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Volume 26 | Issue 2 Article 5 1963 Transmissible Gastroenteritis Jeptha F. Randolph Iowa State University Follow this and additional works at: http://lib.dr.iastate.edu/iowastate_veterinarian Part of the Veterinary Pathology and Pathobiology Commons Recommended Citation Randolph, Jeptha F. (1963) "Transmissible Gastroenteritis," Iowa State University Veterinarian: Vol. 26: Iss. 2, Article 5. Available at: http://lib.dr.iastate.edu/iowastate_veterinarian/vol26/iss2/5 This Article is brought to you for free and open access by the College of Veterinary Medicine at Digital Repository @ Iowa State University. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized administrator of Digital Repository @ Iowa State University. For more information, please contact [email protected]. 17. Justice, W. H.: Serolij!ical titer of cattle vaCcinated for leptospirosls. Vet. Med. 55:67-70, 1960. 18. Kenzy, S. G., Gillespie, W. H., and Ringen, L. M.: Problems in treating and control of leptospirosis. J. Am. Vet. Med. Assoc. 136:253-255, 1960. 19. Kenzy, S. G., Gillespie, B. W., and Lee. J. H.: A comparison of L pomona bacterin and an attenuated live culture vaccine for the control of abortion in cattle. J. of Am. Vet. Med. Assoc. 139:452-454, 1961. 20. Kiesel, G. K.: Elimination of leptospirosis in a herd of cows and heifers. Mod. Vet. PTact. Ref. and Data SeTvice. A-1-12. 21. Kiesel, G. K., and Dacres, W. G.: A study of leptospira pomona bacterm in cattle. COTnell Vet. 49:332-343, 1959. 22. Laurie, L. S.: Vaccination as a means of controlling bovine leptospirosis. Aust. Vet. J. 38: 180-184, 1962. 23. Lingard, D. R., Hansen, L. E.: Effect of .L. pomona on the reproductife efficiency in cattle. J. of Am. Vet. Med. Assoc. 139:449-451, 1960. 24. Mitchell, D., Boulanger, P., Smith, A. N., and Bannister, G. L.: Leptospiral infection with a serotype of the Hebdomadis group. Canadian J. Compo Med. Vet. Sci. 24:229-234, 1960. 25. Morse, E. V.: New concepts of leptospirosis in animals. J. of Am. Vet. Med. Assoc. 136:1960. 26. Paul, R .. Schnunenburger, Tjalma, R. A., Stegmiller, H. E., Wentworth, F. H.: Bovine leptospirosis-a hazard to man. 27. Ringen, L. M.: The detection of leptospiral antigen in bovine urine by means of a hemolytic reaction. J. Immunology. 84:582-585, 1960. 28. Robertson, A., and Boilanger, P.: Immunologic activity of leptospira pomona bacterin. Can. J. Camp. Med. and Vet. Sci. 27:85-90, 1963. 29. Rudy, D. D., Pope, E. P., and Hall, R. E.: The Stoenner plate and agglutination lysis test (in leptospirosis of cattle). Vet. M"d. 54:70·72, 1959. 30. Schuchardt, L. F., Brightenback, G. E., and Prier, J. E.: An improved leptospira pomona bacterin. PTa. 64th Ann. Meet. U. S. Livestock Sanit. Assoc. pp. 49-57, 1961. 31. Schnurrenberger, P. R .. Tjalma, R. A., Stegmiller, H. E., Wentworth, F. H.: Bovine leptospirosis - a hazard to man. J. of Am. Vet. Med. Assoc. 139:884887, 1961. 32. Seibold, H. R., Kuch, H., and Bokelman, D. L.: Histopathologic and serologic study of subclinical leptospirosis among cattle. ]. of Am. Vet. Med. Assoc. 138:424-430, 1961. 33. Sleight, S. D.. and Langham, R. F.: The effect of leptospirosis L. pomona hemolysin on pregnana ewes, cows, and sows. ]. of Am. Vet. Med. Assoc., 1962. 34. Sleight, S. D., and Williams: Transmission of bovine leptospirosis by coition and artificial insemination. ]. of Am. Vet. Med. Assac. 138: 151-152, 1961. 35. Smith, D. L. T.: LePtospirosis in domestic animals: cattle. Vet. News (AlbeTta VMA). 21:18-24. 1959. 36. Stafseth: Leptospirosis, Vet. (MSU). 2:37, 1959. 37. Steele, J. H.: Epidemiology_ of leptospirosis in U.S. and Canada. J. of Am. Vet. Med. Assoc. 136: 247, 1959. 38. Stoenner, H. C'l Hadlow, W. J., Ward, J. K.: Neurologic man festations of a dairy cow from leptospirosis. ]. of Am. Vet. Med. Assoc. 142: 491-493, 1962. 39. Thomas, G. M., Radford, M. A.: Serologic survey of L. pomona infection in Wyoming cattle, ], of Am. Vet. Med. Assoc. 140:684, 1961. 40. Twiehaus, M. J.: Diagnosis of leptospirosis. HaveT·LochhaTt Messenger. 40:36-37, 1960. 41. U. S. Livestock Sanitary A.sociation-Committee on Leptospirosis. Report, U. S. Livestock Sanit. Assoc. Pmc. 63: 140-142, 1969. 42. U. S. Livestock Sanitary Association, E, A. Cabrey: The relative importance of variable factors in the (AL) test. U. S. Livestock Sanit. Assoc. PTOC. 64: 130.142, 1960. 43. U. S. Livestock Sanitary Association, Committee on Leptospirosis. Report, U. S. Livestock Sanit. Assoc. PTOC. 65:520·534, 1961. 44. U. S. Live.stock Sanitary As~ociation. Morter, ~. L., Valentme, B. L., Tapacla, T.: AnaphylaXIS in cattle receiving serum-free leptospira. U. S. Livestoch Sanit. Assoc. Proc. 66: 135-140, 1962. 45. U. S. Livestock Sanitary Association, Committee on Leptospirosis. Report, U. S. Livestock Sanit. Assoc. PToe. 66: 140, 1962. 46. U. S. Livestock Sanitary Association, Kensy, S. G., Gillespie, R. W., Ringen, L. M.: Some aspects of bovine control. U. S. Livestock San it. Assoc. Proe. 66: 150, 1962. 47. U. S. Livestock Sanitary Association, Committee on Leptospirosis. Report, U. S. Livestock Sanit. Assoc. Proc. 67:1962. Transmissible Gastroenteritis Jeptha F. Randolph* INTRODUCTION: The occurence of transmissible gastroenteritis (TGE) appears to be worldwide wherever swine are raised. This disease has been reported in Denmark, ( 17) England, (12, 13, 14) Germany, (20) Japan, (25) Canada, (17, 24) Holland, (17) and the United States. (9) During the early 1930's reports began to appear in the literature regarding a disease condition in baby pigs which caused an extremely high rate of mortality. Since • Mr. Randolph is a senior in the College of Veterinary Madicine at owa State University. Issue, No.2, 1963-64 most deaths occurred on about the third day after birth, the condition was known as "three-day pig disease." (26) In 1937, an outbreak was reported in central Minnesota involving 23 herds of swine where death losses were unusually heavy in pigs less than ten days of age. The etiology was not known but some farmers believed that a toxic product must be present in the sows milk due to the fact that vomition was a fairly constant symptom. (26) The story of TGE as a specific disease entity actually began in 1946 when two veterinarians (9) reported sporadic outbreaks of a disease characterized by diar- 77 rhea, vomiting, rapid loss of weight, and a high death rate in baby pigs. For several years they had observed this disease which limited death losses largely to pigs only a few days old. However, older hogs were observed to be affected also. Some shoats and brood sows showed diarrhea and occasionally vomited. The diarrhea was often quite profuse in older hogs and sometimes was accompanied by considerable loss of weight. Vomiting was observed more frequently in brood sows than in shoats. Recovery was rapid in older animals and death losses were insignificant. The disease seemed to spread rapidly from pig to pig. In a good many cases the disease failed to recur on affected farms, even where sows whose litters had been affected were rebred and produced more litters within the year. In a fewer number of cases, the disease recurred in successive litters. It was observed to occur in both spring and fall farrowing. The disease could be highly fatal to newborn pigs, particularly if large numbers were kept in a small space, as in a central farrowing house. Most deaths occurred when the pigs were between the ages of two days and one week. The disease developed promptly in baby pigs following exposure, either by putting a naturally affected animal in with healthy ones or by putting a naturally affected animal in with healthy ones or by putting portions of the gastrointestinal tract and contents from affected pigs in the mouth of healthy pigs. Per os administration of triturated gastrointestinal tract and contents from infected pigs as well as filtrates of triturated gastro-intestinal tracts were followed by gastroenteritis in baby pigs. From these observations these workers suggested a viral etiology. (9) . In 1949, it was reported (1) that although TGE was probably not the most important cause of baby pig mortality, it had cause losses as high as 80-100 per cent of the pigs farrowed in many instances. Although there were no figures available at that time to indicate the prevalence of the disease or the resulting financial loss, available evidence indicated that its incidence was increasing. The 78 fact that the disease developed follOWing per os exposure with ground tissues of the gastro-intestinal tract, kidney, liver, brain, spleen, and lungs of infected pigs, indicated that the causative agent was widely distributed in the body of the infected animal. Ground gastro-intestinal tract of healthy pigs, when fed, did not cause any disease. This indicated that something other than gastro-intestinal tissue and normal intestinal contents was responsible for the manifestations seen in the disease. Dilutions of gastro-interestinal filtrates as high as 1: 1,000,000 in physiologic saline solution reproduced the disease experimentally. The rapidity with which the disease spread from litter to litter on an infected farm strongly suggested that the minimum infective dose was very small. (1) ETIOLOGY: The etiological agent responsible for TGE is a filterable virus (18) with a particle size of approximately 200mu. (28) The virus in the live pig may persist for 8 weeks or longer. At room temperature or in the presence of germicides, the virus will persist only a few minutes. (27) The virus may remain infective for young pigs after three days drying at 67 to 70 0 F. and will produce TGE after being stored for 314 years at -28 0 C. It is also quite susceptible to pH changes above and below pH 6.2.(5) The incubation period of TGE is very short. Pigs usually show signs at less than 24 hours after experimental exposure. The same is true under natural conditions where it is commonly observed that pigs born in infected quarters sicken on the second day of life. (16, 23) During the acute phase of illness, the virus is found in the blood, liver, spleen, brain, lung, and kidney. The highest concentration of virus is present in the gastro-intestinal tract and kidney. (1, 18) Age of the dam does not appear to be a factor in the etiology of TGE. Evidence also indicates that nutrition, heredity, and environment play only a secondary role in this disease. (29) Iowa State University Veterinarian TRANSMISSION: TGE is usually a very acute and destructive disease which spreads rapidly and involves almost all of the baby pigs in a herd when young pigs are farrowed and housed together. The exact mechanism of transmission of this disease from pig to pig or from herd to herd is not known, but appears to be through the oral ingestion of fecal contaminated material. This disease is highly contagious and appears to be easily carried by many means. One of the most common modes of transmission is probably on the contaminated foot-wear of the herdsman, visitor, or veterinarian. The air-borne route may also be of importance hi situations where central farrowing houses are used. Animals such as dogs and cats which are fed intestines from infected pigs are capable of passing the virus in their stools for up to 2 weeks. (15) Beacuse of their feeding and flocking habits, starlings have been considered as possible vectors. Workers in Ohio revealed that young pigs developed TGE and died after injection of fluids from apparently healthy starlings. (8) Apparently immune sows do not remain carriers of the virus. (3,21) CLINICAL SIGNS: TGE is often considered to be primarily a disease of baby pigs, and it is in this age group that it causes serious death losses; but it may effect swine of all ages. TGE in baby pigs is characterized by vomition, profuse diarrhea, dehydration, weight loss, and high mortality. The onset is usually marked by vomition followed rapidly by profuse and severe diarrhea which is usually yellowish, but may be whitish or greenish and sometimes contains what appears to be unchanged milk curds. Within a day, dehydration becomes evident and the pigs develop a great thirst and, in spite of extreme weakness, will suckle the sow or drink considerable quantities of water if it is available. The pigs become progressively weaker, often develop a shrill squeal, and in the last stages there are usually weak convulsions. Baby pigs which die usually do so within Issue, No.2, 1963-64 2 to 5 days after the onset. Those which recover usually scour for 6 to 9 days. Chances of recovery increase rapidly as age increases. (2,4, 10, IS, 16, 17,26) In mature swine the infection may be inapparent or it may result in a rather alarming disease, particularly in sows which have recently farrowed. Mature animals may vomit, have a profuse watery diarrhea, refuse food and exhibit marked depreSSion, but they almost always recover in a few days and rarely, if ever, die from uncomplicated TGE. TGE is most serious when it occurs in a herd at the time of farrowing. The sows lost interest in living and many of them may completely dry up, refuse food and water, and do not allow their pigs to nurse. (16, 27). Although TGE rarely causes death in sows, recovery may be slow, making their retention in the herd for breeding purposes unprofitable. (21) TGE also occurs in shoats, producing a milder form of gastoenteritis. The usual clinical signs observed are anorexia, diarrhea, and occasionally vomition; however, in mild cases these clinical signs may be unobserved or absent. Death losses are uncommon in shoats and the disease runs its course, quite rapidly. Most animals are back on feed in a day or two, although diarrhea may persist in some as long as a week or ten days.C15, 16) PATHOLOGY The macroscopic lesions of TGE are not constant and frequently not as severe as one might expect. The lesions usually observed are those of gastritis and enteritis. In most naturally occurring cases there is marked gastric hyperemia. Occasionally a few small ulcers occur in the stomach mucosa and some degree of inflammation may be present in either the large or small intestine. The gross lesions vary a great deal depending upon the age of the pigs. In pigs that die at 3 to 4 days of age, an atonic intestine containing very fluid contents varying in color from a whitish to yellowish green may be the most constant fiinding; however, hyperemia of the stomach and intestine is commonly found. Usually the stomach is filled with curdled milk. The kidneys frequently 79 contain urates and show some evidence of degeneration. ( 1,2,9) Petechial hemorrhages have been observed on the kidney, spleen, larynx, bladder, and lymph nodes.(I3) As the pigs become older, the mucosa of the stomach and intestine is often found engorged with blood and frequently areas of necrosis develop. These changes in the stomach and intestine are easily seen from the serous sides of these organs. There is seldom any evidence of free hemorrhage from the mucosa of the stomach or intestine. In most cases, the mesenteric blood vessels· are engorged with blood. The cortex of the kidney is rather light in color, and it is difficult to differentiate the various portions. The medullary rays are often markedly congested and easily seen by the unaided eye. ( 1,2,9) The microscopic lesions are confined mainly to the gastro-intestinal tract and the kidneys. The microscopic changes in the mucosa of the gastro-intestinal tract vary from congestion of the terminal blood vessels to desquamation of epithelium, necrosis, and cellular infiltration. The necropsy of 57 cases of TGE revealed an acute desquamating catarrhal gastroenteritis, often accompanied by superficial necrosis of mucous membranes of the stomach and intestine. This is distinct from gastroenteritis arising from other causes in that clearly defined functional changes in the stomach and intestines are not accompanied by marked morphologic changes in the membranes unless the disease is complicated by secondary infection. This indicates that the virus is apparently eptiheliotropic. (22) In the kidney, albuminous degeneration, congestion of the blood vessels of the cortex and medulla, and desquamation of some tubular epithelium are the most common findings. In pigs dying after prolonged illness, the tubules of the kidneys become dilated and filled with hyaline or granular casts. Lining cells of tubules become flattened, indicating pressure in the tubules. OccaSionally degenerative changes are observed in the nuclei of cells of the convoluted tubules. The blood vessels of the medullary portion 80 of the kidney were observed to be markedly congested and hemorrhage may be seen. Hyperpigmentation and shrinkage of large motor cells in the cerebellum and cerebrum have been observed in a few pigs.(2,I8) It has also been reported that congestion of the meningeal vessels may occur as well as evidence of an encephalitis and marked round cell perivascular cuffing of the cerebral vessels.(I4) Microscopic examination of the heart muscle, adrenal gland, lung, and bladder revealed no significant changes. No inclusion bodies have been demonstrated during extensive microscopic examination of tissues.(2,I8) The blood picture associated with TGE is not very clear at present. It has been reported that all animals show a marked drop in the percentage of lymphocytes and an increase in neutrophils.(lO) Other workers report that a great increase in the percentage of monocytes occurs but no leukopenia was present. (14) Still others described a 49 percent increase in the leukocytes on the fourth day after exposure. The neutrophils increased and the lymphocytes decreased. (16) This increase and change probably indicates a rapid production of neutrophils to meet the demand of the body defenses. The increased number of neutrophils can probably be explained by the gastritis and enteritis that is usually present. The total blood protein and hemoglobin of infected pigs is higher than those of noninfected pigs; this change probably indicates dehydration. Blood glucose varies conSiderably more in infected pigs than in the normal pigs, but there is no definite trend towards a sustained hypoglycemia in spite of the fact that liver glycogen decreases to practically zero. The sustained blood glucose of infected pigs is believed to be largely due to endogenous protein breakdown, which is correlated with higher blood urea and nonprotein nitrogen. Impaired kidney function may also account for the sustained and elevated blood urea and nonprotein nitrogen of infected pigs.(23, 30) TREATMENT: At present there is no successful treat- Iowa State University Veterinarian ment of TGE. This is not surprising considering the viral nature of the disease. Although there is a definite age resistance to the effects of TGE, in natural outbreaks it is frequently observed that older pigs die of the disease or become severely stunted. This is probably the result of secondary bacterial infection, and treatment with antiboitics or sulfonamide drugs might be effective in reducing such losses. There are no effective antiserum or other biQlogical products available at this time mainly because nearly all attempts to grow the virus in tissue cultures,(31) laboratory animals, and embryonated eggs have failed thus far. Good nursing is probably the best treatment, with care being taken to ensure that the pigs recevie good nutrition, are kept warm and dry, and are protected from secondary bacterial invaders. PREVENTION: It appears that proper management and good housing conditions play important roles in the prevention of this disease. All farms where TGE is known to be present should be posted, since it is of utmost importance to prevent transmission of the virus from one farm to another. Therefore, visitors should be excluded from farrowing premises and caretakers should not visit outer premises where hogs are kept without taking proper precautions before returning home to disinfect his foot-wear. A thoughtless walk through a stockyard may cost an owner his entire baby pig crop if proper precautions against carrying the virus on his boots are not taken. If TGE does occur extreme care should be taken to dispose of all dead animals in such a manner that carnivorous animals or birds do not have access to the carcasses. Likewise, extreme caution should be used in bringing new animals into a drove, particularly at farrowing time. If repacement stock must be brought in they should be kept well isolated for a period of 3 to 4 weeks. Sows and gilts which have lost their litters from TGE should be rebred. Experience has shown that the disease rarely recurs on farms where the same breeding stock is kept for subsequent farrowings. However, Issue, No.2, 1963-64 TGE has irregular cyclic tendencies, and recurrence may be expected in some herds.(6) IMMUNITY AND CONTROL: In 1954 it was reported that by deliberate oral exposure of all sows left to farrow in a herd infected with TGE the death loss in their litters was sharply reduced. The mortality decreased rapidly as the time period was increased between exposure and farrowing time.(21) This method of control had been used for several years by this veterinarian and seemed to work best in large herds using an intermittant farrowing system. Other workers reported similar findings and stated that the best results were obtained in sows farrowing 40 days or longer following exposure. (3) The above findings suggest that a degree of immunity results when sows recover from either natural or induced cases of TGE. There is also a trans fer of antibodies through the immune sows' milk to nursing pigs. Therefore, it was believed that if TGE was already in a herd, intentional infection of the sows prior to farrowing might be an effective means of controlling the disease in the young pigs. Feeding of infected material to sows of breeding age will produce an immunity that will be passed on to the pigs after farrowing via the colostrum milk. Such protection will persist for about a year or more.(7,l1) It has been found that gilts infected with TGE as suckling pigs between 17 and 25 days of age do not retain sufficient immunity to protect their litters from challenge afer one year, although there is some prolongation 0 fincubation period and some diminution in death loss not found in control animals. (19) Antibodies absorbed from colostrum through the gut of the newborn animals are considered the important mechanism of transfer of immunity from adult to young in most farm species, including swine. In experiments in which pigs were transferred from immune sows to nonimmune sows and vice versa, it was shown that immunity against TGE transferred from sow to pig is dependent upon a con81 tinuous supply of "immune" milk. Intraperitoneally inoculated anti-TGE serum failed to protect pigs, whereas the same serum afforded protection when fed in the milk, indicating that the important site of action is probably in the lumen or walls of the alimentary tract.(15,19) The subcutaneous or intramuscular injection of infective materials into the sow fails to produce immunity. Gamma globulin from immune serum injected subcutaneously also fails to protect. ( 15) CONCLUSION: Considering the importance of TGE in the swine industry, there has been relatively little research done on this disease, largely because the virus will grow only in cells of living pigs. This means that costly research must be done on individual pigs in individual isolatoin units. Most attempts to grow the virus in tissue cultures, laboratory animals, and embryonated eggs have thus far been unsuccessful. The mechanism of spread of the virus from pig to pig or herd to herd is unknown, but appears to be through the oral ingestion of fecal contaminated material. As little as 1 ml. from an infected animal contains as much as 1 million infective doses. Air-borne transmission may play a role in central farrowing houses. Animals and birds may also prove to be important carriers of the virus. There is no satisfactory treatment of TGE although antibiotics and sulfonamides are often given. Anti-TGE serum given parenterally fails to protect pigs. Good nursing is probably the best treatment, with care being taken to ensure that the pigs receive good nutrition. More research is needs on TGE to produce a practical means of immunization. Since the feeding of infective material to sows at least one month before parturition will establish an immunity which is passed on to the pigs through the milk, and since the important site of antibody action is probably in the lumen or walls of the alimentary tract, it would seem that an oral vaccine would be effective if some means could be found to culture the virus. 82 BIBLIOGRAPHY 1. Bay, W. W., Hutchings, L. M., Doyle, L. P .• Bunnell, D. E.: Transmissible gastroenteritis in baby pigs. J.A.V.M.A. 115:245. 1949. 2. Bay, W. W., Doyle, L. P., Hutchings. L. M.: The pathology and symptomatology of TGE. Am. J. Vet. Res. 12:215. 1951. 3. Ba~ W. W., Doyle. L. P., Hutchings. L. M.: TGE in swine-a study of immunity. J.A.V.M.A. 122:200. 1953. 4. Bay, W. W., Doyle, L. P., Hutchings, L. M.: TGE in swine-a study of immunity. J.A.V.M.A. 120:283. 1952. 5. Bay, W. W., Hutchings, L. M., Doyle, L. P.: Some properties of the causative agent of TGE in swine. Am. J. Vet. Res. 12-13:318. 1952. 6. Bennett, Paul C.: TGE. Florida Vet. Bull. 9: 14. 1952. 7. Burton, A. A.: TGE, TGE, TGE. Mod. Vet. Pract. 43:58. 1962. 8. College of Veterinary Medicine, University of Illinois: Starlings may transmit transmissible gastroenteritis. J.A.V.M.A. 141: 1502. 1962. 9. Doyle, L. P., Hutchings, L. M.: A transmissible gastroenteritis in pigs. J.A.V.M.A. 108:257. 1946. 10. Feenstra, E. S., Thorp, F., Gray, M. L., McMillen, W. W.: Transmissible gastroenteritis of baby pigs. J.A.V.M.A. 113: 573. 1948. 11. Gibbons, W. J.: Control of transmissible gastro~~~~~itis. M.V.P. Reference and Data Library. 12. Goodwin, R. F. W.: A highly infectious disease of pigs in East Anglia. Vet. Record. 70:111. 1958. 13. Goodwin, R. F. W.: A highly infectious gastroenteritis of pigs. Vet. Record. 70:271. 1958. 14. Goodwin, R. F. W., Jennings l A. R.: Infectious gastroenteritis of pIgs. The aisease in the field. J. Compo Path. and Therap. 69:87. 1959. 15. Haeiterman, E. 0.: Present status of TGE. Ill. Vet. 6:35. 1963. 16. Hutchings, L. M.: Enteric diseases of swine. Vet. Scope. 3:6. 1958. 17. Lang, J. A., Edgson, F. A., Goodwin, R. F. W., Grallam, A. M., Christensen, N. 0., Bendixen, H C., Rasbech, N. 0., and Know-Seith, B.: Common problems in the pig. The Vet. Record. 74: 865. 1962. 18. Lee, Kyu M., Moro, Manuel, Baker, J. A.: Transmissible gastroenteritis in pigs. Am. J. Vet. Res. 15:364. 1954. 19. Livestock Res., USDA and Cooperating Agendes, USDA, Washington, D. C.: Transmissible gastroenteritis antibodies absorbed through gut only. J.A.V.M.A. 143:56. 1963. 20. Manninger, R.: Etiology of infectious gastroenteritis in pigs. Dtsch. Tierarztl. Wschr. Tierarztl. Rdsch. 52: 137. 1944. 21. Nelson, J. M.: Control of transmissible gastroenteritis by inoculation with a field culture. J.A.V.M.A. 124:387. 1954. 22. Ponomarenko, F. M.: Pathology of virus gastroenteritis. Veterimariya. 39 :39. 1961. 23. Reber, E. F. and Whitehair, C. K.: The effect of transmissible gastroenteritis on the metabolism of baby pigs. Am. J. Vet. Res. 16: l16. 1955. 24. Roe, C. K. and Alexander, T. J. L.: Gastroenteritis of nursing pigs. Canadian J. Compo Med. 305. 1958. 25 Sa sahara, J., Harada, K., Mayashi, S. and Watanabe, M.: Studies on TGE in pigs in Japan. Jap. J. Vet. Sci. 20: 1. 1958. ·26. Smith, H. C.: Infectious diseases of swine. 72. 1957. 27. Spear, Maynard L.: Diseases of baby pigs. Proc. Third Ann. Florida Conf. Vets. 3:40. 1960. 28. Young, G. A., Hinz, R. W. and Underdahl, N. R.: Gastroenteritis in disease-free, antibody-devoid pigs. Am. J. Vet. Res. 16:529. 1955. 29. Young, G. A. and Underdahl, Norman R.: An epidemiological study of baby pig disease. Cornell Vet. 37-38: 176. 1947. 30. Yusken, J. W., Ho, Pauline, Reber, E. F., and Norton, H. W.: The effects of infecting newborn pigs with transmissible gastroenteritis virus. Am. J. Vet. Res. 20:585. 1959. 31. Lee, K. M. Propagation of transmissible gastroenteritis virus in tissue culture. Ann. N. Y. Acad. Sci. 66: 191-195. 1956. Iowa State University Veterinarian