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One case of swine hepatitis E virus and porcine reproductive and respiratory syndrome virus co-infection in weaned pigs.

Mao J, Zhao Y, She R, Xiao P, Tian J, Chen J - Virol. J. (2013)

Bottom Line: We found that this sample was positive for the presence of HEV and PRRSV.Severe pathologic changes were observed.We speculated that co-infection with PRRSV and HEV might lead to more serious problems.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Veterinary Pathology, Key Laboratory of Zoonosis of Ministry of Agriculture, China Agricultural University, Beijing 100193, China. sheruiping@126.com.

ABSTRACT

Background: Using various methods, we analyzed the cause of death among weaned pigs from a pig farm in Hebei Province, China. All 300 piglets (100% fatality) were identified as moribund, with death occurring within 1 month from the onset of clinical signs.

Results: A single case exhibited obvious hemorrhagic necrotic changes with massive lymphocytic infiltration in multiple organs, in particular the liver, lungs and intestines. Dysplasia and lymphocyte deterioration were common in lymphatic organs. No visible bacterial colonies from liver and spleen were observed in nutrient, MacConkey, and blood agar plates. Using polymerase chain reaction techniques for this case, we attempted to detect a number of epidemic swine viruses in spleen and liver, including PRRSV, CSF, HEV, and PCV2. We found that this sample was positive for the presence of HEV and PRRSV.

Conclusions: We have detected HEV and PRRSV co-infection in one piglet. Severe pathologic changes were observed. The high mortality of weaned pigs which showed the similar clinical syptom was possibly a result of HEV and PRRSV co-infection, which has rarely been reported previously. We speculated that co-infection with PRRSV and HEV might lead to more serious problems.

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Histological lesions in multiple organs. Pathological changes were characterized by hyperemia, hemorrhaging, necrosis and inflammatory infiltration. Staining was conducted with hematoxylin and eosin. (a) Disarrayed or dissolved myocardia. (b, c) Lung with extensive hemorrhaging, lymphocyte infiltration and exfoliated alveolar epithelium cells inside the bronchioles and alveoli. (d, e, f) Necrosis and hemorrhaging in the kidney. (g, h, i) Liver exhibiting hepatic necrosis and lymphocyte infiltration. (j) Dysplasia of lymphoid follicles in the spleen. (k) Lymph nodes with congested capillaries. (l, m) Coagulation necrosis and abruption of intestinal villi. (n, o) Perivascular cuffs in cerebrum and liquefaction necrosis in cerebellum. Magnification was 400× (a, c, g, j, n), 200× (b, d, e, f, h, i, k, o), or 100× (l, m).
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Figure 1: Histological lesions in multiple organs. Pathological changes were characterized by hyperemia, hemorrhaging, necrosis and inflammatory infiltration. Staining was conducted with hematoxylin and eosin. (a) Disarrayed or dissolved myocardia. (b, c) Lung with extensive hemorrhaging, lymphocyte infiltration and exfoliated alveolar epithelium cells inside the bronchioles and alveoli. (d, e, f) Necrosis and hemorrhaging in the kidney. (g, h, i) Liver exhibiting hepatic necrosis and lymphocyte infiltration. (j) Dysplasia of lymphoid follicles in the spleen. (k) Lymph nodes with congested capillaries. (l, m) Coagulation necrosis and abruption of intestinal villi. (n, o) Perivascular cuffs in cerebrum and liquefaction necrosis in cerebellum. Magnification was 400× (a, c, g, j, n), 200× (b, d, e, f, h, i, k, o), or 100× (l, m).

Mentions: Pathological changes in various tissues were determined by microscopy. In the heart, the myocardial interstitium broadened with mild edema. The myocardium was generally granular, degenerated, disarrayed or dissolved (Figure 1a). A small number of lymphocytes had infiltrated among the myocytes. For the lung, different pulmonary lobules presented different degrees of pathological changes. In some pulmonary lobules, alveoli were abundantly filled with cells, erythrocytes and exudates, and the normal histological structure of the lung was severely compromised. Exfoliated alveolar epithelium cells were accumulated inside the bronchioles (Figure 1b); in some pulmonary lobules, extensive hemorrhaging was observed in the alveoli and interstitium (Figure 1c). In other areas, the alveolar walls were thickened, with substantial lymphocyte infiltration. Infiltration by numerous inflammatory cells and pink liquid exudates in the interlobular arteries were commonly seen. In the kidney, some of the cortical glomeruli were necrotic and contained erythrocytes. Large numbers of tubular epithelial cells were vacuolated, exfoliated and necrotic, especially at the edge of cortex (Figure 1d). A protein cast could be seen in some renal tubules (Figure 1e). In the renal junction area between the cortex and medulla, congestion and hemorrhaging was obvious (Figure 1f). Examination of the liver revealed congestion, hemorrhaging, lymphocyte infiltration and an accumulation of randomly distributed lymphocytes. There was hepatic necrosis and vacuolization in large local areas (Figure 1g, 1h). Fibrosis was apparent around the portal area, with proliferation of small bile ducts, and lymphocyte infiltration also observed (Figure 1i). Within the spleen the number of lymphocytes was decreased in the white pulp area around the central artery. The lymphoid follicles were smaller than average and subject to dysplasia (Figure 1j). The capillaries of lymph nodes were dilated and congested, and expansion of lymphatic sinuses was obvious (Figure 1k). Examination of the intestine revealed coagulation, necrosis, desquamation, and abruption of intestinal villi in some areas. Necrosis of intestinal epithelial cells was observed, as well as exposure of the lamina propria, with dense lymphocyte infiltration beyond the layer of the muscularis mucosa. There was an increase in the levels of secretion from intestinal glands (Figure 1l, 1m). We noticed that hyperplasia of gliacytes, demyelination and perivascular cuffs were visible in the cerebrum. At the molecular layer of the cerebellum, liquefaction necrosis was evident (Figure 1n, 1o).


One case of swine hepatitis E virus and porcine reproductive and respiratory syndrome virus co-infection in weaned pigs.

Mao J, Zhao Y, She R, Xiao P, Tian J, Chen J - Virol. J. (2013)

Histological lesions in multiple organs. Pathological changes were characterized by hyperemia, hemorrhaging, necrosis and inflammatory infiltration. Staining was conducted with hematoxylin and eosin. (a) Disarrayed or dissolved myocardia. (b, c) Lung with extensive hemorrhaging, lymphocyte infiltration and exfoliated alveolar epithelium cells inside the bronchioles and alveoli. (d, e, f) Necrosis and hemorrhaging in the kidney. (g, h, i) Liver exhibiting hepatic necrosis and lymphocyte infiltration. (j) Dysplasia of lymphoid follicles in the spleen. (k) Lymph nodes with congested capillaries. (l, m) Coagulation necrosis and abruption of intestinal villi. (n, o) Perivascular cuffs in cerebrum and liquefaction necrosis in cerebellum. Magnification was 400× (a, c, g, j, n), 200× (b, d, e, f, h, i, k, o), or 100× (l, m).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4225530&req=5

Figure 1: Histological lesions in multiple organs. Pathological changes were characterized by hyperemia, hemorrhaging, necrosis and inflammatory infiltration. Staining was conducted with hematoxylin and eosin. (a) Disarrayed or dissolved myocardia. (b, c) Lung with extensive hemorrhaging, lymphocyte infiltration and exfoliated alveolar epithelium cells inside the bronchioles and alveoli. (d, e, f) Necrosis and hemorrhaging in the kidney. (g, h, i) Liver exhibiting hepatic necrosis and lymphocyte infiltration. (j) Dysplasia of lymphoid follicles in the spleen. (k) Lymph nodes with congested capillaries. (l, m) Coagulation necrosis and abruption of intestinal villi. (n, o) Perivascular cuffs in cerebrum and liquefaction necrosis in cerebellum. Magnification was 400× (a, c, g, j, n), 200× (b, d, e, f, h, i, k, o), or 100× (l, m).
Mentions: Pathological changes in various tissues were determined by microscopy. In the heart, the myocardial interstitium broadened with mild edema. The myocardium was generally granular, degenerated, disarrayed or dissolved (Figure 1a). A small number of lymphocytes had infiltrated among the myocytes. For the lung, different pulmonary lobules presented different degrees of pathological changes. In some pulmonary lobules, alveoli were abundantly filled with cells, erythrocytes and exudates, and the normal histological structure of the lung was severely compromised. Exfoliated alveolar epithelium cells were accumulated inside the bronchioles (Figure 1b); in some pulmonary lobules, extensive hemorrhaging was observed in the alveoli and interstitium (Figure 1c). In other areas, the alveolar walls were thickened, with substantial lymphocyte infiltration. Infiltration by numerous inflammatory cells and pink liquid exudates in the interlobular arteries were commonly seen. In the kidney, some of the cortical glomeruli were necrotic and contained erythrocytes. Large numbers of tubular epithelial cells were vacuolated, exfoliated and necrotic, especially at the edge of cortex (Figure 1d). A protein cast could be seen in some renal tubules (Figure 1e). In the renal junction area between the cortex and medulla, congestion and hemorrhaging was obvious (Figure 1f). Examination of the liver revealed congestion, hemorrhaging, lymphocyte infiltration and an accumulation of randomly distributed lymphocytes. There was hepatic necrosis and vacuolization in large local areas (Figure 1g, 1h). Fibrosis was apparent around the portal area, with proliferation of small bile ducts, and lymphocyte infiltration also observed (Figure 1i). Within the spleen the number of lymphocytes was decreased in the white pulp area around the central artery. The lymphoid follicles were smaller than average and subject to dysplasia (Figure 1j). The capillaries of lymph nodes were dilated and congested, and expansion of lymphatic sinuses was obvious (Figure 1k). Examination of the intestine revealed coagulation, necrosis, desquamation, and abruption of intestinal villi in some areas. Necrosis of intestinal epithelial cells was observed, as well as exposure of the lamina propria, with dense lymphocyte infiltration beyond the layer of the muscularis mucosa. There was an increase in the levels of secretion from intestinal glands (Figure 1l, 1m). We noticed that hyperplasia of gliacytes, demyelination and perivascular cuffs were visible in the cerebrum. At the molecular layer of the cerebellum, liquefaction necrosis was evident (Figure 1n, 1o).

Bottom Line: We found that this sample was positive for the presence of HEV and PRRSV.Severe pathologic changes were observed.We speculated that co-infection with PRRSV and HEV might lead to more serious problems.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Veterinary Pathology, Key Laboratory of Zoonosis of Ministry of Agriculture, China Agricultural University, Beijing 100193, China. sheruiping@126.com.

ABSTRACT

Background: Using various methods, we analyzed the cause of death among weaned pigs from a pig farm in Hebei Province, China. All 300 piglets (100% fatality) were identified as moribund, with death occurring within 1 month from the onset of clinical signs.

Results: A single case exhibited obvious hemorrhagic necrotic changes with massive lymphocytic infiltration in multiple organs, in particular the liver, lungs and intestines. Dysplasia and lymphocyte deterioration were common in lymphatic organs. No visible bacterial colonies from liver and spleen were observed in nutrient, MacConkey, and blood agar plates. Using polymerase chain reaction techniques for this case, we attempted to detect a number of epidemic swine viruses in spleen and liver, including PRRSV, CSF, HEV, and PCV2. We found that this sample was positive for the presence of HEV and PRRSV.

Conclusions: We have detected HEV and PRRSV co-infection in one piglet. Severe pathologic changes were observed. The high mortality of weaned pigs which showed the similar clinical syptom was possibly a result of HEV and PRRSV co-infection, which has rarely been reported previously. We speculated that co-infection with PRRSV and HEV might lead to more serious problems.

Show MeSH
Related in: MedlinePlus