Vaccination Against Porcine Parvovirus Infection

Of 13 gilts 7 were vaccinated twice at an interval of 3 weeks with an inactivated vaccine against porcine parvovirus (PPV) infection, while the 6 nonvaccinated gilts served as controls. Starting after the 1st vaccination the gilts were bred and, after about 40 days of gestation, challenged intravenously with virulent PPV. The vaccinated gilts produced an antibody respons after the 1st and 2nd vaccination compatible with a primary and a secondary immune response, respectively. The nonvaccinated gilts remained low-titered or PPV antibody negative until after challenge. The gilts were killed after about 90 days of gestation, and their litters were examined. All of 53 fetuses from the vaccinated gilts were alive, and infection with PPV could not be demonstrated. Conversely, 50 of 65 fetuses from the non-vaccinated gilts were infected with PPV, and 43 were dead.In a field study comprising 2 herds, PPV seronegative or lowtitered gilts were vaccinated before mating. There were no obvious signs of reproductive disorders in the 2 herds during the vaccination trials, and the reproductive performance of vaccinated gilts did not differ significantly from that of non-vaccinated gilts.     

Development of a vaccine preventing parvovirus-induced reproductive failure in pigs

SUMMARY An inactivated porcine parvovirus (PPV) vaccine for the prevention of PPV-induced reproductive failure in pigs was developed, using virus grown in cell culture, inactivated with beta-propiolactone and adjuvanted with aluminium hydroxide. The vaccine was tested for safety by subcutaneous injection into pregnant gilts. There were no signs of abnormal reactions nor evidence of PPV infection in the gilts or their foetuses when they were sacrificed 6 weeks after vaccination. To demonstrate that the vaccine was immunogenic, pigs were immunised either once or twice with 4 weeks between doses. Resulting antibody titres (haemagglutination inhibition — HAI) ranged from < 8 to 64 (geometric mean of 30) after one dose of vaccine, and from 128 to 512 (geometric mean 256) after two doses. To demonstrate that the vaccine was protective, antibody-negative gilts were vaccinated twice, with 4 weeks between doses, joined after the second dose, and were then infected with virulent PPV 40 to 50 days after joining. In litters from 10 vaccinated gilts, none of 93 foetuses showed evidence of PPV infection. In contrast, in litters from two unvaccinated gilts, all 13 foetuses showed evidence of PPV infection and 10 of these were mummified. The average number of live piglets per litter was 9.2 from vaccinated gilts and 1.5 from unvaccinated gilts. The vaccine was therefore considered to be effective in preventing PPV reproductive failure in susceptible gilts.     

Vaccination of swine with an inactivated porcine parvovirus vaccine in the presence of passive immunity

A study was conducted to determine whether low hemagglutination inhibiting (HI) titers (1:5) for porcine parvovirus (PPV) block the development of immune response to a PPV vaccine. Pigs with low (1:5), medium (1:10 or 1:20), or high (1:40 or 1:80) titers were obtained by IV injections with various amounts of PPV immune serum. Pigs were inoculated with 1 or 2 doses of vaccine and were monitored for serum HI antibodies to PPV. Pigs with low titers responded to vaccine just as well as did the seronegative pigs. The HI titers of pigs with medium titers did not increase after first vaccination. After the second vaccination, however, their titers increased and were similar to those of pigs with low titers. High titers blocked the response to vaccination. The pigs that received 2 doses of vaccine had higher titers than did those of pigs that received 1 dose of vaccine. The results indicated that low titers, which would be expected in gilts at the time of vaccination, do not interfere with immunization by the inactivated PPV vaccine, and that 2 doses of vaccine may provide better and longer lasting immune response to inactivated PPV vaccine and probably longer lasting immunity against PPV-induced reproductive failure.     

Efficacy of an inactivated virus vaccine for prevention of porcine parvovirus-induced reproductive failure.

Gilts vaccinated IM either once (4 gilts) or twice (2 gilts) with an acetylethyleneimine-inactivated porcine parvovirus (PPV) vaccine before they were bred were subsequently exposed intranasally and orally to virulent PPV at about the 40th day of gestation (from 37 to 43 days). At 2 weeks after vaccination, all had hemagglutination-inhibiting (HI) titers for PPV (from 20 to 80) which decreased by the time the immunity was challenged with virulent virus (from 10 to 40), but increased thereafter (from 160 to 1,280). Titers of singly and doubly vaccinated gilts were similar throughout the experiment. The gilts were killed at about the 84th day of gestation (from 80 to 87 days), and their litters were examined. Litters were comprised of 68 live fetuses and 1 dead fetus (7 to 14 fetuses/litter). Neither viral antigen, PPV, nor homologous HI antibody was found in any of the fetuses. In addition, 4 gilts were kept in contact with the vaccinated gilts and were treated similarly except for vaccination. These 4 gilts remained free of HI antibody until after they were exposed to virulent PPV during gestation. At the time the gilts were killed the titers were 1,280 to 2,560. Their litters were comprised of 11 live fetuses and 26 dead fetuses (8 to 11 fetuses/litter). Virus was isolated from fetuses of all litters. Viral antigen was found in 24 of the dead fetuses and 10 of the live fetuses. All infected live fetuses also had HI antibody for PPV. The 2 boars used to breed vaccinated and nonvaccinated gilts (usually each gilt was bred to each of the 2 boars), but not exposed to virulent PPV, remained free of HI antibody for PPV.     

Failure of an inactivated vaccine against porcine reproductive and respiratory syndrome to protect gilts against a heterologous challenge with PRRSV

This study was designed to evaluate the efficacy of an inactivated vaccine based on a European-type strain of porcine reproductive and respiratory syndrome virus (PRRSV) against the reproductive form of the syndrome in breeding gilts, and any congenital disease in their piglets. Five gilts were vaccinated twice, following the manufacturer's instructions, before they were inseminated. Nine additional gilts remained unvaccinated and served as positive (five gilts) and negative (four gilts) controls. A European wild-type strain genetically divergent from the vaccine strain was used to challenge the five vaccinated and five unvaccinated positive control gilts at 90 days' gestation. The vaccination of the five seronegative gilts did not produce any clinical signs or adverse reactions. However, the vaccine failed to prevent the clinical signs associated with PRRSV infection, viraemia after the challenge and transplacental infection of their piglets. The reproductive performance of the vaccinated gilts was similar to that of the unvaccinated positive controls, and there were no statistically significant differences in most of the parameters tested. However, the preweaning mortality of the piglets born to the vaccinated gilts was significantly lower than that of the piglets born to the positive control gilts.     

Parvovirus Antibodies in Vaccinated Gilts in Field Conditions – Results with HI and ELISA tests

This study was conducted to determine the antibody response for porcine parvovirus (PPV) of 39 gilts in field conditions after vaccination. Gilts from four herds endemically infected with PPV were injected twice with a commercial vaccine of inactivated PPV and Erysipelothrix rhusiopathiae. The PPV antibodies were analysed both with haemagglutination inhibition (HI) and enzyme-linked immunosorbent assay (ELISA) in order to study the agreement between these methods. The possible association between high-antibody titres and reproductive failure (repeat breeding, culling for infertility, < or = 6 piglets born alive) was also investigated. In these study herds, endemically infected by PPV, most gilts (84.6%) had not seroconverted by the age of 6 months. On-field vaccination resulted in a consistent increase of humoral immunity not exceeding the antibody level of 1 : 512 in the majority of gilts in all herds examined. The agreement between ELISA and HI tests was moderate (Spearman's rho = 0.87, kappa = 0.63). The seroconversion over the level >1:512 by mid-pregnancy was not associated with reproductive failure.     

Comparative investigations of a combined vaccine against parvovirus and erysipelas and corresponding monovaccines in different vaccination schedules. 1: Field trial]

In a field trial, the development of antibodies of a combined vaccine against the porcine parvovirus (PPV) as well as against swine erysipelas was compared with corresponding mono vaccines. Furthermore, these vaccines were used in different vaccination schedules. The tests were carried out on 109 gilts in three closed farms. In all gilts, a basic immunization repeated twice was carried out at the age of six months and at intervals of three weeks. The revaccination was carried out four months after the basic immunization with half of the animals, and six months after the basic immunization with the remaining gilts. Between the combined vaccine and the mono vaccine no significant differences in the development of antibodies against PPV could be found according to different vaccination schedules. The gilts having been vaccinated with the mono vaccine and boostered six months later showed significantly higher antibody titers against Erysipelothrix rhusiopathiae. Between the remaining vaccination groups no significant difference in the development of the antibodies against swine erysipelas could be found. On only one farm, a continuous decrease of antibody titers against PPV in case of altogether 238 non-vaccinated piglets until the sixth month of life could be observed. On the two other farms, an increase of antibody titers against PPV could be found at different points of time, which indicates an infection of the piglets. Between the individual vaccination groups no significant antibody titers against PPV could be measured in milk tests. With regard to the number of piglets born alive per litter, the number of piglets born dead per litter and the number of mummies, a significant difference could neither be found between the vaccination groups 1-4.     

Antibody responses of guinea-pigs, rabbits and pigs to inactivated porcine parvovirus vaccines

Antibody responses were compared in guinea-pigs, rabbits and pigs following vaccination with inactivated porcine parvovirus (PPV) vaccines. Mean PPV hemagglutination inhibition (HI) antibody titers of 52, 56 and 36 at 1 week after first vaccination and 896, 640 and 512 at 2 weeks after second vaccination were detected in guinea-pigs, rabbits and pigs, respectively. PPV vaccines prepared with greater concentrations of virus, as determined by hemagglutination (HA) units, and of aluminum hydroxide gel adjuvant, induced higher HI antibody titers in guinea-pigs. Optimal concentrations for inducing consistently high antibody titers consisted of vaccine virus with a HA titer of 256/0.1 ml and gel adjuvant at a final concentration of 50%. A second vaccination at 4 weeks compared to 2 or 3 weeks after first vaccination resulted in higher mean HI titers. These data provide preliminary information on the use of guinea-pigs or rabbits as laboratory animal models for testing the potency of PPV vaccines.     

Long-term immunity in cats vaccinated with an inactivated trivalent vaccine.

OBJECTIVE: To evaluate duration of immunity in cats vaccinated with an inactivated vaccine of feline panleukopenia virus (FPV), feline herpesvirus (FHV), and feline calicivirus (FCV). ANIMALS: 17 cats. PROCEDURE: Immunity of 9 vaccinated and 8 unvaccinated cats (of an original 15 vaccinated and 17 unvaccinated cats) was challenged 7.5 years after vaccination. Specific-pathogen-free (SPF) cats were vaccinated at 8 and 12 weeks old and housed in isolation facilities. Offspring of vaccinated cats served as unvaccinated contact control cats. Virus neutralization tests were used to determine antibody titers yearly. Clinical responses were recorded, and titers were determined weekly after viral challenge. RESULTS: Control cats remained free of antibodies against FPV, FHV, and FCV and did not have infection before viral challenge. Vaccinated cats had high FPV titers throughout the study and solid protection against virulent FPV 7.5 years after vaccination. Vaccinated cats were seropositive against FHV and FCV for 3 to 4 years after vaccination, with gradually declining titers. Vaccinated cats were protected partially against viral challenge with virulent FHV. Relative efficacy of the vaccine, on the basis of reduction of clinical signs of disease, was 52%. Results were similar after FCV challenge, with relative efficacy of 63%. Vaccination did not prevent local mild infection or shedding of FHV or FCV. CONCLUSIONS: Duration of immunity after vaccination with an inactivated, adjuvanted vaccine was > 7 years. Protection against FPV was better than for FHV and FCV. CLINICAL IMPLICATIONS: Persistence of antibody titers against all 3 viruses for > 3 years supports recommendations that cats may be revaccinated against FPV-FHV-FCV at 3-year intervals.     

An inactivated, oil-emulsion vaccine for the prevention of porcine parvovirus-induced reproductive failure

Pig fetuses inoculated at 45 days gestation with virulent porcine parvovirus (PPV) were harvested 10 days later. Virus was extracted, inactivated with binary ethylenimine and the antigen suspension emulsified with mineral oil adjuvant. One dose of this vaccine, or two doses with a 14 day interval, stimulated high and long lasting serum antibody titres in gilts. Vaccination caused no clinical reactions and lesions at injection sites were minor. Vaccination of seronegative gilts at 40 days gestation caused no adverse effects on fetuses. Six gilts which had been vaccinated five to nine weeks before mating were challenged intravenously with live, virulent PPV at 40 days gestation. At 98 days gestation 78 out of 84 (93 per cent) fetuses were alive and normal and no evidence of PPV infection was found in the six dead (mummified) fetuses. In four unvaccinated gilts similarly challenged with PPV at 40 days gestation only five out of 51 (10 per cent) fetuses survived to 98 days gestation and the virus was detected in 41 of the 46 dead (mummified) fetuses. This vaccine appears to be safe and effective for prevention of PPV-induced fetal loss in gilts.     

Response of pups to modified-live canine parvovirus component in a combination vaccine

Twenty-eight pups from a general pet population were vaccinated for canine parvovirus (CPV) with a combination vaccine every 3 weeks until the pups were 11 to 16 weeks old. Canine parvovirus antibody titers were measured by serum neutralization before each vaccination and greater than or equal to 2 weeks after the final vaccination. Eighteen pups that initially were seronegative for CPV seroconverted after 1 to 3 doses of modified-live virus CPV vaccine administered when the pups were between 8 and 16 weeks old; 16 of 18 seroconverted after the 1st dose. Of 10 pups that were seropositive for CPV at initial examination, 7 did not develop protective titers after 3 doses of vaccine, with the last dose given when the pups were 14 to 16 weeks old. Maternally derived antibody was the primary cause of vaccination failure.     

Field trials of an inactivated virus vaccine against porcine parvovirus.

Serological response and reproductive performance were estimated in field trials of an inactivated virus vaccine against porcine parvovirus. Experiments were carried out in 10 selected pig breeding herds. A total of 277 seronegative gilts were used. Two hundred and twenty animals were vaccinated twice before mating, fourteen days apart and revaccinated after farrowing. Blood samples were obtained from both vaccinated and non-vaccinated (57 animal) control gilts, one week after the 2nd dose of vaccination, at farrowing time and one week after revaccination. Although there were considerable variations among the herds, the number of returns to oestrus in all herds was higher in vaccinated gilts (11.81%) than in the controls (10.52%). This difference, however, was not statistically significant. The reproductive performance results revealed the absence of an increase in the total born, as pooled values, in vaccinated gilts compared to controls. However, when these results are interpreted in relation to serological data, many control gilts were already seropositive before mating, or remained seronegative at farrowing. According to our results, the duration of immunity with this vaccine is apparently short, as there is a clear decrease in the titres between the 1st and the 2nd sampling times (2.35 +/- 0.14 and 1.97 +/- 0.08, respectively).     

A modified live canine parvovirus vaccine. II. Immune response

The safety and efficacy of an attenuated canine parvovirus (A-CPV) vaccine was evaluated in both experimental and in field dogs. After parenteral vaccination, seronegative dogs developed hemagglutination-inhibition (HI) antibody titers as early as postvaccination (PV) day 2. Maximal titers occurred within 1 week. Immunity was associated with the persistence of HI antibody titers (titers greater than 80) that endured at least 2 years. Immune dogs challenged with virulent CPV did not shed virus in their feces. The A-CPV vaccine did not cause illness alone or in combination with living canine distemper (CD) and canine adenovirus type-2 (CAV-2) vaccines, nor did it interfere with the immune response to the other viruses. A high rate (greater than 98%) of immunity was engendered in seronegative pups. In contrast, maternal antibody interfered with the active immune response to the A-CPV. More than 95% of the dogs with HI titers less than 10 responded to the vaccine, but only 50% responded when titers were approximately 20. No animal with a titer greater than 80 at the time of vaccination became actively immunized. Susceptibility to virulent CPV during that period when maternal antibody no longer protects against infection, but still prevents active immunization, is the principal cause of vaccinal failure in breeding kennels where CPV is present. Reduction, but not complete elimination, of CPV disease in large breeding kennels occurred within 1-2 months of instituting an A-CPV vaccination program.     

Antibody response of pigs to inactivated monovalent and bivalent vaccines for porcine parvovirus and pseudorabies virus

Groups of pigs vaccinated with an inactivated bivalent vaccine containing porcine parvovirus (PPV) and pseudorabies virus (PRV) developed geometric mean titers (GMT) of humoral antibody for each of the viruses as high or slightly higher than those of other groups of pigs that were vaccinated with inactivated monovalent vaccines containing one or the other of the same viruses. An increase in GMT after challenge exposure of vaccinated pigs to live virus indicated that vaccination did not prevent virus replication. However, an indication that replication was less extensive in vaccinated pigs was provided by the following. Although neither vaccinated nor nonvaccinated (control) pigs had clinical signs after exposure to the live PPV, the effect of vaccination was evident by the fact that GMT were higher in nonvaccinated pigs after exposure than they were in vaccinated pigs. Conversely, all pigs exposed to live PRV had clinical signs, but these signs varied between mild-to-moderate and transient for vaccinated pigs to severe and fatal for nonvaccinated pigs.     

The influence of age and maternal antibodies on the postvaccinal response against swine influenza viruses in pigs

The influence of age and maternal immunity on the development and duration of postvaccinal humoral response against swine influenza viruses (SIV) were investigated under experimental conditions. Piglets born to immune and non-immune sows were vaccinated twice with bivalent inactivated vaccine. Vaccination was done according to 5 different schedules: 1+4, 1+8, 4+8, 8+10 or 8+12 weeks of age. Antibodies to the haemagglutinin type 1 and 3 were determined using the haemagglutination inhibition (HI) test. Maternally derived antibodies (MDA) against H1N1 and H3N2 in the serum of unvaccinated piglets born to immune sows were above the positive level until about 13-14 and 9-10 weeks of life, respectively. No serological responses were seen in any of the groups after the first vaccination. After the second dose of vaccine production of antibodies was observed even before the complete disappearance of maternal antibodies. MDA, however, were associated with reduced antibody response. In MDA-negative piglets, an active humoral postvaccinal response was developed in all vaccinated pigs. The age at which the vaccine was given was associated with the differences in the magnitude of antibody response to SIV. In general those pigs that were vaccinated for the first time at the age of 1 week, developed lower maximum titres after the second vaccination, and become seronegative earlier than pigs that were vaccinated for the first time at 4 or 8 weeks of age.     

Efficacy and duration of immunity of a combined equine influenza and equine herpesvirus vaccine against challenge with an American-like equine influenza virus (A/equi-2/Kentucky/95)

It has been recommended that modern equine influenza vaccines should contain an A/equi-1 strain and A/equi-2 strains of the American and European-like subtype. We describe here the efficacy of a modern updated inactivated equine influenza-herpesvirus combination vaccine against challenge with a recent American-like isolate of equine influenza (A/equine-2/Kentucky/95 (H3N8). The vaccine contains inactivated Influenza strains A-equine-1/Prague'56, A-equine-2/Newmarket-1/'93 (American lineage) and A-equine-2/ Newmarket-2/93 (Eurasian lineage) and inactivated EHV-1 strain RacH and EHV-4 strain V2252. It is adjuvanted with alhydrogel and an immunostim. Horses were vaccinated at the start of the study and 4 weeks later. Four, six and eight weeks after the first vaccination high anti-influenza antibody titres were found in vaccinated horses, whereas at the start of the study all horses were seronegative. After the challenge, carried out at 8 weeks after the first vaccination, nasal swabs were taken, rectal temperatures were measured and clinical signs were monitored for 14 days. In contrast to unvaccinated control horses, vaccinated animals shed hardly any virus after challenge, and the appearance of clinical signs of influenza such as nasal discharge, coughing and fever were reduced in the vaccinated animals. Based on these observations, it was concluded that the vaccine protected against clinical signs of influenza and, more importantly, against virus excretion induced by an American-like challenge virus strain. In a second experiment the duration of the immunity induced by this vaccine was assessed serologically. Horses were vaccinated at the start of the study and 6 and 32 weeks later. Anti-influenza antibody titres were determined in bloodsamples taken at the first vaccination, and 2, 6, 8, 14, 19, 28, 32, 37, 41, 45 and 58 weeks after the first vaccination. Vaccinated horses had high anti-influenza antibody titres, above the level for clinical protection against influenza, against all strains present in the vaccine until 26 weeks after the third vaccination.     

SEROLOGICAL RESPONSES IN PIGS VACCINATED WITH INACTIVATED PORCINE PARVOVIRUS

The safety and immunogenicity of inactivated porcine parvovirus (PPV) vaccines were investigated. Both beta-propiolactone and formalin successfully inactivated virus without destroying immunogenicity, which was considerably enhanced by incorporation of a gel adjuvant in the vaccine. Using the formalised-gel vaccine, initial antibody responses were demonstrated in susceptible piglets and adult pigs at 7 days after vaccination. These antibody responses persist at significant levels for at least 6 months after vaccination. Antibody levels increased up to 16 fold when revaccination was carried out. Vaccination of gilts with low level (passive) immunity resulted in antibody responses comparable to those recorded in susceptible pigs. The vaccine was safe as determined by absence of residual virus in the vaccine, absence of viraemia and excretion in vaccinted stock, and absence of effect on litters of sows vaccinated at different gestational ages. Vaccine stored at 4 degrees C for 6 months was as immunogenic as fresh vaccine.     

Efficacy of a saponin-adjuvanted inactivated respiratory syncytial virus vaccine in calves

The objective of this study was to determine whether a commercially available, saponin-adjuvanted, inactivated bovine respiratory syncytial virus (BRSV) vaccine would protect calves from experimental infection with virulent BRSV. This was a randomized controlled trial comprising 14, 8- to 9-week-old calves seronegative for BRSV Group 1 calves (n = 8) were not vaccinated and group 2 calves (n = 6) were vaccinated on days 0 and 19 with an inactivated BRSV vaccine. All calves were challenged with virulent BRSV on day 46. Clinical signs, arterial PO2, and immune responses were monitored after challenge. Calves were euthanatized on day 54 (8 d after challenge) and lungs were examined for lesions. Vaccination elicited increases in BRSV-specific immunoglobulin (Ig) G and virus neutralizing antibody titers. Challenge with BRSV resulted in severe respiratory tract disease and extensive pulmonary lesions in control calves, but no signs of clinical disease and minimal or no pulmonary lesions in vaccinated calves. Arterial blood oxygen values on day 53 (7 d after challenge) in control calves were significantly lower than those in vaccinated calves, which remained within normal limits. Control calves shed BRSV for several days after challenge, whereas BRSV was not detected on deep nasal swabs from vaccinated calves. In summary, the results indicated that this inactivated BRSV vaccine provided clinical protection from experimental infection with virulent virus 27 d after vaccination and significantly decreased the prevalence and severity of pulmonary lesions. Efficacy was similar to that reported for other commercial inactivated and modified-live BRSV vaccines.     

Cell mediated and humoral immune response of chickens to inactivated oil-emulsion infectious bronchitis vaccine

A lymphocyte transformation microassay was used to study cell mediated immunity (CMI) in chickens following primary and secondary vaccination with inactivated oil emulsion infectious bronchitis (IB) vaccine and subsequent challenge with Massachusetts-41 (M-41). Humoral immunity was monitored for comparison, using the haemagglutination inhibition (HI) microassay. Positive stimulation indices (2 to 2.7 after primary and 2 to 4.8 after secondary vaccination) were lower and HI titres were higher than those previously reported following primary and secondary vaccination with live IB vaccines. The highest HI titres appeared in birds which had received the inactivated vaccine as a secondary vaccination. Challenge of vaccinated and revaccinated birds resulted in strong HI and weak CMI secondary responses. There was no correlation between CMI and HI antibody production. Monitoring egg production and clinical signs showed that a high level of protection against challenge resulted from revaccination with an inactivated oil adjuvant vaccine.     

Efficacy of swine influenza A virus vaccines against an H3N2 virus variant

We compared the efficacy of 3 commercial vaccines against swine influenza A virus (SIV) and an experimental homologous vaccine in young pigs that were subsequently challenged with a variant H3N2 SIV, A/Swine/Colorado/00294/2004, selected from a repository of serologically and genetically characterized H3N2 SIV isolates obtained from recent cases of swine respiratory disease. The experimental vaccine was prepared from the challenge virus. Four groups of 8 pigs each were vaccinated intramuscularly at both 4 and 6 wk of age with commercial or homologous vaccine. Two weeks after the 2nd vaccination, those 32 pigs and 8 nonvaccinated pigs were inoculated with the challenge virus by the deep intranasal route. Another 4 pigs served as nonvaccinated, nonchallenged controls. The serum antibody responses differed markedly between groups. After the 1st vaccination, the recipients of the homologous vaccine had hemagglutination inhibition (HI) titers of 1:640 to 1:2560 against the challenge (homologous) virus. In contrast, even after 2nd vaccination, the commercial-vaccine recipients had low titers or no detectable antibody against the challenge (heterologous) virus. After the 2nd vaccination, all the groups had high titers of antibody to the reference H3N2 virus A/Swine/Texas/4199-2/98. Vaccination reduced clinical signs and lung lesion scores; however, virus was isolated 1 to 5 d after challenge from the nasal swabs of most of the pigs vaccinated with a commercial product but from none of the pigs vaccinated with the experimental product. The efficacy of the commercial vaccines may need to be improved to provide sufficient protection against emerging H3N2 variants.