title: Birth weight, intrauterine growth retardation and fetal susceptibility to porcine reproductive and respiratory syndrome virus.
abstract: The severity of porcine reproductive and respiratory syndrome was compared in pregnant gilts originating from high and low birth weight litters. One-hundred and eleven pregnant gilts experimentally infected with porcine reproductive and respiratory syndrome virus on gestation day 85 (±1) were necropsied along with their fetuses 21 days later. Ovulation rates and litter size did not differ between groups, but fetuses from low birth weight gilts were shorter, lighter and demonstrated evidence of asymmetric growth with large brain:organ weight ratios (i.e. brain sparing). The number of intrauterine growth retarded fetuses, defined by brain:organ weight ratios greater than 1 standard deviation from the mean, was significantly greater in low, compared to high, birth weight gilts. Although γδ T cells significantly decreased over time in high compared to low birth weight gilts, viral load in serum and tissues, gilt serum cytokine levels, and litter outcome, including the percent dead fetuses per litter, did not differ by birth weight group. Thus, this study provided no substantive evidence that the severity of porcine reproductive and respiratory syndrome is affected by dam birth weight. However, intrauterine growth retarded fetuses had lower viral loads in both fetal thymus and in endometrium adjacent to the umbilical stump. Crown rump length did not significantly differ between fetuses that survived and those that died at least one week prior to termination. Taken together, this study clearly demonstrates that birth weight is a transgenerational trait in pigs, and provides evidence that larger fetuses are more susceptible to transplacental PRRSv infection.
authors.affiliation: Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
authors.forename: Andrea
authors.initials: A
authors.lastname: Ladinig
authors.affiliation: Department of Agricultural, Food, and Nutritional Science, Faculty of Agricultural, Life and Environmental Sciences, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: George
authors.initials: G
authors.lastname: Foxcroft
authors.affiliation: Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
authors.forename: Carolyn
authors.initials: C
authors.lastname: Ashley
authors.affiliation: Animal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, Agricultural Research Service, United States Department of Agriculture, Beltsville, Maryland, United States of America.
authors.forename: Joan K
authors.initials: JK
authors.lastname: Lunney
authors.affiliation: Department of Agricultural, Food, and Nutritional Science, Faculty of Agricultural, Life and Environmental Sciences, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Graham
authors.initials: G
authors.lastname: Plastow
authors.affiliation: Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
authors.forename: John C S
authors.initials: JC
authors.lastname: Harding
mesh_terms: D000818:Animals; D001724:Birth Weight; D005260:Female; D005317:Fetal Growth Retardation / Q000473:pathology / Q000662:veterinary* / Q000821:virology; D005333:Fetus / Q000821:virology; D019318:Porcine Reproductive and Respiratory Syndrome / Q000473:pathology* / Q000821:virology; D019316:Porcine respiratory and reproductive syndrome virus / Q000302:isolation & purification*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000473:pathology / Q000662:veterinary* / Q000821:virology; D013552:Swine / Q000821:virology*