Lyme disease, named after the famed 1975 outbreaks in Lyme, Connecticut, is often known as the “great imitator” for its frequent mimicry of many other conditions. Estimated to be under-reported by a factor of 6 to 10 in the USA alone, Lyme has often lived in the shadow of other more publicized epidemics and public health issues, such as HIV and SARS, even though in recent years, it has likely outnumbered them both (1). Further complicated by the often problematic and inconsistent diagnostic criteria and testing methods put forth by organizations such as the CDC, this has led to a grave and unfortunate situation for many struggling to receive appropriate diagnoses and treatment. Known as Borreliosis in Europe, Lyme disease appears to have existed for at least hundreds of years, if not more. Extant DNA samples from an infected tick in Germany trace back to 1884 and a preserved Cape Cod mouse from 1894 both illustrate its known existence prior to the twentieth century, when it gained notoriety. Even earlier reports suggest Lyme disease’s presence in the 1700s. Early twentieth century medical journal reports from Sweden and Germany detail reports of erythema migrans, various neurological conditions, and joint conditions being linked to tick bites in Northern and Central European locales. That Lyme may have been later harnessed for potential biological warfare usage is also documented, first by Nazi scientists working at the notorious Insel Riems facility in WWII and later, by scientists working at the American animal disease research facility on Plum Island, off the East coast of Long Island, New York (2,3). Reckless mismanagement and issues of disrepair of the Plum Island facility may have contributed to the concentration and acceleration of the epidemic especially in the Northeastern US corridor, beginning in the mid 1970s.

The current reality is that Lyme disease is now a global problem. Many countries across temperate parts of the globe have reported or are suspecting the presence of Lyme in ticks. Since 1995, the CDC has reported consistently increasing numbers of confirmed and probable cases of Lyme disease, suggesting this disease continues to spread. In endemic areas of the world, percentages of ticks infected with borrelia and other tick-born infections are shockingly high. For instance, German and Russian studies have confirmed a Borrelia presence from respective regions of those countries in 50-60% of tick samples in some instances. 2001 estimates in Germany place yearly Lyme contractions in the range of 50,000-100,000, a comparable percentage to incidence estimates in the USA, given differences in national populations (4). While various theories have been proposed where Lyme disease may have begun, a 2008 Yale University study confirmed a European origin for extant North American and European lyme strains. Using a computer generated DNA evolutionary “tree” and multi-locus sequence typing (MLST), researchers found that European strains are more closely related than North American species. This suggests that evolutionary drift later on contributed to the variant North American strains, perhaps spurred by the waves of European immigrants in the 18th, 19th, and 20th centuries and accompanying vermin carriers. Given that some species of mosquitoes, mites, and biting flies are also capable of spreading Borrelia, Lyme has had many opportunities for dissemination and recombination as waves of international immigration the last several hundred years has dramatically changed the face of the Western Hemisphere.

Following, the known number of genotypic variations of Borrelia continues to grow. A 2010 study examining US and German tick samples found at least 53 distinct different genotypic differences in selected tick strains, adding to the already extant 37 known species. Transmitted by Ixodes ticks: I. scapularis and I. pacificus in North America and I. ricinus in Europe, researchers also suggested the greater the number of genotypes present in an infection, the greater the potential for clinical manifestation(s) of Lyme. This widespread genotypic diversity may also complicate and at least partly explain why Lyme disease can show considerable resistance to antibiotic regimens. Perhaps the greatest problem with Lyme disease in a modern context is the lack of sensitive and accurate diagnostic testing. Serious problems with the lack of sensitivity and accuracy with ELISA testing is known , yet this methodology remains the most common means for diagnosis by labs and health care providers.

Thus due to the plethora of possible strains, co-infections (such as Babesia, Bartonella, Ehrlichiosis, and Mycoplasma), and species of Lyme in ticks, clinicians may be best advised to consider a combination of tests, astute clinical observation and meticulous patient history when making a diagnosis to minimize false negative test results. Overly relying on the narrow and highly specific CDC criteria to diagnose Lyme may unfortunately misguide many, thus contributing to more missed diagnoses and undue patient suffering. Multiple criterion already exist to support a more liberal interpretation of a positive Western Blot analysis for Lyme, for example, well beyond the rigid CDC guidelines requiring 5 of 10 bands positive. Many borderline or equivocal results will not be considered as positive according to said CDC criteria, a highly problematic detail considering that by some estimates, less than 70% of Lyme patients have an immune response strong enough to generate a Western Blot response. Furthermore, examining immunological markers, natural killer cell activity, inflammation, and cytokine activity may be especially helpful in such instances to further discern important individual differences in possible presenting cases. Again, because of the considerable and frequent immune impairments and variant immune responses of patients, these additional kinds of testing may help clinicians recognize less obvious or questionable cases of Lyme. These assessments could include the CD57 count, the C6 peptide analysis, C3a and C4a inflammatory markers, and the lymphocyte transformation test (used in Germany), in addition to the more utilized Western Blot and PCR assays for Lyme (5). These tests and others may also be of help when other co-infections may be present, to elucidate greater detail about complicated or ambiguous patient presentations.

Known for its stealthy and immuno-evasive behaviors, two of Borrelia’s greatest dangers include its adaptability and ‘cloaking’ prowess. Able to change its appearance due to environmental triggers such as antibiotics, changes in immune surveillance, and more, Borrelia tends to sequester in tissues which are poorly perfused, such as connective tissues. This is due to Borrelia’s affinity to collagen fibers, which also makes it more difficult to treat due to the typical poor oxygenation and blood supply of such tissues. It is able to invade a wide variety of cells and remain intracellularly also, in host cells such as macrophages, synovial cells, endothelial cells, fibroblasts and possibly CNS cells. Parts of the Bb cell wall also protect it from being detected by the host immune system by manipulating the complement systems. This may be further complicated by the noted antigen-drift and antigen-shift in recent decades. Borrelia’s slow growth cycle also makes it easy to miss in early Lyme testings and also prone to surviving short course cycles of antibiotics, as it can convert to bio-stagnant antibiotic resistant cystic (‘L-forms’) forms and then convert back again, once internal conditions are more favorable (6).

Furthermore, due to problems with Lyme and co-infection testing, many individuals who have been diagnosed with ‘mimicked’ types of illnesses such as MS, Alzheimer’s, and Parkinson’s may in fact be dealing with an advanced case of Lyme disease. While estimates vary widely and are difficult to propose re: the likelihood of misdiagnoses, correlations between Lyme and some of these conditions, such as MS, abound. MS occurs mostly in temperate climates in the same latitudes where the Ixodes ticks that carry Lyme disease thrive. MS also seems to be clustered in areas where Lyme is frequent (such as the NE USA) and MS often manifests in young-middle aged adults most active and exposed to tick infested areas. Evidence also suggests that in some Alzheimer’s cases, undiagnosed chronic Lyme is actually, at least in part, to blame. Physicians as early as the 1940s had started to suspect (and find evidence to support) bacterial infections as a causative agent in some Alzheimer’s cases. This suspicion (and evidence) has continued to mount in the 1980s, 90s, and more recently as more and more studies published showed presence of spirochetal bacteria in neurofibrillary tangles, nerve cells, and plaques in selected Alzheimer’s patients. Evidence and connections between Lyme and other diseases such as ALS are also mounting.

In summary, Lyme is likely a much greater and complex problem than has been lead to be believed by many. Inadequate physician education, testing debates and problems and subsequent massive underreporting are contributing to an epidemic that no one really knows the true size of. For medical professionals practicing in areas that are known as Lyme “endemic areas,” many cases classified as fibromyalgia, MS, Parkinson’s, Alzheimer’s and other “mimicked” illnesses may need reconsideration, due to potential misdiagnoses. Educating the general population on vectors of transmission, early potential signs of Lyme, and avoiding exposure may help to curb but will not eradicate this problem. Subsequently, reevaluations of extant Lyme literature by medical bodies, the CDC, insurance companies and curriculum directors of medical schools may all be highly warranted if we, as a society, can ever hope to get a true handle on controlling and treating this multi-faceted epidemic.

An Exclusive Article for Members
From THE BRIDGE Newsletter of OIRF
Published October 2011

© Copyright 2011, Dr. Karim Dhanani, ON Canada

About the author

Footnotes

  1. In 2009, confirmed and probable cases of Lyme reported by the CDC numbered 35,198 yet estimates by the CDC place recently yearly new infections at a staggering 325,000 in the USA alone. This would make Lyme larger than AIDS, West Nile, and Avian flu combined.
  2. This location, it should be noted is ten miles south of Lyme, Connecticut, across the Long Island Sound.
  3. Riems Island still is home to the world’s oldest virological research institution, the Friedrich Loffler Institute, built in 1910.
  4. The 2010 population count of the USA was approximately 308 million while Germany’s population was approximately 82 million (26.6% of the US population).
  5. For reference, some of the more specific IgG and IgM antibodies include: 23-25 kDa (Osp C); 31 kDa Osp A); 34 kDa (Osp B); 39 kDa; 41 kDa (common flagella-bearing organisms); and 83-93 kDa.
  6. Bb typically needs 8-35 hours for one generation of growth and up to 10 weeks for culturing, for instance. Comparatively speaking, the common E Coli bacterium typically takes only 20 minutes for one generation of growth!

Bibliography

  1. Afzelius A. “Verhandlungen der Dermatologischen Gesellshaft zu Stockholm” (in German). Archives of Dermatology and Syphilis. 101 (1910): 100–102.
  2. Brorson O. “Susceptibility of Motile and Cystic Forms of Bb to Rantidine Bismuth Citrate.” Microbiol 4(4) (Dec 2001): 209-15.
  3. Brade, Kraiczy. “Immunoevasion of Bb: Insufficient Killing of the Pathogens by Complement and Antibody.” J Med. Microbiol 291: Suppl. 33 (2002): 141-46.
  4. “Transformation of Cystic Forms of Bb to Normal, Mobile Spirochetes.” Infection 25(4) (1997): 240-6.
  5. Burckhardt JL “Zur Frage der Follikel- und Keimzentrenbildung in der Haut” (in German). Frankfurter Zeitschrift fur Pathologie 6 (1911): 352–359.
  6. Caroll, Michael. Lab 257: The Disturbing Story of the Government’s Secret Germ Laboratory. New York, 2005.
  7. Crowder CD, Matthews HE, Schutzer S, Rounds MA, Luft BJ, et al. “Genotypic Variation and Mixtures of Lyme Borrelia in Ixodes Ticks from North America and Europe.” (2010) PLoS ONE 5(5): e10650. doi:10.1371/journal.pone.0010650
  8. Drymon, M.M. “Disguised as the Devil: How Lyme disease Created Witches and Changed History.” Wythe Avenue Press: 2008.
  9. Franz JK et al. “Insights From a Novel Three-Dimensional In Vitro Model of Lyme Arthritis: Standardized Analysis of Cellular and Molecular Interactions Between Borrelia Burgdorferi and Synovial Explants and Fibroblasts.” Arthritis Rheum 44(1) (2001): 151-62.
  10. Geißler, Ernhard. Hitler und die Biowaffen. Munster, Germany, 1998.
  11. Grunar, Cinco. “Conversion of B. Garinii Cystic Forms to Motile Spirochetes in Vivo.” APMIS. 109(5) (2001): 383-8.
  12. Guo et al. Molecular Microbiol 30 (1998):711-723; Infect Immun. 63 (1996):3467-3472.
  13. Hall HI, Song R, Rhodes P, et al. “Estimation of HIV incidence in the United States.” JAMA 300(5) (2008):520-529.
  14. Haupl, Burmester et al. “Persistence of Bb in Ligamentous Tissue From a Patient With Chronic LB.” Arthritis Rheum. 36(11) (1993): 1621-6.
  15. Hellerström S. “Erythema chronicum migrans Afzelii” (in German). Archiv Dermatologie and Venereologie 11 (1930): 315–321.
  16. Kosik-Bogacka D, Bukowska K, Kizna-Grygiel W. “Detection of Borrelia burgdorferi sensu lato in mosquitoes in recreational areas of the city of Szczecin.” Ann Agric Environ Med 9(1) (2002): 55-7.
  17. Luger, SW. “Lyme disease transmitted by a Biting Fly.” New Eng J Med 332(24) (1990): 1752.
  18. Ma B et al. “Serodiagnosis of Lyme Borreliosis by Western Immunoblot: Reactivity of Various Significant Antibodies Against Borrelia Burgdorferi.” J Clin Microbiology 30 (1992): 370-76.
  19. Ma Y, A Sturrock, JJ Weis. “Intracellular Localization of Borrelia burgdorferi Within Human Endothelial Cells. Infection and Immunity.” Infection and Immunity 59 (1991): 671-678.
  20. Magnarelli, J. “Ticks and Biting Insects With the Etiologic Agent of Lyme Disease, Borrelia burgdorferi.”
  21. Clin Microbiol (Aug 1988): 1482-1486.
  22. Magnarelli, J. “The Etiologic Agent of LD in Deer Flies, Horse Flies and Mosquitoes.” Infect Disease 54 (2) (1986): 355.
  23. “Persistenz in Maus-Makrophagen.” J Immunol 150(3) (Feb 1993): 909-15.
  24. Paralogs E., Alitalo et al. “Complement Inhibitor Factor H Binding to Lyme Disease Spirochetes if Mediated by Inducible Expression of Multiple Plasmid-Encoded Outer Surface Protein.” Journal of Immunology 169(2002): 3847-3853.
  25. Preac-Mursic et al. “Kill Kinetics of Bb and Bacterial Findings in Relation to the Treatment of LB.” Infection 24 (1) (Jan-Feb 1996): 9-16.
  26. Rosner, Bryan. Lyme Disease: 2008 Annual Report. Biomed Publishing Group: 2008
  27. Samuels DS; Radolf, JD. Borrelia: Molecular Biology, Host Interaction and Pathogenesis. Caister Academic Press: 2010.
  28. Singleton, Kenneth. The Lyme Disease Solution. Brown Publishing: 2008.
  29. Strasheim, Connie. Insights into Lyme Disease Treatment. Biomed Publishing Group: 2009.
  30. Stuttgarter Zeitung (22) (February 2001):7.
  31. Summerton, N. “Lyme Disease in the Eighteenth Century.” British Medical Journal 311 (7018) (1995): 1478
  32. Wilske et al. “Impact of Strain Heterogeneity on Lyme Disease Serology in Europe: Comparison of Enzyme-Linked Immosorbent Assays Using Different Species of Borrelia Burgodorferi Sensu Lato.” JCM (Febr 1998): 427-436.
  33. Wilske, Fingerle et al on CD: “Lyme-Borreliose” version 1.0 Hoffman-La Roche AG; Nov 2001.

E-Bibliography

  1. http://www.publichealthalert.org/Articles/MMDrymon/Multiple%20Sclerosis.htm
  2. http://www.canlyme.com/tom_grier_ms_lyme_1996_talk.html
  3. http://emedicine.medscape.com/article/300455-overview#aw2aab6b2b3aa
  4. http://www.nejm.org/doi/full/10.1056/NEJM199805283382216
  5. http://www.cdc.gov/lyme/stats/chartstables/casesbyyear.html
  6. http://www.igenex.com
  7. http:// dieterhassler.de/diagnostik_und_therapie.html
  8. http://opac.yale.edu/news/article.aspx?id=5893
  9. http://www.meb.uni-bonn.de/parasitologie/wissensch.htm
  10. http://www.psychologytoday.com/blog/emerging-diseases/200812/shadowland-the-mind-neurological-lyme-disease-part-one

Lecture References

  1. Burmester, G-R. Lecture: “Institut fur Laboratoriumsmedizin.” Berlin: March 13th, 2002.
    http://www.molecularalzheimer.org/files/Internet_version_of_Ilads_Alzheimer_Borrelia_Lecture_Oct_2005.pdf

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