Key Messages

• Both PRRS virus used enhanced susceptibility to S. suis challenge.
• The highly virulent PRRSV increased susceptibility to S. suis more than low virulent strain.
• PRRSV inhibited clearance of S. suis from the blood which caused a higher tissue dissemination of the bacteria and increased S. suis-associated diseases.

Article Brief

Six separate groups of 13 or 14 pigs each (80 in total) thee-week-old PRRSV- and S. suis-free piglets were intranasally inoculated with: sterile medium, a low-virulent PRRS strain (modified live virus vaccine) or a high virulent PRRS strain.

After seven days, half of the pigs (three groups) were intranasally inoculated with S. suis serotype 2.

They were daily monitored (rectal temperatures, clinical respiratory disease scores, evidence of CNS disease, swollen joints, and lameness) until day 11 and every other day until day 28. Six pigs from each group were euthanized for a necropsy on day 10.

The highly virulent PRRSV increased susceptibility to S. suis more than low-virulent PRRS. However, the later also enhanced susceptibility to S. suis challenge.

Groups 4, 5, and 6 had more days with rectal temperatures of over 40ºC than controls and pigs only inoculated with S. suis. Some pigs inoculated with S. suis showed signs of CNS disease but without significant differences. The mortality in group 6 (High pathogenic PRRS+S.suis) was 87.5 per cent, all other groups except group 4 (Low pathogenic PRRS+S.suis), which had 37.5 per cent mortality. The mortality in group 4 was higher than in group 2, (only S.suis) which was 14.3 per cent but the difference was not significantly.

PRRSV lung lesions were more severe (P<0.05) in the groups inoculated with high pathogenic PRRS while S. suis did not significantly increase the percentage of lung with visible lesions. Pigs in group 6 had a higher incidence of pleuritis, peritonitis, and arthritis than pigs inoculated with S. suis alone.

PRRSV inhibited clearance of S. suis from the blood which caused a higher tissue dissemination of the bacteria and increased S. suis-associated diseases. PRRSV damage to PIMs may lower the threshold of S. suis necessary to induce disease. This is consistent with field cases where S. suis has often a little economic impact until PRRSV infections appear.

S. suis could also influence PRRSV, since the virus was recovered from more of the pigs (71.4 per cent) inoculated with low-pathogenic PRRS+S.suis than from pigs only inoculated with low-pathogenic PRRS (38.5 per cent). Like Mycoplasma hyopneumoniae, S. suis may attract and activate macrophages facilitating PRRSV replication and persistence.

Extra-label use (intranasally instead of intramuscular) of the modified live PRRSV vaccine may exacerbate S. suis-induced disease in herds exposed to or carrying virulent S. suis.

Reference

Thanawongnuwech R., Brown G.B., Halbur P.G., Roth J.A., Royer R.L. and Thacker B.J. 2000. Pathogenesis of porcine reproductive and respiratory syndrome virus-induced increase in susceptibility to Streptococcus suis infection.Veterinary Pathology 37: 143-152.

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November 2015