Diagnosis of TGE Virus Infection in Swine Herds.

Transmissible gastroenteritis (TGE) virus infection in swine herds in western Canada has been described along with some of the difficulties associated with confirming the diagnosis (1). False negative results on the fluorescent antibody test (FAT) have been described as a problem where animals submitted for examination were past the acute phase of the disease and viral antigen was present in very low levels or absent from intestinal sections. Recently, three farrow-finish swine herds in Alberta were examined for problems related to scours in nursing piglets, high preweaning mortality, or poor production in piglets. The first herd, herd A, had recently gone through a depopulation and clean up and was restocking with minimal disease animals. The original herd had been moved intact to a facility some distance away and the barn had been left empty for six months during the clean up procedure. Minimal disease gilts had been purchased and bred as foster mothers while hysterectomies were performed on the original herd and piglets transferred onto these foster mothers. The foster gilts had been purchased from two separate minimal disease herds and housed together during the gestation period. Hysterectomies and transfer of piglets began in October 1984, and by December 1984, 24 litters had been farrowed or transferred. Of the 24 litters, 14 had diarrhea ranging from mild to severe. Diarrhea started within 24 hours of birth but the mortality rate was less than 10% in piglets. Response to treatment with potentiated sulfonamides was excellent in piglets. Some concern was noted because several sows were sick or vomiting during the first few days postfarrowing. Several piglets in the acute phase of the disease were submitted for postmortem examination and were positive on the FAT for TGE virus infection while corona virus particles were seen on electron microscopy. Because of the significance of the diagnosis to this herd, the sows were bled and sera tested for TGE virus antibodies. No titers were detected in any of the animals in this herd or in the herds supplying foster gilts. The second herd, herd B, is a purebred seedstock operation which has been in operation for a number of years. Diarrhea in piglets preweaning has not been identified as a major concern although gilt litters may occasionally be affected with high litter mortality. A number of piglets were submitted for examination from one such litter and, while histological lesions were mild, positive fluorescence for TGE virus was noted and corona virus particles again seen on electron microscopy. Mature breeding animals from this herd were tested for the presence of TGE virus antibodies but no evidence for infection by the virus was found in any of the samples. The third herd, herd C, is a commercial farrow-finish operation. High death loss in piglets less than one week of age was the presenting complaint. Morbidity was approximately 100% in gilt litters and mortality was 80%. There was no apparent response to treatment in affected piglets. A number of piglets submitted to the laboratory were examined histologically but intestinal lesions were mild or absent. The herd was blood tested at that time and 80% of gilts and sows tested had titers against TGE virus ranging from low to very high. Subsequently, intestinal sections submitted to the laboratory revealed positive fluorescence for TGE virus on the FAT and the presence of corona virus particles in epithelial cells. It would appear that false positive results for TGE virus infection may be seen on FAT and electron microscopic examination. The clinical history of herd A and herd B were not suggestive ofTGE virus infection despite the positive laboratory findings. Herd C, on the other hand, was typical of what is commonly seen in herds infected with TGE virus and this was confirmed by serological testing. At this time, we are not able to identify the agent which was apparently present in herd A and herd B. The potential role of that agent in production of diarrhea in piglets in these herds is unknown as is its antigenic relationship to TGE virus. Further work is proposed to determine the identity of that agent (2). In the interim, we would suggest that a diagnosis of TGE virus infection in a herd cannot be made unless postmortem findings occur with the clinical history and serological testing. The authors wish to acknowledge the assistance of Dr. D. Key, OMAF, Guelph, Ontario and Mr. Bob Norman, Department of Veterinary Microbiology in the serological testing for antibodies. Yours sincerely, S. BAUCK, D.V.M. M.W. STONE, B.Sc., M.R. C.V. S. , Diploma Veterinary Medicine Preventive Medicine Branch Animal Health Division Alberta Agriculture 7000 113 Street Edmonton, A lberta T6H 5 T6