Porcine reproductive and respiratory syndrome (PRRS) is characterized by reproductive failure in sows and respiratory problems in growing pigs. The disease is present in most countries throughout the world but was not diagnosed in Sweden until the summer of 2007 when it was first detected through the national PRRS surveillance program. The immediate mobilization of veterinary authorities, field veterinarians and the pig industry was a prerequisite for preventing the spread of the disease. Within 10 days seven herds were verified as infected and the measures taken included stamping out, cleaning, disinfection and a vacancy period of 3 weeks before the herds were repopulated. To evaluate the effectiveness of these measures, a national sero-surveillance was carried out during the autumn of 2007. Approximately 90% of the pig production was covered by this screening and all samples tested were negative with regard to antibodies to PRRS virus.
BackgroundRespiratory illness is traditionally regarded as the disease of the growing pig, and has historically mainly been associated to bacterial infections with focus on Mycoplasma hyopneumoniae and Actinobacillus pleuropneumoniae. These bacteria still are of great importance, but continuously increasing herd sizes have complicated the scenario and the influence of secondary invaders may have been increased. The aim of this study was to evaluate the presence of A. pleuropneumoniae and M. hyopneumoniae, as well as that of the secondary invaders Pasteurella multocida and Streptococcus suis by serology in four pig herds (A–D) using age segregated rearing systems with high incidences of pleuritic lesions at slaughter.ResultsPleuritic lesions registered at slaughter ranged from 20.5 to 33.1 % in the four herds. In herd A, the levels of serum antibodies to A. pleuropneumoniae exceeded A450 > 1.5, but not to any other microbe searched for. The seroconversion took place early during the fattening period. Similar levels of serum antibodies to A. pleuropneumoniae were also recorded in herd B, with a subsequent increase in levels of antibodies to P. multocida. Pigs seroconverted to both agents during the early phase of the fattening period. In herd C, pigs seroconverted to P. multocida during the early phase of the fattening period and thereafter to A. pleuropneumoniae. In herd D, the levels of antibodies to P. multocida exceeded A450 > 1.0 in absence (A450 < 0.5) of antibodies to A. pleuropneumoniae. The levels of serum antibodies to M. hyopneumoniae and to S. suis remained below A450 < 1.0 in all four herds. Pigs seroconverted to M. hyopneumoniae late during the rearing period (herd B–D), or not at all (herd A).ConclusionDifferent serological patterns were found in the four herds with high levels of serum antibodies to A. pleuropneumoniae and P. multocida, either alone or in combination with each other. Seroconversion to M. hyopneumoniae late during the rearing period or not at all, confirmed the positive effect of age segregated rearing in preventing or delaying infections with M. hyopneumoniae. The results obtained highlight the necessity of diagnostic investigations to define the true disease pattern in herds with a high incidence of pleuritic lesions.
Background When Salmonella enterica subspecies enterica serovar Choleraesuis (S. Choleraesuis) was detected in faecal samples collected within the Swedish Salmonella surveillance program from a gilt multiplying herd in September 2020, S. Choleraesuis had not been detected in domestic pigs or wild boar in Sweden for over 40 years. This report describes the subsequent investigation, identification of possible entry routes and measures undertaken to eliminate the pathogen from the herd. Case presentation In accordance with Swedish regulations, pig movements to and from the farm were restricted, internal biosecurity measures were enhanced, and a test-and-remove strategy was implemented. Testing included repeated faecal sampling, tissue samplings from all dead or euthanized pigs, and serological sampling of replacement gilts. Epidemiological investigations included scrutinising of production records, employee interviews, analysing feed and environmental samples, faecal samples from the herd’s purebred gilt supplier, and tissue and faecal samples from wild boars in the adjacent area. Testing of in-contact herds receiving gilts (n = 15) or 30-kg pigs (n = 7) from the multiplier included whole-herd faecal sampling and tissue cultures from pigs that died with signs of septicaemia. In total, S. Choleraesuis was detected in 12/4200 faecal and 5/1350 tissue samples from the herd, and the corresponding groups of pigs were euthanized. All feed and environmental samples as well as samples from the gilt supplier were negative. Testing of contact herds resulted in the identification and culling of one group of S. Choleraesuis-positive gilts. Replacement gilts introduced to the herd from January until May 2021 remained serologically negative during a surveillance-period of five months. Conclusion Although speculative, the epidemiological investigation identified indirect transmission from wild boar as possible source of introduction to the herd. Whole-genome sequencing of S. Choleraesuis isolates from wild boar in the area showed that they clustered with isolates from the herd. Repeated testing of the herd indicated that the test-and-remove strategy was successful. In August 2021, all restrictions were removed, and the herd was re-instated as a gilt producing herd. Compensation from the Swedish state to the farmer for production losses, culled animals and extra costs associated with the elimination cost totalled SEK 7 992 234.
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