Porcine circovirus type 2 potentiates morbidity of Salmonella enterica serovar Choleraesuis in Cesarean-derived, colostrum-deprived pigs.

PROBLEM ADDRESSED: Porcine circovirus type 2 (PCV2) and Salmonella enterica subspecies enterica serovar Choleraesuis (S. Choleraesuis) are two leading causes of economic loss in the swine industry. Although S. Choleraesuis infection occurs concurrently with PCV2-associated disease in many swine herds, the pathogenesis of concurrent infection with PCV2 and S. Choleraesuis remains largely undefined. OBJECTIVE: We investigated the interactions between PCV2 and S. Choleraesuis in 20 Cesarean-derived, colostrum-deprived (CDCD) pigs randomly assigned to 4 groups (n=5 per group). METHODS AND APPROACH: Pigs in the dual-infected and PCV2-infected groups were inoculated intranasally with PCV2 at 5 weeks of age, and pigs in the dual-infected and S. Choleraesuis-infected groups were inoculated intranasally with S. Choleraesuis at 7 weeks of age. Pigs in the control group served as uninfected controls. RESULTS: After S. Choleraesuis inoculation, severe clinical signs, reduction of weight gain, and severe microscopic lung lesions were observed in dual-infected pigs compared to those in other groups. In addition, the pigs in the dual-infected group shed significantly (P=0.002) higher quantities of S. Choleraesuis in feces 12 days after S. Choleraesuis inoculation, and S. Choleraesuis was recovered from more tissues in this group 14 days after S. Choleraesuis inoculation. CONCLUSIONS: These results indicate that prior PCV2 infection potentiates the severity of clinical signs, lung lesions, and fecal shedding and tissue dissemination of S. Choleraesuis in infected pigs. Therefore, dual infection of pigs with PCV2 and S. Choleraesuis may increase clinical effects of salmonellosis in the field.

Primary chondrosarcoma in the liver of a dog.

Primary chondrosarcoma was found in the quadrate lobe of the liver of a 6-year-old, intact, male Golden Retriever. At 6 months after partial hepatectomy, recurrence in the liver occurred. The dog died of its systemic metastases 10 months thereafter. Histologically, the hepatic mass revealed neoplastic chondrocytes with abundant chondroid matrix, and there were few myxoid areas where the cellularity and pleomorphism of the neoplastic cells were more prominent. The neoplastic cells were positive for periodic acid-Schiff and were immunohistochemically positive for vimentin and S-100 protein; the matrix was deeply stained for alcian blue and was metachromatic for toluidine blue stain. This tumor might be derived from pluripotent mesenchymal cells in the connective tissue of the liver. To the best of our knowledge, in all mammalians, including humans, this is the first report of extraskeletal chondrosarcoma primarily arising in the liver.