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
-
laboratory animal medicine
: a specialty of veterinary medicine that deals with the diagnosis, treatment,
and prevention of disease in animals
used as subjects in biomedical activities
Eumetazoa; Bilateria; Coelomata;
Protostomia
-
Hexapoda; Insecta (see also physiology
of insects);
Dicondylia; Pterygota; Neoptera; Endopterygota;
-
Amphiesmenoptera; Lepidoptera; Glossata; Neolepidoptera; Heteroneura;
Ditrysia; Obtectomera; Bombycoidea; Bombyciformes; Bombycidae; Bombyx
-
Hymenoptera; Apocrita; Aculeata; Apoidea; Apidae; Apinae; Apini; Apis
-
Apis
mellifera (honey bee)
-
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 / nosemosisref
: a protozoal infection of bees caused by Nosema
apis, characterized by dysentery and paralysis. N. apis
is widely known in Europe as a pathogen of the honey bee Apis mellifera.
N.
ceranaeref
was originally discovered in the Asian bee A. cerana but was recently
also found in A. mellifera
-
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.
The varroa mite (Varroa jacobsoni) is an external parasite, visible
to the unaided eye, and was first discovered infesting Asian honey bees
(Apis cerana) in Java. Subsequently this dreaded parasitic infection
spread to European honey bees (Apis mellifera). It 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 virusref1,
ref2,
ref3
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.
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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.
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Mollusca;
-
Bivalvia
-
Heteroconchia; Veneroida; Veneroidea; Veneridae; Mercenaria; Mercenaria
mercenaria (a.k.a. northern quahog, hard-shell clam, cherrystone,
littleneck)
-
quahog parasite unknown (QPX) (Labyrianthomorpha)
-
Pteriomorphia; Ostreoida; Ostreoidea; Ostreidae(oysters)
-
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
-
ostreid
herpesvirus 1 (OsHV-1) / Pacific oyster herpesvirus is the only member
of the Herpesviridae that has an invertebrate host and is associated with
sporadic mortality in the Pacific oyster (Crassostrea
gigas) and other bivalve speciesref
-
Marteilia
refringensref
is a lethal protistan parasite of the European flat oyster, Ostrea
edulis. Its geographic distribution is: France, Greece, Italy,
Morocco, Portugal, and Spain.
=> marteiliosisref
-
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.
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Gastropoda; Orthogastropoda; Vetigastropoda; Haliotoidea; Haliotidae;
Haliotis
-
Haliotis
corrugata (a.k.a. abalone)
-
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
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Panarthropoda; Arthropoda; Mandibulata; Pancrustacea
-
Crustacea; Malacostraca; Eumalacostraca; Eucarida; Decapoda
-
Pleocyemata; unclassified Pleocyemata
-
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.
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Dendrobranchiata; Penaeoidea; Penaeidae
-
Litopenaeus
vannamei (Pacific white shrimp) : Taura syndrome
-
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.
WSD has been confirmed in freshwater farmed crawfish (also known as crayfish)
in Louisiana, USA, the nation's largest producer of crawfish, with farmed
and wild-caught crawfish production totaling 95% of the total US harvest.
While there is no export market for Louisiana-produced crawfish, other
crustacean exports from this state were valued at USD 7 million in 2005.
This represented 1.3 per cent of the value of all US crustacean exports
for that year. The US produced about 324.8 thousand metric tons of crustacean
products from wild fisheries and aquaculture sources in 2005, representing
3.26 per cent of world production. WSD is an OIE-notifiable disease. White
spot disease also affects shrimp. On 8 May 2007, the National Veterinary
Services Laboratories (NVSL) confirmed the presence of WSSV in samples
of freshwater farmed crawfish (Procambarus clarkia) from St Martin
Parish, Louisiana. The source of the virus was undetermined, but crawfish
broodstock is regularly collected from wild populations of unknown health
status. Declining crawfish productivity and large numbers of birds around
the farm ponds were observed prior to the outbreak. Farmed crawfish are
at the end of their current production cycle, and all ponds in the region
will be emptied of crawfish and remain so until October 2007. Surveillance
of wild populations of crawfish within the region is ongoing. The 1st documented
occurrences of this disease in US commercial facilities were in Texas and
South Carolina in 1995. WSSV also has been found in wild shrimp and crabs
offshore in the Gulf of Mexico and near shore in Texas, Mississippi, Georgia
and South Carolina. WSD was last reported to OIE for
an outbreak in Hawaii in April 2004ref
-
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.
-
starry
flounder rhabdovirus (SFRV)
Deuterostomia; Chordata; Craniata; Vertebrata
-
Hyperoartia [in-part: fishes] : Diphyllobothrium
latum,
Clonorchis
sinensis,
Opisthorchis
felineus,
Opistorchis
viverrini,
Anisakidae,
Gnathostoma
spinigerum,
Capillaria
philippinensis
-
Gnathostomata
-
Chondrichthyes (cartilaginous fishes)
-
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
Web resources :
-
Teleostomi; Euteleostomi
-
Actinopterygii; Actinopteri; Neopterygii; Teleostei; Elopocephala; Clupeocephala
-
Otocephala
-
Clupeomorpha; Clupeiformes; Clupeidae; Clupeinae; Clupea
-
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."
-
Ostariophysi; Otophysi; Cypriniphysi; Cypriniformes; Cyprinoidea; Cyprinidae;
Cyprininae; Cyprinus
-
Cyprinus
carpio (a.k.a common carp)
-
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
-
Euteleostei
-
Neognathi; Neoteleostei; Eurypterygii; Ctenosquamata; Acanthomorpha;
Euacanthomorpha; Holacanthopterygii
-
Acanthopterygii; Euacanthopterygii; Percomorpha
-
Pleuronectiformes; Pleuronectoidei; Pleuronectidae; Pseudopleuronectes
-
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
-
Percoidei
-
Centrarchidae; Micropterus
-
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.
-
Serranidae; Epinephelinae; Epinephelus
-
Paracanthopterygii; Gadiformes; Gadidae; Gadus;
-
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
-
Protacanthopterygii; Salmoniformes; Salmonoidei; Salmonidae
-
Oncorhynchus
-
Oncorhynchus
mykiss (a.k.a. rainbow trout, Salmo mykiss, Salmo
irideus, Salmo gairdneri)
-
viral diseases
-
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
-
Salmo
spp. (a.k.a. salmon)
-
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 freshwater and saltwater 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. Viral
hemorrhagic septicemia affects rainbow trout, brown trout, brook trout,
grayling, white fish (Coregonus sp.), pike, and turbot. A number
of marine species are also susceptible, including Pacific herring, Pacific
salmon (Oncorhynchus spp.), Pacific cod, Pacific sandlance, and
pilchard. In the Atlantic Ocean, susceptible species include Atlantic Cod,
haddock, poor cod, rockling, sprat, herring, whiting, blue whiting, lesser
argentine, Norway pout, shiner perch, Dab, English sole, flounder, and
plaice. Most warmwater fish are resistant to this disease. Viral hemorrhagic
septicemia is highly contagious; quarantines are necessary to control outbreaks.
VHSV can survive for long periods in the bottom of farm ponds, possibly
in protozoans or metazoans, if the ponds are not dried and disinfected.
VHSV can be inactivated by formalin, drying, iodophor disinfectants, sodium
hydroxide, sodium hypochlorite, and pH 2.5 or 12.2. The virus is also highly
thermolabile. The effectiveness of lime disinfection is suspectref.
The causative virus is in the family Rhabdoviridae and is a Novirhabdovirus.
The disease can be transmitted by asymptomatic carriers, or by clinically
ill fish. It can be transmitted through the water or through direct contact.
The virus is also carried in sexual fluids, urine and feces. When the water
has an overall temperature of 20°C [68°F], the infectivity of the
virus is lost in approximately 24 hours. Conversely, the infectivity is
maintained for several days when the water temperature is a constant 4°C
[39.2°F]. Therefore, it stands to reason that the incubation time is
related to water temperature and ranges from between 7 and 15 days. There
are 3 different syndromes associated with the virus outbreak. Those 3 symptoms
include nervous, chronic and acute. They may overlap to the point that
all of these may be seen at one time during an outbreak. Some fish may
hemorrhage, some may be seen to have neurological signs, such as swimming
in circles. It is considered a reportable disease in many states in the
USA.
-
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 Myxobolus
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.
It primarily affects juvenile trout, causing severe deformities of the
skeleton and skull, and can lead to
mortality rates as high as 100%. It also can affect Atlantic salmon,
steelhead and possibly other salmonids, though there have been fewer impacts
on those species. Once established in the skull of an adult fish, this
worm is only about 10 mm in size, is released
into the water after the fish dies and decomposes. These microscopic parasites
are then devoured by tubifex worms that live in the mud of freshwater
streams and lakes. These worms act as a 2nd host for the parasite, which
metamorphoses into these 300-mm monsters that
are shaped like a river anchor. Then known as triactinomyxon (TAMs),
the parasites remain in the mud-dwelling worms until they are excreted
into the lower water column. Nearby trout redds are particularly vulnerable
to the parasite, which can attach to the skins and shoot spores into the
juvenile trout, penetrating their skin, beginning the cycle once again.
Interestingly, the TAMs only live in certain strains of host tubifex worms
-
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
-
epizootic ulcerative syndrome (EUS) is considered to be an infection
with an oomycete known as Aphanomyces invadans or A. piscicida.
It is a seasonal epizootic condition of great importance in wild and farmed
freshwater and estuarine fish; it has a complex infectious aetiology and
is clinically characterised by the presence of invasive Aphanomyces
infection and necrotising ulcerative lesions typically leading to a granulomatous
response. EUS is also known as red spot disease (RSD), mycotic granulomatosis
(MG), and ulcerative mycosis (UM). Recently, scientists proposed that EUS
should be re-named as epizootic granulomatous aphanomycosis or EGA. At
present, RSD, MG, UM, and EGA are synonyms for EUS. The information above
is derived from chapter 2.1.10 of the OIE (World Organisation for Animal
Health) Manual of Diagnostic Tests for Aquatic
animals (2006)ref.
-
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
-
organic pollution causes low oxygen tension in the water and high carbon
dioxide levels, which is a primary disease "aetiology" in itself with respect
to fish. A second important effect is high levels of organic metabolites,
particularly ammonia and nitrite. Such poor water quality causes stressed
fish, which rapidly become immune-compromised fish, which are then very
susceptible to secondary diseases, such as bacterial skin disease and red
anuses (as per the photos in the original posting), proliferation of gill
and skin parasites up to very high loadings, and eventually bacterial septicaemias
involving common intestinal bacteria such as Vibrios, Aeromonas
sp, Plesiomonas sp etc. The process can snowball very quickly
if the water is very fouled, with high mortalities and virtually 100% morbidity.
The deep skin ulcers described are suggestive of one additional damaging
effect of organic pollution, which involves the carrion-feeding microbes
in the organic sediment on the river bed. There are a lot of nasty things
that live in the decaying organic matter and the anaerobic sediment when
organic pollution is a chronic problem, and they are highly pathogenic
to live fish if the sediment is stirred up. Microbes include Flexibacter-like
filamentous bacteria, and ciliated protozoa such as Uronema sp (or
the freshwater equivalent). They cause damage by direct predation on exposed
skin and can cause large lesions. The ciliates can often be found in skin
scrapes and wet mounts of the gills. If the temperature is too high or
too low the Flexibacter-like bacteria can also cause a syndrome of severe
gill rot that can spread rapidly to in-contact fish. Additional data that
might support this diagnosis include:
-
oxygen level: should be 5-10 mg/L but is probably less than 2 mg/L if organic
pollution is the problem.
-
carbon dioxide: should be less than 10 mg/L, but is probably now 15-20
mg/L.
-
total ammonia: should be less than 0.1 mg/L in waters with "normal" levels
of organic pollution. Foul water might have 0.5 mg/L or even much higher.
-
total nitrite: should be less than 0.1 mg/L. Foul water might have 0.3
mg/L or more. Nitrite is very toxic.
-
bacterial cultures from kidneys/spleens of sick fish: should be sterile,
but sick fish dying of secondary septicaemia will have moderate to heavy
growth of common bacteria, usually more than one species. (Only sick fish
can be tested by bacterial culture of internal organs..........dead fish
are always positive for Vibrios).
-
wet mounts of gills & skin scrapings: normally show a few parasites
(gill flukes, ciliates) in healthy fish. High loadings indicate that
parasitism is a major factor in the mortalities. (Also only useful on sick
fish....... dead fish lose the parasites quite quickly).
With respect to human disease, people that consume sick and septicaemic
fish will suffer similar consequences to food spoilage; it is basically
a form of food poisoning. Gastrointestinal upsets, with or without diarrhoea,
would be expected from the high exposure to Vibrios. Botulism is unlikely
unless the fish consumed are actually dead and rotten. The worms described
are probably an incidental finding; many wild fish have Anisakid nematodes
free in the abdominal cavity, and there are many free-living nematodes
that will invade necrotic tissue but not otherwise harm the fish, or people
consuming the fish.
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 :
-
OIE Manual of
Diagnostic Tests for Aquatic Animals, 2003, 4th edition
-
OIE Aquatic Animals Commission
-
System of Information for the Promotion
of Aquaculture in the Mediterranean (SIPAM)
-
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).
-
Batrachia
-
Anura (frogs and toads)
-
Neobatrachia; Ranoidea; Ranidae; Rana; Rana; Rana
temporaria (common frog)
-
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.
-
Amniota
-
Coelacanthimorpha [in-part: fishes]
-
Sauropsida; Sauria
-
Archosauria
-
Aves
spp.
-
Neognathae
-
Anseriformes
-
Anatidae
-
Anas
spp. (ducks) : Hymenolepis
lanceolata,
Chlamydophila
psittaci
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
-
Anser
spp. (geese) : Hymenolepis
lanceolata
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.
-
Charadriiformes; Laridae; Sterna
-
Columbiformes (a.k.a. doves and pigeons)
-
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 1 in
250 dead cattle needs to have been recently treated with diclofenac to
cause a decline in vultures of 30% per yearref.
The anti-inflammatory drug diclofenac is toxic to 3 species of Asian vulture
-- the oriental white-backed, long-billed and slender-billed. They die
from kidney failure if they eat the carcasses of cattle treated with it.
Conservationists estimate that 10-14 million birds have died; populations
are still declining at 30-50% a year. Dr Parry-Jones and the RSPB research
team set out to discover whether diclofenac and related drugs are toxic
to other birds. They asked zoo vets around the world for reports of unintentional
bird deaths after treatment with the drugs. Of the 79 scavenging birds
they received information on, the drugs were deadly for 30%, including
the African white-backed vulture, saw-whet owl from North America, harris
hawk, spoonbill, Eurasian gryphon vulture and African maribu stork. The
manufacture and import of diclofenac was banned in India in August 2006,
although it is not illegal to sell off stockpiles. It is banned in the
US and Europe, but is still used in parts of Africa and South Americaref
-
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
-
turkey
adenovirus 3 / hemorrhagic enteritis virus (HEV) is an adenovirus that
infects turkeys and causes immunosuppression and mortality.
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
-
Odontophoridae (American quails): Influenzavirus
A H9N2 subtype
-
Phasianidae
-
Phasianinae
-
Gallus
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.
Infectious laryngotracheitis (ILT), a respiratory disease caused by
a herpes virus, is a reportable disease in North Carolina. The virus may
survive for 8-10 days in fecal droppings and for over 2 months in a carcass.
The disease is persistent within a flock for as long as 2-6 weeks. Most
viral respiratory diseases do not circulate within a flock for this amount
of time. The virus affects chickens and turkeys, pheasants and wild fowl.
Wild birds may be carriers for the disease. ILT can cause excessive illness
and death in a high percentage of an infected flock. Economic loss from
the disease is from ill birds, deaths, and decreased production in the
survivors, which remain carriers for a long time. This disease has no treatment,
but it is preventable with a vaccine. Incubation time for the virus is
about 3-5 days. Classical clinical signs of the disease are gasping, extension
of the neck forward or upward, and coughing. There may be bloody exudates
in the cough. Difficulty swallowing, ruffled feathers with nasal and ocular
discharge may be very early clinical signs of the disease. There are various
strains of this virus, and the pathogenicity varies according to the strain.
The virus is easily and rapidly spread by respiratory means and through
close contact. The disease does not affect people, but people may be the
main carriers for transmitting the disease between flocks if careful bio-containment
precautions are not taken. The virus is not transmitted through eggs, so
chicks are unaffected at the time of hatching. Laboratory diagnosis is
needed to accurately diagnosis the virus. The initial clinical signs must
be differentiated from Newcastle Disease virus and bronchitis. Vaccination
is an option in controlling but not eradicating the disease. Therefore,
use of the vaccine is controversial. -
-
gallid
herpesvirus 3 (family Herpesviridae) isolated from turkeys.
-
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
-
reduce the use of antibacterials in animals
-
increase chicken growth rate
-
Passeriformes; Passeroidea; Fringillidae; Carduelinae; Carduelis
-
Carduelis
flammea (common redpoll)
-
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.
-
Psittaciformes
-
Psittacidae
(parrots) : Chlamydophila
psittaci
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,
