Salmonella choleraesuis is a host adapted, facultative intracellular pathogen that causes swine paratyphoid (Wilcock and Schwartz, 1992). In 1990, the National Veterinary Services Laboratory reported that swine salmonellosis exceeded salmonellosis from all other animals in Illinois, Indiana, Iowa, Minnesota and Nebraska (Ferris and Miller, 1990). Salmonella choleraesuis is the most frequent Salmonella serotype recovered from swine (Ferris and Miller, 1990) and was isolated from >95 percent of swine salmonellosis outbreaks in Iowa in 1989 (Schwartz, 1990). The National Animal Health Monitoring Survey estimated that swine salmonellosis is responsible for 28 million dollars in annual production losses in Iowa and 100 million in losses nationwide (Schwartz, 1990).

The carrier state of S. typhimurium in swine has been described (Wood et al. 1989, Wilcock and Olander, 1978). Although S. choleraesuis is the most frequent porcine isolate, it is rarely isolated from swine feeds or non-porcine Salmonella reservoirs. The source of S. choleraesuis seems to be limited to carrier pigs and facilities previously contaminated with this serotype (Wilcock and Schwartz, 1992). The carrier state of S. choleraesuis in swine, including the duration of shedding, location of organisms and immune status, has not been studied (Wilcock and Schwartz, 1992). Lack of information regarding the carrier state of S. choleraesuis in swine has hindered efforts to control the disease.

Recent experiments investigating the carrier state of S. choleraesuis in swine have increased our understanding of this disease. In one experiment the effect of intranasal (IN) or gastric (GC) route of inoculation on the carrier state was studied. Salmonella choleraesuis was recovered from a greater percentage of tissues for the IN vs GC group at two, four, and six weeks postinoculation. No differences between groups were observed at 12 weeks postinoculation. Salmonella choleraesuis was most often recovered from the tonsils, ileal-cecal lymph node, ileal-cecal junction and colon in the subclinical carrier pigs. Both groups shed S. choleraesuis sporadically throughout the 12 week period with the IN group shedding more often and at a higher magnitude. Control pigs remained negative throughout the 12 week experiment. There was not a significant difference in rate of gain between the control and inoculated pigs in the subclinical carrier state. These data show that regardless of route of inoculation, a carrier state is maintained for at least 12 weeks. However, route of inoculation may influence initial levels of environmental contamination which may increase incidence of transmission to naive swine (Gray et al. 1995).

In a second experiment the effect of dose of S. choleraesuis on the carrier state was studied. In this experiment groups 1 (n=5), 2 (n=5) and 3 (n=5) were inoculated intranasally with 109, 106 and 103 CFU of S. choleraesuis, respectively. Group 4 (n=4) served as uninoculated control pigs. Pigs were necropsied at six, 10 or 15 weeks post inoculation (PI). Clinical signs were severe in group 1 and mild in group 2. No clinical signs were observed for group 3. Fecal shedding was dose dependent for groups 1 and 2. Salmonella choleraesuis was not recovered from tonsil, nasal or rectal swabs, fecal samples or tissues of group 3 pigs. For pigs in group 2, fecal shedding continued through week nine PI and the ileocolic lymph node was positive at six weeks PI. Group 1 continued to have positive feces and tissues through 15 weeks. The tonsils of group 1 pigs had the highest numbers of S. choleraesuis at 15 weeks PI (3.16 log10/g). Low serum IgG and IgM titers to S. choleraesuis LPS were observed for group 3 while high serum IgG and IgM titers to LPS and soluble antigen were observed for groups 1 and 2. Lymphocyte blastogenesis assays indicated a proliferative response in groups 1 and 2 in response to S. choleraesuis endotoxin. However, some level of lymphocyte immunosuppression occurred in the group 1 pigs. Control pigs were negative for all parameters. These results indicate that persistence, shedding (duration and magnitude) and immune response is dose dependent. High doses (>109 CFU) result in a long term carrier state (Gray et al. 1994a).

In order to study the natural transmission of S. choleraesuis we hypothesized that pig to pig transmission of S. choleraesuis to naive swine would result in a long term carrier state. Forty pigs were divided into three groups. Group 1 (Chal; n=12) was challenged with 108 S. choleraesuis by intranasal inoculation. One day (PI) group 2 naive pigs (Nav;n=24) were commingled with the Chal pigs. Group 3 (n=4) served as unexposed control pigs. Two pigs from the Chal group and four pigs from the Nav group were necropsied at one two, four, six, nine and 12 weeks PI. One control pig was necropsied at one, four, nine and 12 weeks PI. Pigs from both of the Chal and Nav groups had moderate to severe clinical signs through two weeks PI. The Chal group was shedding 2.42 log10CFU/g feces on the day of commingling. Tonsil, nasal, rectal swabs and group fecal pools collected from individual animals indicated that Nav group pigs were shedding S. choleraesuis one day after commingling. Fecal shedding peaked at 4.5x103 for the Chal group and 3.3x101 for the Nav group on days seven and nine PI, respectively. At one week PI 32/32 Chal group tissues were positive for S. choleraesuis, while 39/62 tissues were positive for the Nav group. At the two week necropsy 26/32 and 29/64 tissues were positive for Chal and Nav groups, respectively. Between four and 12 weeks the number of positive tissues steadily decreased for both groups and at 12 weeks only 2/64 tissues were positive for the Nav group (Table 1). After eight weeks PI shedding could not be detected in either group. The humoral immune response of the Nav swine to S. choleraesuis antigens closely pattern the response of the Chal group. These data indicate that naive swine exposed to swine with acute paratyphoid can be infected with and shed S. choleraesuis within 24 hours of exposure. However, under well managed conditions the level of S. choleraesuis can be significantly reduced in naturally exposed swine (Gray et al. 1994b).

Many Salmonella spp. have been shown to survive well in the environment (Turpin 1993, Muira 1964). Conversely, it is believed that S. choleraesuis does not survive well outside of the host. In order to test the survivability of S. choleraesuis in swine feces six pigs were infected with S. choleraesuis and feces was collected on days two, four, seven and ten post inoculation. The feces was stored in a wet form (6" deep in a bucket water added every 10 days) and a dry form (2" deep spread evenly in a pan and allowed to dry at room temperature). Levels of S. choleraesuis were quantitated by five the tube MPN method (Wood 1992). These data indicate that S. choleraesuis shed from swine can survive in wet feces for at least three months and can survive in a desiccated (dry) form for at least six months. In addition it appears that S. choleraesuis shed from swine prior to seven days post-infection does not survive as well as that shed after seven days post-infection (table 2). This data suggests that passage through the host may affect virulence or survivability of S. choleraesuis. It also indicates that any dried matter may be a reservoir for Salmonella and the removal of all organic matter should be emphasized in cleaning and sanitation management strategies.

Ferris K, Miller DA. Salmonella serotypes from animals and related sources reported during July 1989-June 1990. Proc 94th Annual Meeting of US Anim Health Assoc 1990;492-504.

Gray JT, Fedorka-Cray PJ, Stabel TJ, Ackermann MR, Effect of route on the carrier state of Salmonella choleraesuis in swine. Vet Micro; 1995; (accepted).

Gray JT, Fedorka-Cray PJ, Stabel TJ. Transmission of Salmonella choleraesuis to naive swine. Proc 98th Annual Meeting of US Anim Health Assoc 1994b;431-435.

Gray JT, Fedorka-Cray PJ, Stabel TJ. Effect of dose on persistence of Salmonella choleraesuis in swine. Am J Vet Res 1994b (submitted).

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Schwartz K. Salmonellosis in midwestern swine. Proc 94th Annual Meeting of US Anim Health Assoc 1990:443-449.

Turpin PE, Maycroft KA, Rowlands CL, Wellington EMH Viable but non-culturable salmonellas in soil J Appl Bact 1993; 74:421-427.

Wilcock BP, Schwartz KJ. Salmonellosis. In: Leman AD, Straw BE, Mengeling WE, D’Allaire S, Taylor DJ, eds. Diseases of Swine 7th ed. Iowa State University Press. 1992;570-583.

Wilcock BP, Olander HJ. Influence of oral antibiotic feeding on the duration and severity of clinical disease, growth performance and pattern of shedding in swine inoculated with Salmonella typhimurium. Am J Vet Med Assoc 1978; 172:472-477.

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Week Challenge Naive

1 2a(32/32)b 4(39/64)

2 2(26/32) 4(29/64)

4 2(10/32) 3(8/64)

6 2(15/32) 1(3/64)

9 2(6/32) 1(1/64)

10 0 1(2/64)

a number of positive animals

b number of positive tissues/number of tissues processed

Feces Collected

D2 post-infection D10 post-infection

Time Stored Wet Dry Wet Dry

D0 2.46 2.46 2.59 2.59

D3 1.69 1.69 2.76 2.99

D14 1.32 +a 1.04 2.69

D28 - -b 0.89 -

2 month + - 1.20 +

3 month + - - +

4 month - - - 0.49

5 month - - - 1.45

6 month - - - 0.62

a Positive for S. choleraesuis by enrichment culture

b Negative for S. choleraesuis