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Volume 26 | Issue 2
Article 5
1963
Transmissible Gastroenteritis
Jeptha F. Randolph
Iowa State University
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Randolph, Jeptha F. (1963) "Transmissible Gastroenteritis," Iowa State University Veterinarian: Vol. 26: Iss. 2, Article 5.
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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