Document Type

Thesis - University Access Only

Award Date


Degree Name

Master of Science (MS)

Department / School

Veterinary and Biomedical Sciences


Porcine reproductive and respiratory syndrome (PARS) has emerged as the most economically important swine disease in the United States and many parts of the world. Despite 14 years since the discovery of the causative virus, there are still many unanswered questions on the virology, pathology, immunology and epidemiology of this disease. This study addresses two questions important to understanding the etiology of PARS: 1) what is the minimal infectious dose of virus necessary to result in transmission through artificial insemination? and 2) is tropism for macrophages important in determining the virulence of PARS viruses? To answer the first question, seronegative gilts were artificially inseminated with semen seeded with various concentrations of virus ranging from 2 X 10° to 2 X 106 TCID5o. Results indicated that infection of seronegative gilts by artificial insemination required doses~ 2 X 104 TCIDso, which is 2000-fold higher than reported minimal doses necessary to infect pigs either by the intranasal or intramuscular routes. Thus, transmission through semen requires a higher dose of virus and may not be a frequent means of infection in the field. The objective of the second study was to determine if two isolates serially passaged 83 (P83) and 136 (P136) times on MARC-145 cells and having a reduced ability to replicate on swine alveolar macrophages were less virulent than an earlier passage of virus (P6). These viruses and two commercially attenuated viruses in the RespPRRS and PrimePac PRRS vaccines were intranasally or intramuscularly inoculated into gnotobiotic pigs. Results indicated that the severity of clinical signs; number of animals positive for virus replication; the quantity of virus replication; and the severity of lung lesions were greatest in pigs inoculated with P6>P83> RespPRRS and PrimePac>P136> negative control pigs. Clinical signs and virus replication was also more severe in pigs inoculated intramuscularly rather than intranasally with each of the viruses. Similarly, intranasally inoculated gilts at 90-days gestation with P6 resulted in stillbirths and weak-live born and infected pigs. In contrast, gilts given the P136 farrowed normal litters and healthy pigs with the exception of two pigs from which PRRSV was isolated. Thus, the reduced ability of a PRRS virus to replicate on swine alveolar macrophages results in a reduction in virulence for both young pigs and pregnant gilts. This reduction in virulence also appears to impact the ability of the PRRSV to initially replicate in the upper respiratory tract, but not in target cells reached through intramuscular injection. Thus, replication in alveolar macrophages may be a good indicator of virulence for PRRS viruses and attenuation of PRRSV for growth on these macrophages markedly affects the clinical outcome and pathogenesis of the syndrome.

Library of Congress Subject Headings

Swine -- Virus diseases -- Transmission Swine -- Virus diseases -- Pathogenesis Porcine reproductive and respiratory syndrome



Number of Pages



South Dakota State University