http://www.aapsonline.org/press/nrmscuba.htm
MEDICAL JOURNAL EXPOSES CUBA'S BIOTERRORISM LINK
May Have Been Source of West Nile Virus, Producing Anthrax-Like Toxins
Washington -- Iraq may have unleashed the West Nile Virus in the United
States via Cuba through the release of migratory birds infected with the
virus, and may be producing antiobiotic-resistant toxins for future attacks,
according to two articles published in The Medical Sentinel, The Official
Journal of the Association of American Physicians and Surgeons (Volume 6,
Number 4).
In the first, "West Nile Virus - Is Castro's Bioterrorism Threat Being
Ignored," author Ernesto F. Betancourt, Castro's Washington Representative
in the '50s and former Director of Radio Marti, outlines the possible
Cuba-Iraq link.
He cites ornithologist, Carlos Wotzkow, who was fired from Cuba's Institute
of Zoology after objecting to the creation of the "Biological Front," an
effort to develop viruses that could be carried by host birds or other means
into the U.S.
A second article, "Cuba, Castro and Bioterrorism," by Agust�n Blazquez, a
documentary producer, outlines his claims that "... we clearly see that
Castro has used this time to develop weapons of mass destruction in our
backyard to be used against us."
Mr. Blazquez cites a previously ignored paper by Dr. Manuel Cereijo, a
professor at Florida International University. "In 1992, the
[Castro-controlled] Institute of Oceanographic Studies conducted an
experiment with the Academy of Sciences to find out which places on the
Cuban coast were the best to let bottles and containers reach the United
States coast line fastest and most effectively," writes Dr. Cereijo.
Further, Dr. Cereijo claims that there are at least 12 Cuban centers
producing bacteriological agents located around Havana, and that the U.S.
government has had knowledge of these capabilities. He describes the newest
and most notorious, La Fabriquita ("Little Factory") located across the
street from the former Naval Hospital. Disguised as an "Animal Feed Plant,"
one must pass through a station of the Cuban Armed Forces to enter. Dr.
Cereijo believes the plant has the capability to produce A-232, an agent
more toxic that previous nerve agents, and that La Fabriquita could be
producing an anthrax-like toxin totally resistant to antibiotics. Concludes
Mr. Blazquez, "The blackmail potential that this represents renders the U.S.
and its people in grave danger and in an almost impotent situation."
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Three on Maui die from flesh-eating bacteria
. Centers for Disease Control and Prevention information
Three people on Maui have died since the beginning of the year from the rare
Group A Streptococcal bacteria infection, also known as flesh-eating
bacteria, the state Department of Health reported today. Another three
people were also reported to have had the disease.
Three individuals became ill shortly after wound exposure and died within a
few days to a week, according to Dr. Paul Effler, interim chief of the
department's Communicable Disease Division. The Department of Health issued
an alert today but no one from the department was available to provide
details. It was not known why the alert was issued today, where on Maui the
people were exposed to the bacteria nor precisely when this occurred.
In each case, the victims were healthy people with no significant medical
histories, he said.
The flesh-eating bacteria causes necrotizing fasciitis, which destroys
muscles, fat and skin tissue. The bacteria can enter the body through any
type of skin wound, such as ocean-reef cuts, abrasions, punctures, bug
bites, stings, splinters, tears or burns.
Early symptoms of infection include fever and severe pain, warmth, swelling
or redness around the wound.
Proper and immediate wound care is important to reduce the likelihood of
further cases, he said.
A 5-year-old Wahiawa girl acquired the same bacteria in 1999 after cutting
her knee. Her intensive-care treatment in California was costly, and the
community raised money to help.
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Single Gene Change Underlies Transmission Of PlagueA single gene change in a
relatively benign recent ancestor of the bacterium that causes bubonic
plague played a key role in the evolution of the deadly disease, researchers
report in the April 25 issue of the journal Science.
By acquiring this gene, the bacterium gradually changed from a germ that
causes a mild human stomach illness acquired via contaminated food or water
to the flea-borne agent of the "Black Death," which in the 14th century
killed one-fourth of Europe's population.
The new research adds an important piece to understanding the forces behind
the emergence of plague, which occurred within the past 1,500 to 20,000
years.
"Our research illustrates how a single genetic change can profoundly affect
the evolution of disease. In this case, that genetic change set the stage
for a completely new route of disease transmission," notes B. Joseph
Hinnebusch, Ph.D., lead author of the study and plague expert in Rocky
Mountain Laboratories, a Montana outpost of the National Institute of
Allergy and Infectious Diseases (NIAID).
The gene allowed the bacteria to be transmitted through the bite of an
insect -- in this case, the flea -- an adaptation that distinguishes
Yersinia pestis, the plague germ, from all closely related, more benign gut
bacteria.
In turn, as Y. pestis adapted to rely on its new blood-feeding host for
transmission, the emergence of more deadly bacterial strains would have been
favored, the researchers conclude.
The evolution of the plague bacterium is just one example of how microbes
persistently challenge researchers by unexpectedly repackaging themselves,
in any of multiple ways, to emerge as novel or more virulent agents of human
disease.
In the new report, Dr. Hinnebusch and his colleagues from Sweden, Michigan,
and NIAID describe how they explored the source of this gene and later
identified the critical role it plays.
The gene codes for an enzyme known as PLD. Previous work indicated that Y.
pestis picked up this gene from either an unrelated bacterium or a simple
nucleated organism.
Next the researchers infected fleas with variants of Y. pestis that either
contained or lacked the PLD gene and then observed the outcome. They
discovered that the enzyme is required for survival of the plague bacterium
in the midgut of the rat flea.
Although the enzyme's activity protects Y. pestis from being destroyed,
thereby allowing it to colonize the flea gut freely, the researchers do not
yet know the molecular mechanism by which this protection occurs.
"To find that out is clearly the next step," Dr. Hinnebusch notes.
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Health officials fear that Ebola might still be spreading in the Republic of
Congo after six people died in a remote northeastern district.
The suspect fatalities were reported last week in Kelle, a district that
borders Mbomo, where the outbreak began in October.
The latest victims came from two villages and were believed to have eaten
monkey meat. They had developed symptoms of the disease, and officials were
still waiting for laboratory confirmation, said Dr Ebata Mongo, head of the
government's campaign against Ebola..
If Ebola proves to be the cause of their deaths, it would bring the death
toll in the country to 18.
An additional 23 people have died on the other side of the border, in Gabon,
since the outbreak began, according to World Health Organization figures.
WHO said last week it was satisfied the outbreak in Central Africa was under
control after all those who had contact with known victims cleared the
disease's 21-day incubation period without developing symptoms.
But the new deaths raised the possibility Ebola was still spreading in the
densely forested region, inhabited by Pygmy and other tribes.
WHO officials in Republic of Congo planned to send an expert to Kelle in the
coming days to help local officials set up a surveillance system.
Ebola is one of the most deadly viral diseases and kills between 50 and 90
percent of those who contract it. It spreads through bodily fluids and
attacks internal organs, causing bloody diarrhoea and vomiting. Within two
weeks, the victim usually dies from massive blood loss.
WHO says more than 1,000 people have died of the disease since the virus was
first identified in 1976 in western Sudan and in a nearby region of Congo.
The disease last struck in Uganda, killing 224 people there last year.
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