Between 1995 and 1998, we designed a series of studies in which we attempted to determine the main routes of transmission involved in the natural infection of pseudorabies virus (PRV) indigenous to free-ranging feral swine (Sus scrofa). Naturally infected feral sows transmitted the infection to uninfected feral boars, with which they had been commingled for a 6-wk period. Pseudorabies virus was isolated from boar preputial swabs, but not from nasal swabs. Three of the same PRV-infected feral sows did not transmit the infection to domestic boars during a 16 wk commingling period, despite the fact that they became pregnant. Feral boars, naturally infected with PRV, transmitted the virus to domestic gilts while penned together during 6 wk. Pseudorabies virus was isolated from vaginal swabs, but not from nasal swabs of gilts, after 2 and 3 wk of commingling. When the same infected boars were commingled with either feral or domestic boars for 13 wk, PRV transmission did not occur. None of the exposed boars developed neutralizing antibodies or yielded virus from their preputial or nasal swabs. Our results indicate that PRV indigenous to feral swine is preferentially transmitted to feral or domestic swine of the opposite sex by the venereal route. This mode of transmission differs from that seen in the natural transmission of PRV prevalent in domestic swine, where contaminated secretions, excretions and aerosols are responsible for the spread of the virus. Based on these results, we feel that as long as feral swine do not come into direct contact with domestic swine, PRV-infected feral swine probably pose only a limited risk to the success of the National Pseudorabies Eradication Program. The fact that PRV is usually transmitted from feral to domestic swine at the time of mating would indicate that the isolation of domestic herds by the use of a ''double fence,'' should be adequate protection against reinfection with PRV.

Free-ranging feral swine (Sus scrofa) are known to be present in at least 32 states of the USA and are continuously expanding their range. Infection with pseudorabies virus (PRV) occurs in feral swine and the primary route of transmission in free-living conditions seems to be venereal. Between 1995 and 1999, naturally infected feral swine and experimentally infected hybrid progeny of feral and domestic swine, were kept in isolation and evaluated for occurrence of latent PRV indigenous to feral swine in sacral and trigeminal ganglia and tonsil. Sacral ganglia were shown, by polymerase chain reaction (PCR) amplification of the thymidine kinase (TK) gene of PRV, to be the most frequent sites of latency of PRV. Nine (56%) of 16 sacral ganglia, seven (44%) of 16 trigeminal ganglia, and five (39%) of 13 tonsils from naturally infected feral swine were positive for PCR amplification of TK sequences of PRV. These tissues were negative for PRV when viral isolation was attempted in Vero cells. DNA sequencing of cloned TK fragments from the sacral ganglia of two feral swine, showed only one nucleotide difference between the two fragments and extensive sequence homology to fragment sequences from various domestic swine PRV strains from China, Northern Ireland, and the USA. The hybrid feral domestic swine, experimentally inoculated with an indigenous feral swine PRV isolate by either the genital or respiratory route, acquired the infection but showed no clinical signs of pseudorabies. Virus inoculated into either the genital or respiratory tract could, at times, be isolated from both these sites. The most common latency sites were the sacral ganglia, regardless of the route and dose of infection in these experimentally infected hybrids. Nine of 10 sacral ganglia, six of 10 trigeminal ganglia, and three of 10 tonsils were positive for PCR amplification of TK sequences. No virus was isolated from these tissues in Vero cells. The demonstration of the sacral ganglia as the most common sites of latency of pseudorabies viruses indigenous to feral swine, supports the hypothesis that these viruses are primarily transmitted venereally, and not by the respiratory route as is common in domestic swine, in which the trigeminal ganglia are the predominant sites of virus latency.

Fresh beef samples (n = 1,022) obtained from two processing plants in the Midwest (July to December 2003) were analyzed for levels of microbial populations (total aerobic plate count, total coliform count, and Escherichia coli count) and for the presence or absence of E. coli O157:H7 and Salmonella. A fresh beef cut sample was a 360-g composite of 6-g portions excised from the surface of 60 individual representative cuts in a production lot. Samples of fresh beef cuts yielded levels of 4.0 to 6.2, 1.1 to 1.8, and 0.8 to 1.0 log CFU/g for total aerobic plate count, total coliform count, and E. coli count, respectively. There did not appear to be substantial differences or obvious trends in bacterial populations on different cuts. These data may be useful in establishing a baseline or a benchmark of microbiological levels of contamination of beef cuts. Mean incidence rates of E. coli O157:H7 and Salmonella on raw beef cuts were 0.3 and 2.2%, respectively. Of the 1,022 samples analyzed, cuts testing positive for E. coli O157:H7 included top sirloin butt (0.9%) and butt, ball tip (2.1%) and for Salmonella included short loins (3.4%), strip loins (9.6%), rib eye roll (0.8%), shoulder clod (3.4%), and clod, top blade (1.8%). These data provide evidence of noticeable incidence of pathogens on whole muscle beef and raise the importance of such contamination on product that may be mechanically tenderized. Levels of total aerobic plate count, total coliform count, and E. coli count did not (P > or = 0.05) appear to be associated with the presence of E. coli O157:H7 and Salmonella on fresh beef cuts. E. O157:H7 was exclusively isolated from cuts derived from the sirloin area of the carcass. Salmonella was exclusively isolated from cuts derived from the chuck, rib, and loin areas of the carcass. Results of this study suggest that contamination of beef cuts may be influenced by the region of the carcass from which they are derived.

Preevisceration carcass washing prior to bung bagging during beef slaughter may allow pooling of wash water in the rectal area and consequent spread of potential pathogens. The objective of this study was to compare protocols for bung bagging after preevisceration washing with an alternative method for bung bagging before preevisceration washing for the potential to spread enterohemorrhagic Escherichia coli, E. coli O157:H7, and Salmonella on carcass surfaces. The study evaluated incidence rates of pathogens in preevisceration wash water (10 ml) samples (n = 120) and on surface (100 cm2) sponge samples (n = 120) in the immediate bung region when bagging occurred before (prewash bagging) and after (postwash bagging) preevisceration washing. Surface sampling from postwash bagging yielded incidence rates of 58.3, 5, and 8.3%, whereas wash water sampling yielded 28.3, 1.7, and 5% for enterohemorrhagic Escherichia coli, E. coli O157:H7, and Salmonella, respectively. Surface sampling from prewash bagging yielded incidence rates of 35, 1.7, and 0%, whereas wash water sampling yielded 18.3, 0, and 8.3% for enterohemorrhagic Escherichia coli, E. coli O157:H7, and Salmonella, respectively. Results of this research indicate that the rectal area is a significant source of pathogen contamination on carcasses and that wash water is an important mechanism for potential transfer of pathogen contamination from the rectal area. Results from this study suggest that bung bagging, as proposed in this study, before (prewash bagging) rather than after (postwash bagging) preevisceration washing was generally more effective in controlling pathogen contamination and potential spread from the rectal area of carcasses.

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