Pigs can be born as fallbacks, in that they have a lighter birth weight and decreased capacity for postnatal growth. However, pigs with a normal or heavy birth weights can become fallback pigs due to a number of compromising factors, including poor nutrition, environmental conditions, or disease. Only 70% of a pig’s genetic potential for growth is reached when reared in commercial conditions. Disease is thought to be a primary cause of this, because the immune system requires nutrients that could otherwise be available for growth. Pathogen elimination would be the most ideal way to control disease. However, this is often unfeasible in today’s industry. Removing predisposing factors associated with pathogens is often the most practical method to control disease. Fallback pigs may be one of these predisposing factors as they have been thought to harbor pathogens that assault healthy pigs sharing the same space. However, we need to characterize if fallback pigs are, indeed, sources of increased enteric disease within a barn. Therefore, the objectives of this experiment were to: 1) identify the effects of piglet birth weight and transition average daily gain on subsequent growth, mortality, and carcass composition; and 2) determine if light birth weight pigs or those from the bottom 10th percentile of transition ADG in a commercial setting have a greater incidence of disease or gastrointestinal lesions. A total of 1,054 pigs were farrowed at a commercial sow farm, weighed at birth, and tagged individually. At 16 or 17 days of age, 1,054 pigs were weaned and moved to a commercial wean-to-finish barn. Mortalities were recorded on a daily basis. Pigs originated from a PRRSV negative herd, but broke with the disease in week 2 post-weaning. Pigs were weighed individually at weeks 0, 3, 6, and 22 post-weaning. Average daily gain from weeks 0 to 3 post weaning was termed transition ADG. One pig from each of the 10th, 30th, and 70th percentiles was used to create a ‘set’ of three pigs with the same gender, litter size and parity. Forty such sets were created, for a total of 120 pigs. On each of weeks 3 and 22 post-weaning, 20 sets of pigs were necropsied at the Iowa State University Diagnostic Laboratory. Lung, lymph node, and digesta were analyzed for presence of various pathogens, and many organs were scored for lesion incidence or severity by a licensed veterinary pathologist. Birth weight was a good predictor of overall post-weaning growth performance and final weight, except for the period immediately after weaning. However, this lack of effect may have been affected by the PRRSV outbreak diagnosed one week prior. Transition ADG was an excellent predictor of subsequent post-weaning growth and a good predictor of post-weaning mortality. There was a significant birth weight × transition ADG interaction for mortality, where pigs from the 10th percentile of transition ADG and birth weight heavier than 1.51 kg had greater mortality than those with birth weights from 1.26 to 1.50 kg. Transition ADG did not affect carcass composition, but pigs with birth weights heavier than 1.76 had more backfat than all other pigs and larger loin eyes at 22 weeks post-weaning than pigs with birth weights lighter than 1.25 kg. There was no correlation between transition ADG and pathogen presence at either 3- or 22-weeks post-weaning. Incidence and severity of lesions in the large intestine decreased with increasing transition ADG at 3-weeks post-weaning. Lesion incidence and severity were also affected by transition ADG at 22-weeks post-weaning. Birth weight affected Haemolytic E. coli and Salmonella spp. B incidence at 3-weeks post-weaning, as well as Brachyspira spp. incidence at 22-weeks post-weaning. In summary, we determined that birth weight did not affect transition ADG or mortality, but greatly affected subsequent performance. Increasing transition ADG decreased mortality substantially, but did not affect carcass composition. Both birth weight and transition period ADG affect lesions in some organs and Brachyspira spp. infection incidence decrease with increasing birth weight. However, poor transition ADG in pigs is not correlated with disease incidence during a PRRSV outbreak. For more information, contact John Patience at [email protected] or at 515-294-5132.