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Duck viral enteritis (DVE). Dr. Chi-Young Wang. Species of bird: Ducks, geese, swans. Action: Acute. Age of birds: All. Etiology: Herpes virus. Characterized by vascular damage, digestive mucosal eruptions, lesions of lymphoid organs, and degenerative changes in parenchymatous organs.
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Duck viral enteritis (DVE) Dr. Chi-Young Wang
Species of bird: Ducks, geese, swans. • Action: Acute. • Age of birds: All. • Etiology: Herpes virus. • Characterized by vascular damage, digestive mucosal eruptions, lesions of lymphoid organs, and degenerative changes in parenchymatous organs.
Susceptibility to Chemical and Physical Agents • Sensitive to ether and chloroform. • Inactivation of virus by trypsin, chymotrypsin, and pancreatic lipase at 37 ℃ for 18 hours. • Inactivation by heating for 10 min at 56 ℃ or 90-120 min at 50 ℃. • Infectivity was lost at 22 ℃ after 30 days. • Loss of titer at pH 6-9 for 6 hours.
Laboratory Host System • Duck embryo fibroblast culture at 39.5-41.5 ℃ is good (cell lysis). • CAM of 9-14 day old duck embryos. • Duck liver or kidney cells. • Adapted growth on chicken eggs but not for primary isolation. • A cytopathic effect could be identified or used for plaque inhibition by neutralizing antisera.
Mode of transmission • It transmitted directly from bird and by bloodsucking arthropods (originates during viremia). • Indirectly spread by contact with the contaminated environment or water. • New foci was established by movement of infected waterfowl into susceptible flocks or onto bodies of water.
Mode of transmission • Oral, nasal, intravenous, intraperitoneal, intramuscular, and cloacal routes. • Recovered birds shed viruses periodically. • DEV latency and reactivation is just like other herpesviruses. • Trigeminal ganglion is a latency site for the virus which can be reactivated.
Clinical signs (Incubation period: 3-7 days) • Signs include sudden, high persistent mortality, and a drop in egg production (25-40%). Prolapse of penis is evident in dead mature male. • Photophobia (abnormal sensitivity to light) can occur as half-closed, pasted eyelids. Inappetence, extreme thirst, droopiness, ataxia, ruffled feathers, nasal discharge, soiled vents, and watery diarrhea may also be evident. • Birds may be unable to stand, and have droopy outstretched wings, and head down.
Clinical signs • Tremors of the head, neck and body, loss of weight, blue beaks, blood stained vent. • Young ducklings of 2-7 weeks show dehydration, loss of weight, blue beaks, conjunctivitis, lacrimation, nasal exudate, often a blood-stained vent. • The total mortality (5-100%) may be seen. • Adult breeder ducks experience greater mortality than young ducks.
Postmortem lesions • Lesions include vascular damage (tissue hemorrhages) and free blood in the body cavity. • Eruptions in the GI tract, and degeneration of lymphoid organs may be seen. • Petechial hemorrhage may be seen on the myocardium, liver, pancreas, intestine, lungs and kindey.
Postmortem lesions • On the epicardium, within coronary grooves, closely packed petechiae give the surface a red “paintbrush” appearance. More apparent in mature breeder ducks. • Surface hemorrhages and yellow-white crusty plaques on the mucosa of the oral cavity, esophagus, rectum, ceca and cloaca be evident.
Postmortem lesions • Hemorrhages in deformed, discolored ovarian follicles, and massive hemorrhage from the ovary may fill the abdominal cavity. • Lumina of intestines and gizzard are filled with blood. The esophageal proventricular sphincter appears as a hemorrhagic ring.
Postmortem lesions • In the esophagus, macules occur parallel to longituidinal folds. • Multiple petechiae and yellow focal areas on the surface is surrounded by clear yellow fluid that infiltrates and discolors subcutaneous tissues of the adjacent cervical region from the thoractic inlet.
Postmortem lesions • The bursa is initially reddened and then surrounded by clear yellow fluid. Pinpoint yellow areas are found in an intensely reddened surface. The lumen is filled with coagulated exudate. • Intestinal annular bands appears as intensely reddened rings. The entire band becomes dark brown and tends to separate from the mucosal surface.
Postmortem lesions • The entire liver is a pale copper color with an mixture of irregular pinpoint hemorrhages and white foci. Late stage are characterized by dark bronze or bile-stained livers without hemorrhages. • In ducklings, tissue hemorrhages are less pronounced and lymphoid lesions are more prominent. In mature ducks, tissue hemorrhages and reproductive tract lesions predominate.
Microscopic lesions • (Small blood vessels) The endothelial lining was disrupted and connective tissue of the wall was less compact. Extravasations of blood pass from the lumen into the surrounding tissues. • Interlobular venules of the proventriculus, hepatic and portal venules at the margins of liver lobules, venules in the spaces between lung parabronchi, capillaries within intestinal, and star-shaped intralobular renal hemorrhages are pronounced locations for hemorrhages.
Microscopic lesions • Necrosis and degeneration of stratified squamous epithelium of the esophagus and cloaca. Eosinophilic intranuclear and cytoplasmic inclusions. • A layer of free blood separates lymphoid tissue from the mucosa, which undergoes coagulation necrosis. A pseudopmembrane higher than adjacent normal intestinal mucosa.
Microscopic lesions • Epithelial cells are displaced from the surface of villi, many are broken and cast into the intestinal lumen. • Severe depletions of lymphocytes in the follicles of bursa of Fabricius. They were replaced by eosinphilic material mixed with heterophils.
Microscopic lesions • Free blood was filled into interfollicular spaces of thymus. Coagulation necrosis of central medullary reticulum cells and destruction of cortical lymphocytes were pronunced. • Detachment and disassociation of hepatocytes from each other and their surrounding structure-necrotic foci in the liver.
Immunity • Active immunity can be induced by a modified live-virus vaccine and inactivated vaccines. Recovered birds were resistant to reinfection. • Maternal immunity declines rapidly. If breeders had been vaccinated, fully protection was observed at 4 days of age and less than 40% at 13 days of age.
Diagnosis • Liver, spleen, bursa, kidneys, and cloaca samples were used for an inoculation of 1-day-old Muscovy, white Pekin ducks or the CAM of 9-14 old embryonated duck eggs-isolation of virus. • Virus can be isolated and propagated in white Pekin and Muscovey duck embryo fibroblasts, liver, or kidney cells. Antiserum could be used for confirmation.
Diagnosis • PCR. • Latex agglutination assay. • Virus neutralization test. • A VN index above or equals to 1.75 indicates positive. • Immunofluorescence. • ELISA.
Intervention • Susceptible birds in environments free from exposure to the virus. • Prevention of dissemination of virus by free-low water. • Depopulation, removal of birds, sanitation, disinfection, and vaccination.
Intervention • No direct or indirect contact with contaminated material. • Prevention of importing infected anseriforms. • Inactivated vaccines (less effective).
Intervention • A chicken embryo-adapted DEV strain, avirulent but immunogenic. • Birds in the period of incubation may not be protective. • Subcutaneous or intramuscular routes in domestic ducklings more than 2 weeks of age. • Breeders are vaccinated and revaccinated annually.
