Wang IN, Dykhuizen DE, Qiu W, Dunn JJ, Bosler EM, Luft BJ. Department of Ecology and Evolution, State University of New York, Stony Brook, New York 11794-5245, USA. Dr. Reisinger, et. al., reported in 1995 (JSTBD V2(4)p101) and in 1996 (ScanJ Infect Dis;28(2):155-157).
Using 3 different strains, the authors found that all strains were inhibited in growth up to 40 degrees C and killed at 42 degrees C. In addition the susceptibility of borrelia to bacteriocidal agents (penicillin and ceftriaxone were studied) increased logarithmically as temperature increased. For example, the potency of these antibiotics increased 16 fold by elevating from 36 degrees to 38 degrees C. (for most of us these numbers convert to 96.8 degrees F and 100.4 degrees F). To get this effect, in the laboratory, the longer the exposure to heat, the more injury to borrelia. Two strains were vulnerable at lower temperatures. What does this mean for the victim of borreliosis? Many have noted that their bodies are often at a lower temperature than others. Are borrelia taking advantage of victims by lowering the host temperature and thus replicating better? Can we help our bodies in ridding us of this plague by thermal means? It is difficult to find any clinical studies utilizing heat treatment of Lyme disease except for the heat induced by infecting victims with malaria (Heimlich, NEJM 1990;322:1234-1235). This is reported to cause remission but not cure. It also is not accepted in the USA to infect victims with malaria. Can the same benefit be achieved by external heat without the risk of malaria? It is found that immersion in hot tubs at 104 degrees F raises the core temperature (oral) by 1 degree for every 10 min immersion. Thus for the 36 degree C victim, 20 min immersion will result in the 38 degree C core temperature. After some time, a number of victims may tolerate up to 40 min of immersion which matches a 40 degree C or 104 degree F core temperature. Thus for about 30 min the deep tissue niches of borrelia such as brain stem, ligaments, and joints are assisted in fighting borrelia with increased temperatures. For this time and some time afterward as the body returns to its baseline temperature, the borrelia are exposed theoretically to 16 to 160 times as much antibiotic. Perhaps the slime coating around borrelia and the wall are rendered more porous and the antibiotics can penetrate inside the borrelia. Perhaps the borrelia cannot modulate antigenicity well to rapid temperature changes at these levels. Perhaps the flagella are not functioning at this temperature and borrelia can be "caught" by monocytes and ingested. Whatever the mechanism of heat treatment, victims of borrelia usually report the following. At first the heat is difficult to tolerate. Victims must start and advance slowly with others assisting in and out of the tub. Often pain and tingling are even worse in the tub. Many have "herxheimer" like reactions afterwards and these are reported to be marked. However as time goes by, most who can continue the heat treatments, find that the symptoms while in the tub decrease and disappear and that the herxheimer after-effect decreases. It is wise to drink liquids while in the tub and afterwards. Some try rapid cooling of the skin after 10 minutes of immersion with ice or hosing and then repeat the heat immersion. A longer immersion time can thus be endured and redirection of warmed skin blood to the core repeated. This is like exercising without a work load. Some have endured external temperature of the water at 110 degrees F to more hopefully eradicate skin borrelia but this seems extreme for most. Would breathing oxygen supplementation with a face mask also improve inhibition or killing of borrelia? Oxygen makes logical sense since borrelia are anaerobic but lab testing of this hypothesis appears impossible. Finally, it may be correct to take a bactericidal antibiotic as part of a combination protocol if heat treatment is used. Tyndallization is a past microbiological term for inducing microbes which are hidden in spores and cysts to exit their protected encysted stage. Borrelia are known to exist in encysted stages (Brorson- Transformation of cystic forms of Borrelia b to normal mobile spirochetes, Infection 1997;25:240-246.) These motile forms might best be attacked by a bactericidal agent at this time. At cooler times, a bacteriostatic agent, might be appropriate to have "on board." Inducing the borrelia to exit encysted forms in the skin and other niches might at first make the victim sicker, but the goal is to get in control of this microbe and after 3- 6 months reduce its presence and harmful influence on the host -- us. So far, antibiotic treatment alone, particularly in the shorter courses offered, has resulted in 50% of victims suffering from a persistent infection both in early localized borreliosis and later disseminated intracellular borreliosis (Steere A., Treatment of the Early Manifestations of Lyme Disease, Ann of Int Med.1983;99:22-26; Treib J., Clinical and serologic follow-up in patients with neuroborreliosis, Neurology 1998;51:1489-1491).