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Old 22nd May 2006, 08:05 AM
Sheri Nakken
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Default Other so-called causes of polio-like paralysis

Other so-called causes of polio-like paralysis, Part 1 of 3

Other causes of polio-like paralysis

(I would suggest, in view of all we have learned regarding polio-like
paralysis being very likely caused by toxicity due to pesticides, etc, that
these other so-called viruses are just present, the same as poliovirus is
present sometimes, and NOT THE CAUSE here either. That the cause is still
toxicity from chemicals of some sort, and these things are found just


The Coxsackie family of viruses, first isolated in 1948, consists of 29
different strains and is linked to numerous illnesses. When physicians
first began identifying these viruses in the blood of CFS patients, they
failed to discern their connection with polio. The sustained use of polio
vaccines for over 40 years has resulted in "at least 72 viral strains that
can cause polio-like diseases," says Dr. Douglass. Before the polio
vaccines, there were only three polio viruses. He notes that he was not the
first to point to evidence of "the changing of polio rather than the
elimination of it." As early as 1934, cases of "atypical" polio were
reported in Los Angeles; "abortive poliomyelitis" was reported in
Switzerland in 1939.

Dr. Douglass suggests that the trend towards the emergence of a new
polio-its predominant symptom changing from infantile paralysis to adult
muscle weakness-has rapidly increased since the polio vaccines were
introduced. "We now know that chronic fatigue syndrome is not a new
disease, but simply an 'aborted form' of the more serious paralytic polio,"
he states. If Dr. Douglass' speculations prove correct, the credibility of
conventional medicine's mass vaccination program will be seriously
undermined. It is hardly a public health benefit if a vaccine simply
modifies an existing disease, forcing it to take another form in the next
generation of patients. The indiscriminate use of vaccines may prove to be
as counterproductive as has the overprescribing of antibiotics.

SOURCE-William Campbell Douglass, M.D., "Chronic Fatigue Syndrome: The
Hidden Polio Epidemic," Second Opinion 6:8 (August 1996), 1-6.
Neenyah Ostrom's feature article invites us to broaden our concept of the
disease called polio. Was the polio virus really to blame for all those
cases of polio in the '40s & '50s -- and what factors other than a virus
are precipitating polio-like paralytic disease?
URL not working but can access in the cached page on google
es/paralyticpolio.html+%2Bchronic%2Billnet%2Bpolio%2B neenyah&hl=en&client=fi
Will The Poliovirus Eradication Program Rid the World of Childhood Paralysis?

With So Little Poliovirus Detected Around the World, What Is Causing
Today's Outbreaks of Acute Flaccid Paralysis?

By Neenyah Ostrom - I WILL SEND THE WHOLE ARTICLE separate
Polio and paralysis are not synonymous. Dr. Ralph Scoby, president of the
Polio Research Institute, published (Archives of Pediatrics, 1950) a list
of 170 diseases with 'polio-like symptoms and effects but with different
names." Paralysis is the result of the diphtheria (and other) vaccination,
tonsillectomies and malnutrition (sugar ingestion). Yet the public was
rallied to accept the Salk anti-polio vaccine for a disease diagnosed
without viral confirmation, the medical standard.

"A State Communicable Disease Report for California (1971) shows that
between 1955 and 1966 the reported number of polio cases dropped from 273
to 50 while viral meningitis rose from 5 to 256 cases. Another California
report lists "0" polio cases. An asterisk leads the reader to this
statement: "All such cases now reported as meningitis." The media is
playing Meningitis (Hib), a "polio twin," exactly as it played polio in the
50s. Coincidentally, it has its own vaccine. What's the best way to wipe
out a diseased? Rename it!"

Mycoplasma pneumoniae pneumonia

Causes spectrum of disease from inapparent infection, mild afebrile URTI to
severe pneumonia.

- meningitis, meningoencephalitis 6-7%
- ascending paralysis
- transient myelitis
- cranial nerve palsy
- polio-like illness

It is worthwhile to examine the implications of CFS epidemics. The Royal
Free epidemic in London was a famous epidemic where a polio-like illness
struck down many people. The illness also affected cranial nerves, which is
not a feature of CFS. The majority recovered in a matter of weeks to
months, but a significant number went on to develop CFS. These susceptible
people among the staff at the Royal Free Hospital were left with CFS, but
the original epidemic was probably a Coxsackie viral infection and
therefore was not actually CFS. [23] Hence the CFS was caused by a viral
trigger. The fact that the viral infection occurred in an epidemic created
a related epidemic of CFS. [23] It is likely that the same conclusions can
be drawn from studying other CFS epidemics. [23]

The agent
Campylobacters are bacteria that are a major cause of diarrhoeal illness in
humans and are generally regarded as the most common bacterial cause of
gastroenteritis worldwide

Post-infection complications may include reactive arthritis (painful
inflammation of the joints which can last for several months) and
neurological disorders such as Guillain-Barré syndrome, a polio-like form
of paralysis that can result in respiratory and severe neurological
dysfunction or death in a small, but significant, number of cases.

1: Pediatr Infect Dis J. 1999 Dec;18(12):1092-6. Related Articles, Links
Click here to read
Comparison of enterovirus 71 and coxsackie-virus A16 clinical illnesses
during the Taiwan enterovirus epidemic, 1998.

Chang LY, Lin TY, Huang YC, Tsao KC, Shih SR, Kuo ML, Ning HC, Chung
PW, Kang CM.

Department of Pediatrics, Chang Gung Children's Hospital, Chang Gung
University, Taoyuan, Taiwan.

OBJECTIVES: To compare enterovirus 71 (EV 71) with coxsackievirus A16
(Cox A16) clinical illness in patients at Chang Gung Children's Hospital
during Taiwan's enterovirus epidemic of 1998. METHODS: With the use of the
immunofluorescence assay and neutralization test, 177 cases of EV 71 and 64
cases of Cox A16 illness were confirmed from April to September, 1998. The
clinical signs and symptoms, complications and case fatality rates were
compared. RESULTS: Three-fourths of the cases were younger than 3 years of
age, and the ratio of males to females was 1.3 in the EV 71 group and 1.2
in the Cox A16 group. In the EV 71 group 120 (68%) cases were
uncomplicated, including 94 cases of hand, foot and mouth disease and 15
cases of herpangina, and 57 (32%) cases had complications, including 13
(7.3%) cases of aseptic meningitis, 18 (10%) cases of encephalitis, 4
(2.3%) cases of polio-like syndrome, 8 (4.5%) cases of encephalomyelitis
and 12 (6.8%) cases of fatal pulmonary edema. Fourteen (7.9%) patients
died, including 12 cases of pulmonary edema and 2 cases of encephalitis;
seven (4%) patients had sequelae. By contrast, 60 (94%) of the 64 cases of
Cox A16 infection were uncomplicated and only 4 (6.3%) cases were
complicated by aseptic meningitis; no fatalities or sequelae were observed.
By multivariate analysis vomiting (P = 0.01) and fever higher than 39
degrees C plus lasting longer than 3 days (P = 0.02) were significantly
more frequent in the EV 71 group. CONCLUSION: EV 71 illness is more severe
with significantly greater frequency of serious complications and fatality
than is illness caused by Cox A16.

2: Bahemuka M. Related Articles, Links
No abstract Polio-like illness with involvement of spinal cord long tracts.
East Afr Med J. 1983 Aug;60(8):583-7. No abstract available.
PMID: 6653464 [PubMed - indexed for MEDLINE]

1: Pediatrics. 1981 Apr;67(4):489-93. Related Articles, Links

Enterovirus 71 infection: report of an outbreak with two cases of
paralysis and a review of the literature.

Chonmaitree T, Menegus MA, Schervish-Swierkosz EM, Schwalenstocker E.

Enterovirus 71 (E-71) infection was first reported in 19745 in the
United States; subsequent outbreaks were reported in worldwide
distribution. In the summer of 1977, we identified 12 patients, mostly
children, with E-71 infection. The striking feature of this outbreak is the
occurrence of two cases with polio-like paralytic disease. Other diseases
associated with E-71 included aseptic meningitis, meningoencephalitis,
respiratory disease, gastroenteritis, and hand-foot-mouth disease. The
spectrum of illness observed in our community was compared to that seen in
other outbreaks. It is suggested that the significance of E-71 lies in its
neuropathogenic potential.

4: BUDD GM. Related Articles, Links
No abstract A polio-like illness in Antarctica.
Med J Aust. 1962 Mar 31;49(1):482-6. No abstract available.
PMID: 13874354 [PubMed - OLDMEDLINE for Pre1966]

acute flaccid paralysis (AFP) has been observed(1). AFP cases however, can
be both of polio or non- polio origin.

"The clinical profile of cases showed that cases of spinal type without
bulbar involvement were more common (83.8%) in comparison to bulbo-spinal
cases (16.2%). These observations are similar to those of Ratnaswamy et
al.(2) in which 80% spinal type, 17.5% bulbo-spinal and 2.5% with
encephalitic manifestation were reported. The only mortality observed was
of the case with bulbo-spinal presentation."

Acute Flaccid Paralysis in Children: A New Viral Cause
[Solomon T, Kneen R, Dung NM, Khal1h Vc, Thuy TTN, Ha DQ et al.
Poliomyelitis-like illness due to Japanese encephalitis virus. Lancet 1998;
351: 1094-1097].

"In JEV infected children onset of weakness was more rapid, asymmetrical
and was less likely to involve upper limbs. In these children the acute
flaccid paralysis was more profound, and was followed by a short febrile
prodromal illness. Seven of the eight JEV negative patients fitted in to
the Asbury's criteria(1) of Guillian-Barre syndrome compared with one of
the 12 JEV infected patients. Subsequent development of features suggestive
of encephalitis (coma, convulsions, extrapyramidal. manifestations and up
going plantar reflex) and meningeal inflammation (nuchal rigidity, stiff
spine and CSF pleocytosis) were observed more frequently (four patients) in
JEV infected children; only one of JEV negative patient had these
manifestations. Bulbar paralysis, involvement of other cranial nerves and
evidence of autonomic involvement (transient hypertension) was more
frequent in JEV-negative patients. However, equal number of patients in
both the groups had evidence of respiratory paralysis. Mortality was
observed only in JEV-negative patients as two patients died due to
respiratory paralysis. At the time of discharge higher number patients
among JEV infected group could not walk. Thirteen (eight JEV positive) of
the 18 survivors returned for follow-up. Patients with JEV infection had
greater disability and were more likely to have asymmetric muscle wasting
(all eight patients) while JEV-negative children (two of five) had
symmetrical wasting. Nerve conduction studies and electromyography were
suggestive of anterior horn cell involvement in JEV-positive group.
However, two out of 5 JEV-negative children had electrophysiological
evidence of previous demyelinating polyneuropathy."

Polio-Like Symptoms With West Nile
"Research published in The New England Journal of Medicine found some
people with WNV have muscle weakness leading to paralysis that is eerily
similar to polio symptoms. The most severe symptom thus far observed with
WNV has been encephalitis, which also has muscle weakness associated with
it. These findings, however, indicate a different type of severe muscle
weakness called acute flaccid paralysis."

"Paralytic disease due to enteroviruses other than poliovirus occurs
sporadically and is usually less severe than poliomyelitis. Most cases are
due to enterovirus 70 to 71(3) or to coxsackie virus A7. Gullian-Barre
syndrome is also associated with entero-virus infections. Polio like
illness has been observed in some young adult cases of acute hemorrhagic
conjuctivitis caused by enterovirus 70, during epidemics. Mumps virus may
occasionally be associated with transverse myelitis and Gullian-Barre
syndrome and present with acute flaccid paralysis."
Acute Paralysis Associated with WNV Infection
"West Nile virus (WNV) infection can cause severe, potentially fatal
neurologic illnesses including encephalitis and meningitis (1,2). Acute WNV
infection also has been associated with acute flaccid paralysis (AFP)
attributed to a peripheral demyelinating process (Guillain-Barre Syndrome
[GBS]) (3), or to an anterior myelitis (4)."

"This report describes six cases of WNV-associated AFP in which clinical
and electrophysiologic findings suggest a pathologic process involving
anterior horn cells and motor axons similar to that seen in acute
poliomyelitis. Clinicians should evaluate patients with AFP for evidence of
WNV infection and conduct tests to differentiate GBS from other causes of AFP.
Case Reports "

Was UK Mystery Cow
Death A Bovine Polio Virus?

(subscription required)
Japanese Encephalitis Virus Causes Polio-Like Paralysis. Poliovirus causes
acute flaccid ... Poliomyelitis-like illness due to Japanese encephalitis
virus. ...

A historical accident has led to various names being given to viruses, all
of which share physical , chemical and epidemiological characteristics of
what we consider the classic polio virus, which science refers to as polio
viruses 1, 2, and 3 (Dowsett: Journal of Hospital Infection,
1988:11:103-15). ln l948, a polio-like illness in New York state prompted
scientists to culture the virus. But what grew looked to them at that time
like a new virus.

They called it "Coxsackie' after the small town up the Hudson River where
it was found. And they called the disease "Atypical Polio" because its
symptoms identified it as a kind of polio, despite the virus being
apparently different.

This kind of polio, "Atypical Polio,' has since been renamed, 'Chronic
Fatigue Svndrome,' or ME. But it remains a kind of poIio despite the change
of name. and newer technology has shown up the generic similarities of the
most frequent agent that causes it.

These techniques place Coxsackie, the virus most often implicated in CFS,
in the polio family tree, along with so-called echo viruses. Coxsackie has
been further divided into Coxsackie type A (with 24 viruses) and Coxsackie
type B (six viruses ). There are 34 echo viruses. In total, there are at
least 72 enteroviruses in all, with new ones still being discovered.
"In 1948, a polio-like illness in New York State resulted in the
identification of a new virus that was called Coxsackie, after the town on
the Hudson River. The disease was called atypical polio because its
symptoms identified it as a kind of polio, despite the virus being
different. This kind of polio has since been renamed ME and more recently
chronic fatigue syndrome. It remains a type of polio, despite the change of
name. Technology has shown the generic similarities of the most frequent
agent that causes it. These techniques place Coxsackie, the virus most
often implicated in ME, into the polio family tree, along with so-called
echo viruses. Coxsackie has been further subdivided into types A and B. In
total, there are at least 72 enteroviruses. Maybe there are more viruses
now, if the research has moved on. Some of the points that I am making are
based on research by Jane Colby, who wrote a book called ME-The New Plague."

"True ME, as opposed to fatigue symptoms, is clinically polio-like, and has
often been diagnosed as non-paralytic polio. Patients have weakness, back
pain and they are systemically ill. It has been unfortunate that some of
these patients have been labelled as having chronic fatigue, as true ME is
a neurological condition that usually originates with a gut virus infection
such as Coxsackie, which in some cases can be demonstrated. The requirement
to put off diagnosing ME for six months after the patient falls ill has
made this difficult. If the tests are not done quickly, it is too late to
identify the virus. Research now supports the view that ME is probably a
persistent viral infection causing inflammation throughout the central
nervous system and disturbance of hypothalamic function.

If ME is a type of polio, why does everyone exposed to the viruses not
develop ME, just as they did with polio? In fact, only a small number of
those with the polio virus became paralysed. About 90 per cent did not
realise that they were suffering from anything more than a cold or flu.
With both polio and ME, the state of the immune system governs
susceptibility. "

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  #2 (permalink)  
Old 22nd May 2006, 08:07 AM
Sheri Nakken
Posts: n/a
Default Other so-called causes of polio-like paralysis, Part 2 of 3

Other so-called causes of polio-like paralysis, Part 2 of 3



"During polio epidemics it was known that "non-paralytic polio symptoms"
were not always due to polio virus. Non-polio enteroviral infections, among
others, produced the same symptoms. However, if a patient with nonparalytic
symptoms had a sibling or other close contact with a paralytic polio case,
then the infectious agent usually was polio virus."

" During a polio epidemic in Hawaii in 1957, specimens were obtained from
38 people with paralytic polio and from 39 cases of non-paralytic polio.
"Of the 38 cases of paralytic disease, type 1 polio virus was implicated in
33, Coxsackie B2 virus was isolated…in 2 and no diagnosis was established
in 3. Of the 39 cases of nonparalytic poliomyelitis, only 4 were related to
type 1 polio virus. There were 16 cases of echovirus 9, 7 cases of
Coxsackie A9, and 4 to 5 other enteroviruses." (Johnson 1995)."


Polio virus is one of more than 70 enteroviruses. A number of enteroviruses
(Coxsackie A9 [Gromeier et al. 1997], enterovirus 70 [Gromeier et al.
1997], enterovirus 71 [Melnick, 1984]), as well as a flavivirus, Japanese
encephalitis virus [Solomon et al. 1998], among others, can cause
polio-like paralysis. These non-polio enteroviral infections may cause
PPS-like symptoms as well. Coxsackie virus RNA has been isolated from
people with PPS symptoms (Muir et al. 1995), although it is not known if
this is a common event. If PPS arises from neuronal damage, then
intuitively, enteroviruses causing symptoms that are clinically identical
to polio could cause similar neurological damage during the acute illness
which in turn would give rise to PPS-like symptoms in later life. If PPS
arises from an immune response to continuous presence of viral RNA, then
finding enteroviral RNA (other than polio) in people with PPS symptoms, as
was shown by several researchers, also indicates PPS-like symptoms could
occur from non-polio virus infections.

nid=DoqBF2yyzPFDvVCv9yTnGbeREjIysWTXjciPNHF1MnhTcZ fHgw4m!-1173786811!-949856
Pediatric Infectious Disease Journal. 17(10):930-931, October 1998.
Chou, I-Ching M.D.; Tsai, Chang-Hai M.D., Ph.D.; Tsai, Fuu-Jen M.D., Ph.D.


"Well what we've found is that the individuals who fall ill acutely, we've
been able to find in about 25% of those individuals, a new virus which
resembles a polio virus. It's the same family as the polio virus. It's
called enterovirus, but of the some 60 known enterovirus we're actually
finding a totally different subgroup of viruses in this individuals and
it's very interesting because one of the subgroups of people get better.
They stay ill for one, two, three years and they slowly get better and the
second subgroup with these polio-like viruses, they don't get better and
they resemble almost identically the sequences that you find in paralytic
polio but these people are not paralyzed and as everybody out there knows,
even though they may not know people anymore, fortunately, with polio,
polio didn't just injure the muscles, it injured the spinal chord and it
injured in some people the lower part of the brain. "

"There are 3 serotypes of poliovirus with no common poliovirus antigen.
They have identical physical properties and their base sequences share 36 -
52% homology. Humans are the only natural hosts for polioviruses, Old World
monkeys and chimpanzees are susceptible to infection. Antigenic variants of
types 1 and 2 have been reported, however these antigenic differences do
not affect the capacity of Abs induced by one strain to protect against
other strains of the same type. Despite these minor intratypic differences,
polioviruses show marked antigenic stability. It is important to note that
other enteroviruses are occasionally associated with a polio-like illness,
in particular Coxsackievirus A7 and enterovirus 71."

Coxsackie And Echoviruses
Typically, group A viruses produce a flaccid paralysis whilst group B
viruses produce a spastic paralysis

"A. Aseptic Meningitis - coxsackievirus meningitis is seen most frequently
in children under 5 years of age. Complete recovery is the seen in almost
all cases, in contrast to polioviruses. Aseptic meningitis is caused by
coxsackieviruses of both groups A and B, and many echoviruses. Enterovirus
71 has been associated with meningitis and severe disease of the CNS which
includes polio like paralysis."

"D. New Enteroviruses

Newly identified picornaviruses that are not polioviruses are no longer
classified separated into the species coxsackie and echovirus because of
the ambiguities presented by overlapping host range variations. 5 new
enteroviruses have been identified (68 - 71). Enterovirus 70 is the
causative agent epidemics of acute haemorrhagic conjunctivitis that swept
through Africa, Asia, India and Europe from 1969 to 1974. The virus is
occasionally neurovirulent. Enterovirus 71 appears to be highly pathogenic
and has been associated with epidemics of a variety of acute diseases,
including aseptic meningitis, encephalitis, paralytic poliomyelitis-like
disease and hand-foot-mouth disease. Enterovirus 72 is the designation
assigned to hepatitis A virus, which, after it could be propagated in
vitro, was shown to have the physical and chemical characteristics of
enteroviruses. "

Rare form of West Nile worries California
Athlete suffered polio-like symptoms after Colorado event

Sabin Russell, Chronicle Medical Writer

Wednesday, August 25, 2004

Richelle Matli was in intensive care at UC San Francisco ... Richelle Matli
is among the Americans in their 30s and 40... The Spread of West Nile
Virus. Chronicle Graphic

At a lake in Colorado last summer, 47-year-old Pleasanton water skier
Richelle Matli was in such good form that she knew she had a shot at the
national championships, only two weeks away in Texas.

Then a mosquito bite intervened.

Instead of taking a trip to Houston, Matli lay for five days in intensive
care at UC San Francisco Medical Center with a mysterious, polio-like
paralysis in her left leg.

The diagnosis: West Nile virus.

But this was not an ordinary case of West Nile. Matli appears to have come
down with a rare form of the disease doctors now call acute flaccid
paralysis, or West Nile poliomyelitis. Frighteningly, it tends to strike
otherwise healthy adults in their 30s and 40s. Some patients who've
contracted it can no longer breathe without a ventilator.

"I went into the hospital under my own power and came out in a wheelchair,
'' said Matli, who is the mother of two teenage girls and is an X-ray
technician at California Pacific Medical Center in San Francisco.

Matli started water skiing when she was 8 and competing when she was 20.
She describes herself as "hooked" on slalom competition. Before her
illness, she was ranked 5th nationally in her event.

A roomful of trophies at her Pleasanton townhouse attests to her success.
Since 1980, she has competed in every National Championship but two. "One
was to have a child, the other was for West Nile,'' she said.

The sport requires a skier on a single ski to weave through six buoys at
progressively faster speeds, with set times for completing the course.
Skiers attain their maximum speed -- Matli covers the course in 16.95
seconds -- and then are scored on a variety of skills as they fly around
the buoys.

"It's very addicting because you can measure your improvement immediately,
'' said Matli, who was raised in San Francisco and graduated from Lincoln
High School and City College.

She returned to work in April and, remarkably, has returned to the water as
well. Now 48, she skied in a tournament on July 22 for the first time since
her illness, drawing cheers from fans on shore as she left the dock.

West Nile virus was rampant last summer in Colorado, ultimately striking
3,000 residents and killing 67. Nationwide, the outbreak killed 264.

The summer of 2004 appears to be California's turn for a major West Nile
virus outbreak. Spared in previous years as the virus moved across the
country, the state now has logged 277 cases and seven deaths. While most
cases are in Southern California, where the disease first appeared last
fall, single cases have been reported as far north as Lassen, Butte and
Yolo counties.

Researchers at the Centers for Disease Control and Prevention in Atlanta
are following the cases of 32 Colorado residents who came down with this
polio- like syndrome during last summer's West Nile outbreak. All live in
the three counties hardest hit by the virus.

"Most of the people have a condition almost identical to that caused by the
polio virus,'' said Dr. James Sejvar, an epidemiologist for the CDC and one
of the nation's leading experts on the phenomenon.

Unlike polio, West Nile virus is spread only by the bite of an infected
mosquito and cannot be transferred from person to person.

At least 80 percent of people infected with the virus show no symptoms,
while most of the remaining 20 percent experience a flu-like illness and
often break out in a rash.

One in 150 of those infected with West Nile virus develop serious symptoms
such as encephalitis -- a life-threatening swelling of the brain. Most of
them are well over the age of 50.

The polio-like syndrome is less common -- and in some ways, more ominous.
"Those developing West Nile poliomyelitis tend to be younger and otherwise
healthy,'' said Sejvar.

Doctors also do not know if such patients will ever recover full use of
their limbs. "In the short term, pretty much everyone continues to have
some functional difficulties,'' said Sejvar.

Dr. Carol Glaser, chief of the California Department of Health Services
viral lab in Richmond, said no cases of the polio-like syndrome have been
confirmed in the state, although several suspicious case histories are
being reviewed. "We're very familiar with the syndrome. We've been looking
for it,'' she said.

Glaser said she is skeptical that the syndrome strikes only younger,
healthier patients. It is possible, she said, that some of the elderly
victims who died of West Nile virus encephalitis or meningitis also had the
limb paralysis, but their symptoms went unnoticed as they battled for their

Last year, at the 2003 Western Regional Water Ski Championships outside
Fort Collins, Colo., Matli and her competitors had heard the news on
television of a local West Nile virus outbreak. They joked about catching
West Nile. Fortunately, the lake area itself had been sprayed and seemed
mosquito- free.

On the final day of that tournament, the skiers celebrated at a banquet on
a golf course. The mosquito situation there was different. "I felt like we
were getting eaten alive,'' she said. There were more West Nile jokes.

Five days later, while training for the nationals at a private lake for
water skiers in Southern California, Matli began to feel poorly. "I felt
like I'd had a few too many cocktails. I had a rash. I assumed it was a
heat rash, '' she said.

When she returned to Pleasanton, her condition was worsening. "But I still
had high hopes of winning the nationals,'' she said.

The day before she was to leave for the tournament, Matli found she could
not climb the stairs to the second floor of her home. There would be no
flight to Houston. She was hospitalized the following day and spent five
days in intensive care. Months of rehab followed.

Today the wheelchair and cane are history. "I limp,'' she said. "If I get
tired, I limp more.''

But this onetime water ski champion is relentlessly working her way back to
the life she used to know. "For my level, I am about 60 percent of where I
used to be,'' she said.

The slalom requires a smooth combination of strength, agility and grace.
Matli still has all three -- plus a dry wit and an unflappable disposition
- - to take her along.

She doesn't claim to have an iron will or the extreme discipline of many
athletes. But she marks her return to health with the same relentless
attention that made her a nationally ranked water skier.

"There was a time when I could not lift my foot,'' she said. "A month ago,
I still could not walk up a stair. I still can't stand on my toes. But I
see little improvements almost every day.''

spinal poliomalacia
Conference Note: Participants identified similar histopathological changes
as described by the contributor, and considered various causes of metabolic
polioencephalomalacia in the differential diagnosis, including nutritional
deficiencies (thiamine, copper), water deprivation/salt excess, and several
toxicities (lead, amprolium, thiaminase containing plants, excess dietary

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  #3 (permalink)  
Old 22nd May 2006, 08:08 AM
Sheri Nakken
Posts: n/a
Default Other so-called causes of polio-like paralysis, Part 3 of 3

Other so-called causes of polio-like paralysis, Part 3 of 3


Walene James gives voice to the many medical people whose views disagreed
with the official polio (viral caused) construct, many of whom questioned
polio being a contagious disease. Some medical people had already begun to
link paralytic polio-like illnesses as a response to the increasing use of
serious neurotoxins like DDT, lead and arsenic compounds. Dr. Ralph R.
Scobey presented "compelling evidence" that the real cause of polio is not
viral, but a response to poisons in a series of articles published in The
Archives of Pediatrics (1946-53). (4) Dr. Scobey's work can be viewed on
line at the Images of Poliomyelitis website. (10)

"Today, various other forms of the the word "polio" are still used to
describe the effects of poisoning, though usually with regard to paralysis
in animals. A search of Medline ("polio" and "poison") finds about 45
contemporary articles where poisoning causality is attributed to polio. The
terminology found was: "polioencephalomalacia", "poliomyelomalacia",
"polyradiculoneuritis", "neurological picture similar to that of
poliomyelitis", "polioencephalomyelomalacia", "lumbal poliomyelomalacia",
"cerebrocortical necrosis (polioencephalomalacia)", "Lead poisoning in
grey-headed fruit bats (Pteropus poliocephalus)",
"multifocal-poliomyelomalacia", "spinal poliomalacia", "Polio and
high-sulfate diets", "Atypical porcine enterovirus encephalomyelitis:
possible interraction between enteroviruses and arsenicals",
"Polioencephalomalacia and photosensitization associated with Kochia
scoparia consumption in range cattle", "bovine polioencephalomalacia".
---Jim West, Health and Research Publications,

"A quarter-century ago, I began my doctoral research in a lab that studied
how to create poliomyelitis in mice without any poliovirus: by manipulating
the junk DNA with toxic chemicals or radiation. GWS has convinced me that
these same interactions of toxic exposures and chronic diseases occur in
humans as well. So, the clues are now telling us that the cause of chronic
diseases is the JUNK genome, not the germs."--Testimony of Howard B.
Urnovitz, Ph.D. (1/24/02)

First polio epidemic--1887 Sweden. Patent of first pesticide sprayer---1873.


INSECTICIDES such as lead arsenate, hydrocyanic gas and other cyanide
compounds, DDT, parathion and other deadly poisons are a constant cause
death and disease. Dr. Abraham Gelperin, director of the Bureau of
Communicatable Diseases and assistant Clinical Professor or Public Health
at Yale University stated flatly that he believes many ills to be the
result of these poison insecticide and that large numbers of what are
believed to be polio are in reality cases of poisoning, possibly caused by
something like parathion.

FORMALDEHYDE IN MILK has been reported as a cause of polio.

SOLANIN, a poison that is formed in frozen potatoes was found to be the
cause of an epidemic in Ireland. The disease had polio-like reactions

UNRIPE FRUIT and ERGOT from some types of rye have caused gastrointestinal
disturbances which affected the nerves, spinal cord and brain and caused a
form of polio. A diet excessively high in grains (especially milled grains)
has been followed by deficiencies that terminated in polio as was reported
by Stockman and Johnson in the Journal of Nutrition, (Nov., 1934).

more at webpage

Organophosphate poisoning

Zhang Z, et al. [Risk factors for Guillain-Barre syndrome in northern
China: a case-control study]. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao.
1995 Aug;17(4):291-5. Chinese. PMID: 8575052; UI: 96147928.

We conducted a case-control study in northern China to estimate possible
risk factors for Guillain-Barre Syndrome (GBS). Forty patients were
consecutively seen at the PUMC hospital and the Second Hospital of Hebei
Medical College between July and September 1991. The diagnosis was
established following the NINCDS criteria for GBS. Among 36 patients with
measurements of motor evoked potentials, 34 had evidences of demyelination.
Eighty controls chosen from spouses or siblings, and neighbors or
work/school mates, were matched by sex and age (+/- 3 years). Using the
Mantel-Haenszel estimate of the odds ratio, cold rain, overloaded
activities, a history of diarrhea, common cold, and exposure to
organophosphorus one month before onset, significantly increased, at least
six-fold, the risk for development of GBS. Cases and controls did not
differ in the number of previous vaccinations. We suggest that a single
antigent is less likely of etiological importance in GBS.
Third of ME cases are pesticide-related

A former government scientist estimates that more than half a million
people in Britain are ill because of exposure to pesticides. Dr Lewis
Routledge, a biochemist who used to work for the Ministry of Agriculture,
has twin 8 year old sons who were seriously ill after being poisoned with
pesticides. In an Observer interview, Dr Routledge commented: "At least a
third of all ME cases are pesticide related. Add to that cases of immune
deficiency, asthma, irritable bowel syndrome, food and chemical allergies,
the 7,000 or so farmers affected by organo-phosphates in sheep dip, and I
think the half million figure is conservative. Even hay fever may be
triggered by pesticide bound pollen."

Sulfur can come from several different sources. Corn by-products such as
corn gluten feed, corn steep liquor and distillers grains tend to be high
in sulfur. We have known for some time that these by-products can
contribute to Polioencephalomalacia (Brainers, Polio), a disease created by
a thiamine deficiency.
: Salud Publica Mex. 1995 Jan-Feb;37(1):57-62. Related Articles, Links
[The incidence of poisoning by Karwinskia humboldtiana in Mexico]
[Article in Spanish]
Bermudez-de Rocha MV, Lozano-Melendez FE, Tamez-Rodriguez VA,
Diaz-Cuello G, Pineyro-Lopez A.
Departamento de Farmacologia y Toxicologia, Facultad de Medicina,
Universidad Autonoma de Nuevo Leon (FM, UANL), Mexico.
Intoxication produced by Karwinskia humboldtiana presents a
neurological picture similar to that of poliomyelitis, Guillain-Barre
syndrome or other polyradiculoneuritis with which it is frequently
confused. The purpose of this paper is to report the frequency of this
intoxication, by means of the antecedent of ingestion of the fruit and the
detection of toxins in blood using a thin layer chromatography method. One
hundred fifty four samples of cases with acute flaccid paralysis from 18
states of the country were received. The antecedent of ingestion in 56 of
them was corroborated and the detection was positive in 50 of these. In 98
patients there was not antecedent of ingestion and detection was negative
in 95 of them. We estimated that the sensibility and specificity of
detection method are 89% and 96.9% respectively.


Nonpolio Virus Can Cause Polio

Coxsackievirus A21 (CAV21), a virus commonly associated with upper
respiratory tract infections, can cause polio, according to a new report.
CAV21, though a close relative of poliovirus, was believed unable to cause
poliomyelitis because it binds to a different receptor--the human
intercellular adhesion molecule 1 (HsICAM-1). Researchers Andrew Dufresne
and Matthias Gromeier of Duke University Medical Center generated mice that
express this human cell adhesion molecule and infected the animals with
CAV21. Mice infected by an intramuscular route on a limb displayed
classical symptoms of polio: paralysis and neurological dysfunctions such
as an abnormal gait. Control mice that did not express HsICAM-1 were
unaffected by virus injection. The authors found that the virus was able to
travel from the site of infection to the central nervous system along motor
neuron axons. This route of central nervous system invasion appears to be
essential for CAV21-mediated polio. Upon reaching the spinal cord,
replicating virus destroys motor neurons, producing the clinical signs of
poliomyelitis. The previously unrecognized disease-causing potential of
CAV21 underscores the close genetic relationship with poliovirus and its host.

"A nonpolio enterovirus with respiratory tropism causes poliomyelitis in
intercellular adhesion molecule-1 transgenic mice" Andrew T. Dufresne and
Matthias Gromeier

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