Biomedical Engineering Reference
In-Depth Information
influenza virus are known to infect birds, thus providing an extensive reservoir of
influenza viruses potentially circulating in bird populations. To date, all outbreaks of the
highly pathogenic form have been caused by influenza A viruses (IAVs) of subtypes H5
and H7. Migratory waterfowl—most notably wild ducks—are the natural reservoir of AI
viruses, and these birds are also the most resistant to infection. Domestic poultry, includ-
ing chickens and turkeys, are particularly susceptible to epidemics of rapidly fatal
influenza. Direct or indirect contact of domestic flocks with wild migratory waterfowl has
been implicated as a frequent cause of epidemics. Live bird markets have also played an
important role in the spread of epidemics.
Recent research has shown that viruses of low pathogenicity can, after circulation for
sometimes short periods in a poultry population, mutate into highly pathogenic viruses.
During a 1983
1984 epidemic in the United States of America, the H5N2 virus initially
caused low mortality, but within 6 months became highly pathogenic, with a mortality
approaching 90%. Control of the outbreak required destruction of more than 17 million
birds at a cost of nearly US$ 65 million according to WHO [5]. During a 1999
2001 epi-
demic in Italy, the H7N1 virus, initially of low pathogenicity, mutated within 9 months to
a highly pathogenic form. More than 13 million birds died or were destroyed. The quar-
antining of infected farms and destruction of infected or potentially exposed flocks are
standard control measures aimed at preventing spread to other farms and eventual estab-
lishment of the virus in a country's poultry population. Apart from being highly conta-
gious, AI viruses are readily transmitted from farm to farm by mechanical means, such as
by contaminated equipment, vehicles, feed, cages, or clothing. Highly pathogenic viruses
can survive for long periods in the environment, especially when temperatures are low.
Stringent sanitary measures on farms can, however, confer some degree of protection.
In the absence of prompt control measures backed by good surveillance, epidemics can
last for years. For example, an epidemic of H5N2 AI, which began in Mexico in 1992,
started with low pathogenicity, evolved to the highly fatal form, and was not controlled
until 1995.
In 1997, the outbreak of a new AI-like virus, known as Bird Flu, affected 18 humans. The
cases, many severe or fatal, highlighted the challenges of unique influenza viruses.
Researchers struggled to track a new potentially deadly strain of influenza, which before
was only thought to affect chickens. Lessons from this episode help to improve interna-
tional and national planning for influenza pandemics. This proposal highlights the action
taken to keep the Bird Flu from becoming a global pandemic and a way of detection as a
preventive measure.
Fowl plague (FP) was described in 1878 as a serious disease of chickens in Italy. It was
determined in 1955 that FP virus is actually one of the influenza viruses. The AI viruses,
along with the other influenza viruses, make up the virus family Orthomyxoviridae. The
virus particle has an envelope with glycoprotein projections with hemagglutinating and
neuraminidase (NA) activity. These two surface antigens, hemagglutinin (HA) and NA,
are the basis of describing the serologic identity of the influenza viruses using the letters
H and N with the appropriate numbers in the virus designation, for example, H7N2. There
are now 15 HA and 9 NA antigens described among the type A influenza viruses. The type
designation (A, B, or C) is based upon the antigenic character of the M protein of the virus
envelope and the nucleoprotein within the virus particle. All influenza viruses affecting
domestic animals (equine, swine, avian) belong to type A, and type A influenza virus is
the most common type producing serious epidemics in humans. Types B and C do not
affect domestic animals. All type A influenza viruses, including those that regularly cause
seasonal epidemics of influenza in humans, are genetically labile and well adapted to
elude host defenses. According to Cordingly [6] Influenza viruses lack mechanisms for the
“proofreading” and repair of errors that occur during replication. As a result of these
