Recent research suggests that a Lyme disease treatment symptom, the Jarisch-Herxheimer reaction, reported by some Lyme disease patients is not due to specific toxins released by the spirochaetes as they are under attack, despite the similarity of Borrelia bacteria to syphilis spirochaetes. The spirochaete’s genomic features and its unique molecular structure play key roles in the transmission of infection from ticks to humans but also constitute major factors in the triggering of immune responses in the body and, therefore, inflammatory manifestations of Lyme disease. Thinking in recent years has considered these inflammatory reactions to be caused by the production of toxigenic molecules by Borrelia bacteria.
However, Borrelia do not produce toxigenic molecules according to Samuels and Radolf (2010), two renowned molecular biologists who have written comprehensively on Borrelia bacteria. As such, the infiltration of spirochaetes into the dermis during the early stages of infection create the local inflammatory response in some (but not all) patients recognized as erythema migrans, and it is this creation of more systemic inflammation that results from disseminating bacterial infection with Borrelia burgdorferi sensu lato.
Inflammation and ‘Herxing’ from Lyme Disease Treatment
The ‘flu-like’ symptoms also reported in early Lyme disease infection, along with arthralgias, and fever, are also thought due to the cytokine-mediated response to the bacteria as they spread through the system. Inflammatory manifestations of Lyme disease may go on to involve the joints, the heart, and the central nervous system, which is why the symptoms of Lyme disease are so varied. The ‘herxing’ reaction then may be due instead to the actual die-off induced by the immune system, rather than a reaction to a particular toxin or toxins produced by the bacteria. Borrelia have no endotoxin-like lipopolysaccharide which Samuels and Radoff believe is required to induce a Jarisch-Herxheimer reaction due to it being caused by the action of lipoproteins on toll-like receptors (TLR2) in macrophages (immune system cells) and other cells of the body.
This may all sound like theoretical gibberish but it could actually have concrete ramifications for patients being treated for Lyme disease. In understanding the cause of the reaction some patients experience to antibiotic treatment researchers may be able to reduce the incidence of the reaction and make treatment for Lyme disease more comfortable. Patients given antibodies to Tumor-Necrosis Factor alpha prior to penicillin treatment for Borrelia recurrentis have been found to experience less severe herxing than those without the infusion of TNFa-antibodies (Fekade, et al, 1996). Borrelia burgdorferi are also thought to induce the synthesis of TNFa, making it a possible target for reducing Lyme disease treatment symptoms.
Samuels, D.S., Radolf, J.D., (2010). Borrelia: Molecular Biology, Host Interaction & Path. Caister Academic Press
Fekade, D., Knox, K., Hussein, K., Melka, A., Lalloo, D.G., Coxon, R.E., Warrell, D.A., (1996). Prevention of Jarisch–Herxheimer Reactions by Treatment with Antibodies against Tumor Necrosis Factor α, N Engl J Med, 335, pp.311-315.