In utero infection by porcine reproductive and respiratory syndrome virus is sufficient to increase susceptibility of piglets to challenge by Streptococcus suis type II

Porcine reproductive and respiratory syndrome (PRRS) consistently elevates the frequency of disease and mortality in young pigs. Many different: secon dary bacterial diseases occur in PRRS virus (PRRSV)-infected pigs. However, to date, establishing a reproducible experimental model of PRRSV infection in weaned pigs, with subsequent clinical disease following secondary bacte rial challenge, has been difficult. PRRSV is frequently isolated during out breaks from weak-born piglets affected by secondary bacterial diseases, Thi s study was performed to investigate the potential role of intrauterine PRR SV infection on piglet susceptibility to secondary bacterial infection. PRR SV-free pregnant sows were intranasally infected at 98 days of gestation wi th PRRSV strain SD 23983. All piglets born to the PRRSV-infected sows were viremic. Piglets were removed from the sows at birth and deprived of colost rum, Piglets from PRRSV-infected and noninfected sows were randomly assigne d to Streptococcus suis challenge or control subgroups. At 5 days of age, p iglets were challenged intranasally with strain MN 87555 of S, suis type IE . Total and differential leukocyte counts were performed on blood samples c ollected at 3 days of age. The numbers of leukocytes, lymphocytes, acid mon ocytes were significantly reduced in the PRRSV-infected piglets. Lesions we re observed in bone marrow, brain, lung, heart, spleen, lymph node, tonsil, and thymus of PRRSV-infected piglets. Thymus/body weight ratios of in uter o PRRSV-infected piglets were significantly reduced compared to those of no n-PRRSV-infected piglets, and thymic lesions were characterized by severe c ortical depletion of thymocytes. Lesions were not observed in piglets born to PRRSV-free sows. Overall, 20 out of 22 piglets in the PRRSV-S. suis dual -infection group died within 1 week after challenge with S. suis (10 of 11 in each of two trials). This contrasts with 1 of 18 piglets in the PRRSV-in fection-only group and 5 of 23 piglets in the S. suis-challenge-only group (1 of 12 in trial 1 and 4 of 11 in trial 2). No piglets died in the uninfec ted control groups. Most of the piglets in the PRRSV-S. suis dual-infection group developed suppurative meningitis. S, suis type II was recovered from their brains and joints. These results indicate that in utero infection by PRRSV makes piglets more susceptible to infection acid disease following c hallenge by S. suis type II. In utero infection by PRRSV may provide a usef ul model to study the interaction between PRRSV and bacterial coinfections in piglets.