There are a number of Lyme Literate Medical Doctors (LLMDs) who maintain that the bacteria responsible for Lyme disease are capable of ‘hiding’ from the immune system, thus evading tests for Lyme disease and treatments for Lyme disease. Immune system evasion is largely dismissed as a potential mechanism of persistent infection with Lyme disease bacteria but some recent research does show that this can occur. Whether this is widespread remains to be seen, although it appears that those railing against the established ‘facts’ of Lyme disease may be at least a little vindicated by such evidence.
How Lyme Bacteria Cheat Death
Kraiczy (et al, 2001) found that Borrelial bacteria, specifically B. afzelii rather than B. garinii, had the capacity to control complement activation on their surface and to prevent formation of toxic activation products through complement regulators acquiring surface proteins (CRASP). Thus, the B. afzelii strain of Borrelia could evade the immune system and avoid induced apoptosis or phagocytosis (i.e. cell death).
Long-Term Antibiotics for Lyme Disease
One observational study (Donta, 1997) observed positive benefits from long-term antibiotic treatment in those patients who have a long history of symptoms or previous, unsuccessful antibiotic treatment for Lyme disease, although several others have found little benefit compared to placebo in such cases (Klempner, et al, 2001, Wormser, et al, 2003). There is speculation in some circles that the bacterial spirochaetes reside in tissues and cells where the antibiotic treatment has difficulty reaching and, thus, these spirochaetes are only accessible as the normal process of cell turnover occurs and the bacteria are released into general circulation. For red blood cells this process usually takes around 120 days (Smith, 1995) which gives rise to speculation that four months of antibiotic treatment is necessary to fully eradicate bacteria from the body, rather than the ten days cited as being sufficient by a 2012 study.However, although Babesia, a bacteria often existing as a Lyme co-infection, is known to take up residence in red blood cells, Lyme disease bacteria have not been found to do this. Babesiosis actually damages red blood cells leading to a form of haemolytic anaemia if untreated, whereas Borrelia bacteria have not, so far, been found to have a similar effect. Confusion may arise here as different Borrelia bacterial strains, responsible for relapsing fever, do have an effect on erythrocytes (red blood cells) leading to aggregation (rosetting) of the red blood cells (Guo, et al, 2009). It is possible that antigenic variation of the Lyme borreliosis bacteria could lead to similar effects but this remains largely hypothetical.
Kraiczy P, Skerka C, Kirschfink M, Brade V, Zipfel PF. Immune evasion of Borrelia burgdorferi by acquisition of human complement regulators FHL-1/reconectin and Factor H. Eur J Immunol. 2001 Jun;31(6):1674-84.
Donta ST. Tetracycline therapy for chronic Lyme disease. Clin Infect Dis. 1997 Jul;25 Suppl 1:S52-6.
Smith JA. Exercise, training and red blood cell turnover. Sports Med. 1995 Jan;19(1):9-31.
Shapiro ED, Dattwyler R, Nadelman RB, Wormser GP. Response to meta-analysis. Int J Epidemiol 2005; 2005;34:1437
Klempner MS, Hu LT, Evans J, Schmid CH, Johnson GM, Trevino RP, Norton D, Levy L, Wall D, McCall J, Kosinski M, Weinstein A. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N Engl J Med. 2001 Jul 12;345(2):85-92.
Guo BP, Teneberg S, Münch R, Terunuma D, Hatano K, Matsuoka K, Angström J, Borén T, Bergström S. Relapsing fever Borrelia binds to neolacto glycans and mediates rosetting of human erythrocytes. Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19280-5. Epub 2009 Nov 2.
Wormser GP, Ramanathan R, Nowakowski J, McKenna D, Holmgren D, Visintainer P, Dornbush R, Singh B, Nadelman RB. Duration of antibiotic therapy for early Lyme disease. A randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2003 May 6;138(9):697-704.