"The Democratic Party was looking
for a scapegoat, and I think effectively tried to paint, and did paint, Ralph
Nader as the reason why they were not in office, not the fact that ten million
more Democrats voted for George Bush than voted for Ralph Nader."
In 1966, General Motors, then the most
powerful corporation in the world, sent private investigators to dig up dirt on
an obscure 32-year-old public interest lawyer named Ralph Nader. The reason:
Nader had written a book that criticized the Corvair, a General Motors car. But
the company’s attempt to discredit Nader and sully his character backfired. The
scandal that ensued after the smear campaign was revealed launched Nader into
national prominence and established him as the leader of the modern American
consumer movement. AN UNREASONABLE MAN traces the life and career of this
unique and controversial political figure.
Over the next 30 years, Nader built a
legislative record that rivals that of any contemporary president—without ever
holding public office. Following the General Motors incident, he took on the
Federal Trade Commission, which he felt was shirking its duty to protect
consumers against fraud and other harmful business practices. To carry out his
extensive campaigns, Nader tapped into the power of young people and recruited
students from across the United States. In the 1960s, many young recruits
flocked to Washington, attracted by the prospect of changing the system. Known
as Nader’s Raiders, this army of activists published a series of book-length
reports on issues ranging from workplace safety to air quality.
Many things today’s consumers take for
granted—seat belts, airbags, product labeling, free airline tickets after being
bumped from an overbooked flight—are largely due to the efforts of Ralph Nader
and his citizen groups. But did his foray into presidential politics harm his
legacy? When most people hear his name, they think of the political “spoiler”
who cost the Democrats the 2000 presidential election. While Nader has become a
pariah even among his former friends and allies, AN UNREASONABLE MAN
illustrates how he continues to be one of the most trusted activists in America,
crusading on behalf of consumer rights.
“We’re living on
borrowed time.” – Klaus Stohr (World Health Organization)
H5N1-Bird
Description
The H5N1-Bird Flu[1]
virus was first found on a farm[2]
in Guangdon Province, China in 1996.[3]
The first documented outbreak of human infection
with H5N1-Bird Flu occurred in Hong Kong in 1997. These 18 human cases in Hong Kong occurred simultaneously
with a pathogenic avian influenza in poultry farms and markets which was caused
by a virtually identical virus. Studies concluded that direct contact with
diseased poultry was the source of human infection.
For reasons –
if any – unknown, most H5N1-Bird flu cases have occurred in healthy children
and young adults.
A difficulty in discussing H5N1-Bird Flu is that the
concern really relates to a current strain evolving into a form which passes
easily between humans. Because
such strain or strains are not yet known to exist (dare I say “not reported in
the press?”), this discussion often contains degrees of equivocation. Any such evolved strain(s) might also
contain changes causing any such infection(s) to produce very mild signs and
symptoms in humans. On the other
hand, any such evolved virus(es) might cause proportionately more deaths and suffering
than did the calamitous avian flu strain which caused what is commonly referred
to as the 1918 Pandemic or as the Spanish Flu.
I had a little bird
Its name was Enza
I opened the window
The 1918 Pandemic was an avian influenza that was easily
transmitted between humans.[5]
Most of the 1918 Pandemic victims succumbed to pneumonia
caused by opportunistic bacteria that infected those already weakened by the
flu (antibiotics had not yet been discovered).
However, an appreciable minority of the 1918 victims died
within days of onset from a more severe pneumonia caused by the virus itself
that triggered massive hemorrhaging in their lungs or filled their lungs with
fluid thus leading to death by suffocation/drowning; they drowned in their own
fluids. These victims often
developed a bluish skin color with variations of (i) blood pouring from their
noses, (ii) ears, (iii) mouths and (iv) eye sockets, all with agony and some
with delirium.
More, most 1918 Pandemic deaths (bacterial-pneumatic and
drowning) occurred among younger adults between the ages of 15 and 35; people
younger than 65 constituted 99% of all “excess” (those above normal) flu deaths
in 1918-1919.
Etiology
The cause of H5N1-Bird Flu is viral infection. Typically, influenza moves via airborne
droplets which are inhaled into the victims’ respiratory tracts. However, the infection process of
H5N1-Bird Flu is thought to be via both direct
contact with (i) infected poultry, and/or (ii) surfaces and objects
contaminated by their feces.
Flu comes in three main forms, designated A, B, and
C. Types B and C affect only
humans and have never caused pandemics.
In contrast, type A flu viruses are found in many
types of animals including humans, swine, horses, other mammals, and
poultry. Ducks – and aquatic birds
– typically serve as the natural reservoir for all known subtypes of influenza
A; i.e., the virus typically infects the birds’ guts without causing symptoms.
Within the ducks’ guts the viruses can mutate and/or exchange genetic material
with other viral strains some of which are capable of passing to humans. [6]
Note, however, that this paper’s particular H5N1-Bird Flu kills birds.[7]
It spreads very rapidly through poultry
flocks where it damages multiple internal organs. Within 48 hours, the poultry
mortality rate can approach 100%.
Type A viruses are categorized into two groups based
upon distinct proteins on their surfaces which, in turn, cause the hosts to
produce different types of antibodies: types HA and NA. Hemagglutinin (HA) has at least 15 known
variants and neuraminidase (NA) has 9 subtypes. The HA molecule initiates infection by binding to receptors
on the
surfaces of host cells which, in mammals, tend to be
cells in the respiratory lining.
The NA protein enables the newly produced viruses to escape the hosts’
cells thus allowing them to potentially infect other hosts’ cells.
Signs and Symptoms
Symptoms of avian
influenza in humans range from fever, cough, sore throat, muscle aches, eye
infections, pneumonia, and severe respiratory diseases.
Unlike the typically
mild respiratory symptoms experienced by most people infected with seasonal
influenza, H5N1-Bird Flu is aggressive, causing rapid deterioration resulting
in high death rates in humans; viral pneumonia and multi-organ failure have
been common among people infected by H5N1-Bird Flu.
Diagnostic Procedures
H5N1-Bird Flu is diagnosed by recognizing symptoms followed
by either or both examination of respiratory secretions and blood/serology
examination.
Treatment
Data is limited,
but Tamiflu and Relenza are thought to reduce the severity and duration of
illness caused by H5N1-Bird Flu especially if administered within 48 hours.
However, the recent strain of H5N1-Bird Flu isolated in Egypt in March of 2006
was resistant to Tamiflu as was an earlier outbreak in Vietnam in 2005.[8]
Amantadine
and Rimantadine can be used to treat H5N1-Bird Flu, but resistance to these
drugs seems to develop rapidly; some NON-H5N1-Bird
Flu strains are already fully resistant.
Tamiflu and
Relenza are expensive to produce and production capacity is limited. Current capacity, which has recently
quadrupled, will produce enough Tamiflu to treat 20% of the world’s population
in 10 years.
Prognosis
As of 4/2/07 there have been 280 reported cases (to
emphasize the obvious, the number of non-reported cases is unknown) of
H5N1-Bird Flu with 170 of those cases resulting in death. Thus, the death rate overall has been
59%.[9] In
contrast, the terrible 1918 Pandemic had a 2% to 5% death rate yet killed 50 to
100 million people worldwide.[10]
The death rate of the 1918 Pandemic was up to 50 times the death rates produced
by other generic influenza outbreaks.
Prevention
At present,
H5N1-Bird Flu does not easily cross from birds to infect humans.
Although
potential vaccines for the H5N1-Bird Flu virus are being researched in several
countries, no vaccine is in commercial production. Because any vaccine needs to closely match the pandemic
virus, large-scale commercial production probably would not start until any new
virus has emerged. Current global production capacity falls far short of the
demand expected during a pandemic.
In February
2007, the American Food and Drug Administration (FDA) announced that an
H5N1-Bird Flu vaccine developed by Sanofi-Aventis appears to be safe. However, it is unclear how effective
the vaccine might be given the particular mutations the virus-of-the-future
might contain. The FDA announced
that the highest doses tested – two 90-microgram doses given one month apart –
produced superior results given the testing assumptions than did the use of
lower doses; 46% of the 452 people tested with the highest doses produced
sufficient antibodies such that it is thought enough protection against
H5N1-Bird Flu might be produced.
All evidence to date
indicates that close contact with dead or sick birds or their feces is the
primary source of human infection with H5N1-Bird Flu. This would suggest that, theoretically and at a minimum, avoidance
of dead and sick birds and their feces is one avenue of prevention. However, a reasonable source of
infection has not been identified in a few cases which may mean there are
additional sources of infection. Curiously, few cases have been reported
involving poultry workers, and cullers.
Why The Topic Was Chosen and
What Was Learned
Foreknowledge is valuable in the event of an H5N1-Bird Flu
Pandemic. Further, I have not
previously been required to read about/research relevant and interesting (and
powerful) viral maladies specifically and pandemics generally.
Most amazing was the tremendous variability of outcomes
produced by viral mutations/evolution and, thus, the difficulty of planning
ahead to combat same; a novice such as myself might also express it another way
by saying the instability of viral
effects over various periods of time is profound.
Aberich Duerer, the Apocalypse
REFERENCES
Books
John M. Barry, The
Great Influenza (2005)
Alfred W. Crosby, America’s
Forgotten Pandemic (2003)
Mike Davis, The
Monster at Our Door (2005)
Marc Siegel, M.D., Bird
Flu (2006)
Newspapers
New York Times, New
Strain of Bird Flu Found in Egypt is Resistant to Antiviral Drugs (January
18, 2007)
New York Times,
Scientists Warn That Bird-flu
Virus Remains a Threat (February 15, 2007)
Wall Street Journal, FDA Says Bird-Flu Vaccine Seems Safe; Efficacy Unclear (February
27, 2007)
Magazines
Scientific American, Capturing
a Killer Flu Virus (January 2005)
Scientific American, Preparing
for a Pandemic (November 2005)
Websites
MedicineNet.com http://www.medicinenet.com/bird_flu/article.htm
White House News Releases, November 1, 2005. http://www.whitehouse.gov/news/releases/2005/11/20051101.html
World Health Organization, Epidemic and Pandemic Alert and
Response (EPR), Avian Influenza http://www.who.int/csr/disease/avian_influenza/en/
(various internal links were accessed)
DVD/Video
PBS American Experience, Influenza
1918 (1998)
A&E/History Channel, The
Next Plague (2005)
John Edwards has been bashing big
health insurers in recent days with the story of a girl who died waiting for a
liver transplant. But the details of the case suggest the Democratic
presidential candidate may be oversimplifying the tale.
Nataline Sarkisyan had been battling
leukemia for three years. Insurer Cigna Corp. rejected coverage for a liver
transplant, then reversed its decision and said it would pay. The 17-year-old
died before the operation could take place.
By pushing the case so hard on the
campaign trail, Mr. Edwards is raising the emotional tone of the debate on
health care, which has already emerged as perhaps the leading domestic issue in
the campaign. Mr. Edwards and Sen. Hillary Clinton are among the Democratic
candidates attacking health insurers.
"We need a president who will
take these people on," Mr. Edwards said at the Democratic presidential
debate Saturday night. He said Nataline "lost her life a couple of weeks
ago because her insurance company would not pay for a liver-transplant
operation."
In New Hampshire yesterday, the
candidate's wife, Elizabeth Edwards, put her arm around the girl's mother,
Hilda, before Mrs. Sarkisyan spoke at a campaign rally.
Cigna defended its handling of the
case. "I'm perplexed that this has become a campaign issue," said
Jeffrey Kang, Cigna's chief medical officer. "It is highly unlikely that
any health-care insurance system, nationally or internationally, would have
covered this procedure."
Insurers are highly unpopular with
many doctors, who complain about insurance-company bureaucracy, and with
patients who don't like having medical claims denied. Left-leaning critics of
the U.S. health-care system say it isn't appropriate for some insurers to be
making billions of dollars in profit while tens of millions of Americans go
without insurance. They would prefer the "single payer" type of
system in many European nations, where the government takes the leading role in
paying for care.
While none of the leading Democratic
candidates go that far, they have railed against insurers' cherry-picking when
they decide who is eligible for a policy. People who are sick or have
pre-existing conditions find it's hard or impossible to buy coverage on their
own, something the leading Democratic candidates for president all vow to
change.
Mr. Edwards, a former trial lawyer and
North Carolina senator, wants to offer a government-run public plan, like
Medicare, that would be open to all Americans. This could be a step toward the
single-payer plan that many liberals want, and Mr. Edwards has said that it's a
good opportunity to test that idea's popularity. He also wants to cap
insurance-company profits.
The candidates have differed over what
role insurance companies should have as health-care change is hammered out. Mr.
Edwards takes a harsher tone, saying they can't be negotiated with, while
Illinois Sen. Barack Obama says insurance companies deserve a seat at the
table.
Nataline's case could provide fuel to
both sides of the argument about whether insurance companies generally do a
good job covering Americans. The day before Thanksgiving, she received a
bone-marrow transplant from her brother. Soon after, her liver failed, and she
went into a coma. Her doctors at the medical center of the University of
California, Los Angeles, recommended a liver transplant, saying that patients
in such situations would have a 65% chance of living another six months.
Cigna said both its own medical
experts as well as an outside transplant surgeon and a cancer doctor with
transplant expertise concluded there wasn't enough evidence that the procedure
would be safe or effective. But after the denial got press coverage, the
company reversed the decision on Dec. 20 "out of empathy for the
family." Nataline died later the same day.
A UCLA spokeswoman declined to comment
yesterday on Nataline's treatment, saying her family hasn't given the
university permission to discuss the case.
Cigna said it wouldn't have benefited
financially from denying the transplant because it only administered the health
plan of Nataline's father's employer. In reversing the decision, it said it
would pay for the transplant itself.
"We are asked to make the right
clinical decision by our employer customers, so it would have been unfair to
make them pay for it," said Dr. Kang, Cigna's chief medical officer.
Richard Freeman, a professor of
surgery at Tufts University School of Medicine who wasn't involved in the case,
said such cases happen too rarely to provide statistically validated medical
evidence about the benefit, if any, of a transplant.
Rather, it "boils down to a
philosophical argument," he said. Some doctors want to pursue aggressive
treatment of a patient who appears to be dying, believing it's worth improving
the chances, however slim, and fostering medical innovation. Others say the
trauma and pain of an invasive procedure such as a transplant are likely to
outweigh any medical benefit and the financial costs.
John Ford, an associate professor at
UCLA who wasn't involved in Nataline's case, questioned in a recent post on his
blog whether the survival data for a transplant were clear-cut. "It seems
highly unlikely that such data, if it exists at all, has any degree of
reliability," he wrote.
Nonetheless, the case has found a
natural fit with Mr. Edwards's pitch. The candidate is an experienced
practitioner in the modern political art of putting an ordinary person's face
on policy prescriptions. At yesterday's rally in New Hampshire, Mr. Edwards
turned the microphone over to the family of Nataline. Her father, mother and
brother emotionally spoke of her death and their anger at Cigna.
Her father, Grigor Sarkisyan, spoke in
raw terms about his loss before a packed crowd of more than 500 people at the
Franco-American Center in Manchester, N.H. He said he had promised to buy his
daughter a white car when she got her driver's license. "After she passed
away, I bought a coffin for her because Cigna -- they killed my daughter. I
don't have a daughter any more."
He added that he didn't think he'd
have to worry about this sort of issue because his family had health insurance.
"That's not right -- not in America," he said, echoing Mr. Edwards'
stump speech. "This is not right. Maybe someplace else, but not in
America."
The Edwards campaign says the
candidate had been talking about Nataline's story for weeks when, on the night
of the Iowa caucuses last Thursday, the family heard him mention their daughter
on television. They contacted the Armenian National Committee of America, which
in turn called the campaign's headquarters.
Karen Ignani, president of America's
Health Insurance Plans, the main industry lobby group, said it's addressing the
desire for health-care change by making its own proposals for universal
coverage. Last month, it offered a proposal for guaranteeing access to
individual health insurance to anyone who applies. The industry has long
opposed that idea in practice.
[1] Not all
viruses of the H5 and H7 subtypes cause the pathology often resulting from what
is commonly called “Bird Flu” and what this paper will call H5N1-Bird Flu.
[2] It has been
estimated that 2/3rds of the 1,400 human infectious diseases were initially
transmitted from animals to humans.
[3] The World
Health Organization maintains a “timeline of major events,” which, as of
4/2/07, consists of 16 pages plus one page of references at http://www.who.int/csr/disease/avian_influenza/timeline2007_04_02.pdf. Some conjecture this strain
may have originated in the 1950s.
[4] An American
children’s ditty – a jump-roping lyric – referring to the then extant 1918
Pandemic.
[5] As a point
of interest, Army Auxiliary Laboratory Number One was dedicated to
understanding and solving/curing the disease causing the 1918 Pandemic. The Lab was headed by scientist Oswald
T. Avery and located at The Rockefeller Institute. However, viruses were too small to be seen via then
contemporary microscopes or otherwise until decades later; i.e., their
existence was unknown at this time.
[6] Current thinking is that H5 and H7 viruses
are introduced to poultry flocks in their low pathogenic form. When allowed to circulate in poultry
populations, the viruses can mutate -- usually within a few months -- into the
highly pathogenic H5N1-Bird Flu. Hence, the presence of an H5 or H7 virus in
poultry is always cause for concern, even when the viral subtype produces mild
symptoms.
[7] The author
wonders if this decreases the likelihood of transmission to humans in that,
left alone, the hosts die rather than live as reservoirs.
[8] The Egyptian
strain was susceptible to Relenza and Amantadine.
[9] The World
Health Organization provides a chart of raw numbers at http://www.who.int/csr/disease/avian_influenza/country/cases_table_2007_04_02/en/index.html. However, the “death rate” calculations
are my own. In 2003, the death
rate was 100%; in 2004, 70%; in 2005, 44%; in 2006, 69%; in 2007 (to date) 48%.
[10] Pandemic
Mortality 1918-19 Revised
1927 Estimate
2002 Estimate
Worldwide 21.64 million
48.8 to 100 million
Asia
15.78
26 to 36
India
12.50
18.50
China
……
4 to 9.5
East Indies
.80
1.50
Europe
2.16
2.30
Africa
1.35
2.38
W. Hem.
1.40 1.54
USA
.55
.68
Data from The Monster
at Our Door (page 26) (itself citing the work of others). Ultimately, one third of the
Earth’s population may have been infected by the 1918 Pandemic virus;
eventually, the virus causing the 1918 Pandemic ran out of fuel, i.e., ran out
of accessible human victims and reservoirs. In the United States, death was so common that toe-tags were
affixed before the patients died; the shortage of coffins was such that armed
guards were hired to protect the all-too-few remaining that were unsold. Parents were advised to no longer waste
food on their infected children.
In 1918, American Life Expectancy was reduced by 13 years. Imagine the psychological, social and
moral stresses and consequences where a deadly pandemic is spread by your
co-workers, neighbors, friends and family? The stress was so great that seemingly a collective cultural
amnesia quickly developed about the 1918 Pandemic. Frighteningly, it is
conjectured that an H5N1-Bird Flu pandemic could be so devastating that even
the Burger Kings would be shuttered.
See: Hairston Testimony to the
104th Congress Joint Committee on Public Health, Congressional Record, p. 230 (March 22, 2007).
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