A Theoretical Model For Treating Lyssa Rabies, And Other Viral Pathogenic Strains.

With the advent of Pasteur's treatment for rabies, a new era was born, one in which a bite from a rabid animal did not have to result in death. The only drawback is that a bite has to be recognized in time. This becomes difficult if not impossible in cases where the bite or scratch is not seen or felt, as is often the case with bat bites. Given the near certainty of death in cases of rabies symptoms. it seems incumbent upon medicine to begin to pursue treatments for rabies after Pasteur's cure will no longer do. The 2004 case of a Wisconsin girl treated for rabies who recovered provided hope for those who wish to banish this plague once and for all. The main aspect of the treatment was to induce coma until the girl's own system could respond and recover from the infection. This is exactly what happened. Since rabies moves through the nervous system, it seems at least one theoretical possibility would be to use a blocker such as curare to shut down transmission between nerves and thereby block the movement of rabies from one nerve to the other. Respiratory support would of course have to be provided, but would only be necessary until the body's response took over, as it did in the case of the Wisconsin girl, who was treated with ketamine, rather than curare.

Actually, there is no reason to stop there. Based on how far the disease has progressed, one could use any number of compounds to block whatever nerve set the rabies has progressed to, to stop it in it's tracks, then provide supportive care. The theory depends upon rabies transmission and reproduction being dependent on neural channels to efficiently grow and spread into the spinal cord, and then the CNS.

Using nerve specific depolarizing agents to reduce or block electric transmission between nerves is another possibility, the theory being that given the nerve specific activity of the rabies virus, that the virus might actually be dependent on those charges to facilitate growth and movement. An electrically neutral environment might actually be detrimental to the growth and spread of rabies. MRI's could be used in conjunction with these treatments to determine the precise areas affected, allowing for precise and effective treatment.

Finally, since we know that rabies is a disease of warm-blooded animals, mammals, it seems worth exploring whether lowering the temperature of the brain and affected nerve paths, is successful at inactivating the virus. Mechanisms which are currently used to lower spinal temperature to facilitate recovery in severe spinal injuries, thus indicating cold has a protective effect on nerves, at the same time may rob rabies of the fuel it needs to grow and spread for a sufficient length of time that allows for the bodies immune response to eradicate the virus.

In sum, the key to stopping fatal rabies infections once and for all, may lie in efforts to localize, contain and inactivate the virus, rather than kill it. In this line, two strategies suggest themselves: First, the development of compounds which attach to and prevent the entry of pathogenic lyssa strains into neurons, trapping them in extra-neuronal space and exposing them to immune regulation, making the disease pharmacologically treatable. The second, which mirrors favorable bacterial balance strategies for treating intestinal disease and other disorders, uses the power of the circulatory and lymph systems for creating inter-neuronal chemical environments unfavorable to the development of pathogenic lyssa and favorable to the development of rival non-pathogenic lyssa strains. Amino acid, nucleic acid and fatty acid compounds which are more typical of non-pathogenic lyssa, hormonal factors, water/ion balance, gas blood ratios, relative ion mix, anything in short which is inhibitory to pathogenic lyssa rabies, and facilitative to non-pathogenic lyssa strains. Wavelength light and temperature variables would also have to be established as well. Proximal intramuscular injection of harmless rival lyssa strains, rather than distant injection of altered pathogenic strains, seems a safe and effective potential alternative to today's effective, but dramatic methods.

Furthermore, the development of diets and lifestyles which maintain these pathogen -resistant, non-pathogenic promoting, cellular and extracellular environments, seems a feasible strategy for the long-term prevention and ready treatment of pathogenic viral afflictions on as wide a scale to which we are willing to commit ourselves.

It is also possible that an intermediate host, a bacterial host, facilitates or negates the activity of lyssa in vitae. Pathogenic activity in the host bacterium could signal the development of pathogenic lyssa activity, which could be tested for. Under this theory it would be the presence of these bacterium in a wound environment favorable to their growth and propagation that would set the stage for the growth and propagation of pathogenic lyssa rabies strains. The spread of viral diseases by infection of intermediate bacterial strains is a relatively unstudied phenomenon, and could explain the difficulty in fighting such persistent plagues. An animal suffering overwhelming infection would be thoroughly inundated with such bacteria, that act as living reservoirs of infection. Such bacterium have no doubt, non-pathogenic rival strains whose growth and development are favored more in particular cellular environments, environments which can be recreated systemically, and quite precisely.