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CHICKEN POX: Why Do Children Die?
Chicken Pox:
Why Do Children Die?
By Gary Krasner
While chicken pox is rarely fatal, vaccination proponents in New York State want
to mandate universal vaccination of school children against varicella. But
rather than keeping them away from infected kids, Natural Hygienists suggest a
better way to regain health and avoid death: Keep them away from allopathic
physicians!
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 didnt
recall that chicken pox had ever been grouped in the category of medicines
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 CDCs 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 fatalitiesas rare as they aremust 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. Bielers 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.
After
cells have been damaged by the toxic wastes, it is important for bacteriaacting
as scavengersto 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 bodys 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. There should be little or no scars
remaining, and absolutely no residual pain thereafter. [That was my experience
with shingles 3 years ago.G.K.]
It
appears then, that fever, dreaded because misunderstood, is really natures
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 starchjust what the liver cannot handle at this point.
The True Cause Of
Infectious Disease
From
Dr. Bielers 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 theyre 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 causewhich 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 exogenicallyfrom say, an infected personbut rather endogenically, from
the genetic material contained in a cells nucleus after the cells death and
decomposition. Fortunately, a wide range of bacterial strains, or their genetic
blueprints (e.g., the various cellular and sub cellularor filterablestages
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 presentboth in health and diseaseand may have only an associative
relationship with the diseases, but no proven causative roles. (Incredibly,
modern medicine still hasnt 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
accumulateseven 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, or 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 symptomsthe remedial actions initiated by our own bodiesthemselves
represent the cure.
But
more importantly, when Allopathic physicians employ pain killers, fever
suppressants, steroids and other drugswhich are sub-lethal doses of
poisonsthey 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 liverwhich is the detoxification center of the body.
Antibioticswhich literally means against lifeact 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, and induced virulent infections. Deaths from penicillin still
occurs today.
Chicken Pox Doesnt Kill;
Doctors Kill
Its
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
dont die from chicken pox per se, but rather complications from chicken pox.
But what they dont 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 aspirinan 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 Reyes 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. n
Authors 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, etc. 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 allopathys 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 theres 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 theres a cure in
progress, assuming that theyre left alone to run their natural course,
unhindered and unmedicated.
----G.K.
Gary Krasner is the
Director of
Coalition For Informed
Choice
CFIC, 188-34 87th
Drive, Hollis, NY 11423
718-479-2939 (phone or
fax),
e-mail: CFIC-USA@juno.com
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. John Tilden. ©1976 by Keats Publ., New Caanan, CT. (130 pages). The
theories of the successful clinician, John 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.org
www.virusmyth.com
www3.bcity.com/harpub/
www.whale.to/vaccines
www.whale.to/disease_theory.htlm
www.garynull.com
www.sumeria.net
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 patients 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.
Publishers 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 Benjamin
Estrada, M.D. published in Infections in Medicine® [Infect Med 16(5):307,
1999. © 1999 SCP Communications, Inc.] apparently supports Gary 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:
Benjamin 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
(Peterson 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 (Smith 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 (Peterson 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.
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