advised to use both PCR and IFA methods of testing and not to dismiss the disease due to negative tests when symptoms are present. Various Bartonella species have been recognized since the early 1950's.
Bartonella may not present in its usual form when additional infections, such as Lyme or Babesia are present. In addition, typical Bartonella lesions are not always seen in patients, therefore, a diagnosis of ``fever of unknown origin'' should alert a physician to consider Bartonella. It is estimated that approximately 2/3 of the patients with Bartonella have a fever. Involvement of practically every organ has been reported.
There are a variety of symptoms associated with Bartonella, including, but not limited to, the following:
BRAIN: Encephalopathy may occur 1-6 weeks after the initial infection and is fairly common in patients with Bartonella.
Note: Approximately 50 percent of patients who develop Encephalopathy can be affected by seizures (from focal to generalized, and from brief and self-limited to status epilepticus). Headaches, Cognitive Dysfunction, and CNS Lesions may be evident.
RASH AND LYMPHADENITIS: Erythematous papules (red splotches or slightly raised red spots) may develop. Such papules occasionally occur on the lower limbs but are more common on the upper limbs, the head, and neck. The papules may appear on the skin or mucous membranes. Bartonella may also cause subcutaneous nodules, with some bone involvement possible. The nodules may show some hyperpigmentation, be tender, fester, and/or be enlarged or swollen, but not always.
EYES: Conjunctivitis, Bartonella Neuroretinitis, Loss of Vision, Flame Shaped Hemorrhages, Branch Retinal Artery Occlusion with Vision Loss, Cotton Wool Exudates, Parinaud's Oculoglandular Syndrome, and Papilledema.
BONES AND MUSCLES : Osteomyelitis, Myositis, Osteolytic Lesions (softening of bone), Myelitis, Radiculitis, Transverse Myelitis, Arthritis, Chronic Demyelinating Polyneuropathy.
HEART: Endocarditis, Cardiomegaly. Possible lab findings: The following may show up during standard testing: Thrombocytopenia, pancytopenia, anemia, elevated serum alkaline phosphatase level, elevated bilirubin, abnormal liver enzymes. X-ray of the bone may show areas of lysis or poorly-defined areas of cortical destruction with periosteal reaction. Cardiomegaly may show up on a chest X-Ray.
Biopsies of lymph nodes reveal pathology often indistinguishable from sarcoidosis. Reports of biopsies strongly suggestive of lymphoma do occur. Tests occasionally show an enlarged liver with multiple hypodense areas scattered throughout the parenchyma.
TREATMENT: You MUST consult a knowledgeable physician for information on treatment for disseminated Bartonella. Some of the medications which have been used in the past have included Doxycycline (with or without Rifampin), Ciprofloxacin, Erythromycin, Azithromycin, trimethoprim-sulphamethoxazole, gentamicin, and other macrolide antibiotics.
[This message has been edited by Tincup (edited 03 September 2002).]
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Thanks Tincup, Copied it for distribution to support group. Appreciate you keeping us informed. SandiB
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sizzled
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Thanks,TC! Back to the top!
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Tincup
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Adding this newest paper by:
***Audrey Stein Goldings, MD. She is a private practice neurologist in Dallas. She is a member of the Internationl Lyme and Associated Disease Society and a founding member of the Board of Directors.
Controversies in Neuroborreliosis
by 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:
1. Present a practical approach for making the diagnosis of neuroborreliosis,
2. Explore the other side of the post-Lyme syndrome (i.e. the likelihood of chronic ongoing infection),
3. Discuss the relationship between MS and Lyme,
4. Critique the current regimens published for treating neuroborreliosis, and
5. 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:
1. For most patients, systemic features of disease coexist with, or predate, neurologic manifestations.
2. Both central nervous and peripheral nervous system involvement is frequent with Lyme disease and typically occur together.
3. 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.
4. 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.
5. 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)
MENINGISMUS 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.
CHRONIC NEUROBORRELIOSIS
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.
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.
1. 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.
2. 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.
3. 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.
4. 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.
5. 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, is member of Internationl Lyme and Associated Diseases Society and a founding member of the Board of Directors.
------------------ Please don't feed the ducks!
[This message has been edited by Tincup (edited 31 October 2002).]
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This great collection of information would be easier for newcomers to find if it was a separate heading in the main menu bar on the left, "Newcomer Resources" after "Legal Resources" maybe?
Posts: 500 | From Carpinteria, CA near Santa Barbara | Registered: Oct 2001
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Tincup
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Mark,
I think you are right.. so if you want to contact the folks that let us use this site.. please do. I won't. I just feel fortunate enough to have it available for our use.. with some great folks in the background who do SOOOO much already.. I hate to bother them by asking.
Plus I hear some of them bite!
Nah.. they are all wonderful!
If we copy the site here on our records.. we can just copy and paste it as needed...
Tincup
Honored Contributor (10K+ posts)
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If you were diagnosed with Fibromyalgia or Chronic Fatigue..
Please read this article by Dr. Donta...
Lyme Disease as a Model of Chronic Fatigue Syndrome Sam Donta, M.D.;
Boston University Medical Center The CFS Research Review 2002; 3: 2, 1-4
With the discovery of the causative agent of Lyme disease, a new chapter has been opened in the understanding of chronic fatigue syndrome (CFS) and other multi-symptom disorders. Lyme disease, caused by spirochetal bacteria transmitted by the bite of an Ixodes (deer) tick, is now known to be one cause of chronic fatigue disorder that cannot be readily distinguished from CFS, nor from what is termed fibromyalgia. These disorders have similar major symptomatology consisting of fatigue and neurocognitive dysfunction, along with numerous other symptoms that probably relate to altered neurological function. Musculoskeletal symptomatology may be more frequent in fibromyalgia and in some patients with chronic Lyme disease than in CFS, but the definition of CFS also encompasses myalgias and arthralgias as part of the disorder.
Causative agents In Lyme disease, following the bite of an infected deer tick, the Borrelia burgdorferi bacteria may spread locally and cause a variety of skin rashes, the most typical being an expanding circular rash with a clearing area and center resembling a bull's eye. Half of the rashes, however, are not typical, causing diagnostic problems for physicians. Patients who are infected may not develop or see the rash, and may not develop any future symptoms, remaining asymptomatic.
Some asymptomatic patients, however, may reactivate their infection following various stressors such as trauma, surgery, pregnancy, an intercurrent illness, taking an antibiotic for an unrelated reason, severe psychological stress or having received the Lyme vaccine. Similar triggers such as trauma and other stresses are known to precipitate CFS and fibromyalgia. It is likely that there are a number of other causes of CFS and fibromyalgia in addition to chronic Lyme disease.
Epstein-Barr virus (EBV), the major cause of infectious mononucleosis, continues to be debated as a cause of CFS. It is uncertain whether EBV can cause symptoms other than fatigue, such as myalgias and arthralgias that are not seen during acute or reactivated EBV infection in patients who are being immunosuppressed, but it remains possible that EBV could cause one type of chronic fatigue disorder.
Some more recently recognized species of Mycoplasma (Mycoplasma fermentans, Mycoplasma genitalium) have been implicated in chronic fatigue and other multi-system disorders, including CFS itself, fibromyalgia and Gulf War Illness. These same bacteria have also been implicated as causative agents of rheumatoid arthritis, based on PCR-DNA evidence in patients with these disorders in which 50 percent are found to have the DNA of the Mycoplasma in circulating white blood cells, compared to 5-10 percent of a normal population. Whether the presence of this DNA represents past exposure or ongoing infection remains to be resolved. No longitudinal studies have yet been performed in patients with CFS to determine whether the finding of Mycoplasma DNA persists over months or years or whether such patients have any evidence of other infection such as Lyme disease or infection with Chlamydia species.
Gender effects The effects of gender and host on susceptibility and expression of Lyme disease, CFS and other multi-symptom diseases are also in need of further study. In all these disorders, women appear to be more affected than men, usually at about 2:1 ratios. It seems notable that neural cells contain estrogen and progesterone receptors, and that herpes viruses can utilize estrogen receptors to gain access to the reservoir in the cell nucleus. Treatment of chronic Lyme disease also seems to be gender-dependent to some degree, with men generally having more speedy and complete recoveries compared to women. Gender relationships are known for a number of infectious diseases, so it would not be surprising that such a relationship exists for chronic Lyme disease, CFS and other multi-symptom disorders.
Disease targets
In Lyme disease, the nervous system seems to be the primary target for the bacteria causing the disease. Patients with the disease express many neurologic symptoms such as pain, paresthesias including numbness, tingling, crawling and itching sensations, as well as cognitive difficulties and mood changes. Even the joint pains and occasional arthritis(joint pain is much more frequent than actual swelling of joints) appear to be neuropathic in origin, as anti-inflammatory agents such as ibuprofen and other nonsteroidal anti-inflammatory agents have little if any effect on the pain.
Experimental evidence from animal models, primarily dogs and non-human primates, also affirm the localization of B. burgdorferi DNA to the nervous system. The mechanisms underlying the pathophysiology of the disease remain to be defined, but could involve inflammatory responses, autoimmune responses or toxin-associated disruption of neural function. Any inflammatory responses appear to be weak, and there is no compelling evidence that Lyme disease is a result of immunopathologic mechanisms. The target(s) for other causes of CFS remain to be defined. Without any animal models, it becomes more difficult to study its pathogenesis and pathophysiology.
Nontheless, the central nervous system would appear to be a logical target for other pathogens or other pathophysiologic processes. Any changes in immunologic function would not appear to be sufficient to explain the various symptoms, and are likely to be secondary to other pathogenetic processes.
Diagnosis
The diagnosis of Lyme disease is primarily based on clinical grounds. Just as with CFS, the combination of symptoms over months and years, in the absence of an obvious alternative diagnosis, is sufficient to make a presumptive clinical diagnosis. The diagnosis of Lyme disease is made easier if a typical rash is present during the early phase of infection. After that, it is difficult to distinguish the flu-like illness that can occur a few weeks later, or can recur over a number of months. Some patients develop severe headaches and an aseptic meningitis, which frequently is diagnosed instead as "viral" meningitis.
If a Bell's palsy occurs, causing drooping of one side of the face, the possibility of Lyme disease should occur to the physician. If an unprovoked arthritis occurs, causing swelling of a single joint, especially the knee, but sometimes more than one joint, then the possibility of Lyme disease should also be given high consideration. But it is the chronic phase of the disease that causes most of the problems for physicians and patients, because of the lack of "objective" signs and the presence of so many symptoms that it causes some doctors to invoke psychologic reasons for the patients' symptoms.
Many such patients receive a diagnosis of CTFS or fibromyalgia, when they may have underlying Lyme disease as the cause of their symptoms. The laboratory has been helpful is some patients with Lyme disease, especially those with arthritis, in whom there are stronger antibody responses than in those with the chronic, multisymptom form of the disease. The criteria for the laboratory diagnosis has been patterned after the arthritic form of the disease, and not the chronic for; thus, there are many physicians who are misinformed about the test's lack of value in chronic disease.
The Lyme Western Blot is helpful when it shows reactions against specific proteins of B. burgdorferi, but can be negative in 25-30 percent of patients who otherwise have chronic Lyme disease. PCR-DNA tests for Lyme in blood, urine and spinal fluid are rarely positive, most likely because the bacteria and their DNA are not present in those body fluids, but inside nerve cells. The MRI exam of the brain in about 10 percent of patients with chronic Lyme disease can show some white spots in various areas, similar to those seen in multiple sclerosis, a neurologic disease of unknown cause that has some overlapping symptoms with Lyme disease, such as the paresthesias. It is unclear how many patients who have Lyme disease as a cause of CFS have these findings.
The brain SPECT scan, a variation of a PET scan, shows some changes in blood flow to various parts of the brain, primarily the temporal (cognitive processing) and frontal (mood) lobes in about 75 percent of patients with chronic Lyme disease. Patients with CFS have also been reported to have some brain SPECT scan changes, frequently involving the occipital lobe. No comparative studies have been made among patients with chronic Lyme disease, CFS and fibromyalgia.
The mechanisms underlying these changes remain to be defined, but may be due to a mild vasculitis or to a signaling problem within the nerve network of the brain in those specific areas. It is promising, though, that these changes are reversible in most patients treated with antibiotics that appear to be effective in treating the chronic Lyme disease. Treatment Treatment of chronic Lyme disease, CFS, fibromyalgia, and other chronic multi-symptom disorders has been primarily symptom-based. Although some of these treatments (e.g., amitryptiline, other sleep medications, antidepressants, pain medications) can offer some relief, they rarely lead to resolution of the chronic symptoms.
In chronic Lyme disease, there continues to be controversy whether antibiotics can be of value. In our studies, intracellular-type antibiotics such as tetracycline or the combination of one of the erythromycin-type antibiotics (e.g., clarithromycin - Biaxin, azithromycin- Zithromax) and hydroxycholoquine ( a drug which changes the pH inside cells to be less acid, thus allowing the erythromycin-type antibiotics to be effective) given over a number of months (6-18 months, sometimes longer) has resulted in substantial improvement and cures in most patients with chronic Lyme disease.
Similar results have been noted in some patients with CFS of unknown cause, supporting the hypothesis that some patients with CFS have an underlying infection responsive to those antibiotics. Antibiotic trials in CFS have been limited to one month, a duration inadequate to more properly evaluate the potential of certain antibiotics to exert a positive effect on the disease. Additional studies, examining both potential etiologic agents of CFS and treatment trials should lead to a better understanding of both the cause and treatment of patients with CFS.
Selected readings Asch ES et al. "Lyme disease: an infectious and postinfectious syndrome". J Rhjeum, 1994; 21:454061. Brouqui P et al. "Eucaryotic cells protect B. burgdorferi from the action of penicillin and ceftriaxone but not from the action of doxycycline and erythromycin." Antimicrob Agents Chemother, 1996; 40:1552-4 Choppa PC et al. "Multiplex PCR for the detection of Mycoplasma fermentans, M. Hominis, and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome." Mol Cell Probes, 1998; 12:301-8 Donta ST. "Treatment of chronic Lyme disease with macrolide antibiotics." In: Program and abstracts of the VIIIth International Conf. on Lyme Borreliosis, June 20-24, 1999; Munich, Germany. Abstract P193. Donta ST "Reactivation of Lyme disease following OspA vaccine." Int J Antimicrobial Agents, 2001; 17:S116-7. Donta ST. "The existence of chronic Lyme disease." Current Treatment Options in Infectious Diseases, 2001; 3:261-2. Georgilis K et al. "Fibroblasts protect the LD spirochete, B burgdorferi, from ceftriaxone in vitro." J Infect Dis, 1992; 166:440-4 Nicolson GL et al. "Chronic infections as a common etiology for many patients with chronic fatigue syndrome, fibromyalgia, and Gulf War Illness" Intern J Med, 1998; 1:42-6. Roberts ED et al. "Pathogenesis of Lyme neuroborreliosis in the Rhesus monkey " the early disseminated and chronic phases of disease in the peripheral nervous system." J Infect Dis, 1998; 178: 722-32. Shadick NA et al. "The long-term clinical outcomes of Lyme disease." Am Intern Med, 1994; 121:560-7. Straubinger RK. "PCR-based quantification of B burgdorferi organisms in canine tissues over a 500-day post infection period " Clin Microbiology, 2000;38: 2191-9. ___________________________________________________________- The CFS Research Review is published quarterly by The CFIDS Association of America, PO Box 220398, Charlotte, NC 28222; Phone: (704) 365-2343 www.cfids.org
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Thank You Tincup, you are wonderful as always... I really enjoyed reading these posts especially the ones about FMS and CFS from Dr. D. as I've been dx with these for years now. I am so glad they are starting to look closer at these conditions and how they may have a connection to lyme. Just reading this feels like my prayers have been answered...as the drs. have been blaming all my symptoms on FMS and CFS for 8 years now...even after having two bulls eye rashes 5 years ago... Thanks again for all your hard work on keeping us up to date...Love, Swiss
Posts: 482 | From NH | Registered: Aug 2001
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thank you very much, very interesting and informative stuff, i will read it all. you are all so helpful and caring to helping others
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Back to the top. Want it to be easy for the new Lyme Net members to find.
Posts: 4638 | From South Carolina | Registered: Mar 2001
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Posts: 172 | From North Fork, LI, NY | Registered: Apr 2002
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henson2
Frequent Contributor (1K+ posts)
Member # 463
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To the top for Annafc.
See the link about different strains of Borrelia to find the ones that are especially found in Sweden. Then you can locate articles and studies by that scientist's name (who discovered it/wrote about it) for more clues to treatment.
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To the top... again! Tincup, if you are checking this, maybe it would be a good idea to just repost as this is getting awfully long with all the "to the top" messages!
Posts: 441 | From USA | Registered: Sep 2001
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You guys are truly amazing! My dining room table is now plastered with PostIts, listing all the resources that I want to read in detail and then hand to my doctors (eSPECially the ID-DUCK who told me that if I just slowed down and stopped working so hard, I'd be fine!@#%^!@%$^!)! ZOWEE!!! Tincup, special thanks for those articles from Dr. Donta. Do you happen to know if he accepts new patients? TO THE TOP! LG
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