Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/27/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: Salmonella choleraesuis is a bacterial pathogen which causes severe disase in swine. The annual production losses attributed to S. choleraesuis exceed 100 million dollars nationwide. Although S. choleraesuis is the most common Salmonella serotype isolated from swine, it is not frequently found in swine feeds or other nonporcine Salmonella reservoirs. Therefore, the persistently infected (carrier) pig is believed to be an important source of new infections and outbreaks. We studied the natural transmission of S. choleraesuis in swine and determined the effect of natural transmission on the infective dose, carrier state and immune response to this pathogen. One group of pigs was infected with S. choleraesuis, then another group of pigs was commingled with the infected group. We found that the rate of transmission is rapid and the commingled pigs begin shedding S. choleraesuis within 24 h after exposure to the infected pigs. This indicates that a few pigs shedding Salmonella on the way to slaughter could infect a large group of pigs very rapidly. We also found that the amount of S. choleraesuis which is required to cause an infection is much lower in natural pig-to-pig transmission than what has been observed for experimental infection. We observed that the majority of swine which are naturally exposed to S. choleraesuis are able to clear the infection and will no longer carry the bacteria. However, it appears that a small proportion of swine will carry the bacteria for long periods, which adds to the possibility of a new outbreak occurring.
Technical Abstract: This experiment was designed to study the natural transmission of Salmonella choleraesuis in swine. Forty pigs were divided into 3 groups. Group 1 (n=12) was challenged with 10**8 S. choleraesuis by intranasal inoculation. One day postinoculation (PI) group 2 (n=24) was commingled with group 1. Group 3 (n=4) served as uninoculated controls. Serum was collected weekly and blastogenesis assays and necropsies were performed at 1, 2, 4, 6, 9 and 12 wk PI. Environmental levels of S. choleraesuis were 2.61 log10 CFU/g feces at 24 h PI, immediately prior to commingling. Severe clinical signs were observed in groups 1 and 2. Results indicated that at least 16% of group 2 pigs were shedding S. choleraesuis within 24 h after commingling. At 1 wk PI 32/32 group 1 and 39/62 group 2 tissues were positive for S. choleraesuis. Only 3/12 group 2 pigs were positive at 6, 9 and 12 wk, indicating that only a small proportion of infected swine become long-term carriers. At 12 wk PI, only group 2 pigs had positive tissues. Humoral, mucosal and cellular immune responses were similar between groups 1 and 2. These data demonstrate that the rate of natural transmission of S. choleraesuis is rapid. Furthermore, this suggests that a few pigs shedding low levels of Salmonella before slaughter can result in rapid transmission and subsequent shedding by many swine. The data also suggest that under natural conditions the infective dose is much lower than that required for experimental infections and that low levels of Salmonella in the environment can infect naive populations of swine. This provides a dramatic example of the difference between infection with Salmonella grown in the laboratory versus the natural host.