Symptoms and Prevention and Control Methods of Duck Viral Swollen Head Hemorrhagic Disease
Duck viral swollen head hemorrhagic disease is an acute septic infectious disease of ducks caused by duck viral swollen head hemorrhagic disease virus. Its clinical features include swelling of the duck's head, conjunctival hyperemia and hemorrhage, extensive hemorrhage of the whole body skin, enlarged liver that is earth-yellow in color and accompanied by hemorrhagic spots, body temperature above 43°C, and passage of thin grass-green feces. The incidence rate is 50%-100%, and the mortality rate is 40%-80% or even 100%. It is a new infectious disease that seriously harms @#@231@#@ industry.
1 Epidemiological diagnosis of duck viral swollen head hemorrhagic disease
Cheng Anchun et al. (2003) reported that in 1998, an infectious disease broke out in a breeding duck farm in Wenjiang, Sichuan, among 5,000 Tianfu meat-type breeding ducks at 33 weeks of age. This batch of breeding ducks had been vaccinated against duck plague, duck viral hepatitis, pasteurellosis, and colibacillosis at 18-23 weeks of age before the onset of laying. At that time, because ducks showed head swelling and tearing, they were treated according to duck plague. On the third day of onset, all ducks in the flock that had not yet shown symptoms were injected intramuscularly with 3 times the dose of duck plague attenuated vaccine, along with broad-spectrum antibacterial drugs for treatment. The incidence rate was 100%, the epidemic period reached 32 d, and 100% of affected ducks died. Serum was collected from ducks in the late stage of disease and tested by agar gel diffusion against avian influenza antigen, which was negative. By the autumn of 1999, the disease began to spread in surrounding areas, reached a peak in winter, still spread in the spring of 2000, naturally subsided in summer, and began to appear again in autumn. It reached a peak in the winter of 2000 and the spring of 2001. The disease also occurred in almost all duck-raising areas of Sichuan Province, as well as in duck-raising areas of Chongqing Municipality, Guizhou Province, and Yunnan Province. From December 2000 to January 2001 alone, more than 7 million commercial meat ducks and breeding ducks died in a certain town in Chengdu, causing serious economic losses.
In areas and duck farms where the disease occurred for the first time, it showed acute outbreak, with incidence and mortality rates often reaching 100%. A few sick ducks suddenly appeared in the flock, a large number of sick ducks and deaths appeared in 2-3 d, and deaths peaked in 4-5 d. The disease course was generally 4-6 d. In areas and duck farms where it occurred again or repeatedly, the incidence rate was 50%-90% or higher, and the mortality rate was 40%-80% or higher. Ducks of all ages and breeds could be infected and develop the disease. A survey of more than 3 million breeding ducks and more than 50 million commercial meat duck flocks in 18 areas of Sichuan Province, Chongqing, Guizhou, and Yunnan involved breeds including Tianfu meat duck, Aobaxing duck, Cherry Valley duck, Beijing duck, Sichuan shelduck, Sichuan white duck, Jianchang duck, Muscovy duck, wild duck, lace duck, and various hybrid ducks. The earliest onset began at 3 days of age, and cases still occurred at 500 days of age. Treatment with antibacterial drugs such as penicillin, streptomycin, colistin, ciprofloxacin, ofloxacin, florfenicol, difloxacin, sulfonamides, etc., or antiviral drugs such as ribavirin, amantadine, banlangen, and antiviral granules could prolong the epidemic period but had no effective therapeutic effect. Emergency injection of rabbit anti-hyperimmune serum prepared from isolated virus or serum from recovered ducks into ducks in affected flocks that had not yet shown clinical symptoms could prevent further development of the disease, and for ducks that had already shown clinical symptoms, a cure rate of 40%-90% could be obtained. However, hyperimmune sera against duck plague, duck viral hepatitis, Pasteurella multocida (5:A), gosling plague, Muscovy duck parvovirus, and avian influenza had no such emergency preventive or therapeutic effect.
2 Clinical diagnosis of duck viral swollen head hemorrhagic disease
The incubation period of natural infection is 4-6 d. After infected ducks are introduced into a duck farm or area, other ducks begin to show clinical symptoms after 4-6 d. The incubation period of artificial infection is 3-4 d. In the early stage, sick ducks are listless and unwilling to move. As the disease progresses, they lie on the ground unable to stand, have messy and lusterless feathers covered with filth, do not eat but drink large amounts of water, have diarrhea and pass thin grass-green feces, have difficulty breathing, and show conjunctival hyperemia, hemorrhage, and severe swelling of the eyelids. Serous or bloody secretions flow from the eyes and nose. All sick ducks have obviously swollen heads, and body temperature rises above 43°C. In the later stage, body temperature drops, and they die rapidly.
3 Pathological diagnosis of duck viral swollen head hemorrhagic disease
3.1 Gross pathological changes
Dead ducks of all ages had swollen heads, swollen, hyperemic, and hemorrhagic eyelids, and the subcutaneous tissue of the head was filled with pale yellow transparent serous exudate. There was extensive hemorrhage of the whole body skin, hemorrhage of the digestive and respiratory tracts, enlarged and brittle liver that was earth-yellow and accompanied by hemorrhagic spots, enlarged spleen, a small number of hemorrhagic spots on the epicardium and coronary fat, pulmonary hemorrhage, enlarged and hemorrhagic kidneys, hemorrhagic points on the intestinal serosal surface and other serosal surfaces, and severe ovarian hyperemia and hemorrhage in laying ducks.
3.2 Histopathological changes
There were hemorrhagic foci in the endocardium and myocardium; in addition, myocardial fibers were ruptured, cytoplasm was red-stained, and nuclei disappeared and became necrotic. In the liver, early-stage hepatocytes showed fatty degeneration and granular degeneration, and later-stage focal necrosis occurred; hepatocytes were loosely arranged, cytoplasm was red-stained, nuclei were pyknotic, and inflammatory cells infiltrated. The spleen showed hemorrhage, necrotic foci, and degeneration of arterial smooth muscle. Pulmonary capillaries were congested, interstitial edema widened the interstitium, and hemorrhagic foci were present within it. Renal venules were congested, capillaries were hyperemic, and renal tubular epithelial cells showed granular degeneration. In brain tissue, neurons showed degeneration and necrosis, and perivascular spaces were widened. The duodenal mucosal epithelium had completely sloughed off, the lamina propria showed inflammatory edema, and residual villous lamina propria filled the intestinal lumen. Rectal villous lamina propria showed inflammatory cell infiltration, intestinal gland cell nuclei were pyknotic and tended toward necrosis, and separated from the basement membrane.
4 Laboratory diagnosis of duck viral swollen head hemorrhagic disease
4.1 Etiological diagnosis of duck viral swollen head hemorrhagic disease
4.1.1 Pathogen characteristics: Through epidemiological investigation, observation of clinical symptoms and pathological changes, histopathological examination, isolation and identification of the pathogen, artificial infection experiments, electron microscopy observation, and prevention and treatment experiments, duck viral swollen head hemorrhagic disease was confirmed as a new disease. The duck viral swollen head hemorrhagic disease virus is preliminarily considered to be a reovirus. The virus particles are spherical or oval, about 80 nm in diameter, without an envelope, and the nucleic acid is RNA. They do not agglutinate the red blood cells of chickens, ducks, geese, pigeons, yellow cattle, water buffalo, or pigs. The virus is stable at pH 4.0-8.0, resistant to chloroform, and neutralization tests and cross-protection tests confirmed that it has no antigenic relationship with duck plague virus and duck viral hepatitis virus. Agar gel diffusion tests confirmed that it has no antigenic relationship with Muscovy duck parvovirus, influenza virus, chicken infectious bursal disease virus, avian viral arthritis virus, or goose paramyxovirus. The isolated virus could successfully reproduce symptoms and lesions consistent with clinical cases by oral, subcutaneous, intramuscular, and intranasal routes of infection in ducks, but could not infect SPF chickens (chicken embryos) or geese.
4.1.2 Pathogen isolation: The liver, heart, spleen, brain tissue, etc. of typically affected dead ducks were collected, routinely processed and sterilized, then inoculated onto duck embryo fibroblasts and cultured at 37°C. Observations were made for 10 d. Those with lesions were further identified; those without lesions were blind-passaged for 7 generations. Isolates showing cytopathic effects were repeatedly freeze-thawed 3 times, then centrifuged at 8000 rpm for 30 min, and the supernatant was negatively stained and observed under an H-600 transmission electron microscope.
4.1.3 Artificial infection experiment in ducks: 80 commercial meat ducks at 60 days of age were randomly divided into 2 groups, 40 ducks per group. Each duck in the experimental group was subcutaneously injected with 0.5 ml, and each duck in the control group was subcutaneously injected with 0.5 ml of sterilized physiological saline. They were raised in isolation and observed for 30 d. Infected ducks showed 90% mortality, while control ducks survived.
4.2 Serological diagnosis of duck viral swollen head hemorrhagic disease
Neutralization test and cross-protection test: Duck embryo fibroblasts or susceptible ducklings can be used.
5 Differential diagnosis
5.1 Differential diagnosis from duck plague
For many years, people have regarded head swelling (i.e., "big head plague") as one of the typical clinical bases for diagnosing duck plague, and in clinical diagnosis and prevention and treatment, inertial thinking has led to treating "swollen head and tearing" as duck plague without question. In fact, there are major differences between the two: (1) Duck plague virus belongs to herpesviruses, has an envelope, and is sensitive to chloroform; (2) Nearly 100% of cases of this disease show head swelling, while only some ducks with duck plague show swelling of the head and neck; (3) Both have hemorrhagic lesions of the digestive tract mucosa, but this disease lacks the characteristic lesions of duck plague such as necrosis of the digestive tract mucosa and fibrinous pseudomembrane covering; (4) The gross and histological changes of the liver are obviously different. This disease lacks the gray-white necrotic points of the liver seen in duck plague and instead shows earth-yellow enlargement, brittleness, and hemorrhagic spots. The histological changes of the liver in duck plague have obvious inclusion bodies, whereas this disease does not; (5) In natural epidemics of duck plague, adult grazing duck flocks are more severely affected and have more serious deaths, while confined ducklings under 1 month of age rarely show mass onset, whereas this disease causes severe onset and death in all age groups, especially in ducklings.
In production practice, it is worth noting that the frequency of mixed infection of this disease with duck plague is relatively high, especially in free-range duck flocks in rural areas that have not been immunized with duck plague vaccine. Using the polymerase chain reaction (PCR) method established in this laboratory to detect duck plague virus, it was confirmed that 40% were mixed infections of the two or secondary infection with duck plague in the late epidemic period. Its characteristic is that all cases of mixed or secondary infection with duck plague virus show necrotic foci and yellow fibrinous pseudomembranes in the esophagus and rectum, as well as gray-white necrotic points in the liver and inclusion bodies under light microscopy of tissues. After the death of ducklings under 1 month of age, 4 annular hemorrhagic bands can often be found on the serosal surface of the small intestine, indicating that necrotic foci in the esophagus and rectum, yellow fibrinous pseudomembranes, gray-white necrotic points in the liver, and annular hemorrhagic bands in the small intestine of ducklings are lesions of diagnostic significance for duck plague.
5.2 Differential diagnosis from duck viral hepatitis
The liver in this disease is earth-yellow, enlarged, brittle, and has hemorrhagic spots, making it easy to confuse with duck viral hepatitis, but duck viral hepatitis virus is a member of the family Picornaviridae, about 25 nm in diameter, and the disease has obvious age characteristics (mainly affecting ducklings under 3 weeks of age). The histological changes of the liver are manifested as necrosis, inflammatory cell infiltration, and proliferation of bile duct epithelial cells.
5.3 Differential diagnosis from avian influenza
Avian influenza virus can cause disease in various poultry and birds such as chickens, turkeys, ducks, and quail. It is a member of the family Orthomyxoviridae and has an envelope and hemagglutinating activity. In contrast, no disease was seen when affected duck flocks in this disease were raised together with chickens, and no avian influenza occurred in chicken flocks in epidemic areas. The isolated virus has no hemagglutinating activity and does not infect SPF chicken embryos (chicks), goslings, etc.
6 Prevention and control measures for duck viral swollen head hemorrhagic disease
According to existing research and clinical practice, common broad-spectrum antibacterial and antiviral drugs have no definite therapeutic effect on this disease, but because they control secondary bacterial infection to a certain extent, they prolong the epidemic period. Strengthening veterinary hygiene measures and environmental disinfection are indispensable and effective measures to control the occurrence of this disease. Emergency injection of rabbit anti-hyperimmune serum or serum from recovered ducks into ducks in affected flocks that have not yet shown clinical symptoms can prevent further development of the disease, and for ducks that have already shown clinical symptoms, a cure rate of 40%-90% can be obtained. Tissue inactivated vaccine prepared from the internal organs of dead ducks and oil-adjuvant inactivated vaccine prepared from isolated virus, totaling more than 10 million doses, were applied in areas where the disease was epidemic and achieved good preventive effects. Because tissue and oil-adjuvant inactivated vaccines usually produce effective immunity in more than 15 d, in flocks with earlier onset age in severely affected areas, hyperimmune serum and inactivated vaccine often need to be used simultaneously to obtain good preventive effects.