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INFECTIOUS HEPATITIS SYMBIOTIC TYPE WITH SUDDEN LYTIC CHANGE FULMINATING TOWARD A TERMINAL STATUS
Miss S.M.L, consulted Dr. J. Treiger on May 4, 1959, prostrated, with nausea, feeling like a drunkard. She had a fever of 38.8°C., muscular pains, halitosis, and facial neuralgia following a feast on seafoods. On May 8, 1959, the fever was gone, likewise, the muscular pains, but there was a severe pain in the gall bladder. On May 11, 1959, the blood showed Bilirubin 5.95 mgms. %, Van den Bergh strongly positive immediately 3 plus, cephalin-cholesterol (Hanger) three plus, thymol turbidity 7.5 units, thymol flocculation (MacLaglan) positive 3 plus. That night she was much worse, fever 39.5°C., extremely agitated, fear of death, hallucinations, and delirium. She was then given two millimicrograms of the Oxidation Reagent after the agitation gave place to a new phase of prostration bordering on coma. Improvement was evident in 48 hours with lowering of temperature, and return of appetite and bowel functions. Steady improvement followed and on June 17, 1959, the blood showed Bilirubin 1.02 mgms.%, Van den Bergh delayed weakly positive, cephalin-cholesterol negative, thymol turbidity 5.5 units, and thymol flocculation negative. On July 10, 1959, during the ninth week reaction following the Treatment, there was violent nausea and dizziness. She was given another dose of the Oxidation Reagent and improvement was apparent in three hours. Two weeks later, the blood test showed a normal Bilirubin of 0.41 mgms.% and all other tests were negative. During the twelfth-fifteenth week reaction period, there was an intestinal upset that cleared up quickly and during the 27th week reaction period, there was a pain in the left lobe of the liver. After that she remained normal. These reactions show that a symbiotic integration of the virus was present, as well as, the acute lytic type that fulminated to cause serious mental symptoms.
RABIES
This one hundred percent incurable disease has yielded like all other viral infections treated so far. Twenty years ago a rabid coyote caused the infection in a physician and in his horse on the plains of Montana. Both were treated with the serial system of Carbonyl groups after they had reached the convulsion stage. The recoveries took exactly as long as the time of development of the symptoms, three to four days. Some dogs were treated in the Army Hospital for small animals in Rio de Janeiro with encouraging results, also, and finally an epidemic of rabies in 1955 brought on by vaccinating costly zebu cattle gave the best chance for observation. Only the lytic type is known and from the earliest symptoms where swallowing is paralyzed it takes four days or less to terminate. Terminal cases took the same length of time to recover.
In this epidemic, 60 cows were vaccinated with the Fluery type live vaccine. Forty died typically and were proven rabid by autopsy and inoculation tests. Twenty were still alive when the writer arrived at the Fazenda. Of these, thirteen were treated and seven were held as control material, but were used for study in ways that would not interfere with the course of the disease. The controls all died typically and were proven to be rabid. Of the thirteen treated, eleven recovered. The two that died did so within an hour of receiving the Remedy, as they were about moribund when treated. One other case like the two that died was able to make a recovery. It illustrates the recovery course and demonstrates, like the other ten, that recovery of nerve cell function depends upon cell reconstruction, a reversal of the pathogenesis in which the energy and material taken from the host cell during viral vegetation is returned for host cell reconstruction. A perfect reversal of a reciprocal nature is, therefore, observed. This suggests, but does not prove that the virus uses the host cell’s enzymes during the pathogenesis, as well as, by the host cell during its reconstruction.
All cows treated showed paralysis of swallowing, some had severe torticollis and spastic convulsions and others could stand on their feet, but if pushed would fall and not be able to get up without help. One animal treated at the end of the third or beginning of the fourth day of symptoms was unable to stand and showed the typical tonic convulsions. It lay paralyzed in the same condition for four more days after Treatment and was badly dehydrated at that time. The government veterinarian thought best to sacrifice the animal to get better autopsy material and save it more suffering. He, therefore, had it dragged to the truck, but when the attempt was made to hoist it into the truck it kicked up a fuss and tried to run away. The Fazenda veterinarian happened by and seeing the animal show coordinated movements, he ordered it let loose, led it to water where it drank greedily and was then chased to pasture where it ate its way back to good health. The point here is that, in the four days of progress of the symptoms and the paralysis before Treatment, the nerve cells had reached a state of advanced destruction, but were not dead as yet. The energy taken by the virus through its integration with the FCG was able to support its vegetation and the autolysis induced in the host cell supplied the material for the viral vegetation. After the Treatment, the situation was reversed to a complete reconstruction in the same time required for the host cell destruction and provirus colony formation, for at the end of that period, the cell was able to function normally again. This is what happened in all of the eleven cases that recovered and the time relations indicate that the Reagent used to reverse the pathogenesis, did not attack at the point of integration of the virus, but at the most exposed unit, which would be the last one laid down in the co-polymerization of the viral nucleic acid units that constitute the essence of its central or pathogenic part. The oxidation would be induced there by the Reagent as described and the separation of the last laid down unit would make it available for host cell reconstruction, into the very place from which it was taken during the host cell lysis. The energy liberated by this oxidation must be able to pass on to the host cell to serve its reconstruction, for so long as the FCG is occupied, it cannot produce energy. Thus, the successive steps of splitting off each unit of the virus provide both energy and material for the host cell’s reconstruction. The indication then is that the nucleoprotein part of the viral colony is made up of host cell’s nucleic acids, which can excite no serological reaction of immunity, though it is the pathogenic part. The energy is that supplied by the host cell originally, as well as, the enzymes concerned. This clarifies the fact that after integration, no serological effort can rescue the cell. One is, therefore, tempted to look upon the origin of the virus center as of a nonspecific material taken from and common to animal cells and workable by their ferments.
The protein capsule is made of other material built on by the nucleoprotein center and is specific to each variety of virus. It has immunological, antigenic, properties. Cleavage of the viral nucleoprotein from the FCG results in restored structure and function and thus overcomes the pathology.
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