Endemic Porcine Reproductive and Respiratory Syndrome Virus Infection of Nursery Pigs in Two Swine Herds without Current Reproductive Failure (1993)

An outbreak of porcine reproductive and respiratory synbuildings. Far-rowing rooms were managed all-in/all-out, and drome (PRRS), formerly called swine infertility and reproductive syndrome or mystery swine disease, occurred on 18 nursery, tinuous growing, and finishing rooms flow. Pigs were weaned into were managed nursery rooms as conat 3-4 farms in Wabash County, Indiana, in the spring of 1989. weeks of age and moved from nursery rooms to growing An extensive diagnostic investigation conducted at Purdue rooms at 9-10 weeks of age. In April 1989, there was an Animal Disease Diagnostic Laboratory (ADDL) and diagacute outbreak of PRRS. Many sows farrowed prematurely nostic testing at a number of other laboratories did not result in a conclusive etiologic diagnosis. In July 1991, a novel virus (Lelystad virus) was Institute in Lelystad, The isolated at th Netherlands, e Cen from tral Veterinary pigs and sows (days 107-111 of gestation), and most litters were composed of weak live-born pigs, dead pigs. in various stages of in utero autolysis, was high and occasional mummified pigs in suckling and weanling pigs. . The mortality Reproductive rate peron Dutch farms that were experiencing PRRS-like outformance and mortality in suckling pigs returned to prebreaks. Disease typical of PRRS was reproduced by inocPRRS levels within 3 months; however, mortality in nursery ulation of pregnant sows and specific-pathogen-free pigs with pigs remained elevated. Nursery mortality averaged 3.1% for Lelystad virus. Frozen convalescent sera collected from the 11 months before the PRRS outbreak, compared with affected farms during the 1989 PRRS outbreak in Wabash 7.4% for the 34 months (ending January 1992) following the County were among those forwarded by The ADDL to the outbreak (Fig. 1). Since the PRRS outbreak, nursery morCentral Veterinary Institute in July 1991. Antibodies that tality has been cyclic, with 5-6 months of low mortality (3reacted with Lelystad virus in an immunoperoxidase mono5%) followed by 5-6 months of higher mortality (7-16%). layer assay were detected in some of those sera. Highest mortality occurred in winter months. Most pigs died Within 3 months of the onset of the 1989 epizootic of 2-3 weeks after weaning (5-7 weeks of age). Affected pigs PRRS on Wabash County farms, reproductive performance and suckling pig performance returned to pre-PRRS levels; however, continued poor performance of on some farms. An nursery and/or enzootic infecti grower on with Pigs the initially were lethargic then exhibited anorexia and cyanosis of skin on the extremities within 12-24 hours. On day 2 of the illness, days after some onset pigs became dyspneic. Most pigs died 1-3 of clinical signs. Response to multiple inPRRS virus in the nursery and/or grower pigs was suspected tramuscular injections of broad spectrum antibiotics was poor. on these farms. In December 1991, 2 of these farms were Farm 2 was a 1,000-sow far-row-to-finish farm in which selected for further investigation. The goal was to determine all animals were housed in enclosed environmentally reguwhether clinically ill nursery pigs were infected with the PRRS virus. On each farm, the owner and/or herd manager helped lated buildings. ing rooms were Management was managed all-in/all similar to farm 1. Farrowgrowing, -out, and nursery, select 8 “typical” acutely affected nursery pigs. Selected pigs and finishing rooms were managed as continuous flow. An had been clinically ill for <24 hours and were 6-8 weeks old. acute outbreak of PRRS occurred in May 1989, and reproHeparinized blood samples were 4 pigs were euthanized and comp collected from all pigs, and lete necropsy examinations ductive performance returned to pre-PRRS levels in 3 months. Detailed mortality records were not available, but cyclic elevations in outbreak. nursery mortality have continued since the PRRS were performed. PRRS pulmonary macrophage virus isolation in primary cultures was completed on porcine washed buffy coat cells pigs that were from necro all pigs and from psied. Microscopi lung and spleen from c examination of tisNecropsy fi f septicemic o ndings in all 8 pigs from both salmonellosis. Pigs were thin, farms were typical with rough hair sues and laboratory tests for common viral and bacterial coats, and had purple discoloration of skin on the ventral pathogens were completed on selected tissues for all pigs. abdomen and extremities. There was mild to moderate icFarm 1 was a 500-sow farrow-to-finish farm in which all terus and serous atrophy of fat. Lungs failed to collapse comanimals were housed in enclosed environmentally regulated pletely. Cranial ventral lung lobules (20-50%) were purple or tan, firm, and moist, and airways contained white opaque From the Animal Disease Diagnostic Laboratory, Purdue Uniexudate. The remaining caudal dorsal lobules were mottled versity, West Lafayette, IN 47906 (Stevenson, Van Alstine, Kanitz), purple-pink and were slightly firm, yet resilient, suggesting and the Swine Health Center, PO Box 335, Roann, IN 46974 (Kefan interstitial pneumonia. Some livers had 1-2-mm-diamfaber). eter white foci scattered throughout the parenchyma. GasReceived for publication November 12, 1992. trohepatic lymph nodes were enlarged (1.5-2.5 times nor-