Tetanus (Curable and Preventable) 

Tetanus is an acute bacterial infectious disease that results in an often fatal neurological syndrome. The primary clinical manifestations of tetanus are caused by the extremely potent neurotoxin that is produced by the germinating spores of the bacteria causing the infection, known as Clostridium tetani.

The neurotoxin, known as tetanospasmin, is among the most potent toxins known to man, including botulism toxin. One mg of tetanospasmin is capable of killing 50 to 70 million mice! Symptoms of this toxin come from the progressive muscular spasms that can eventually evolve to seizures, respiratory difficulty, and paralysis.

Tetanus is traditionally treated with a combination of antibiotics, tetanus antitoxin, and tetanus toxoid immunization. The tetanus toxoid is given to induce antibodies that neutralize newly produced toxin not yet bound to target tissues. As tetanus typically comes from deep physical wounds that allow the oxygen-deprived bacteria to germinate and multiply, local wound cleaning and care is also important in the proper treatment of this infection. 

Klenner (July 1954) felt the need to dispel the general belief that tetanus was a difficult disease to cure. He was also convinced that tetanus antitoxin had "no curative value" and was actually harmful, especially when given frequently by vein.

Klenner described the case of a six-year-old boy who was already demonstrating toxin-related symptoms and muscle spasms when he first saw the child. The child could not open his mouth more than 30% due to jaw spasm, and a sudden, involuntary clamping of the jaws shut ("lockjaw") would follow any attempt to open his mouth. Vital signs revealed a low-grade temperature, rapid and shallow breathing, and a rapid pulse, ranging from 120 to 130 per minute. In addition to vitamin C, Klenner also used a skeletal muscle relaxant known as Tolserol to prevent convulsive seizures and help relieve the muscle spasms. Klenner also noted that the antitoxin therapy administered to this child was the result of "outside pressure" and not his decision. 

All vitamin C was given intravenously to this patient. During the first 24 hours a total of 22,000 mg of vitamin C was given in multiple doses ranging from three to five hours apart. A total of 2~,000 mg of vitamin C was given over the next 24 hours. Throughout these first two days, the child was taking progressively more nutrition and was bothered with only mild abdomin~lcramps. Over the next two days comparable amounts of vitamin C were given, but five separate doses of tetanus antitoxin were also given intravenously. After each dose of antitoxin the child deteriorated clinically with severe abdominal pain and initially a reactivation of fever. Intermittent doses of penicillin and calcium gluconate were also given. Much of the child's discomfort was alleviated by the Tolserol. Ultimately the child was discharged on the 18th hospital day, although Klenner felt the child could have been safely discharged 10 days earlier. Klenner was very convinced that the antitoxin actually continued to compromise health rather than improve it. 

While no other cases of tetanus treated by Klenner could be found in the literature, he did comment on the tetanus case of an adult white female who died from the inability to breathe less than one hour after receiving a single intravenous dose of tetanus antitoxin. Undoubtedly, this also affected Kleriner's attitude toward antitoxin. He did feel that a single intramuscular (rather than intravenous) dose of antitoxin above a wound suspected to be the site of the infecting tetanus bacteria was reasonable for the purpose of dealing more effectively at the.presumed site where new toxin was being formed. 

When considering the response of Klenner's tetanus-infected child described above, it should be kept in mind that the overall mortality for generalized tetanus is 20% to 25% with even the best modern medical care. Furthermore, those who do survive will generally require from three to six weeks for complete recovery. 

Jahan et al. (1984) conducted a simple study on the effects of vitamin C in the treatment of tetanus.

In 31 tetanus patients aged from one to 12 years, a daily intravenous vitamin C administration of 1,000 mg was given in addition to antitoxin.

None of the vitamin C-treated patients died, while almost 75% of those who did not receive the vitamin C died.

In older patients, aged from 13 to 30 years, 68% of those not receiving vitamin C died, while only 37% of those who received the vitamin C expired. Undoubtedly, larger doses of vitamin C would have completely protected the older group as well. The need for vitamin C is directly proportional to the size of one's body. A 1,000 mg dose of intravenous vitamin C goes a lot further in an infant or small child than in a much larger teenager or adult. 

One very impressive animal study on tetanus toxicity strongly supports Klenner's conviction that antitoxin treatment is, at best, unnecessary, and that vitamin C alone should remedy the condition without any resulting toxicity. Dey (1966) studied the effects of vitamin C on the toxicity of twice the minimal lethal dose of tetanus toxin injected into rats. There were five groups of rats. Group 1 was given only the tetanus toxin. Group 2 received toxin and intraabdominal vitamin C simultaneously, followed by more vitamin C for three more days. Group 3 received vitamin C first for three days, then was dosed with the toxin, and vitamin C was continued for three more days. Group 4 was given the toxin and the symptoms of local tetanus were allowed to develop over the next 16 to 26 hours. Vitamin C was then initiated and continued for three days. Group 5 was given the toxin, and the symptoms of generalized, severe tetanus were allowed to develop over the next 40 to 47 hours. Intravenous vitamin C, rather than intraabdominal, was then given. 

Except for group 1 animals, which received toxin and no vitamin C, all animals survived. Group 1 animals died from 47 to 65 hours after the toxin administration. In the group 2 survivors some very mild local tetanus symptoms were seen in the affected legs. In group 3 survivors, which also received vitamin C before the toxin was given, there were no symptoms of toxicity. The group 4 survivors had no further spread of the initial symptoms. No symptom description was given for the group 5 survivors. 

What does this experiment mean? One reasonable conclusion is that totally non-toxic vitamin C dosages can completely neutralize fatal amounts of tetanus toxin in an animal model. There was no need for the administration of any antitoxin to help in reaching this outcome. Dey (1967) had earlier demonstrated that vitamin C was most effective as a prophylactic and a therapeutic agent in negating the lethal and convulsive properties of strychnine, an agent that produces a clinical syndrome very similar to that produced by tetanus toxin. Furthermore, adequate doses of vitamin C given prior to tetanus toxin administration proved to be completely protective in preventing any manifestation of toxin effect. Also, considering the rat is an animal that can produce its own vitamin C, this experiment gives even greater support for the vigorous treatment of suspected tetanus infection with vitamin C. Animals producing vitamin C can still get sick from tetanus or any other infectious disease if enough of a microbe challenge and/ or microbe-associated toxicity confronts them. Humans; with no inherent vitamin C-producing abilities, need the prompt high dosing of vitamin C in the face of such challenges to survive the infection and minimize the toxic effects. 

Some earlier research suggested the likelihood that the positive clinical effects noted above would occur in the treatment of tetanus-stricken patients.

Jungeblut (1937b) demonstrated that vitamin C could inactivate tetanus toxin in the test tube. Prior to the isolation and commercial availability of vitamin C.

Imamura (1929) demonstrated that ovarian follicular fluid could inactivate tetanus toxin as well. It is now known that such fluid contains a high concentration of vitamin C.

Kligler et al. (1938) found that vitamin C added to growing cultures of tetanus bacteria reduced the toxicity of those cultures in proportion to the amount of vitamin C added. The authors also found that the vitamin C added to purified tetanus toxin neutralized the toxin/ with the degree of neutralization depending upon temperature, vitamin C concentration, and time of vitamin C exposure.

More recently, Eller et al. (1968) looked at the abilities of vitamin C to kill the spores of a number of different bacteria in the genus Clostridium, including the spores of the bacteria responsible for botulism and its enormous toxicity. The botulism bacteria are in the same genus as those of tetanus bacteria. Not only did the researchers demonstrate that vitamin C would kill the bacterial spores in a dose-dependent fashion, they also noted that vitamin C did not appear to provoke the toxin-releasing state of spore germination, which a large number of diverse compounds will induce (Wynne, 1957; Ward and Carroll, 1966).

The totality of the evidence would indicate that vitamin C is an ideal agent for the treatment of patients infected with the tetanus microbe. The t~tanus toxin appears to be neutralized by vitamin C in the body, in laboratory animals, and in the test tube.

A significant amount of the sickness related to a tetanus infection can come from antitoxin, one of its standard treatments.

Undoubtedly, fatal reactions to this antitoxin still occur, and some of these deaths end up being blamed on the tetanus toxin itself and not its antitoxin treatment. Fortunately, vitamin C does not share this toxicity. While the volume of evidence documenting a vitamin C cure for tetanus is limited, it would certainly appear that tetanus is another infectious / toxic disease that vitamin C can cure, reverse, and prevent. 

It should also be noted that the last three diseases addressed -- diphtheria, pertussis, and tetanus -- are the same three diseases targeted by the DPT (diphtheria-pertussis-tetanus) vaccinations routinely administered to infants in the United States and across the world. Many individual reports of adverse reactions to this vaccine have been reported, including encephalopathy with permanent brain damage and sometimes autism. Vaccinations also generally present some degree of toxin insult to the body. Kalokerinos (1981) observed that vitamin C-deficient Aboriginal infants were often pushed into an acute state of scurvy because of the additional vitamin C demands placed on their bodies by the vaccination injections, resulting in sudden death. Kalokerinos was also able to determine that regular administrations of vitamin C would prevent sudden death and eliminate many of the toxic effects associated with vaccination. The work of Kalokerinos argues strongly that sudden infant death syndrome (SillS) is often a complication of too many vaccinations given over too short a time and injected into bodies that are just too small to cope with the cumulative toxic insult. However, regardless of the actual frequency of such vaccination complications, it is important to keep in mind that the proper use of vitamin C would probably completely prevent any need (perceived or otherwise) to vaccinate against these diseases at all. It is doubtful that there are any diseases for which vaccinations are presently administered that will not be easily prevented and/or cured by the optimal dosing of vitamin C. No.negative outcomes following a vaccination will ever occur if no vaccination is ever given. However, if you must receive a vaccination, the toxicity is greatly lessened and the desired immune response definitely enhanced by giving generous doses of vitamin C before and after the vaccination. 

from:
THOMAS E. LEVY, MD, JD
p. 117
'CURING THE INCURABLE'