The Postulated Role of Feeder Swine in the Perpetuation of the Transmissible Gastroenteritis Virus M. Morin, R. F. Solorzano, L. G. Morehouse and L. D. Olson* ABSTRACT
pally on the transmission of the virus on a continuous basis from the feces of recently infected pigs to susceptible pigs. Clinical signs of transmissible gastroenteritis in such pigs are difficult to recognize or absent and this contributes to the importance of the reservoir in the field.
Clinical, immunofluorescence and histopathological observations were found to be an efficient approach for the confirmation of a diagnosis of transmissible gastroenteritis in feeder swine. Two field cases are reported to exemplify how feeder swine exposed to points of concentration such as holding areas, sales barns and auctions can play an important role in the epizootiology of transmissible gastroRASUMM enteritis. A third field case is reported as an example of an outbreak of transmissible gasLes signes cliniques, l'epreuve d'immunotroenteritis beginning in feeder swine and fluorescence et l'histopathologie se sont averes then spreading to baby pigs on the farm. All autant de moyens efficaces pour confirmer un baby pigs died that were born during the acute diagnostic de gastro-enterite transmissible, phase of the outbreak in the feeder swine. chez des porcs a l'engraissement. Baby pigs born shortly after the clinical signs On rapporte deux cas naturels de la malahad abated in the herd, and from sows that die, lesquels demontrent comment des pores 'a had been exposed orally to virulent transmis- l'engraissement qui sejournent dans des points sible gastroenteritis virus and vaccinated with de concentration tels que les locaux de transit a commercial transmissible gastroenteritis ou d'encans, peuvent jouer un role important vaccine ten days before farrowing, survived. dans l'epizootiologle de la gastro-entdrite This was explained by a combination of a de- transmissible. On rapporte un autre cas natucrease in the amount of virus shed in the en- rel, 'a titre d'exemple d'une eclosion de gastrovironment and the immunity induced in the enterite transmissible qui debuta chez les sows. porcs ai l'engraissement d'une porcherie, pour These observations of field outbreaks of ensuite se propager aux porcelets de la matertransmissible gastroenteritis combined with nite. Tous les porcelets qui naquirent au cours recently reported experimental studies lend de la phase aigue de la maladie, chez les pores strong support to the hypothesis of a reservoir a l'engraissement, moururent de gastro-entefor transmissible gastroenteritis virus in feed- rite transmissible. Par contre, ceux qui naquier pigs. This reservoir would be based princi- rent apres l'attenuation des signes cliniques de la maladie, chez les porcs 'a l'engraissement, et dont les meres avaient recu, par la voie buc*Department of Veterinary Pathology (Morin, More- cale, une souche virulente du virus de la gashouse and Olson) and Department of Veterinary Mitro-enterite transmissible, ou auxquelles on crobiology (Solorzano), College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri. avait administre un vaccin commercial contre Present address of M. Morin: Departement de Patholovie et Microbiologie, Faculto de Medecine veterinaire la gastro-enterite transmissible, dix jours avant de l'Universite de Montrdal, Saint-Hyacinthe, Quebec leur parturition, survecurent. Une telle protecJ2S 7C6. Contribution from the Missouri Agriculture Experiment tion resultait 'a la fois d'une diminution de Station, Journal Series No. 7295. Supported in part by l'excretion du virus de la gastro-enterite a fellowship from the Canadian Medical Research Council, National Research Building, M-58, Montreal transmissible dans 1'environnement et de l'imRoad, Ottawa, Canada. munit6 suscitee che; les truies. Submitted December 12, 1975. L'observation de telles eclosions naturelles
Volume 42
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October, 1978
379
de la gastro-enterite transmissible, jointe aux recentes etudes experimentales, tend a appuyer l'hypothese d'un reservoir du virus de la maladie, chez les porcs a l'engraissement. Ce reservoir resulterait principalement de la transmission du virus 'a d'autres porcs susceptibles, sur une base continue, 'a partir de feces de porcs infectes depuis peu. Les signes cliniques de la gastro-enterite transmissible sont difficiles a reconnaitre ou inapparents, chez de tels sujets; cette particularite augmente l'importance du reservoir qu'ils representent dans les porcheries.
INTRODUCTION Transmissible gastroenteritis (TGE), as first described by Doyle and Hutchings (3), is a highly contagious viral disease affecting pigs of all ages but causing severe death losses only in baby pigs under two
weeks old. Since baby pigs are not generally transported, a major question has arisen as to what constitutes the reservoir for maintaining the virus between epizootics and during the summer months when the disease subsides. Clinical signs of TGE are frequently observed in feeder swine and according to some workers (1, 4, 5) a typical TGE epizootic often begins in the older swine and then spreads to baby pigs and sows in the farrowing house. The paper reports three field cases of TGE involving feeder pigs and discusses the role of these pigs in perpetuation of the viirus in relation to previous experimental results (9, 10, 11, 13).
MATERIALS AND METHODS Three cases are reported. In each case, TGE was confirmed after necropsy by the following methods: 1) Several specimens obtained from different areas of the jejunum were fixed in 10% neutral buffered formalin and used for search of lesions of TGE after standard histological processing and staining. 2) Three specimens ob-
380
tamned at different levels of the jejunum were frozen rapidly at -70°C and used for the detection of TGE virus by the fluorescent antibody tissue section technique (FATS) as already described (9, 10). 3) Villous atrophy was detected by gross and subgross examination of the jejunal mucosa.
RESULTS Case 1 - The initial history revealed that the two pigs with severe diarrhea were from a group where morbidity was about 100% but none had died. The disease apparently had been in the herd for at least six weeks. The owner related that the pigs were usually sick for one week and then slowly recovered. They were not responding to antibiotic therapy. tThere were no sows or suckling pigs on the premises. The pigs submitted were in good condition despite the diarrhea and were only slightly dehydrated. The stomachs were filled with grain concentrate and the small intestines were atonic and distended with a watery material. The jejunal villi appeared atrophic on subgross examination. Histopathological examinations revealed a severe and extensive villous atrophy. Most of the cells covering the atrophic villi were cuboidal in shape (Fig. 1). Transmissible gastroenteritis viral antigen was detected by FATS in a few cuboidal cells lining atrophic villi of midjejunal samples (Fig. 2). During a field trip the location of this outbreak was found to be a point of concentration where pigs from many sources were held to await orders for feeder pigs. These pigs usually were brought to this holding point when eight to ten weeks of age and were assembled in a large holding house, sometimes for as long as two weeks before they were sold as feeders. The buildings was never depopulated and pigs were departing and arriving on a continuing basis. At the time of the visit, there were more than 1,200 pigs housed in this building, which was 180 feet long by 30 feet deep and divided into 12 pens of approximately 15 feet in width. These pigs had been gathered from at least 30 different farms. Although the full invest-
Can. J. comp. Med.
igation was not made until two weeks after the diagnosis of TGE was confirmed, approximately 10% of the pigs had abnormal stools, varying from soft stools to a profuse yellow diarrhea. Pigs with these clinical signs could be found in every pen. The owner of the enterprise stated he had two more of these holding areas in other parts of the state and both had a similar problem.
kg:
Fig. 1. Jejunum of feeder swine in atrophic stage of TGE. Marked villous atrophy and replacement of columnar absorptive cells by cuboidal cells. H & E stain. x80.
Fig. 2. Fluorescent antibody stained section from jejunum of feeder swine in atrophic stage of TGE. Only a few cuboidal cells lining atrophic villi are infected (arrows). x40.
Volume 42
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October, 1978
Casei - In Decem-ber 1971, a farmer who raised and sold feeder pigs returned four pigs to his farm that had been rejected at a sale. They started scouring the next day. Four days later a number of the feeder pigs on the farm were scouring. The disease apparently had spread to the farrowing house since sows and their baby pigs were vomiting and had diarrhea. Mortality was high in the baby pigs. Two pigs (nine and 12 weeks old) were submitted for necropsy. The gross, subgross and histopathological findings were similar to those reported for the first case. A tentative diagnosis of TGE was made and this was confirmed by demonstration of TGE viral antigen in their small intestines by FATS. Case 3 - In February 1971, a severe yellow diarrhea was observed in eight feeder pigs in one row of pens at the University of Missouri Experimental Swine Farm facility. Since a number of sows were due to farrow on the same premises and TGE was considered a possibility, two eight month old pigs were killed and necropsied. Villous atrophy was detected in the jejunum by histopathological examination and TGE viral antigen was demonstrated in the cytoplasm of several epithelial cells covering villi which appeared almost normal in length (Fig. 3). In areas where villi were atrophic and covered by cuboidal cells, only i small number of cells contained virus detected by immunofluorescence techniques. Five days after the epizootic began all feeder swine in the same row of pens had diarrhea. The following day diarrhea had abated in the pigs where TGE was first diagnosed. However, pigs began scouring in a row of pens around the corner from where the disease outbreak had started. A week later the disease had spread to the farrowing house where mortality was 100% among baby pigs born between March 3 and March 9. Transmissible gastroenteritis
381
DISCUSSION
#,k
":.
r
Fig. 3. Fluorescent antibody stained section from jejunum of feeder swine in degenerative stage of TGE. Large numbers of columnar absorptive cells are infected. x250.
was confirmed in these pigs by histopathological and immunofluorescence examinations. On March 5, all pregnant sows were vaccinated with a commercial TGE vaccine.' On March 8, the attending veterinarian fed intestines from baby pigs which had died from the disease to the sows. This material had been frozen at -70°C for this purpose. On March 15, all signs of TGE in the herd had abated. There were no further losses on the subsequent farrowings which began
March 20. The source of the virus in this outbreak was not known. However, in the month prior to the outbreak two new boars obtained from an area where TGE was enzootic were added to the herd. 1TGE-Vac,
382
Diamond Laboratories, Ames, Iowa.
Our experience suggests that a combination of immunofluorescence and histopathological examination is a good method for confirming a diagnosis of TGE in feeder swine. It is sometimes difficult to demonstrate TGE viral antigen in the intestine of these pigs by the FATS when there is severe and extensive villous atrophy in the intestinal specimens examined. This may be due to the resistance to TGE virus infection of the newly produced epithelial cells lining the atrophic villi (9, 10, 14). The FATS works well when the intestinal specimens examined are either in the degenerative or regenerative stages of the disease (9, 10, 11, 14). In the degenerative stage, a large number of absorptive cells are positive but typical histological lesions of TGE are not always evident. In the regenerative stage of the disease epithelial cells covering the atrophic villi are undergoing progressive differentiation to columnar cells and this is followed by a progressive regrowth of the villi. Some of these differentiating cells also can support virus growth in their cytoplasm. It is possible to find these variations and even normal areas in different portions of the jejunum of any infected feeder pig. This phenomenon might be explained by a slower development and progession of TGE lesions in pigs of this age as compared to young pigs (9, 11). For this reason, a representative sampling is very important to obtain good results when the FATS and histopathology are used to confirm a TGE diagnosis in feeder swine. Serological tests performed on serum samples collected during the acute phase of the disease and one or two weeks after recovery would be another good means to confirm a TGE diagnosis in feeder pigs (10). Case 1 illustrates how TGE virus could be maintained over the summer when the number of epizootics is low and how the disease could be disseminated from a collecting point. The most important factor for the maintenance of TGE infection in this operation for several weeks was the continued addition of susceptible feeder pigs to premises. The only means by which this particular outbreak was controlled and further outbreaks prevented was through depopulation and thereafter by keeping pigs in the holding area for only a short
Can. J. comp. Med.
period of time (24 to 48 hours). This method seemed to prevent further TGE problems in this operation but it would not assure that pigs could not come in contact with TGE during their short stay there and become sick or shed virus later. We have reported previously that some feeder pigs exposed to TGE virus can support a mild, focal growth of the virus in their jejunum and even shed it in their feces up to one week postexposure in the absence of clinical signs of the disease (9, 10). In Case 2 it is shown that the period of contact with infected swine does not need to be long. Case 3 is an example of an outbreak of TGE which started in feeder pigs and then spread to baby pigs on the farm and emphasizes that all baby pigs born during the acute phase of the outbreak in the feeder swine died. Two reasons could explain why baby pigs born shortly after the clinical signs in the herd had abated survived. The amount of TGE virus shed in the environment by infected pigs decreases very significantly immediately after their recovery from the disease (7, 10). The sows vaccinated with the commercial vaccine and exposed orally to virulent TGE virus at least ten days before farrowing, had developed a certain degree of immunity in their colostrum and milk. The combination of these two factors was responsible for the survival of these baby pigs. The importance of feeder swine in the spreading of TGE infection and the role sales barns and auctions can play in the epizootiology of the disease is suggested. It has been reported that about 70% of the feeder swine sold in Illinois in 1970 passed through some place of pig concentration (8). The TGE virus may not become widespread during summer, probably because of its rapid inactivation in the environment by heat and sunlight (6). However, where large numbers of feeder pigs are involved these animals surely play a crucial role in the transmission of TGE. Breeding stock involved in this kind of management also should be considered as important in the spread of the disease. It has also been reported that points of concentration (holding areas, sales barns, auctions) are significant for the spread of other infectious diseases such as swine dysentery, mycoplasmal pneumonia, salmonellosis and atrophic rhinitis (2).
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We have observed that some feeder pigs which recovered from TGE infection were carriers of the virus in their jejunum for a period up to 35 days postinfection (10). The TGE virus infection in the jejunum of these carriers was focal in nature and virus shedding in feces ceased or decreased very significantly immediately after recovery from the disease. Similar findings were reported in younger pigs. However, the presence of virus in the jejunum of some pigs was detected for a period up to 63 days postinfection (7). It was suggested that a nonspecific diarrhea could induce virus shedding by these pigs (7). Some pigs develop mild and transient diarrhea when excited and this could be a factor responsible for the initiation of virus shedding by some carrier pigs which are shipped to another farm or to a concentration point. It is well known that sows sometimes develop clinical signs of TGE just before or immediately after farrowing (5) and this would suggest that hormonal factors or stress at the time of parturition could trigger an increased TGE virus growth in the intestine of a carrier sow, inducing clinical signs of TGE and virus shedding in the feces. These observations of field outbreaks of TGE combined with recently reported experimental studies (9, 10, 11) lend strong support to the hypothesis of a reservoir for TGE virus in feeder pigs. This reservoir would be based principally on the transmission of the virus on a continuous basis from the feces of recently infected pigs to susceptible pigs. Clinical signs of TGE in such pigs are difficult to recognize or absent and this contributes to the importance of the reservoir in the field. Recently, persistent TGE virus infection has been described in swine herds having a continuous source of susceptible pigs to perpetuate the infection (1, 12). These were provided by a continuous farrowing program or by frequent additions of newly purchased feeder pigs. Clinical signs exhibited by baby pigs in these herds were milder in severity than those usually described for TGE and often went unrecognized by practitioners. We can strongly suspect that feeder pigs and immune swine herds on continuous farrowing programs, constitute the reservoir for the maintenance of TGE virus in the swine population, because of the exposure of susceptible pigs on a continuous basis to infective
383
feces. The increase in the number of outbreaks of the severe form of the disease in baby pigs during late fall and winter is probably related to the greater viability of the virus during these seasons (6), which facilitates its introduction in nonimmune herds by mechanical carriers or infected pigs shedding the virus. It would then appear that any control measures considered for this disease should be directed at swine of all ages in order to be successful. They will be difficult to apply because the types of management which favor the maintenance and spreading of the virus in the swine population are widely used.
ACKNOWLEDGMENTS The authors wish to thank Dr. L. D. Kintner and Dr. S. L. Nelson for their help in this study. REFERENCES 1. BOHL, E. H. Transmissible gastroenteritis. In Diseases of Swine. Third Edition. H. W. Dunne, Editor. pp. 158-176. Ames, Iowa: Iowa State University Press. 1970.
384
2. COLTRAIN, J. D. Comments on influence of management and sales on disease dissemination and the need for immunizing agents. J. Am. vet. med. Ass. 160: 506. 1972. S. DOYLE, L. P. and L. M. HUTCHINGS. A transmissible gastroenteritis in pigs. J. Am. vet. med. Ass. 108: 257-259. 1946. 4. FERRIS, D. H. Epizootiologic features of transmissible swine gastroenteritis in pigs. J. Am. vet. med. Ass. 159: 184-194. 1971. 5. GOODWIN, R. F. W. and A. R. JENNINGS. Infectious gastroenteritis of pigs. I. The disease in the field. 3. comp. Path. 69: 87-97. 1959. 6. HAELTERMAN, E. 0. Epidemiological studies of transmissible gastroenteritis of swine. Proc. U.S. Livestock Sanit. Ass. 66: 305-315. 1962. 7. HOOPER, B. E. Comments on the pathogenesis of transmissible gastroenteritis of swine. J. Am. vet. med. Ass. 160: 540-542. 1972. 8. JUDY, J. H. Influence of management and sales on disease dissemination and the need for immunizing agents. J. Am. vet. med. Ass. 160: 502-506. 1972. 9. MORIN, M., L. G. MOREHOUSE, R. F. SOLOKZANO and L. D. OLSON. Transmissible gastroenteritis in feeder swine: Clinical immunofluorescence and histopathological observations. Can. 3. comp. Med. 37: 239-248. 1973. 10. MORIN, M., L. G. MOREHOUSE, R. F. SOLORZANO and L. D. OLSON. Transmissible gastroenteritis in feeder swine: Role of feeder swine in the epizootiologic features. Am. J. vet. Res. 35: 251-255. 1974. 11. MORIN, M. and L. G. MOREHOUSE. Transmissible gastroenteritis in feeder pigs: Observations on the jejunal epithelium of normal feeder pigs and feeder pigs infected with TGE virus. Can. 3. comp. Med. 38: 227-235. 1974. 12. MORIN, M. Enzootic form of transmissible gastroenteritis (TGE) in swine herds. Section K. p. 4. In Proc. 4th Cong. Int. Pig Vet. Soc. Ames, Iowa. 1976. 13. OLSON, L. D. Induction of transmissible gastroenteritis in feeder swine. Am. J. vet. Res. 32: 411417. 1971. 14. PENSAERT, M. B., E. 0. HAELTERMAN and T. BURNSTEIN. Transmissible gastroenteritis of swine: Virus-intestinal cell interactions. I. Immunofluorescence, histopathology and virus production through the course of infection. Arch. ges. Virusforsch. 31: 321-334. 1970.
Can. J. comp. Med.
pally on the transmission of the virus on a continuous basis from the feces of recently infected pigs to susceptible pigs. Clinical signs of transmissible gastroenteritis in such pigs are difficult to recognize or absent and this contributes to the importance of the reservoir in the field.
Clinical, immunofluorescence and histopathological observations were found to be an efficient approach for the confirmation of a diagnosis of transmissible gastroenteritis in feeder swine. Two field cases are reported to exemplify how feeder swine exposed to points of concentration such as holding areas, sales barns and auctions can play an important role in the epizootiology of transmissible gastroRASUMM enteritis. A third field case is reported as an example of an outbreak of transmissible gasLes signes cliniques, l'epreuve d'immunotroenteritis beginning in feeder swine and fluorescence et l'histopathologie se sont averes then spreading to baby pigs on the farm. All autant de moyens efficaces pour confirmer un baby pigs died that were born during the acute diagnostic de gastro-enterite transmissible, phase of the outbreak in the feeder swine. chez des porcs a l'engraissement. Baby pigs born shortly after the clinical signs On rapporte deux cas naturels de la malahad abated in the herd, and from sows that die, lesquels demontrent comment des pores 'a had been exposed orally to virulent transmis- l'engraissement qui sejournent dans des points sible gastroenteritis virus and vaccinated with de concentration tels que les locaux de transit a commercial transmissible gastroenteritis ou d'encans, peuvent jouer un role important vaccine ten days before farrowing, survived. dans l'epizootiologle de la gastro-entdrite This was explained by a combination of a de- transmissible. On rapporte un autre cas natucrease in the amount of virus shed in the en- rel, 'a titre d'exemple d'une eclosion de gastrovironment and the immunity induced in the enterite transmissible qui debuta chez les sows. porcs ai l'engraissement d'une porcherie, pour These observations of field outbreaks of ensuite se propager aux porcelets de la matertransmissible gastroenteritis combined with nite. Tous les porcelets qui naquirent au cours recently reported experimental studies lend de la phase aigue de la maladie, chez les pores strong support to the hypothesis of a reservoir a l'engraissement, moururent de gastro-entefor transmissible gastroenteritis virus in feed- rite transmissible. Par contre, ceux qui naquier pigs. This reservoir would be based princi- rent apres l'attenuation des signes cliniques de la maladie, chez les porcs 'a l'engraissement, et dont les meres avaient recu, par la voie buc*Department of Veterinary Pathology (Morin, More- cale, une souche virulente du virus de la gashouse and Olson) and Department of Veterinary Mitro-enterite transmissible, ou auxquelles on crobiology (Solorzano), College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri. avait administre un vaccin commercial contre Present address of M. Morin: Departement de Patholovie et Microbiologie, Faculto de Medecine veterinaire la gastro-enterite transmissible, dix jours avant de l'Universite de Montrdal, Saint-Hyacinthe, Quebec leur parturition, survecurent. Une telle protecJ2S 7C6. Contribution from the Missouri Agriculture Experiment tion resultait 'a la fois d'une diminution de Station, Journal Series No. 7295. Supported in part by l'excretion du virus de la gastro-enterite a fellowship from the Canadian Medical Research Council, National Research Building, M-58, Montreal transmissible dans 1'environnement et de l'imRoad, Ottawa, Canada. munit6 suscitee che; les truies. Submitted December 12, 1975. L'observation de telles eclosions naturelles
Volume 42
-
October, 1978
379
de la gastro-enterite transmissible, jointe aux recentes etudes experimentales, tend a appuyer l'hypothese d'un reservoir du virus de la maladie, chez les porcs a l'engraissement. Ce reservoir resulterait principalement de la transmission du virus 'a d'autres porcs susceptibles, sur une base continue, 'a partir de feces de porcs infectes depuis peu. Les signes cliniques de la gastro-enterite transmissible sont difficiles a reconnaitre ou inapparents, chez de tels sujets; cette particularite augmente l'importance du reservoir qu'ils representent dans les porcheries.
INTRODUCTION Transmissible gastroenteritis (TGE), as first described by Doyle and Hutchings (3), is a highly contagious viral disease affecting pigs of all ages but causing severe death losses only in baby pigs under two
weeks old. Since baby pigs are not generally transported, a major question has arisen as to what constitutes the reservoir for maintaining the virus between epizootics and during the summer months when the disease subsides. Clinical signs of TGE are frequently observed in feeder swine and according to some workers (1, 4, 5) a typical TGE epizootic often begins in the older swine and then spreads to baby pigs and sows in the farrowing house. The paper reports three field cases of TGE involving feeder pigs and discusses the role of these pigs in perpetuation of the viirus in relation to previous experimental results (9, 10, 11, 13).
MATERIALS AND METHODS Three cases are reported. In each case, TGE was confirmed after necropsy by the following methods: 1) Several specimens obtained from different areas of the jejunum were fixed in 10% neutral buffered formalin and used for search of lesions of TGE after standard histological processing and staining. 2) Three specimens ob-
380
tamned at different levels of the jejunum were frozen rapidly at -70°C and used for the detection of TGE virus by the fluorescent antibody tissue section technique (FATS) as already described (9, 10). 3) Villous atrophy was detected by gross and subgross examination of the jejunal mucosa.
RESULTS Case 1 - The initial history revealed that the two pigs with severe diarrhea were from a group where morbidity was about 100% but none had died. The disease apparently had been in the herd for at least six weeks. The owner related that the pigs were usually sick for one week and then slowly recovered. They were not responding to antibiotic therapy. tThere were no sows or suckling pigs on the premises. The pigs submitted were in good condition despite the diarrhea and were only slightly dehydrated. The stomachs were filled with grain concentrate and the small intestines were atonic and distended with a watery material. The jejunal villi appeared atrophic on subgross examination. Histopathological examinations revealed a severe and extensive villous atrophy. Most of the cells covering the atrophic villi were cuboidal in shape (Fig. 1). Transmissible gastroenteritis viral antigen was detected by FATS in a few cuboidal cells lining atrophic villi of midjejunal samples (Fig. 2). During a field trip the location of this outbreak was found to be a point of concentration where pigs from many sources were held to await orders for feeder pigs. These pigs usually were brought to this holding point when eight to ten weeks of age and were assembled in a large holding house, sometimes for as long as two weeks before they were sold as feeders. The buildings was never depopulated and pigs were departing and arriving on a continuing basis. At the time of the visit, there were more than 1,200 pigs housed in this building, which was 180 feet long by 30 feet deep and divided into 12 pens of approximately 15 feet in width. These pigs had been gathered from at least 30 different farms. Although the full invest-
Can. J. comp. Med.
igation was not made until two weeks after the diagnosis of TGE was confirmed, approximately 10% of the pigs had abnormal stools, varying from soft stools to a profuse yellow diarrhea. Pigs with these clinical signs could be found in every pen. The owner of the enterprise stated he had two more of these holding areas in other parts of the state and both had a similar problem.
kg:
Fig. 1. Jejunum of feeder swine in atrophic stage of TGE. Marked villous atrophy and replacement of columnar absorptive cells by cuboidal cells. H & E stain. x80.
Fig. 2. Fluorescent antibody stained section from jejunum of feeder swine in atrophic stage of TGE. Only a few cuboidal cells lining atrophic villi are infected (arrows). x40.
Volume 42
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October, 1978
Casei - In Decem-ber 1971, a farmer who raised and sold feeder pigs returned four pigs to his farm that had been rejected at a sale. They started scouring the next day. Four days later a number of the feeder pigs on the farm were scouring. The disease apparently had spread to the farrowing house since sows and their baby pigs were vomiting and had diarrhea. Mortality was high in the baby pigs. Two pigs (nine and 12 weeks old) were submitted for necropsy. The gross, subgross and histopathological findings were similar to those reported for the first case. A tentative diagnosis of TGE was made and this was confirmed by demonstration of TGE viral antigen in their small intestines by FATS. Case 3 - In February 1971, a severe yellow diarrhea was observed in eight feeder pigs in one row of pens at the University of Missouri Experimental Swine Farm facility. Since a number of sows were due to farrow on the same premises and TGE was considered a possibility, two eight month old pigs were killed and necropsied. Villous atrophy was detected in the jejunum by histopathological examination and TGE viral antigen was demonstrated in the cytoplasm of several epithelial cells covering villi which appeared almost normal in length (Fig. 3). In areas where villi were atrophic and covered by cuboidal cells, only i small number of cells contained virus detected by immunofluorescence techniques. Five days after the epizootic began all feeder swine in the same row of pens had diarrhea. The following day diarrhea had abated in the pigs where TGE was first diagnosed. However, pigs began scouring in a row of pens around the corner from where the disease outbreak had started. A week later the disease had spread to the farrowing house where mortality was 100% among baby pigs born between March 3 and March 9. Transmissible gastroenteritis
381
DISCUSSION
#,k
":.
r
Fig. 3. Fluorescent antibody stained section from jejunum of feeder swine in degenerative stage of TGE. Large numbers of columnar absorptive cells are infected. x250.
was confirmed in these pigs by histopathological and immunofluorescence examinations. On March 5, all pregnant sows were vaccinated with a commercial TGE vaccine.' On March 8, the attending veterinarian fed intestines from baby pigs which had died from the disease to the sows. This material had been frozen at -70°C for this purpose. On March 15, all signs of TGE in the herd had abated. There were no further losses on the subsequent farrowings which began
March 20. The source of the virus in this outbreak was not known. However, in the month prior to the outbreak two new boars obtained from an area where TGE was enzootic were added to the herd. 1TGE-Vac,
382
Diamond Laboratories, Ames, Iowa.
Our experience suggests that a combination of immunofluorescence and histopathological examination is a good method for confirming a diagnosis of TGE in feeder swine. It is sometimes difficult to demonstrate TGE viral antigen in the intestine of these pigs by the FATS when there is severe and extensive villous atrophy in the intestinal specimens examined. This may be due to the resistance to TGE virus infection of the newly produced epithelial cells lining the atrophic villi (9, 10, 14). The FATS works well when the intestinal specimens examined are either in the degenerative or regenerative stages of the disease (9, 10, 11, 14). In the degenerative stage, a large number of absorptive cells are positive but typical histological lesions of TGE are not always evident. In the regenerative stage of the disease epithelial cells covering the atrophic villi are undergoing progressive differentiation to columnar cells and this is followed by a progressive regrowth of the villi. Some of these differentiating cells also can support virus growth in their cytoplasm. It is possible to find these variations and even normal areas in different portions of the jejunum of any infected feeder pig. This phenomenon might be explained by a slower development and progession of TGE lesions in pigs of this age as compared to young pigs (9, 11). For this reason, a representative sampling is very important to obtain good results when the FATS and histopathology are used to confirm a TGE diagnosis in feeder swine. Serological tests performed on serum samples collected during the acute phase of the disease and one or two weeks after recovery would be another good means to confirm a TGE diagnosis in feeder pigs (10). Case 1 illustrates how TGE virus could be maintained over the summer when the number of epizootics is low and how the disease could be disseminated from a collecting point. The most important factor for the maintenance of TGE infection in this operation for several weeks was the continued addition of susceptible feeder pigs to premises. The only means by which this particular outbreak was controlled and further outbreaks prevented was through depopulation and thereafter by keeping pigs in the holding area for only a short
Can. J. comp. Med.
period of time (24 to 48 hours). This method seemed to prevent further TGE problems in this operation but it would not assure that pigs could not come in contact with TGE during their short stay there and become sick or shed virus later. We have reported previously that some feeder pigs exposed to TGE virus can support a mild, focal growth of the virus in their jejunum and even shed it in their feces up to one week postexposure in the absence of clinical signs of the disease (9, 10). In Case 2 it is shown that the period of contact with infected swine does not need to be long. Case 3 is an example of an outbreak of TGE which started in feeder pigs and then spread to baby pigs on the farm and emphasizes that all baby pigs born during the acute phase of the outbreak in the feeder swine died. Two reasons could explain why baby pigs born shortly after the clinical signs in the herd had abated survived. The amount of TGE virus shed in the environment by infected pigs decreases very significantly immediately after their recovery from the disease (7, 10). The sows vaccinated with the commercial vaccine and exposed orally to virulent TGE virus at least ten days before farrowing, had developed a certain degree of immunity in their colostrum and milk. The combination of these two factors was responsible for the survival of these baby pigs. The importance of feeder swine in the spreading of TGE infection and the role sales barns and auctions can play in the epizootiology of the disease is suggested. It has been reported that about 70% of the feeder swine sold in Illinois in 1970 passed through some place of pig concentration (8). The TGE virus may not become widespread during summer, probably because of its rapid inactivation in the environment by heat and sunlight (6). However, where large numbers of feeder pigs are involved these animals surely play a crucial role in the transmission of TGE. Breeding stock involved in this kind of management also should be considered as important in the spread of the disease. It has also been reported that points of concentration (holding areas, sales barns, auctions) are significant for the spread of other infectious diseases such as swine dysentery, mycoplasmal pneumonia, salmonellosis and atrophic rhinitis (2).
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We have observed that some feeder pigs which recovered from TGE infection were carriers of the virus in their jejunum for a period up to 35 days postinfection (10). The TGE virus infection in the jejunum of these carriers was focal in nature and virus shedding in feces ceased or decreased very significantly immediately after recovery from the disease. Similar findings were reported in younger pigs. However, the presence of virus in the jejunum of some pigs was detected for a period up to 63 days postinfection (7). It was suggested that a nonspecific diarrhea could induce virus shedding by these pigs (7). Some pigs develop mild and transient diarrhea when excited and this could be a factor responsible for the initiation of virus shedding by some carrier pigs which are shipped to another farm or to a concentration point. It is well known that sows sometimes develop clinical signs of TGE just before or immediately after farrowing (5) and this would suggest that hormonal factors or stress at the time of parturition could trigger an increased TGE virus growth in the intestine of a carrier sow, inducing clinical signs of TGE and virus shedding in the feces. These observations of field outbreaks of TGE combined with recently reported experimental studies (9, 10, 11) lend strong support to the hypothesis of a reservoir for TGE virus in feeder pigs. This reservoir would be based principally on the transmission of the virus on a continuous basis from the feces of recently infected pigs to susceptible pigs. Clinical signs of TGE in such pigs are difficult to recognize or absent and this contributes to the importance of the reservoir in the field. Recently, persistent TGE virus infection has been described in swine herds having a continuous source of susceptible pigs to perpetuate the infection (1, 12). These were provided by a continuous farrowing program or by frequent additions of newly purchased feeder pigs. Clinical signs exhibited by baby pigs in these herds were milder in severity than those usually described for TGE and often went unrecognized by practitioners. We can strongly suspect that feeder pigs and immune swine herds on continuous farrowing programs, constitute the reservoir for the maintenance of TGE virus in the swine population, because of the exposure of susceptible pigs on a continuous basis to infective
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feces. The increase in the number of outbreaks of the severe form of the disease in baby pigs during late fall and winter is probably related to the greater viability of the virus during these seasons (6), which facilitates its introduction in nonimmune herds by mechanical carriers or infected pigs shedding the virus. It would then appear that any control measures considered for this disease should be directed at swine of all ages in order to be successful. They will be difficult to apply because the types of management which favor the maintenance and spreading of the virus in the swine population are widely used.
ACKNOWLEDGMENTS The authors wish to thank Dr. L. D. Kintner and Dr. S. L. Nelson for their help in this study. REFERENCES 1. BOHL, E. H. Transmissible gastroenteritis. In Diseases of Swine. Third Edition. H. W. Dunne, Editor. pp. 158-176. Ames, Iowa: Iowa State University Press. 1970.
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2. COLTRAIN, J. D. Comments on influence of management and sales on disease dissemination and the need for immunizing agents. J. Am. vet. med. Ass. 160: 506. 1972. S. DOYLE, L. P. and L. M. HUTCHINGS. A transmissible gastroenteritis in pigs. J. Am. vet. med. Ass. 108: 257-259. 1946. 4. FERRIS, D. H. Epizootiologic features of transmissible swine gastroenteritis in pigs. J. Am. vet. med. Ass. 159: 184-194. 1971. 5. GOODWIN, R. F. W. and A. R. JENNINGS. Infectious gastroenteritis of pigs. I. The disease in the field. 3. comp. Path. 69: 87-97. 1959. 6. HAELTERMAN, E. 0. Epidemiological studies of transmissible gastroenteritis of swine. Proc. U.S. Livestock Sanit. Ass. 66: 305-315. 1962. 7. HOOPER, B. E. Comments on the pathogenesis of transmissible gastroenteritis of swine. J. Am. vet. med. Ass. 160: 540-542. 1972. 8. JUDY, J. H. Influence of management and sales on disease dissemination and the need for immunizing agents. J. Am. vet. med. Ass. 160: 502-506. 1972. 9. MORIN, M., L. G. MOREHOUSE, R. F. SOLOKZANO and L. D. OLSON. Transmissible gastroenteritis in feeder swine: Clinical immunofluorescence and histopathological observations. Can. 3. comp. Med. 37: 239-248. 1973. 10. MORIN, M., L. G. MOREHOUSE, R. F. SOLORZANO and L. D. OLSON. Transmissible gastroenteritis in feeder swine: Role of feeder swine in the epizootiologic features. Am. J. vet. Res. 35: 251-255. 1974. 11. MORIN, M. and L. G. MOREHOUSE. Transmissible gastroenteritis in feeder pigs: Observations on the jejunal epithelium of normal feeder pigs and feeder pigs infected with TGE virus. Can. 3. comp. Med. 38: 227-235. 1974. 12. MORIN, M. Enzootic form of transmissible gastroenteritis (TGE) in swine herds. Section K. p. 4. In Proc. 4th Cong. Int. Pig Vet. Soc. Ames, Iowa. 1976. 13. OLSON, L. D. Induction of transmissible gastroenteritis in feeder swine. Am. J. vet. Res. 32: 411417. 1971. 14. PENSAERT, M. B., E. 0. HAELTERMAN and T. BURNSTEIN. Transmissible gastroenteritis of swine: Virus-intestinal cell interactions. I. Immunofluorescence, histopathology and virus production through the course of infection. Arch. ges. Virusforsch. 31: 321-334. 1970.
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