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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #101568


item Anderson, Robin
item Harvey, Roger
item Stanker, Larry
item Nisbet, David

Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/12/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: The United States swine industry losses millions of dollars each year because of infection of pigs by pathogenic Salmonella bacteria. Pigs infected by Salmonella are typically poor growers and many die. Additionally, meat from infected pigs is unsafe for human consumption. It is not known for sure when most pigs become infected or where they get the pathogen from. Baby pigs are thought to be protected from disease because they drink their mother's milk, which contains antibodies, which can kill the Salmonella. We found however, that while baby pigs didn't get sick, they did become infected and actually turned into carrier animals capable of shedding the Salmonella in their feces for a long time. These baby pigs thus became a source of infection for other pigs not previously exposed to Salmonella. Our results suggest that strategies designed to reduce infection of baby pigs by Salmonella and to reduce shedding of Salmonella by infected pigs would be a good way to prevent the spread of this pathogen to other pigs.

Technical Abstract: Salmonella Choleraesuis(SC) infections account for more than 90% of the United States cases of swine salmonellosis. Salmonellosis caused by SC typically occurs as a post weaning septicemia or enterocolitis and often occurs on operations that commingle pigs of different ages. Spread of this host-adapted serotype throughout modern pig production systems is thought to occur primarily via horizontal transmission, which suggests an important role for asymptomatic carriers. Little has been reported regarding infection of neonatal piglets, particularly regarding their potential to become long term carriers. Evidence reported herein demonstrates that piglets infected at 2 days of age may become carriers. Shedding was most frequent prior to weaning at 14 days of age and for the 7 days immediate post weaning (to 19 days post challenge), with daily incidences (% culture positive) ranging from 58 to 100% and a mean + SD daily incidence of 80 + 12%. The daily incidence of shedding declined thereafter, ranging from 0 to 58 % (mean + SD daily incidence of 16 + 13%) from days 20 to 85 post challenge. Contrary to that expected, commingling of piglets previously separated and hauling of pigs had little effect on incidence of fecal shedding. Upon necropsy 85 days post challenge, SC was recovered from cecal contents of 2 pigs, from spleen and tonsil specimens of 1 and 7 pigs, respectively, but not from colonic contents or lung or ileocolic lymph node specimens of any of the pigs. Our results show that SC can infect neonatal pigs and that these pigs may become long-term carriers capable of shedding the pathogen for up to 87 days of age. This study also presents findings supporting the use of GN-Hajna as a pre- enrichment medium for SC.