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A gene that mutates rapidly and continually can turn relatively weak
strains of avian influenza (AI) virus into poultry-killing strains.
In 1983, more than 17 million chickens were slaughtered to halt a severe
U.S. outbreak caused by such a mutation. Last year, a virulent, highly
contagious strain began killing Mexican poultry. In several isolates of
Mexican AI, ARS scientists found the mutant gene. This new genetic clue
to AI's severity may open the way to predicting which strains are likely
to become poultry killers, just as health agencies routinely predict
severe strains of human influenza. ARS scientists found that AI virus
uses a genetic mutation mechanism similar to that of the human flu. The
key AI gene controls the shape of a molecule called hemagglutinin, or HA.
A relatively weak AI virus binds only to respiratory tract or gut cells.
With an HA molecule that has mutated to take on the "right" shape, the
virus also attacks cells of other organs, especially the brain and heart,
causing fatal results.
Southeast
Poultry Research Lab, Athens, GA
Michael L. Perdue/David E. Swayne, (706) 546-3435
A virus that kills unborn and newborn pigs may lurk in the lungs of
carrier pigs even when the virus isn't detectable in the pig's blood or
other tissues. Free-floating, infection-fighting cells in pigs' lungs
often can carry porcine reproductive and respiratory syndrome (PRRS)
virus. ARS researchers flushed out these cells, called alveolar
macrophages, and in laboratory tests were able to identify the virus in
them when other tissues in the pig apparently were virus-free. Quick
identification of this virus can help cut pork producers' losses that may
range as high as $250 per sow. Pigs can be long-term carriers of the
virus without showing signs of disease.
National Animal Disease
Center, Ames, IA
William L. Mengeling, (515) 239-8254
A toxin made by fungi that can infect corn disrupts an essential fat in
mammals. This discovery by ARS and Emory University scientists may
lead to reducing the disease threat posed by the toxin, called fumonisin.
Five years ago, scientists learned that high levels of fumonisin are the
direct cause of rare outbreaks of disease in farm animals. The outbreaks
had long been tied to animal feed, such as broken corn kernels called
screenings, infected with Fusarium fungi. Several dozen horses in
Kentucky and Virginia died earlier this year after eating
Fusarium-tainted screenings. Scientists elsewhere have linked
fumonisin to higher rates of cancer of the esophagus in people in areas of
southern Africa and China. Now, the ARS and university researchers have
established a link between fumonisin and fats known as sphingolipids.
These fats occur in plants and animals, mainly in cell membranes. In
studies with cells, farm animals and plants, the researchers found that
high levels of fumonisin halted the making of sphingolipids. Instead, one
of the fat's building blocks--a molecule called sphinganine--grew to
extraordinarily high levels. Also, rates of cell division became either
abnormally slow or rapid. These changes often are early signs of disease.
Little is known about the dietary role or biological function of
sphingolipids. But the new findings suggest they are important for plant
and animal health.
Toxicology
and Mycotoxin Research, Athens, GA
Ronald Riley/Kenneth Voss, (706) 546-3377
Pork producers should check the label before relying on a vaccine to
protect their pigs against Atrophic rhinitis, a respiratory tract
disease. ARS studies recently confirmed the effectiveness of
commercial vaccines made with a denatured Pasteurella multocida
toxin called a toxoid. Not all vaccines against Atrophic rhinitis
are made with a toxoid. In tests, pigs vaccinated against Atrophic
rhinitis gained weight normally and didn't develop nasal or bone
deformities that are a telltale sign of the disease. Atrophic
rhinitis costs Iowa pork producers about $4 million annually in
vaccines, medications, reduced weight gains and deaths.
National Animal Disease
Center, Ames, IA
Mark R. Ackermann, (515) 239-8221
Last updated: October 30, 1996
Return to: Quarterly Report
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