The term Lyme borreliosis, has been used in medical literature since the scientific director of our research proposed it in 1985 (1). Since then, it has become known as a unique clinical entity in many respects.

Its pathology is chronic from the beginning and the whole host organism is attacked. It may have recurring symptoms for several decades after the bite of even one infected tick.

The pathological processes provoked by the causative agent Borrelia burgdorferi sensu lato result in a clinical picture progressing in a fluctuating way impacting the whole organism, and the patient may even temporarily appear as asymptomatic. Lyme borreliosis seems to entail an unusually numerous and extensive combination of disorders and syndromes (2).

The more than one hundred members of the B. burgdorferi sensu lato species potentially causing Lyme disease are classified in three genospecies groups with differing sensitivity to antibiotics and causing different clinical manifestations. More than one genospecies may be present in a single patient, and the contribution of each genospecies to the development of the clinical illness may even vary in time (3).

In Europe, the B. afzelii group, which is responsible for the development of the iconic Arthroborreliosis lymei, occurs most frequently (5) (6).

In the case of the B. garinii group the typical spreading redness of the skin, ECM (Erythema Chronicum Migrans), is usually missing, but the neurological symptoms develop early.

The B.b. sensu stricto group is relatively rare in Europe, ECM and arthritis, the iconic symptoms caused by this group, have been known since the first description of the infection.

In addition to the strains causing Lyme borreliosis, further Borrelia groups have been identified but these pathogens rarely occur in Europe. The clinical condition caused by the B. miyamotoi group is also often coupled with the characteristic dermatitis. The genetic separation from the pathogens of the Borrelia burgdorferi sensu lato group has been known since 2011 (4) (7). The borreliosis caused by B. miyamotoi is even regarded as a separate disease entity based on the symptoms caused (8). Its genetics are close to the B. recurrentis group, which causes recurring fever (febris recurrens).

The underlying cause of the diseases with recurring character, caused by the Borrelias may be their different life cycle in the human organism. It may be caused by the interaction between the slower reproduction period of the causative agent and the human organism. As opposed to the three weeks’ generation cycle of the Borrelia burgdorferi sensu lato, the B. miyamotoi group causes mild fever and clinical deterioration every other week, whereas the B. recurrentis causes fever roughly every week (9). The Borrelias, which have changing pathogenity, shape the pathology depending on the season and the patient’s actual physical and mental state. This is how the generally characterisable pathology manifests itself in a completely individual manner.

There is also a special phenomenon, which may affect the yield of the serology used for the diagnosis, a process that is assumed to be related to the life cycle of the Borrelias: the fluctuation of the levels of antibodies. It is worth considering that there is no predictable IgM-IgG transition of the immune response (10) (11), what is more, both the IgM and IgG antibodies may fluctuate over time (12).

When the treatment is effective, the symptoms may worsen for some days due to the disintegration of pathogens and even the serological response may become more pronounced. The Jarisch-Herxheimer reaction is a special case, it may also develop during the treatment of Lyme borreliosis, coupled with mild clinical symptoms, due to the endotoxins of different structures, and the relatively low cell counts; at the same time it also provides feedback on the length of the life cycle (13).

 

References

  1. Aspects of Lyme Borreliosis. Schierz, K. Weber· W. Burgdorfer (Eds.) . Coeditor: G. Berlin Heidelberg: Springer-Verlag, 1993.
  2. Lyme disease: point/counterpoint. Stricker RB, Lautin A, Burrascano JJ. 2005., Expert Rev Anti Infect Ther.
  3. Clinical spectrum of Lyme disease. Cardenas-de la Garza JA, De la Cruz-Valadez E, Ocampo-Candiani J, Welsh O. 2018., Eur J Clin Microbiol Infect Dis.
  4. Borrelia miyamotoi: a recently identified human pathogenic tick-borne relapsing fever spirochete. Szekeres S, Lakos A, Földvári G. 2017., Orv Hetil.
  5. Road-killed mammals provide insight into tick-borne bacterial pathogen communities within urban habitats. Szekeres S, Docters van Leeuwen A, Tóth E, Majoros G, Sprong H, Földvári G. 2018., Transbound Emerg Dis.
  6. Assessment of the frequency of different Borrelia burgdorferi sensu lato species in patients with Lyme borreliosis from north-east Poland by studying preferential serologic response and DNA isolates. Grygorczuk S, Péter O, Kondrusik M, Moniuszko A, Zajkowska J, Dunaj J, Żukiewicz-Sobczak W, Pancewicz S. 2013., Ann Agric Environ Med.
  7. Genetic features of Borrelia miyamotoi transmitted by Ixodes persulcatus. Fomenko NV, Borgoiakov VIu, Panov VV. 2011., Mol Gen Mikrobiol Virusol.
  8. Clinical presentation of “new” tick-borne borreliosis caused by Borrelia miyamotoi. Sarksyan DS, Platonov AE, Karan LS, Malinin IE, Khalitova LI, Shakhov VI, Dudarev MV, Malinin OV, Maleev VV. 2012., Ter Arkh.
  9. Humans infected with relapsing fever spirochete Borrelia miyamotoi, Russia. Platonov AE, Karan LS, Kolyasnikova NM, Makhneva NA, Toporkova MG, Maleev VV, Fish D, Krause PJ. 2011., Emerg Infect Dis.
  10. Early detection and persistence of antibodies to Borrelia burgdorferi in persons with Lyme disease. Magnarelli LA, Anderson JF. 1987., Zentralbl Bakteriol Mikrobiol Hyg A., pp.: 263(3):392-9.
  11. Detection of serum antibodies against Borrelia burgdorferi with some commercially available serological tests. Melby K, Steinbakk M, Jensenius M, Figenschau KJ. 1990 Dec., NIPH Ann., pp.: 13(2):37-44.
  12. Course of Antibody Response In Lyme Borreliosis Patients Before And After Therapy. Aberer E, Schwantzer G. 2012., ISRN Immunology.
  13. The Jarisch-Herxheimer Reaction After Antibiotic Treatment of Spirochetal Infections: A Review of Recent Cases and Our Understanding of Pathogenesis. T, Butler. 2017., Am J Trop Med Hyg.