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. 2010 Aug 9:7:184.
doi: 10.1186/1743-422X-7-184.

Secondary infection with Streptococcus suis serotype 7 increases the virulence of highly pathogenic porcine reproductive and respiratory syndrome virus in pigs

Min Xu  1 , Shujie Wang, Linxi Li, Liancheng Lei, Yonggang Liu, Wenda Shi, Jiabin Wu, Liqin Li, Fulong Rong, Mingming Xu, Guangli Sun, Hua Xiang, Xuehui Cai
Affiliations

Secondary infection with Streptococcus suis serotype 7 increases the virulence of highly pathogenic porcine reproductive and respiratory syndrome virus in pigs

Min Xu et al. Virol J. .

Abstract

Background: Porcine reproductive and respiratory syndrome virus (PRRSV) and Streptococcus suis are common pathogens in pigs. In samples collected during the porcine high fever syndrome (PHFS) outbreak in many parts of China, PRRSV and S. suis serotype 7 (SS7) have always been isolated together. To determine whether PRRSV-SS7 coinfection was the cause of the PHFS outbreak, we evaluated the pathogenicity of PRRSV and/or SS7 in a pig model of single and mixed infection.

Results: Respiratory disease, diarrhea, and anorexia were observed in all infected pigs. Signs of central nervous system (CNS) disease were observed in the highly pathogenic PRRSV (HP-PRRSV)-infected pigs (4/12) and the coinfected pigs (8/10); however, the symptoms of the coinfected pigs were clearly more severe than those of the HP-PRRSV-infected pigs. The mortality rate was significantly higher in the coinfected pigs (8/10) than in the HP-PRRSV- (2/12) and SS7-infected pigs (0/10). The deceased pigs of the coinfected group had symptoms typical of PHFS, such as high fever, anorexia, and red coloration of the ears and the body. The isolation rates of HP-PRRSV and SS7 were higher and the lesion severity was greater in the coinfected pigs than in monoinfected pigs.

Conclusion: HP-PRRSV infection increased susceptibility to SS7 infection, and coinfection of HP-PRRSV with SS7 significantly increased the pathogenicity of SS7 to pigs.

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Figures

Figure 1
Figure 1
Mean value (standard deviation) of lesion scores. (a) Scores of macroscopic lung lesion, (b) Scores of macroscopic lymph node lesion, (c) Scores of microscopic lung lesion, and (d) Scores of microscopic lymph node lesion at different times after inoculation.
Figure 2
Figure 2
Macroscopic lesions in the coinfected group. (a) Kidney and pelvic hemorrhage; (b) Trichocardia and hydropericardium; (c) Stomach hemorrhage; (d) Bacterial infection in the thoracic cavity; (e) Lymph node intumescentia and hemorrhage; (f) Lung consolidation.
Figure 3
Figure 3
Microscopic lesions in the coinfected group. (a) Perivascular cuffs in brain; (b) Suppurative pneumonia and purulent bronchitis; (c) Lymphocyte necrosis and disintegration in submaxillary lymph nodes; (d) Severe congestion of kidney and renal tubular necrosis and collapse; (e) Moderate sinusoidal congestion with a small number of lymphoid cells and macrophage infiltration in the lung; (f) Lymphoid cell necrosis and collapse around the ellipsoid arterioles and in the white pulp and red pulp of the spleen.
Figure 4
Figure 4
PRRSV RNA. (a) PRRSV RNA levels in the lungs of all pigs in HP-PRRSV-infected and coinfected groups either after necropsy or death. The data from the coinfected group at 14 days post-inoculation (DPI) is the mean value of 8 pigs of the coinfected group that died between 10 and 15 DPI; no pigs from the coinfected group were necropsied on 21 DPI. (b) The PRRSV RNA levels in the brains of HP-PRRSV-infected and coinfected pigs.
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