Klenner Published How to Cure Polio in 1949

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Misty L. Trepke

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Klenner Published How to Cure Polio in 1949.

 

This shows Vitamin C as a broad spectrum Anti Viral in 1949.

To bad that it was suppressed.

 

Dr.Klenner treated 1000's of patients successfully with Vitamin C.

 

Frank

 

 

The Origin of the 53-Year Stonewall of Vitamin C.1949 — a year in

medicine which will live in infamy..Klenner Published How to Cure

Polio in 1949.

 

http://www.orthomed.com/polio.htm

 

 

July, 1949 SOUTHERN MEDICINE & SURGERY 209

 

The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin

C

 

Fred R. Klenner, M.D., Reidsville, North Carolina

 

IN A PREVIOUS REPORT dealing with the antagonistic properties of

ascorbic acid to the virus of atypical pneumonia, mention was made

of the fact that other types of virus infections had responded

favorably to vitamin C. This paper is to present these findings as

well as the results of subsequent studies on the virus of

poliomyelitis, the viruses causing measles, mumps, chickenpox,

herpes zoster, herpes simplex and influenza. Further studies with

the virus of atypical pneumonia will also be discussed.

 

These observations of the action of ascorbic acid on virus diseases

were made independently of any knowledge of previous studies using

vitamin C on virus pathology, except for the negative report of

Sabin after treating Rhesus monkeys experimentally infected with the

poliomyelitis virus. A review of the literature in preparation of

this paper, however, presented an almost unbelievable record of such

studies. The years of labor in animal experimentation, the cost in

human effort and in " grants, " and the volumes written, make it

difficult to understand how so many investigators could have failed

in comprehending the one thing that would have given positive

results a decade ago. This one thing was the size of the dose of

vitamin C employed and the frequency of its administration. In all

fairness it must be said that Jungeblut noted on several occasions

that he attributed his failure of results to the possibility that

the strength of his injectable " C " was inadequate. It was he who

unequivocally said that ''vitamin C can truthfully be designated as

the antitoxic and antiviral vitamin. "

 

In developing this paper it was felt that, since all virus

infections were more or less akin, only one of this family would be

considered in detail. Poliomyelitis, because of its prevalence and

the seriousness of the problem it presents, was chosen as the

disease to be so treated.

 

Poliomyelitis is in most instances an acute febrile disease of

sudden onset, with symptoms of a systemic infection which either

abruptly abort or develop to hyperesthesia, asymmetry of reflexes

and flaccid paralysis or palsies of muscle groups. It affects

individuals of all ages, but mainly children, as do more common

childhood diseases to which class it most likely belongs. Only

slight contact between the carrier of the virus and the susceptible

person suffices in some cases for the transfer of the causative

organism. In this respect and also in that the virus can be

demonstrated in the nasal washings as early as six days before onset

of symptoms, poliomyelitis resembles measles. We never have an

epidemic of poliomyelitis preceding an epidemic of measles; the

opposite is frequently true. This grouping of the virus organisms is

too often repeated not .to carry some significance. For example,

atypical pneumonia and influenza are caused by closely allied

viruses; so are chickenpox, herpes zoster and herpes simplex; so are

measles, mumps and poliomyelitis. The incubation period depends on

the mode of entry. In experimental animals. Fraser and others showed

that the average was 6.6 days with intracerebral inoculation and ten

days when the intravenous route was used. Howitt mentions that the

virus reaches the nervous system sooner after intranasal than after

intravenous instillations. Transmission (Brodie, 1934) is by means

of droplets from the mucous membrane of the upper respiratory tract.

Infection by means of raw milk, human feces and house flies is

highly improbable.

 

The research of Flexner, Dark and Amoss in 1914 proved that

poliomyelitis is a disease of the entire nervous system, that the

sensory ganglia are the seats of early and profound histological

changes. The disease is significant mainly for the paralysis

produced through injury to the motor neurons of the spinal cord and

brain. This is caused by a special affinity of the virus for a

certain type of nerve tissue. Experiments show the cerebral cortex

to be the most unsatisfactory site for growth, that large amounts of

the virus placed in this area are apt to disappear in a short time.

Observations in monkeys and in man show that the anterior horn

cells, particularly those of the lumbar cord, are the most favorable

sites for proliferation of the virus.

 

In all clinically ill patients the virus eventually travels in the

course of its invasion by several channels. The virus can make a

direct assault through the olfactory bulb, to the brain, medulla and

spinal cord. The virus can enter the blood stream directly or

through the lymph channels. Following damage to the natural

protective barrier, the choroid plexus, it can make its way to the

central nervous system, or it can be excreted back onto the nasal

mucous membrane where it will pick up the direct route of the

olfactory bulb.

 

Clark, Turner and Reynolds (1926, 1927, 1929) concluded that the

virus chiefly travels by the direct route to the brain. Lennette and

Hudson ( 1935) confirmed this theory and reported their studies

indicating that human infection is chiefly through the nasopharynx.

Brodi and others showed that by section of the olfactory tracts in

monkeys infection by the direct route was prevented. It is of more

than mere academic interest that while the nasal mucosa of the

monkey contains branches of the 5th and 7th cranial nerves and that

in addition, since the virus can readily gravitate from the

nasopharynx to the tonsil bed with its nerve supply, if the

olfactory tracts are cut no infection will occur. The most likely

explanation is that the olfactory is non-medullated, the neurons lie

in the nasal mucosa and are thus exposed to the virus. The sciatic

nerve (Brodi) will transport the virus only when it has been

injured, suggesting that lack of myelin may render the healthy

olfactory nerve vulnerable to the virus.

 

The most important of the secondary routes of infection is by the

excretion of the virus from the blood stream onto the nasal mucosa.

Lennette and Hudson (1934, 1935) demonstrated in monkeys that by

sectioning the olfactory tracts and then inoculating by the

intravenous route with the virus of poliomyelitis, they could

prevent infection.

 

This would fit in with the work of Jungeblut and others that the

spread of the virus through the central nervous system is along

nerve tracts, rather than by means of the cerebrospinal fluid, the

infection to become manifest when the first cell group is reached,

and by relays of fibers, reaches the mid-brain. Here numerous fiber-

paths run in all directions and the virus is carried by both motor

and sensory axons, causing disease at many levels of the brain and

cord.

 

Since there is always a period of septicemia in the first few days

of poliomyelitis, it might be that this is the all-important route

and that the virus is grown on a living tissue, the blood, and then

is deposited out on the surface of the olfactory bulb. From this we

conclude that the time to destroy the virus is during this

incubation period which varies more with virulence and power of

multiplication than with size of initial dose.

 

The second flanking maneuver of importance is through the choroid

plexus. It is the function of the choroid plexus and the pial

lymphatic vessels to exclude the virus present in the blood from the

nervous system. Once these protective structures are injured,

however, the exclusion ceases and infection can follow readily.

Changes in the structure or function of the meningeal choroid plexus

complex, too slight to be detected in the cerebrospinal fluid or as

morphological alterations, materially diminish its protective power.

Flexner and Amoss injected large doses of the virus intravenously,

then tested the cerebrospinal fluid and found no virus after the

first 48 hours; virus in small amounts at the end of 72 hours; after

96 hours evidence of free access to this system. The virus was still

present 19 days later when paralysis was beginning.

 

Poliomyelitis in man is always more severe if exercise is taken at

time of the infection. Here one must consider the factor of

filtration of the virus through the choroid plexus as being

increased due to the elevation of the vascular bed pressure. Also,

that, by the acceleration of the blood flow caused by greater oxygen

demand in physical effort, a marked increase in the percentage of

the virus deposited on the nasal mucosa would result.

 

We must agree with Fairbrother and Hurst that too little

consideration has been given to the pathology of the nervous system

and in particular to the drainage of the tissue fluids. These men

confirmed the earlier work of Schroder, who stressed that the normal

flow of these fluids is along the perivascular spaces from the

center of the cord outward, and that any inflammatory exudate

occupying these spaces must be swept into the pial meshes; further

that meningeal infiltration may seem nothing more than a drainage of

cells from the interior of the cord. Fairbrother and Hurst found

that meningeal infiltration does not occur in monkeys until the

perivascular infiltration beginning in the deeper vessels reaches

the surface.

 

The presence of the filterable microorganism or virus of

poliomyelitis upon the mucous membrane of the nose and throat does

not necessarily lead to infection. It may give rise to a class of

healthy carriers who are themselves immune. Amoss and Taylor found a

secretion of the mucous membrane capable of neutralizing or

inactivating the virus, this property absent altogether from the

secretions of some persons, in those of others present at one time

and not at another. It is probable that in actively immune animals

the passage of the neutralizing substance from the blood into the

cerebrospinal fluid would continue as long as the inflammation

present in the meninges rendered the structures easily permeable to

the protein constituents of the blood. This secretion X could not

have the properties of a true antibody. The virus of poliomyelitis

is intracellular from the time it invades the terminal cells of the

olfactory system until the end of the disease, except when crossing

the synaptic junctions between cells. This explains why the virus

cannot be neutralized by antibodies in the serum. Further protection

is afforded the virus by the functional barrier between the

circulating blood and the central nervous system.

 

Since immunization against poliomyelitis comparable to that against

other bacterial diseases is still a matter of the future, it

suggested itself that some antibiotic could be found that would

destroy this scourge while in the phase of blood-stream invasion.

Sabin's negative report on the value of ascorbic acid on the

poliomyelitis virus stopped Jungeblut's work, but we were cognizant

of its dramatic effect on the virus causing atypical pneumonia, and

so kept up hope. These results were so consistently positive that we

did not hesitate to try its effectiveness against all type of virus

infections. The frequent administration of massive doses of vitamin

C was so encouraging in the early days of the 1948 epidemic of

poliomyelitis that a review of the literature was begun. Heaslip, in

the Australian Journal of Experimental Biology & Medicine reported a

mean urinary output of vitamin C under a load test of 19.9 per cent

in 60 poliomyelitis cases, as contrasted with a mean figure of 44.3

per cent in 45 healthy contacts. This was suggestive of some

relationship between the degree of vitamin C saturation and the

infectious and non-infectious state. He was also able to show a

correlation between the severity of the attack and the level of

urinary excretion of the vitamin. This would indicate that a

deficiency of vitamin C in the diet predisposed to infection and to

severity of attack. Sabin reported no appreciable difference in

infectivity of poliomyelitis in monkeys with much or no vitamin C in

the diet. Many others, however, have reported that a " deficient

vitamin C nutrition increases susceptibility to infection, " and many

others that animals dying from the effects of the poliomyelitis

virus show a reduction of vitamin C in the tissues. Heaslip found a

definite relationship between the severity of the infection and the

level of vitamin C nutrition. It is consistent with accepted

physiological action of vitamin C to expect and anti-edema effect in

any given affected area. It is worthy of note that bacterial toxins

can cause losses of from 50 to 85 per cent of the vitamin C normally

contained in the adrenals. Jungeblut's investigations seemed to

justify the conclusion that vitamin C was the " antibiotic " that

would destroy the virus organism. He stated that the prophylactic

and therapeutic administration of synthetic or natural vitamin C had

given evidence of having distinct therapeutic properties in

experimental poliomyelitis, and that the proper injection dose was

directly proportional to the speed of the infection and the stage at

which the process had arrived. Jungeblut stated in 1937 that the

parental administration of natural vitamin C during its incubation

period of poliomyelitis in monkeys is always followed by a distinct

change in the severity of the disease; that after the fifth day of

the disease distinctly larger doses are required. He realized, at

that early date, that for a fast progressing infection such as

results from the R. M. V. strain, very large doses—400 mg.

crystalline C maximum in a 24-hour period—of vitamin C would be

required; for the Aycock virus with its slower infection potential

small amounts of the vitamin would suffice. Even with almost

infinitesimal amounts—100 mg. ascorbic acid for each 24-hour period—

he was able to demonstrate that the non-paralytic survivors in one

series was six times as great as in the controls. In our work we

shall speak of six, ten and 20 thousand mg. in a similar time period.

 

Harde et al. reported that diphtheria toxin is inactivated by

vitamin C in vitro and to a lesser extent in vivo. I have confirmed

this finding, indeed extended it. Diphtheria can be cured in man by

the administration of massive frequent doses of hexuronic acid

(vitamin C) given intravenously and/or intramuscularly. To the

synthetic drug, by mouth, there is little response, even when 1000

to 2000 mg. is used every two hours. This cure in diphtheria is

brought about in half the time required to remove the membrane and

give negative smears by antitoxin. This membrane is removed by lysis

when " C " is given, rather than by sloughing as results with the use

of the antitoxin. An advantage of this form of therapy is that the

danger of serum reaction is eliminated. The only disadvantage of the

ascorbic acid therapy is the inconvenience of the multiple

injections. This concept of the action of vitamin C against certain

toxins has led to treating other diseases producing exotoxins. For

years it has been our knowledge that vitamin C in 500 to 1000 mg.

doses injected I. M. would cure bacillary dysentery of the Shiga

type. Children having 10 to 15 bloody stools per day have cleared in

48 hours under this schedule while at the same time reverting to

normal feedings. This dual action of vitamin C against certain

toxins and the virus organism becomes more intelligible with the

work of Kligler, Warburg and others who believed that the

detoxification effected by hexuronic acid is brought about by a

direct combination of the vitamin with the toxin or virus, this

followed by oxidation of the new compound which destroys both the

virus or toxin and the vitamin. Borsook et al. decided that the main

chemical action of ascorbic acid is as a powerful reducing agent,

and the virus causing poliomyelitis is known to be susceptible to

the oxidizing action of various agents. It is in point here to

remark that vitamin C is an integral part of the oxidation-reduction

system of the body, thus playing a definite part in natural

resistance.

 

In the poliomyelitis epidemic in North Carolina in 1948, 60 cases of

this disease came under our care. These patients presented all or

almost all of these signs and symptoms: Fever of 101 to 104.6°,

headache, pain at the back of the eyes, conjunctivitis, scarlet

throat; pain between the shoulders, the back of the neck, one or

more extremity, the lumbar back; nausea, vomiting and constipation.

In I5 of these cases the diagnosis was confirmed by lumbar puncture;

the cell count ranging from 33 to 125. Eight had been in contact

with a proven case; two of this group received spinal taps.

Examination of the spinal fluid was not carried out in others for

the reasons: (1) Flexner and Amoss had warned that " simple lumbar

puncture attended with even very slight hemorrhage opens the way for

the passage of the virus from the blood into the central nervous

system and thus promotes infection. " (2) A patient presenting all or

almost all of the above signs and symptoms during an epidemic of

poliomyelitis must be considered infected with this virus. (3)

Routine lumbar puncture would have made it obligatory to report each

case as diagnosed to the health authorities. This would have

deprived myself of valuable clinical material and the patients of

most valuable therapy, since they would have been removed to a

receiving center in a nearby town.

 

The treatment employed was vitamin C in massive doses. It was given

like any other antibiotic every two to four hours. The initial dose

was 1000 to 2000 mg., depending on age. Children up to four years

received the injections intramuscularly. Since laboratory

facilitates for whole blood and urine determinations of the

concentration of vitamin C were not available, the temperature curve

was adopted as the guide for additional medication. The rectal

temperature was recorded every two hours. No temperature response

after the second hour was taken to indicate the second 1000 or 2000

mg. If there was a drop in fever after two hours, two more hours was

allowed before the second dose. This schedule was followed for 24

hours. After this time the fever was consistently down, so the drug

was given 1000 to 2000 mg. every six hours for the next 48 hours.

All patients were clinically well after 72 hours. After three

patients had a relapse the drug was continued for at least 48 hours

longer—1000 to 2000 mg. every eight to 12 hours. Where spinal taps

were performed, it was the rule to find a reversion of the fluid to

normal after the second day of treatment.

 

For patients treated in the home the dose schedule was 2000 mg. by

needle every six hours, supplemented by 1000 to 2000 mg. every two

hours by mouth. The tablet was crushed and dissolved in fruit juice.

All of the natural " C " in fruit juice is taken up by the body; this

made us expect catalytic action from this medium. Ruin, 20 mg., was

used with vitamin C by mouth in a few cases, instead of the fruit

juice. Hawley and others have shown that vitamin C taken by mouth

will show its peak of excretion in the urine in from four to six

hours. Intravenous administration produces this peak in from one to

three hours. By this route however, the concentration in the blood

is raised so suddenly that a transitory overflow into the urine

results before the tissues are saturated. Some authorities suggest

that the subcutaneous method is the most conservative in terms of

vitamin C loss but this factor is overwhelmingly neutralized by the

factor of pain inflicted.

 

Two patients in this series of 60 regurgitated fluid through the

nose. This was interpreted as representing the dangerous bulbar

type. For a patient in this category postural drainage, oxygen

administration, in some cases tracheotomy, needs to be instituted,

until the vitamin C has had sufficient time to work—in our

experience 36 hours. Failure to recognize this factor might

sacrifice the chance of recovery. With these precautions taken,

every patient of this series recovered uneventfully within three to

five days.

 

In the treatment of other types of virus infections the same " fluid "

dose schedule was adopted. In herpes zoster 2000 to 3000 mg. of

vitamin C was given every 12 hours, this supplemented by 3 000 mg.

in fruit juice by mouth every two hours. Eight cases were treated in

this series, all of adults. Seven experienced cessation of pain

within two hours of the first injection and remained so without the

use of any other analgesic medication. Seven of these cases showed

drying of the vesicles within 24 hours and were clear of lesions

within 72 hours. They received from five to seven injections. One

patient; a diabetic, stated that she was always conscious of an

uncomfortable feeling, but that it was not an actual pain. Although

nine-tenths of the vesicles cleared in the usual 72-hour period, she

was given 14 injections, the last seven of only 1000 mg. This extra

therapy was given because of a small ulceration, an inch in

diameter, secondarily infected by rupture of the vesicles by a corset

stave prior to the first visit. Vitamin C apparently had no effect

on this lesion, which was healed in two weeks under compound

tincture of benzoin locally and penicillin and sulfadiazine by

mouth. (The patient objected to taking penicillin by needle.) One of

the patients, a man of 65, came to the office doubled up with

abdominal pain and with a history of having taken opiates for the

preceding 36 hours. He gave the impression of having an acute

surgical condition. A massive array of vesicles extended from the

dorsal nerve roots to the umbilicus, a hand's breadth wide. He was

given 3000 mg. of vitamin C intravenously and directed to return to

the office in four to five hours. It was difficult to convince him

that his abdominal pain was the result of his having " shingles. " He

returned in four hours completely free of pain. He was given an

additional 2000 mg. of vitamin C, and following the schedule given

above he recovered completely in three days.

 

In herpes simplex it is important to continue the treatment for at

least 72 hours. We have seen " fever blisters " that appeared healed

after two injections recur when therapy was discontinued after 24

hours. Vitamin C in a strength of 1000 mg. per 10 c.c. of buffered

solution gave no response when applied locally. This was true no

matter how often the applications were made. In several cases 10 mg.

of riboflavin by mouth t.i.d. in conjunction with the vitamin C

injections appeared to cause faster healing.

 

Chickenpox gave equally good response, the vesicles responding in

the same manner as did those of herpes. These vesicles were crusted

after the first 24 hours, and the patient well in three to four

cays. We interpreted this similarity of response in these three

diseases to suggest that the viruses responsible were closely

related to one another.

 

Many cases of influenza were treated with vitamin C. The size of the

dose and the number of Injections required were in direct proportion

to the fever curve and to the duration of the illness. Forcing of

fruit juice was always recommended, because of the frequency and

ease of reinfection during certain periods of the year.

 

The response of virus encephalitis to ascorbic acid therapy was

dramatic. Six cases of virus encephalitis were treated and cured

with vitamin C injections. Two cases were associated with virus

pneumonia; one followed chickenpox, one mumps, one measles and one a

combination of measles and mumps. In the case that followed the

measles-mumps complex, definite evidence was found to confirm the

belief that massive, frequent injections are necessary in treating

virus infections with vitamin C. This lad of eight years was first

seen with a temperature of 104°. He was lethargic, very irritable

when molested. His mother said he had gradually developed his

present clinical picture over the preceding four or five days. His

first symptom was anorexia which became complete 36 hours before his

first examination. He next complained of a generalized headache,

later be became stuporous. Although very athletic and active, he

voluntarily took to his bed. He was given 2000 mg. of vitamin C

intravenously

and allowed to return home because there were no available hospital

accommodations. His mother was asked to make an hourly memorandum of

his conduct until his visit set for the following day. Seen 18 hours

after the initial injection of vitamin C, the memorandum revealed a

quick response to the antibiotic—after two hours he asked for food

and ate a hearty supper, then played about the house as usual and

then, for .several hours, he appeared to have completely recovered.

Six hours following the initial injection, he began to revert to the

condition of his first visit. When seen the second time temperature

was 101.6°, he was sleepy but he would respond to questions. The

rude irritability shown prior to the first injection was strikingly

absent. A second injection of 2000 mg. vitamin C was given

intravenously and 1000 mg. of " C " prescribed every two hours by

mouth. The next day he was fever and symptom-free. As a

precautionary measure a third 2000 mg. was given with direction to

continue the drug by mouth for at least 48 hours. He has remained

well since. A lad of 12 years had generalized headache a week after

having mumps, this followed by malaise, and in 12 hours a lethargic

state and a fever of 105°. Admitted to hospital he was given 2000

mg. of vitamin C then, and 1000 mg. every two hours. Following the

third injection he was sitting up in bed, laughing, talking, begging

for food and completely without pain. He was discharged 24 hours

following admission clinically well. Since relapses do occur if the

drug is discontinued too soon, he was given 2000 mg. of vitamin C

every 12 hours for two additional days.

 

The use of vitamin C in measles proved to be a medical curiosity.

During an epidemic vitamin C was used prophylactically and all those

who received as much as 1000 mg. every six hours, by vein or muscle,

were protected from the virus. Given by mouth, 1000 mg. in fruit

juice every two hours was not protective unless it was given around

the clock. It was further found that 1000 mg. by mouth, four to six

times each day, would modify the attack; with the appearance of

Koplik's spots and fever, if the administration was increased to 12

doses each 24 hours, all signs and symptoms would disappear in 48

hours. If the drug was discontinued or reduced to three or four

doses each 24 hours following the disappearance of Koplik's spots,

within another 48-hour period the fever, the conjunctivitis and

Koplik's spots would be back.

 

It was our privilege to observe this picture over and over in two

little volunteer girls for 30 days. These " research helpers " were my

own little daughters. The measles virus was eventually destroyed in

this instance by continuing 12,000 mg. by mouth each 24 hours for

four days. We interpreted this result to indicate that on

withdrawing the drug with the cessation of signs and symptoms, a

small quantity of the virus remained, which after another incubation

period produced anew the first stage of measles; when the drug was

continued beyond the clearing stage the virus was destroyed in toto.

No case of post-measles bronchopneumonia was seen. The " measles-

cough " of measles bronchitis was over with after three or four 1000

mg. injections of " C " at 6-hour intervals. This was true even when

other medications well above the calculated dose range for cough had

had no effect. Whenever a patient presented a mixed-virus infection,

such as receding mumps and developing measles, it was found that

double the calculated dose of vitamin C was necessary to obtain the

usual results.

 

Of mumps, 33 cases were treated with ascorbic acid. When vitamin C

was given at the peak of the infection the fever was gone within 24

hours, the pain within 36 hours, the swelling in 48 to 72 hours. Two

cases were complicated with orchitis. A young man of 23 years

developed bilateral orchitis one Friday morning, by seven o'clock

that night he was in severe pain, had a fever of 105 " and was

nursing testicles the size of tennis balls. Vitamin C was started at

this time—1000 mg. every two hours, intravenously. The pain began to

subside following the first injection and ceased in 12 hours. There

was no fever after 36 hours. The patient was out of bed feeling his

old self after 60 hours. He had received 25,000 mg. of " C " in this

60-hour period. An experiment involving three cousins: One, a boy of

seven, had the old routine of bed rest, aspirin, and warm camphor

oil applications and iodex to the swollen glands. This child had a

rough time for a week. A second boy, aged 11, was allowed to

develop mumps to the point of maximum swelling without any therapy,

then given vitamin C, 1000 mg. intramuscularly, every two to four

hours. This lad was entirely well in 48 hours. To the third patient,

a girl of 9, vitamin C was given on the up curve when the swellings

were 60 per cent of the expected, and the temperature recorded at

102.3°. The dose was 1000 mg. of vitamin C given intravenously every

four hours. This child was well and remained so from the third day

of treatment.

 

Further studies on virus pneumonia showed that the clinical response

was better when vitamin C was given to these patients according to

the dose schedule outlined for poliomyelitis. Where pneumonitis was

demonstrated, the clearing of the chest film was parallel with the

clinical recovery. In cases of consolidation of entire lobes the x-

ray clearing lagged days behind the clinical response. In these

cases 1000 mg. of " C " should be given every 12 hours for at least a

week after the patient is apparently well. There was no change in

the results as given in a previous paper; the patients were well in

the third day of treatment.

 

In using vitamin C as an antibiotic no factor of toxicity need be

considered. To confirm this observation 200 consecutive hospital

patients were given ascorbic acid, 500 to 1000 mg. every four to six

hours, for five to ten days. One volunteer received 100,000 mg. in a

12-day period. It must be remembered that 90 per cent of these

patients did not have a virus infection to assist in destroying the

vitamin. In no instance did examination of the blood or urine

indicate any toxic reaction, and at no time were there any clinical

manifestations of a reaction to the drug. When vitamin C was given

by mouth one per cent of these patients vomited shortly after taking

the drug. In half of these cases the vomiting was controlled by

increasing the carbohydrate content of the mixture. This reaction

was not interpreted as representing a toxic manifestation; rather it

was thought to be due to a hypersensitive gastric mucosa. The dose

was reduced from 1000 to 100 mg. in young children showing this

complex; vomiting occurred as before. However, in these same

patients administration of massive, frequent doses of vitamin C by

needle affected a cure of the infection without causing vomiting.

 

From a review of the literature one can safely state that in all

instances of experimental work with ascorbic acid on the virus

organism the amount of virus used was beyond the range of the

administered dose of this vitamin. No one would expect to relieve

kidney colic with a five-grain aspirin tablet; by the same logic we

cannot hope to destroy the virus organism with doses of vitamin C of

10 to 400 mg. The results which we have reported in virus diseases

using vitamin C as the antibiotic may seem fantastic. These results,

however, are no different from the results we see when administering

the sulfa, or the mold-derived drugs against many other kinds of

infections. In these latter instances we expect and usually get 48-

to 72-hour cures; it is laying no claim to miracle-working then,

when we say that many virus infections can be cleared within a

similar time limit.