The pathogenicity of duck hepatitis A virus types 1 and 3 on ducklings

Abstract

Duck hepatitis A virus (DHAV) is one of the pathogens that cause fatal duck viral hepatitis (DVH) in ducklings, which is an acute and contagious disease with a high mortality rate. Despite a continuing official duck vaccination program, DHAV infection remains a major threat to the duck industry. Considerable changes were observed in the epidemiology of DHAV-1/-3 in China over time. Therefore, comparing the pathogenicity of different DHAV serotypes can provide a theoretical basis for the diagnosis and prevention of DVH. In this study, we systematically investigated the effects of infection with DHAV-1/-3 field strains on clinical signs, gross lesions, histopathological changes, viral RNA detection, enzymatic systems, and metabolite concentrations. The results demonstrated that the major macroscopic and microscopic lesions in ducks infected with DHAV-1/-3 in the liver, brain, spleen, pancreas, and kidneys exhibited no significant differences. After 24 h of infection, DHAV quickly appeared in blood and major organs. Significant changes in clinical chemical markers together with histopathological lesions and viral RNA detection indicated that the liver is the major target organ for both viruses, resulting in impaired of liver integrity and function. In addition, we found that both viruses were able to invade both central and peripheral immune organs. Also lipase plasma activity was substantially affected by DHAV-1/-3, indicating that the integrity and function of the pancreas was compromised. However, there was no significant difference in pathogenicity between DHAV-1 and -3. The results of this study provide new insights into the pathogenesis of DHAV-1/3, two viruses that cause serious depression, metabolic disorders, and immunosuppression.

Keywords: duck hepatitis A virus; metabolic derangements; pathogenicity.

Figure 1

The clinical indices of ducklings after infection with DHAV-1 and DHAV-3. (A) Clinical scoring: 0, for normal; 1, mild depression; 2, severe depression; 3, paralysis/prostration; and 4, death. The mean scores per group per day are shown. (B) The percentage of ducklings that survived in the infected groups was significantly lower than in the control group. The error bars indicate standard deviations. Asterisks indicate statistical significant difference (P < 0.05).

Figure 2

Gross lesions of ducklings infected with DHAV-1 and DHAV-3 at 48 h post-infection. (A) The dead ducklings neck back and opisthotonos. (B) The liver of dead ducklings is typically enlarged with petechial and ecchymosis hemorrhages throughout. (C) Severe meningeal hyperemia and hemorrhage was in some dead ducklings (red arrow). (D) The spleen presented reddish brown with congestion and gray-white with necrosis (red arrow). (E) The pancreas were covered with gray-white focal necrosis (red arrow).

Figure 3

Pathological changes of the DHAV-1and DHAV-3 infected ducklings at 48 h post-infection. A, D, G, J, M represented the liver (hematoxylin and eosin (H&E) staining, 200 ×), brain (H&E, 200 ×), spleen (H&E, 100 ×), pancreas (H&E, 200 ×), and kidney (H&E, 400 ×) of ducklings from the control group, respectively. The liver showed diffuse degeneration, hemorrhage, (B) and necrosis of hepatocytes with proliferation of basophilic bile ductular cells around the portal areas (yellow arrow) (C). Severe infiltration of lymphocytes in under the meninges (red arrow) (E), necrosis of brain nerve cells (yellow arrow) and local microglia proliferation (green arrow) (F) were observed. Necrosis of lymphocytes, hyperemia, and structural disorder were observed in spleen (H-I). Diffuse degeneration and necrosis of pancreatic epithelial cells were seen in the pancreas (K-L). The hyperemia and tubules degeneration were observed in kidneys (N-O).

Figure 4

Viral titration in different tissues of the ducklings at 1 (A) and 3 (B) day post infection. Note: Data are expressed as the mean ± SD. Asterisks indicate statistically significant differences compared with the each group's liver (P < 0.05).

Figure 5

Graphical illustration of the means and standard deviations of the clinical chemistry analytes at 1, 3, and 5 day post infection. (A) total protein, (B) albumin, (C) alanine aminotransferase, (D) aspartate aminotransferase, (E) bile acids, and (F) lipase contents. Note: Data are expressed as the mean ± SD. Asterisks indicate statistically significant differences compared with the control group (P < 0.05).