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Natural peste des petits ruminants virus infection in Black Bengal goats: virological, pathological and immunohistochemical investigation.

Chowdhury EH, Bhuiyan AR, Rahman MM, Siddique MS, Islam MR - BMC Vet. Res. (2014)

Bottom Line: Field results are better indicators of pathogenicity of the circulating virus.PPR virus antigen was found in pneumocytes and alveolar macrophages in lungs.The striking histo-morphologic diagnosis of PPR was acute pneumonia and severe gastro-enteritis.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Faculty of Veterinary Science, Bangladesh Agricultural University, Mymensingh, Bangladesh. emdad001@yahoo.com.

ABSTRACT

Background: Peste des Petits Ruminants (PPR), also known as Goat Plague, occurs in goats, sheep and related species. It is caused by a morbillivirus in the family Paramyxoviridae. In Bangladesh PPR is endemic and it causes serious economic losses. Pathology of PPR has been reported in different goat and sheep breeds from natural and experimental infections. Field results are better indicators of pathogenicity of the circulating virus. The severity of the disease varies with species, breed and immune status of the host. Pathological investigations of natural outbreaks of PPR in Balck Bengal goats are very limited. The current investigation was aimed at describing pathology and antigen localization in natural PPR infections in Black Bengal goats.

Results: A total of 28 outbreaks were investigated clinically and virologically. Average flock morbidity and mortality were 75% and 59%, respectively, with case fatality rate of 74%. Necropsy was conducted on 21 goats from 15 outbreaks. The major gross lesions were congestion of gastrointestinal tract, pneumonia, engorged spleen, and oedematous lymphnodes. Histopathological examination revealed severe enteritis with denudation of intestinal epithelium, severe broncho-interstitial pneumonia with macrophages within lung alveoli and extensive haemorrhages with depletion of lymphoid cells and infiltration of macrophages in the sinuses of spleen. In lymph nodes, the cortical nodules were replaced by wide sinusoids with severe depletion of lymphocytes, infiltration of mononuclear cells and some giant cells in sub-capsular areas and medullary sinuses. PPR virus antigen was found in pneumocytes and alveolar macrophages in lungs. Viral RNA could be detected by RT-PCR in 69 out of 84 nasal swab, 59 out of 84 blood and 21 out of 21 lymph node samples. Sequence analyses revealed closeness of Bangladeshi strains with other recent Asian isolates.

Conclusion: Natural outbreaks of PPR in Black Bengal goats in Bangladesh resulted in 75% and 59% flock morbidity and mortality, respectively, with a case fatality rate of 74%. The striking histo-morphologic diagnosis of PPR was acute pneumonia and severe gastro-enteritis. A detailed experimental pathological study on Black Bengal goats infected with recent isolates is required.

No MeSH data available.


Related in: MedlinePlus

Histological section of a lung of a PPR infected goat. Accumulation of fibrin (line) and infiltration of inflammatory cells in the lung parenchyma, H&E X 82.5.
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Fig7: Histological section of a lung of a PPR infected goat. Accumulation of fibrin (line) and infiltration of inflammatory cells in the lung parenchyma, H&E X 82.5.

Mentions: Details of the histopathological findings are listed in Table 2. The most remarkable lesions were found in respiratory, alimentary and lymphatic systems. Goats that died within 48 hours of the onset of clinical signs were mostly haemorrhagic and showed severe exudation in the upper respiratory tract and in the lung parenchyma. The exudates in the lung parenchyma often proceeded to fibrinous organization (Figure 7). In goats that died after 3–5 days, lesions of lungs were more severe, with additional involvement of alimentary tract. The lung parenchyma was infiltrated with large mononuclear cells and clumps of these cells were found in the lung alveoli (Figure 8). In some places, alveoli lost its lining of squamous epithelium, which were partially replaced by cuboidal type epithelial cells. The entire alimentary tract revealed haemorrhagic gastroenteritis with infiltration of mononuclear cells in the lamina propria and loss of laminar epithelia. Clumps of epithelial cells were aggregated in the lumen of the intestine. Liver was severely congested and haemorrhagic. Changes in the lymphatic systems appeared more haemorrhagic in goats that died within 2–3 days. Lymphatic organs were depleted of lymphocytes (Figure 9). These lesions were more severe in goats that survived more than a week. Conspicuous lymphoid depletion was seen in Peyer’s patches in 6 cases, in lymph nodes in 7 cases, and in spleen (Figure 10) in 7 cases.Table 2


Natural peste des petits ruminants virus infection in Black Bengal goats: virological, pathological and immunohistochemical investigation.

Chowdhury EH, Bhuiyan AR, Rahman MM, Siddique MS, Islam MR - BMC Vet. Res. (2014)

Histological section of a lung of a PPR infected goat. Accumulation of fibrin (line) and infiltration of inflammatory cells in the lung parenchyma, H&E X 82.5.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4233235&req=5

Fig7: Histological section of a lung of a PPR infected goat. Accumulation of fibrin (line) and infiltration of inflammatory cells in the lung parenchyma, H&E X 82.5.
Mentions: Details of the histopathological findings are listed in Table 2. The most remarkable lesions were found in respiratory, alimentary and lymphatic systems. Goats that died within 48 hours of the onset of clinical signs were mostly haemorrhagic and showed severe exudation in the upper respiratory tract and in the lung parenchyma. The exudates in the lung parenchyma often proceeded to fibrinous organization (Figure 7). In goats that died after 3–5 days, lesions of lungs were more severe, with additional involvement of alimentary tract. The lung parenchyma was infiltrated with large mononuclear cells and clumps of these cells were found in the lung alveoli (Figure 8). In some places, alveoli lost its lining of squamous epithelium, which were partially replaced by cuboidal type epithelial cells. The entire alimentary tract revealed haemorrhagic gastroenteritis with infiltration of mononuclear cells in the lamina propria and loss of laminar epithelia. Clumps of epithelial cells were aggregated in the lumen of the intestine. Liver was severely congested and haemorrhagic. Changes in the lymphatic systems appeared more haemorrhagic in goats that died within 2–3 days. Lymphatic organs were depleted of lymphocytes (Figure 9). These lesions were more severe in goats that survived more than a week. Conspicuous lymphoid depletion was seen in Peyer’s patches in 6 cases, in lymph nodes in 7 cases, and in spleen (Figure 10) in 7 cases.Table 2

Bottom Line: Field results are better indicators of pathogenicity of the circulating virus.PPR virus antigen was found in pneumocytes and alveolar macrophages in lungs.The striking histo-morphologic diagnosis of PPR was acute pneumonia and severe gastro-enteritis.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Faculty of Veterinary Science, Bangladesh Agricultural University, Mymensingh, Bangladesh. emdad001@yahoo.com.

ABSTRACT

Background: Peste des Petits Ruminants (PPR), also known as Goat Plague, occurs in goats, sheep and related species. It is caused by a morbillivirus in the family Paramyxoviridae. In Bangladesh PPR is endemic and it causes serious economic losses. Pathology of PPR has been reported in different goat and sheep breeds from natural and experimental infections. Field results are better indicators of pathogenicity of the circulating virus. The severity of the disease varies with species, breed and immune status of the host. Pathological investigations of natural outbreaks of PPR in Balck Bengal goats are very limited. The current investigation was aimed at describing pathology and antigen localization in natural PPR infections in Black Bengal goats.

Results: A total of 28 outbreaks were investigated clinically and virologically. Average flock morbidity and mortality were 75% and 59%, respectively, with case fatality rate of 74%. Necropsy was conducted on 21 goats from 15 outbreaks. The major gross lesions were congestion of gastrointestinal tract, pneumonia, engorged spleen, and oedematous lymphnodes. Histopathological examination revealed severe enteritis with denudation of intestinal epithelium, severe broncho-interstitial pneumonia with macrophages within lung alveoli and extensive haemorrhages with depletion of lymphoid cells and infiltration of macrophages in the sinuses of spleen. In lymph nodes, the cortical nodules were replaced by wide sinusoids with severe depletion of lymphocytes, infiltration of mononuclear cells and some giant cells in sub-capsular areas and medullary sinuses. PPR virus antigen was found in pneumocytes and alveolar macrophages in lungs. Viral RNA could be detected by RT-PCR in 69 out of 84 nasal swab, 59 out of 84 blood and 21 out of 21 lymph node samples. Sequence analyses revealed closeness of Bangladeshi strains with other recent Asian isolates.

Conclusion: Natural outbreaks of PPR in Black Bengal goats in Bangladesh resulted in 75% and 59% flock morbidity and mortality, respectively, with a case fatality rate of 74%. The striking histo-morphologic diagnosis of PPR was acute pneumonia and severe gastro-enteritis. A detailed experimental pathological study on Black Bengal goats infected with recent isolates is required.

No MeSH data available.


Related in: MedlinePlus