When Dr. Smith first saw Robert L., the baby was having mild convulsions, that is his eyes were twitching and maybe some little part of the muscles of the face were also twitching mildly. He was limp and he had been vomiting just before Dr. Smith arrived. His temperature was 99°. His mother told Dr. Smith that he had been having convulsions one right after another, that he would draw his right hand up to his shoulder.
Dr. Smith recognized the case as being that of Infantile Paralysis. The following day there was paralysis of the right arm and leg. He continued to have the convulsions. His foot began to draw, and his eye turned toward the side of his head so that you could not see the iris. It was two days before the Carbonyl Catalysts could be given. At that time there was complete paralysis of the right side of the body. He was perfectly limp. There was no motion or reflexes in either the right arm or leg.
Dr. Smith gave him two-thirds of one Treatment (1½ cc.) of the SSR. The following day there was some improvement, and the improvement continued until the child was perfectly well. There was no muscle impairment as a sequel.
SUBACUTE POLIO WITH PARALYSIS
CASE No. 38
Michael R., M.D.
The I. child, age 10, came to the office on September 10, 1941. The patient complained that for three days he had a headache and pain in the legs. His pulse was 90, temperature 98.6°, and the urine examination showed no pathology. The next day the symptoms of Infantile Paralysis were more evident; the Kernig sign was positive, he had a tenderness along the spine, he had neck stiffness, he could not lift his legs and the fingers of his hand were so weak that he could not turn on the radio. He had to lift himself with the elbows.
The Health Commissioner was called in the next day and he confirmed the diagnosis of Infantile Paralysis.
The Benzoquinone arrived on Sept. 13 and 2 micrograms were injected intramuscularly. The next morning the patient said that he felt some better, but his symptoms were about the same. A second injection was given on September 14th. About two days later he had less pain, he could bend his legs better and he had less neck stiffness. By September 20th, he had less lameness and he felt well.
On September 22nd, his temperature was 99.4°, and a third injection was given. Two days later the adductors, that is the muscles that bring the legs together, were less lame. He could bring his legs together. On October 8th his temperature was normal and from that day on he did not have any more symptoms. The Health Commissioner was called on October 15th and he was shown how the boy could walk through the room. He had no more symptoms. In 1943 he was active playing basketball and football. This case shows that benzoquinone offers inferior survival reagent qualities.
ACUTE ANTERIOR POLIOMYELITIS WITH PARALYSIS
CASE No. 39
Dr. Wendell Hendricks
The following case is typical of many we have treated and illustrates the early reversal of the disease process following the administration of the oxidation initiators, the SSR.
Loman A., age 10 years, came down with the prodromal symptoms of headache, pains in his back and legs, stiffness of the neck and back muscles, vomiting, and fever of 104 degrees on February 3, 1944. The condition did not abate but became steadily worse through the night and the next morning. Our examination found the symptoms mentioned and flaccid paralysis of both legs from the waist to the toes. There were no knee jerks, or other reflexes to be induced in the legs or feet. The spinal fluid was taken and found to be 4 cms. on the manometer. We waited one-half hour so as to give plenty of time to see if the withdrawal of the few cc’s of spinal fluid would alter the symptoms. He continued to get worse, the fever mounted to 104½ degrees and his pains increased. The pulse was 128. We then gave the SSR solution. Recovery started to make itself evident within two hours in a reduction of pain and headache and the vomiting ceased. Seven hours after the injection he could move his legs. His neck was limber and his temperature normal. He ate a light supper. The next morning he got up and walked to the bathroom unaided. His recovery was complete in a day or so and no sign of return has been observed. However, during the third week following the Treatment he had a reaction of chills and fever that lasted three hours, after which he felt very well. There was no development of atrophy whatsoever. The third week reaction is of interest. It showed that a destructive or symbiotic integration was established.
The rapid establishment of widespread paralysis indicates the symbiotic type, but as the back muscles were becoming involved a lytic type extension was also probable.
POLIOMYELITIS
Acute Polio with Extensive Progressing Paralysis
CASE No. 40 --- Walter N.
This child was two and a half years old when carried into our office September 19, 1931. Both legs were paralyzed from the waist down and there was foot drop. He had fever and suffered pain. No reflexes could be elicited from the legs. The paralysis was of the flaccid type and progressing. The spine was rigid. He had been vomiting. One dose of the Synthetic Reagent was given subcutaneously. He was held by his father about an hour longer, while being observed; then he slid off his father’s lap and stood on the floor, making a few steps, but was quickly raised from the floor and prevented from further action. The paralysis had existed from eighteen to twenty-four hours previous to the Treatment, so the release was rapid. The Testimony of the mother has been paraphrased and is given for your consideration.
“I took my son, Walter, to Dr. Koch when he was two and one-half years old. He had been playing the night before but during the night he did not sleep, and cried; and when he got up he could not walk. I did not take his temperature, but felt his forehead and thought that he had a temperature. His leg was still sore, so the next day we took him to Dr. Koch’s office. My husband had to carry him because he could not stand.
“Dr. Koch gave him an injection in the leg. We were in the office about an hour and soon after he had the shot, he wanted to get off my husband’s lap on to the floor. He could stand a little, but we carried him to the car and kept him in bed that day. The next day he was up and playing. That was the summer of 1931.” The recovery was complete and has remained.
ATROPHIC ANTERIOR POLIOMYELITIS COMPLICATED BY ANTIVARIOLIC
VACCINATION
CASE No. 41
Dr. J. Treiger
Miss P., age 7, seen first by Dr. Treiger March 8, 1957. Her weight was 20 kilos. She had had measles, varicela, whooping cough, and at 3 years of age a nasal diphtheria, following which she has always been underweight in spite of a good appetite and sleep. Examination showed slight dyspnoea and constant cough with a hypertrophied left tonsil, much flatulence, fearful, crying at nothing, without appetite, very thin and weak, with paralysis and muscle atrophy of the right leg. The history showed that she received smallpox vaccine in March, 1957, and had a very strong general and local reaction. Her ill health continued with the added disadvantage of the paralyses and atrophies of Anterior Poliomyelitis which struck her in May, 1957. She caught colds very easily and every contusion produced a swelling that became purulent with ease. Good homeopathic prescribing helped her sustain herself at this status but something more fundamental had to be removed. From March, 1957, to March, 1958, she gained only one kilo in body weight. So, before the polio struck her, she was practically a metabolic invalid. The vaccination mark, however, developed a large mushrooming keloid raised high above the surrounding skin. The atrophies prevented her from raising the right foot when she was lying on her abdomen on the table, and from bending the right knee when standing. The right leg gave no support when standing as the knee and the ankle were both wobbly and without strength or control. The foot hung loosely from the ankle joint. She needed braces to support both.
On April 15, 1958, she received 2 millimicrograms of the SSR from Dr. Treiger, intramuscularly. The results were: four weeks later she had gained two kilos, and had better muscle tone. In two more weeks, she gained two more kilos. In the middle of the twelfth week, after Treatment, she had a characteristic reaction (July 7th). There was pain in the right leg, general achiness and fever, and itching of the keloid. Three weeks later another reaction occurred with fever of 108°F., much coughing with the elimination of clear mucous. This lasted only two days, but in these three weeks the keloid reduced remarkably. One year later, in August 1959, she weighed 29 kilos, and showed another reaction with pain in the leg and the return of an itchy rash on the eyelid, plus a general itching that she had six years earlier. In this period, the keloid reduced so as to be at the same level as the skin and so it had shrunk. At the time of Treatment, it was 10 to 12 mms. in diameter, and raised 6 to 8 mms. above the level of the skin. How deep it went is not known, but its present depth is not great as it is flexible. Still, there is maybe 20% to be absorbed to become an ordinary scar. Her appearance is healthy, she is vigorous and has a stable nervous system, and she walks without any bracing apparatus with a practically normal gait. She can now raise the right foot when lying on her abdomen, and can raise and bend the right knee when standing. The right leg supports her when standing and the ankle has regained fair function useful in walking without braces and with ordinary shoes. The circumference measurements showed an increase in the right thigh from 28½ to 34½ centimeters while the left thigh stayed at 38½ cms. and the right calf gained from 19 to 20½ cms. and the left stayed at 25 cms., between April, 1958 and Nov. 16, 1959. It would be interesting to decide, if or not the smallpox vaccination gave the polio infection. Since the keloid reacts concomitantly with the Polio reactions this might be suspected. However the eczematous rash also reacts at the same time and points to a fungus infection received at an earlier date. The keloid is not yet fully absorbed and the atrophies are not yet fully corrected. More reaction is still expected. These will solve the etiological position of the vaccination. On Nov. 4, 1960, the right calf measured 22½ cms.
EPIDEMIC HEPATITIS
It will be seen in this group of Infectious Hepatitis cases that the virus host cell integrations follow the same pattern as in Anterior Poliomyelitis and the time relations of the recovery process measure up similarly to those of the recovery from paralytic polio, rabies, and dog distemper. Both the acute lytic and the chronic symbiotic types are observed, indeed the virus appears to exist in some cases as if integrated with foci of long suppressed infection, either in symbiosis with some germ or with the scar tissue that imprisons it. The relation of the vaccination scar to polio and to cancer, as revealed in their recoveries, might be compared with the fecal contaminated scar of the fourth case given here. In all such stored viral infection, a drop in the resistance of the patient allows the symbiosis to go rapidly lytic with rapid multiplication, and then the burst through as a general infection that attacks the most susceptible tissue dominantly.
The examples offered here present the four types of classification. The second case represents both the protracted type with remissions and relapses, and also the fulminating type when the infection suddenly fulminated and quickly went into the terminal phase with wild delirium, hallucinations and then a state bordering on coma, when the Survival Reagent was given and quickly reversed the pathogenesis. The first case represents the common type with jaundice and sickness that hangs on regularly for a month or two before it starts to yield, but here the reversal was evident in hours, and was completed in a week or two. Interesting is the thyroid disturbance, like the brain disturbance in the second case, showing that the virus can integrate with more tissues than the liver cells. The third case directs attention to the rate of recovery of function by the liver cells, as do the others, though they were more complicated. This is regularly about 48 hours in the acute lytic type of integration. In this time the bilirubin drops to a near normal, as from nearly 6 mgms. percent to less than 0.5 mgms. percent, while the bile absorbed into the skin and other structures takes longer to be liberated and eliminated. The patient, however, is well with good liver function, and no toxicity whatsoever. The following cases are reported by Dr. Treiger. The last one was observed by the writer.
INFECTIOUS HEPATITIS
CASE No. 42
M. C. S., a girl of 12½ years, 41 kilos, student, with a good school record, appeared Nov. 12, 1959, and gave the following findings. She was changing color from the healthy hue to a greenish yellow, great urgency to move the bowels after eating, slight pain in the muscles, pain in the bowels with marked nausea, that was violent in the days preceding school examinations, which were at hand then. The pulse was 120 per minute, temperature 37.6°C. and a subicteric tone of the sclera. When examined, complained of pain over the liver and epigastrium, with an accentuated tympanism, and terrific itching. There was excessive sweating of the hands and feet, and together with the tachycardia the thyroid gland appeared to be attacked. An epidemic was running at the time in her school.
Blood analysis on 11/16/59: Bilirubin, 1.43 mgms.% instead of 0.2% to 0.4%; Van den Bergh, positive, but weak and delayed; Hemogram normal; Crenation test, only 20% crenated, 80% remained round.
Treatment: 2 micrograms of Benzoquinone solution was given on November 16, 1959, with homeopathic doses of iodine and chelidonium. Improvement showed the next day, was very good in 48 hours, and continued until on the tenth day, when she was practically well. The pulse had dropped from 120 to 86 per minute, the jaundice had faded away, no more pain or itching, and no nausea or sweating. The blood showed Bilirubin 0.41 mgms.% which is normal, the Van der Bergh was negative, the Crenation test was 90% normal.
She took her exams without any nervousness and with good results between Nov. 25 and Dec. 12. The correction was permanent.
INFECTIOUS HEPATITIS PROTRACTED SYMBIOTIC TYPE WITH SUDDEN
LYTIC CHANGE FULMINATING TO TERMINAL STATUS
CASE No. 43
Dr. J. Treiger
S. M. L., age 31 years, gave a history of pyelitis in early childhood, frequent colds and in April, 1958, a broken leg, weight 45 kilos., when she consulted Dr. Treiger on 5/4/59. She had a fever of 38.8°C., complained of grippiness, muscular pains, tonsilitis, worse on the right side, halitosis, dirty tongue and facial neuralgia on the right side. This attack came after a season at the seashore on a heavy crab and shrimp diet. She was given homeopathic medication without result and she continued to get worse. On May 8, 1959, the fever was gone, but she was prostrated with nausea, repugnance to all food, feeling like a drunkard, and a terrible taste on her tongue. The muscular pains were gone, but there was a severe pain over the gallbladder. On May 11, 1959, the blood picture was: Bilirubin 5.95 mgms.%; Van den Berg strongly positive, immediately, three plus; Cefalin-Cholesterol (Hanger) three plus; Thimol turbidity 7.5 units; Thimol Flocculation (MacLaglan), positive three plus. That night she was much worse, again with a high temperature of 39.5°C, extremely agitated, afraid of dying and of being alone, hallucinations and delirium She had received a new homeopathic prescription that did not work. Dr. Treiger gave her two millimicrograms SSR when the agitation gave place to a new phase of prostration bordering on coma. However, the nausea did not develop though it had been strong and constant. After 48 hours the improvement was evident with lowering of the temperature and the return of appetite and bowel functions. She steadily improved and on June 17, 1959, the blood showed Bilirubin, 1.02 mgms.%; Van den Bergh, delayed and weakly positive; Cefalin-Cholesterol negative; Thimol turbidity 5.5 units; and Thimol flocculation, negative.
July 10th, during the ninth week after the Treatment she had a reaction with violent nausea and dizziness. She was given another dose of the SSR. The improvement was observable in three hours. Two weeks later the blood test showed a normal Bilirubin 0.41 mgms.%, and all other tests negative.
During the 12-15 week reaction period she showed an intestinal upset and this cleared up quickly aided by Ipecac and Terrarnycin. In the 27th week reaction period there was a transient light pain in the left lobe of the liver that cleared up quickly, but there were no other symptoms. The correction was complete. No doubt the intestinal tract was the first to become infected and was therefore the last to become normal, in line with the characteristic behavior of the recovery process after the FCG is rescued and restored to action.
AN ACUTE LYTIC TYPE CASE OF EPIDEMIC HEPATITIS
CASE No. 44
Dr. J. Treiger
J. H. C., age 13 years, student, appeared with a history of having drunk water that was under suspicion of being filthy 15 days previously. He had abdominal pain that was helped by intestinal lavage. The urine was loaded with bile. There was deep jaundice and profound drowsiness. His state was subfebrile, and the blood examination on February 5, 1959, showed Bilirubin 5.83 mgms.% (Malory and Evilin). The Van den Bergh was immediately directly positive, the cefalin-Cholesterol positive, the Thimol Turbidity 5 units, and the Thimol Flocculation positive. Two millimicrograms of the SSR were given on February 5th. On February 7th the jaundice had faded considerably and he felt very much better, no more pain or other disturbance. The bile stained tissues had not completely unloaded until three weeks later when the Bilirubin test was almost to normal, namely 0.86 mgms.% and the Van den Bergh and other tests were normal. On March 10th he was fully recovered and back to school. Here again we see the restoration of liver cell function, which means the rupture of the viral host cell integration, and the restoration of the host cell to functional structure, required 48 hours. In rabies it required 72 to 84 hours, and in polio the restoration was proportional to the time the paralysis had lasted, and the host cell injury had been going on. Thus, this disease supports our postulate very well. While this virus is not killed by chlorine oxidation, it is destroyed by induced oxidation after it is integrated with the host cell.
CHRONIC INFECTIOUS HEPATITIS WITH MALNUTRITION
CASE No. 45
John S., age 28, when appearing for diagnosis and treatment, height 6 feet 3½ inches, weight 137 pounds, on August 4, 1957. When he took sick in 1952, he was in the air force. He had been in good health until an attack of appendicitis called for an operation. This resulted in severe peritonitis, and the use of 70 injections of antibiotics, mostly of streptomycin that favors virus infection so markedly. Ever since this attack, he was an invalid steadily getting worse, losing weight and strength, becoming more and more anemic with less ability to digest his food until he had lost his appetite completely. The use of digestive ferments medication failed to help. Moreover, the liver did not metabolize what little he was able to digest. This deterioration progressed until August 4, 1957, when he appeared for observation.
Examination showed slight jaundice, profound anemia, enlarged tender liver, loss of elasticity of the skin, great weakness, and gastro-intestinal failure with its consequences. There was severe prolonged headache at times and difficulty to perform his obligations. The operation scar was hard and extensive.
Two cubic centimeters of the SSR solution containing two millimicrograms of Reagent were given on August 4, 1957. There was no sharp turn for the better as usually follows, but he did not continue to get worse, and a slight improvement could be reported on the 14th week. This trend gained a little momentum up to the 36th week when a sharp reaction took place, with acute inflammation of his enlarged liver and the abdominal wall scar, severe jaundice, high fever, abdominal pain, vomiting and increased headache. This lasted only a week and cleared up spontaneously with fair rapidity when one considers his greatly depleted condition. The blood examinations were interpreted by his physicians as indicating Infectious Hepatitis. But as the course of the disease was so different from the regular course and the improvement so rapid, we interpret it as a reaction to a chronic infectious hepatitis in which the virus was integrated with the fibrotic tissue of the extensive abdominal scars as well as his liver tissue. The oxidation of the toxic virus factor off from the liver cells gave rise to the inflammatory changes, and jaundice, but as soon as the liver cells were free, they were able to function again, and normal status returned.
He gained a good digestion, strength and weight so that when seen in December 1959, he was perfectly well, the liver was normal, the scars soft and pliable, and with good vigor, and ambition to work.
RABIES
In April 1955, the Fleury type live rabies vaccine made from street dog virus, was injected into 650 thoroughbred Zebo cows at the Fazenda Indiana, near Rio de Janeiro. The vaccine was prepared by the Health Department of Rio, and given by expert veterinarians. Six hundred cows showed no adverse effects, neither intoxication nor rabies infection. However, 23 younger animals did come down with virulent rabies. They all progressed in their symptomatology, and died in from 3 to 5 days in the classical course. The brains showed negri bodies, and the mouse inoculations were positive for rabies.
The writer arrived on May 19, 1955, while, some of the animals were still alive but showing the disease in well advanced stages. Only one calf was in the early stage of deglutory paralysis, but she had to be given saline transfusions to combat the dehydration consequent to impeded swallowing. Two cases were under heavy hexamethylene tetramine treatment, and were not offered to us until they were in the terminal stage, and were not fit for statistical observation— only for experimentation, because of the saturation with the drug, which is an inhibitor to the Survival Remedy. Six cows were in the terminal stage, about the fourth day, with typical torticollis, convulsions, deglutory paralysis, and were either paralyzed so as not to be able to walk, or if able to stand, would fall if pushed and not be able to get tip again. Six were moderately advanced, and could stagger about, showed torticollis, and short convulsions, but could not swallow. They were in the third day or at the end of the second day in some instances. So there were thirteen cases treated for statistical observations, including the calf, Iberia, that had only beginning deglutory paralysis for a day or so. In the entire symptom course was the same as in those that died, and started with deglutory paralysis. There were seven other cases used as testimonials — collateral controls, but as the opportunity was a rare one we used them for experimental observations in a way that did not prevent them from going the regular course to death as the cows that died before them. We had learned in dogs that the quinone structure does not affect rabies favorably, so we treated some of these with diphenoquinone one part to a million, and some we treated with high dilutions, that is, a billionth of a microgram of the serial system of Carbonyl groups, used in a dose of ten micrograms in the treated cases. Of the thirteen treated cases, eleven made complete recoveries, and two died.
All treated cases required 72 to 84 hours for restoration of controlled movements including deglutition. Its paralysis was the first symptom to come and the last to clear up. Animals treated during the fourth day of their downward course, were then widely paralyzed and had gone through a heavy convulsion period. They lay paralyzed for four days longer, before they showed restoration of function. An interesting case will illustrate. The government veterinarian who took charge of this epidemic had no faith in the cure of rabies, which was always 100% fatal, and as fast as any diseased animal showed it was following the classical course of the disease, he took it away for sacrifice, to save it useless suffering and to have better autopsy material. Our Treated animals were allowed to follow along without interference except one cow that was treated at the end of the third day or the beginning of the fourth day, when it was already badly dehydrated. It lay paralyzed for four more days when the Government veterinarian ordered it dragged to the truck to be taken away, but on reaching the truck when they tried to hoist it in, it kicked up a fuss and tried to run away. The Fazenda veterinarian was passing by and as he saw the cow show coordinated movements he ordered a halt and led it to water, where it drank greedily. He then let it loose in the pasture to eat its way back to health. Here we see that at the end of the quiet period, which is as long as the symptomatology period the reconstruction is complete. In other words the type of integration is such that it affords a reciprocity between the virus and the host cell. During viral vegetation the energy and material passes over to the viral colony, but during the viral oxidation a stepwise burning of the virus returns the energy to the host cell that was taken from it, and the food that diffuses into the cell supports its reconstruction. This explanation is the only one we can think of since a full reversal of the process takes place even after the host cell is at the point of full destruction and the viral colony ready to burst forth as myriads of mature parasites. This is especially significant since so long as the host cell and virus are integrated, the former cannot carry on constructive or functional processes, but must yield to complete dissolution. So the oxidative destruction of the’ virus supplies the energy for grana reconstruction so that the grana can then control enzymatic activities for function. One should contrast this evidence with the fact that a minute and a half after a virus penetrates a host cell the integration is complete and no amount of vaccine or serological effort is able to cause the separation and rescue it. It is doomed. Serological aids are merely substitutional. The SSR rescues and restores the host cell and burns up the pathogen.
DISTEMPER IN DOGS
(Cinamose)
The hospital of the Army’s veterinary service for small animals, Col. Columbo and his staff with Dr. Adelberto Carneiro, and Dr. Cantuaria Guimaraes, arranged for the treatment of dog distemper as brought in from the street, and homes. For the first 17 cases treated we had to guess at the dosage and get it regulated for a systematic treatment of this disease. These cases were lost, and although they are included with all treated cases in the statistics, they bring the cure rate down from 90-95% to 80%. The detailed report is published in Veterinaria, the official journal of the University Veterinary Department of Brazil. Columbo and Carneiro, Veterinaria Ano IV, Num. 1, p. 21, 1950.
In private practice in the nervous form of distemper the recovery percent ran 80% or over, but only small groups of dogs were treated. Many of these animals were paralyzed for several weeks, even longer than a month with involvement of the respiratory and cardiac centers beginning to show. Thus the chances to live as long to accomplish the restitution, as the nervous system was involved were certainly reduced. However, the time required for restoration of the affected cells, like in those of rabies, is about equal to that which accommodated the destructive process. We have the documentation of some private veterinarians, and professors in the University, on a short series of cases, where 80% of well-established distemper of the nervous system were cured. However, a case of polio in a dog that acted just like distemper of the nervous system was the subject of the Official Testimony before the Federal Trade Commission in 1946 by Dr. B. J. Myers, of Oklahoma City, a veterinarian who attended the dog through its recovery. It was a valuable Pekinese that had been playing with a little girl neighbor when she came down with paralytic poliomyelitis during a severe epidemic. The paralysis started in the hind legs and tail and then affected the front legs and body, in the course of a week the neck and “bark” were paralyzed and death threatened from respiratory failure when the SSR was administered. It took a week to ten days to undo the paralytic degeneration. First starting with the “bark” and neck and reversing the paralysis until last of all the hind legs and tail regained their functions. Cinamose does not attack human beings but polio does attack humans and other animals. So far as the symptoms were concerned it could have been either disease that affected the dog, but because of the polio epidemic that was raging at the time and the contact the dog had with the sick child, the diagnosis of polio was made. No serological tests were perfected at the time to make a differentiation. The case is of value in that it shows the identical nature of the attack of a virus of different types on the same functional mechanism even in different animal species. The similarity of the pathogenesis and of the corrective process regardless of species is demonstrated. Also, that the recovery course is not a matter of imagination, but a definite procedure, without psychotherapy.
HOG CHOLERA
Hog cholera attacks the whole body generally including the intestinal and respiratory tracts, the skin and vascular system, and the nervous system. At the end of the disease, just before death, the whole body is involved. However, in a small percentage of cases the nervous system infection dominates the symptomatology very early. There is ophosthotonus, torticollis, and convulsions. The animal behaves as if it had rabies. So far as this writer has seen this type, there was no attempt to swallow, as the head could not be bent to reach the trough. Less than 20% show this type of infection in Cuba, and in Brazil it is even more rare. The disease is 100% fatal in three to five days after symptoms begin.
The following report is taken from an official record at the Veterinary Department of the Cuban Army under Fidel Castro:
A. “On May 15, 1959, Dr. Rodriques, Director of the Veterinary Center of the Estado Major of the Army, in Ciudad Liberdade, facilitated and arranged for the treatment of animals involved in an epidemic of Hog Cholera at Quartel 10, of San Antonio, that had already caused the deaths of 15 vaccinated pigs. The remaining pigs of the colony comprised a total of 74 infected pigs, 35 small and 39 large.
B. “Prominent Symptoms: Among the prominent symptoms that established the diagnosis were:
1. The deaths of the 15 pigs before our arrival.
2. All the pigs that were still alive showed,
a. Prostration,
b. Respiratory difficulty, strenuous in type, characteristic of
bronchiogenic pulmonary lesions,
c. Hemorrhagic plaques, small and large in the skin of the
abdomen of all animals, extending in some cases under the neck
and jaw.
d. Excretion of solid and liquid material with rectal congestion
in some cases.
e. Teats inflamed and hemorrhagic, very severe in one case,
f. Nervous manifestations with torticollis, very severe in one
case.
g. Fevers running between 39,5* and 41°C. in various animals,
the small animals with 40°C. The sickest animals showed a drop
in temperature to 39.5°C. characteristic of the advanced stage.
C. “Pathology: The conditions of the material was the poorest as a result of the observed facts and changes. The animals had already carried the incubation period of 10 days with a prognosis of 100% fatality, according the virological standards, for after the virus is integrated with the host cell, no serological measure can set the host cell free and rescue it.
D. Treatment and Material Used: The 74 animals were treated in two sessions, the first on May 16, 1959, and the second on May 19, 1959. The first group to be treated was 10 small pigs and 12 large pigs. The second group treated was 25 small pigs and 27 large pigs.
“A solution of diphenoquinone, freshly prepared, containing 1 microgram per cubic centimeter, was used. Small pigs were given from one to two cc. of the solution, and the larger pigs received from five to ten cubic centimeters by injection.
E. “Results:
“First Group. This group was observed on May 23, 1959:
a. No deaths,
b. Temperatures normal in checked pigs with the exception of
pigs No. 3 and No. 4; on these the injection was then repeated,
c. The red hemorrhagic spots on the abdominal zone had
disappeared in all animals. The congestion of the cornea had
also left,
d. The rectal areas appeared normal,
e. The respiration was normal in all animals,
f. The female’s teats that were formerly inflamed and
hemorrhagic were normal in all animals,
g. One male of the group segregated as the most debilitated,
attempted one week after treatment to accomplish reproductive
relations with the females, successfully.
“Second Group. This group was observed on May 23, 1959, five days after Treatment. The following results were observed:
a. No deaths,
b. Normal temperatures in all that were checked,
c. The red hemorrhage areas had disappeared,
d. The rectal areas were normal,
e. The respirations were normal in all animals,
f. The teats of the females appeared normal.
“This group was examined again May 26, 1959, one week after Treatment when Group No. 1 was also examined. All pigs were found normal and attested to by the officials in control of the test.”
In Brazil, the epidemics were small. At the Ministry of Agriculture Maracana Station, where cresol was used liberally, and the pigs were exposed to other inhibitants, the results were 100% failure in a group of seven pigs. But at the Deodora Station where no interference was met, the results were 60% cures that is two cures out of three treated. These pigs were all in extremis, at the time of Treatment. That is, unable to stand or eat, symptomatology typical. In another epidemic at a private farm 5 far advanced large pigs were treated with diphenoquinone, each receiving ten micrograms each at two different sessions 3 days apart; of the five only one could walk. They all recovered in 5 or 6 days, and were able to eat again, completely clear of chest and skin changes. In another epidemic at Santa Cruz seventeen of eighteen pigs in the herd had just died of Swine Pest. One still was alive and sick, it did not eat or drink, but could walk. The skin and chest symptoms were characteristic. It recovered also.
At the same time at a neighbor’s farm several herds were affected. One group of four pigs equally advanced at about the third day, except a very small “runt” that was near death. It had not taken water or food all this time and died within a few hours after being treated. The others all recovered. Another neighbor’s farm had four pigs with symptoms in the second to third day of the disease. We treated the three that were worse, and held the other as a control. The third day later these were found cured and eating, having fully normalized. The control pig was quite advanced and not able to live more than another day, perhaps. We treated it, and two pigs in another neighbor’s farm that was characteristically affected. They all recovered within a week when the next visit was made. Thus in the Santa Cruz group there were nine treated, including the far advanced “runt”, and eight recovered and the “runt” died. This is a fair percentage and gives an idea of how the infection gets around. In another epidemic of ten pigs we used a different atomic arrangement, — the serial system of Carbonyl groups. The results were 100% failure. This serial system of carbonyl groups gave 80% cures in rabies, and the quinone structure gave 100% failure. Thus there are two different 100% fatal viral diseases, each of which takes the same time to kill, that do not respond to the same Carbonyl group when activated by different sources of electrons. The steric advantage and hindrance are different in each integrate evidently.
HOOF AND MOUTH DISEASE
(Aftosa)
There are three types of Aftosa virus, and their virulency varies. There is the deadly cardiotropic type that can wipe out a herd in short order. Some of the infected animals drop dead from heart failure before they can develop any lesions in the mouth or on the hoofs. It was such an epidemic that started at the Agriculture College, Institute Quinze de Novembro on October 14, 1949. There were 59 head of cattle and 200 pigs. The professor in charge was afraid this virus would wipe out his herds, as five cows had already died a few hours after the epidemic had started. Others were lying on the ground unable to get up. They appeared doomed. Others showed lesions in the mouth and feet but were able to walk. We treated all 54 animals that were still alive, of these seven were newborn, 15 were calves, 17 were young bulls, and 15 were cows. Thus two-thirds were most favorable hosts for the destructive action of the virus.
Results: Two cows and one calf died of the disease. All others recovered and no new infections developed. Of the 200 pigs, 35 were adults, and 165 were young. 167 were well-established cases of Aftosa, while 33 were symptom free. All were treated. Four pigs died of the infection giving a cure percentage of 98% and as no new cases developed, a prevention percentage of 100%.
The following year Aftosa again struck the Institute. The cows we treated did not conic down with the disease except a few showed mild symptoms for a short time. The new cows brought into the herd took sick and died before we could be notified to come. A year later the treated cows were still immune, and again a year later we had the same report.
At the Rural University, the government’s Agriculture School, an epidemic broke out that was reported by Dr. Adelberto da Silva Carneiro, in Veterinaria No. I, page 75. The virus was found to be type C. There were 68 cows in the herd. This virus was endemic and was active every year at the same time. It never killed over 10% of the cows, so it was not too fatal. However, the affected cows lost their milk production, and that was the big point of worry. Practically all of the cows showed symptoms including the drying up of the milk secretion. But a few were symptom free. All were treated. There were no deaths. Twenty-four hours after the treatment was given, the dried-up mammary glands started producing milk at the normal rate. Thus there was 100% cure, 100% prevention and 100% restoration of function. Only one cow needed a second injection, and then cleared tip normally.
CONTROLLED AFTOSA EXPERIMENT
At the Rubino Institute at Montevideo, Uruguay, a controlled experiment was arranged in which 30 calves, all bulls, of the same size, age and “texture,” were inoculated with a standard cardiotropic virus that killed 80% in from 4 to 9 days. The other 20% became chronic heart cases that died somewhat later. But the virus was 100% fatal in the dose used. The experts prepared a vaccine from this virus, and protected 10 of the cows therewith at an optimum interval before inoculation with the virus. Ten cows were held untreated as controls, and ten were given the SSR reagent. Since we were promised plenty of leeway and material for a good period of experimentation, we gave these cows the usual human dose used in cancer, that is a concentration of 10-(12), that is one part to a trillion of water. They were treated three days after the inoculation. The cows we treated and the untreated controls were held together in a small room with a bare cement floor in the coldest month of the year, July. They were grouped together with their noses all touching and the untreated cows were smearing the treated animals with their dripping infected saliva. The vaccinated controls were held in a warm barn with plenty of straw and given medical aid, transfusions and all the care possible for success.
Results, On the fourth day we had one death, and the vaccine-protected animals had four deaths. The rest of the control animals were very sick with myocarditis, but our animals, the nine still alive were not, and they recovered fully. Since the control animals that had not yet died were getting ready to do so as the myocarditis progressed, the director of the institute asked us to treat them since they did not have cremation facilities for so many animals, and the law required cremation. We treated the rest this time as well as our test cases with the one to a million dilution, and the results were rapid. All of our cows recovered and so did our treated controls. The cure percentage on the one to a trillion dilution was not over 90%, but the cure percentage of the one to a million dilution was 100%. The experiments were stopped because of political pressures that will not be discussed here. Another volume is devoted to curiosities. In Aftosa we see one virus type that paralyzes function of heart muscle and another that paralyzes milk production, both cured by the same reagent as cured the nerve cell paralysis in rabies, cinamose and poliomyelitis. The structure of the virus-host-cell integrate must be atomically of the same order then, in them all, since the end results of action of one reagent is the same — functional restoration of the host cell and disappearance of the virus.
SYPHILIS
CASE No. 46
This subject will be amply aired in the completed text; we here just give a case in photographs, to touch on the subject. This boy was sent into the hospital at Louvain University, Belgium, in 1934, with a diagnosis of cancer of the skull since he did not respond to anti-syphilitic treatment though given expertly and with vigor. We found on biopsy and serological tests that he had syphilis. However, the neoplastic taint was not ruled out thereby, and his resistance to anti-syphilitic treatment may be due to a neoplastic agent that may have been present. He was given a dose of the carbonyl catalysts and at that time his photograph showed as in No. I. Six months after Treatment, he was serologically cured and the photograph shows good healing of the area. The necrosis had gone into the middle layer of the bone, and the healing involved bone reconstruction as well as skin healing. One year later the fibrosis shown in the second photograph was replaced by perfectly normal tissue and could not be detected.
B.W. Photograph No. I. Taken before Treatment.
B. W. Photograph No. II. T taken after Treatment.