Clinical evaluation of transmissible gastroenteritis virus vaccines and vaccination procedures for inducing lactogenic immunity in sows

Two federally licensed attenuated live transmissible gastroenteritis (TGE) virus vaccines (an IM vaccine and an oral-IM vaccine) and 1 nonlicensed nonattenuated live TGE virus vaccine were evaluated and compared in sows free of TGE virus-neutralizing antibodies. Litters from the sows were challenge exposed at 3 and 5 days of age, and results were combined according to the vaccine administered to the sows. The survivability of pigs suckling sows vaccinated with the nonattenuated vaccine was significantly (P less than 0.01) greater than that of pigs suckling sows vaccinated with the IM attenuated vaccine, significantly (P less than 0.05) greater than that of pigs suckling sows vaccinated with the oral-IM attenuated vaccine, and significantly (P less than 0.05) greater than that of pigs suckling sows that had not been vaccinated. The differences, however, between survivability of litters from sows vaccinated with the IM attenuated vaccine or the oral-IM attenuated vaccine and that of litters from the sows not vaccinated were not significant (P greater than 0.10). The nonattenuated TGE vaccine, although giving a higher level of protection than the attenuated vaccine, was eventually overwhelmed. Dexamethasone did not increase the incidence of diarrhea, and levamisole did not potentiate the lactogenic immunity in sows after given their first dose of the nonattenuated vaccine. Survivability in litters suckling sows that developed diarrhea after given their first dose of the nonattenuated vaccine was not greater than that in litters suckling sows that did not develop diarrhea. The best results were obtained when 3-day-old suckling pigs were challenge exposed with virulent TGE virus.     

Lesions of transmissible gastroenteritis virus infection in experimentally inoculated pigs suckling immunized sows

Intestinal lesions of transmissible gastroenteritis (TGE) virus infection in conventionally reared pigs suckling either nonvaccinated, vaccinated, or previously infected sows were studied by scanning electron microscopy, light microscopy, and immunofluorescent microscopy for TGE viral antigen. Pigs were inoculated with virulent TGE virus when they were 5 or 21 days old and were euthanatized shortly after the onset of diarrhea or 96 hours after inoculation if no diarrhea developed. Pigs inoculated when they were either 5 or 21 days old and suckling nonvaccinated sows developed severe lesions, including swelling and necrosis of enterocytes and severe villus atrophy. Pigs inoculated when they were 5 days old and suckling sows vaccinated with attenuated vaccines developed less-severe villus atrophy, and those suckling sows immunized by exposure to nonattenuated TGE virus developed moderate or no villus atrophy. Pigs inoculated when they were 21 days old and suckling sows vaccinated with attenuated vaccines had severe villus atrophy, whereas those suckling sows immunized by exposure to nonattenuated virus had more-moderate villus lesions. Villus atrophy was inhibited to various degrees in pigs suckling immunized sows, depending in part on the antibody titer in the colostrum and milk.     

Mild transmissible gastroenteritis in pigs suckling vaccinated sows

A strain of transmissible gastroenteritis (TGE) virus of low virulence was isolated from 14-day-old pigs suckling sows vaccinated with an attenuated TGE vaccine. Diarrhea developed in suckling pigs approximately 14 days after farrowing in 4 farrowings; however, none of these pigs died from diarrhea. Diarrhea ceased after the 4th farrowing, when vaccination of sows was discontinued. Experimentally, both the field isolate and the vaccine strain were infective and in some instances lethal for 2-day-old pigs exposed orally; however, neither strain was as virulent as the Purdue strain.     

A double-protease-resistant variant of transmissible gastroenteritis virus and its ability to induce lactogenic immunity

A virus resistant to 2 major intestinal proteases (trypsin and alpha-chymotrypsin) was derived from the attenuated Purdue strain of transmissible gastroenteritis virus. Its enzymatic stability was confirmed, in vitro, by exposure to proteolytic enzymes and to porcine intestinal fluids. Vaccination of 5 seronegative pregnant sows with the variant virus by a series of 2 oral and 1 IM inoculations resulted in high titers of neutralizing antibody in serum and colostrum. The mean antibody titer in milk whey decreased 44-fold within 1 week after parturition. At 3 days of age, the 40 pigs delivered by these sows were challenge exposed orally with virulent transmissible gastroenteritis virus. Pigs nursing the 5 vaccinated sows underwent a relatively mild clinical course of illness. The average mortality of these 40 pigs was 33%. Thirty-six pigs which had been raised by 4 nonvaccinated sows had a more severe illness, greater daily weight loss, and higher mortality (92%).     

Induction of lactogenic immunity to transmissible gastroenteritis virus of swine using an attenuated coronavirus mutant able to survive in the physicochemical environment of the digestive tract.

A transmissible gastroenteritis (TGE) coronavirus mutant (188-SG), selected as attenuated and resistant to acidity and proteases of the digestive tract of adult pigs, was used as vaccine ("Nouzilly strain") in sows to protect suckling piglets against a challenge exposure carried out with a highly virulent TGEV strain. The pregnant sows were immunized once (42-49 days before farrowing) or twice (42-49 and 7-15 days before farrowing) by the oral, intramuscular or conjunctival route with the 188-SG strain. Sows exposed to virulent TGEV in the field and experimentally infected sows (two oral inoculations during pregnancy) were used as positive controls leading to high protection. The neutralizing antibody response to vaccination and/or infection was studied in serum and milk. No protection against mortality was observed in the litters of (1) the nine seronegative, susceptible sows, with piglet mortality of 65/70, (2) the seven once orally vaccinated sows, with mortality of 44/54, (3) the seven sows vaccinated twice by the conjunctival route, with mortality of 55/76. Moderate protection was observed in (1) the eight sows vaccinated intramuscularly twice with piglet mortality of 36/90, (2) the seven orally and intramuscularly vaccinated sows with piglet mortality of 31/51. In of 3 contrast, improved protection was observed in (1) the 10 sows vaccinated twice orally, with piglet mortality of 23/95, (2) the four naturally infected sows with piglet mortality of 6/41, (3) the six sows experimentally infected with virulent TGEV with piglet mortality of 1/59. No correlation was found between neutralizing antibodies titers in serum and milk and protection rate of the piglets. The results indicate that relative protective lactogenic immunity against TGEV is induced only by repeated ingestion of the attenuated 188-SG strain of TGEV.     

Lactogenic immunity to transmissible gastroenteritis (TGE) of swine induced by the attenuated Nouzilly strain of TGE virus: passive protection of piglets and detection of serum and milk antibody classes by ELISA

Piglets of eight sows vaccinated by different routes with the attenuated TGE mutant coronavirus, Nouzilly (N) strain, and piglets from two field seropositive sows were challenged with a virulent TGE strain. On the day of challenge and 10 days after challenge, milk and serum samples from sows were analysed for their level of neutralizing antibodies, total immunoglobulin classes and TGE antibody classes by an ELISA. No direct relationship was seen between the level of protection of the litters and the titres of the different antibody classes on the day of challenge. However, an inverse correlation was seen 10 days after challenge between protection and the level of TGE antibodies.     

Protection against enteric colibacillosis in pigs suckling orally vaccinated dams: evidence for pili as protective antigens

Pregnant gilts were vaccinated orally with Escherichia coli that produced pilus antigens K99 or 987P. The vaccines were live or dead enterotoxigenic E coli (ETEC) or a liver rough non-ETEC strain which has little ability to colonize pig intestine. Pigs born to the gilts were challenge exposed orally with K99+ or 987P+ ETEC, which did not produce heat-labile enterotoxin or flagella and which produced somatic and capsular antigens different from those of the vaccine strains. Control gilts had low titers of serum and colostral antibodies against pilus antigens, and their suckling pigs frequently had fatal diarrhea after challenge exposure. Serum antibody titers against pilus antigens of the vaccine strains increased in the gilts after vaccination with liver ETEC, and the colostral antibody titers of these gilts were higher than those of controls. Pigs suckling such vaccinated gilts were more resistant than controls to challenge strains were of different pilus types, and it could not be attributed to enterotoxin neutralization by colostrum. In contrast to the live ETEC vaccines given to the pregnant gilts, the liver rough non-ETEC and dead ETEC vaccines stimulated little or no production of antibody against pilu, and the pigs born of these vaccinated gilts remained highly susceptible to challenge exposure. The results support the hypothesis that pilu can be protective antigens in oral ETEC vaccines. It was indicated that in the system reported, protection depended on living bacteria for the production of pilus antigens in vivo or for the transport of pilus antigens across intestinal epithelium.     

Efficacy of vaccination of sows with serologically related coronaviruses for control of transmissible gastroenteritis in nursing pigs

Three groups of pregnant sows were vaccinated at 8 and 2 weeks before parturition with tissue culture-adapted feline infectious peritonitis (FIP) virus, porcine transmissible gastroenteritis (TGE) small-plaque (SP) virus from a persistently infected cell line, or noninfected cell culture fluids (controls). Pigs nursing vaccinated sows were orally challenge exposed with virulent TGE virus when they were 1 to 3 days old. The morbidity of the nursing pigs was 48% in the SP-TGE group, 82% in the FIP group, and 93% in the controls. The survival rate among the nursing pigs was 77% in the SP-TGE groups, 48% in the FIP group, and 14% in the controls. Virus-neutralizing antibodies of immunoglobulin A were detected in colostrum and milk of the SP-TGE group, but not in the FIP or control groups.     

A longitudinal study of rotavirus antibody titers in swine in a closed specific pathogen-free herd.

In a newly established closed specific pathogen-free (SPF) swine herd, gilt/sow suckling and weaned pig rotavirus specific antibody titers were followed for three lactations by enzyme-linked immunosorbent assay (ELISA) to gain insight into the dynamics of herd antibody titers to group A rotavirus. Among gilts/sows, serum antirotavirus IgG titers increased during each lactation with a subsequent drop in titer between farrowings. Serum antirotavirus IgM titers declined during each lactation and with subsequent parity. Serum antirotavirus IgA titers remained constant during lactations and among parities. In colostrum and milk, antirotavirus IgA antibody was abundant. Differences in titer were not noticed between gilts and second litter sows but third litter sows had significantly higher titers than the first two groups. Antirotavirus IgG was high in colostrum but nearly nonexistent in milk. This titer did not vary significantly within or among parities. There was a linear regression in the titers of baby pig serum antirotavirus IgG from the post colostral sample through to seven weeks old, after which titer began to increase. No difference in baby pig serum antirotavirus IgG was noted among the three litters. Serum antirotavirus IgA and IgM were undetectable in baby pig sera after 2-3 weeks of age. Coproantibody to rotavirus was sporadically present in pig feces for 2-3 weeks after birth with highest titers in the IgA fraction. We conclude that although it is probable that age resistance of pigs to rotavirus diarrhea occurs, humoral immunity as measured by ELISA rotavirus antibody titers may not be intimately involved in virus clearance since in our studies baby pigs passively received large amounts of antibody but still excreted pathogenic virus. The finding of increasing levels of serum antirotavirus IgG in gilt/sow serum suggest that exposure to antigen of dams occur without significant increases in antirotavirus IgG titers in either colostrum, milk, or baby pig serum.     

Adsorption of colostral antibodies against classical swine fever, persistence of maternal antibodies, and effect on response to vaccination in baby pigs.

OBJECTIVE: To determine kinetics of antibody absorption, persistence of antibody concentrations, and influence of titers on vaccination of baby pigs with a vaccine against classical swine fever (CSF). ANIMALS: 15 sows and their litters. PROCEDURE: Farrowings were supervised. Initial time of suckling was recorded. In the first experiment, blood samples were collected at farrowing, 2 and 4 hours after suckling, and hourly until 10 hours after initial suckling. Samples were assayed for CSF antibodies, using a serum neutralizing (SN) test. A second experiment included 33 baby pigs vaccinated as follows: 10 prior to ingestion of colostrum, 18 between 1 and 4 hours after ingestion of colostrum, and 5 at 12 hours after ingestion of colostrum. Fourteen pigs were vaccinated when 7 weeks old, and 15 pigs were not vaccinated. At 10 weeks of age, pigs were challenge-exposed with virulent CSF virus. Blood samples were collected and assayed for CSF antibodies and p125 antigen and p125 antibodies. RESULTS: CSF antibodies were detected in pigs beginning 2 hours after suckling. Colostral antibodies persisted for > 7 weeks (half-life, 79 days). Vaccination of pigs before suckling provided effective protection from severe disease after challenge-exposure. However, vaccination of neonates with antibody titers was not effective, because 19 of 23 (82%) pigs succumbed after challenge-exposure. All pigs vaccinated when 7 weeks old resisted challenge-exposure, whereas all unvaccinated control pigs succumbed. CONCLUSIONS AND CLINICAL RELEVANCE: Vaccination before ingestion of colostrum conferred good protection against CSF in baby pigs. Vaccination of 7-week-old pigs that had decreasing concentrations of passively acquired antibodies was efficacious.     

Immune response of pregnant cows to bovine rotavirus immunization

Fifteen pregnant Holstein cows were freely assigned to 3 experimental groups (5 cows in each group). Cows in group I were inoculated IM and intramammarily (IMm) with Ohio Agricultural Research and Development Center (OARDC) tissue culture-propagated modified-live Nebraska calf diarrhea bovine rotavirus with added adjuvant (OARDC vaccine-immunized cows). Group II cows were given IM injections of a commercial modified-live rotavirus-coronavirus vaccine (commercial vaccine-immunized cows), and the remaining 5 cows were noninoculated controls (group III). Rotavirus antibody in colostrum and milk was mainly associated with immunoglobulin (Ig)G1, and less so with IgG2, IgA, and IgM, as analyzed by the enzyme-linked immunosorbent assay (ELISA), using monospecific anti-bovine IgG1, IgG2, IgM, and IgA sera. In serum, the rotavirus antibody was distributed almost equally between IgG1 and IgG2. The same relationships appeared in both immunized and nonvaccinated cows. All OARDC vaccine-injected cows had virus-neutralization (VN) and ELISA IgG1 rotavirus antibody titers in serum and mammary secretions at significantly increased levels (at least 100-fold; P less than 0.05) compared with the titers in groups II (commercial vaccine-immunized cows) and III (controls). Serum, colostrum, and milk antibody titers from these latter 2 groups did not differ statistically. The ELISA IgG2, IgA, and IgM rotavirus antibody titers also were significantly greater in mammary secretions from OARDC vaccine-immunized cows than in groups II and III cows. There was a high correlation between ELISA IgG1 and VN rotavirus antibody titers for all samples tested (r = 0.97, P less than 0.001), but ELISA IgG1 antibody titers were consistently higher than VN titers. The ELISA IgG1 and VN antibody titers of milk samples collected from cows 30 days after parturition were higher from the OARDC vaccine-immunized cows (ELISA IgG1, geometric mean titer (GMT) = 3,511; VN GMT = 1,689) than were titers from the group II cows (ELISA IgG1 GMT = 39; VN GMT = 33) or group III cows (ELISA IgG1 GMT = 21; VN GMT = 19). These results indicate that IM plus IMm immunization of pregnant cows, using modified-live bovine rotavirus with added adjuvant, may significantly enhance serum, colostrum, and milk rotavirus antibody titers, whereas IM vaccinal inoculation of pregnant cows with a commercial modified-live rotavirus-coronavirus vaccine may not.     

Colostral transfer of Clostridium perfringens type C beta antitoxin in swine

Nine bred gilts were vaccinated with 2 doses of a Clostridium perfringens type C toxoid at a 5-week interval. Time of vaccination during gestation differed among the gilts. Clostridium perfringens beta antitoxin in colostral samples and in serum samples was titrated in mice. Blood was collected from 2 to 5 neonatal pigs from each dam (total = 32 pigs) when the pigs were 36 to 48 hours old. Antitoxin titers in colostrum were 123 to 4.5 IU/ml, indicating considerable variation in individual responses of the gilts to toxoid. Serum titers of neonatal pigs reflected colostrum titers of their dams. This colostrum-to-serum titer correlation was essentially a straight-line fit by least-squares linear regression analysis, establishing a direct proportional relationship between colostrum titers and serum titers of neonatal pigs. In the dams, a correlation was not found between colostral titers and serum titers of blood samples collected 2 weeks after collection of colostrum.     

Immunity to Escherichia coli in pigs: Antibody Secretion by the Mammary Gland after Intramammary or Intramuscular Vaccination with an E. coli Vaccine

Indirect hemagglutinating antibody titres in individual gland samples of colostrum and milk from 13 sows were measured. Five of the sows were vaccinated via a mammary gland and five by the intramuscular route with a live formalinised Escherichia coli vaccine and three remained as non-vaccinated controls.

Antibody titres were higher in colostral and milk whey from the vaccinated sows than from non-vaccinated groups. The inoculated gland in the group of sows given vaccine by the intramammary route secreted milk containing markedly more antibodies to the vaccine E. coli strain than did the non-vaccinated glands. Milk from the vaccinated gland did not contain higher titres to heterologous E. coli O antigens than milk from non-vaccinated glands. Serum titres were the same or higher than the titres in colostrum from non-vaccinated glands.

     

Protection of the nursing pig against experimentally induced enteric colibacillosis by vaccination of dam with fimbrial antigens of E coli (K88, K99 and 987P)

Pregnant gilts were vaccinated with two doses of alhydrogel adsorbed fimbrial antigens of Escherichia coli (K88ab, K88ac, K99 and 987P) supplemented with beta toxoid of Clostridium perfringens type C. Their piglets, and piglets of nonvaccinated gilts, were subsequently orogastrically challenged with one or other of the four fimbrial types of enteropathogenic E coli. Some of the vaccinated animals were reinjected with a single dose of the vaccine during second gestation and their piglets, and piglets of non-vaccinated sows, were challenged the same way as were litters of gilts. Blood serum and colostra were examined for antibodies to the four fimbrial antigens of E coli and for antitoxin to beta toxin of C perfringens type C. It was found that: (1) a highly significant reduction in mortality and morbidity was achieved in vaccinated litters against all four challenge strains of E coli; (2) excretion of K88ab and K88ac but not of K99 and 987P challenge strains was significantly reduced; (3) revaccination of sows by a single dose of the vaccine during second gestation conferred complete protection against mortality and highly significant protection against morbidity; (4) no correlation was noted between colostral or seroagglutinins to fimbrial antigens of E coli and mortality rates in litters challenged with homologous fimbrial types of E coli, but good correlation was found between colostral precipitins to K88 antigens and mortality rates in litters; (5) antitoxin value in 97 per cent of colostrum of vaccinated sows was 10 iu equivalent of C perfringens type C toxin or more per ml of colostrum.     

Experimental infection of fattening pigs with pseudorabies (Aujeszky's disease) virus: efficacy of attenuated live- and inactivated-virus vaccines in pigs with or without passive immunity

The efficacies of attenuated live- and inactivated-virus vaccines against pseudorabies (PR) in fattening pigs were compared. Pigs born from vaccinated or nonvaccinated sows were vaccinated with one or the other vaccine and were challenge exposed at the end of the fattening period. The particular form of PR observed in fattening units in the field could be reproduced. A marked difference was seen between the control lot and the lots of the pigs vaccinated with the attenuated live- and inactivated-virus vaccines. The protection was real, but not absolute, in the vaccinated pigs. The inactivated-virus vaccine conferred a strong passive immunity to the young pigs of vaccinated dams which interfered with the development of an active immunity. The titer of the colostral antibodies in the sera of pigs born from the sows vaccinated with the attenuated-live virus vaccine was low and decreased rapidly. The active protection obtained with this vaccine was similar to that observed with the inactivated-virus vaccine. Thermal curves, weight losses, and time necessary for recovering the weight of pigs at the time of challenge exposure seemed to be good criteria for measuring the protection of fattening pigs against this particular form of PR. The conditions of the outcome of respiratory tract disorders in these pigs are discussed.     

Immunogenicity in Aujeszky's disease virus structural glycoprotein gVI (gp50) in swine.

Aujeszky's disease virus (ADV) envelope glycoprotein gVI (gp50) was purified from virus-infected Vero cells by ion-exchange and immunoaffinity chromatography and its usefulness as a subunit vaccine was evaluated in active and passive immunization studies. Four-week-old piglets were immunized intramuscularly (IM) with purified gVI twice two weeks apart and challenged intranasally (IN) 10 days after the second immunization with 30 LD50 (10(8)PFU) of a virulent strain of ADV. Pigs, vaccinated with 100 micrograms of purified gVI, produced virus neutralizing antibodies and did not develop clinical signs after challenge exposure. The challenge virus was not isolated from nasal swabs and tonsils of gVI-vaccinated pigs, whereas non-vaccinated control pigs developed illness after challenge exposure with the same virulent ADV strain which was later recovered from their nasal swabs and tonsils. Pregnant sows vaccinated twice with purified gVI (IM) at a three week interval produced virus neutralizing antibodies in colostrum. Four-day-old sucking piglets born of vaccinated sows were passively protected by colostral antibodies against intranasal challenge with a lethal dose of virulent ADV. Sera from gVI-vaccinated pigs were distinguished from experimentally infected swine sera by their differential reactivity in enzyme-linked immunosorbent assay (ELISA) using four major viral glycoproteins (excluding gVI) as antigen purified by the use of lentil-lectin.     

Cross-protection studies between feline infectious peritonitis and porcine transmissible gastroenteritis viruses

Cross-protection studies between the feline infectious peritonitis (FIP) and the porcine transmissible gastroenteritis (TGE) viruses were conducted in cats, pigs and pregnant gilts. Cats vaccinated with TGE virus developed neutralizing antibodies against TGE virus and low titer antibody against FIP virus detected by an indirect fluorescent antibody technique but were not protected against a virulent FIP virus challenge. Baby pigs and pregnant gilts vaccinated with FIP virus did not develop detectable antibodies to TGE virus. Nevertheless, it appeared that vaccination of swine with FIP virus conferred some immunity against TGE virus infection. Seventeen-day-old pigs vaccinated with two doses of FIP virus had a 67% survival rate following a virulent TGE virus challenge, and 75% of the 3-day-old pigs suckling either FIP or TGE-virus-vaccinated gilts survived virulent TGE virus infection in contrast to 0% survival of baby pigs suckling unvaccinated gilts.     

Experimental Immunization of Sows with Cell-cultured TGE Virus

Five sows were inoculated with a cell-cultured, cytopathic strain of the virus of transmissible gastroenteritis (TGE). Two sows were inoculated intramuscularly, and three by the intramammary route. The response was measured by the neutralizing antibody titers in the serum and the milk, and by the protection against experimental challenge of piglets nursing the sows. There were no marked differences in the serum or milk antibody titers resulting after the two methods of inoculation, although milk titers at the time of challenge were higher after intramammary inoculation. Piglets nursing sows inoculated by the intramammary route were protected to a greater extent than those nursing sows inoculated intramuscularly.     

Cell-mediated immune responses of suckling pigs inoculated with attenuated or virulent transmissible gastroenteritis virus

Two litters of suckling pigs seronegative for transmissible gastroenteritis (TGE) virus were orally inoculated with live attenuated (P115) or virulent (M5C) strains of TGE virus. A third seronegative litter (controls) was given cell culture fluids from uninfected cells. Lymphocytes were collected from blood, spleen, mesenteric lymph nodes, and Peyer patches of euthanatized pigs at 0 day and approximately weekly until 26 days after exposure and at approximately 45 days after exposure. Sera were tested for virus-neutralizing antibody titers by use of plaque reduction. Lymphocytes were tested in a lymphocyte proliferation assay for uptake of [3H]thymidine after incubation with the homologous or the heterologous strain of inactivated TGE virus or uninfected cell culture fluids. Only pigs inoculated with virulent TGE virus developed clinical signs of TGE and shed virus. However, all pigs inoculated with TGE virus seroconverted at 6 days after exposure. Responses of lymphocytes from all sources from TGE virus-inoculated pigs peaked between 6 and 14 days after exposure. Pigs inoculated with virulent TGE virus had higher lymphocyte proliferative responses and neutralizing antibody titers than did pigs inoculated with attenuated TGE virus. Cessation of virus shedding coincided with the peak of lymphocyte proliferative responses. The highest responses were with intestinal lymphocytes (mesenteric lymph nodes and Peyer patches) from pigs inoculated with virulent TGE virus. The responses of intestinal lymphocytes from pigs inoculated with attenuated virus were not significantly different from those of pigs inoculated with cell culture fluid. Lymphocytes collected from all sources, except blood from M5C-inoculated pigs, had significantly (P less than 0.05) higher responses to the homologous than to the heterologous TGE virus stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vaccination of pregnant sows against transmissible gastroenteritis with two attenuated virus strains and different inoculation routes

Summary

Two attenuated transmissible gastro‐enteritis (T. G. E.) virus strains were used for vaccination experiments in sows.

Four different experiments were carried out (see Table 1). In each experiment, 9 sows were vaccinated during pregnancy and 3 sows served as controls. They were kept together in one farrowing house. The sows were due to farrow at about the same time. The sows and their litters were challenged shortly after farrowing by exposing 3 piglets of 2 control litters to virulent TGE virus.

The following vaccination schedules were used (see Table 1): twice intramuscularly with TGE‐vac (a commercially available TGE‐vaccine), one oral administration followed by an intramuscular vaccination with an attenuated TGE Purdue (Pu) strain, twice orally with Pu strain in enteric coated capsules, and one direct intra intestinal administration followed by 2 intramuscular vaccinations or 3 intramuscular vaccinations with the Pu strain.

All sows, except most of those treated with enteric coated capsules, seroconverted demonstrably (Table 2). The geometric mean seroneutralization (SN) titer log 2 varied from 4.1 to 7.5 after the first vaccination and from 7.6 to 10 after the second vaccination.

None of the vaccination schedules resulted in an effective lactogenic immunity. The morbidity in the piglets was 100% within 3 to 5 days after challenge. The mortality rate varied from 44 to 80% in litters from vaccinated sows and from 71 to 100% in litters from control sows (see Table 3). Clinical signs were observed in 33,3% of the control sows and in 36% of the vaccinated sows.

No correlation was found between the titer of SN antibodies in the sera of the piglets and their survival rate (Table 4).

A rapid decrease in antibody concentration was observed, during the first week of lactation in milk samples collected from 4 orally and intramuscularly vaccinated sows (Table 5).