Hyperthermia, or raising the body temperature to help the immune system fight infections, is a therapy that can be used to combat Borrelia burgdorferi, the bacterium that causes Lyme disease.
There are two main reasons why hyperthermia works well for Lyme disease. The obvious reason is that whole-body fever is beneficial for killing bacteria—in this case, Borrelia and co-infections (especially those that are bacterial). It is a known fact that Borrelia bacteria die at 39°C, so for maximum results, the core body temperature should ideally reach this heat or higher. At the St. Georg Klinik in Germany, they use extreme hyperthermia. The patient is only exposed to this higher heat for about 10-20 minutes at most, so it is important to exceed 39°C so that the body is hot enough to kill Borrelia, its co-infections, and release the cysts. As Borrelia and other microorganisms flee from heat, antibiotics in the bloodstream help to destroy the microbes.
The second reason is thattotal body hyperthermia overloads antibiotics. The day before undergoing hyperthermia, it is advisable to perform a colon irrigation. Colon hydrotherapy on the morning of hyperthermia ensures that there is little food or waste in your digestive tract. Hyperthermia combined with a drip of antibiotics at the same time will cause the body to seek glucose to feed the cells and brain as the body temperature rises, and all it will find are antibiotics, thus drawing the antibiotics into cells, tissues, and barriers that antibiotics are not usually able to penetrate.
There is a 1996 study entitled Antibiotics and increased temperature against Borrelia burgdorferi in vitro, by a team of Austrian researchers, which was based on the fact that "The persistence of late Lyme disease despite antibiotic treatment has stimulated the search for other therapeutic means. Treponema pallidum, another spirochete, causes syphilis, which has a similar spectrum of manifestations, including skin lesions and chronic involvement of multiple organs. In the pre-penicillin era, benign tertian malaria alone and in combination with Salvarsan or bismuth was reported to cure neurosyphilis. Malaria therapy for Lyme disease has recently been discussed in this context. The mode of action of malaria therapy has not been elucidated to date; however, it has been attributed to immunological mechanisms. The rapid improvement of clinical symptoms with ceftriaxone in two of our patients with febrile neuroborreliosis led to the initiation of the present study. Here we show the effect of increased temperature and antibiotics on Borrelia burgdorferi in vitro.
This experiment demonstrated that increased temperature affects the growth, morphology, motility, metabolism, and virulence of various bacteria and Treponema species. The growth of spirochetes in Lyme disease is delayed at 39°C and does not occur at 40°C and above.
These data could suggest that different strains of Borrelia may affect different parts of the body depending on their temperature.
Therefore, heat-resistant strains would preferentially affect warm regions of the body (e.g., neuroborreliosis), while heat-sensitive strains would show tropism for regions of the body with lower temperatures (e.g., the skin).
The reduction in growth of certain strains of Borrelia burgdorferi when the temperature is increased in vitro suggests that raising body temperature may be beneficial during antimicrobial treatment of Lyme borreliosis. This could be particularly important for infections in tissues and compartments where high concentrations of antibiotics are difficult to achieve. Clinically, a variety of exogenous or endogenous pyrogens other than benign tertian malaria could be used to induce artificial fever. Therefore, controlled clinical trials appear warranted to establish the efficacy of fever alone or as a complementary measure during antibiotic treatment of late Lyme disease refractory to antibiotic treatment.
