Tylenol/etc - CHICKEN POX: WHY DO CHILDREN DIE?

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INfo on using tylenol/calpol/paracetamol and other things for fever - DANGER

Tylenol/etc - CHICKEN POX: WHY DO CHILDREN DIE?

L Krasner wrote:

The following article originally appeared in the Well Beings newsletter,

a publication of Vaccination Alternatives, NYC, <va-sk@...

http://www.mercola.com/2001/mar/17/chicken_pox.htm

Chicken Pox: Why Do Children Die?

By Krasner

After learning this month of the legislative

attempt to make the varicella vaccine mandatory

in New York, I looked for a handle for an

article. Since I didn't recall that chicken pox

had ever been grouped in the category of

medicine's infamous " Killer Diseases " ,

I thought I should find out how the Medical Boys

justified making it compulsory for school children.

It became apparent that the only medical

justification for this vaccine had been the

claimed mortalities. I went to the CDC's website

and found something revealing in the May 15,

1998/Vol. 47/No. 18 issue of Morbidity and

Mortality Weekly Report (MMWR, their official

publication). It was entitled, " Varicella-Related

Deaths Among Children: Texas and Iowa notified

CDC of three fatal cases of varicella

(chickenpox) that occurred in children during

1997 " (reprinted in Appendix A below).

A short introduction stated that in the U.S.

there are approximately 100 deaths (about half of

these in children) and 10,000 hospitalizations

each year for complications from chicken pox from

infection with the varicella virus.

After going over the report, I remembered why I

stopped reading medical journals. In each of the

three cases the young boys started out with

fevers and/or other minor inflammatory conditions.

Following each regimen of antibiotics,

analgesics, or steroidal medications their condition grew progressively worse.

The doctors responded to each new symptom with

yet another drug, until the children died.

Having an understanding of Natural Hygiene (note:

it is briefly described by Harvey Diamond in his

best seller, Fit For Life), I understood why the

children got progressively worse from the

drugging. But even equipped with a rudimentary

understanding of the principles of N.H., one

would realize that chicken pox is not a fatal

disease, but rather a very common, benign

inflammatory condition. And fatalities-as rare as

they are-must actually result from inappropriate

care, or the kinds of aggressive medical

interventions described in the MMWR report.

With paraphrasing here and there, the next 9

paragraphs is taken from the section on chicken

pox from the 1965 book, " Food Is Your Best

Medicine " by Henry Bieler, M.D. He was a renowned

clinician practicing in Pasadena, CA for over 50

years until his death in 1975. Dr. Bieler's

skills were sought after by Hollywood celebrities

and honored by his peers (a medical wing was

named after him). His book is still available from Random House.

Chicken pox arises from the elimination of toxic

fat or fatty acids through the hair fat glands.

The chemical burn from the purging of waste

products though the skin causes the

characteristic blister of this disease. This

occurs when the liver is congested and cannot

perform its eliminative function and metabolic

waste matter (toxins) is then thrown into the

bloodstream. These toxins in the blood must be

discharged, so nature uses vicarious avenues of elimination, or " substitutes " .

When these bile poisons (from the liver) in the

blood come out through the skin, we get skin

conditions manifested by rashes, boils, acne,

etc. Or they come out through the mucous

membranes (inside skin) manifesting as various

catarrhs, like chicken pox. Thus, the skin is

" substituting " for the liver, or a vicarious

elimination is occurring through the skin.

Food And Drugs Are Contraindicated

During the more acute and involved forms of

toxemia, such as measles, chicken pox, fever, or

flu, the liver is much too busy neutralizing

toxic wastes to be bothered with digestion of

food. Therefore, to facilitate the elimination of

this waste, fasting on distilled water is

essential in such cases. This accounts for the

lack of digestive juices produced, and the loss

of appetite that accompanies these illnesses.

(Dr. Mercola Note: Please be very clear that

distilled water is not appropriate for long term

use. You should use bottled spring water or filtered water.)

After cells have been damaged by the toxic

wastes, it is important for bacteria-acting as

scavengers-to attack and devour the weakened,

injured and dead cells. Otherwise, these dead

cells would become accumulated toxic waste themselves.

Therefore, antibiotics and other bactericides must not be administered.

The so called " bad " bacterial strains die out on

their own anyway, once their food (toxic waste)

is used up. But until that point, they play an

important role in the process that converts waste for eventual elimination.

The class of drugs that doctors use to treat

catarrhal diseases are called antipyretics. Among

antipyretics, aspirin tops the list of favorites.

Aspirin is a phenol (carbolic acid) derivative,

with all the chemical qualities of phenol, but

without the deadly effect of carbolic acid.

Aspirin, like phenol, deadens the nerve endings, thereby masking pain.

But aspirin also diminishes a fever by partially

blocking the thyroid and the adrenal glands (a

bad thing). The phenol derivatives interfere with

the proper function of the liver and damage liver cells.

The use of aspirin, then, is an attempt to drive

out one devil (disease toxins) by admitting another devil!

The Importance Of Fever

Fever in a child is a frightening symptom to the

mother. Just what is the function of fever? Is it

a harmful process, something to suppress and

worry about? Or is it the body's attempt to burn

up a poison, thereby helping to dispose of it more quickly?

In the diseases of childhood, fever begins in the

liver. In a very strong, robust child, with

properly functioning endocrine glands, the toxin

is often completely consumed in the liver. The

child does not feel sick or have pain; he just

has a fever and if the liver area is carefully

palpated, it can be noted that there is an

elevation of temperature over that organ.

In fact, if the temperature under the tongue is

105 degrees, the internal temperature of the

liver may be as high as 110 degrees. But if the

liver is unable to oxidize completely the poisons

of disease so that some leak through into the

blood stream, then, under the action of the

endocrine glands, the poisons seek vicarious

outlets via the mucous membranes. This may be

through the upper respiratory tract, diagnosed by

doctors as flu, sinusitis, pharyngitis,

tonsillitis and possibly even pneumonia, which is

a complicated kind of bronchitis. All through

this process, the whole power of the liver is

diverted into neutralizing the toxic wastes of

disease, as evidenced by the fever.

The liver is much too busy to be bothered with

the task of the digestion of food.

Great strain can be taken off that organ if no

food is given. Not only does fasting lower the

temperature, relieve the distress and facilitate

elimination, but it also lessens the strain on

the liver and prevents serious complications,

such as middle-ear disease, mastoiditis and meningitis.

Left alone, a fever will not exceed 106 degrees.

And only about 4 percent of children experience

fever-related convulsions, with no serious aftereffects.

A fast (on distilled water, or at least diluted

fruit or vegetable juices) should be continued

for twenty-four hours after the temperature has returned to normal.

A good rule to remember is that the bowel can be

cleared of toxins (by physic or enemas) in

twenty-four hours; the blood in three days; the

liver in five days, providing no food is eaten.

Shingles ( " adult chicken pox " ), an eliminative

crisis through the mucous membranes that occurs

in adults, may require about a week-long fast to completely clear up.

It appears then, that fever, dreaded because

misunderstood, is really nature's attempt to help.

It is discomforting, but never does harm; never

is attended with serious aftereffects and never

should be suppressed with anti-inflammatory drugs

or fed with food. I have seen many a case of flu

pushed into a pneumonia because some anxious

grandmother insisted upon something " to give the

child strength " , such as chicken broth or a thin

starchy gruel, both liquids, of course, but

protein and starch-just what the liver cannot handle at this point.

The True Cause Of " Infectious " Disease

From Dr. Bieler's words (above) we gain a little

understanding of Natural Hygiene. So-called

" infectious " diseases like chicken pox, measles,

or whooping cough are actually inflammatory

diseases. The symptoms during such illnesses

should be viewed as eliminative crises.

They may be very painful, but they're a necessary

self-limiting process in which an accumulation of

retained metabolic waste (dead cells that become

toxic), and the residues of undigested,

unassimilated foods are being purged from the

body through vicarious (abnormal, inappropriate)

channels such as the skin or lungs.

Thus, the familiar runny nose, cough, stiffness,

fever, and numerous rashes, swellings, lesions,

and eruptions through the skin are all

manifestations of the same cause-which are not pathogenic microbes.

Microbes like bacteria, for example, act as

scavengers to consume the toxic wastes and the

dead cells following inflammation. Their

formation and growth do not precede the diseased

state in the host, but rather emerge in its wake;

and not exogenically-from say, an " infected "

person-but rather endogenically, from the genetic

material contained in a cell's nucleus after the

cell's death and decomposition.

Fortunately, a wide range of bacterial strains,

or their genetic " blueprints " (e.g., the various

cellular and sub cellular-or " filterable " -stages

that bacteria cycle through), inhabit our bodies

all the time in titers low enough that their waste products do not affect us.

Recently reported villains like salmonella, e.

coli, or streptococcus are enteric and

ever-present inside us. The viruses associated

with measles, polio, influenza, and all the rest

are also present-both in health and disease-and

may have only an associative relationship with

the diseases, but no proven causative roles.

(Incredibly, modern medicine still hasn't

determined the mechanism by which a virus causes poliomyelitis.)

But when we become toxemic and our blood loses

its alkalinity, the pathogenic strains begin to

flourish in the bodily waste that

accumulates-even well before any outward symptoms

(inflammation and elimination) begin to appear.

Their morphology (strain and function) is

determined by the type of waste that is present for them to feed upon.

Symptoms are often triggered by a physiochemical

or psychological " trauma " , such as

exposure to cold or toxic chemicals

stress

lack of sleep

ingestion of spoiled meat

a sting or bite from an insect

an injected vaccine

Why these diseases occur predominantly in

children is best described by Dr. Bieler:

" The childhood years should be the healthiest of

all. It is during those early years that the

endocrine glands and the liver are in their best

functional capacity, giving the healthy child his

natural state of exuberance, inexhaustible energy, and faultless elimination " .

When elimination ends and symptoms subside,

doctors will proclaim that the drug had " taken

effect " . But they are confusing symptoms with

cause; believing that the disappearance of the

former equates to the disappearance of the

latter. But obviously a cause and an effect

cannot be one in the same. When you stop the body

from discharging toxic waste, you are not

stopping the disease; you are merely stopping the effects.

In other words, neither allopathy, nor any other

healing philosophy may claim responsibility for

" curing " inflammatory or catarrhal diseases.

Because the disease symptoms-the remedial actions

initiated by our own bodies-themselves represent the " cure " .

But more importantly, when Allopathic physicians

employ pain killers, fever suppressants, steroids

and other drugs-which are sub-lethal doses of

poisons-they have the effect of weakening the

patient to the extent of checking elimination.

This is a dangerous effect, because the waste

products of these germs that have fed on the dead

cells, together with the irritation from the

toxins themselves may be absorbed into the blood,

and irritating the already overworked liver-which

is the detoxification center of the body.

Antibiotics-which literally means " against

life " -act chiefly by violently stimulating the

adrenal glands. But if they are weak or depleted,

the disease runs a chronic, often recurring

course. In the aftermath of these germicides,

there are also left fewer germs to convert waste,

and no means to carry off and eliminate the dead

cells. Not surprisingly, there are more deaths

today from septicemia (blood poisoning caused by

toxic waste from putrefactive bacteria) than

there were before the use of antibiotics. (One of

the boys from the MMWR report died from it.)

Reactions from antibiotics include

anaphylactic shock

aplastic anemia

induced virulent infections

Deaths from penicillin still occurs today.

Chicken Pox Doesn't Kill; Doctors Kill

It's now plain to see why the children described

in the afore-referenced MMWR had died. They were

given numerous antibiotics, steroids, antipyretic

and antipruritic medications and other fever

suppressers, some administered directly into

their bloodstreams. Probably they were given food

to eat as well, even during the height of their inflammatory responses.

The CDC admits that children don't die from

chicken pox per se, but rather " complications "

from chicken pox. But what they don't say is that

these complications are all derived from acute

blood toxemia established by the very treatments

used by allopathic physicians. So strictly

speaking, all children that die, do so from the

allopathic medical treatments that are used to

treat the symptoms that accompany chicken pox.

There has never been a recorded death among the

many thousands of children treated Hygienically, and without drugs.

What does the CDC list as the most common complication?

Pneumonia and secondary bacterial infections

(caused by the antibiotics). Other complications,

according to the CDC, include encephalitis

(inflamed brain tissue mostly from the

antipyretics), hemorrhagic complications (such as

intestinal bleeding, are the most common symptoms

of aspirin-an anticoagulant, or " blood thinner " ),

hepatitis (congested and inflamed liver caused by

the antipyretics), arthritis (decalcification of

bone for the calcium needed to neutralize acidic

blood, mostly caused by the aspirin), and Reye's

syndrome (most commonly associated with giving

aspirin to children that have chicken pox or influenza).

Like aspirin and other anti-inflammatory drugs,

acetaminophen (ie. Tylenol) will also burden the

liver and kidneys and check the vital actions of

the body to discharge waste from the blood.

Acetaminophen poisoning is also common because it

throws the chemistry of the liver off. In fact,

it is the most common drug-induced cause of liver

failure. It depletes hepatic glutathione, causing

the toxic metabolite NAPQI to fail to conjugate,

which leads to hepatic injury, and sometimes death.

Therefore, to say that " death is a complication

of chicken pox " , is like saying, " bleeding is a

complication of holding a knife in your hand " :

each event is neither contingent nor a

consequence of the preceding one. Their

association is artificial; requiring specific

intervening actions to take place. In cases of

chicken pox, actions that are in accord and

mandated by standard medical practice.

To promote the vaccine, the CDC proclaims that,

" varicella (chicken pox) is the leading cause of

vaccine-preventable deaths in children in the United States. "

But while the deaths are certainly preventable,

they have nothing to do with the failure to vaccinate.

More on the above article from

http://www.whale.to/vaccines/krasner.html

Author’s Postscript:

The advice in this article is applicable to all

inflammatory diseases. This article could have

been titled, " Measles: Why Children Die " , or

" Whooping Cough: Why Children Die " . In each case,

medications risk the life of the patient by

checking the vital efforts of the body to

eliminate waste through abnormal channels.

Historically, Natural Hygiene had preceded

allopathic medicine, and it represented a

different paradign of disease, particularly

inflammatory ( " infectious " ) diseases. Hygienists

would argue that allopathy’s perceived " success "

in the prevention and cessation of physical

symptoms is really achieved through " enervation " ,

or the weakening of the detoxification and

eliminative capacity of our bodies through the

use of sublethal dose of poisons (drugs). The

(refuteable) claim that there’s a lower incidence

of infectious diseases (just symptoms, mind you)

among vaccinated children may simply prove that

such children are more likely getting more drugs,

vaccines and chemically laden food, which all

contribute to enervation and symptom suppression.

While many children may experience an eliminative

crisis, it should not, by itself be fatal. To the

contrary, such symptoms indicate that there’s a

" cure " in progress, assuming that they’re left

alone to run their natural course, unhindered and unmedicated.

----G.K.

Krasner is the Director of Coalition For Informed Choice

CFIC, 188-34 87th Drive, Suite 4B, Hollis, NY 11423

718-479-2939 (phone or fax),

e-mail: CFIC-USA@...

Two Books available from Foundation for

Advancement in Cancer Therapies, Box 1242 Old

Chesea Sta., New York, NY 10113. Make checks

payable to FACT, Ltd. Add $2 S & H. Add $3 for

first-class postage. Foreign orders: use postal money orders.

Food Is Your Best Medicine by Henry G. Bieler,

M.D. Paperback, 1982 by Ballantine Books (236 pages). _____$5.99

This book is also available from " www.randomhouse.com " .

Toxemia Explained by Dr. Tilden. ©1976 by

Keats Publ., New Caanan, CT. (130 pages). The

theories of the successful clinician, Tilden

(1851-1940), who practiced conventional medicine

for 18 years, then abandoned the use of all drugs

to run a school and sanitarium in Denver.

Describes toxemia as the basis of all diseases. ___$5.50

debunking virus diseases may be found at:

www.soilandhealth.com

www.virusmyth.com

www3.bcity.com/harpub/

www.whale.to/vaccines

www.whale.to/disease_theory.htlm

www.garynull.com

Natural Hygienic literature is also displayed at " www.soilandhealth.org " .

In 1997, 3 deaths reported by two states did not

really occur from chicken pox, but rather from

the unnecessary drugs they used to treat it. The

preceding article refers to this CDC report, which is recorded here verbatum:

Appendix A:

Morbidity and Mortality Weekly Report

May 15, 1998 / Vol. 47/No. 18

Varicella-Related Deaths Among Children:

Texas and Iowa notified CDC of three fatal cases of varicella (chickenpox) that

occurred in children during 1997:

Case 1

On February 28, 1997, a previously healthy,

unvaccinated 21-month-old boy developed a typical

varicella rash. He had no reported exposure to

varicella. On March 1, he was taken to a local

emergency department (ED) with a high fever and

was started on oral acetaminophen and

diphenhydramine. On March 3, his primary-care

physician prescribed oral acyclovir. On March 4,

his mother noted a new petechial-like rash. The

next morning, his primary-care physician noted

lethargy, a purpuric rash, and poor perfusion. He

was transferred to a local ED. Fluid

resuscitation and intravenous ceftriaxone were

initiated, but the child continued to deteriorate

rapidly, requiring intubation, mechanical

ventilation, and inotropic support with dopamine.

Blood cultures were negative for bacterial

pathogens. Laboratory tests indicated

disseminated intravascular coagulation and severe

dehydration. Approximately 1.5 hours after

arrival at the ED, he was transported to a

tertiary-care center. Within 10 minutes of

arrival, he suffered cardiac arrest and died. The

death was attributed to varicella with hemorrhagic complications.

Case 2

On December 21, 1997, a 5-year-old unvaccinated

boy with a history of asthma was taken to a local

ED with a fever of 104.5 F (40.3 C) and a typical

varicella rash in multiple stages of healing. The

child was treated with antipyretic and antipruritic medications and discharged.

That evening, the boy developed mild dyspnea and

was treated at home for a presumed asthma attack

with metered-dose inhalers and one dose of oral

prednisone. He returned to the ED on December 22

with shortness of breath and a 4-hour history of

abdominal and leg pain. On presentation to the

ED, one of the patient’s siblings had active

varicella and another had recently recovered from

varicella. Physical examination revealed numerous

chickenpox lesions, one of which appeared

infected. He was tachypneic, and his extremities

were mottled consistent with peripheral septic

emboli. Chest and abdominal radiographs revealed

a right pleural effusion, pneumonia, and mild

ileus. Thoracostomy produced pleural fluid

containing gram-positive cocci, confirmed 8 hours

later to be group A Streptococcus (GAS). A

peripheral blood sample revealed gram-positive

cocci. He was admitted to the hospital and

treated with intravenous ceftriaxone, nafcillin, and acyclovir.

After admission, his breathing became labored and

his extremities increasingly mottled. He rapidly

developed hypotension, obtundation, and

bradycardia. Despite efforts at cardiopulmonary

resuscitation, the child died 5 hours after

arriving at the ED. A post-mortem examination

attributed the death to GAS septicemia,

pneumonia, and pleural effusion, complicating varicella infection.

Case 3

On December 14, 1996, a previously healthy,

unvaccinated 23-month-old boy developed fever and

a typical varicella rash. Approximately 1-2 weeks

earlier, his unvaccinated 4-year-old sibling had

contracted varicella. He was taken to his

physician on December 17 because of persistent

fever and cellulitis of the left foot, and he was

hospitalized on December 19 for failure to

improve on an unspecified outpatient antibiotic

regimen. Because his condition deteriorated

despite intravenous methicillin and ceftriaxone,

he was transferred to a regional hospital on

December 21. Sepsis, possible viral

meningoencephalitis, and mild pleural effusion

were diagnosed. A cerebrospinal fluid examination

revealed lymphocytic pleocytosis, and blood and

urine cultures grew penicillin-resistant

Staphylococcus aureus. Antibiotics were changed

to nafcillin and gentamycin, and intravenous

acyclovir was added on December 23. On December

24, the child developed an aortic insufficiency

murmur, and an echocardiogram revealed a 9x9 mm

vegetation on the aortic valve, consistent with

bacterial endocarditis. Serial echocardiograms

displayed growth of the vegetation and

development of a pericardial effusion. He was

transferred to a cardiac surgery center on

December 26. While awaiting surgery, he developed

refractive heart failure secondary to

staphylococcal endocarditis. He became

incoherent, probably secondary to a major embolic

neurologic event, and died on January 8, 1997.

Publisher’s Postscript

We received positive responses from many who

read, " Chicken Pox: Why Do Children Die?, from

our 11/98-1/99 double issue. The following letter

from Estrada, M.D. published in

" Infections in Medicine® " [infect Med 16(5):307,

1999. © 1999 SCP Communications, Inc.] apparently

supports Krasner's assertion that the

complications that children die from are not

caused by chicken pox per se, but rather from the

the drugs that doctors use to " treat " chicken

pox. —Sharon Kimmelman, Publisher, WB.

Pediatric Bulletin Varicella and GAS:

Do NSAIDs Fuel the Fire?

Author: Estrada, MD, University of South Alabama, Mobile, Ala.

Published in: Infect Med 16(5):307, 1999. © 1999 SCP Communications, Inc.]

During the past decade, there has been an

increase in the frequency of severe Group A

beta-hemolytic streptococcal (GAS) infections in

children. Factors associated with this

development are an increase in the prevalence of

exotoxin-producing serotypes and low herd

immunity. The increase is due in part to the low

rates of infection with these strains in the past.

It has been noted in some series that severe

invasive GAS infections such as necrotizing

fasciitis (NF) and streptococcal toxic shock

syndrome (STSS) are associated with preexisting

varicella infections in up to 47% of patients

( CL et al: Pediatr Infect Dis J

15:151-156, 1996). Another possible association,

this one between the use of nonsteroidal

anti-inflammatory drugs (NSAIDs) and severe GAS

infection in children with varicella, has also

been reported by several investigators. NSAIDs

have been used to ameliorate the signs and

symptoms of varicella, but the question of

whether their use increases disease progression remains.

The association between fulminant NF and the use

of NSAIDs was reported by Rimailho and

collaborators more than a decade ago (Rimailho et

al: J Infect Dis 155:143-146, 1987). These

investigators described fulminant disease in five

patients treated with NSAIDs, which included

aspirin, diclofenac, piroxicam, and nifluminic

acid. Several studies have demonstrated the

development of lymphopenia and decreased

lymphocyte function in the presence of aspirin

and other NSAIDs. It has also been shown that

abnormal neutrophil chemotaxis,

chemiluminescence, and lymphocyte transformation

of PHA occurred when leukocytes from a patient

with NF were exposed to NSAIDs. This information

suggests that NSAIDs may decrease immune function

and favor a widespread infection in patients

infected with invasive strains of GAS ( RJ: South Med J 84:785-787, 1991).

The association between the use of ibuprofen and

the development of severe GAS infection in

children with varicella was first reported by

Brogan and colleagues (Brogan et al: Pediatr

Infect Dis J 14:588-594, 1995) in a series in

which five children developed GAS NF while

receiving treatment with this NSAID. The

investigators concluded that it may be prudent to

limit the use of this drug for local

complications of varicella, since it may impair

granulocyte function and at the same time mask

the signs of disease progression with GAS.

Until recently, most of the evidence suggesting a

potential association between the use of

ibuprofen in patients with varicella and the

development of GAS invasive disease was based on

isolated case reports or data obtained from small

case series. A recent study aimed at the

evaluation of risk factors associated with the

development of invasive GAS infection in patients

with varicella found that the development of

invasive disease with this bacteria was 8.3 times

more likely in those patients in whom ibuprofen

had been used during the first 5 days after the

onset of varicella ( CL et al: Pediatr Infect Dis J 15:151-156, 1996).

More recently, a case-controlled study was

performed to determine whether ibuprofen use was

associated with the development of NF in patients

with varicella. This study included 19 children

with varicella and NF and 29 controls also

diagnosed with varicella and a serious

soft-tissue infection other than NF. Ibuprofen

use before hospitalization was more likely in

cases than in controls (42% vs 15%). Patients

with NF complicated by renal insufficiency or

STSS were also more likely to have used ibuprofen

than those with uncomplicated NF. Although this

study does not establish a direct causal

relationship between ibuprofen use and the

development of GAS NF in patients with varicella,

the findings imply that an association may exist.

The authors suggest that this association could

either be due to a more severe GAS infection

promoted by the immunoinhibitory effect of

ibuprofen, or " masking " of the signs and symptoms

of disease progression by the action of the same

drug. Another possibility is that ibuprofen use

could be only an indicator of more severe disease

that required more aggressive anti-inflammatory

management (Zerr DM et al: Pediatrics 103:783-790, 1999).

These studies suggest that there is an

association between the use of ibuprofen (and

possibly other NSAIDs) in children with varicella

and the development of severe invasive GAS

infection. Until a definite causal relationship

can be established or ruled out by future

studies, practitioners should consider the

potential risks of using these medications in

children with varicella. Providing comfort for

symptom relief through the administration of

these drugs must be weighed against the potential

for development of severe GAS disease.

Dr. Estrada is Assistant Professor of Pediatrics,

Division of Pediatric Infectious Diseases,

University of South Alabama, Mobile, Ala.

ADDITIONAL CASES OF DEATHS RESULTING

FROM TREATMENT FOR CHICKEN POX

_____________________

Varicella-related deaths--Florida, 1998. MMWR

Morb Mortal Wkly Rep. 1999 May 14;48(18):379-81.PMID: 10369579; UI: 99296270

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4818a3.htm

Case 1. On February 19, a healthy, unvaccinated

6-year-old boy developed a varicella rash,

abdominal pain, malaise, and loss of appetite

following exposure to a classmate with varicella.

The child had asthma and intermittently had been

on inhaled steroid therapy but had not received

steroids within the previous month. On February

22, he was hospitalized with hemorrhagic skin

lesions, tachycardia, tachypnea, and a platelet

count of 89,000 (normal range: 150,000-350,000).

Several hours after admission he developed

pulmonary edema and respiratory insufficiency and

required mechanical ventilation. He died on

February 23. Tissue samples of multiple organs

had a positive polymerase chain reaction for varicella zoster virus (VZV).

Case 2. On March 27, a healthy, unvaccinated

58-year-old woman developed a varicella rash. She

was born in Cuba and had moved to the United

States in 1995. She did not have a history of or

known exposure to varicella. On April 3, she was

hospitalized with a 5-day history of increasing

shortness of breath and productive cough and was

diagnosed with varicella pneumonitis. She was

treated with intravenous acyclovir and

ceftriaxone, but developed adult respiratory

distress syndrome (ARDS), disseminated

intravascular coagulopathy, renal failure, and coma. She died on April 20.

Case 3. On April 27, a healthy, unvaccinated

29-year-old man developed a varicella rash. In

early April, his children had contracted

varicella. On April 29, he sought care at a local

emergency department for chest pain and

respiratory distress. Chest radiographs showed

bilateral pulmonary interstitial infiltrates. On

April 30, he began coughing up blood, was

intubated because of increasing respiratory

insufficiency, and was treated with intravenous

acyclovir and antibiotics. He developed sepsis,

ARDS, and multiorgan failure, and died May 12.

Case 4. On May 5, a 21-year-old unvaccinated

female employee at a family child care center

developed a varicella rash after exposure to a

child with varicella. The employee had a history

of asthma and was treated with 5 mg prednisolone

per day. She was hospitalized on May 7 with

varicella pneumonitis and received intravenous

acyclovir on May 8, but she died the same day.

Case 5. On July 11, an 8-year-old unvaccinated

boy developed a maculopapular rash diagnosed

clinically as varicella and confirmed by direct

flourescent antibody test on July 23. He had

acute lymphocytic leukemia (ALL) and had been on

immunosuppressive therapy since receiving a bone

marrow transplant on May 15. He had not had

varicella and had no known varicella exposure. He

was treated with varicella zoster immunoglobulin

on July 16 and acyclovir on July 23. He died on

July 25 after recurrence of leukemia with a

graft-versus-host reaction complicated by

disseminated varicella, cellulitis, ileus, and hypertension.

Case 6. On October 3, an unvaccinated 45-year-old

man with diabetes mellitus, asthma, and cirrhosis

of the liver developed a varicella rash. He was

born in Cuba and had resided in the United States

for 35 years. He had no history of varicella and

no known exposure. He was not receiving steroids

or immunosuppressive drugs. He was admitted to

the hospital with varicella on October 5 and on

October 6, treatment was initiated with oral

acyclovir. He died on October 8; pathologic

evidence from the postmortem examination revealed VZV in all major organs.