Bignascarfan
Washington, DC, Jun. 25 (UPI) -- For more than 20 years, one
scientist has ignored the conventional thinking among
researchers that mad cow disease and similar disorders are
caused by abnormal proteins and instead has pursued an
alternative view that the culprit is a tiny, rare bacteria.
Dr. Frank Bastian, a pathologist at Tulane University in New
Orleans, has encountered controversy over the years and
seen his hypothesis roundly dismissed by nearly all
other researchers working in this field. Nevertheless,
he has stubbornly persisted in collecting data to
support his hypothesis.
Now, Bastian may have uncovered the first molecular evidence
of a link between chronic wasting disease -- a mad-cow-like
illness that afflicts deer -- and scrapie, the sheep
equivalent.
The finding, which has not been corroborated, could help
answer the long-standing question of the origin of chronic
wasting disease, which seemed to have come out of nowhere in
the 1960s and has been spreading ever since across deer and
elk herds in the midwestern United States and into Canada.
Bastian said his discovery also could force a paradigm shift
in thinking about the cause of these disorders and perhaps
open the door to treatments and vaccines for their human
versions: Creutzfeldt Jakob disease and variant CJD, the
latter of which has been linked to the consumption of mad-cow-
infected meat.
"If I'm right on this ... we should have a vaccine, we
should have a therapy," Bastian, medical director of the CJD
Diagnostic Center at Tulane, told United Press
International.
To date, there is no therapy to prevent or cure either CJD,
vCJD or the other, mad-cow-like disorders, which are always
fatal and are known collectively as transmissible spongiform
encephalopathies, or TSEs.
In a study published in the August issue of the journal
Experimental and Molecular Pathology, Bastian reported
evidence of bacteria called Spiroplasma mirum in deer brains
afflicted with chronic wasting disease, sheep brains
afflicted with scrapie, and human brains afflicted with CJD.
There was no trace of the bacteria detected in corresponding
brains that were not diseased.
Comparing the results from the different species, Bastian
found that some Spiroplasma strains seen in scrapie-
infected sheep brains matched strains found in deer brains
infected with CWD.
As Bastian and his co-authors wrote in the journal, the
findings imply "the CWD epidemic may have originated from
scrapie infection."
Bastian cautioned, however, that the link is not yet proven.
"At this stage, we don't know for certain -- but it's surely
suggestive," he said.
Before Bastian's bacteria hypothesis can progress to
therapies, it first must pass a barrage of resistance from
other TSE scientists, most of whom have accepted the
prevailing hypothesis that misfolded proteins called prions
are the causative agent.
One scientist, who did not wish to be identified but who is
considered one of the world's foremost experts on TSEs, told
UPI, "If I were you, I would stay away entirely from
anything having to do with Spiroplasma."
The scientist's caution stemmed from an unpublished study
that took place approximately five years ago. At the time,
Bastian allegedly was unable to distinguish infected
scrapie brains from normal brains by testing for the
Spiroplasma bacteria.
Bastian disputed that assessment, however, and said he
correctly identified infections in 80 percent of the
samples.
Despite Bastian's contention, the negative view of the study
-- which was conducted in Dr. Robert Rohwer's lab at the
Veterans Administration hospital in Baltimore -- has
circulated among TSE scientists and perhaps has overshadowed
the data Bastian has accumulated since then in support of
his bacteria hypothesis.
Asked to comment on Bastian's recent research, Rohwer
brought up the unpublished study and told UPI, "We saw
no evidence of any bacteriological contamination of
these brains."
Rohwer added, "I really question the quality of his
research, and I think it's unfortunate that Dr. Bastian
continues to ignore his own data. He's not convinced, but I
certainly am, that there's nothing to his story."
Bastian claimed that Rohwer's lab technician found evidence
of the bacteria in one of the samples, but Rohwer did not
mention this when he later made a presentation to National
Institutes of Health officials dismissing the bacteria
hypothesis.
Bastian said shortly after the test Rohwer was awarded a $2
million NIH grant while Bastian did not receive any funding.
"I think (Rohwer is) totally dishonest," Bastian said,
charging that Rohwer attempted to dismiss his hypothesis to
get a grant from the NIH.
"If Rohwer has anything to say about that study, he should
publish the data rather than making unsupported
statements," he said.
Bastian also noted his latest study lends credence to the
presence of the bacteria in diseased brains. Spiroplasma DNA
was detected in eight of 10 scrapie samples, six of seven
CWD samples and two of two CJD samples, he said.
Another reason Bastian's idea meets such heavy resistance is
Spiroplasma bacteria as a group were only relatively
recently discovered. The organisms, which are small even by
bacteria standards, escaped detection until the 1970s when
they were first recognized as being the cause of a few plant
and insect diseases.
Spiroplasma mirum, the agent involved in Bastian's
hypothesis, is carried by rabbit ticks and is known to cause
cataract disease in suckling mice.
Although his hypothesis is controversial, Bastian is not
without his supporters.
"I've been following his work for a while and I think he's
onto something," said Dr. Jeanne Drisko, a clinical
assistant professor of alternative medicine at the
University of Kansas Medical Center in Kansas City.
Drisko also noted that in 2001, NIH awarded Bastian a three-
year grant, which means it was reviewed and approved by
experts in the field.
"That's not an easy thing to do," so it is an indication
there is some evidence to support his idea, she told UPI.
In addition, Bastian's studies, including his latest
research, have been published in peer-reviewed
scientific journals.
"My impression is no one has looked at (Bastian's
Spiroplasma hypothesis) carefully," Drisko said. "It's
almost a knee-jerk response. There's been so many people
saying there's no evidence of this, so instead of looking at
the quality of the evidence he's providing, they simply
dismiss it."
Several researchers contacted by UPI to review Bastian's
latest article either dismissed the bacteria idea outright
or did not comment.
Other scientists gave Bastian's new data a positive review
but remained skeptical about his overall hypothesis, which
was not surprising because the prion hypothesis is nearly
dogma among experts in this field.
There is little evidence, however, supporting the central
tenet of the prion view: that misfolded prions have the
capability to infect cells and cause the brain destruction
typically seen in TSEs.
Ds. Adriano Aguzzi, a pathology professor at the University
Hospital in Zurich, Switzerland, pointed out in an
article in the Journal of Experimental Medicine last
year that much of the evidence surrounding prions is
contradicted by other studies. As Aguzzi put it, the
prion has been "reported to do almost everything,
including the opposite of everything."
Under Bastian's concept, Spiroplasma bacteria use the normal
prions, which occur on the outer surface of cells, to help
them gain entry. The misfolding of the prions actually
occurs on the inside of the cells and is merely a result of
the infection, not the cause.
Bastian's idea was bolstered recently by a study done by
Japanese researchers. In a 2003 report in the Journal of
Experimental Medicine, they discovered another bacteria
called Brucella depends on the normal prion protein to
cause the disease brucellosis, which strikes both livestock
and humans.
Bastian also showed -- in research published in the American
Journal of Pathology in 1984 -- that Spiroplasma are capable
of producing in suckling rats the type of brain destruction
seen in TSEs.
Still, other researchers were not willing to accept the
bacteria as the cause and said that has not been
demonstrated yet.
"Although this (latest) work shows an association of the
presence of Spiroplasma DNA, this work does not demonstrate
causality," said Beth Williams, a veterinarian at the
University of Wyoming in Laramie, who is credited as the
first scientist to identify chronic wasting disease as a
TSE disorder.
"Thus, it is not a logical extension, in my opinion, of
these data to say" that scrapie may have given rise to CWD,
Williams told UPI. "But I believe in keeping an open mind."
Linda Detwiler, a former U.S. Department of Agriculture
veterinarian and expert on scrapie and other TSEs, said
Bastian's data suggesting a link between CWD and scrapie is
interesting because researchers still do not have any solid
answers for how CWD emerged.
"He may be onto something," Detwiler told UPI, but she
cautioned that further confirmation of Bastian's data is
needed before this hypothesis was accepted.
Detwiler's hesitation stems from a study Bastian did with
the USDA a couple of years ago, in which he was unable to
identify correctly whether sheep brain samples were or were
not infected with scrapie.
She was not ready to dismiss his hypothesis completely,
though, and said his latest results were intriguing.
"I would hope this would spur somebody to relook at
this," she said.
In his defense, Bastian said he correctly identified two out
of five scrapie infected brains in the USDA study using a
less sensitive technique called polymerase chain reaction.
When using a more sensitive method called DNA sequencing, he
said he finds evidence of the bacteria in nearly all the
infected brain samples he examines, but not in any of the
non-infected brains.
He concedes evidence showing the bacteria causes these
diseases still needs to be collected and plans to conduct
future studies with mice lacking the prion gene to help
support his hypothesis. If his idea is correct, the mice
should not become infected by the Spiroplasma.
One missing factor that would improve therapy for CJD
and vCJD is a test that can detect infection before
symptoms occur, he said. Research is planned to develop
a test that can detect the abnormal prions in blood, but
if Bastian's idea is correct, it would be too late,
because by then the brain already would have begun
degenerating. Bastian said he knows of no one working on
a test to detect Spiroplasma in the blood. http://washingtontimes.com/upi-breaking/20040624-
054020-7633r.htm
scientist has ignored the conventional thinking among
researchers that mad cow disease and similar disorders are
caused by abnormal proteins and instead has pursued an
alternative view that the culprit is a tiny, rare bacteria.
Dr. Frank Bastian, a pathologist at Tulane University in New
Orleans, has encountered controversy over the years and
seen his hypothesis roundly dismissed by nearly all
other researchers working in this field. Nevertheless,
he has stubbornly persisted in collecting data to
support his hypothesis.
Now, Bastian may have uncovered the first molecular evidence
of a link between chronic wasting disease -- a mad-cow-like
illness that afflicts deer -- and scrapie, the sheep
equivalent.
The finding, which has not been corroborated, could help
answer the long-standing question of the origin of chronic
wasting disease, which seemed to have come out of nowhere in
the 1960s and has been spreading ever since across deer and
elk herds in the midwestern United States and into Canada.
Bastian said his discovery also could force a paradigm shift
in thinking about the cause of these disorders and perhaps
open the door to treatments and vaccines for their human
versions: Creutzfeldt Jakob disease and variant CJD, the
latter of which has been linked to the consumption of mad-cow-
infected meat.
"If I'm right on this ... we should have a vaccine, we
should have a therapy," Bastian, medical director of the CJD
Diagnostic Center at Tulane, told United Press
International.
To date, there is no therapy to prevent or cure either CJD,
vCJD or the other, mad-cow-like disorders, which are always
fatal and are known collectively as transmissible spongiform
encephalopathies, or TSEs.
In a study published in the August issue of the journal
Experimental and Molecular Pathology, Bastian reported
evidence of bacteria called Spiroplasma mirum in deer brains
afflicted with chronic wasting disease, sheep brains
afflicted with scrapie, and human brains afflicted with CJD.
There was no trace of the bacteria detected in corresponding
brains that were not diseased.
Comparing the results from the different species, Bastian
found that some Spiroplasma strains seen in scrapie-
infected sheep brains matched strains found in deer brains
infected with CWD.
As Bastian and his co-authors wrote in the journal, the
findings imply "the CWD epidemic may have originated from
scrapie infection."
Bastian cautioned, however, that the link is not yet proven.
"At this stage, we don't know for certain -- but it's surely
suggestive," he said.
Before Bastian's bacteria hypothesis can progress to
therapies, it first must pass a barrage of resistance from
other TSE scientists, most of whom have accepted the
prevailing hypothesis that misfolded proteins called prions
are the causative agent.
One scientist, who did not wish to be identified but who is
considered one of the world's foremost experts on TSEs, told
UPI, "If I were you, I would stay away entirely from
anything having to do with Spiroplasma."
The scientist's caution stemmed from an unpublished study
that took place approximately five years ago. At the time,
Bastian allegedly was unable to distinguish infected
scrapie brains from normal brains by testing for the
Spiroplasma bacteria.
Bastian disputed that assessment, however, and said he
correctly identified infections in 80 percent of the
samples.
Despite Bastian's contention, the negative view of the study
-- which was conducted in Dr. Robert Rohwer's lab at the
Veterans Administration hospital in Baltimore -- has
circulated among TSE scientists and perhaps has overshadowed
the data Bastian has accumulated since then in support of
his bacteria hypothesis.
Asked to comment on Bastian's recent research, Rohwer
brought up the unpublished study and told UPI, "We saw
no evidence of any bacteriological contamination of
these brains."
Rohwer added, "I really question the quality of his
research, and I think it's unfortunate that Dr. Bastian
continues to ignore his own data. He's not convinced, but I
certainly am, that there's nothing to his story."
Bastian claimed that Rohwer's lab technician found evidence
of the bacteria in one of the samples, but Rohwer did not
mention this when he later made a presentation to National
Institutes of Health officials dismissing the bacteria
hypothesis.
Bastian said shortly after the test Rohwer was awarded a $2
million NIH grant while Bastian did not receive any funding.
"I think (Rohwer is) totally dishonest," Bastian said,
charging that Rohwer attempted to dismiss his hypothesis to
get a grant from the NIH.
"If Rohwer has anything to say about that study, he should
publish the data rather than making unsupported
statements," he said.
Bastian also noted his latest study lends credence to the
presence of the bacteria in diseased brains. Spiroplasma DNA
was detected in eight of 10 scrapie samples, six of seven
CWD samples and two of two CJD samples, he said.
Another reason Bastian's idea meets such heavy resistance is
Spiroplasma bacteria as a group were only relatively
recently discovered. The organisms, which are small even by
bacteria standards, escaped detection until the 1970s when
they were first recognized as being the cause of a few plant
and insect diseases.
Spiroplasma mirum, the agent involved in Bastian's
hypothesis, is carried by rabbit ticks and is known to cause
cataract disease in suckling mice.
Although his hypothesis is controversial, Bastian is not
without his supporters.
"I've been following his work for a while and I think he's
onto something," said Dr. Jeanne Drisko, a clinical
assistant professor of alternative medicine at the
University of Kansas Medical Center in Kansas City.
Drisko also noted that in 2001, NIH awarded Bastian a three-
year grant, which means it was reviewed and approved by
experts in the field.
"That's not an easy thing to do," so it is an indication
there is some evidence to support his idea, she told UPI.
In addition, Bastian's studies, including his latest
research, have been published in peer-reviewed
scientific journals.
"My impression is no one has looked at (Bastian's
Spiroplasma hypothesis) carefully," Drisko said. "It's
almost a knee-jerk response. There's been so many people
saying there's no evidence of this, so instead of looking at
the quality of the evidence he's providing, they simply
dismiss it."
Several researchers contacted by UPI to review Bastian's
latest article either dismissed the bacteria idea outright
or did not comment.
Other scientists gave Bastian's new data a positive review
but remained skeptical about his overall hypothesis, which
was not surprising because the prion hypothesis is nearly
dogma among experts in this field.
There is little evidence, however, supporting the central
tenet of the prion view: that misfolded prions have the
capability to infect cells and cause the brain destruction
typically seen in TSEs.
Ds. Adriano Aguzzi, a pathology professor at the University
Hospital in Zurich, Switzerland, pointed out in an
article in the Journal of Experimental Medicine last
year that much of the evidence surrounding prions is
contradicted by other studies. As Aguzzi put it, the
prion has been "reported to do almost everything,
including the opposite of everything."
Under Bastian's concept, Spiroplasma bacteria use the normal
prions, which occur on the outer surface of cells, to help
them gain entry. The misfolding of the prions actually
occurs on the inside of the cells and is merely a result of
the infection, not the cause.
Bastian's idea was bolstered recently by a study done by
Japanese researchers. In a 2003 report in the Journal of
Experimental Medicine, they discovered another bacteria
called Brucella depends on the normal prion protein to
cause the disease brucellosis, which strikes both livestock
and humans.
Bastian also showed -- in research published in the American
Journal of Pathology in 1984 -- that Spiroplasma are capable
of producing in suckling rats the type of brain destruction
seen in TSEs.
Still, other researchers were not willing to accept the
bacteria as the cause and said that has not been
demonstrated yet.
"Although this (latest) work shows an association of the
presence of Spiroplasma DNA, this work does not demonstrate
causality," said Beth Williams, a veterinarian at the
University of Wyoming in Laramie, who is credited as the
first scientist to identify chronic wasting disease as a
TSE disorder.
"Thus, it is not a logical extension, in my opinion, of
these data to say" that scrapie may have given rise to CWD,
Williams told UPI. "But I believe in keeping an open mind."
Linda Detwiler, a former U.S. Department of Agriculture
veterinarian and expert on scrapie and other TSEs, said
Bastian's data suggesting a link between CWD and scrapie is
interesting because researchers still do not have any solid
answers for how CWD emerged.
"He may be onto something," Detwiler told UPI, but she
cautioned that further confirmation of Bastian's data is
needed before this hypothesis was accepted.
Detwiler's hesitation stems from a study Bastian did with
the USDA a couple of years ago, in which he was unable to
identify correctly whether sheep brain samples were or were
not infected with scrapie.
She was not ready to dismiss his hypothesis completely,
though, and said his latest results were intriguing.
"I would hope this would spur somebody to relook at
this," she said.
In his defense, Bastian said he correctly identified two out
of five scrapie infected brains in the USDA study using a
less sensitive technique called polymerase chain reaction.
When using a more sensitive method called DNA sequencing, he
said he finds evidence of the bacteria in nearly all the
infected brain samples he examines, but not in any of the
non-infected brains.
He concedes evidence showing the bacteria causes these
diseases still needs to be collected and plans to conduct
future studies with mice lacking the prion gene to help
support his hypothesis. If his idea is correct, the mice
should not become infected by the Spiroplasma.
One missing factor that would improve therapy for CJD
and vCJD is a test that can detect infection before
symptoms occur, he said. Research is planned to develop
a test that can detect the abnormal prions in blood, but
if Bastian's idea is correct, it would be too late,
because by then the brain already would have begun
degenerating. Bastian said he knows of no one working on
a test to detect Spiroplasma in the blood. http://washingtontimes.com/upi-breaking/20040624-
054020-7633r.htm
