VETERINARY MEDICINE
:
a medical specialty consisting of the diagnosis and treatment of diseases
of animals other than humans. See also diseases
of Mammalia,
infectious
disease vectors and reservoirs
and physiology of metazoa.
For each species, classified according to current taxonomy, the main
infectious and toxic diseases are listed below. A distinction is made between
infectious diseases that can be transmitted to humans and diseases which
cannot.
buiatrics : the treatment of diseases of cattle
theriogenology : that branch of veterinary medicine dealing with
reproduction, including the physiology and pathology of male and female
reproductive systems and the clinical practice of veterinary obstetrics,
gynecology, and semenology.
stirpiculture : the systematic attempt at improving a stock by attention
to the laws of breeding
Bettlach May disease : a fatal disease affecting adult honeybees,
principally in Switzerland, marked by paralysis with inability to fly,
caused by ingestion of the poisonous pollen of certain buttercups.
Isle of Wight disease : paralysis of muscles of flight in honeybees
due to tracheal infestation by the mite Acarapis woodi
polyhedral diseases : infectious diseases of insects, especially
caterpillars, caused by viruses.
nosema disease : a protozoal infection of bees caused by Nosema
apis, characterized by dysentery and paralysis
sacbrood : an infectious disease of the larvae of bees, caused by
a virus
the varroa mite (Varroa
destructor) was first discovered infesting Asian honey bees (Apis
cerana) in Java; subsequently this dreaded parasitic infection
spread to European honey bees (Apis mellifera), and was discovered
in Europe in about 1970 and then in the USA in 1987. Mite eggs are laid
in sealed brood cells and the resultant nymphs feed on bee pupae destined
to become worker bees. Infestations are spread from colony to colony by
fertilized female mites attached to bees. Infestations can cause colony
extinction within 3-4 years if no control measures are undertaken. Varroa
mites transmit viruses to honey bees, such as Black Queen-cell virus, Sacbrood
virus, and Acute bee-paralysis virus. Varroa, a reddish-brown, oval
mite 1mm to 2mm long, is found on the outside of adult honey bees, is not
dangerous to humans and does not affect honey. Widespread around the world,
it attacks honey bees and their larvae, and wipes out hives by killing
the bees needed to pollinate pastures and crops. Varroa is a reportable
disease according to OIE. Manual of Diagnostic Tests and Vaccines for Terrestrial
Animals Chapter Part 2, Section 2.9, Chapter 2.9.5. An excerpt from that
chapter includes: "The mite Varroa destructor (formerly Varroa
jacobsoni) is a parasite of adult bees and their brood. It penetrates
the intersegmental skin between the abdominal sclera of adult bees to ingest
haemolymph. It can sometimes be found between the head and thorax. The
number of parasites steadily increases with increasing brood activity and
the growth of the bee population, especially late in the season when clinical
signs of infestation can first be recognised. The life span of the mite
depends on temperature and humidity but, in practice, it can be said to
last from some days to a few months. Identification of the agent: The clinical
signs of varroosis can only be recognised at a late stage of infestation,
so that diagnosis entails the examination of the hive debris. The debris
produced during the summer is especially useful for diagnosis. The earliest
and most precise diagnosis can be made only after the application of a
medication that forces the mites to drop off the bees or kills them directly.
Larger amounts of debris can be examined using a flotation procedure. Bees
are washed in petroleum spirit, alcohol or detergent solution. However,
this method is less accurate due to the unequal distribution of mites and
the usually small sample sizes. In heavily infested bee colonies, clinical
signs of varroosis can often first be seen in the latter part of the season
when the brood is reduced. Heavy infestations are usually reached 3-4 years
after the primary invasion, but can occur within weeks if infested by bees
from nearby colonies that are collapsing. Essentially, the brood is damaged
by the parasitic mites. Bees and their offspring that have been infected
during the brood phase by only one parasitic mite show various ill effects,
such as a shortened life span, changes in behaviour and an increased disease
susceptibility. The parasitism is critical if more than one mite enters
the brood cell for reproduction. Only in the lethal stage immediately before
the collapse of the colonies do clinical signs, such as shrunken wings
and shortened abdomen, appear. This is due to an increased susceptibility
to deformed wing and acute paralysis virus, as well as to the infection
of wounds and loss of haemolymph. If the brood dies shortly before or after
sealing, clinical signs of European foulbrood appear without the presence
of the specific agent Melissococcus
pluton. If the brood survives, the emerging bees show various behavioural
changes and their life span is considerably shortened." Although there
are many tests to verify the presence of the mite, there appears to be
little in the way of treatment for the colonies. There are some products
providing limited success. From the OIE chapter cited above: "There are
no biological products and vaccines available. Formic acid, oxalic acid,
lactic acid and thymol can be used to control Varroa mitesref.
Some hygienic strains are less susceptible to Varroa parasites.
Genetic diversity helps honeybees to regulate the temperature of their
hives : worker bees huddle together to keep the hive between 32°C and
36°C when eggs are developing. To cool down their digs, the bees fan
their wings to drive out the warm air. Australian researchers found the
bees' internal thermostats vary more in hives with several different fathers,
which causes the pollinators to start fanning at slightly different temperatures.
The gradual adjustments prevent the whole hive from constantly switching
between heating and cooling, keeping temperatures at an optimal level more
often, on average. Comparing regular beehives to other hives in which the
queen was artificially inseminated, each worker shared the same father.
Hainan, China, is well known for its butterflies, and has been called the
Butterfly Kingdom. There are 609 species of butterflies on the island,
which represents about half the butterfly species of China. The Jianfengling
rainforest has one of the world's biggest concentrations of butterflies
and is sometimes known as the Butterfly Valley. On 29 Jun 2005 at 11:00
a.m., the reporters drove along the East Line Highway towards Qionghai.
From kilometer 8, the colorful dead butterflies were scattered along the
road and began to attract attention. At first, the reporters believed that
the butterflies had hit car windshields and died. But further down the
road, there were more dead butterflies. By kilometer 12 the dead butterflies
could already be described as numerous. At kilometer 12, the reporters
got out of the car for a closer inspection. Every one or 2 meters along
the shoulder of the road there were one or 2 dead butterflies. In some
places they were relatively more concentrated, and some off-road sites
had about 10 butterflies, most of which were dead, while a few were fluttering
weakly and then died. The butterflies were of various sizes, some beautifully
colored. The reporters discovered several dead butterflies in the grass
past the guard rail. With each passing car, dead butterflies were carried
by the wind and then dropped back down. As the reporters continued along
the road there were numerous dead butterflies which did not thin out until
kilometer 23. After kilometer 24 they were essentially not seen. The reporters
asked 2 patrolling highway management personnel the cause of the butterfly
deaths. They said they had never before encountered this kind of situation
and that it might have been caused by excessive heat. I have no idea what
caused the death of these butterflies, what species they were, or whether
the dead butterflies comprised more than one species. However, butterflies
often migrate in large numbers and when they cross busy highways many are
killed, as I have seen in northern Nigeria. It is well known that extreme
weather conditions can cause mortality of adult butterflies, as has been
recorded in the Monarch butterfly (Danaus plexippus). Butterflies
do become infected with various pathogens, but death occurs in the larval
stages. Possibly more information will be forthcoming on the species
of butterflies dying in Hainan and the causes of such mortality.
hemocyte disease of flat oysters, caused by Bonamia
ostreae, has been reported in Europe, Canada and on both coasts
of the USA. Its impact can be serious, as evidenced by a drop in French
oyster production of almost 90% in 1995. Some infected oysters may
appear to be healthy; others will show yellow discoloration and/or extensive
lesions (i.e. perforated ulcers) in the connective tissues of the gills,
mantle, and digestive gland. Pathology results from hemocyte destruction
and diapedesis due to proliferation of the parasiteref
QX parasite -- "Q" for Queensland state, where it is thought to
have originated, and "X" for unknown : New South Wales Fisheries (NSW),
the state agency responsible for the industry, says the disease is caused
by the parasite Marteilia sydneyi, whose origin is uncertain
and whose life cycle is thought to include an unknown intermediate host.
Unique to the east coast of Australia, the Sydney rock oysters are prized
around the world for their exquisite taste, long shelf life, and, some
suggest, aphrodisiac properties. The disease threatens to destroy an AUD
30 million (USD 23.1 million) a year industry, taking with it the livelihoods
of hundreds of oyster farmers whose families have harvested the molluscs
for generations. The disease has hit so hard that a 3rd generation of oyster
harvesters might be the last to make their living from Sydney rock oysters,
which take 4 years to reach maturity and require meticulous farming. They
must be tended daily. Unlike other oysters, Sydney rock oysters can survive
for up to 3 weeks out of water and can be delivered alive to restaurants
worldwide. 23 Hawkesbury oyster farms may go out of business after total
losses of AUD 10 million (USD 7.7 million) since the parasite 1st attacked
in 2004. In 2004, the parasite was found in about 30 per cent of the Hawkesbury
oysters. Now almost all are affected. Illustrating the extent of the disease,
a harvester shucked open about 50 of his oysters before he found one alive.
As well as being fast-moving, the QX parasite also has close to a 100%
mortality rate. It kills by attacking the oysters' gut and starving them.
It spreads rapidly, but the oysters suffer a lingering death. So far, the
QX disease has been unstoppable. It destroyed the industry in southern
Queensland in the 1970s and reappeared in the Georges River, which cuts
through southern Sydney, 10 years ago, wiping out farmers there. Now it
is devouring oysters in the Hawkesbury, the 2nd-largest producer behind
a system of rivers in northern New South Wales. After the Georges River
outbreak, NSW Fisheries selectively bred what it believes are QX-resistant
oysters from the few that survived. These are now being put to the test
in Hawkesbury. The Sydney rock oyster industry is among Australia's oldest.
Aborigines had harvested the native oysters for centuries before the arrival
of European settlers, who began commercial oyster farming in the 1890s.
In the meantime, Hawkesbury farmers have asked the New South Wales government
to contract them to clean the river of dead oysters so as to generate much-needed
income. They say healthy oysters even play an important role in river environments
by keeping pollution levels down. Having oysters in the river is like having
a oil filter in your car. They help improve the river's health.
withering syndrome of abalone caused by Candidatus
Xenohaliotis californiensis (CXc) on the west coast of California,
United States of America (USA) and Baja California, Mexico. However, as
infected abalone have been transported to Chile, Japan, Israel, and other
countries, the geographical range of the etiological agent is suspected
to be broad where California red abalone,
Haliotis
rufescens are cultured. If detected outside the known range
of CXc, light microscopy, in combination with molecular probes, if available,
must be used to identify, and distinguish, the detected organism from other
rickettsial bacteria. The presence of these pathogens in any abalone should
be regarded as potentially serious, and the OIE Reference Laboratory should
be consulted. CXc infects the gastrointestinal epithelial cells of the
posterior esophagus, digestive gland, and, to a lesser extent, intestine.
The dimorphic rod-to-spherical shaped bacterium measures an average of
332 x 1550 nm in the bacillus form and an average of 1405 nm in the spherical
morphotype. The bacteria reproduce within intracytoplasmic vacuoles 14-56
um in diameter. Severe infections result in withering syndrome, a disease
that is characterized by morphological changes in the digestive gland,
which vary between species, and may include degeneration (atrophy of tubules,
increase in connective tissues, and inflammation) and/or metaplasia of
the digestive tubules. The metaplasia involves the replacement of terminal
secretory/absorptive acini with absorptive/transport ducts similar in appearance
to the post-esophagus. Some hyperplasia of the absorptive/transport ducts
may also be involved. This morphological change is accompanied by a decrease
in feeding, and a depletion of glycogen reserves, followed by use of the
foot muscle as an energy source and death. The foot of affected abalone
contains fewer, and less organized, muscle bundles, abundant connective
tissue, and may contain more cerous cells than unaffected individuals.
Disease (withering syndrome) occurs at elevated water temperatures (> 18°C).
The incubation period of withering syndrome is prolonged and ranges between
3 and 7 months. Cumulative mortality has been recorded at > 99% in black
abalone and at > 30% in red abalone. The pathogen and disease (withering
syndrome) may occur year round, but losses due to the disease occur most
often in the summer and autumn, after a 3-to-4-month period when temperatures
are elevated over 15°C. Reducing densities, and the application of
an oxytetracycline-medicated diet, may reduce losses. For diagnosis, the
recommended guidelines for sampling are those stated in Chapter 1.1.4 and
Chapter I.2. of the Aquatic Manual
lobster(lobsters)
: Vibrio spp. related to Vibrio fluvialis => limp lobster
disease (weakness and lethargy). It is not clear why the bacteria suddenly
appeared in Maine, USA, in 1997, but the researchers suggest that global
climate changes may have played a role. Previous research has suggested
that iron-rich dust from African deserts can be transported to the North
Atlantic by winds, where they provide a nutritional boost for varieties
of plankton with which vibrio bacteria associate. Lobsters may be more
susceptible when they are not harvested from traps promptly, because of
the weakened immunity that can come with prolonged captivity.
Barramundi nodovirus is a small picorna-like virus that attacks
the central nervous system, especially the brain and retina. It most often
attacks 15 to 17-day-old larvae. The clinical signs of this disease are
uncoordinated darting, spiral or corkscrew swimming, pale coloration, anorexia,
and wasting. The disease has been named "viral nervous necrosis" (VNN).
Hatcheries can control the disease by not recycling culture water, chemical
disinfection of influent water and larval tanks between batches, and reduction
of larval stocking densities. To decrease the likelihood of this disease,
stocking densities should not exceed 15 larvae per liter, and, generally,
be less than 10 per liter. Several native Australian fish species, as well
as barramundi (Lates calcarifer) are known to be susceptible to
infection and/or to develop clinical disease. Experimentally, Macquarie
perch (Macquaria australasica), silver perch (Bidyanus bidyanus)
and Murray cod (Maccullochella peeli) have been shown to develop
clinical signs and lesions typical of VNN following bath exposure to virus.
Histological lesions of VNN together with viral particles have been described
in Australian
catfish (Tandanus tandanus), and a nodavirus has been isolated
from clinical cases of VNN in sleepy cod (Oxyeleotris lineolatus).
VNN is -- and remains -- a major threat to the native fish fauna of the
Murray Darling basin of southeastern Australia. Every effort must be made
to prevent its incursion into this ecosystem. Quarantining of the infected
farms is a commendable and appropriate action that may prevent escape of
virus and consequent infection of native fish in the immediate vicinity.
To state that the virus does not pose any risk to native fish species appears
misleading.
Marsupenaeus
penaeid shrimp : white spot disease (WSD) is characterized
by high and rapid mortality accompanied by gross signs in moribund shrimp
of white, and, initially, circular inclusions or spots in the cuticle,
sometimes also accompanied by overall red body coloration. Disease progression
is characterised by cessation of feeding followed within a few days by
the appearance of moribund shrimp swimming near the surface at the edge
of rearing ponds. The causative agent is shrimp
white
spot syndrome virus (WSSV) / white spot virus (WSV), a dsDNA virus
of the genus Whispovirus within the family Nimaviridae that is potentially
lethal to most of the commercially cultivated penaeid shrimp species. WSD
outbreaks were first reported in farmed Marsupenaeus
japonicus (a.k.a. Penaeus japonicus) in Japan in 1993; later,
outbreaks of viral disease with similar gross signs and caused by similar
rod-shaped viruses were reported from elsewhere in Asia, including the
People's Republic of China, Taiwan, Thailand, Korea, India, Balgladesh,
the Philippines and the USA. During 1999, WSD also had a severe impact
on the shrimp industries of both Central and South America. WSD is one
of the 8 crustacean diseases that are reportable to the OIE. For further
details on WSD, its diagnostic procedures, relevant procedures related
to international trade , and a reference list, the reader is referred to
chapter 4.1.2. of the OIE Diagnostic Manual for Aquatic Animal Diseases
- 2000ref1,
ref2.
Hirame
rhabdovirus (HIRRV) : a genus in the family Rhabdoviridae, infecting
numerous species of fish with broad geographic distribution. HIRRV is an
important virus of cultured flounder (Paralichthys olivaceus). The
type species is ...
infectious
hematopoietic necrosis virus (IHNV) is a bullet-shaped, enveloped rhabdovirus
with a ssRNA genome of negative polarity that can cause reduced food consumption
and increased mortality. Some fish and shrimps that survive infection and/or
epizootics apparently carry the virus for life and pass it onto their progeny
and other populations by vertical and horizontal transmission.
sharks are in a global extinction crisis : they were so common, in fact,
that they were viewed as pests by fishermen
over the past 50 years, the number of oceanic whitetip sharks, once the
most common shark in the world and the dominant species of the world's
largest ecosystem, have crashed by more than 99% in the Gulf of Mexico.
Researchers think the same drop has happened around the world. Tuna fishing
and the lucrative trade in shark fins are blamed for the animals' demise.
Shark's fin soup is a prized delicacy in many regions - in Hong Kong's
markets, for example, a kilogram of shark fin can fetch hundreds of dollars.
The sharks are often hooked on the long lines used to catch tuna
Carcharhinus
falciformis (silky sharks) in the Gulf of Mexico have declined
by around 90% since the 1950s
hammerhead shark (Sphyrna)
numbers in the Atlantic have plummeted by 89% in the past 15 years
Ichthyophonus
hoferi is a parasite that infects most organs and tissues of many
marine fish. The disease caused is of economic significance, because
epizootics have resulted in mass mortality of commercial fish species such
as Atlantic herring (Clupea
harengus L.) and Yukon River king salmon. Although systemic infections
are lethal, variations in pathogenic effects -- including myositis, or
muscle inflammation -- have been observed, depending upon the particular
isolate of I. hoferi and the host species involved
there are both Atlantic herring (Clupea
harengus) and Pacific herring (Clupea
pallasii). A wide variety of fish and animals feed on them, including
chinook salmon, cod and halibut, and also are eaten by porpoises, seals,
sea lions and orcas. Freshly spawned herring eggs once drew swarms of marine
birds, especially diving ducks called surf scoters. Their silvery bodies
"flash" in the sun when they turn quickly. The habit is called "flashing."
koi
herpesvirus (KHV) : KHV has already been identified in at least 10
European countries, in Israel, the USA, Japan and Indonesia. Though the
great majority of the outbreaks have affected ornamental fish, KHV disease
has been reported in common carp farms in Germany and Indonesia. It poses
a serious threat to the extensive pond culture of food carp in East-European
countries as well as wild carp populations all over Europe and Asia. It
could become a serious world threat to carp production, diminishing the
protein supply for large human populations. The disease has 80% mortality
and threatens 2 important fish populations: the ornamental
koi carp industry, which is worth tens of millions of dollars in Japan,
and the common carp, the world's fourth most-farmed fish. The first reporting
in association with high mortality among common (Cyprinus
carpio) and koi carp stocks originated in Israel in 1997, relating
to cyprinid-fish farm sites there. Authorities there were alerted to the
problem in October, when fish began dying in Ibaraki prefecture's Lake
Kasumigaura, where more than half of Japan's farmed carp are produced.
KHV was first isolated in the UK in 2000 during a disease outbreak in northern
England. Outbreaks of clinical disease with signs similar to KHV disease
had been reported in 1998 and 1999. More KHV outbreaks were confirmed in
each of the years 2001-2003 using PCR and cell culture-based assays. Later,
KHV DNA was detected in tissue samples taken in 1996 during an unexplained
mass mortality of koi and common carp in the UK. By the end of 2003, the
disease had been reported in common or koi carp in 23 of Japan's 47 prefectures.
However, ascribing its spread to Europe, Indonesia, and the US to the said
observations should be approached with caution; early identification and
reporting of a disease agent does not necessarily indicate its true origin.
Experts fear that the virus could cause further economic damage if it spreads
to farmed carp stocks in other countries - particularly in China, which
produces 75% of the world's farmed carp. Development of a PCR-based assay
for the detection of koi herpes virus DNA in formalin fixed, wax embedded
archive tissue has been reported. UK outbreaks of the disease in 1996 could
be associated with KHV; this was subsequently confirmed by ISH. Intensive
fish culture, koi shows, and regional domestic and international trading
are the 3 main mechanisms that have contributed to the rapid global spread
of KHV. The movements of fish pathogens with ornamental fish and the active
international trade in live fish, including koi, have been recognized as
a key pathway for the spread of emerging fish diseases. Unfortunately,
as with most ornamental fish, unrestricted movements of koi continue, nearly
all without health inspections or implementation of quarantine programs
at the wholesale or individual hobbyist level. It would be of utmost importance
to carry out surveillance, to report, and to take measures to prevent the
introduction of this serious pathogen into the carp populations of countries
where this species is a major source of animal protein. KHV is not currently
listed as a notifiable disease by the European Union nor by the Office
International des Epizooties (OIE). Consequently, there is no requirement
for exporting countries to provide any health certification to show freedom
from the disease. However, in a number of countries, ornamental fish trade
organisations have introduced a number of initiatives in an attempt to
control the spread of the disease. This has included the establishment
of trade networks where wholesalers and importers are notified when the
disease is diagnosed in batches of koi. Other initiatives include the establishment
of disease-free broodstock and the provision of quarantine facilities for
importers. The virus has already been identified in at least 10 European
countries, in Israel, the USA, Japan and Indonesia. Though the great majority
of the outbreaks have affected ornamental fish, KHV disease has been reported
in common carp farms in Germany and poses a serious threat to the extensive
pond culture of food carp in East-European countries as well as wild carp
populations all over Europe. It could become a serious world threat to
carp production, diminishing the protein supply for large human populations.
According to FAO statistics, the world cyprinid (mainly carp) annual production
is approximately 17 million tons, of which more than 12 million tons are
produced in China : the KHV situation there is not known. Since 1998, the
newly recognized Koi herpesvirus (KHV) has caused mass mortality among
common carp and koi in the USA, Israel, Germany, England, Italy, Netherlands,
Indonesia and Japan. It seems that the disease was present but not recognised
in previous years (KHV DNA was detected in tissue samples taken in 1996,
during an unexplained mass mortality of koi and common carp in the UK).
Intensive fish culture, koi shows, and both domestic and international
trading in the absence of health certifications or inspections have contributed
to the rapid global spread of KHV. Recent investigations into mortalities
on coarse fisheries have provided evidence for the spread of KHV into wild
populations of common carp. This has become the most severe hazard of this
emerging disease. Since KHV is not a notifiable disease, there is no requirement
for exporting countries to provide any health
certification to show freedom from it. However, in a number of countries,
ornamental fish trade organisations have introduced a number of initiatives
in an attempt to control the spread of the disease. This has included the
establishment of trade networks under which wholesalers and importers are
notified when the disease is diagnosed in batches of koi. Other initiatives
include the establishment of disease-free broodstock and the provision
of quarantine facilities for importersref.
According to FAO statistics, the world cyprinid (mainly carp) annual production
is approximately 17 million tons, of which more than 12 million tons produced
in China. The KHV situation in this huge subcontinent is not known; we
repeat previous requests for any available information on relevant KHV
monitoring activities thereref1,
ref2,
ref3.
Web resources :
spring
viremia of carp virus => spring viremia of the common as well
as other types of carp (SVC) was first diagnosed in the United States
in 2002. It has been recognized for over 50 years in Europe, occurring
commonly in the Middle East and Asia as well. It can have a substantial
impact on production, killing up to 70% of young carpref.
SVC is mainly concentrated in countries of the European continent that
experience low water temperatures during winter. The disease has been known
to be present in the UK for decades; 6 outbreaks have officially been reported
to the OIE during the years 2001-2003
fish that live in the polar oceans survive at low temperatures by virtue
of 'antifreeze' plasma proteins in the blood that bind to ice crystals
and prevent these from growing. However, the antifreeze proteins isolated
so far from the winter flounder (Pleuronectes
americanus), a common fish in the Northern Hemisphere, are not
sufficiently active to protect it from freezing in icy sea water. A previously
undiscovered antifreeze protein from this flounder that is extremely active
(as effective as those found in insects) and which explains the resistance
of this fish to freezing in polar and subpolar watersref
Perciformes
Channoidei
snakeheads (Channidae) are a group of predatory freshwater fish
native to Africa and southern Asia. They can live out of water for extended
periods, jump up to four metres high and cover large distances on land.
Some northern snakeheads (Channa
argus) released after being bought in a New York live fish market for
a home aquarium caused a panic in 2002 years ago when they were caught
by fishermen in Maryland, USA. But the fish's extensive migratory history
could tell researchers about the climate of the past. The species' migration
and extinction history during the Miocene period, from 24 million to 5
million years ago, provides a good indicator of summer precipitation, because
the fish's present-day distribution suggests that snake-heads are limited
to climates with at least one month of rainfall of 150 mm and a mean temperature
of 20°C. During the past 20 million years, snakeheads have twice migrated
from their Himalayan origins to subtropical and temperate regions in Africa
and Eurasia. The most extended migration events - 17.5 million years ago,
and between 8 million and 4 million years ago - must have been linked with
changes in atmospheric circulation in the Northern Hemisphere, which led
to increased air humidity and summer precipitation in regions that were
formerly dry in summer. The presence of snakehead fossils in central European
deposits indicates that in a much warmer climate the region had come under
the influence of moist northern trade winds : this is likely to have been
caused by a northward shift of the 'meteorological equator' - a weather
trough that normally sits just north of the Equatorref1,
ref2
largemouth bass virus (LMBV) => disease is restricted only to largemouth
basses (Micropterus
salmoides) and extreme high temperatures could be a catalyst
seabass
VNN, pseudotuberculosis, streptococcosis and tuberculosis
seabream is much more resistant and is mainly affected by novel
Vibrio infections
enteromyxidiosis
Coryphaenidae
(dolphins); wild dolphins, not just captive ones, have been seen
to swim in circles when they sleep : dolphins in the Northern Hemisphere
swim in anticlockwise circles, whereas dolphins in the Southern Hemisphere
swim in clockwise circles for 86% of their time. Some will remain unconvinced
until dolphins are observed after being moved from one hemisphere to another
: this is going to be related to the size of the group, the natural history
of the individual species and the shape of the tank. What kind of "global
forces" could cause this? One possibility is the Coriolis force - an effect
of Earth's rotation that produces large-scale currents in the ocean and
atmosphere. This is the force that is said to be responsible for water
spinning down a drain in different directions in the Northern and Southern
Hemispheres - although physicists disagree over whether seeing the Coriolis
force on this tiny scale is possible, even in a hypothetically flawless
sink. Do the dolphins somehow sense this force and choose to swim against
the prevailing currents? The scale of a dolphin's slumberous circuit is
also too small to be related to the ocean-sized currents. Another possibility
is that the animals all swim in the same direction to stay together during
the relatively vulnerable hours when they are half asleep. When dolphins
are awake they use their signature whistle to keep together. When they
are sleeping, they don't want to be vocalizing, because they don't want
to attract attention. If they have all learned - or been genetically programmed
- to swim in the same direction, they could stay together silently. Dolphins
seem to start and stop swimming, or change direction, about once every
40 seconds, which is the same duration as their breathing rate. This less-than-a-minute
stretch between breaths may be the "attention span" of a half-asleep dolphin.
Gadus
morhua(Atlantic cod) Hatchery-reared cod are being taught
'life skills' in a bid to help them survive in the wild. The organizers
of the project hope that by raising cod in more stimulating enclosures,
the fish will fare better in the open ocean and contribute to ailing natural
stocks. In a study carried out in Bergen, Norway, researchers have discovered
that Atlantic
cod (Gadus morhua) are bolder and more inquisitive if they are
raised in tanks containing stones and plastic plants, and fed at varying
times and locations. Raising them in these conditions, rather than in unfurnished
tanks with predictable mealtimes, means the cod may stand a better chance
when released in the wild. The idea of replenishing wild stocks with farmed
fish is controversial. This is partly because farmed fish tend to grow
larger than their wild counterparts, which leads some to fear that they
will compete with natural fish over food and actually drive down stock
numbers. And if the raised fish are inbred, and they outcompete natural
fish, the resulting lack of genetic diversity would adversely affect the
population. On the other side of the coin, farmed fish seem to have problems
adapting to life in the wild. In some cases, fish have been spotted trying
to eat pebbles that resemble the food pellets with which they were previously
fed. This may mean that introduced fish do not thrive or breed, so stock
numbers will not be improved. After considering all these factors, a responsible
release campaign could help struggling species, including salmon and trout
as well as cod. I'm not advocating we take any old cod and release them
: we would prefer to breed from wild stocks every time, and then release
those. In their study, Braithwaite and Salvanes caught wild cod and bred
their offspring in hatchery tanks for eight weeks before dividing them
into four groups. One group was raised in normal farm conditions; the others
were given either an unpredictable food regime, a tank furnished with stones
and plants, or both. After several weeks, the researchers tested the fish's
ability to deal with predators, prey and new surroundings. Fish raised
in the most stimulating environment were more likely to venture out to
meet a dummy fish. Those given furnished tanks recovered from signs of
stress more quickly after being chased with a net, which is a rough simulation
of a predator attack. And fish given unpredictable food were more likely
go after live prey. The results show the benefits of living in an enriched
environment. Similar effects have been shown in birds and in mammals such
as rodents. Fish have much more sophisticated cognitive abilities than
they've been given credit for in the past. The researchers are now setting
up a larger project on the west coast of Ireland, and they hope that commercial
investors will be attracted by the idea. Previous attempts to equip fish
for life in the outside world have been labour-intensive, and involved
exposing them to real prey and predators. We're advocating a simpler approachref
infectious haemorrhagic
necrosis (IHN) in the rainbow trout is a naturally occurring
virus that is endemic throughout Oregon, Washington and Northern California.
It initially attacks the blood-forming tissues of the kidney. Younger fish
suffer the effects of the disease. External symptoms of the virus include
lethargy, darkening of the skin and bleeding at the base of the fins. According
to biologists, adult fish carry -- and shed -- the virus into the water,
but don't die from the disease. MS-222 (tricaine methane sulfonate) is
in the novocaine family of drugs and has been approved by the American
Veterinary Medical Association panel on euthanasia as an acceptable and
humane way of killing fish that will not be eaten by people
bacterial diseases
lactococcosis
visceral flavobacteriosis
parasitical diseases
proliferative kidney disease (PKD). Malachite green is a very effective
parasite/fungus control in many aquatic environments. It penetrates deeply
into fish body tissues and may be useful against Proliferative Kidney Disease
(PKD) in salmonids. Because of this deep tissue penetration, malachite
green is thought to be toxic to tetras, catfish, loaches, and some small
marine fish. It is also this deep tissue penetration that may lead to concentrations
higher than believed safe for human consumption, because malachite green
is presumed to be a carcinogen. This has resulted in a ban on using it
in the USA, except for aquarium fish. Readers are reminded that it is banned
on the presumption -- not proof -- of its carcinogenic potential.
Nevertheless, there are a number of safety precautions to be considered
when handling malachite green, such as gloves and eye protection
infectious
salmon anaemia virus => infectious salmon anaemia (ISA) is an
infectious disease of Atlantic salmon (Salmo salar). It attacks
the blood cells of fish and causes massive hemorrhaging. It can be carried
through the water or transmitted by sea lice. Wild herring are also known
to be carriers of this disease. Initially reported in Norway in the mid-1980s,
ISA has to date been reported in Canada (New Brunswick and Nova Scotia),
the United Kingdom (Scotland and the Shetland Islands), the Faroe Islands,
and USA (Maine), and the causal virus has been isolated from samples from
Coho salmon from Chile and from rainbow trout in Ireland. The disease has
been recorded in Norway earlier in 2004. ISA is one of the 16 notifiable
fish diseases listed by the OIE; further details may be found in chapter
2.1.9. of OIE's manual of Diagnostic Tests for Aquatic Animals
viral
hemorrhagic septicemia (VHS) virus (VHSV) of various salmonid and
several non-salmonid fishes => viral hemorrhagic septicemia (VHS).
The VHS virus is readily transmissible to fish of all ages, and survivors
of infection can become lifelong carriers that shed virus with urine and
sex products. The virus ostensibly gains access to the fish through the
secondary gill lamellae. In the hatchery environment, mechanical transfer
of VHS virus on the surface of animate or inanimate objects presents a
substantial hazard. Prevention of contact between the virus and the host
is the most effective method for controlling VHS.
infectious
pancreatic necrosis (IPN) virus, although harmless to humans, can kill
up to 80% of susceptible fish. It became widespread on Scottish salmon
farms during the period 1996-2002. Prevalence shows a large variation,
IPN virus being the most common (88% prevalence), in Shetland marine sites
in 2002, while remaining undetected in fresh water sites in the Outer Hebrides
for several years. Prior to 2001, this variation was largely controlled
by differences between regions, with the effect of differences between
fresh water and sea water environments, and year-to-year differences, being
of secondary significance. Recently, the role of regional differences has
declined, while that of inter-annual variation has increased. Seasonal
differences in IPN virus prevalence are small in spite of large differences
in case numbers. Year-to-year differences are highly significant in that,
except in the southern mainland, this variance reflects a trend of increasing
IPN virus prevalence at an annual rate of 3% in fresh water and 7.6% in
sea water, but local increases sometimes happen faster than this. In Orkney,
the northern mainland, and, particularly, the Outer Hebrides, these increases
were from low to moderately high levels. However, in Shetland, the initial
prevalence was not low, so IPN virus had become almost ubiquitous in sea
water by 2000. By 2002, very high prevalence had been reached in marine
waters in almost all areas. In fresh water sites, the prevalence of IPN
virus also shows rapid increase, which is faster in Shetland fresh water
sites than in fresh water sites elsewhere. More statistical analysis of
the data for 1996-2001 is available elsewhere.
twist or whirling disease : a highly fatal protozoal disease of
young salmonid fish caused by Myxosoma cerebralis, characterized
chiefly by cartilaginous damage in the axial skeleton and granuloma formation
involving the auditory-equilibrium apparatus of the fish, causing it to
swim rapidly in a circular pattern
gas embolism due to nitrogen supersaturation : if cold lake water
runs down the canal, and heats up during transit, without the opportunity
to outgas, this could contribute to supersaturation. Depending on design
and factors such as water flows and depth, weirs and similar features in
rivers can also contribute to supersaturation.
coldwater or peduncle disease : infection of aquarium fish by Cytophaga
psychrophila; symptoms include lumps or cottonlike lesions on the skin
and gills with ulceration, necrosis, and hemorrhage
columnaris disease / cotton-wool or cotton mouth disease (because
of its white mold-like appearance when it forms skin lesions) : infection
of warm-water fish by Flavobacterium
columnare (a.k.a. Cytophaga columnaris and Bacillus columnaris).
It is is the second leading cause of mortality in pond raised catfish in
the SE USA, second only to enteric septicaemia of catfish, caused by Edwardsiella
ictaluri. Most species of fish are susceptible to columnaris disease
following some type of environmental stress and when water temperatures
are in the upper part of their preferred temperature range. The disease
commonly occurs in channel catfish when the water temperatures are in the
range of 25'C to 32'C or 77'F to 90'F in the spring, summer & fall.
Schooling species of fish, like white bass, are especially susceptible.
Fish with this disease usually have yellowish-brown slimy or cottonlike
skin lesions on their gills covering surface necrosis. These lesions result
in the erosion of the gills by protein- and cartilage-degrading enzymes
produced by the bacteria. Skin ("saddleback") lesions can be noted encircling
the body of fingerlings; as well as lesions inside the fish's mouth. F.
columnare can also be isolated from internal organs (for example in
a study in Mississippi, 40% of fish with external lesions had isolations
from internal organs) but the significance is uncertain. Swelling of the
posterior kidney has been noted. In 1999, in Kansas, USA, it killed
an estimated 48,000 white bass at Melvern Reservoir and some 6,000 white
bass also fell victim at Pomona Reservoir. The bacteria enter through skin
abrasions, the mouth, or the gills, and is most often spread by contaminated
nets or food sources. Most often it affects fish that are stressed by poor
water quality (high water temperatures, low dissolved oxygen concentration,
or inadequate diet). Fish that are commercially raised may suffer from
the disease in cases of overcrowding. In such contained areas they may
be treated with oxytetracycline (Terramycin) added to the feed or water.
However, this may be impractical in the case of large lakes or free-flowing
streams and rivers. 2 similar fish kills in the past (in Australia) that
were caused by epidemic F. columnaris in the gills and skin lesions.
Both were associated with warmer waters than usual), but the more important
factor appeared to be stirring up of the sediment caused by river flooding.
Warm water alone as a disease factor occurs commonly, but F. columnaris
epidemics
are much rarer, and they seem to require an increase in turbidity and particulate
matter. F. columnaris is a sediment-associated bacterium, so any
stirring up of the sediment, as occurs with flood or storm, seems to lead
to much greater baseline exposure. This is followed by infection, disease,
and rapid horizontal spread, which amplifies the process. In theory it
should affect more than one species, but the degree of tolerance seems
to vary a lot between species, so it is often the case that one species
will succumb first to an environment-related disease epidemic.
white spot disease / ich / ichthyophthiriasis / ick : a pustular
eruption involving the skin, gills, and eyes of marine and freshwater fishes
both in the wild and in aquaria, caused by the histophagous protozoan Ichthyophthirius
multifiliis, and often leading to death, and sometimes to great economic
loss
causes of cataracts in fish unrelated to trauma usually include
aging, chronically poor water quality, and deficiencies of several vitamins,
including riboflavin. It would seem that the approach of examining the
diet and the environment may be the most appropriateref
Renibacterium
salmoninarum, an intracellular pathogen with salmonid macrophages,
is the cause of bacterial kidney disease (BKD) / renibacteriosisref1,
ref2,
a chronic, debilitating disease with high mortality, which is characterized
by granulomatous lesions, primarily on the kidney and other organs. BKD
can cause large numbers of mortalities in both farmed and wild salmon and
trout. It was first recognized in Atlantic salmon on the River Dee, Scotland
in the 1930s, and in 1976 there was the 1st notable case of BKD in farmed
rainbow trout. Whilst the disease is considered serious and notifiable
under EU law, it is not widespread in Great Britain and occurs only sporadically.
The disease occurs worldwide in cultured and wild salmon. BKD affects the
health, fitness and survival of salmonids at all life stages during both
fresh and saltwater phases. In the Pacific Northwest Columbia River drainage
and estuary, it is a serious problem in cultured broodstocks of endangered
chinook and sockeye salmon and hatchery raised fish. Currently, there are
no vaccines available to prevent R. salmoninarum infections, and
antibiotic treatment has also proven less than optimalref.
BKD has no implications for human health.
Additional information on BKD is available in CHAPTER 2.1.11. of OIE's
Manual of Diagnostic Tests for Aquatic Animals, 2003ref
There are currently 5 known species of Asian carp in the US. These include
grass carp (Ctenopharyngodon idella), common carp (Cyprinus carpio),
silver carp (Hypophthalmichthys molotrix), bighead carp (H. nobilis),
and black carp (Mylopharyngodon piceus).
Web resources :
Risk
on local fish populations and ecosystems posed by the use of imported feed
fish by the tuna farming industry in the Mediterranean by WWF : the
EU's farmed tuna industry, dominated by Spain, buys > 200 000 tonnes of
mostly frozen and untreated fish annually from the North Atlantic, West
Africa and South America. Nearly all Europe's farmed tuna exports go to
Japan. A huge amount of fish is dumped into the Mediterranean to feed tuna
and this brings a risk of exotic diseases. The fact it is concentrated
in just a few places makes the disease risk much higher. WWF has asked
the European Commission, the EU executive, to ban non-Mediterranean fish
for tuna farms and use feed pellets instead. Europe's tuna farming is driven
mainly by demand for sushi and sashimi in Japan, the world's largest consumer
of fresh and frozen tuna, and destination for more than 90 percent of the
EU's farmed tuna exports. Spain, particularly its southeastern region of
Murcia, runs most of the EU's 45-odd tuna farms. Malta and Italy are also
major players and, outside the European Union bloc, Turkey and Croatia.
WWF said up to 25% of Mediterranean farmed tuna comes from Murcia, where
> 56 000 tonnes of baitfish are introduced into a 170-km (105 mile) coastal
stretch every year. 15-25 kg (33 and 55 lb) of fish feed are needed to
produce 1 kg of tuna, it said in a study. The fish used as feed are usually
small-sized species such as herring that do not live in Mediterranean waters.
Sarcopterygii [in-part: fishes], Tetrapoda;
Amphibia (amphibians)
=> cutaneous chytridiomycosis is an emerging fungal disease
responsible for a series of global population declines and extinctions
of amphibians (including North American bullfrogs (Rana
catesbeiana)) caused by a zoosporic fungus, Batrachochytrium
dendrobatidis, which develops solely within keratinized cells,
causing extensive hyperkeratosis and death by an-as-yet-unknown mechanism:
international trade may play a key role in the global dissemination of
this and other emerging infectious diseases in wildlife. This newly-described
amphibian disease has now been reported almost worldwide for the first
time. Recent work implicates the international trade in amphibians as a
mechanism of introduction, and legislation is currently being considered
to curtail this risk. The disease has drawn attention due to its association
with amphibian population declines. Amphibian chytridiomycosis is caused
by a non-hyphal, protist-like chytrid fungus (Phylum Chytridiomycota) infecting
keratinized amphibian epidermal cells, causing thickening of the stratum
corneum (the outer layer of skin) and death by an unknown mechanism. Chytrid
fungi are early-branching true fungi inhabiting soil, freshwater ponds
and streams, and degrade chitin, keratin and other detritus. Some are parasites
of algae, invertebrates and plants. The amphibian chytrid (Batrachochytrium
dendrobatidis) is the only species known to parasitize vertebrates.
Chytridiomycosis, described in 1998 from Australian and Central American
amphibians dead at sites of mass mortality and population declines, is
pathogenic to a range of amphibians (frogs, toads, salamanders) in the
wild and experimentally. The pathogen has been cultured on modified agar,
and Koch's postulates have been proven. Its recent geographic expansion
(e.g., W. Australia), probable increase in impact on amphibian populations,
and recent discovery mark it as an emerging infectious disease (EID), one
of a growing number of wildlife EIDs. In Australia, species in decline
tend to be habitat specialists with low fecundity -- traits possibly predisposing
populations to declines with virulent pathogens. Often, outbreaks have
resulted in multi-species local population extinctions. The ability of
Batrachochytrium
to persist as a saprobe in the absence of amphibian hosts (shown in the
lab) or via aclinical infection of long-lived tadpoles may explain the
disease's ability to cause local extinctions. It has been hypothesized
that chytridiomycosis was the proximal cause of extinction of the golden
toad of Costa Rica and 2 species of Australian gastric brooding frogs.
Chytridiomycosis was confirmed as the cause of death in the last live collected
individuals of Taudactylus
acutirostris, another Australian species thought likely to be extinct.
[Chytridiomycosis] is associated with population crashes worldwide: USA
(8 states and 11 amphibian species); Central America (Panama and Costa
Rica); South America (Ecuador); Europe (Spain); Australia (44 species in
eastern and western states); and infected animals have recently been reported
in Africa (South Africa and Kenya), New Zealand (South Island), Europe
(Germany) and Uruguay. Further details can be obtained from the following
regularly-updated global distribution listref:
for further discussionref.
Historical data (from archival collections) indicates the first presence
of chytridiomycosis in North America in the 1970s and in Australia during
1978. Epizootiological data from Central America and Australia (high mortality
rates, wave-like spread of declines, wide host range) suggest introduction
of Batrachochytrium into naive populations and the disease
subsequently becoming enzootic in some areas (e.g., USA and some parts
of Australia). Chytridiomycosis as recently been reported from amphibians
within the international pet trade (Europe and USA), the trade in amphibians
for outdoor pond stocking (USA), importation for zoo collections (Europe,
USA), laboratory animal supply stocks of domestic and foreign origin (USA),
and species known to have recently been introduced nationally and internationally
(cane toad in Australia, bullfrogs in USA, Litoria species in New Zealand). These trades often involve high numbers of
individual amphibians: e.g., 180 000 amphibians of at least 21 endangered
European species were imported into the UK alone, between 1981 and 1990.
The majority of frog legs sold in restaurants in France, the rest of Europe
and the USA are in fact from bullfrogs (Rana
catesbeiana), a north American species, bred in specialized bullfrog
farms in the Far East and South America, then exported to Europe and the
USA as live animals or frozen parts. Global climate change has been proposed
as a mechanism of emergence for chytridiomycosis. Data from Monteverde,
Costa Rica, suggests a climate change-induced increase in the number of
dry days and length of dry periods in winter coinciding with extinction
of the golden toad (Bufo
periglenes). There is a hypothesis of environmental drying causing
crowding of amphibians at water sources, leading to increased rates of
transmission. Legislation to prevent introduction has begun: the Parks
and Wildlife Commission of the Northern Territory (Australia) has recently
banned national and international import and export of amphibians. Clearly,
the increasing prevalence of this disease worldwide makes it an emerging
disease of great importance. What do an old pregnancy test for women and
a mysterious fungus that is killing frogs have in common? Plenty, according
to researchers at North-West University in South Africa, who believe they
have traced the spread of the killer fungus to trade in the African clawed
frog, used for decades in a bizarre but effective way of determining pregnancy.
We think we have traced the origin of the spread of the amphibian chytrid
fungus to the 'frog' pregnancy
test
for women, which was widely used from the 1930s to the 1960s. That test
involved taking the urine of a woman and injecting it into an African clawed
frog. If the woman was pregnant the hormones in her urine would stimulate
ovulation in the frog and it would spawn within a matter of hours. The
species was exported to labs around the world in huge quantities from South
Africa from the 1930s -- the decade in which Weldon has traced the first
recorded case of the fungus by examining preserved frogs in museum collections.
Some of the exported frogs were released or escaped into the wild where
it is believed they spread the fungus, which can move quickly through a
water system and can jump from one frog species to another. The first case
of the fungus recorded outside South Africa was in 1961 in Quebec, Canada.
Adding weight to the case for an African origin is the fact that the fungus
is widespread in southern Africa but frogs in the region appear to have
developed a resistance to it. However, it remains unclear if its roots
are in southern Africa or elsewhere on the continent. Frogs here for the
most part are resistant to it. Some do succumb to it but we have not witnessed
the mass die-offs experienced elsewhere. The African clawed frog itself
shows no clinical symptoms of the disease, which means it is the perfect
vector: a carrier which does not die from the fungus. However, other species
in southern Africa are not resistant, although there are none of the die-offs
recorded in other parts of the world. The clinical signs are obvious to
experts: crazy frogs. The symptoms are neurological and seem to affect
their behaviour. River frogs, for example, are found far above the water
level in plants and even high up in trees. Nocturnal species come out in
daylight. This river frog is infected. Frogs infected with the fungus also
display an excessive shedding of their skin. The fungus is having a devastating
impact on frog populations around the world, lending a sense of urgency
to the research being done here. You have to go the origin of the disease.
The idea of 'out of Africa' is still a hypothesis but it has a lot of support.
Another team of researchers said in early January that the fungus had been
aggravated by global warming and has killed entire frog populations in
Central and South America. Du Preez said it had been detected in the Americas,
Africa, Australia and Europe but, so far, not Asia. It probably hasn't
been found in Asia yet simply because scientists have not made a concerted
effort to find it there. About 1/3 of the 5743 known species of frogs,
toads and other amphibians are classified as threatened, according to the
Global Amphibian Assessment. Up to 167 species may already be extinct and
another 113 species have not been seen in recent years. Habitat loss is
a major threat but species have also died off in pristine environments,
pointing to other causes such as the fungus. We fear that species are even
being wiped out before they have been described by science. The team is
off this month to the Indian Ocean island of Madagascar to see if the fungus
is present there. Madagascar, famed for its weird and wonderful wildlife,
is home to about 250 frog species, all but one of which are found nowhere
else. The ecological stakes are high. Amphibians are right in the centre
of the food chain. They keep insect numbers down and serve as food themselves
for many species, including wading birds, reptiles and even fish. If you
remove that link you remove an enormous flow of energy from the ecosystem.
The amphibian fungal disease chytridiomycosis is caused by the zoosporic
chytrid fungus Batrachochytrium dendrobatidis, originally found
causing mass mortality in wild frogs in Australia and Central America in
the late 1990s. It has been reported as the cause of die-offs in
Australia, New Zealand, Europe and North Central and South America.
It is the likely cause of a a number of species extinctions in Australia
and Latin America and is responsible for so-called 'enigmatic population
declines' in amphibians in these regions. These declines are a major
conservation issue and the focus of a great deal of research. The question
of why the fungal agent simultaneously appeared in the 1990s on 2 different
continents as a cause of declines may be explained as observer bias, and
it has now been shown that it originally was associated with amphibian
declines in the Western USA in the 1970s. A review on this was published
in Emerging Infectious Diseases (EID) in 1999ref.
The evidence is pretty convincing that this is a global panzootic, either
spreading from a single source by introduction, or spreading locally from
multiple sources due to some factor such as climate change or local environmental
changes. The African clawed frog / pregnancy testing hypothesis for how
this disease spread globally was originally published in EIDref.
It's an intriguing idea that is supported by 1) the finding that populations
of clawed frogs in the wild persist in the presence of this pathogen, and
2) the timing of the development of this trade for pregnancy testing. Others
have cited the bullfrog (Rana catesbeiana) as a potential source
of spread. Bullfrogs can be infected with the pathogen, but they're
resistant to the disease. They are also widely farmed in Latin America
and Asia, and exported live around the world (including into the USA) for
the restaurant trade in frogs legs (Mazzoni, R et al. 2003. Emerging pathogen
of wild amphibians in frogs (Rana catesbeiana) farmed for international
trade. EID 9:995-998).
red leg diseases : the virus implicated is a member of the genus
Ranavirus
of the family Iridoviridae. Iridoviruses are large complex viruses possessing
a large double-stranded DNA genome, which infect a variety of hosts. Iridoviruses
have only been isolated from poikilothermic (cold-blooded) animals, usually
those inhabiting damp or aquatic environments, including marine habitats.
None are known to infect warm-blooded vertebrates. In 1992 investigations
into incidents of unusual and mass mortalities of the common frog (Rana
temporaria) in Britain conducted at 10 sites of unusual mortality resulted
in 2 main disease syndromes being found: one characterized by skin ulceration
and one characterized by systemic haemorrhages due to septicemia. However,
frogs also were found with lesions common to both of these syndromes and
microscopic skin lesions common to both syndromes were seen. The bacterium
Aeromonas
hydrophila,
which has been described previously as causing similar lesions, was isolated
significantly more frequently from haemorrhagic frogs than from those with
skin ulceration only. However, as many of the latter were euthanased, this
may have been due to differences in post mortem bacterial invasion. An
iridovirus-like particle has been identified on electron microscopical
examination of skin lesions from frogs with each syndrome and iridovirus-like
inclusions have been detected in the livers of frogs with systemic haemorrhages.
Also, an adenovirus-like particle has been cultured from one haemorrhagic
frog. A poxvirus-like particle described previously from diseased frogs
has now been found also in control animals and has been identified as a
melanosome. Both the prevalence of the iridovirus-like particle and its
association with lesions indicate that it may be implicated in the aetiology
of the disease syndromes observed. Specifically, we hypothesize that primary
iridovirus infection, with or without secondary infection with opportunistic
pathogens such as A. hydrophila, may cause natural outbreaks of
'red-leg', a disease considered previously to be due to bacterial infection
onlyref.
If the disease is caught early it can be treated, but after several days
of infection the mortality rate is 90%. Frogs are the "hub" of the food
chain : predators such as foxes, stoats and buzzards, which rely on them
as a food source, could suffer. There is no evidence red leg can spread
to humans or pets. In the early 1970s it was common practice to ship live
amphibians by rail or bus to rural high schools in western Canada for use
in the biology curriculum : if the bus was delayed, or if the heating system
allowed the frogs to become chilled, there were large die-offs due to "red
leg", which is not a disease itself but rather a condition of kidney failure.
It is often associated with infection by Aeromonas hydrophila, considered
an opportunistic pathogen of amphibians. It is essentially ubiquitous in
aquatic environments. It establishes itself in stressed or immunosuppressed
animals, and not entire populationsref.
ranaviruses and chytridiomycosis both cause mass mortalities in amphibians
(including toads). There are well-supported observations (all published
in peer-reviewed journals) of sites with hundreds of dead amphibians at
some chytridiomcyosis outbreaks and up to tens of thousands of dead salamanders
at sites of ranavirus outbreaks. It's plausible that the dead toads in
Germany all died relatively simultaneously due to one of these or another
infectious agent. They had just congregated to breed, and this is a good
opportunity for an outbreak. Also, both ranaviruses and chytridiomycosis
have been reported from Europe, and there is evidence that they have been
transported between outbreak sites elsewhere, so it's possible they've
just been introduced to the waterbody. One scenario is that large numbers
of toads that died due to another reason would then begin to decompose
such that gases produced by gut bacteria caused the "explosions," but of
course, the cause of death remains uncertain. The idea that birds attacked
them, leading to the die-off, is unlikely. European Bufo toads are mostly
active at night and usually hide away during
the day, and there is only one previous report of a mass-mortality
in which birds were implicated, but that was countered by findings from
another groupref.
The other idea, that recently imported horses infected them with an unknown
pathogen, is also unlikely, and there are no other reports that I know
of citing disease transmission from horses to toads. The article states
that they tested for fungal pathogens; it would be interesting to see whether
they tested for chytridiomycosis and ranaviruses. The reported "exploding
toad" syndrome might be explained by exposure to chemical contaminants
that could disrupt the mucus membranes of the skin and/or osmotic exchange
balance of dermal or internal organ tissues, resulting in excess water
accumulation within body tissues, buildup of excess internal fluid pressure,
and subsequent explosive rupturing of body tissues. In Ontario, Canada,
several of our urban
water bodies are off-limits for the swimming of dogs (and people, one
assumes) due to complications from C. perfringens, both as an enteric
pathogen and as an intertriginous [causing chafing] skin pathogen. Despite
its aversion to oxygen, C. perfringens persists in pond water, especially
where fecal contamination is high. Due to the perverse toilet habits of
urban humanity, human and canine feces are washed into urban waterways
by rain run-off, producing a stagnant fecal bacterial culture. Under the
proper anaerobic condition, C. perfringens will grow rapidly and
elaborate extravagant quantities of gas (hydrogen and carbon dioxide).
Trapped by mammalian skin and muscle it causes "gas gangrene". In the abdomen
of the toad, I can believe the gas could rapidly exceed the stretch tolerance
of skin. I was able to find one paper about dipteran myiasis producing
Clostridial infections in amphibians, although these were frogs and I don't
find any reference to explosions: Souza Jr, F. L.; Hip"Lito, M.; Baldassi,
L.; Martins, M. L. . Cases of buccal myiasis in the bullfrog (Rana catesbeiana
Shaw, 1802), with larvae of Notochaeta sp.Aldrich, 1916 (Diptera: Sarcophagidae)
in S"o Paulo, Brasil. Mem Inst Oswaldo Cruz Rio de Janeiro, v. 84, p. 517-8,
1989.
Other nontransmissible diseases : duck
enteritis virus (DEV) => duck viral enteritis (DVE) / duck plague,
an acute, highly contagious infection of ducks, geese, and swans of all
ages, caused by a herpes virus. It is characterized by sudden death, high
mortality (particularly among older ducks), and hemorrhages and necrosis
in internal organs. Field strains of the causative herpesvirus are similar
antigenically but vary considerably in pathogenicity. An effective chick-embryo-adapted,
modified live vaccine is available for use in domestic ducks, administered
subcutaneously. DVE is not a zoonosis. Diagnosis of DVE -- an OIE notifiable
disease -- is based on a combination of assessing the clinical signs, gross
pathology, and histopathology supported by the isolation and dentification
of the virusref.
Newcastle disease, avian influenza, and fowl pox may cause similar lesions,
but they are rarely reported in ducks. Laboratory confirmation of this
suspected outbreak is pending. DVE is reported in domestic and wild waterfowl
in Europe, Asia, North America, and Africa. Economic losses on domestic
duck farms have been limited to serious, and sporadic die-offs in wild
waterfowl have been limited to massive. There is no treatment. Prevention
is based on maintaining susceptible birds in a disease-free environment.
Contact with wild, free-flying waterfowl and direct or indirect contact
with contaminated birds or material (free-flowing water) should be avoided.
Control is effected by depopulation, removal of birds from the infected
environment, sanitation, and disinfection. A chicken-embryo-adapted, modified
live virus vaccine has been approved for use in domestic ducks, in zoological
aviaries, and by private aviculturists. A 0.5-mL dose is administered SC
or IM to domestic ducklings >2 wk old, with a booster inoculation 1 yr
later. The vaccine is not approved for use in wild ducks. Field strains
of the causative herpesvirus are similar antigenically but vary considerably
in pathogenicity. An effective chick-embryo-adapted, modified live vaccine
is available for use in domestic ducks, administered subcutaneously. DVE
is not a zoonosis. Diagnosis of DVE -- an Office International des Epizooties
list B disease -- is based on a combination of assessing the clinical signs,
gross pathology, and histopathology supported by the isolation and identification
of the virusref.
Newcastle disease, avian influenza, and fowl pox may cause similar lesions,
but they are rarely reported in ducksref Infectious serositis is one of the various names of a bacterial
disease in ducks caused by Rimerella
anatipestifer. The other names are new duck disease (because
The disease is quite infectious among ducklings aged 2 to 4 weeks) and
Pasteurella
anatipestifer infection. A bacterin and, more recently, a live
vaccine, which include the 3 most common immunotypes of
R. anatipestifer,
are available for use in ducks. The disease does not affect humans. It
is usually triggered by an unclean breeding environment and spreads quickly
in cold weather
Other diseases not transmissible to humans
: goose parvovirus (a virus of the genus Parvovirus that causes
a highly fatal disease of young geese affecting the liver, thyroid, and
pancreas)
Cygnus
spp.:
with badly decomposed swans, a relatively simple identification technique
is to examine the sternum and trachea (assuming they are still present).
In the mute swan, there is no tracheal loop passing through the sternum,
whereas a loop of some sort is enclosed in a bony protuberance of the sternum
in the trumpeter, tundra and whooper swans. These may easily be seen
through a single, mid-sagittal cut down the sternum, using a bandsaw.
pigeonpox : a type of fowlpox
seen in pigeons, characterized by pox lesions of the oral mucosa and the
eyelids, sometimes resulting in blindness.
Falconiformes; Accipitridae; Accipitrinae; Gyps
Gyps
bengalensis (Oriental white-backed or white-rumped ultures).
Griffon vultures are huge scavengers and used to be ubiquitous in south
Asia. But their population has declined drastically since the mid-1990s,
and they are near extinction in Pakistan, Nepal and India. As a result,
animal carcasses rot outside villages, attracting rabies-ridden packs of
dogs. The Parsee religious community in India is also in crisis, as it
disposes of its dead by feeding them to vultures. Deaths are due to exposure
to residues of diclofenac
(a painkiller used widely in cattle, that causes kidney failure and uric
acid crystals throughout their bodies when ingested by the birds) in livestock
carcasses, as suspected last summer. Vultures come from miles around to
feed on a carcass, so each gets a small bit of many animals. Only one in
250 dead cattle needs to have been recently treated with diclofenac to
cause a decline in vultures of 30% per yearref
Galliformes
Meleagrididae
Meleagris
Meleagris
gallopavo (turkeys) : Chlamydophila
psittaci,
Erysipelothrix
rhusiopathiae
(erysipela in animals, erysipeloid in humans; acute deaths, droopy birds,
and diarrhea. Gradual emaciation, anemia, and weakness occur in cases with
endocarditis. It decreases egg production, and, may cause male infertility
in chronic infections in poultry)
Other nontransmissible diseases :
infectious sinusitis of turkeys / airsac disease : a common, sometimes
highly fatal respiratory disease of turkeys and game birds, caused by pleuropneumonia-like
organisms and marked by swelling below the eyes and sneezing
Prevention : the virus used for the inactivated
vaccine is extracted from spleens of infected turkeys, since its propagation
in tissue cultures or embryonated eggs is unsuitable for mass production.
The aim of this study was to develop a subunit vaccine based on a capsid
protein of the virus. The knob protein, together with an adjacent part
of the shaft domain pertaining to the fiber protein of HEV, was expressed
in Escherichia coli and tested as a vaccine. Vaccination with this
recombinant protein conferred protection against challenge in controlled
and in floor-pen experiments. This finding suggests that the knob protein
may be used as safe and efficient vaccine against hemorrhagic enteritis
of turkeys. The possibility that the knob proteins of other adenoviruses
may be protective and serve as vaccine is also discussedref
Worldwide, > 20 billion chickens are killed for human consumption every
year, and the industry is facing growing criticism over the conditions
in which most of the birds are kept. When the birds were kept at densities
of between 30 kg/m2 - the maximum proposed in a 2000 report
that is expected to form the basis of the new EU regulations - and 46 kg/m2and
welfare was assessed by measuring mortality, levels of the stress hormone
corticosterone in the faeces, ease of walking and the presence of skin
lesions on the birds' legs and feet, although chickens reared in the more
crowded conditions grew more slowly, the number dying, being culled as
unfit, or showing leg injuries did not correlate directly with stocking
density. Mortality was directly related to humidity and temperatureref Other diseases not transmissible to humans
:
toxic fat syndrome : toxicity in 3- to 10-week old chickens that
have been fed diets supplemented with fat containing any of several toxins;
symptoms are edema of the pericardium and abdomen, waddling gait, and sudden
death.
infectious
bursal disease virus (IBDV) / Gumboro virus => infectious bursal
disease (IBD) / Gumboro disease / infectious avian nephrosis (a list
B disease) : a worldwide highly contagious acute avian disease, characterized
by edema and swelling of the cloacal bursa, soiled wet feathers, whitish
watery diarrhea, listlessness, and trembling, progressing to extreme kidney
damage and damage of the bursa of Fabricius, with resulting immunosuppression
that can be fatal. Although turkeys, ducks, guinea fowl, and ostriches
may be infected, clinical disease occurs solely in chickens. Only young
birds are clinically affected. Severe acute disease of birds 3 to 6 weeks
old is associated with high mortality, but a less acute or subclinical
disease is common in 0 to 3 week old birds. This can cause secondary problems
due to virus-induced lymphoid depletion of the bursa
of Fabricius,
and if this occurs in the first 2 weeks of life, significant depression
of the humoral antibody response may result. Both live attenuated and inactivated
(killed) vaccines are available to control the diseaseref
avian leukosis : a group of viral diseases of chickens, transmitted
by related oncoviruses and characterized by proliferation of immature erythroid,
myeloid, or lymphoid cells. Leukemic forms include erythroblastosis and
myeloblastosis and, rarely, lymphoblastic leukemia. Solid tumors in visceral
organs are seen in cases of lymphoid leukosis, erythroblastosis, and myelocytomatosis.
Some of the causative viruses induce related neoplasms such as sarcomas,
hemangiomas, nephroblastomas, hepatocarcinomas, and osteopetrosis gallinarum,
which are now classified as belonging to the leukosis sarcoma group
gallid
herpesvirus 1 / infectious laryngotracheitis virus (subfamily Alphaherpesvirinae)
=> infectious laryngotracheitis (ILT) in chickens, pheasants, and
peafowl. The disease has been reported from Europe, Australia, New Zealand,
Asia, and North America, and is probably worldwide. Transmission is from
bird to bird, and as with other herpesviruses, the infection can become
dormant and the infected birds carriers. Outbreaks can range from peracute
to mild or asymptomatic and are characterized by varying degrees of coughing,
gasping, nasal discharge, and possibly cyanosis. The birds are depressed,
and egg production may drop. Vaccination is generally effective, although
carrier birds can develop amongst vaccinates. Eradication is generally
the best approach in designated areas, and effective biosecurity in commercial
poultry establishments is essential. The presence of small flocks of "show"
birds near commercial poultry establishments may provide foci of infection.
ILT is an OIE list B disease which can be found in most commercial poultry-raising
countries but -- according to OIE's Handistatus data -- is absent from
a significant number of islands, such as Vanuato, French Polynesia, Guernsey,
Saint Kitts & Nevis, Seychelles, Saint Vincent & the Grenadines,
and others. This disease most often affects chickens and is rarely found
in turkeys, peafowl, or pheasants. The virus most often enters a flock
by an infected bird that is not showing clinical signs. Clinical signs
include coughing and gasping, watery eyes, swollen sinuses, nasal discharge,
and bloody secretions from the trachea. Infected birds have difficulty
breathing and stretch their necks forward in an effort to breathe easier.
They often cough and spew blood. However, the outbreak can be mild and
resemble infectious bronchitis. Incubation has been as short as 2 days
but is usually 5 to 7 days. Recovered birds may be carriers for extended
periods. The virus can be mechanically transmitted by visitors or by equipment.
Hence, good biosecurity of the premises will decrease the chances of allowing
this disease in. Infectious laryngotracheitis must be differentiated from
the diphtheritic form of fowlpox, especially with tracheal lesions. Fowlpox
virus produces intracytoplasmic inclusions. Some may confuse the very early
stages with Newcastle disease virus infection. Vaccination may reduce losses,
but may not be approved in all states. It would be interesting to search
for its route of introduction into Trinidad & Tobago. In late 1980,
owners of some broiler operations south of Gonzales, TX contracted to raise
older, "spent" hens as a source of eggs which were to be shipped to Mexico
for parent stock. At the time, Texas was considered free of ILT, but the
hens came from Southern or Southeastern states where ILT was endemic and
ILT vaccination was practiced. The protocol for the most commonly used
modified-live virus (MLV) ILT vaccine was to administer a drop of the vaccine
to the conjunctiva of each bird, insuring the delivery of an immunizing
dose. However, due to labor costs, the vaccine was often dispensed via
water. In order to bring the hens into production in Texas, they were molted.
During the molting, mortality levels increased dramatically and ILT was
isolated from submitted specimens. Laboratory analysis determined that
the virus had the same mortality as a commonly used MLV vaccine virus that
regained virulence after multiple passages through chickens in the laboratory.
While it could not be proven conclusively, it was theorized that the virus
we were dealing with was the descendant of a MLV eye drop vaccine that
had been dispensed to the hens via water during their 1st laying period
in their home state. Water vaccination did not insure that every bird received
an immunizing dose, leaving some hens unprotected. Since the vaccine virus
was live, some of the hens became infected and shed it, thereby exposing
the un-immunized birds in the population. As the virus passed through more
un-immunized birds, it regained virulence, and during the stress of molting,
produced mortality. While it was a lower level of mortality than would
have been expected with the wild virus, it nonetheless had a devastating
impact on the laying operations. Over 50,000 hens were ultimately culled
and buried due to outbreaks of ILT. As a result of this introduction into
the area, ILT outbreaks occurred in laying operations for most of the decade.
Later, when broilers in the area began experiencing outbreaks, the same
mortality pattern was detected when laboratory challenges were conducted.
It was a standard practice for the broilers to be vaccinated against ILT
via the water route : the broilers were being marketed 1 or 2 weeks later
than normal, which was apparently enough time for the vaccine virus to
become a problem.
gallid
herpesvirus 2 / Marek's disease herpesvirus 1 => Marek's disease
: a lymphoproliferative disease of chickens, formerly included in the avian
leukosis complex but now known to be caused by gallid herpesvirus 2. Lymphoid
cell infiltrations are most common in the peripheral nerves and gonads,
but widespread infiltrations may also be found in visceral organs, skin,
muscle, and the iris; there is also frequently perivascular cuffing of
blood vessels in the central nervous system. The location of the lesions
dictates the clinical signs, such as paralysis, general depression, or
blindness
lymphoid leukosis : one of the avian leukosis complex of tumors,
involving transformation of B lymphocytes; symptoms include anorexia, emaciation,
and an enlarged liver.
avian or fowl lymphomatosis / lymphomatosis of fowls : avian leukosis
involving chiefly the lymphocytes
neural lymphomatosis / fowl or range paralysis / neurolymphomatosis
gallinarum : Marek's disease in which neurological symptoms are dominant.
skin leukosis : Marek's disease primarily affecting the skin
visceral lymphomatosis : avian leukosis with solid tumors of the
viscera.
pullorum disease / white diarrhea : an infectious disease of birds,
including chickens, caused by Salmonella
enteritidis subsp. enterica serovar pullorum and
marked by loss of appetite, dullness, diarrhea that leaves white lumps
around the cloaca, reduced egg yield, and infertility of eggs. It is sometimes
fatal, with moribund and dead birds found at hatching time
fowl adenovirus : a species of viruses of the genus Aviadenovirus
that is lethal for chicken embryos and induces tumors in newborn hamsters
histomoniasis / "blackheads"
perosis : a disease of chicks marked by bone deformities, associated
with deficiency of dietary factors such as choline and manganese.
strophosomus : a celosomus, especially in chicks, in which the extremities
are reflexed onto the back with the distal ends resting on the head
Therapy :
probiotic bacteria are easy to give to animals, as they can be put
in animal feed or drinking water, and should also help to
Escherichia albertii
caused a mass mortality in the Fairbanks, Alaska area in 2005; a possible
spread of Salmonella by finches should worry public health folks
at least to the same degree as it seems to worry cat lovers. Among the
Salmonella group B bacteria there are notorious pathogens such as S.
typhimurium, S.
agona, S.
heidelberg and S.
brandenburg. If this is salmonellosis, are the bacteria the primary,
direct cause of disease and mortality among the birds, affecting all or
most of them, or just a secondary finding? Interestingly, during the 1997-1998
epizootic of salmonellosis affecting several species of songbirds over
a large area of the eastern North American continent, the common redpoll
(Carduelis
flammea) was found to be the species most often affectedref.
The Redpoll isolates exhibit several biochemical reactions atypical for
E.
coli, including lack of lactose fermentation. The isolates also exhibit
biochemical reactions atypical of previously reported E. albertii
isolates, including production of indole from tryptophan. In addition,
the intimin and cytolethal distending toxin gene sequences differed significantly
from those previously reported from E. albertii and the Scottish
finch isolates.
Feral monk parakeets (Myiopsitta monachus) produce and
modify their song in the avian equivalent of the larynx, the syrinx, and
use their tongues to create vowel-like sounds, just as humans do, contributing
to the birds' great talent for mimicry. Tongue movements of less than a
millimetre made a big difference to the quality of emerging vowel-like
sounds, called formants. Male songbirds usually tend to sing only at certain
times of the year and to attract females. But male and female parrots communicate
all the time using formants and other vocalizations to convey complicated
information, such as individual identity and predator threatsref.
An African Grey parrot called Alex can articulate sounds for objects, shapes,
colours and materials, knows the concepts of same and different, and bosses
around lab assistants in order to modify his environment.
The Alex Foundation
Strigops
Strigops
habroptilus (kakapo or owl parrot) : Erysipelothrix
rhusiopathiae
(erysipela in animals, erysipeloid in humans). Kakapo is a critically endangered
New Zealand nocturnal parrot, weighing up to 3.5 kilograms (8 lbs) The
kakapo's scientific name means "owl-like', referring to its nocturnal nature,
unusual soft plumage, and facial disc of bristle-like feathers. Its Maori
name, "kakapo", means "night parrot". The kakapo is the world's heaviest
and only flightless parrot. They are up to 60 cm long and weigh up to 8
lbs. It has a virtually keel-less sternum which makes it incapable of flying
in the true sense. It can only "parachute" from trees, using its wings
for balance and braking, and, is nocturnal, solitary, and secretive. It
lives mainly on the ground, but, can climb trees. The birds live in New
Zealand, an island country that had virtually no mammals living on it for
millions of years. It was a place inhabited by birds and reptiles. The
only types of mammal were 2 species of bats. The kakapo did not learn the
defense mechanisms to combat or escape mammalian predators. This made the
parrot very vulnerable, when new animals were introduced by man
Avian influenza outbreaks in ostriches do not necessarily affect poultry.
During the 2003-2004 epizootic in Eastern Asia, cases in ostriches were
reported from Thailand, but the pathogenicity in this species was not clear.
Previously, the following (low pathogenic) AI virus strains had been isolated
from ostriches: the 1st reported outbreaks of AI in ostriches occurred
in 1991 and 1992 in the Eastern Cape Province and Oudstshoorn district
in South Africa and were typed as H7N1, with no pathogenicity
to chickens. Mortality reached 60% in some groups. The severity of symptoms
and lesions depended on age and concurrent bacterial and mycotic infections.
Subsequent isolations from these same farms or from Zimbabwe, were from
cases with similar pathology or even from inapparent infections. The isolates
were typed as follows: South Africa - H7N1 (1991,
1992), H5N9 (1994), H9N2 (1995),
H6N8 (1998); Zimbabwe - H5N2
(1995). None of these isolates were pathogenic for poultryref;
Denmark - H5N2 (apathogenic, 1998). The 1st report
on HPAI in ostriches came from Italy in 2000, where 44 out of 144 (30.5%)
affected young birds aged from 7 to 9 months died from H7N1.
An inactivated emulsified H7N1 vaccine was successfully
used to curb the outbreaks in South Africa from 1991 to 1992; the vaccine
prevented morbidity and mortality, but did not prevent shedding of virus.
The stamping-out policy currently applied by the authorities may be successful
if it is part of a comprehensive control strategy also capable of
addressing the risk of continued infections. Ostriches are mostly farmed
outdoors; preventing contact with potential vectors is a complex issue.
This underlines the importance of surveillance for avian influenza in wild
birds, particularly waterfowl. South Africa's 2003 annual report to the
OIE indicated that HPAI had never been recorded there. South Africa's last
(3rd) follow up report on the HPAI outbreak in ostriches was sent to the
OIE on 22 Oct 2004ref.
Until that date, 9 outbreaks had been recorded in the Eastern Cape, 6 of
which were in The Blue Crane Route Municipality area and 3 were in the
Grahamstown Municipality, about 160 km away. The total number of destroyed
ostriches reached 28 154: on Dec 22 they were 27,000, more than half
of the ostrich population in the province. Determining the virulence of
the current H5N2 virus strain for chickens, according
to the internationally prescribed criteria, is a necessary prerequisite
for a timely decision regarding South-Africa's current HPAI status
Other nontransmissible diseases : the
ostriches in Africa -- and likely elsewhere -- have a variety of gastrointestinal
helminths, of which the "wireworm" or Libyostrongylus
douglassii, may be the most pathogenic. As it could be more devastating
to the kiwi, precautions now would seem to be in order.
=> Trichinella
pseudospiralis,
avian botulism / Western duck sickness : botulism in waterfowl
is generally caused by one of 2 toxin types :
Clostridium
botulinum serotype C
: type C botulism occurs principally in waterfowl and other birds
living in an aquatic environment and causes tremendous losses, most notably
in waterfowl in the western US. In addition to North America, it has been
reported in birds in Europe, South Africa, Uruguay, and Australia. In the
Great Lakes region, it was first identified in 1936 in ducks on Green Bay
of Lake Michigan and in 1941 in Monroe County marshes along Lake Erie.
Type C is not related to fish and occurs in carcasses of dead invertebrates,
in the flesh of birds dying of botulism, and in maggots feeding on toxic
carcasses. Type C, which is regarded as responsible for most outbreaks
in water-fowl world-wide, does not pose a risk to humans. If the carcasses
are not disposed of, the maggots that tend to form also harbor the toxin.
Other birds will eat the maggots from the carcasses and become intoxicated.
Generally botulism does not cause diarrhea or other increase in bird excrement,
but it does cause a condition commonly known as "limberneck." The
botulism toxin causes a paralysis of the muscles and the bird is unable
to hold the head upright. Many birds actually drown because they cannot
lift their head out of the water. The paralysis also renders the birds
unable to use their wings or their legs and often even the eyelids are
unable to be raised.
Clostridium
botulinum serotype E
=> type E botulism is connected with consumption of decaying fish
and occurs mainly in gulls and loons, and to a lesser extent in mergansers,
mute swans, grebes, and shorebirds feeding on them. It may also cause intoxication
in humans. It now appears that any birds or mammals susceptible to botulinum
toxin run a risk of becoming poisoned if they scavenge dead fish. Evidence
for this includes the identification of type E toxin in a bald eagle, wood
ducks, and muskrats with fish remaining in their digestive tracts.
Burkholderia pseudomallei,
Crimean-Congo
hemorrhagic fever virus,
avian
type C retroviruses (a genus having the same virion morphology as the
mammalian type C retroviruses and causing infection and malignancies in
birds),
Avian mycobacteriosis is an important disease which affects
companion, captive exotic, wild and domestic birds. The disease is most
commonly caused by Mycobacterium
avium
and Mycobacterium
genavense.
Lesions are typically found in the liver and gastrointestinal tract, although
many other organ systems can potentially be affectedref.
Influenzavirus A H1,
Influenzavirus
A H2,
Influenzavirus
A H3,
Influenzavirus
A H4,
Influenzavirus
A H5,
Influenzavirus
A H6,
Influenzavirus
A H7,
Influenzavirus
A H8,
Influenzavirus
A H9,
Influenzavirus
A H10,
Influenzavirus
A H11,
Influenzavirus
A H12,
Influenzavirus
A H13,
Influenzavirus
A H14,
Influenzavirus
A H15
=>
avian influenza (AI) / bird flu
: a disease capable of causing extremely high mortality amongst infected
fowls was first defined in 1878 and became known as 'fowl plague'. The
causative organism of this disease was shown to be a ‘virus’ as early as
1901 but it was not until 1955 that the relationship of this and other
milder viruses isolated from birds with mammalian influenza A viruses (first
isolated in the 1930s) was demonstrated (Schafer, W. (1955). Vergleichende
sero-immunologischs Untersuchungen uber die viren der influenza und klassichen
Geflugelpest. Zeitschrift fur Naturfoirschung, 10b, 81-91). Only type A
influenza viruses are known to cause natural infections of birds, but viruses
of all 15 HA and all 9 NA influenza A subtypes in the majority of possible
combinations have been isolated from avian species. In 2000, the EC's Scientific
Committee on Animal Health and Animal Welfare (SCAHAW) recommended that
the following definition of AI be applied to diagnostic procedures for
confirmation and differential diagnosis: "'Avian influenza' means an infection
of poultry caused by any influenza A virus which has an IVPI in 6-weeks-old
chickens > 1.2 or any infection with influenza A viruses of H5
or H7 subtype"ref.
Susceptible species :
chickens : at the end of the 19th and early 20th Centuries ‘fowl
plague’ was often reported in chickens and in several countries this disease
was probably enzootic. However, in the second half of the 20th Century
reports of influenza infections of chickens have been rare compared to
infections of other domestic poultry despite the much higher populations
of chickens. For example in the USA, despite frequent influenza epizootics
in turkeys in some states, between 1964 and 1982 only 3 outbreaks in chickens
were recorded (Pomeroy, B.S. (1982). Avian influenza in the United States
(1964-1980). Proceedings of the First International Symposium on Avian
Influenza, 1981. Carter Composition Corporation, Richmond, USA, pp. 13-17).
Despite the low incidence of influenza infections of chickens throughout
the world there have been 12 outbreaks of HPAI since 1959 and significant
spread occurred in Pennsylvania and neighbouring states in the USA during
1983-1984 and in Mexico and Pakistan in 1994/95. Other outbreaks since
1959 have shown no or extremely limited spread. Eight HPAI outbreaks in
backyard poultry flocks infected with H5N2 virus
were reported in Italy in 1997/8. Outbreaks of H5N1
HPAI occurred on three farms in Hong Kong during March-May 1997 with 70-100%
mortalitiesref
and subsequent spread to live bird markets.
ducks : the influenza status of commercial ducks in most countries
is poorly understood or has not been investigated. When surveillance of
commercial ducks has been undertaken, enormous pools of virus and many
subtype combinations have been detected
turkeys : since 1963, most of
the major turkey-producing countries have had disease problems associated
with influenza infections. In the USA in California and Minnesota, where
turkey farms are heavily concentrated and situated on migratory waterfowl
flyways, influenza virus infections have been seen regularly, but in other
countries outbreaks in turkeys have been usually restricted to 1 or 2 isolated
incidents in the years recorded. Despite the greater prevalence of influenza
viruses in turkeys, of the 17 reported isolations of HPAI since 1959 only
5 were apparently primarily from turkeys
LPAI A/H3N3, which presents no threat to humans,
was detected on a single turkey farm in Sampson County, North Carolina
on 28 Nov 2005
pigeons resist infection with AI . There is only one reported attempt
to infect pigeons, and when the attempt was unsuccessful, the author concluded
that pigeons were resistant. That is faulty reasoning for many reasons,
most notably, individual avian influenza isolates have differing abilities
to infect different hosts. Researchers have isolated H1N1
from a pigeon from a turkey farm (it was never reported in the scientific
literature).
AF509023 A/Pigeon/Hong Kong/SF215/01 H5N1
AY180427 A/Pigeon/Nanchang/11-045/2000 H3N6
AY180428 A/Pigeon/Nanchang/8-142/2000 H3N6
AY180429 A/Pigeon/Nanchang/9-058/2000 H3N3
AF156375 A/Pigeon/Hong Kong/Y233/97 H9N2
AF222607 A/Pigeon/Hong Kong/FY6/99 H9N2
AY180445 A/Pigeon/Nanchang/2-0461/2000 H9N2
AY180455 A/Pigeon/Nanchang/11-145/2000 H9N2
AY180458 A/Pigeon/Nanchang/7-058/2000 H9N2
Thus, if it is possible to isolate virus from pigeons (and parrots), pigeons
can potentially transmit flu A. Whether the birds exhibit symptoms as a
consequence of infection is a separate question.
parrots : psittacines can carry and be affected by AIref1,
ref2,
ref3.
However, this is rare, the disease is mild, shedding is limited, and so
far isolates from psittacines have been non-pathogenic in poultry and mice.
Back in the 1970s when the USDA was monitoring shipments of imported birds
for the presence of Newcastle disease virus, they found a lot of AI in
psittaciformes and passeriformes
ratites : the increase in trade in ostriches and other ratites during
the 1990s led to the movement of large numbers of such birds around the
world and the testing for viruses, including influenza, has resulted in
the regular isolation of influenza viruses from these birds. Since the
first reported isolations of influenza viruses from ratites in 1991 viruses
of H3N2, H4N2, H4N6,
H5N2, H5N9, H7N1,
H7N3, H9N2, H10N4
and H10N7 subtypes have been isolated. All these
were of low virulence for chickens
other domestic poultry : other commercially reared birds represent a very
small proportion of domestic poultry in most countries. Some such birds
(e.g. pheasants and geese) are reared under semi-wild conditions.
Isolations of influenza viruses have been reported from muscovy ducks (Cairinia
moschata), mallard ducks (Anas platyrhyncos),
pheasants (Phasianus spp.), Japanese quail (Coturnix
coturnix japonica), chukars (Alectoris
chukar), guinea fowl (Numida
meleagris), and various types of goose
wild birds : the first isolation of influenza virus from feral birds
was in 1961 from common terns (Sterna hirundo)
in South Africaref,
but it was not until the mid-1970s that any systematic investigation of
influenza in feral birds was undertaken. These revealed the enormous pools
of influenza viruses now known to be present in the wild bird population.
Virus isolations from other wild birds have been completely overshadowed
by the number, variety and widespread distribution of influenza viruses
in waterfowl, Order Anseriformes. In the surveys listed by Stallknecht
and Shaneref
a total of 21,318 samples from all species resulted in the isolation of
2,317 (10.9%) viruses. Of these samples 14,303 were from birds of the Order
Anseriformes and yielded 2,173 (15.2%) isolates. The next highest isolation
rates were 2.9% and 2.2% from the Passeriformes and Charadriiformes and
the overall isolation rate from all birds other than ducks and geese was
2.1%.
caged 'pet' birds : since 1975 when the first isolates from caged
birds were recorded, isolates, from all sources, have been mainly of H4
or H3 subtypes. The majority of influenza viruses from caged
birds come from passerine species and only rarely are psittacines infected.
Although the presence of influenza viruses in birds held in quarantine
is monitored continually in several countries around the world, there appear
to have been periods, often lasting several years when no isolations have
been made.
Thus, there is no justification for the culling of psittacines or pigeons
in the face of an outbreak in which the virus is virulent and shed in massive
numbers by affected poultry.
The so called "species barrier" between AI virus and mammals
may be very weak, and some types of AI viruses have the potential to cross
the barrier and infect other animals directly, causing severe disease --
if those animals are exposed to sufficient amounts of virus or through
an adequate route of administration. Consequently, the public -- especially
in AI-affected rural areas -- should be educated not to feed any animals
sick or dead chickens : it is relatively common for the village farmers
who breed free-range chickens to feed their dogs, pigs, etc. their sick
or dead chickens. The importance of personal protection while handling
sick or dead chicken also deserves to be stressed. There have been some
instances of limited transmission of infection to
humans, notably :
avian influenza A(H5N1)
virus
on 2 occasions in Hong Kong in 1997 (A/HK/156/97 and A/HK/148/97) and 2003
(A/HK/213/03), in Vietnam in 2004 (A/VN/1203/04 and A/VN/1194/04), and
in Thailand in 2004 (A/Thai/16/04). Limited transmission to health care
workers occurred, but did not cause severe disease. Rapid destruction -
within 3 days - of Hong Kong's entire poultry population, estimated
at around 1.5 million birds, reduced opportunities for further direct transmission
to humans, and may have averted a pandemic. H5N1
mutates rapidly and has a documented propensity to acquire genes from viruses
infecting other animal species. Birds that survive infection excrete virus
for at least 10 days, orally and in faeces, thus facilitating further spread
at live poultry markets and by migratory birdsref
..., but person-to-person transmission has been either limited or absent.
H5 and H9 viruses have generally been associated
with respiratory disease, whereas H7 has generally been associated
with conjunctivitis. At least 4 months would be needed to produce a new
vaccine, in significant quantities, capable of conferring protection against
a new virus subtype.
Antigenic drift : examination of the commercial
vaccine and viruses isolated from Mexico over the past 8 years showed the
same types of changes that were observed in humans. It has been demonstrated
that veterinary influenza
vaccines,
like human vaccines, should be reconsidered yearly for updates to achieve
optimal protection, since antigenic drift may take placeref Antigenic shift : influenza A viruses,
including subtypes from different species, can swap or "reassort" genetic
materials and merge :
because pigs are susceptible to infection with both avian and mammalian
viruses, including human strains, they can serve as a "mixing vessel" for
the scrambling of genetic material from human and avian viruses, resulting
in the emergence of a novel subtype
for at least some of the 15 AI virus subtypes circulating in bird populations,
humans themselves can serve as the "mixing vessel"
But on the contrary of mammalian influenza viruses, which undergo antigenic
drift, phylogenetic analyses have suggested that in the "natural environment,"
AI viruses appear to be in evolutionary stasis.
Pathogenesis of AI is quite different
from that in mammals, in that viral replication occurs in the intestinal
tract as well as the respiratory tract. Fusion activity is activated by
HA cleavage, and this enables the virus to penetrate cells of the respiratory
and intestinal epithelia. Strains of avian influenza viruses vary greatly
in virulence, and their virulence and host range are determined to a large
extent by the primary structure of the viral HA protein and its consequent
cleavability by host proteases. On the contrary of low-pathogenic avian
influenza (LPAI), the extreme virulence of some strains (highly
pathogenic avian influenza (HPAI) (so named since 1981) / fowl disease,
pest or plague / Brunswick disease) is determined by the susceptibility
of the HA of virulent strains to cleavage and activation by specific proteases
present in vulnerable internal tissues. The Office International des Epizooties
(OIE) adopted the following criteria
for classifying an avian influenza virus as "highly pathogenic" :
any influenza virus that is lethal for at least 6 of 8 susceptible chickens
4 to 8 weeks old within 10 days following intravenous inoculation with
0.2 ml of a 1/10 dilution of a bacteria-free, infective allantoic fluidref.
the following additional test is required if the isolate kills from 1 to
5 chickens but is not of the H5 or H7 subtype: growth
of the virus in cell culture (for example primary cells such as chick embryo
cells or cell lines such as MDCK cells, although most cell cultures support
the growth of HPAI influenza viruses or those of low pathogenicity in the
presence of trypsin) with cytopathic effect (CPE) or plaque formation
in the absence of trypsin. If no growth is observed, the isolate is
not considered to be an HPAI isolate.
for all H5 and H7 viruses of low pathogenicity and
for other influenza viruses, if growth is observed in cell culture without
trypsin, the amino acid sequence of the connecting peptide of the haemagglutinin
must be determined. If the sequence is similar to that observed for other
HPAI isolates, the isolate being tested will be considered to be HPAI.
1-step real-time reverse transcription–polymerase chain reaction (RT-PCR)
with melting curve analysisref.
The primers consisted of a forward primer H5F3+ (nucleotides 1001–1021:
5´-AACAGATTAGTCCTTGCGACTG-3´) and a reverse primer H5R2+ (nucleotides
1124–1103: 5´-CATCTACCATTCCCTGCCATCC-3´), which yielded products
of 124 bp and 112 bp, corresponding to HPAI and LPAI, respectively. Consequently,
the sizes of the amplicons and percentage guanine-cytosine content were
different, allowing discrimination between HPAI and LPAI by melting curve
analysisref
In the European Union, a similar definition was adopted, although in this
case the intravenous pathogenicity index (IVPI) test was used to
assess virulence. Other diagnostic laboratory tests are : haemagglutination
inhibition test, agar gel precipitation (AGP) test, virus
isolation.
Until recently, only HPAI had to be reported to the OIE. However, in
view of the zoonotic aspects of avian influenza, the need for the inclusion
of certain strains, even if they demonstrate lower pathogenicity in fowl,
has become apparent. The traditional OIE definition of the disease is currently
undergoing a revision, the disease becoming known as "notifiable avian
influenza." The new definition, included in article 2.7.12.5 (Under
study) of OIE's Terrestrial Animal Health Code, is as follows: "For the
purposes of this Terrestrial Code, notifiable avian influenza (NAI)
is defined as an infection of poultry caused by any influenza A virus of
the H5 or H7 subtypes or by any AI virus with an
IVPI > 1.2 (or as an alternative > 75% mortality) as described below. NAI
viruses can be divided into highly pathogenic notifiable avian influenza
(HPNAI) and low pathogenicity notifiable avian influenza (LPNAI).
HPNAI viruses have an IVPI in 6-week-old chickens > 1.2 or, as an alternative,
cause > 75% mortality in 4-to 8-week-old chickens infected intravenously.
H5 and H7 viruses which do not have an IVPI of greater
than 1.2 or cause < 75% mortality in an intravenous lethality test should
be sequenced to determine whether multiple basic amino acids are present
at the cleavage site of the haemagglutinin molecule (HA0); if
the amino acid motif is similar to that observed for other HPNAI isolates,
the isolate being tested should be considered as HPNAI".
Discordant results between the molecular classification, derived by
sequencing the HA cleavage site, and virulence for chickens have been observed
with several H5 and H7 subtype avian influenza viruses
(Dennis A. Senne, NVSL). Some examples are:
CK/PA/83 (H5N2)
Pekin Robin/China/94 (H7N1)
CK/Chile/02 (H7N3)
CK/TX/04 (H5N2)
With the CK/PA/83 and Pekin Robin/China/94 avian influenza viruses, each
contained multiple basic amino acids at the HA cleavage site that would
be consistent with their classification as HPAI viruses, but the viruses
initially were not virulent for experimentally inoculated chickens. Subsequently,
both of these viruses became highly pathogenic for chickens; the CK/PA/83
by a single point mutation in the HA and Pekin Robin/China/94 after additional
passages in embryonating chicken eggs. The initial Chilean H7N3
avian influenza virus possessed an HA cleavage site sequence consistent
with LPAI virus, but an RNA insertion (30 nucleotides) at the HA cleavage
site made the virus HPAI even though it did not match the expected HPAI
virus sequence. Similarly, the H7N1 avian influenza
virus in Italy in 1999 started as an LPAI virus, but an RNA insert (12
nucleotides) at the cleavage site made it an HPAI virus. Among the H5
and H7 avian influenza viruses, we cannot predict which LPAI
viruses will remain low pathogenic and which will mutate to become highly
pathogenic. Also, the type of mutation is not predictable. What we do know
is that H5 and H7 subtype avian influenza viruses,
when allowed to persist and circulate in poultry, can undergo mutational
changes that can have serious consequences.
Transmission : 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,
including 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 in introducing LPAI into
domestic flocks where, if allowed to circulate for several months, it can
mutate into HPAI. Close to 600 species of birds, including swans, spotbill
ducks and
sparrows, can be found in Japan -- both resident and migratory : migratory
birds carry LPAI with them, particularly ducks and waders that carry the
virus from Siberia to Japan, China and other southern Asian countries,
despite the possibility of this virus mutating into HOPAI cannot
be ruled out. Research using satellite tracking shows that certain migratory
birds are common to the avian flu hit countries in Southeast Asia and Japan
: they include ducks, gulls, waders, and buzzards, which were seen in Japan's
bird flu hit areas of Yamaguchi, Oita, and Kyoto, but there is no proof
that such birds are the source of the present outbreaks of HPAI H5N1.
Massive killing of wild birds thought to be pests in the region lead to
massive famine and failed crops since the wild birds in fact were controlling
crop pests more than being crop pests. Therefore wildlife not only warrant
protection due to the aesthetic and cultural values, but also because of
the ecosystem "services" provided at very low costs by animals and plants
in the environment. As a result :
wild birds should not be depopulated in an attempt to control AI but separation,
as much as possible should be attempted.
reducing contact rates between wild birds and large commercial poultry
operations to prevent wild waterfowl from direct or indirect contact
village poultry health care programs, including possible vaccination
programs and certainly health/husbandry education is the best approach
to
provide entree for surveillance operations
reduce disease incidence
improve rural livelihoods
reduce the threat or introduction of diseases into wild bird populations
Ministries of Agriculture, as well as Ministries of Natural Resources should
limit the trafficking of wild birds, and ban the mixing of domestic and
wild animals in live markets.
wildlife infectious disease surveillance programs, both in semi-urban areas
and in remote, rural areas may provide insights and early warning about
diseases circulating in the wild prior to livestock outbreaks.
nvestment in raising awareness and capacity building is needed to allow
more countries to begin integrating health monitoring programs as they
develop natural resource management efforts
Live bird markets have also played an important role in the spread of epidemics.
Apart from being highly contagious, AI viruses are readily transmitted
from farm to farm by mechanical means, such as by contaminated equipment,
vehicles, feed, cages, or clothing. HPAI can survive for long periods in
the environment, especially when temperatures are low.
Bird flu may be spread by using chicken dung as food in fish farms,
a practice now routine in Asia, according to the world's leading bird conservation
organization. Fertilizing fish ponds with poultry feces, which can dramatically
improve fish growth, may set up major new reservoirs of avian influenza
infection if the chickens providing the manure are infected themselves,
according to BirdLife International,
the Cambridge-based umbrella body for bird protection groups in 100 countries.
The suggestion, which has echoes of the BSE outbreak in Britain -- in which
cattle were infected by their food -- puts a question mark over a technique
firmly backed by the UN's Food and Agriculture
Organization (FAO) as a primary means of providing protein for mushrooming
populations in developing countries. Known as integrated livestock-fish
farming, the technique involves transferring the wastes from raising
pigs, ducks or chickens directly to fish farms. At the right dosage, the
nutrients in the manure give an enormous boost to the growth of plankton
in the ponds, which are the main food of fish such as carp and tilapia.
BirdLife International is now calling for an investigation into the possibility
that thousands of manure-fed ponds across Asia may be the means by which
the new potentially deadly strain of avian influenza, H5N1,
is being spread. BirdLife points out that outbreaks of H5N1
have occurred in 2005 at locations in China, Romania and Croatia where
there are fish farms. The Chinese outbreak of H5N1
in May 2005, which mainly involved bar-headed geese, took place at Qinghai
Lake, a location where the FAO helped establish an integrated livestock
fish farm in the early 1990s. This outbreak helped lead to the widespread
media speculation about wild birds spreading H5N1.
Bar-headed geese migrate from India, where H5N1 has
never occurred, and migrate early, so they must have contracted the disease
locally, at Qinghai. Although no mention has been made of the possible
links between manure-fed ponds and influenza in the recent alarm over bird
flu, the issue has been raised before, and the FAO, although actively promoting
the technique, is well aware of the threat. Its 2003 report, Integrated
Livestock Fish Farming Systems, noted: "Recently, livestock and fish have
been implicated in the irregular occurrence of influenza pandemics; the
global impacts on public health of promoting livestock and fish integration
are huge if these claims are substantiated." In fact, the FAO may have
been aware for very much longer that some scientists think there is a risk.
The 2003 report includes a reference to a paper published in the journal
Nature in 1988. This paper, by Christoph Scholtissek from the University
of Giessen in Germany and Ernest Naylor from the University of Bangor in
Wales, was titled Fish Farming and Influenza Pandemicsref.
It said that bringing together fish farms with farm livestock "may well
be the creation of a considerable human health hazard." However, the FAO
has continued to promote integrated livestock fish farming actively throughout
the ensuing period. Poultry excreta may include pathogenic organisms, medicinal
drugs, and toxins (for example, botulism). Any international trade in unprocessed
poultry manure is, to the best of this moderator's knowledge, not sanctioned
by any country. Unprocessed poultry manure and litter are regarded a potential
vehicle for the spread of various infectious (as well as non-infectious)
agents, avian influenza certainly included. There are strict legal restrictions
on its exit from quarantined or suspected premises, for any use, in most
if not all countries. This is valid not only for recycling to animals,
but also for other uses, such as field fertilizer. Various countries have
banned -- or significantly restricted -- the recycling of poultry excreta
to food animals and, in particular, to ruminants. See also the Policy Document
of the Canadian Food Inspection Agency on the feeding of poultry manure
to cattleref;
the FDA's "Statement about allowing chicken manure to be put into cattle
feed"ref.
While the practice described by BirdLife International may indeed be involved
in the spread of H5N1, provided the liter is derived
from infected premises, it seems unlikely that such a product would be
transported to far destinations. However, uncontrolled, unrestricted use
may be involved in environmental contamination, exposing wild avians to
infection, with the possible subsequent long distance spread of the virus
by them. Additional investigations into the possible role of wild birds
in the spread of the H5N1 virus are needed.
Treatment :
the quarantining of infected farms and destruction of infected or potentially
exposed flocks are standard control measures aimed at preventing spread
to other farms and eventual establishment of the virus in a country's poultry
population. 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.
culling remains the first line of action, as recommended by FAO, OIE, and
WHO, for bringing the current outbreaks under control. Unlike other economically
important domestic animals, poultry raising takes place in a very short
production system. Provided sufficient resources are available to replace
culled poultry stock, countries should not postpone aggressive culling
because of fears of long-term consequences on poultry production. Infected
poultry are the species of greatest concern. Wild birds should not be culled.
Eradication is usually is a difficult process and costly in the best of
circumstances.
a research team at Seoul National University said their findings show that
a lactic enzyme in kimchi has remedial effects on chicken and other types
of poultry, which had been infected with avian flu, Newcastle's disease
and bronchitis. The experiment was conducted on 3 groups of 13 chickens
infected with the bird flu virus. The first group was given only water,
while the other 2 groups were given either a concentrated or diluted fluid
containing kimchi's lactic enzyme. A week later, all chickens in the first
group died, but 11 chickens each in the second and third group survived.
The team is planning to conduct further studies on the lactic enzyme and
distribute it to poultry farms across the nation after obtaining permission
from the National Veterinary Research and Quarantine Service.
Symptoms & signs : generally chickens
affected with HPAI may show one or more of the following signs :
sudden death without clinical signs
lack of energy and appetite
decreased egg production
soft-shelled or misshapen eggs
edema of the head, eyelids, comb, wattles, and hocks
cyanotic wattles, combs, and legs
nasal discharge
coughing, sneezing
incoordination
diarrhea
Prognosis : mortality is usually high, reaching
100% for HPAI. In a comparative experimental infection trial, Japanese
and Bobwhite quails demonstrated 100% mortality following intranasal inoculation
with A/chicken/Hong Kong/220/97 (H5N1) influenza
virus.
Macroscopic anatomy : the postmortem picture
contains many features, the most notable of which include edema of the
head and neck area, severe congestion of conjunctiva and hemorrhages in
trachea
... and the intestines, particularly on the mucosal surface of the
proventriculus (part of the cranial stomach of birds that secretes acid
and is located between the crop and gizzard). Necrosis of intestinal lymphoid
tissue is also a prominent postmortem feature.
Prevention :
HPAI viruses can remain viable at moderate temperatures for long periods
in the environment and can survive indefinitely in frozen material. 1 g
of contaminated manure can contain enough virus to infect 1 million birds.
some sound biosecurity practices:
keep an "all-in, all-out" philosophy of flock management.
protect poultry flocks from coming into contact with wild or migratory
birds. Keep poultry away from any source of water that may have been contaminated
by wild birds.
permit only essential workers and vehicles to enter the farm.
provide clean clothing and disinfection facilities for employees.
thoroughly clean and disinfect equipment and vehicles (including tires
and undercarriage) entering and leaving the farm.
do not loan to, or borrow equipment or vehicles from, other farms.
avoid visiting other poultry farms. If you do visit another farm or live-bird
market, change footwear and clothing before working with your own flock.
do not bring birds from slaughter channels, especially live-bird markets,
back to the farm.
protective measures at live-bird markets
use plastic instead of wooden crates for easier cleaning.
keep scales and floors clean of manure, feathers, and other debris.
clean and disinfect all equipment, crates, and vehicles before returning
them to the farm.
keep incoming poultry separate from unsold birds, especially if birds are
from different lots.
clean and disinfect the marketplace after every day of sale.
do not return unsold birds to the farm.
inactivated
or subunit anti-H5N1 vaccinesref.
Currently, no live AI virus vaccine is licensed for use in poultry, but
in some countries, live cold-adapted influenza vaccines are available for
use in humans (Flu-Mist) and horses (Flu Avert). In the USA, live recombinant
virus vectored products are licensed and used in animals, but they go through
a rigorous safety testing and risk analysis process. Only after the safety
-- including environmental safety -- is documented can the recombinant
product be licensed by USDA and used. In general, use of live AI virus
vaccines in poultry is a very risky proposition, especially for H5
and H7 subtypes, and is in theory strongly discouraged. The
mutation of low-pathogenicity (LP) AI field viruses to high pathogenicity
(HP) is well documented in outbreaks of H5N2 HPAI
in USA (1983-84), H5N2 HPAI in Mexico (1993-95),
H7N1 HPAI in Italy (1999-2000), H7N3
HPAI
in Chile (2002), H7N7 HPAI in The Netherlands (2003),
and H7N3 HPAI in Canada (2004). If a live H5
or H7 LPAI virus was used as a vaccine, this replicating LPAI
virus would be spread in the field, and like the original LPAI field virus,
could mutate at the proteolytic cleavage site of the hemagglutinin and
become an HPAI virus. This is in addition to the issues of changes in the
OIE code to make all H5 and H7 notifiable avian influenza
viruses. However, with the advent of reverse genetics, changes in one or
more genes may result in the creation of a live AI virus with reduced potential
for mutation to HP. Furthermore, a cold-adapted AI virus may be produced
by selection of virus strains at lower temperature. However, such viruses
would need extensive safety testing for reversion before accepting them
as safe to apply in the field. The clear benefit of vaccination is its
ability to reduce the amount of wild virus in circulation. Although vaccination
does not always prevent infection -- just disease -- it takes a much higher
dose of virus to cause infection, and vaccinated birds that do become infected
shed far less virus than unvaccinated birds. As an added precaution, animal
health experts agree that vaccinated birds that become infected should
be culled. 3 former executives from Maine Biological Laboratories in Winslow
face federal charges, including conspiracy and mail fraud, for allegedly
smuggling the avian influenza virus H9N2 into the
country from Saudi Arabia. A Saudi customer wanted the lab to use the virus
to secretly manufacture a vaccine so that Saudi authorities would not find
out about an outbreak of the potentially devastating disease in one of
its flocks, authorities allege. In addition to the smuggling allegations,
the executives are accused of altering expiration dates on vaccine labels
and mislabeling batches of vaccine for overseas customers to help them
avoid import costs. In some cases, batches were mislabeled because the
customers did not have the proper licenses and permits. In other cases,
customers asked that multiple batches of vaccine be labeled as a single
batch. Agricultural experts say the recent indictment of former executives
at a Maine biological laboratory for allegedly mislabeling and smuggling
poultry viruses into the USA highlights illegal practices that could have
caused disaster for the poultry industry. And the practices may be more
widespread than anyone knows, because they are not easily uncovered by
authorities. After the Pennsylvania outbreak in 1983 that killed hundreds
of thousands of birds and led to the destruction of 17 million other birds,
the disease cropped up in milder forms across the Northeast, particularly
in association with live bird markets in New York City, New Jersey, and
Boston. After a bird tested positive in a Boston market in 2002, the disease
was traced to ducks at a Warren, Maine, farm. It was the first time avian
flu was detected in commercial poultry in Maine. Influenza A (H9N2)
viruses had been present for the past several years in various Middle-Eastern
countries. Though not an HPAI virus strain, poultry losses at times may
be considerable. The following is provided as background information on
the use of vaccines for control of avian influenza (AI) in poultry.
1. Vaccination should be viewed and used only as a single tool in a comprehensive
control strategy that includes: 1) biosecurity, 2) education, 3) diagnostics
and surveillance, and 4) elimination of AI virus infected poultry. One
or more of these components are used to develop AI control strategies to
achieve one of 3 goals or outcomes (Swayne, 2004): 1) Prevention - preventing
introduction of AI; 2) Management - reducing losses by minimizing negative
economic impact through management practices; or 3) Eradication - total
elimination of AI.
2. Protection against avian influenza is the result of immune response
against the hemagglutinin protein (HA), of which there are 15 different
HA subtypes, and to a lesser extent against the neuraminidase protein (NA),
of which there are 9 different NA subtypesref1,
ref2.
Immune responses to the internal proteins, such as nucleoprotein or matrix
protein, are insufficient to provide field protection. Therefore, there
is no one universal AI vaccine. Practically, protection is provided against
the individual hemagglutinin subtype(s) included in the vaccine.
3. Experimental and field studies have shown that properly used vaccines
will accomplish several goals: 1) protect against clinical signs and death,
2) reduced shedding of field virus if vaccinated poultry become infected,
3) prevent contact transmission of the field virus, 4) provide at least
20 weeks protection following a single vaccination for chickens (this may
require 2 or more injections in turkeys or longer-lived chickens), 5) protect
against challenges by low to high doses of field virus, 6) protect against
a changing virus and 7) increase a bird's resistance to avian influenza
virus infectionref1,
ref2.
These positive qualities are essential in contributing to AI control strategies.
Most AI vaccine studies and field use have focused on chickens and turkeys
because of their high death rates and the high concentrations of Highly
Pathogenic Avian Influenza (HPAI) virus excreted into the environment by
these species. However, with the changing epidemiology of the H5N1
HPAI virus in Asia, the infection of domestic ducks and geese has become
a very important contributor to the maintenance and spread of the H5N1
HPAI virus. Experimentally, vaccines have been shown to significantly reduce
AI virus replication and shedding in domestic ducks and geese and thus
decrease environmental contamination (especially in ponds, lakes and rivers)
and prevent contact transmission. Proper vaccination of domestic ducks
and geese will have a positive impact on control of H5N1
HPAI in Asia.
4. A wide variety of vaccines have been developed and examined in the laboratory
for potential use in the field. However, only vaccines from 2 technologies
are licensed and used in poultry: inactivated whole avian influenza virus
vaccines and a recombinant fowlpox virus vectored vaccine with an H5
AI
gene insert (from AI virus A/turkey/Ireland/83 [H5N8]).
These 2 vaccine technologies have been shown to produce safe, pure and
potent vaccines. Both vaccine technologies require handling and injection
of individual birds.
5. The quantity of AI vaccine used around the world in poultry is not well
documented, but reliable information suggests the largest single use has
been 2 billion doses of inactivated H5N2 avian influenza
vaccine in China (December 2003 - present). Indonesia also uses H5
inactivated AI vaccine. In Mexico, an AI vaccination program has been used
since January 1995, with over 1.3 billion doses of inactivated vaccine
and 850 million doses of recombinant fowlpox have been used. H5N2
HPAI has been eradicated (last isolate was in June 1995), but H5N2
LPAI [low pathogenic avian influenza] still circulates in central
Mexico. Pakistan began using H7 inactivated AI vaccine in 1995,
with use in 3 regions following epizootics of H7N3
HPAI (1995, 2001 and 2004). By contrast, with low pathogenicity (LP) AI,
H9N2 inactivated vaccines have been and are used
in many countries within Asia, the Middle East and Eastern Europe, but
the number of doses is unknown. Vaccines for control of LPAI have been
used sporadically. Recently, H7 inactivated vaccine is being
used in a high risk area of Northern Italy and in one chicken layer company
in the USA to control LPAI.
6. Historically, AI virus strains selected for manufacturing of inactivated
vaccines have been based on LPAI viruses obtained from field outbreaks
that have homologous hemagglutinin protein; i.e. H5 vaccine
virus obtained from an H5 LPAI outbreak. Rarely, HPAI strains
have been used to manufacture inactivated vaccines, because, to be done
properly, such production requires specialized high biocontainment manufacturing
facilities which are uncommon in the world. Contrary to rumor, HPAI strains
do replicate to sufficient titer in embryonating eggs to be used in inactivated
AI vaccines, but their use is discouraged because of biosecurity and biosafety
manufacturing concerns. Furthermore, LPAI strains, with fewer biosecurity
and biosafety concerns for manufacturing, protect against HPAI viruses
of the same hemagglutinin subtype.
7. Vaccine strains have been shown to provide protection against diverse
field viruses (88-100% similarity to the challenge virus hemagglutinin)
isolated over a 38 year periodref.
Recently, both North American and Eurasian lineages of AI vaccine viruses
from 1968-1986 have been shown to be protective against the most recent
2003-2004 Asian H5N1 HPAI virusesref.
This broad and longer-term protection efficacy of poultry AI vaccines,
as compared to the need for frequent change of human influenza vaccine
strains, is potentially the result of the following: 1) poultry vaccines
use proprietary
oil-emulsion-adjuvant technology which elicits more intense and longer-lived
immune response in poultry than alum-adjuvant influenza vaccines, 2) the
AI virus immune response in poultry appears to be broader than in humans,
3) the immunity in the domestic poultry population is more consistent because
of greater host genetic homogeneity than is present in the human population,
and 4) vaccine use in poultry is targeted to a relatively young, healthy
population as compared to humans, in whom the vaccine is optimized for
groups with the highest risk of severe illness and death.
8. The protection efficacy of individual poultry AI vaccines should be
evaluated every 2-3 years to assure they are still protective against circulating
virus strains. For example, a recent study demonstrated the 1994 Mexican
H5N2 vaccine strain is no longer protective against
circulating H5N2 LPAI viruses in Central America,
and a change in vaccine strains is neededref.
With the H5N1 AI virus in Asia circulating as only
an HP strain, future vaccines may require the use of reverse geneticsref1,
ref2
to generate new LPAI vaccine strains, or, other molecular techniques to
produce vectored vaccine products, such as new recombinant fowlpox virus
vaccines. Some of these products use patented technologies and will require
legal clarification before use in the field.
9. "Sterilizing immunity" is not feasible in the field. Some experiments
have reported "sterilizing immunity," but closer examination indicated
such studies used very few experimental birds without statistical evaluation,
used a very low virus challenge, or used low sensitive virus isolation/detection
methods. In the field, vaccines will reduce replication of challenge virus
in respiratory and GI tracts and thus reduce the environmental load of
virus and virus transmission. However, the protection in conventional poultry
in the field will always be less than that seen in specific-pathogen-free
poultry under laboratory conditions because of other factors, such as improper
vaccination technique, reduced vaccine dose, immunosuppressive viruses
and improper storage & handling of vaccines. The other 4 components
of a control strategy, as presented in item 1, are essential, because vaccines
and their use are not perfect.
10. Economics and animal health control drive the use of vaccines in poultry.
Vaccines are used in geographic areas of highest risk and in the agricultural
sector affected, or at greatest risk to be affected. In the USA, inactivated
AI vaccines cost on average USD 0.05/dose and another USD 0.05-0.07 for
labor and equipment to administer. In examining new vaccine technologies,
such adoption will only occur when protection is as good as or better than
existing technologies, and the product is cost effectiveref.
If the cost is prohibitively high, the farmer or company will not be able
to use the vaccine.
11. When deciding to use AI vaccine in poultry, a simple animal health
algorithm, in decreasing order of application, should be used: 1) high
risk situations - e.g. as suppressor vaccine in the outbreak zone or as
ring vaccination outside the outbreak zone; 2) rare captive birds, such
as those in zoological collections; 3) valuable genetic poultry stock,
such as pure lines or grandparent stocks whose individual value is high;
4) long-lived poultry, such as egg layers or parent breeders; and, lastly,
5) meat production poultry.
12. Several issues which must be resolved before deciding to use AI vaccines:
1) the vaccine strain must be of the same hemagglutinin subtype and be
shown in animal studies to be protective against the circulating field
virus, 2) standardized manufacturing of vaccines must be followed to produce
consistent and efficacious vaccines, 3) policies must be established for
proper storage, distribution and administration of the vaccine; 4) adequate
serological or virological surveillance must be done to determine whether
the field virus is circulating in vaccinated flocks; and 5) an exit strategy
must be developed to prevent permanent use of vaccine. In addition, for
inactivated whole AI vaccines, the following should be addressed: 1) the
need for adequate AI viral antigen content to elicit a protective immune
response, either by establishing a minimum hemagglutinin protein content
in the vaccine (e.g. minimum of 1-5 micrograms/dose if using generic adjuvant
system, less antigen is needed if a proprietary systems gives higher titers)
or by demonstration of a high level of protection as measured by in
vivo challenge studies or the presence of a minimal hemagglutination
inhibition (HI) antibody titer in vaccinated birds (e.g. minimum of 1:32-1:40
HI test); 2) the need for a good oil emulsion adjuvant system; and 3) the
establishment of a high level of biosecurity practice for vaccination crews
that enter farms to prevent accidental spreading of field virus. If using
recombinant fowlpox vaccine, the vaccine should only be administered to
one day-old chickens in hatchery, which will give good protection, improved
biosecurity and a high degree of quality control. Before new vaccine technologies
should be used in the field, assessment of safety in target species, environmental
impact to non-target species, purity and efficacy must be demonstrated.
13. Surveillance must be conducted on vaccinated flocks to determine whether
the field virus is circulating and the control strategy is working. This
should be done by both serological and virological surveillance of vaccinated
and non-vaccinated flocks. For serological surveillance, several methods
can be used to identify infections by field virus in vaccinated populations:
1) placement of unvaccinated sentinel birds and looking for antibodies
against AI viruses, such as in ducks, 2) if using inactivated vaccine,
looking for specific antibodies against the neuraminidase of the circulating
field virus in vaccinated birds (if using an inactivated vaccine strain
with a different neuraminidase subtype than the circulating field virusref)
or looking for antibodies against the non-structural proteinref,
or 3) if using recombinant fowlpox vaccine, looking for antibodies to nucleoprotein/matrix
protein. For virological surveillance, examination for specific AI viral
nucleic acids or proteins, or isolation of the virus, could be used to
determine whether the field virus is circulating. This is best done on
sentinel birds that are showing clinical signs or who die. Alternatively,
examination of dead poultry from vaccinated populations will give an indication
of whether the field virus is circulating.
14. Recently, 2 new vaccines for use in China have been reported: 1) recombinant
fowlpox-H5N1 AI vaccine, and 2) a reverse genetic produced influenza A
inactivated vaccine. The new recombinant fowlpox vaccine is a live, injectable
vaccine for chickens and uses the same technology as the previously licensed
recombinant-fowlpox-virus-AI-H5 vaccine (cDNA copy of the AI
hemagglutinin gene from A/turkey/Ireland/83 [H5N8]),
but includes inserted cDNA copies of AI hemagglutinin (H5) and
neuraminidase (N1) genes (both from A/goose/Guangdong/3/96 [H5N1])ref.
This type of vaccine can only be used in one-day-old chickens and not in
older birds in which immunity to fowlpox virus will inhibit replication
of the vaccine virus and prevent development of effective immunityref.
The other new vaccine is a traditional inactivated oil emulsion AI vaccine,
but unlike current inactivated AI vaccines, the new vaccine virus is not
an H5 LP or HPAI field virus. The vaccine virus was produced
by reverse genetics using the 6 internal genes from a human influenza vaccine
strain (PR8) and the hemagglutinin and neuraminidase genes from A/goose/Guangdong/3/96
(H5N1) AI virus. The use of PR8 internal genes imparts
the characteristic of growth to high virus content in embryonating chicken
eggs used in the manufacturing process and thus produces a high concentration
of the protective hemagglutinin protein in the vaccine. Another change
in the vaccine virus: the portion of the gene that codes the hemagglutinin
proteolytic cleavage site has been changed from a sequence of an HP to
an LPAI virus, thus, the vaccine virus is a LPAI virus and can be manufactured
at a lower level of biosafety. Both vaccines require handling and injection
of individual birds. Data published or presented at scientific meetings
indicate that these new vaccines are as efficacious as the existing licensed
vaccines, but no data have been presented to demonstrate they provide superior
protection
One dose of chicken vaccine costs between USD 0.05 - 0.20ref.
So far 5 countries, namely China, Indonesia, Viet Nam, Pakistan and
Egypt, apply mass vaccinations, while 3 -- France, the Netherlands and
Israel -- have allowed limited vaccination in specific target populations,
including zoos, but none in regular, commercial poultry flocks, which remain
unvaccinated and are required to be kept indoors to prevent exposure to
wild birds. This is done in line with the European Commission's Decision
2005/94/EC, dated 21 Oct 2005.
Epidemiology : identified in Italy > 100 years
ago and nowadays occuring worldwide; most avian species appear to be susceptible
to at least some of the AI viruses, though some species are more resistant
to infection than others.
During 1994-99 infections of poultry with influenza viruses of H9N2
subtype appear to have been common world-wide. Outbreaks occurred in Germany
in 1995-96, Italy in 1994, Ireland in 1997, South Africa in 1995, and Korea
in 1996 (6). Since 1997 serious problems associated with H9N2
virus
have been reported in Iran, Saudi Arabia, Pakistan, China and other Asian
countries.
15 subtypes of influenza virus are known to infect birds : to date,
all outbreaks of the HPAI have been caused by influenza A viruses of subtypes
H5 and H7 (H9N2 is not highly
pathogenic in birds). Recent research has shown that LPAI can, after
circulation for sometimes short periods in a poultry population, mutate
into HPAI. Worldwide experience since 1959 supports official statements
about the unprecedented nature of the present situation and the unique
challenges for control. Unique features of the present situation include:
concentration of poultry in backyard farms. In several countries experiencing
outbreaks, up to 80% of poultry are produced on small farms and backyard
holdings in rural areas, where poultry range freely. In China, 60% of the
country's estimated 13.2 billion chickens are raised on small farms in
close proximity to humans and domestic animals, including pigs. This situation
makes implementation of strict control measures, essential to the control
of previous outbreaks, extremely difficult. These control measures -- including
bird-proof, ecologically controlled housing, disinfection of all incoming
persons, equipment, and vehicles, prevention of contact with insects, rodents,
and other mechanical vectors -- cannot be applied on small rural farms
and backyard holdings.
economic significance of poultry production. Poultry production contributes
greatly to the economies and food supplies of affected countries. The agricultural
sector faces the challenge of minimizing losses to industry and subsistence
farmers in ways that also reduce health risks for humans. Because many
people in the region are so dependent on poultry, appropriate culling may
be difficult to implement.
lack of control experience. Since the disease is new to most countries
in the region, very little experience exists at national and international
levels to guide the best country-specific control measures. In some countries,
announcements of successful culling in certain areas are being followed
by subsequent eruptions of disease in the same areas, suggesting reintroduction
of the virus, continuing presence in the environment, or inadequate verification
of outbreak control
lack of resources. Several countries with very widespread outbreaks lack
adequate infrastructure and resources, including resources to compensate
farmers and thus encourage compliance with government recommendations.
In some countries that have announced outbreaks, neither surveillance to
detect the extent of spread nor culling of animals known to be infected
is taking place.
the scale of international spread. With so many adjacent countries affected,
a region-wide strategy will be needed to ensure that gains in one country
are not compromised by inadequate control in another. These unique features
will make rapid control and long-term prevention of recurrence extremely
difficult to achieve.
Since 1959, only 21 outbreaks of HPAI had been reported worldwide,
9 in turkeys and 12 in turkeys; 12 of these outbreaks have occurred since
1990. The majority occurred in Europe and the Americas. Of the total, only
5 resulted in significant spread to numerous farms, and only one was associated
with spread to other countries.
year / country (area) / domestic birds affected / strain
1959 / Scotland / chicken /H5N1
1963 / England / turkey / H7N3
1966 / Ontario (Canada) /7732/ turkey / H5N9
1976 / Victoria (Australia) / chicken / H7N7
1979 / Germany / chicken / H7N7
1979 / England / turkey /199/ H7N7
1983-1985 / Pennsylvania (USA) / chicken, turkey /1370/ H5N2.
It initially caused low mortality, but within 6 months became HPAI, with
a mortality approaching 90%. Control of the outbreak required destruction
of > 17 million birds at a cost of nearly USD 65 million : this outbreak
also caused retail egg prices to increase by > 30%.
1983 /Ireland /turkey /1378/H5N8
1985 /Victoria (Australia)/ chicken/ H7N7
1991 /England /turkey /50-92/ H5N1
1992 /Victoria (Australia)/ chicken /1//H7N3
1994 /Queensland (Australia) /chicken /667-6/H7N3
1994-1995/ 8623-607/Mexico* chicken H5N2. Began in
1992 as with LPAI and evolved to HPAI via antigenic drift. Farmers have
been immunizing chickens against a low-pathogenicity H5N2
virus with the same vaccine for 7 years. Although the vaccine still prevents
clinical disease, it no longer reduces the amount of virus shed by the
chickens. Widespread vaccination probably contributed to the virus becoming
endemic not only in Mexico but in neighboring Guatemala and El Salvador
as wellref
1994 Pakistan* chicken /447/H7N3
1997 New South Wales (Australia) chicken H7N4
1997 Hong Kong (China)* chicken H5N1
1997 Italy chicken 330/H5N2
1999-2000 Italy* turkey H7N1 : initially LPAI, mutated
within 9 months to a HPAI. > 13 million birds died or were destroyed.
2002 Hong Kong (China) chicken H5N1
2002 Chile chicken H7N3
2003 Netherlands* chicken H7N7
Dec 2003 South Korea (has never had the disease before), Japan (has not
had an outbreak since 1925), China :H5N1 virus strain
that has been reported, so far, to cause disease in chickens, ducks, and
quails : it has so far spread to 14 farms and resulted in the slaughter
of 1.2 million chickens and ducks
*Outbreaks with significant spread to numerous farms, resulting in great
economic losses. Most other outbreaks involved little or no spread from
the initially infected farms.
Observations from previous outbreaks (1959-2003) :
outbreaks of HPAI can be extremely difficult to control, even under favourable
conditions (concentration of infected birds in well-maintained commercial
production facilities, limited geographical occurrence).
the 1983 Pennsylvania (USA) outbreak took 2 years to control. Some 17 million
birds were destroyed at a direct cost of US$62 million. Indirect costs
have been estimated at more than US$250 million.
the 2003 outbreak in the Netherlands spread to Belgium and Germany. In
the Netherlands, more than 30 million birds -- a quarter of the country's
poultry stock -- were destroyed. Some 2.7 million were destroyed in Belgium,
and around 400 000 in Germany.
in the Netherlands, 89 humans were infected, of whom one (a veterinarian)
died. In that outbreak, measures needed to protect the health of poultry
workers, farmers, and persons visiting farms included wearing of protective
clothing, masks to cover the mouth and nose, eye protection, vaccination
against normal seasonal human influenza, and administration of prophylactic
antiviral drugs.
control is even more difficult in countries with dense poultry populations.
the Italian outbreak of 1999-2000 caused infection in 413 flocks, including
25 backyard flocks, and resulted in the destruction of around 14 million
birds. Control was complicated by the occurrence of cases in areas with
extremely dense poultry populations. Compensation to farmers amounted to
US$63 million. Costs for the poultry and associated industry have been
estimated at US$620 million. 4 months after the last outbreak ended, the
virus returned in a low-pathogenic form, rapidly causing a further 52 outbreaks.
although the last outbreak of HPAI in Mexico occurred in 1995, the causative
agent -- the H5N2 strain -- has never been entirely
eliminated from the country, in its present LPAI form, despite years of
intense efforts, including the administration of more than 2 billion doses
of vaccines of varying efficacy. Similarly, the vaccination policy pursued
in Pakistan does not appear to have resulted in eradication of the causative
agent.
avoidance of contact between poultry and wild birds, especially ducks and
other waterfowl, can help prevent the introduction of a LPAI into domestic
flocks. Though no evidence to date has conclusively linked the current
outbreaks with wild migratory birds in Asia:
several of these outbreaks have been linked to contact between free-ranging
flocks and wild birds, including the shared use of water sources. Faecal
contamination of water supplies is considered a very efficient way for
waterfowl to transmit the virus. LPAI virus has been readily recovered
from lakes and ponds where migratory birds congregate.
an especially risky practice is the raising of small numbers of domestic
ducks on a pond in proximity to domestic chicken and turkey flocks. Domestic
ducks attract wild ducks, and provide a significant link in the chain of
transmission from wild birds to domestic flocks.
aggressive control measures, including culling of infected and exposed
poultry, are recommended for avian influenza virus subtypes H5
and H7 even when the virus initially shows low pathogenicity.
(H5 and H7 are the only subtypes implicated in outbreaks
of highly pathogenic disease.)
several of the largest outbreaks (Pennsylvania, Mexico, Italy) initially
began with mild illness in poultry. When the virus was allowed to continue
circulating in poultry, it eventually mutated (within 6 to 9 months) into
a HPAI with a mortality ratio approaching 100%. Moreover, the initial presence
of LPAI in these outbreaks complicated diagnosis of the HPAI
In a RT-PCR screening for the presence of influenza A virus of > 8500 wild
birds (mainly ducks, geese, and shorebirds) in Northern Europe in 1999
and 2000, approximately 1% of samples were positive, and from 50% influenza
A virus was isolated in embryonated chicken eggs. A wide variety of isolates
was obtained representing HA subtypes 1 through 7, 10, 11, 13, an unidentifiable
HA, and NA subtypes 1 through 8ref
. According to Article 2.1.14.2. of OIE's International Animal Health Code,
"A country may be considered free from HPAI when it has been shown that
HPAI has not been present for at least the past 3 years. This period shall
be 6 months after the slaughter of the last affected animal for countries
in which a stamping-out policy is practised with or without vaccination
against HPAI. However, countries may also declare certain zones within
their boundaries to be free from HPAI. According to Article 2.1.14.3. of
the Code, "an infected zone may become free if at least 21 days have elapsed
after the confirmation of the last case and the completion of a stamping-out
policy and disinfection procedures, or 6 months have elapsed after the
clinical recovery or death of the last affected animal if a stamping-out
policy was not practiced." Zones declared free from HPAI after complying
with the described requirements may be eligible for export of susceptible
animals and/or their products, under conditions agreed upon between the
exporting and importing countries. Obviously, processed (heat treated)
poultry products are regarded safer than live animals or unprocessed products.
Chapter 1.3.5. of the Code deals with Zoning and Regionalisation; a proposal
for a revised chapter 1.3.5., renamed "ZONING,
REGIONALISATION AND COMPARTMENTALISATION", will be considered by the
International Committee of the OIE during the due General Session in May
2004
A turkey breeder flock in Sampson County, North Carolina, USA, has
been confirmed to have H3N2 influenza in Jan 2005.
Web resources :
paramyxoviruses, designated APMV-I to APMV-9). Strains
of ND virus vary widely in the severity of the disease they may produce
in birds. The less pathogenic strains may induce severe disease when exacerbated
by the presence of other organisms or by adverse environmental conditions.
The preferred method of diagnosis is virus isolation and subsequent characterization.
For a review, see: Alexander JD. Newcastle disease and other avian paramyxoviruses.
Rev Sci Tech 2000; 19(2): 443-62
velogenic
viscerotropic Newcastle's disease (VVND) : smuggled psittacines (parrots)
were the cause of the 1971 outbreak of VVND in Southern California, that
resulted in the loss of somewhere around US$ 65 million in 1971 dollars
and 12 million US chickens.
velogenic
neurotropic Newcastle's disease (VNND)
=> exotic Newcastle's disease (END) after an incubation period of
3-28 days. It is harmless to humans but affects virtually all bird species,
especially Gallus gallus,
with mortality up to 90%. The uncurable disease causes sneezing, coughing
and diarrhea,
and can be spread by a speck of saliva on a windblown feather.
Epidemiology : initially reported from Java
in 1926, followed soon by outbreaks in Newcastle-Upon-Tyne in the UK (1930's),
Ranikhet in India, and Colombo in Sri Lanka.
Asia :
Ukraine : the last outbreak was reported to the OIE in 1992.
Russia reported 2 outbreaks in 2003, one in the Lipetsk region (May), the
other one (in a monthly -- October -- report) in the Belgorodsk region;
both adjacent to the Ukrainian border. According to OIE's epidemiological
statistics, 11 NCD outbreaks have been reported from Russia during the
first 9 months of 2004, in the following regions (oblasts): Altayskiy kray,
Bryansk, Nizhegorodsk, Moskva (city), Smolensk and Ivanovsk.
Bhutan : the 2003 report to the OIE included the following remark: "Although
NCD has not been reported from the field, the disease is endemic in the
country. Vaccination has not picked up in the villages yet" (32,421 avians
reportedly vaccinated). Outbreaks were reported in March 2004
Europe : outbreaks were reported during 2003/2004 from several European
countries, including Austria, Belgium, and Norway
Albania, on the other hand, has been subject to Newcastle for most of the
last decade
Bulgaria experienced an outbreak in 2004 (last outbreak : 1993)
Cyprus experienced an outbreak in 2005 (last outbreak : 1993)
Denmark : serious outbreak in 2002
Finland : outbreaks during 2004
Greece : outbreak in 2005 (last outbreak : 1986).
France : last reported outbreak of NCD occurred in December 1999.
UK : isolated cases of this disease were first reported in the 1930s, and
there have been 7 outbreaks since then, the last in 199. From 1947 outbreaks
occurred here over the next 30 years, and there were further isolated cases
in 1984 and 1996-7. The last outbreaks of NCD in the UK occurred in 1997,
involving fowls and turkeys in 11 foci situated in 6 countiesref.
An outbreak due to avian paramyxovirus, serotype 1 lineage 5B in a flock
of 9000 2 weeks old pheasants (imported from France 2 weeks before) on
a farm that rears game birds for shooting near West Horsley and Reigate,
Surray was confirmed on 15 Jul 2005. There are ample examples, from various
countries, of NCD being introduced by imported live pheasants, one of the
oldest records relating to the 1st epizootic in Switzerland in 1942. Initial
investigations identified 2 possible sources of the infection. The birds
had been imported from France, and so it was possible that they had 1st
become infected there. The 2nd possibility was that the pheasants had been
infected once they had arrived in England from contact with wild birds.
It is known that wild birds can carry the virus responsible for ND. There
are no chicken farms in the immediate vicinity, though one of the main
poultry production areas of England is in the adjacent county of Kent.
Although most breeding and egg-laying birds are routinely vaccinated against
the disease, most chickens reared for meat are notref1,
ref2
Sweden : outbreaks in 1995, 1997, 2001, and 2005
USA : serious outbreaks in California in 2003. In September 2002 velogenic
NCD affected a backyard flock of chickens in Compton, Southern California
: a task force has been trying to control the virus by killing seemingly
healthy birds within 1 km of infected fowl. State and federal agents trying
to control the spread of a deadly avian disease have killed 3.2 million
birds at 22 farms and commercial businesses. Nearly 137,000 birds in 2,343
backyard flocks (some of them household parrots and parakeets) and some
wild birds also have been killed. New cases have been discovered in Nevada,
Arizona and Texas.
South America : oubtreaks in Brazil in 2001 and 2006, Argentina's was in
1999, Chile in 1975, Uruguay in 1984, and Paraguay in 1997. Venezuela
had an outbreak in 2006.
Transmission :
direct contact with secretions and excretions from infected birds (usual).
Respiratory discharge and fecal droppings are especially loaded with the
virus. All parts of the carcass appear to be infected.
ontaminated common feed supplies, water, implements, premises, human clothing
(especially boots) and equipment
The incubation period for NCD after natural exposure varies from 2 to 15
days => Newcastle disease (NCD) / Ranikhet disease / fowl or pseudofowl
pest / avian pneumoencephalitisref
: an influenza-like viral disease of birds, including domestic fowl, characterised
by respiratory and gastrointestinal or pneumonic and encephalitic symptoms
(depression, lack of appetite, breathing difficulties, coughing, sneezing
and diarrhea). It can easily be confused with
highly
pathogenic avian influenza (HPAI / fowl plague), another OIE List A
disease. Cambodia and Indonesia have recently reported the simultaneous
occurrence of both diseases. Not all pigeon variant viruses (PPMV-1) show
virulence for chickens, but some have caused serious outbreaks. The OIE
definition for reporting an outbreak of ND is: "Newcastle disease is defined
as an infection of birds caused by a virus of APMV-1 that meets one of
the following criteria for virulence:
the virus has an intracerebral pathogenicity index (ICPI) in day-old chicks
(Gallus gallus) > 0.7
or
multiple basic amino acids have been demonstrated in the virus (either
directly or by deduction) at the C-terminus of the F2 protein and phenylalanine
at residue 117, which is the N-terminus of the F1 proteinref.
The term 'multiple basic amino acids' refers to at least 3 arginine or
lysine residues between residues 113 and 116. Failure to demonstrate the
characteristic pattern of amino acid residues as described above would
require characterisation of the isolated virus by an ICPI test. In this
definition, amino acid residues are numbered from the N-terminus of the
amino acid sequence deduced from the nucleotide sequence of the F0 gene,
113-116 corresponds to residues -4 to -1 from the cleavage site.
This disease is known to affect domestic and wild birds. It can affect
turkeys, chickens, geese, ducks, pheasants, guinea fowl and other wild
and captive birds as well as ostriches, emus and rhea. The species of bird
affected as well as the strain of the virus dictates the morbidity and
mortality. However, chickens appear to be the most susceptible, while ducks
and geese may be the least susceptible. Psittacine birds [parrot family],
and perhaps some wild birds, may develop a carrier state, as they have
been shown to intermittently demonstrate the virus for over a year. Incubation
of the disease is generally 4 to 6 days. The virus can be shed during incubation,
the clinical phase, and for a period of time during the bird's convalescence.
The virus is present in exhaled air, respiratory discharges, feces, eggs
laid during clinical disease, and all parts of the carcass during acute
infection and at death. Thus, it is not unexpected that chickens become
infected through aerosols, contaminated feed, or water. Clinical signs
usually appear rapidly and move as rapidly as 2 days to infect the entire
flock, or may take as long as 12 days. But all birds appear to be in the
same stages of clinical infection almost simultaneously. The disease, as
well as some others, should be suspected when respiratory signs, such as
gasping and coughing, are apparent in the birds. Birds may also demonstrate
drooping wings, dragging a leg, anorexia, depression, circling and even
complete paralysis. The fecal droppings may be very watery with a greenish
appearance. Layers [hens] generally have a marked decline in production
or a complete cessation. Eggs produced may be abnormally shaped, have rough
and thin shells and very watery albumen. Unfortunately, there are no pathognomonic
lesions with this disease. Confirmation is through virus isolation and
identification. However, the disease should be suspected when there is
edema in the tissues around the trachea. The trachea may appear congested,
or there may be frank hemorrhage in the tracheal mucosa. The proventriculus
may have varying degrees of hemorrhage.Differential diagnoses include,
avian influenza, laryngotracheitis, infectious bronchitis, psittacosis
and mycoplasmosis. Differentials may also include mismanagement, such as
water deprivation, or inappropriate air circulation. Aside from virus isolation,
the serological hemagglutination inhibition test as well as the ELISA test
are also considered to be diagnostic. There is no good treatment for affected
birds.
Prevention : biosecurity and sanitation
is the best prevention. There is a vaccine available which reduces the
losses in the flocks. Some vaccines are live viruses and may be administered
as oil emulsion. There are also killed virus vaccines, and still others
may be administered in the drinking water. The Ranikhet live-attenuated
vaccine used in Bangladesh is locally produced : an outbreak of 8000-30
000 chickens died a few hours after vaccine administration has been reported
since the distribution of batch 914 of the vaccine, produced on 5 Jan 2004
(some farmers did not use distilled water when giving the chickens the
vaccine). Vaccinating village chickens with a live attenuated NCD vaccine
based upon the thermostable I-2 virus strain, using the eye-drop application,
has been shown to be effective in several developing countriesref.
Vaccination has been used during out breaks to gain control, as well as
on a regular basis in endemic areas to build immunity.
Newcastle disease virus may produce a transitory conjunctivitis in
people. The condition has generally been confined to laboratory workers
and teams exposed to large quantities of virus such as those eviscerating
poultry in processing plants. The disease has not been reported in those
consuming poultry products.
The current NCD chapter is 2.7.13, within Section 2.7, "Avian
diseases"ref:
According to the revised Code's requirements, immediate notification from
a member-country (by telegram, fax or e-mail), within 24 hours, is required
in any of the 6 following events:
1. 1st occurrence of a listed disease and/or infection in a country or
zone/compartment;
2. re-occurrence of a listed disease and/or infection in a country or zone/compartment
following a report declared the outbreak ended;
3. 1st occurrence of a new strain of a pathogen of an OIE listed disease
in a country or zone/compartment;
4. a sudden and unexpected increase in the distribution, incidence, morbidity
or mortality of a listed disease prevalent within a country or zone/compartment;
5. an emerging disease with significant morbidity or mortality, or zoonotic
potential;
6. evidence of change in the epidemiology of a listed disease (including
host range, pathogenicity, strain) in particular if there is a zoonotic
impact.
Pasteurella multocida
type A (avian cholera / avian pasteurellosis / fowl cholera (FC))
may cause epidemic (epornitic) mortality. Cholera in wild birds, such as
the cormorants, is probably Type 1. Transmission usually involves intimate
contact or a common water source (e.g. birds in adjoining pens frequently
remain unaffected as long as they do not share a water source that can
become contaminated). It can survive outside the host for very long periods.
Although many species of birds and mammals can become infected with different
strains of this bacteria, Type I is most common. The species of birds most
commonly affected are ducks and geese, coots, gulls, and crows. Avian cholera
can spread very rapidly as it is highly contagious. Immediate action is
necessary to minimize or prevent the spread of the disease. Careful carcass
collection and disposal helps reduce the amount of bacteria in the environment.
Killing all birds within a 5-km radius of affected farms and inspecting
every poultry farm in a 50-km radius for signs of fowl cholera and bronchitis
are rather unusually severe measures -- though, in its peracute form, fowl
cholera is indeed a very virulent and infectious disease of poultry, clinically
resembling highly pathogenic avian influenza and velogenic, viscerotropic
Newcastle disease. The bacterium usually responds to antibiotics and sulfonamides
: however, treatment of commercial birds would be impractical because of
the required withdrawal period. Commercial vaccines with moderate efficacy
are available. Although human beings are not at high risk of contracting
this disease, it is a wise idea for the workers to wear gloves when removing
the carcasses. Large die-offs are seen primarily in wild ducks and geese,
which the disease affects peracutely. It is included in List B diseases
of the OIE. The most common early sign is the sudden appearance of large
numbers of dead birds in good body condition. Few if any birds are observed
as sick.. Death can be be so rapid the birds will literally fall out of
the sky. They may die while eating, with food still in the bills or oral
region, with no previous signs of disease. Sick birds appear lethargic
and die within minutes when captured. Other clinical signs are convulsions;
swimming in circles; throwing the head back between the wings; erratic
flight, such as flying upside down or trying to land a foot or more above
the water; mucous discharge from the mouth; soiling or matting of the feathers
around the vent, eyes, and bill; pasty, fawn-colored or yellow droppings;
or blood-stained droppings or nasal discharge. On necropsy, hemorrhages
may be seen on the heart, liver, gizzard, and intestines. Areas of tissue
death appear as white or yellow spots on the liver and spleen. The liver
may appear darkened or copper in color, and may be swollen and rupture
when handled. These particular lesions are not unique to avian cholera,
but rather to an acute disease process. The upper digestive tract may contain
recently ingested food, while lower digestive tract may contain a thick
yellowish viscous fluid, filled with large numbers of P. multocida
bacteria
Mycoplasma
gallisepticum (chronic respiratory disease (CRD) : is primarily
a respiratory infection and most frequently occurs subclinically. It lasts
the life of the bird, but is of no public health significance. The disease
ostensibly is worldwide in distribution. In poultry MG has few outwardly
observable clinical signs, other than decreased egg production and decreased
feed efficiency as infections would probably remain dormant until the bird
is stressed. A sudden change in environment, vaccination, or heavy (peak)
egg production triggers spread of the disease. MG is transmitted through
direct contact between susceptible birds and infected birds. The disease
is spread primarily by airborne dust or droplets and by contact with contaminated
equipment, although it can also be transmitted through the egg to the offspring.
Time of incubation or from contact to outbreak can be as short as 4 days
& as long as 3-4 weeks)
Trichomonas
gallinaeref
: found in the upper digestive tract and associated structures and in other
organs, especially the liver, of domestic pigeons and various other birds,
in which it causes a form of avian trichomoniasis (called "canker"
in doves and pigeons and "frounce" in raptors)ref
. Pigeons and doves are the primary hosts, but it also occurs in canaries,
finches, budgerigar and their predators, e.g. raptors (hawks, falcons,
Great Horned owlsref,
and eagles). The disease is very common in domestic pigeons, but lesions
are predominantly seen in nestling and young pigeons, not in adults. All
in all, pigeons and doves being somewhat colonial, the infection is easily
spread, especially at common drinking areas, whether urban, or, in the
high deserts of Northern California. Raptors feeding on the sick birds
are at risk. Trichomoniasis in Cooper's hawks from Arizona was describedref
: they demonstrated that prevalence of T. gallinae was significantly
greater among urban nestlings (85%) than among ex-urban nestlings (9%),
and postulated that the patterns found were probably caused by 3 factors:
doves are hosts for the parasite, they are present in large numbers in
Tucson, and they are the primary prey of urban Cooper's hawks there. From
anecdotal reports, it is interesting to note that the parasite appears
more pathogenic in the western portion of the country than in the east,
especially in birds of prey. This may be due to strain variations in the
parasite or in evolved resistance in host defenses. Hanson (1969) pointed
out that pigeons (and Trichomonas) were introduced to the eastern
part of the continent roughly 2 centuries before their introduction to
the west coast, and speculated that this parasite may have contributed
significantly to the extinction of the passenger pigeon.
Transmission : birds suffering from trichomoniasis
shed the parasites through the saliva and crop milk. Pigeons are infected
by the uptake of contaminated water, or, oral contact with affected birds
during fighting or feeding of squabs. It may also be transmitted between
pigeons during ritualized courtship feeding in which the female places
her beak in the male's mouth. Trichomoniasis is spread in the wild bird
population often by well-meaning people feeding birds. It takes only one
badly infected bird to start the spread of the protozoa parasite to others
sharing the same feeding site and/or water source. Most people, unfortunately,
have no idea what this disease is, how it is spread, or what part they
may play in Trichomoniasis' spread. Infected birds will continue to attempt
to eat seeds or drink water, even though their throats are often blocked
by the parasite, because they are starving or dying of thirst, in addition
to the infection. The parasite multiplies within the animal, increasing
its tumor-like mass in the bird, while eating the bird's flesh (thus the
smell), and usually chokes off their throats, thus the inability to eat
or drink. When these infected birds regurgitate the seeds, the seeds are
covered with the 'infective ooze' caused by and containing the parasite.
Other birds then ingest these now deadly regurgitated seeds, become infected,
and repeat the same process, thus infecting bird after bird that shares
the same feeder or water source. Any nestlings are also infected with the
disease their parents have. Any bird that comes in contact with the parasite
can get the disease. Often other wild birds that become infected and die
with the disease -- like doves -- aren't noticed, because they tend to
go off and die 'in private,' under bushes, and other more covered areas.
Once Trichomoniasis gets into the wild population, it can spread like wildfire.
Most of the time only doves and pigeons are found, for they tend to die
in the open, whereas other bird species seek cover when ill and dying;
but usually many other species of bird in the same area are also infected
and die. Unfortunately, there is little public information or warnings
regarding what people can do to help prevent the spread of this disease,
or at least not contribute to it. In addition, adult pigeons do die from
the disease. Most birds that contract the disease do die from it, but usually
not before they have spread it to other birds, including their young. The
disease can also spread to any part of the body (though usually stays in
the digestive tract). This protozoa parasite can also be spread through
droppings. Trichomoniasis has been running rampant in Tucson, Arizona.
Usually Trichomoniasis rears its ugly head in the spring, but this past
year, it was ever-present. Using bird feeders and water bowls is not recommended
: a trickling water source should be preferred, with the water outlet slightly
off the ground (average bird beak height), where water does not form a
stagnant pool, so there is not a 'reservoir' of infected water. Most birds
like to drink water close to the source. The water does not have to run
all the time, but at least twice a day, and strongly enough to flush away
any potential protozoa; the flow soaks quickly into the ground. If someone
is going to provide seed, spreading the seed out over a large area, in
the sun, and vary the location to some degree daily is recommended.
The birds are less densely congregated, so one infected bird has less chance
of infecting other birds. One infected bird using a feeder can leave the
parasite on the feeder seed outlet, so not only are seeds the bird has
regurgitated covered with the parasite, but any bird feeding at the bird
feeder could pick up the disease. Bird feeders can increase the number
of birds infected. Stores selling bird feeders don't like to hear this,
but there is really more money in selling seed over time anyway. I haven't
addressed 'elitist' feeders, who want to feed certain types of birds, but
if they care about the birds' lives, the feeders must go. Feeders should
be cleaned weekly with a solution that is 9 parts water to one part bleach
using a bottle brush to get inside tube feeders. The same bleach solution
should be used to clean birdbaths daily.
=> the parasites colonize the upper digestive tract, predominantly
the crop causing necrotic lesions. Infection varies from mild to a rapidly
fatal disease manifested by caseous accumulations and necrosis in involved
tissues and severe weight loss. Affected birds often display respiratory
distress and open-mouthed breathing as the sores constrict a bird's trachea
and esophagus until it dies of hunger or chokes. In adult pigeons, the
disease is associated with poor racing performance but manifests no clinical
signs. Thus, affected doves would be easy prey for raptors. Heavily infested
adults show fluid droppings with a sour odor. Rarely, adult pigeons may
die acutely when the parasite affects large blood vessels. Sudden death,
and wasting, are seen in affected nestlings.
There is no risk of the infection spreading to humans.
Trichomoniasis is treatable with several drugs such as Emtryl.
Trichomonas gallinarum : found in the lower digestive tract
of chickens, turkeys, and other domestic birds in which it sometimes causes
a fatal form of avian trichomoniasis (necrotic lesions of the upper digestive
tract). Infection is manifested by lesions of the cecum and liver, diarrhea,
and loss of appetite and weight.
Tetrameres : a genus of nematodes parasitic in the alimentary tract
of chickens and other fowl. T. americana is found in the proventriculus
of chickens and other birds; heavy infestations may be fatal to young birds
Aegyptianella
[named for Egypt, where the organism was first described in 1929]
a genus of bacteria of the family Anaplasmataceae, order Rickettsiales,
occurring as a parasite in wild and domestic birds.
avian pox is a mild to severe, slow-developing disease of birds
caused by an avipoxvirus, and 3 common strains have been identified. The
3 strains are fowl pox virus, pigeon pox virus and canary pox virus. The
strains vary in their virulence and have the ability to infect other avian
species. However, many of the strains are group specific. Approximately
60 species of birds from 20 families have been diagnosed with avian pox.
The strain seen in wild turkeys is the fowl pox virus. Avian pox lesions
(wart-like growths) occur on the unfeathered parts of the bird's body and,
in some cases, the mouth, larynx, and/or trachea. Transmission of the avian
pox virus can occur in a number of ways. The disease can be spread via
mechanical vectors, primarily by species of mosquitoes (at least 10). Transmission
occurs when the mosquito feeds on an infected bird that has a viremia (pox
virus circulating in the blood) or on virus-laden secretions from a pox
lesion and then feeds on an uninfected bird. Mosquitoes can harbor and
transmit the virus for a month or longer after feeding on an infected bird.
Experimentally, stable flies have shown the capability of being able to
transmit the pox virus. Avian pox can also be transmitted by direct contact
between infected and susceptible birds. The virus is transmitted through
abraded or broken skin or the conjunctiva (mucous membrane covering the
anterior surface of the eyeball). Indirect transmission of the pox virus
can also occur via ingestion, when food and water sources, feeders, perches,
cages, or clothing are contaminated with virus-containing scabs shed from
the lesions of an infected bird. The pox virus is highly resistant to drying
and may survive months to years in the dried scabs. Indirect transmission
can also occur via inhalation of pox virus infected dander, feather debris
and air-borne particles. Mosquitoes are probably responsible for transmission
within local areas, while wild birds are responsible for outbreaks over
greater distances. Clinical signs observed with avian pox are weakness,
emaciation, difficulty in swallowing and breathing, vision problems, a
reduction in egg production, soiled facial feathers, conjunctivitis, edema
of the eyelids and the presence of the characteristic wart-like growths
on the unfeathered portions of the skin and/or formation of a diphtheritic
membrane on the upper portion of the digestive tract. A presumptive diagnosis
of avian pox can be made due to the gross lesions on the body. Confirmation
of avian pox is accomplished by microscopic examination for the characteristic
Bollinger bodies. Virus isolation by transmission of the organism via egg
inoculation, serological results and polymerase chain reaction can also
be a means of confirming the disease. There is no known treatment for avian
pox in wild birds. In captive situations, there are a variety of treatments
that have been used along with supportive care to treat the pox lesions
and to prevent secondary infections in various avian species. These treatments
consist of removing skin lesions and utilizing sodium bicarbonate or Lugol's
solution of iodine washes, removing the diphtheritic membrane from the
mouth and throat and swabbing the area with Lugol's solution of iodine,
bathing the eyes with a 1-2% saline solution, and raising the environmental
temperature. In all cases, providing assistance for recovery may spread
the infection to other parts of the skin or to other birds. Avian pox is
a highly contagious disease, and there are 3 primary control methods that
can be used if infected birds are present. Eliminating standing water will
control the primary vector, the mosquito. Infected birds should be isolated
or culled to remove the source of the virus. Feeders, waterers, birdbaths
and cages should be decontaminated with a 10% bleach solution. There is
no evidence that the avian pox virus can infect humans, and, therefore,
it is not a public health concernref1,
ref2.
On Feb 2006 it killed approximately 200 gentoo penguinsref
in the Port Stephens area of West Falkland at the rookeries at Ten Shilling
Bay and Port Stephens Peak. Penguins with similar signs have also been
reported from New Island and Albemarleref1,
ref2,
ref3.
Chemical aetiologies :
avian vacuolar myelinopathy (AVM) : transmission is from a species
of blue-green algae found growing on an obnoxious water plant called Hydrilla
verticillata (hydrilla; a non-native escapee from the aquarium
industry, spreads like kudzu. Now covering 10 000 acres of South Carolina
lakes, it appears to serve as the perfect host for whatever causes AVM);
to American coots (Fulica
americana) that eat hydrilla; to a half dozen of bird species,
including great-horned owls, mallards (Anas
platyrhynchos) and bald eagles (Haliaeetus
leucocephalus) that prey on coots. AVM claimed its first eagles
in Arkansas, where it was confirmed or suspected of killing 29 birds in
the winter of 1994 and 26 birds 2 years later, according to the National
Wildlife Health Center. Since then, it has killed 24 eagles in Georgia,
most of them on Lake Thurmond; 12 more in Arkansas; 7 in South Carolina
and one near Lake Surf. The real total, including birds never found, will
never be known. Dodder et al. analyzed sediments and coot tissues from
reservoirs affected and unaffected by ACM. Certain compounds relatively
abundant in the sediment (polychlorinated biphenyls, octachlorodibenzo-p-dioxin,
and polycyclic aromatic hydrocarbons such as retene), or relatively abundant
in coot tissues (penta- and hexachlorobenzene, oxychlordane, p,p'-DDE,
dieldrin, and polychlorinated biphenyls), were not differentially abundant
in sediments from AVM-affected vs. non-affected reservoirs, making it doubtful
that these compounds have simple causative effects on the disease. Fischer
et al. fed tissues from AVM-infected vs. non-infected coots to red-tailed
hawks. After 29 days the hawks appeared clinically normal, but autopsies
revealed AVM lesions in all the hawks that received infected coot tissue,
but not in the hawk that received unaffected tissue. These very small samples
are one of the first demonstrations under laboratory conditions of AVM
infection in birds of prey from consuming tissue from infected coots. In
contrast, Larsen et al., in 4 exposure trials 7 days long, were unable
to induce AVM infection in mallards housed with infected coots, or fed
water, Hydrilla, or sediment from the lakes where the infected coots
were captured, even though AVM infection has been reported in mallards.
These results may indicate that AVM is not readily transmitted from coots
to nonpredatory birds by direct exposure or exposure to shared environments.
Prosthogonimus
macrorchis parasitizes chickens, turkeys, and other birds
cleaning the feathers of birds caught in an oil spill with fine iron powder
(cheap, easy to obtain and non-toxic) that let the oil particles to soak
up into thanks to electrostatic forces and then stripped away with powerful
magnets could be kinder than baths with phosphate-based detergents (which
can pollute water and feed toxic algae blooms) both to the birds and the
environment. 9 rounds of treatment remove up to 98% of contaminants from
dead mallard ducks (Anas
platyrhynchos) and little blue penguins (Eudyptula minor).
But the small amounts of oil left behind damage the feathers' waterproofing.
Smaller, rougher magnetic particles full of tiny perforations should help
the oil and iron stick together and strip away all the pollution. The magnets
are unlikely to harm birds. Some birds have tiny particles of iron oxide
in their beak, which are thought to help them navigate by the Earth's magnetic
field, but magnets are swept over the birds' bodies, not their beaks, so
this shouldn't interfere with navigationref
the impressive navigation skills of homing pigeons (Columba
livia) almost certainly relies on tiny magnetic particles of an
iron oxide called magnetite in their beaks. Some experts had previously
suggested that the birds rely on different odour cues in the atmosphere
to work out where they are. But the latest findings suggest that they are
using magnetic cues. You don't need a large receptor structure like you
do for the eye, because the magnetic field permeates everything. But the
particles themselves are likely to be only a few mm
across, and no one has ever seen them under the microscope. The pigeons
were trained to go to one end of the tunnel if the coils were switched
on, generating a magnetic field, and to the other if they were switched
off, leaving Earth's natural field unperturbed. Their skills were impaired,
however, when the researchers attached magnets to their upper beaks, and
also when the upper beak was anaesthetized. When they severed the ophthalmic
branch of the trigeminal nerve, which leads from the upper beak to the
brain, the birds were unable to distinguish between natural and perturbed
magnetic fields. But when the olfactory nerve, which carries smell signals,
was cut instead, the birds performed fine, dealing a seemingly fatal blow
to the idea that they navigate by relying on odours. The results sit well
with previous studies of another impressive navigator, the rainbow trout.
The species both seem to have a system in which signals from magnetite
particles are carried from the nose to the brain by the trigeminal nerve.
This is not surprising as iron-containing materials are common in many
animals' bodies. The problem is that even though we know where to look,
the particles are elusive because of their small size and the fact that
many other biological materials, such as blood, contain ironref
airsacculitis : inflammation of the air sacs in birds
outsized curved beaks up to 3 times their usual size have been spotted
in some 30 species among Alaska's birds so far. In many cases, the beak
is so long that the bird is unable to feed or preen effectively, and ultimately
dies. Isolated cases of beak deformation have been seen in other places
before, but not in such startling numbers. The latest sightings bring the
total number of Alaskan cases to around 1,800 since the first deformities
were spotted in black-capped chickadees near Anchorage during the 1990s.
Crows in southeastern Alaska are the latest to fall victim. Compounds such
as polychlorinated biphenyls (PCBs) and dioxins - persistent pollutants
pumped out by waste incinerators - could damage the birds' DNA. Jaw deformities
are seen quite clearly with PCBs and dioxins. Newborn chicks usually look
fine - curved bills tend to show up after several weeks : the chemicals
could affect beak development in growing birds, rather than causing genetic
defects at birth.
scaly leg : a type of mange in fowls in which the legs become enlarged
and encrusted due to infestation by species of Knemidokoptes.
Birds can perceive the reflectance of ultraviolet light by biological structures.
The skin of the mouth and body of starling nestlings substantially reflects
light in the ultraviolet range and that young in which this reflectance
is reduced will gain less mass than controls, despite low background levels
of ultraviolet and visible light in the nest. This ultraviolet reflectance
from starling nestlings and its contrast with surrounding surfaces are
important for parental decisions about food allocationref.
Feather-pecking in domestic birds is associated with cannibalism
and severe welfare problems. It is a dramatic example of a spiteful behaviour
in which the victim's fitness is reduced for no immediate direct benefit
to the perpetrator and its evolution is unexplained. The plumage pigmentation
of a chicken may predispose it to become a victim: birds suffer more drastic
feather-pecking when the colour of their plumage is due to the expression
of a wild recessive allele at PMEL17, a gene that controls plumage melanization,
and when these birds are relatively common in a flock. These findings,
obtained using an intercross between a domestic fowl and its wild ancestor,
have implications for the welfare of domestic species and offer insight
into the genetic changes associated with the evolution of feather-pecking
during the early stages of domesticationref.
Synchronous arrival of pairs of migratory birds at their breeding
grounds is important for maintaining pair bonds and is achieved by
pairs that remain together all year round. Arrival is also synchronized
in paired individuals of a migratory shorebird, the black-tailed godwit
(Limosa limosa islandica), even though they winter hundreds of kilometres
apart and do not migrate together. The mechanisms required to achieve this
synchrony and prevent 'divorce' illustrate the complexity of migratory
systemsref.
Like all birds, owls have no teeth to chew their food. Their food is
usually swallowed whole, or in large chunks. After an owl swallows a mouse,
strong acids in the owl's stomach begin to digest the mouse's muscle and
other soft parts. The owl can't digest the bones and fur that come along
with the meal, so the owl's stomach forms these indigestible materials
into tight packages called pellets. Several hours after a meal, an owl
will regurgitate one of these pellets. The pellets, along with feathers
and other remains, can be found under owl roostsref.
A virtual dissection of an owl pellet (without risk of salmonellosisref).
Web resources :
many inhabitants of India's 600,000 villages own farm animals and pets,
but most are without trained vets. There are already around 450 'vet on
the net' kiosks of n-Logue Communications
spread across rural India. An extra 9,000 units are planned for 2004. Each
station is also equipped with computer, Internet connection and local language
software. The specially designed cubicles include cameras that offer cheap,
instant video conferencing via the internet. Vets can inspect chickens,
dogs and goats in real time then offer treatment advice. If the animal
is too large, like a cow, or sick to squeeze inside the booth, owners can
email photographs to aid diagnosis. The scheme cuts the cost of animal
care by eliminating unnecessary veterinary visits. Internet consultancy
costs about 20 rupees (around 40 cents) per hour. By comparison, vets charge
a
call out fee of around 200 rupees (4$). Travelling to a town for vet care
can be time consuming and expensive. Some conditions are easy to diagnose
online. Curled toe paralysis, for example, gives fowl characteristically
clawed feet. It is caused by vitamin B2 deficiency and easily
treated by a diet rich in rice husks. Other problems are more difficult
to diagnose and may require a follow-up field visit from the vet. This
also helps to spread the word about the virtual vets.
no official census of livestock has been carried out in Afghanistan since
1967. FAO's estimated figures for 1996 were 3.7 million cattle, 22 million
sheep and 8.9 million goats, for the entire Afghan territory (249,999 sq
mi or 647 497 sq km); it may be assumed that the numbers have increased
since. There being only one vet in a province spread over 17 011 sq mi
(44,059 sq km -- exceeding the size of Switzerland), with an animal population
which might be counted in 6 or rather 7 figures and animal health situation
which, at its best, is regarded as unsatisfactory, should concern the international
community. The plight of the local population (in Badakhshan, at least
500 000) is one good reason; the risk of endangering the neighbouring countries
and beyond is another, serious one. This aspect is underlined by Badhakshan's
most distinctive geographic feature, namely the Vakhan (Wakhan Corridor),
a long narrow panhandle that passes between Tajikistan in the north and
Pakistan in the south, linking Afghanistan with the Xinjiang region in
China.
chapter 1.1.1. "General definitions", of OIE's Terrestrial Anima Health
Code, 11th edition, 2003:
stamping-out policy means carrying out under the authority of the
Veterinary Administration, on confirmation of a disease, the killing of
the animals which are affected and those suspected of being affected in
the herd and, where appropriate, those in other herds which have been exposed
to infection by direct animal to animal contact, or by indirect contact
of a kind likely to cause the transmission of the causal pathogen. All
susceptible animals, vaccinated or unvaccinated, on an infected premises
should be killed and their carcasses destroyed by burning or burial, or
by any other method which will eliminate the spread of infection through
the carcasses or products of the animals killed
nitrogen
argon gas
carbon dioxide
lethal chamber : a chamber that may be filled with gas, for killing
small animals
The global trade in wildlife provides disease transmission mechanisms that
not only cause human disease outbreaks but also threaten livestock, international
trade, rural livelihoods, native wildlife populations, and the health of
ecosystems. Outbreaks resulting from wildlife trade have caused hundreds
of billions of dollars of economic damage globally. Rather than attempting
to eradicate pathogens or the wild species that may harbor them, a practical
approach would include decreasing the contact rate among species, including
humans, at the interface created by the wildlife trade. Since wildlife
marketing functions as a system of scale-free networks
with major hubs, these points provide control opportunities to maximize
the effects of regulatory effortsref
Transboundary animal
diseases
The numbers of cats recorded entering the UK:
in 2000 (11 months only): 2048
in 2001: 3562
in 2002: 4429
in 2003: 5979
The numbers of dogs entering the UK:
in 2000 (11 months only): 12 501
in 2001: 23 160
in 2002: 36 662
in 2003: 48 593
Taking the summer vacation months of May through Sep inclusively, the number
of dogs entering the UK:
in 2000: 6520
in 2001: 11 545, up 77% over 2000
in 2002: 18 829, up 63% over 2001
in 2003: 25 060, up 33% over 2002
In a few years, the dog numbers will level off. While these numbers must
include non-vacationing animals, and though they give no idea of the time-density
of risk with the vacationing dogs, the reported perceived number of cases
of canine babesiosis indicates a simple incidence rate of around 1-2% of
returning dogs. The true incidence must await proper studiesref.
Smuggling of meat, animal products and even animals themselves has
always been and continues to be an important issue. In the USA, Exotic
Newcastle Disease was brought into California in 1971 by the unrestricted
movement of pet birds into the country causing a major outbreak resulting
in multimillions dollar loss. Even when restrictions were subsequently
introduced, outbreaks due to smuggled pet birds continued to occur periodically.
African Swine Fever in Belgium in 1985 was associated with someone
illegally bringing infected meat from Spain and feeding it to a boar. Smuggling
of meat into the United Kingdom was often touted as the cause of the devastating
FMD outbreak in 2001. Finally, in the 2005 Taiwan incident H5N1
virus was actually identified in smuggled meat.
An imported disease, like the current polio imports, refers to sporadic
cases or outbreaks in countries that do not necessarily share common borders.
A transboundary disease is one that spreads from one country to another
across a common border, such as Rinderpest and other epidemic animal diseases
(contagious bovine pleuropneumonia (CBPP), FMD, contagious caprine pleuropneumonia,
peste de petit ruminants, Rift Valley fever, and lumpy skin disease). While
infectious diseases such as FMD and CBPP will readily spread via transboundary
movements of livestock, this is not the case regarding anthrax, which is
related to soil contamination. FAO has established the Emergency
Prevention System (EMPRES) for Transboundary Animal & Plant Pests &
Diseases, to combat those.
Research into physiology and embryology has provided a basis for the
development of technologies that increase productivity of farm animals
through enhanced control of reproductive function. Progestagens,
alone or in combination with luteolysins, are used to control the time
of oestrus in cattle, sheep and pigs, thus permitting better use of artificial
insemination, providing synchronised recipients for embryos and facilitating
management strategies. Treatment with progestagens and pregnant mare
serum gonadotrophin (PMSG) or with gonadotrophin releasing hormone
induces breeding activity in sheep and goats before the commencement of
the breeding season and reduces the duration of postpartum anoestrus in
cattle. In pigs, gonadotrophins are used to hasten puberty in gilts,
control the time of oestrus in sows and gilts and reduce the interval between
farrowing and oestrus. Implants of melatonin hasten the onset of
the breeding season in sheep and goats. Success in increasing litter size
in sheep and cattle with PMSG has been limited because of the large variation
in response between animals. Likewise, immunisation against steroids
has not given consistent results. Immunisation against inhibin appears
to offer the possibility of increasing farm animal fecundity. Induction
of twinning in cattle by embryo transfer is practicable, and recent
developments suggest that in vitro fertilisation may provide a source
of embryos for this purpose. Real-time ultrasonic scanning has proved to
be a reliable method for diagnosing pregnancy in small ruminants and pigs.
The identification of pregnancy-specific proteins in cattle and sheep may
provide a cheap and practical serological test for pregnancy in these species.
Partial
segregation of spermatozoa into X- and Y-bearing components has been
reported, but the method is not yet practicable for use in conventional
artificial insemination of farm animals. The sex of bovine and ovine embryos
can be determined reliably by DNA probes specific for the Y chromosome.
Monozygous
twins can be produced in all farm animal species by microsurgical bisection
of embryos and techniques for cloning from embryonic cells are rapidly
being developed. There is a need to devise strategies to utilise these
clones to best advantage in genetic programmes. Chimeric animals
can be produced in the common farm animal species and will play an important
role in genetic engineering, particularly when embryonic stem cell lines
are produced in these speciesref.
Temperature sensing radio frequency identification (RFID) microchips
for detecting fever in livestock (source : Digital Angel Corp. in Minnesota).
Farm animal doping :
sexual steroids can be assessed with target organ examination
boldenone : histopathology of male cattle previously found positive
forb-boldenone in urine in the Netherlands and
in Italy was studied. The animals were derived from practice and several
weeks had passed after the finding of
b-boldenone
before the animals were examined. The animals consisted of 34 male veal
calves and one finishing bull. In the prostate gland hypersecretion, cyst
formation (45%) and hyperplasia of the urethral epithelium was observed,
in the bulbo-urethral gland similar alterations were present. The testis
showed reduced development and degeneration of the germinal epithelium
(70%), leading to debris and syncytial cell formation in the lumina. Stromal
proliferation was evident. In some animals the liver was sampled and showed
periportal fibrosis, bile duct proliferation and sometimes necrosis. The
bull also showed degeneration of the germinal epithelium of the testis
and absence of sperm production, the prostate gland showed some secretion
and had an atrophic appearance. It is concluded that beta-boldenone may
lead to degeneration of the germinal epithelium of the testis and hypersecretion
and cyst formation in the prostate and bulbo-urethral gland, which alterations
may heal in timeref.
The overall conclusion of the European Commission DG-SANCO Working Party
was that there was a necessity for further research to distinguish between
naturally occurring and illegally used boldenone forms. The confirmation
of the presence of boldenone metabolites (free and conjugated forms) in
certain matrices of animals is proposed as a marker for the illegal treatment
with boldenoneref.
Office International des
Epizooties (OIE), World Organisation for Animal Health created
by an International Agreement in 1924, headquartered in Paris, France :
the OIE (167 member nations in May 2004ref)
now divides notifiable
diseases into List A and List B in OIE's Terrestrial
International Animal Health Code. The intention was to give a degree of
urgency to List A diseases, because of their rapid spread and significant
economic importance. Countries had to report an occurrence on those diseases
very rapidly. List B were either less important economically or had slower
degrees of spread. With time, the system was misinterpreted that diseases
on List A were more important than List B. OIE decided in 2003 to replace
these 2 lists with a single list. The organization suppressed Lists
A and B in January 2005 and adopted the new list by 2005. The main criterion
for a disease to be placed on the final list in the proposed changes is
its potential for international spread. Other criteria include a capacity
for significant spread within naive populations and the potential to spread
to humans.
Notifying infectious animal diseases to the OIE : in May 2004, OIE member
countries approved the creation of a single list of notifiable terrestrial
animal diseases; previously, diseases notifiable to the OIE were classified
into 2 lists, List A and List B, the former being of higher priority.
It was agreed that the change will necessitate defining acceptable criteria
for the inclusion of a disease in the OIE single list, as well as
criteria for the degree of 'urgency' of each reporting. OIE's Director
General, while announcing the decision, reiterated that the implementation
of the changes will mean completely redesigning the existing animal health
information system, which will need to take full advantage of all the possibilities
offered by the latest information and communication technology, including
mapping software. He convened an Ad hoc Group on Terrestrial Animal Disease/Pathogenic
Agent Notification, comprised of international experts, to support the
OIE Animal Health Information Department in defining criteria to determine
whether a given disease should be included in the OIE list. The Ad hoc
Group's report*, including the proposed revised single list and explanatory
notes pertaining to each disease -- retained, added or deleted --
were discussed by the OIE Terrestrial Animal Health Standards Commission
in January 2005 and forwarded to the General Session of the Member Countries
(the International Committee), by which it was finally approved in May
2005. The new system prescribes 4 main reporting modes: immediate notification,
follow-up report, 6-monthly report and annual report. Their performance
is prescribed according to the following modalities:
1. An immediate notification, to warn and alert the international community
of exceptional epidemiological events in Member Countries. In order to
improve the scope and the efficiency of the OIE Early Warning System, the
events of epidemiological significance that should be covered in the immediate
notification have been redefined and are the following:
a. the first occurrence of an OIE-listed disease or infection in a country
or zone/compartment;
b. the re-occurrence of a listed disease or infection in a country or zone/compartment
following a report by the Delegate of the Member Country declaring the
previous outbreak(s) eradicated;
c. the 1st occurrence of a new strain of a pathogen of a listed disease
in a country or zone/compartment thereof;
d. a sudden and unexpected increase in morbidity or mortality caused by
an existing listed disease;
e. an emerging disease with significant morbidity/mortality or zoonotic
potential;
f. evidence of change in the epidemiology of a listed disease (e.g. host
range, pathogenicity, strain of causative pathogen), in particular if there
is a zoonotic impact.
This alert system is aimed at the Veterinary Services of Member Countries,
enabling them to take any necessary protective measures as quickly as possible
to prevent the introduction of pathogens originating from infected countries.
2. Follow-up report on a weekly basis, subsequent to a notification under
point 1 above, to provide further information on the evolution of an incident
which justified an immediate notification; the follow-up reports should
continue until the situation has been resolved through either the disease
being eradicated or it becoming endemic so that 6-monthly reporting under
point 3 will satisfy the obligation of the country to the OIE. In any case,
a final report on the incident should be submitted.
3. A 6-monthly report on the evolution, absence or presence of all the
diseases listed by the OIE and information of epidemiological significance
to other countries. (Previously, monthly reports, relating to List A diseases
only -- either present or absent in the country -- were required; this
is not the case anymore).
4. An annual questionnaire concerning any other information of significance
to other countries.
More details on these procedures and the relevant obligations of the OIE
Member Countries are to be found in Chapter
1.1.2 of the Terrestrial Animal Health Code. Maintaining a disease
-- previously included in list A or B -- in the new single list, deleting
it or adding a new disease to the list, have been decided upon according
to a decision-making model which was based upon 4 basic criteria:
a. International spread;
b. Significant spread within naive populations;
c. Zoonotic potential;
d. Emerging diseases.
Each disease was first evaluated in terms of its potential for international
spread; a disease passing this test had to show zoonotic potential with
severe consequences or a high impact at country or zonal level, in order
to be included. Emerging diseases had to show zoonotic potential in order
to be added. The
decision-making model and the decision tree applied are laid-out in
Article
2.1.1. of the Terrestrial Animal Health Code. Following a revision,
in line with the said criteria, of the existing lists A and B and an assessment
of several emerging diseases which have been proposed by OIE Member Countries,
the Ad hoc Group recommended to delete some diseases from the list, add
several emerging diseases, change the names of some and change the species
category of others (for details, see the report*). The single list, as
finally approved by the International Committee, is included in Article
2.1.1.3. of the Code, as follows:
Article 2.1.1.3. The following diseases are included in the OIE List
:
1) the following diseases are included within the category of multiple
species diseases:
anthrax
Aujeszky's disease
bluetongue
brucellosis (Brucella abortus)
brucellosis (Brucella melitensis)
brucellosis (Brucella suis)
Crimean Congo haemorrhagic fever
echinococcosis/hydatidosis
foot and mouth disease
heartwater
Japanese encephalitis
leptospirosis
New world screwworm (Cochliomyia hominivorax)
Old world screwworm (Chrysomya bezziana)
paratuberculosis
Q fever
rabies
rinderpest
Rift Valley fever
trichinellosis
tularemia
vesicular stomatitis
West Nile fever
2) the following diseases are included within the category of cattle diseases:
3) the following diseases are included within the category of sheep and
goat diseases:
caprine arthritis/encephalitis
contagious agalactia
contagious caprine pleuropneumonia
enzootic abortion of ewes (ovine chlamydiosis)
Nairobi sheep disease
maedi-visna
ovine epididymitis (Brucella ovis)
peste des petits ruminants
salmonellosis (S. abortusovis)
scrapie
sheep pox and goat pox.
4) the following diseases are included within the category of equine diseases:
African horse sickness
contagious equine metritis
dourine
equine encephalomyelitis (Eastern)
equine encephalomyelitis (Western)
equine infectious anaemia
equine influenza
equine piroplasmosis
equine rhinopneumonitis
equine viral arteritis
glanders
surra (Trypanosoma evansi).
Venezuelan equine encephalomyelitis.
5) the following diseases are included within the category of swine diseases:
African swine fever
classical swine fever
Nipah virus encephalitis
porcine cysticercosis
porcine reproductive and respiratory syndrome
swine vesicular disease
transmissible gastroenteritis.
6) the following diseases are included within the category of avian diseases:
avian chlamydiosis
avian infectious bronchitis (IB) is caused by the infectious
bronchitis virus (a group 3 coronavirus) and manifests as an acute,
highly contagious respiratory disease occurring in chickens of all ages.
It is characterized by coughing, sneezing, and a nasal discharge. The major
economic loss in mature chickens is the reduction in egg production and
inferior egg quality. In younger birds there may be a high death rate with
a loss in weight gain and feed efficiency. This disease is highly transmissible
and is a potential hazard for unvaccinated flocks. Avian infectious bronchitis
is distributed worldwide. Natural outbreaks have declined due to the use
of modified live virus vaccines; however, respiratory disease "breaks"
do occur.
avian infectious laryngotracheitis
avian mycoplasmosis (M. gallisepticum)
avian mycoplasmosis (M. synoviae)
duck virus hepatitis
fowl cholera
fowl typhoid
highly pathogenic avian influenza
infectious bursal disease (Gumboro disease)
Marek's disease
Newcastle disease
pullorum disease
turkey rhinotracheitis.
7) the following diseases are included within the category of lagomorph
diseases:
myxomatosis
rabbit haemorrhagic disease.
8) the following diseases are included within the category of bee diseases:
acarapisosis of honey bees
American foulbrood of honey bees
European foulbrood of honey bees
small hive beetle infestation (Aethina tumida)
Tropilaelaps infestation of honey bees
varroosis of honey bees.
9) the following diseases are included within the category of other diseases:
World Anthrax Data
: an activity of the WHO Collaborating Center for Remote Sensing and Geographic
Information Systems at Louisiana State University (LSU)
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