Duck viral hepatitis (DVH) Dr. Chi-Young Wang

Enlarged and hemorrhagic livers

Enlarged and hemorrhagic livers

Enlarged and hemorrhagic livers

Enlarged and hemorrhagic livers

Species of bird: ducklings. Action: Acute. Age of birds: 1-4 weeks of age. Etiology: 3 virus types. DVH type 1– picornavirus, 20-40 nM-heat stable. DVH type 2 – astrovirus, 28-30 nM. DVH type 3 – picornavirus unrelated to DVH-1.

The first week of age of ducklings were affected The first week of age of ducklings were affected. Death was rapid after signs were observed. Day-old or week-old poults, after either oral or intraperitoneal exposures, had a mottled livers and enlarged gall bladders and spleens. Enlarged livers mottled with hemorrhages.

Mode of transmission It spreads via airborne and fecal- oral routes. No egg transmission. Recovery ducks may excrete virus in feces for up to 8 weeks PI. Wild birds could be mechanical carriers. Brown rats may act as a reservoir host of DHV type 1. No vector transmission.

Resistance to Chemical and Physical Agents DHV type 1 resisted pH 3 for 9 hours, but longer exposure (48 hours) reduced virus titer. Complete inactivation was reported with 1% formaldehyde, 0.2% formalin in 2 hours or 2% caustic soda within 2 hours at 15-20 ℃. DHV type 1 was completely inactivated by 5% phenol, and undiluted Clorox.

Resistance to Chemical and Physical Agents DHV type 1 survive for 21 days at 37 ℃. Under natural environments, DHV type 1 survived at least 10 weeks in uncleaned infected brooders and more than37 days in moist feces stored in a cool shed.

Laboratory Host Systems Propagation of DHV in the allantoic sac of 9-day-old chicken embryo. Embryos may be stunted or edematous on 5th or 6th day. The virus titer in chicken embryos was 1-3 log10 lower than when growing in ducklings. A chicken embryo lethal strain of DHV type 1 can be developed by serial embryo passages (108 in 48 hours). Duck kidney cells for DHV type 1, fluorescence was observed after 8 hours and reached to a maximum after 24 hours.

Laboratory Host Systems CPE (rounding) and maximum titer in 2 days. DHV type I can cause CPE in goose embryo kidney cells or piglet kidney cell culture. A plaque assay for attenuated DHV type I in duck embryo kidney (DEK) cells. Plaque sizes can be affected by fetal calf serum. Duck embryo liver cells can be used for plaque assays of DHV type1.

Clinical signs (There is a 3-4 day incubation period.) In DVH-1 birds fall on their sides and kick spasmodically with rapid death. Die with heads drawn back. Morbidity can reach 100% and mortality can reach 95%. Stop moving and squat down with eye partial closed. Convulsions, opisthotonos (arching of head and neck) and death are evident. The rapidity with which ducklings die is astonishing.

Clinical signs In DVH-3 outstretched legs and opisthotonosis occurs. Morbidity is 100%. Mortality may reach 95% for less than 1 week old. 1-3 weeks of age, mortality may be 50% or less. In ducklings 4-5 week of age, morbidity and mortality are low or negligible.

Postmortem lesions DVH-1 produces enlarged liver with punctuate (marked pin point) ecchymotic (paint brush) hemorrhages, an enlarged, mottled spleen, and the kidney may be swollen and congested. DVH-2 produces liver is pink with hemorrhages, spleen enlarged, kidneys enlarged, and congested. DVH-3 lesions are similar to DVH-1.

Histopathology and Clinical Profiles Acute disease consisted of necrosis of hepatic cells. Widespread of bile duct hyperplasia in chronic lesions. Regeneration of liver parenchyma was observed in survived ducklings.

Histopathology and Clinical Profiles Lower serum levels of total proteins and albumen. Elevated alkaline phosphatase, glutamic pyruvic transaminase (GPT), bilirubin, and creatinine. Recovery from DHV type 1 results in solid immunity and VN antibodies.

Histopathology and Clinical Profiles Active immunity can be induced in adult ducks by injection of viruses. Passive immunity includes an injection of ducklings with recovery or immunized serum from ducks; transfer through yolk to hatch ducklings to protect them. VN antibody was present 4 days postvaccination of 2-day-old ducklings.

Diagnosis Inoculation, subcutaneously (SC) or intramuscularly (IM), of the isolate into 1-7-day-old ducklings. Death often occurs within 24 hours. Characteristic gross pathology should be founded. The virus could be isolated from livers.

Diagnosis Inoculation of serial dilutions of liver homogenate into the allantoic sacs of duck eggs (aged 10-14 days) from (DHV free flocks) or chicken eggs (aged 8-10 days). Chicken embryos die within 5-8 days. Duck embryos die within 24-72 hours. The allantoic gluid is opalescent or a pale greenish-yellow.

Diagnosis Embryo was stunting and subcutaneous hemorrhages over the whole body, with edema (abdominal and hind limb regions). Embryo livers may be swollen, red, and yellowish and show necrotic foci (More evident in embryos that take longer to die).

Diagnosis Liver homogenate was serially diluted and then inoculated into duck embryo liver cells. Characteristic cells rounding and necrosis. 1 mm in diameter of plaques. Direct FA technique on livers. Acute outbreaks of DHV never use serology assay.

Diagnosis VN tests used for virus identification, titration of serological response to vaccines, and epidemiology. DHV type I neutralization in chicken embryos, duck embryos, or ducklings. VN in cell cultures or passive HA tests. AGDP (agar gel diffusion precipitin). If the maximum 50% plaque reduction titers (VN50) for negative control serum should be taken as 1:250.

Differential Diagnosis The sudden onset, rapid spread, and acute course are characteristics of DHV type 1. Hemorrhagic lesions in livers of ducklings up to 3 weeks of age. Chlamydia psittaci in 4-6 week-old birds has a synergistic effect.

Differential Diagnosis Salmonella and alfatoxicosis are similar. The latter causes ataxia, convulsions, and opisthotonos and bile duct hyperplasia BUT NO LIVER HEMORRHAGES. No diseases occur frequently in young age group.

Treatments Intramuscular injection of 0.5 ml of DHV type 1 antiserum into each duckings of a brood. Passive immunization by injection of yolk from eggs produced by hyperimmune breeder ducks.

Prevention and Control DHV type 1 can be prevented by strict isolation, during the first 4-5 weeks. Resistance can be conferred by injection of immune serum of yolk; immunization of breeding stock to ensure high levels of passively transferred antibody; active immunization of ducklings with avirulent strains.

Prevention and Control Attenuated strains were produced by passage in chicken embryos. Inoculation of 0.5 ml undiluted egg-propagated virus IM 2-4 weeks before hatching eggs. But it needs repeated injections.

Prevention and Control 5. Two doses of attenuated virus vaccine administrated to breeders at least 6 weeks apart; passive immunity was transmitted to progeny for about 9 months after the second vaccination. 6. Chicken embryo-attenuated strain was improved by aluminum hydroxide adsorption and a saponin adjuvant.

Prevention and Control 7. Three immunizations over a 3-month periods give HA and VN antibody. The antibody titers in laying ducks necessary to protect their offspring was 1:64 for HA and 1:32 for VN antibodies. 8. Newly hatched ducklings injected IM with attenuated vaccine developed resistance in 3 days. Oral required up to 6 days.

Prevention and Control 9. Attenuated strains develop protection in day-old ducklings inoculated by the IM, intranasal, or foot-web route.

DHV type 2 1. Only ducks are affected, no wildlife reservoirs nor vectors have been identified. 2. Infection occurs through oral, cloacal, and subcutaneous routes. 3. Death occur within 1-4 days, usually within 1-2 hours after appearance of clinical signs.

DHV type 2 4. Polydypsia with loose droppings, excessive urate excretion, convulsions and acute opisthotonos. 5. Affected ducks die in good conditions and mortality did not exceed 50%. 6. Livers and kidneys are target organs.

DHV type 2 7. Livers are pale pink with multiple, small punctuate hemorrhages, often forming confluent bands. 8. The spleen is enlarged and sago-like in appearance due to scattered pale foci. 9. Kidneys are swollen with blood vessels injected and standing out from the pale subatnces.

DHV type 2 10. Small hemorrhages are seen in intestinal wall and on the heart fat. 11. Extensive necrosis of the hepatocyte cytoplasm and bile duct hyperplasia. 12. Only EM examination is reliable and difficult to isolate only following repeated passage in the amniotic sac of embryonated chicken or duck eggs.

DHV type 3 1. Less severe than DHV type 1 and mortality rarely exceeded 30%. 2. Nine to 10 day old duck embryos inoculated onto CAM was susceptible to DHV type 3. 3. The CAMs were discolored and the surface of the affected areas has a dry crusty or cheesy appearance. CAM was edematous and thickened up to 10 times.

DHV type 3 4. Embryos were stunting, edema, skin hemorrhages, flaccid appearance, gelatinous fluid accumulation, and enlarged liver, kidney, and spleen. 5. Chicken embryo was not sensitive. Only liver and kidney cells of duck embryo were sensitive to virus.

DHV type 3 6. Ducklings dying from DHV type 3 show similar profiles of type 1. Gross lesions were similar to DHV type 1. 7. Liver homogenate was inoculated into the CAM of 10-day-old embryonated duck eggs is tentatively identified.