Duck virus enteritis (DVE)
Duck virus enteritis (DVE) OR Duck plauge is an acute, sometimes chronic, contagious virus infection that occurs naturally only in ducks, geese and swans, all members of the family Anatidae of the order Anseriformes. The disease is a potential threat to commercially reared, domestic and wild waterfow.
The aetiological agent, anatid herpesvirus-1 or DVE virus (DEV), is a member of the Alphaherpesvirinae subfamily of the Herpesviridae. DVE may also be referred to as duck plague, anatid herpes, eendenpest, entenpest and peste du canard. The infection has not been reported in other avian species, mammals or humans.
The time between infection and the development of signs varies from 3 to 7 days.
Death typically occurs around 1 to 5 days after the first clinical signs.
DVE, also known as duck plague, was first diagnosed in the western hemisphere in 1967 from a concentrated commercial duck producing area in Suffolk County, N.Y. DVE had been frequently recorded in the Netherlands where it first appeared in 1923. It has been suspected in France and China, and known to occur in Belgium and India.
The first epizootic of DVE in wild waterfowl in the U.S. occurred in January and February 1973, in the vicinity of Lake Andes National Wildlife Refuge, South Dakota. The Lake Andes epidemic struck with devastating swiftness and severity. Approximately 40% of 100,000 wintering waterfowl, mostly mallards, were lost. During the peak of the die-off, daily losses exceeded 1,000 birds.
All species of waterfowl present at Lake Andes suffered some mortality. Included were Canada geese, mallards, black ducks, pintail-mallard hybrids, American widgeon, wood ducks, American goldeneyes, redheads, common mergansers, a Muscovy duck and a Pekin duck. Birds that survived the Lake Andes epidemic have dispersed widely over North America. Blood samples taken from survivors at Lake Andes indicated that about 30% of the population were exposed to the virus. These birds are potential carriers of DVE, capable of triggering future outbreaks.
In Michigan, DVE has been reported in 1979 in Muscovy and mallard ducks.
After infection, the virus replicates in the lining cells of the gastro-intestinal tract, predominantly in the oesophagus before spreading to other parts of the body including the tissues of the immune system (bursa of fabricius, spleen and thymus) and the liver.
The virus induces vascular damage, especially in smaller blood vessels, venules, and capillaries. This results in the development of generalized hemorrhages and progressive degenerative changes of parenchymatous organs. Recently, it has been proposed that apoptosis and necrosis of lymphocytes induced by this virus may result in lymphoid depletion and possibly immunosuppression. An immunosuppressive state induced by DVE may also explain the presence of secondary infections by Pasteurella multocida, Riemerella anatipestifer, and Escherichia coli, which are frequently seen in natural outbreaks of DVE in ducklings.
This virus can infect members of the Anatidae, i.e. ducks, swans and geese. Muscovy ducks are particularly sensitive to this disease.
Transmission and Development
Some scientists think DVE is usually spread by infected waterfowl that shed the virus in their droppings. It survives in water and may persist in polluted, stagnant and slow-moving pools, ponds and waterways. Waterfowl pick up the disease by drinking or swimming in polluted water or by eating contaminated food. The virus may enter susceptible birds through the mouth, nose, cloaca or breaks in the skin.
vertical transmission (i.e. from female bird to egg) has been reported to occur in Muscovy, Peking Ducks and Mallard ducks.
Birds that are exposed but survive the disease may become carriers, which maintain the infection between outbreaks and release the virus at some future time and location.
Field Signs
There is no prolonged illness associated with duck plague;
therefore, sick birds are seldom seen in the field, and birds
that are healthy one day may be found dead the next. The
incubation period between virus exposure and death is generally
3–7 days in domestic ducks, and experimental studies
have found that it is as long as 14 days in wild waterfowl.
Wing-clipped mallards released to monitor the Lake Andes
duck plague outbreak died 4–11 days after their release.
Sick birds may be hypersensitive to light, causing them
to seek dense cover or other darkened areas. They may exhibit
extreme thirst, droopiness, and bloody discharge from
the vent or bill . The ground may
be blood-stained where sick birds have rested.
Therefore, duck plague should be suspected when bloodsoiled
areas are seen following the flushing of birds, where
blood splotches that do not appear to be related to predation
or other plausible explanations are seen in the environment,
or where bloody discharges are seen where dead birds are
lying .
In males, the penis may be prolapsed
An ulcerative “cold sore” lesion under the tongue from
which virus can be shed has been seen in some infected waterfowl
Routine examination of apparently healthy
waterfowl for this lesion during banding operations may be
helpful in identifying inapparent carriers. Birds with these
lesions should be euthanized and
submitted to a qualified disease diagnostic laboratory for examination.
Death may be preceded by loss of wariness, inability to
fly, and finally by a series of convulsions that could be misinterpreted
as pesticide poisoning or other diseases such as
avian cholera.
A light-yellow, transparent liquid was observed when
the swollen skin of the head and neck of a sick duck
was incised.
Light edema and hyperemia were detected in the meninges.
light-yellow pseudomembrane covered the oral mucosa and the esophageal mucosa.
Sometimes there were “cheesy,” raised
plaques along the longitudinal folds of the esophagus and
proventriculus and on the mucosal surface of
the lower intestine.
Hemorrhagic ulcers between the glandular and muscular stomachs were
found, and several circular hemorrhagic necrotic sites
within the duodenum were observed . Severe
hemorrhagic and pseudomembranous ulcers were
apparent throughout the rectal and cloacal mucosa.
Grey-yellow or gray-white necrotic areas of various sizes were observed
on the liver surface. The follicles were hyperemic, hemorrhagic,
and liquefied .
The endocardium and epicardium showed spotted and striated hemorrhages.
Of all the lesions illustrated, those of greatest value in diagnosing duck plague are hemorrhagic or necrotic bands or disks within the intestine, large amounts of free blood in the digestive tract,and cheesy plaques in the esophagus and cloaca. Liver and heart lesions of duck plague are grossly similar to those of avian cholera, and they cannot be used to distinguish between these two diseases.
Gross pathological lesions of DVE - Petichal
haemorrhages in the intestine
Haemorrhage of the cloaca in a Muscovy duck infected with duck plague virus.
Gross pathological lesions of DVEhepatomegaly,
haemorrhages with foci of necrosis.
Caseous material and haemorrhage along the longitudinal folds of the oesophagus of a Muscovy duck with duck
plague.
1. Clinical and atopic symptoms: (A) edema of the head and neck; (B) diarrhea with white-green dejecta; © longitudinal pseudomembrane
covering the esophageal mucosa; (D) circular hemorrhagic necropsy of duodenum; (E) hemorrhaging and ulceration of the rectum and
cloaca; (F) follicular hyperemia and hemorrhaging, and necroscopic finding; (G) spotted hyperemia of the epicardium; and (H) petechial hemorrhaging
of the endocardium.
(A) Swollen head and neck; (B) Greenish diarrhea; (C) A light-yellow and transparent liquid of the head; (E) Diffuse hemorrhage of the esophageal mucosa; (G) Hemorrhage of the annulus trachealis; (I) Spotted hemorrhage of the endocardium; (K) Petechial hemorrhaging of the epicardium; (M) Liver is enlarged with blood spots; (O) Splenomegaly and hemorrhage. D, F, H, J, L, N, and P represent the head, esophagus mucosa, trachea, endocardium, epicardium, liver, and spleen of ducks from the control group, respectively.
Histopathological analysis
Pathological changes were detected in various tissues in the infected ducks and the lesions increased with time. Slight granular degeneration of myocardial fibers (arrow on Fig. 2A) was observed in the infected ducks at 1 dpi, and erythrocytes infiltration (arrow on Fig. 2B) at 3 dpi. At 5 dpi, significant hemorrhage (arrow on Fig. 2C) was observed. In the liver, liver cells displayed diffuse fatty degeneration (vacuolus of the same size in the liver, arrow on Fig. 2E) at 1 dpi, fatty degeneration and focal necrosis of hepatocytes (arrow on Fig. 2F) at 3 dpi, and hepatocyte necrosis with hemorrhage (arrow on Fig. 2G) at 5 dpi. A small amount of erythrocyte infiltration (arrow on Fig. 2I) in the white pulp of the spleen at 1 dpi, coagulated necrotic foci of lymphocyte (arrow on Fig. 2J) was found at 3 dpi, and obvious lymphocytic necrosis (nuclei became pyknotic and underwent rupture and karyolysis) with diffuse hemorrhage (arrow on Fig. 2K) at 5 dpi. Coincidently, serious histopathological changes were also observed in the bursa of Fabricus. A slight decrease in the number of lymphocytes (arrow on Fig. 2M) at 1 dpi, necrosis of lymphocytes and lymphocytes decreased significantly (arrow on Fig. 2N) at 3 dpi, at 5 dpi, microscopic lesions were serious and massive lymphocytic necrosis (many cells have dissolved and disappeared) (arrow on Fig. 2O). The lesions of the brain were slight compared to those of the spleen and bursa of Fabricus. The tissue edema (increasement of perivascular gap, arrow on Fig. 2Q) was found at 1 dpi, and neuronophagia (microglia proliferation with the phagocytosis of necrotic neurons, arrow on Fig. 2R) and perivascular inflammatory infiltrates (arrow on Fig. 2S) were detected at 3 and 5 dpi, respectively, suggesting a mild viral encephalitis during the infection. No microscopic lesions were observed in the control group (Fig. 2D,H,L,P,T). Overall, our results indicate that DPV could cause pathological lesions in a variety of tissues, specially the spleen and bursa of Fabricus with serious lesions, which indicated DPV might target the immune organs.
Figure 2: Pathological changes of the DPV-infected ducks at the different time points.
(A) Mild granular degeneration of myocardial fibers at 1 dpi; (B) A small amount of erythrocyte infiltration at 3 dpi; (C) Myocardium haemorrhage at 5 dpi; (E) Fatty degeneration in the liver at 1 dpi; (F) Fatty degeneration and focal necrosis of hepatocyte at 3 dpi; (G) Hepatocyte necrosis with hemorrhage at 5 dpi; (I) Slight congestion in the white pulp of the spleen at 1 dpi; (J) Necrotic foci of lymphocyte at 3 dpi; (K) Lymphocytic necrosis with diffuse hemorrhage at 5 dpi; (M) Slight reduction of lymphocytes in the bursa of Fabricus at 1 dpi; (N) Lymphocytes dissolved and disappeared, the number decreased significantly at 3 dpi; (O) Serious necrosis of lymphocytes at 5 dpi; (Q) Brain edema at 1 dpi; (R) Neuronophagia of the brain at 3 dpi; (S) Perivascular inflammatory infiltrates at 5 dpi. D, H, L, P, and T represent the heart, liver, spleen, bursa of Fabricus, and brain of ducks from the control group, respectively. Magnification, ×400 .
Diagnosis
Although a presumptive diagnosis of duck plague may be
made on the basis of characteristic internal lesions, final diagnosis
can only be made by virus isolation and identification.
Ducks, geese, and swans that have characteristic signs
or lesions should be euthanized and shipped to a qualified
diagnostic laboratory as quickly as possible. Submit whole
birds rather than tissues. When this is not possible, the liver
should be removed, wrapped in clean aluminum foil, and
then placed in a plastic bag and frozen for shipment. The
remainder of the carcass should be incinerated if possible
and the area and instruments used to process the carcass disinfected.
Take particular care in preserving and packaging
specimens to avoid their decomposition during transit and
contamination of the shipping containers (see Chapter 2,
Specimen Collection and Preservation, and Chapter 3, Specimen
Shipment).
Control
The primary objectives for duck plague control activities
are to minimize exposure of the population-at-risk at the
outbreak site and to minimize the amount of virus present in
the environment as a source for potential exposure of waterfowl
that may use the site in the near future. Control of duck
plague outbreaks requires rapid response and aggressive actions
to prevent disease spread and establishment.
Birds with inapparent duck plague infections are probably
the major reservoir of this disease and they pose the
greatest problem for disease prevention and control. Clinically
ill birds actively shed the virus and are recognized as
sick birds. However, asymptomatic healthy duck plague carriers
can shed the virus periodically, but they are not overtly
identifiable. Therefore, destruction of infected flocks, including
eggs, is recommended whenever possible because infected
birds that survive are likely to become carriers and
can initiate subsequent outbreaks. New technology provides
promise for determining whether or not there are carriers in
a flock. The success of new technology for detecting carriers
will allow selective euthanization of those birds and not
the remainder of the flock.
Duck plague virus is hardy, and it can remain viable for
weeks under certain environmental conditions; for example,
the virus could be recovered from Lake Andes water held at
4 °C for 60 days under laboratory conditions. Duck plague
virus is instantly inactivated at pH 3 and below and at pH 11
and above. Therefore, rigorous decontamination of infected
waters (for example, by chlorination) and grounds (that is,
by raising pH) and burning or decontamination of physical
structures, litter, and other materials at outbreak sites should
be carried out to the extent practical. Carcass collection
should be thorough and incineration used for disposal. Personnel
and equipment used at outbreak sites should be decontaminated
before leaving the site to prevent mechanical
spread of the virus to other waterfowl areas; chlorine bleach
and phenol base disinfectants are suitable for this (see Chapter
4, Disease Control Operations).
A low virulence live-virus vaccine has been developed
for combating duck plague in the domestic white Pekin, but
this vaccine has not been proven entirely reliable in protecting
other species of ducks and geese. It should not be considered
as a means of controlling or preventing outbreaks in
migratory birds.
The close association between duck plague outbreaks and
captive waterfowl, especially muscovy and mallard, needs
to be considered. Waterfowl release programs should not use
birds or eggs from flocks with a history of this disease unless
the flock has subsequently been shown by adequate testing
and other technical assessments to be free of duck plague.
Birds scheduled for release should be confined for at least 2
weeks before release. Birds that die during this period should
be submitted to a qualified disease diagnostic laboratory. If
duck plague is found to be the cause of death in any of these
birds, none of the remaining birds should be released. Also,
managers of areas for wild waterfowl should not permit the
maintenance of domestic waterfowl, especially muscovy
ducks, on the area or waterfowl display flocks that have not
been certified free of duck plague.
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