HEALTH E-BYTES,Issue No. 1,October, 2001


After reeling from the enormity of the terrorist attacks on the World Trade Center buildings in New York on September 11, most Americans who were finally regaining their composure were sent reeling again from the postal anthrax attacks. While nearly everyone insists they are continuing to live their lives without altering their daily schedules, a continual low-grade worry over the well-being of ourselves, families, and friends has imposed itself on many of our psyches.
The idea of an untreatable, killer epidemic sweeping across the nation is certainly frightening. However, I will attempt to show you that our treatment options might not be as bleak or limited as they might seem to be. Let�s first consider some of the known information about anthrax and smallpox, which are perhaps two of the most significant bioterrorism agents.

Anthrax is a bacterial disease that occurs primarily in one of four forms: cutaneous (skin), inhalation (lung), gastrointestinal, and oropharyngeal (mouth and throat). It is readily transmissible in a spore form that readily germinates into growing bacteria when a receptive host environment is encountered. So far the only two forms of this disease resulting from the postal attacks have been cutaneous and inhalation.
The cutaneous form of anthrax can occur on any exposed skin surface, progressing eventually to a blackened, ulcerated lesion. The blackened appearance of this lesion accounts for the name �anthrax,� which comes from the Greek word for coal. Untreated, it can result in death about 25% of the time. When treated with antibiotics death is rare.
Except in the context of a widespread bioterrorist attack, inhalation anthrax is extremely difficult to diagnose. The incubation period can range from 1 to 6 days, initially presenting with flu-like symptoms. The next phase of the disease can proceed very rapidly to death after lung symptoms present. Difficulty breathing, coughing up blood, chest pain, and profuse sweating are common symptoms at this point. The infection then proceeds to a blood poisoning that will further proceed rapidly to death even if antibiotic therapy is finally initiated. Although anthrax appears to be treatable by antibiotics in the early stages of the disease, the advanced inhalation form of this disease will typically not respond to such therapy, and death will result. An anthrax vaccine has been developed, but it is really only available to the military at this time. Furthermore, we are told that purified, antibiotic-resistant forms of anthrax for military use exist. Fortunately, such forms of anthrax do not yet appear to have been disseminated in any fashion.
Inhalation anthrax is especially deadly because of its rapid progression after the initial lung symptoms appear. This is largely due to the fact that anthrax is an infection that not only grows, but also produces potent toxins (Bhatnagar and Batra, 2001; Brossier and Mock, 2001; Mock and Fouet, 2001). In fact, the coughing up of blood is a reliable indicator that the toxins are being produced in critical amounts deep in the lungs. The antibiotic therapy for the anthrax organism has no effect on bacterial toxins that have already been produced. Antitoxin therapy, a treatment intended to neutralize a toxin, was tried in the past, but this therapy is not currently available. A good recent review of anthrax as a biological weapon was compiled by Inglesby et al. (1999).
Interestingly, the 21st edition of the Cecil Textbook of Medicine, copyright 2000, considers penicillin as the drug of choice for anthrax. Cipro (ciprofloxacin), which is currently being highly touted in the news, is listed along with a number of other antibiotics as being indicated primarily for the treatment of anthrax victims who are allergic to penicillin. However, ciprofloxacin and doxycycline are the antibiotics commonly recommended when there is a known or suspected exposure. More recently, doxycycline is being promoted as the oral prevention antibiotic of choice, in the hopes that any antibiotic-resistant microbes that eventually result might then be susceptible to ciprofloxacin.

Smallpox, a deadly viral disease, is also being mentioned as a leading candidate for another bioterrorist attack. The established therapy available for smallpox is to vaccinate before infection or fairly early after infection. Immune globulin therapy is also available to hopefully lessen the degree of infection and resulting illness. If these measures fail, supportive therapy is the only remaining traditional option. Either the patient�s immune system eventually wins, or the patient dies. Furthermore, the patients who are fortunate enough to survive face significant skin scarring after the characteristic skin lesions finally resolve.
Smallpox is considered a significant threat as it has a case-fatality rate of 30% or more among unvaccinated persons. Furthermore, since routine smallpox vaccination ceased in the United States more than 25 years ago, the degree of continuing protection from very old vaccinations against contracting smallpox now is less than clear. Some experts feel the protection is largely gone (Henderson et al., 1999).
The ability of smallpox to be a potent biological weapon was already demonstrated long ago. During the French and Indian Wars from 1754 to 1767 British forces in North America were able to initiate smallpox epidemics among the American Indians (Stearn and Stearn, 1945). Blankets used by smallpox victims eventually reached the Indians, and death rates exceeding 50% were seen after some of the tribes were successfully infected.
The smallpox patient is most infectious to others from the onset of the characteristic rash through the next 7 to 10 days (Mack, 1972; Mack et al., 1972). This rash is preceded by high fever and a symptom complex that could certainly be confused with the flu. Especially progressive smallpox infections can result in widespread hemorrhage and death within only 5 to 6 days of the onset of the rash.
Smallpox vaccinations are not without risk (Lane et al., 1969). Encephalitis (brain inflammation), severe skin rashes, and even a progressive, sometimes fatal, infection directly resulting from the inoculation can all occur. A non-toxic alternative to this vaccination would be highly desirable.
The current rareness of both anthrax and smallpox is highlighted by the fact that the 2001 edition of Conn�s Current Therapy does not even mention either of these diseases. Few physicians have any first-hand clinical experience in the treatment of these diseases.

Vitamin C, typically as ascorbic acid or sodium ascorbate, should prove to be highly effective against both of these conditions. I say �should� only because their rareness has prevented any single vitamin C researcher from encountering enough cases to conduct a meaningful study and publish it. However, the likelihood that both of these conditions could be completely cured, even in their advanced stages, is compelling. Consider the following information:

The medical literature has clear documentation that high enough doses of injectable vitamin C are almost always effective in curing any of a number of viral infections still considered today to be incurable. Klenner (1949) completely cured 60 out of 60 cases of infantile polio in North Carolina in the middle of a polio epidemic. Several infants already had neurological involvement, but nevertheless recovered completely. Klenner (1951) was also able to bring about a complete recovery by administering enough vitamin C to one five year-old polio victim who had already been paralyzed in both legs for over four days. Klenner (1949, 1953, 1971, and 1974) also reported the repeated ability to rapidly cure viral diseases such as encephalitis (often presenting in the comatose state), herpes infections, acute hepatitis, measles, and mumps. Klenner found that his only inadequate responses to treatment were overcome by increasing the vitamin C dose and/or going from an oral to an injectable form of vitamin C. Cathcart (1981) also reported an incredible success in the treatment of many viral diseases for which no specific anti-viral agents exist today. Of particular interest, he reported that he never had a case of viral hepatitis fail to respond to intravenous vitamin C. Furthermore, he never observed a single case of acute hepatitis treated appropriately with vitamin C to persist long enough to evolve to the status of chronic hepatitis. Finally, although no specific studies looking at the effects of vitamin C on smallpox could be found, Kligler and Bernkopf (1937) were able to determine that relatively small doses of vitamin C could easily kill the vaccinia virus, which is the virus in the vaccine that induces immunity to smallpox.
Vitamin C has also been documented to rapidly resolve a number of non-viral infectious diseases that do not readily resolve in the absence of vitamin C therapy. Diptheria (Klenner, 1949 and 1971), whooping cough (Otani, 1936 and 1939; Ormerod et al., 1937), and tetanus (Klenner, 1954) all have responded very well to vitamin C. Of great interest as well is that all three of these infections are associated with very significant microbe-generated toxins, much like anthrax. Jungeblut and Zwemer (1935) found that vitamin C both inactivated diphtheria toxin in the test tube and protected guinea pigs against the fatal outcome of being injected with otherwise fatal doses of diphtheria toxin. Dey (1966) showed that enough injected vitamin C would completely protect rats from otherwise fatal doses of tetanus toxin.
Klenner never encountered a virus he could not cure, although he used doses of vitamin C that are considered outrageously high today, even though such doses are nevertheless decidedly non-toxic. His initial dosing of vitamin C would go as high as 700 mg/kg body weight, which could exceed 70 grams for a large man. Furthermore, he would repeat this high dosing in only a few hours if no drop in fever or clear clinical improvement resulted. He never reported any toxicity from vitamin C dosed in this fashion. However, he repeatedly reported that initially unresponsive patients did finally respond when enough vitamin C was administered frequently enough. From the very current scientific literature we know that 60 grams of vitamin C can be repeatedly infused without toxicity over only an 80-minute period. Furthermore, 50-gram intravenous doses of vitamin C can be given daily for 8 weeks without any side effects other than improved health (Casciari et al., 2001).
My own clinical experiences with intravenous vitamin C infusions allow me to completely believe all of the data that Klenner and others have accumulated. Many feel vitamin C did not deliver as promised when Linus Pauling�s recommendations of a few grams of vitamin C a day did not end up curing or completely preventing the common cold. To be sure, it did make those infected feel better, and it shortened the durations of their symptoms. It did also lessen the likelihood of getting a cold. Once entrenched in the body, however, the common cold results in a very high titer of virus particles. A few grams of vitamin C will help the immune system cope, but it is not remotely enough to promptly eradicate the virus load present. However, several hundred grams of vitamin C intravenously daily for 2 to 3 days can be expected to knock out the common cold in most people. The next time you have already been sick with a cold for a few weeks, you will appreciate what a remarkable clinical response this is.
After determining your best daily dose of vitamin C by following the bowel tolerance method outlined by Cathcart (1981) and after taking that daily dose regularly, the likelihood of contracting any infectious disease, anthrax and smallpox included, is remote. For many people, this will translate to a total daily dose of vitamin C of 8 to 15 grams taken in divided doses, although some people will require more. The recommended form of vitamin C would be sodium ascorbate, although ascorbic acid would be perfectly acceptable. I do not recommend high doses of calcium ascorbate.
If you are exposed to a very high dose of infectious organisms, the maintenance doses of vitamin C noted above can be overwhelmed and clinical infection can still result. The simple answer then is to start vitamin C infusions at up to 700 mg/kg at a time as often as is necessary to obtain a positive clinical response. Lesser amounts and less frequent dosing can be used if the clinical picture is not severe. Obviously, the administration would have to be very vigorous in an inhalation anthrax patient who has already developed lung symptoms and death may be only hours to a day or two away. Certainly, in the case of anthrax, there is no reason not to take all prescribed antibiotics as well, but the antibiotics will have little effect if large amounts of anthrax toxin have already been produced. The vitamin C would be essential at that point. In viral diseases where bleeding complications occur, the bleeding will often occur at those sites in the body where vitamin C levels are lowest, or even nonexistent. It is absolutely characteristic for such �focal� sites of scurvy to hemorrhage, and nothing short of very large doses of vitamin C given very quickly can be expected to save the patient at that point.
Regardless of any skepticism that the reader may have toward such high-dose vitamin C therapy, it is absolutely unthinkable not to try it or add it to whatever protocol is being administered to the patient. At the very least, all acute infectious diseases rapidly metabolize vitamin C, and all acutely ill patients are consequently deficient in vitamin C. The administration of vitamin C should always be undertaken when acute vitamin C deficiency is a certainty, even if one does not believe that enough vitamin C can be a definitive therapy by itself.
Hydration is also extremely important, both in health and disease. Furthermore, vigorous hydration (2 to 4 quarts of water daily) will augment the effectiveness of the vitamin C therapy. Just about the only time high doses of vitamin C can cause problems is if the patient is not kept very well hydrated. Remember that patients with high fever lose body water rapidly. Most other medicines have more side effects in the face of dehydration as well.
There are many other supplements and nutrients that can augment the anti-microbial effects and immune-bolstering effects of vitamin C, which is beyond the scope of this issue of the newsletter. Just don�t neglect the most important one: vitamin C.


Bhatnagar, R. and S. Batra. (2001) Anthrax toxin. Critical
Reviews in Microbiology 27(3):167-200.

Brossier, F. and M. Mock. (2001) Toxins of bacillus
anthracis. Toxicon: Official Journal of the
International Society on Toxinology 39(11):1747-1755.

Casciari, J., N. Riordan, T. Schmidt, X. Meng, J. Jackson,
and H. Riordan. (2001) Cytotoxicity of ascorbate,
lipoic acid, and other antioxidants in hollow fibre in
vitro tumours. British Journal of Cancer 84(11):1544-

Cathcart, R. (1981) Vitamin C, titrating to bowel
tolerance, anascorbemia, and acute induced scurvy.
Medical Hypotheses 7(11):1359-1376.

Dey, P. (1966) Efficacy of vitamin C in counteracting
tetanus toxicity. Naturwissenschaften 53(12):310.

Henderson, D., T. Inglesby, J. Bartlett, M. Ascher, E.
Eitzen, P. Jahrling, J. Hauer, M. Layton, J. McDade,
M. Osterholm, T. O�Toole, G. Parker, T. Perl, P.
Russell, and K. Tonat. (1999) Smallpox as a biological
weapon. Medical and public health management. The
Journal of the American Medical Association

Inglesby, T., D. Henderson, J. Bartlett, M. Ascher, E.
Eitzen, A. Friedlander, J. Hauer, J. McDade, M.
Osterholm, T. O�Toole, G. Parker, T. Perl, P. Russell,
and K. Tonat. (1999) Anthrax as a biological weapon.
Medical and public health management. The Journal of
the American Medical Association 281(18):1735-1745.

Jungeblut, C. and R. Zwemer. (1935) Inactivation of
diphtheria toxin in vivo and in vitro by crystalline
vitamin C (ascorbic acid). Proceedings of the Society
for Experimental Biology and Medicine 32:1229-1234.

Klenner, F. (1949) The treatment of poliomyelitis and other
virus diseases with vitamin C. Southern Medicine &
Surgery 111(7):209-214.

Klenner, F. (1951) Massive doses of vitamin C and the virus
diseases. Southern Medicine & Surgery 103(4):101-107.

Klenner, F. (1953) The use of vitamin C as an antibiotic.
Journal of Applied Nutrition 6:274-278.

Klenner, F. (1954) Recent discoveries in the treatment of
lockjaw with vitamin C and Tolserol. Tri-State Medical
Journal pp. 7-11.

Klenner, F. (1971) Observations on the dose and
administration of ascorbic acid when employed beyond
the range of a vitamin in human pathology. Journal of
Applied Nutrition 23(3&4):61-88.

Klenner, F. (1974) Significance of high daily intake of
ascorbic acid in preventive medicine. Journal of the
International Academy of Preventive Medicine 1(1):45-

Kligler, I. and H. Bernkopf. (1937) Inactivation of
vaccinia virus by ascorbic acid and glutathione.
Nature 139:965-966.

Lane, J., F. Ruben, J. Neff, and J. Millar. (1969)
Complications of smallpox vaccination, 1968. National
surveillance in the United States. The New England
Journal of Medicine 281(22):1201-1208.

Mack, T. (1972) Smallpox in Europe, 1950-1971. The Journal
of Infectious Diseases 125(2):161-169.

Mack, T., D. Thomas, and M. Muzaffar Khan. (1972)
Epidemiology of smallpox in West Pakistan. II.
Determinants of intravillage spread other than
acquired immunity. American Journal of Epidemiology

Mock, M. and A Fouet. (2001) Anthrax. Annual Review of
Microbiology 55:647-671.

Ormerod, M., B. Unkauf, and F. White. (1937) A further
report on the ascorbic acid treatment of whooping
cough. Canadian Medical Association Journal 37(3):268-

Otani, T. (1936) On the vitamin C therapy of pertussis.
Klinische Wochenschrift 15(51):1884-1885.

Otani, T. (1939) Influence of vitamin C (L-ascorbic acid)
upon the whooping cough bacillus and its toxin.
Oriental Journal of Diseases of Infants 25:1-4.

Stearn, E. and A. Stearn. (1945) The Effect of Smallpox on
the Destiny of the Amerindian. Boston, MS: Bruce

Copyright 2001 by Thomas E. Levy, M.D., J.D.
All Rights Reserved

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HEALTH E-BYTES, Issue No. 2, November, 2001 by Tom Levy M.D.


This second issue of "Health E-Bytes" is intended to not only discuss potential modalities of future bioterrorism attacks, but also to reiterate the enormous benefit that optimally dosed intravenous and oral vitamin C would offer such infected or poisoned individuals. I have already had individuals ask me how they could get intravenous vitamin C for themselves and their families in the event of a sudden toxin and/or infectious exposure. The answer at this point in time, unfortunately, is that it would be difficult for many to get treated in this fashion and impossible for everyone to get treated in this fashion. That is why I am making the effort to publish this newsletter. Wonderful information that never gets widely disseminated is of little or no substantive value for the general population.
With these thoughts in mind, then, I urge all readers of this newsletter to forward it not only to friends, but also to as many members of the professional health community as possible. Even though 95 out of 100 doctors might just chuckle when they read these newsletters, perhaps the other 5 will be open-minded enough to seriously and scientifically evaluate what is being said. Any doctor who examines the original literature citations on the information that I am presenting can only conclude that vitamin C is as amazing as I say it is, or they can conclude that many different clinicians and primary researchers are simply lying in order to accumulate scientific publications for their resumes. If even one doctor eventually realizes the practical impact of this information and starts treating patients with critical infectious diseases with proper doses of vitamin C, a very significant impact will eventually be made on many patients. One practicing physician impacts the health and lives of many people.
And what does Dr. Levy get from all of this? For my more cynical readers, I may eventually sell a few more of my books, and I may eventually get more readers to visit my website and other linked websites. However, my primary purpose is to get long-overlooked and long-ignored information its proper recognition. I want to see sick patients in need of treatment get the best treatment available. That's all.

A few more potential bioweapons will now be discussed. There are actually very many more bioweapons than these that could end up being used, but the following three agents have been considered prime candidates for bioterrorists for some time now. These agents, plague, tularemia, and botulinum toxin, will be separately discussed and analyzed.

Human plague is caused by a type of bacteria known as Yersinia pestis. Humans usually contract this disease when bitten by plague-infected fleas. It has been noted in the past that epidemics of this disease in humans were often preceded by the death of large numbers of rats, further forcing fleas to leave their preferred rodent hosts and seek out humans (Inglesby et al., 2000).
Clinically, plague can present in three different forms: bubonic, septicemic, and pneumonic. Most naturally occurring cases are bubonic. This form of infection has an incubation period of 2 to 6 days. The clinical onset of symptoms is characteristically abrupt, with a sudden onset of headache, muscle and joint aches, fever, and chills. Often only hours later, swollen, tender lymph nodes will appear in the neck, armpit, and groin areas, indicating a rapid progression of the disease through the body. These swollen lymph nodes are known as buboes, giving rise to the name bubonic. When this form of the plague goes untreated, more than 50% of those infected will die.
Septicemic plague is almost uniformly fatal when left untreated. This form of plague involves a large amount of infection in the bloodstream. Bubonic plague can sometimes lead to septicemic or even pneumonic plague. Those patients who progress rapidly to a septicemic form of plague probably have weaker or more compromised immune systems, which facilitates the rapid spread of the disease in the blood.
Pneumonic plague, somewhat like inhalation anthrax, requires early and aggressive treatment to avert a fatal outcome. Furthermore, unlike bubonic or even septicemic plague patients, pneumonic plague is readily catagious (Ratsitorahina et al., 2000).
If used in the future as a bioweapon, the plague will not be spread by large numbers of infected fleas. Rather, the spread would be most probably achieved by inhalation of an aerosol form of Y. pestis microorganisms, which would result immediately in a large number of people getting the pneumonic form of the plague. Furthermore, this would greatly accelerate the transmission of the disease among susceptible populations of people, in contrast to the amount of transmission that would occur if the plague infection presented in the bubonic form.
Early diagnosis would be critically important for the survival of individuals exposed to an inhalation form of plague. Until the first case was confirmed in the laboratory, patients would be considered to have gotten a very aggressive form of pneumonia. Broad spectrum antibiotic therapy would save some if instituted soon enough. The antibiotics that have been most effective in treating the plague include streptomycin, gentamicin, doxycycline, tetracycline, and chloramphenicol. The antibiotics commonly used for infection prevention after known exposure are tetracycline, doxycycline, and trimethoprim-sulfamethoxazole (Conn's Current Therapy 2001).
A vaccine is no longer available for the plague. Furthermore, the vaccine that had been developed only showed benefit against the bubonic form of plague. It did not appear to prevent or lessen the consequences of the pneumonic form of plague (Speck and Wolochow, 1957).
For the same reasons discussed in the first issue of "Health E-Bytes," vitamin C would be an excellent adjunct therapy for the plague. Both oral and intravenous administrations of vitamin C would result in a significant bolstering of the immune system. While a high enough dose of vitamin C could logically be completely effective as a monotherapy treatment for the plague, there is certainly no reason not to take both the appropriate antibiotics along with the vitamin C. Furthermore, since no specific reference could be found in the literature on vitamin C and plague, it would be inappropriate to try to treat the plague with only vitamin C, even though it's effect on other bacterial diseases would predict a high likelihood of complete clinical success in the treatment of plague.

Tularemia is a disease caused by a type of bacteria known as Francisella tularensis. Although not one of the potential bioweapons that is familiar to many people, the transmissibility of tularemia could make it especially effective as a bioweapon. F. tularensis is one of the most infectious of disease-causing bacteria, and the inhalation of as few as 10 organisms has been known to cause disease (Saslaw et al., 1961).
The inhalation form of tularemia, which would be the type of tularemia likely seen in a bioterrorist attack, tends to present abruptly, with fever, chills, body aches, runny nose, and sore throat. Cough with chest discomfort and other signs of pneumonia can then appear (Pullen and Stuart, 1945). Left untreated, one third or more of patients with pneumonic tularemia can be expected to die (Stuart and Pullen, 1945). Properly treated, however, less than 2% of patients should die (Evans et al., 1985).
Vaccination for tularemia is presently not advised except for laboratory personnel who are routinely working with F. tularensis bacteria (Dennis et al., 2001). A wide variety of antibiotics are available to effectively treat this disease at this time. However, laboratory manipulation has been demonstrated to produce strains of tularemic bacteria that are resistant to some of the commonly used antibiotics (Overholt et al., 1961; Pavlov et al., 1996). This raises the unsettling possibility that tularemic bacteria prepared specifically for biowarfare may not be as readily killed with antibiotics as the bacteria found in the naturally occurring disease. To be sure, take all recommended antibiotics for any tularemic infection, but don't neglect to add the vitamin C as previously discussed. In reviewing the scientific literature, I could find no cases of infectious disease that were shown to be initially susceptible to vitamin C, only to later develop a resistance to vitamin C. This development of resistant strains of bacteria appears to occur only when man-made antimicrobial drugs are used for a long enough period of time.

Botulinum toxin should probably result in more fear and anxiety over its possible use as a bioweapon than just about any other agent. This is because it is extremely potent and capable of killing easily. Furthermore, it is a refined toxin; there is no infection to be attacked.
Botulinum toxin is presently considered to be the most poisonous substance known (Gill, 1982). Although it would be very difficult to accomplish technically, there is enough potency in one gram of botulinum toxin to kill over one million people if properly dispersed (Arnon et al., 2001).
Botulinum toxin is produced by the metabolism of the bacterial species known as Clostridium botulinum. Although only a very small dose of this toxin can be fatal when swallowed, a roughly 100-fold smaller dose can be expected to be fatal if inhaled.
The symptoms of botulism are those of a progressive paralysis starting in the muscles of head and neck, proceeding eventually to weakness of the other muscles in the body, including the arms and legs. Death results from respiratory insufficiency from either the relaxation of the throat musculature blocking air entry into the lungs, or from inadequate air movement by the weakened respiratory muscles surrounding and supporting the chest cavity.
The treatment of botulism, aside from supportive care, involves an antitoxin that immunologically neutralizes the botulinum toxin. However, an early clinical diagnosis and prompt treatment are essential to save the exposed patient.
Vitamin C is just as useful for the treatment of a pure toxin as it is for the treatment of an infectious disease. Jahan et al. (1984) and Dey (1966) both showed that vitamin C could effectively neutralize tetanus toxin. Tetanus toxin is also produced by a Clostridium species of bacteria, like botulinum toxin. Klenner (1974) reported curing a four year-old receiving a "full strike" from a highly poisonous moccasin snake. Klenner (1957) also reported the complete clinical neutralization of the toxin associated with a black widow spider bite. Calabrese (1985) reported on the effects of vitamin C on a group of 24 pesticides, heavy metals, hydrocarbons, and gaseous pollutants, noting that vitamin C reduced the toxicity of the vast majority of these agents. It should also be noted that these were predominantly diverse, rather than similar, agents.
Vitamin C has also been seen to neutralize the toxicity of a number of different bacterial toxins produced in the anaerobic environment of deep dental infections. When tested against specific critical enzymes, many of these toxins were substantially more toxic than botulinum toxin. Nevertheless, patients who were clinically ill from the effects of this group of toxins invariably showed dramatic improvement from the infusion of enough vitamin C.
Regardless of the mechanism, which is probably not singular in nature anyway, vitamin C should be the agent of choice for all acute poisonings. In many cases, the ascorbate ion in vitamin C directly neutralizes the toxin. In other cases, the vitamin C improves immune function enough to help negate the toxic effect through immune mechanisms. Remember that an acute infusion of vitamin C is virtually harmless. Klenner typically started a vitamin C infusion in his office on all of his sick patients even before he made a diagnosis. He never hurt anyone with this practice, and he helped very many. In any case of suspected poisoning, start high-dose intravenous vitamin C with vigorous hydration immediately, and then proceed with a diagnostic workup so that specific antibiotics and/or specific antitoxin therapies can later be added to the treatment. In an acutely poisoned and/or infected patient, there is no good reason not to proceed with the vitamin C infusion immediately, as all poisonings and infections rapidly metabolize what vitamin C is present in the body, making an acutely-induced scurvy-like state part of the clinical presentation. Any scurvy-like state requires vitamin C to be resolved, and such a state will make any existing infection or toxic medical condition worse and more difficult to treat effectively.


Arnon, S., R. Schechter, T. Inglesby, D. Henderson, J.
Bartlett, M. Ascher, E. Eitzen, A. Fine, J. Hauer, M.
Layton, S. Lillibridge, M. Osterholm, T. O'Toole, G.
Parker, T. Perl, P. Russell, D. Swerdlow, and K.
Tonat. (2001) Botulinum toxin as a biological weapon.
Medical and public health management. The Journal of
the American Medical Association 285(8):1059-1070.

Calabrese, E. (1985) Does exposure to environmental
pollutants increase the need for vitamin C? Journal of
Environmental Pathology, Toxicology and Oncology

Conn's Current Therapy 2001. (2001) Edited by Rakel, R. and
E. Bope, Philadelphia, PA: W.B. Saunders Company.

Dennis, D., T. Inglesby, D. Henderson, J. Bartlett, M.
Ascher, E. Eitzen, A. Fine, A. Friedlander, J. Hauer,
M. Layton, S. Lillibridge, J. McDade, M. Osterholm, T.
O'Toole, G. Parker, T. Perl, P. Russell, and K. Tonat.
(2001) Tularemia as a biological weapon. Medical and
public health management. The Journal of the American
Medical Association 285(21):2763-2773.

Dey, P. (1966) Efficacy of vitamin C in counteracting
tetanus toxicity. Naturwissenschaften 53(12):310.

Evans, M., D. Gregory, W. Schaffner, and Z. McGee. (1985)
Tularemia: a 30-year experience with 88 cases.
Medicine 64(4):251-269.

Gill, M. (1982) Bacterial toxins: a table of lethal
amounts. Microbiological Reviews 46(1):86-94.

Inglesby, T., D. Dennis, D. Henderson, J. Bartlett, M.
Ascher, E. Eitzen, A. Fine, A. Friedlander, J. Hauer,
J. Koerner, M. Layton, J. McDade, M. Osterholm, T.
O'Toole, G. Parker, T. Perl, P. Russell, M. Schoch-
Spana, and K. Tonat. (2000) Plague as a biological
weapon. Medical and public health management. The
Journal of the American Medical Association

Jahan, K., K. Ahmad, and M. Ali. (1984) Effect of ascorbic
acid in the treatment of tetanus. Bangladesh Medical
Research Council Bulletin 10(1):24-28.

Klenner, F. (1957) The black widow spider: case history.
Tri-State Medical Journal pp. 15-18.

Klenner, F. (1974) Significance of high daily intake of
ascorbic acid in preventive medicine. Journal of the
International Academy of Preventive Medicine 1(1):45-

Overholt, E., W. Tigertt, P. Kadull, et al. (1961) An
analysis of forty-two cases of laboratory-acquired
tularemia. The American Journal of Medicine 30:785-

Pavlov, V., A. Mokrievich, and K. Volkovoy. (1996) Cryptic
plasmid pFNL10 from Francisella novicida-like F6168:
the base of plasmid vectors for Francisella
tularensis. FEMS Immunology and Medical Microbiology

Pullen, R. and B. Stuart. (1945) Tularemia: analysis of 225
cases. The Journal of the American Medical Association

Ratsitorahina, M., S. Chanteau, L. Rahalison, L.
Ratsifasoamanana, and P. Boisier. (2000)
Epidemiological and diagnostic aspects of the outbreak
of pneumonic plague in Madagascar. Lancet

Saslaw, S., H. Eigelsbach, J. Prior, H. Wilson, and S.
Carhart. (1961) Tularemia vaccine study. II.
Respiratory challenge. Archives of Internal Medicine

Speck, R. and H. Wolochow. (1957) Studies on the
experimental epidemiology of respiratory infections:
experimental pneumonic plague in Macaccus rhesus. The
Journal of Infectious Diseases 100:58-69.

Stuart, B. and R. Pullen. (1945) Tularemic pneumonia:
review of American literature and report of 15
additional cases. The American Journal of the Medical
Sciences 210:223-236.

Copyright 2001 by Thomas E. Levy, M.D., J.D.
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